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        <title>Neurochemical Research via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Neurochemical Research' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Neurochemical+Research&t=Neurochemical+Research&s=Search&f=source]]></link>
        <lastBuildDate>Tue, 07 Feb 2012 07:05:46 +0100</lastBuildDate>
        <item>
            <title>Protective Effects of Salvianolic Acid B on Schwann Cells Apoptosis Induced by High Glucose.</title>
            <link>http://www.medworm.com/index.php?rid=5621827&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22252725%26dopt%3DAbstract</link>
            <description>Authors: Sun LQ, Zhao J, Zhang TT, Qu L, Wang X, Xue B, Li XJ, Mu YM, Lu JM
    Abstract
    Diabetic peripheral neuropathy (DPN) is one of the most common and debilitating microvascular complications of diabetes, and there is no effective therapy for the prevention or treatment of DPN. Oxidative stress triggers several pathways of injury and may be the unifying factor of hyperglycemia. The aim of this study was to investigate protective effect of Salvianolic acid B (Sal B) on the high glucose (HG)-induced oxidative stress-induced mitochondrial pathway activation and Schwann cells (SCs) apoptosis in vitro. We found that Sal B inhibited the HG-induced oxidative stress by reducing ROS and 8-hydroxy-2-deoxy Guanosine (8-OHdG) production, and mitochondrial depolarization and apoptosis in SCs i...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5621827</comments>
            <pubDate>Wed, 18 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Cholesterol, GM1, and Autism.</title>
            <link>http://www.medworm.com/index.php?rid=5621826&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22252726%26dopt%3DAbstract</link>
            <description>Authors: Schengrund CL, Ali-Rahmani F, Ramer JC
    Abstract
    Disruption of cholesterol metabolism has been hypothesized to contribute to dementia, possibly due to its role in maintaining membrane fluidity as well as the integrity of lipid rafts. Previously, we reported an apparent inverse relationship between membrane cholesterol levels and those of GM1, another lipid that can be found in rafts. This paper describes the observation that red blood cell (RBC) membranes isolated from blood drawn from children diagnosed with autism have on the average significantly less cholesterol and significantly more GM1 than RBC membranes isolated from blood obtained from control children. While cholesterol in the circulation does not cross the blood brain barrier, a generalized defect in its synthesi...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5621826</comments>
            <pubDate>Wed, 18 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5621826</guid>        </item>
        <item>
            <title>Contralateral Retinal Dopamine Decrease and Melatonin Increase in Progression of Hemiparkinsonium Rat.</title>
            <link>http://www.medworm.com/index.php?rid=5621825&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22252727%26dopt%3DAbstract</link>
            <description>Authors: Meng T, Zheng ZH, Liu TT, Lin L
    Abstract
    Both dopamine (DA) and melatonin (MLT) are abundant neuromodulators located in vertebrate retina. The retinal DA deficiency and variations in MLT levels have been linked to Parkinson's disease (PD). No studies have investigated the ipsilateral and contralateral DA and MLT in retina and their relationships in 6-hydroxydopamine (6-OHDA) induced hemiparkinsonian rats. We established PD rat model by unilateral injection of 6-OHDA into the right substantia nigra and the right medial forebrain bundle. Eye tissue was collected and the levels of MLT and DA were measured twice daily at 10:00 and 22:00. The concentrations of DA and its metabolites, 3,4-dihydroxyphenylacetic (DOPAC) and homovanillic acid (HVA), as well as MLT were determined b...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5621825</comments>
            <pubDate>Wed, 18 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5621825</guid>        </item>
        <item>
            <title>On the Structural Elucidation of GalNAc-GD1a.</title>
            <link>http://www.medworm.com/index.php?rid=5621829&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22249764%26dopt%3DAbstract</link>
            <description>Authors: Li YT
    PMID: 22249764 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5621829</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5621829</guid>        </item>
        <item>
            <title>Classic 18.5- and 21.5-kDa Myelin Basic Protein Isoforms Associate with Cytoskeletal and SH3-Domain Proteins in the Immortalized N19-Oligodendroglial Cell Line Stimulated by Phorbol Ester and IGF-1.</title>
            <link>http://www.medworm.com/index.php?rid=5621828&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22249765%26dopt%3DAbstract</link>
            <description>This study supports a role for classic MBP isoforms in cytoskeletal and other protein-protein interactions during membrane and cytoskeletal remodeling in OLGs.
    PMID: 22249765 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5621828</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5621828</guid>        </item>
        <item>
            <title>Effects of DL-3-n-Butylphthalide on Vascular Dementia and Angiogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5621832&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22246225%26dopt%3DAbstract</link>
            <description>Authors: Zhang L, Lü L, Chan WM, Huang Y, Wai MS, Yew DT
    Abstract
    3-n-Butylphthalide (NBP) is a compound extracted from Chinese celery and is used as an anti-hypertensive herbal medicine for treating stroke patients. The aim of this study is to demonstrate the effects and mechanisms of this compound through in vitro and in vivo experiments. Culture experiments were performed by adding hydrogen peroxide (H(2)O(2)) to SH-SY5Y cells. From the MTT assay result, enhanced cell survival was observed with DL-NBP treatment, regardless of whether they are added before, simultaneously with or after the addition of H(2)O(2). For the in vivo experiment, Spontaneously Hypertensive rats and Wistar Kyoto control rats with chronic cerebral ischemia, which were induced by bilateral transection of t...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5621832</comments>
            <pubDate>Sat, 14 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5621832</guid>        </item>
        <item>
            <title>It's a Lipid's World: Bioactive Lipid Metabolism and Signaling in Neural Stem Cell Differentiation.</title>
            <link>http://www.medworm.com/index.php?rid=5621831&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22246226%26dopt%3DAbstract</link>
            <description>Authors: Bieberich E
    Abstract
    Lipids are often considered membrane components whose function is to embed proteins into cell membranes. In the last two decades, studies on brain lipids have unequivocally demonstrated that many lipids have critical cell signaling functions; they are called &quot;bioactive lipids&quot;. Pioneering work in Dr. Robert Ledeen's laboratory has shown that two bioactive brain sphingolipids, sphingomyelin and the ganglioside GM1 are major signaling lipids in the nuclear envelope. In addition to derivatives of the sphingolipid ceramide, the bioactive lipids discussed here belong to the classes of terpenoids and steroids, eicosanoids, and lysophospholipids. These lipids act mainly through two mechanisms: (1) direct interaction between the bioactive lipid and a specific ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5621831</comments>
            <pubDate>Sat, 14 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5621831</guid>        </item>
        <item>
            <title>Comparison of the Immunoreactivity of Trx2/Prx3 Redox System in the Hippocampal CA1 Region Between the Young and Adult Gerbil Induced by Transient Cerebral Ischemia.</title>
            <link>http://www.medworm.com/index.php?rid=5621830&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22246227%26dopt%3DAbstract</link>
            <description>Authors: Yan BC, Park JH, Ahn JH, Lee YJ, Lee TH, Lee CH, Cho JH, Kim MJ, Kim TY, Kang IJ, Won MH
    Abstract
    In the present study, we compared the immunoreactivities and levels of Trx/prx redox system, thioredoxin 2 (Trx2), thioredoxin reductase 2 (TrxR2) and peroxiredoxin 3 (Prx3), as well as neuronal death in the hippocampal CA1 region between the adult and young gerbil after 5 min of transient cerebral ischemia. At 4 days post-ischemia, pyramidal neurons (about 90%) in the adult stratum pyramidale of the CA1 region showed &quot;delayed neuronal death (DND)&quot;; however, at this time point, few pyramidal neurons showed DND in the young stratum pyramidale. At 7 days post-ischemia, about 56% of pyramidal neurons showed DND in the young stratum pyramidale. The immunoreactivities of all the...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5621830</comments>
            <pubDate>Sat, 14 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5621830</guid>        </item>
        <item>
            <title>Dopamine Affects the Change of Pain-Related Electrical Activity Induced by Morphine Dependence.</title>
            <link>http://www.medworm.com/index.php?rid=5621833&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22240902%26dopt%3DAbstract</link>
            <description>Authors: Zhang Y, Zhang F, Yang C, Jin H, Yang Y, Xu M
    Abstract
    Morphine is among the most effective analgesics. However, many evidences suggest that, besides the well-know analgesic activity, repeated opioids treatment can induce some side effects such as dependence, hyperalgesia and tolerance. The mechanism of noxious information transmission in the central nervous system after dependence is not clear. An important neurotransmitter, dopamine (DA) participates not only in the process of opioid dependence but also in pain modulation in the central nervous system. In the present study we observed changes of electrical activities of pain-excitation neurons (PENs) and pain-inhibition neurons (PINs) in the caudate nucleus (Cd) following the development of morphine dependence. We also o...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5621833</comments>
            <pubDate>Fri, 13 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5621833</guid>        </item>
        <item>
            <title>The Roles of Neutral Sphingomyelinases in Neurological Pathologies.</title>
            <link>http://www.medworm.com/index.php?rid=5621835&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22237969%26dopt%3DAbstract</link>
            <description>Authors: Horres CR, Hannun YA
    Abstract
    The neutral sphingomyelinases (N-SMases) are a group of Mg(2+)-dependent enzymes with a pH optimum in the neutral range. N-SMases catalyze the conversion of sphingomyelin to ceramide and have been found particularly enriched in brain tissue. N-SMase activity has been implicated in many physiological and pathological processes affecting the brain and nervous system. In this review, we discuss the proposed functions of N-SMase with a particular emphasis on its role in neurological disorders, such as age-related neurodegeneration, Alzheimer's disease, HIV-associated dementia, atherosclerosis, ischemia-reperfusion injury, and cancer.
    PMID: 22237969 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5621835</comments>
            <pubDate>Thu, 12 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5621835</guid>        </item>
        <item>
            <title>Administration of Histidine to Female Rats Induces Changes in Oxidative Status in Cortex and Hippocampus of the Offspring.</title>
            <link>http://www.medworm.com/index.php?rid=5621834&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22237970%26dopt%3DAbstract</link>
            <description>Authors: Rojas DB, Gemelli T, de Andrade RB, Campos AG, Dutra-Filho CS, Wannmacher CM
    Abstract
    Histidinemia is an inherited metabolic disorder biochemically characterized by high concentrations of histidine in biological fluids. Usually affected patients are asymptomatic although some individuals have mental retardation and speech disorders. Considering the high prevalence of histidinemia and the scarce information on the effects of maternal histidinemia on their progeny, we investigated various parameters of oxidative stress in brain cortex and hippocampus of the offspring from female rats that received histidine (0.5 mg/g of body weight) in the course of pregnancy and lactation. At 21 days of age we found a significant increase of thiobarbituric acid reactive substances (TBARS)...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5621834</comments>
            <pubDate>Thu, 12 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5621834</guid>        </item>
        <item>
            <title>Ganglioside GM1/Galectin-Dependent Growth Regulation in Human Neuroblastoma Cells: Special Properties of Bivalent Galectin-4 and Significance of Linker Length for Ligand Selection.</title>
            <link>http://www.medworm.com/index.php?rid=5621836&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22234579%26dopt%3DAbstract</link>
            <description>This study reveals complete functional divergence between galectins differing in the spatial mode of lectin-site presentation and dependence of reactivity to distinct counter-receptor(s) on linker length. Due to the documented presence of galectin-4 in the nervous system and its affinity for sulfatide these in vitro results indicate the potential for a distinct functionality profile of this lectin in vivo, giving further research direction.
    PMID: 22234579 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5621836</comments>
            <pubDate>Wed, 11 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5621836</guid>        </item>
        <item>
            <title>Protective Effects of mGluR5 Positive Modulators Against Traumatic Neuronal Injury Through PKC-Dependent Activation of MEK/ERK Pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5578309&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22228200%26dopt%3DAbstract</link>
            <description>Authors: Chen T, Cao L, Dong W, Luo P, Liu W, Qu Y, Fei Z
    Abstract
    Several previous studies utilizing selective pharmacological antagonists have demonstrated that type 5 metabotropic glutamate receptors (mGluR5) are potential therapeutic targets for the treatment of numerous disorders of the central nervous system, but the role of mGluR5 activation in traumatic brain injury (TBI) is not fully understood. Here in an in vitro TBI model, the mGluR5 agonist (RS)-2-chloro-5- hydroxyphenylglycine (CHPG) and the positive allosteric modulators 3-cyano-N-(1,3- diphenyl-1H-pyrazol-5-yl) benzamide (CDPPB) were used to investigate the neuroprotective potency of mGluR5 activation. Data showed that CHPG and CDPPB suppressed the increase of LDH release and caspase-3 activation induced by traumati...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578309</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578309</guid>        </item>
        <item>
            <title>Drug Resistance in Glioblastoma: A Mini Review.</title>
            <link>http://www.medworm.com/index.php?rid=5578308&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22228201%26dopt%3DAbstract</link>
            <description>Authors: Haar CP, Hebbar P, Wallace GC, Das A, Vandergrift WA, Smith JA, Giglio P, Patel SJ, Ray SK, Banik NL
    Abstract
    Glioblastoma multiforme (GBM) is recognized as the most common and lethal form of central nervous system cancer. Currently used surgical techniques, chemotherapeutic agents, and radiotherapy strategies have done very little in extending the life expectancies of patients diagnosed with GBM. The difficulty in treating this malignant disease lies both in its inherent complexity and numerous mechanisms of drug resistance. In this review, we summarize several of the primary mechanisms of drug resistance. We reviewed available published literature in the English language regarding drug resistance in glioblastoma. The reasons for drug resistance in glioblastoma include dr...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578308</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578308</guid>        </item>
        <item>
            <title>Chronic Effects of Pyridoxine in the Gerbil Hippocampal CA1 Region after Transient Forebrain Ischemia.</title>
            <link>http://www.medworm.com/index.php?rid=5578310&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22228142%26dopt%3DAbstract</link>
            <description>Authors: Yoo DY, Kim W, Nam SM, Chung JY, Choi JH, Yoon YS, Won MH, Hwang IK
    Abstract
    In a previous study, we reported that the administration of pyridoxine (vitamin B(6)) to mice for 3 weeks significantly increased cell proliferation and neuroblast differentiation in the dentate gyrus without any neuronal damage. In the present study, we investigated the restorative potentials of pyridoxine on ischemic damage in the hippocampal CA1 region of Mongolian gerbils. Gerbils were subjected to 5 min of transient ischemia, and surgical operation success was assessed by ophthalmoscope during occlusion of common carotid arteries and spontaneous motor activity at 1 day after ischemia/reperfusion. Pyridoxine (350 mg/kg) or its vehicle (physiological saline) was intraperineally administered...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578310</comments>
            <pubDate>Sun, 08 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578310</guid>        </item>
        <item>
            <title>TNF-α Expression in Schwann Cells is Induced by LPS and NF-κB-Dependent Pathways.</title>
            <link>http://www.medworm.com/index.php?rid=5578319&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22219126%26dopt%3DAbstract</link>
            <description>Authors: Qin Y, Hua M, Duan Y, Gao Y, Shao X, Wang H, Tao T, Shen A, Cheng C
    Abstract
    Lipopolysaccharide (LPS) is recognized by Toll-like receptor 4 and activates mitogen-activated protein kinase, which leads to the induction of proinflammatory cytokine gene expression. In vivo, Schwann cells (SCs) at the site of injury may also produce tumor necrosis factor-α (TNF-α). However, the precise mechanism that regulates TNF-α synthesis is still not clear. The nuclear transcription factor-κB (NF-κB) is an important transcription factor which is involved in the regulation of host immune responses. In the present study, we found that LPS possessed a comparable specific activity for activation of NF-κB-dependent gene expression in SCs. We also observed IκB-α/IκB-β degradation and t...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578319</comments>
            <pubDate>Thu, 05 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578319</guid>        </item>
        <item>
            <title>Role of a Neural Cell Adhesion Molecule Found in Cerebrospinal Fluid as a Potential Biomarker for Epilepsy.</title>
            <link>http://www.medworm.com/index.php?rid=5578318&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22219127%26dopt%3DAbstract</link>
            <description>Authors: Wang W, Wang L, Luo J, Xi Z, Wang X, Chen G, Chu L
    Abstract
    The neural cell adhesion molecule (NCAM-1) plays an important role in cell adhesion and synaptic plasticity. We designed this study to evaluate NCAM-1 as a potential biomarker for epilepsy. We performed a quantitative evaluation of the levels of NCAM-1 in cerebrospinal fluid (CSF) and serum and noted differences in patients with epilepsy compared to control subjects. We used sandwich enzyme-linked immunosorbent assays to measure NCAM-1 concentrations in CSF and serum samples of 76 epileptic patients (subdivided into the following subgroups: drug-refractory epilepsy, DRE; first-diagnosis epilepsy, FDE; and drug-effective epilepsy, DEE) and 44 control subjects. Our results show that cerebrospinal fluid-NCAM-1 (CSF-N...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578318</comments>
            <pubDate>Thu, 05 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578318</guid>        </item>
        <item>
            <title>Neuronal Damage Using Fluoro-Jade B Histofluorescence and Gliosis in the Striatum After Various Durations of Transient Cerebral Ischemia in Gerbils.</title>
            <link>http://www.medworm.com/index.php?rid=5578317&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22219128%26dopt%3DAbstract</link>
            <description>Authors: Ohk TG, Yoo KY, Park SM, Shin BN, Kim IH, Park JH, Ahn HC, Lee YJ, Kim MJ, Kim TY, Won MH, Cho JH
    Abstract
    Ischemic damage occurs well in vulnerable regions of the brain, including the hippocampus and striatum. In the present study, we examined neuronal damage/death and glial changes in the striatum 4 days after 5, 10, 15 and 20 min of transient cerebral ischemia using the gerbil. Spontaneous motor activity was increased with the duration time of ischemia-reperfusion (I-R). To examine neuronal damage, we used Fluoro-Jade B (F-J B, a marker for neuronal degeneration) histofluorescence staining. F-J B positive cells were detected only in the 20 min ischemia-group, not in the other groups. In addition, we examined gliosis of astrocytes and microglia using anti-glial fibril...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578317</comments>
            <pubDate>Thu, 05 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578317</guid>        </item>
        <item>
            <title>Oxidative Modification of Cysteine 111 Promotes Disulfide Bond-Independent Aggregation of SOD1.</title>
            <link>http://www.medworm.com/index.php?rid=5578316&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22219129%26dopt%3DAbstract</link>
            <description>Authors: Chen X, Shang H, Qiu X, Fujiwara N, Cui L, Li XM, Gao TM, Kong J
    Abstract
    Converging evidence indicates that SOD1 aggregation is a common feature of mutant SOD1-linked fALS, and seems to be directly related to the gain-of-function toxic property. However, the mechanism inducing the aggregation is not understood. To study the contribution of oxidative modification of cysteine residues in SOD1 aggregation, we systematically examined the redox state of SOD1 cysteine residues in the G37R transgenic mouse model at different stages of the disease and under oxidative stress induced by H(2)O(2). Our data suggest that under normal circumstance, cysteine 111 residue in SOD1 is free; however, under oxidative stress, it is prone to oxidative modification by providing the thiolate anio...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578316</comments>
            <pubDate>Thu, 05 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578316</guid>        </item>
        <item>
            <title>Dysfunctional Nucleus Tractus Solitarius: Its Crucial Role in Promoting Neuropathogentic Cascade of Alzheimer's Dementia-A Novel Hypothesis.</title>
            <link>http://www.medworm.com/index.php?rid=5578315&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22219130%26dopt%3DAbstract</link>
            <description>Authors: Daulatzai MA
    Abstract
    The pathophysiological mechanism(s) underlying Alzheimer's disease (AD) still remain unclear, and no disease-modifying or prophylactic therapies are currently available. Unraveling the fundamental neuropathogenesis of AD is an important challenge. Several studies on AD have suggested lesions in a number of CNS areas including the basal forebrain, hippocampus, entorhinal cortex, amygdale/insula, and the locus coeruleus. However, plausible unifying studies on the upstream factors that involve these heterogeneous regions and herald the onset of AD pathogenesis are not available. The current article presents a novel nucleus tractus solitarius (NTS) vector hypothesis that underpins several disparate biological mechanisms and neural circuits, and identifies...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578315</comments>
            <pubDate>Thu, 05 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578315</guid>        </item>
        <item>
            <title>Oxidative Damage in Muscular Dystrophy Correlates with the Severity of the Pathology: Role of Glutathione Metabolism.</title>
            <link>http://www.medworm.com/index.php?rid=5578314&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22219131%26dopt%3DAbstract</link>
            <description>Authors: Renjini R, Gayathri N, Nalini A, Srinivas Bharath MM
    Abstract
    Muscular dystrophies (MDs) such as Duchenne muscular dystrophy (DMD), sarcoglycanopathy (Sgpy) and dysferlinopathy (Dysfy) are recessive genetic neuromuscular diseases that display muscle degeneration. Although these MDs have comparable endpoints of muscle pathology, the onset, severity and the course of these diseases are diverse. Different mechanisms downstream of genetic mutations might underlie the disparity in these pathologies. We surmised that oxidative damage and altered antioxidant function might contribute to these differences. The oxidant and antioxidant markers in the muscle biopsies from patients with DMD (n = 15), Sgpy (n = 15) and Dysfy (n = 15) were compared to controls (n = 10). Protein ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578314</comments>
            <pubDate>Thu, 05 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578314</guid>        </item>
        <item>
            <title>Restraint Stress in Rats Alters Gene Transcription and Protein Translation in the Hippocampus.</title>
            <link>http://www.medworm.com/index.php?rid=5578313&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22219132%26dopt%3DAbstract</link>
            <description>In this study, male Wistar rats were exposed to restraint stress (RS) for 5 h daily for different time periods. At the end of the exposure periods, the amounts of β-actin, cofilin, amyloid precursor protein (APP) and mitogen-activated protein kinase 1 (MAPK-1) RNAs and proteins were investigated. The mRNA expressions of β-actin, cofilin and MAPK-1 followed U-shaped time course. Acute (3 days) and chronic (21 days) RS caused a fourfold and tenfold increases, respectively, in hippocampal β-actin mRNA expression. In the case of cofilin mRNA expression, elevations were detected in the hippocampus on days 3, 7 and 21. The APP mRNA level was increased on day 21. On protein level, chronic stress elevated the levels of β-actin, cofilin and APP in the hippocampus. These results suggest that ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578313</comments>
            <pubDate>Thu, 05 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578313</guid>        </item>
        <item>
            <title>Ischemia-Induced Inhibition of Mitochondrial Complex I in Rat Brain: Effect of Permeabilization Method and Electron Acceptor.</title>
            <link>http://www.medworm.com/index.php?rid=5578312&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22219133%26dopt%3DAbstract</link>
            <description>In this study we have examined the effect of global brain ischemia/reperfusion on biochemical properties of the mitochondrial respiratory complex I (CI) in rat hippocampus and cortex. Since the inner mitochondrial membrane forms the permeability barrier for NADH, the methodology of enzymatic activity determinations employs membrane permeabilization methods. This action affects the basic character of electrostatic and hydrophobic interactions inside the membrane and might influence functional properties of membrane embedded proteins. Therefore we have performed the comparative analysis of two permeabilization methods (sonication, detergent) and their impact on CI enzymatic activities under global brain ischemic-reperfusion conditions. We have observed that ischemia led to significant decrea...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578312</comments>
            <pubDate>Thu, 05 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578312</guid>        </item>
        <item>
            <title>Age-Related Decline in DNA Polymerase β Activity in Rat Brain and Tissues.</title>
            <link>http://www.medworm.com/index.php?rid=5578311&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22219134%26dopt%3DAbstract</link>
            <description>Authors: Vyjayanti VN, Swain U, Rao KS
    Abstract
    Fidelity of DNA polymerases is vital for maintaining genomic integrity. Deficient DNA repair leads to age related disorders or cancer. If the age at which the decline in activity of predominant DNA repair enzymes starts is identified, and the deficient proteins supplemented, then the manifestation of these diseases can be delayed promoting healthy aging. DNA polymerase β (pol β) is a predominant repair enzyme in brain. DNA pol β activity declines with age in rat brain/neurons but the exact age during the life time of rat when this decline begins is not known, and comparison of this activity was not made between post mitotic and proliferating tissues therefore the pattern of pol β with age was studied in rat brain and tissues. The ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578311</comments>
            <pubDate>Thu, 05 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578311</guid>        </item>
        <item>
            <title>Comparison of Neurogenesis in the Dentate Gyrus Between the Adult and Aged Gerbil Following Transient Global Cerebral Ischemia.</title>
            <link>http://www.medworm.com/index.php?rid=5578320&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22215251%26dopt%3DAbstract</link>
            <description>Authors: Choi JH, Yoo KY, Lee CH, Park JH, Yan BC, Kwon SH, Seo JY, Cho JH, Hwang IK, Won MH
    Abstract
    In the present study, we compared differences in cell proliferation, neuroblast differentiation and neuronal maturation in the hippocampal dentate gyrus (DG) between the adult and aged gerbil induced by 5 min of transient global cerebral ischemia using Ki-67 and BrdU (markers for cell proliferation), doublecortin (DCX, a marker for neuroblast differentiation) and neuronal nuclei (NeuN, a marker for mature neuron). The number of Ki-67-immunoreactive ((+)) cells in the DG of both the groups peaked 7 days after ischemia/reperfusion (I/R). However, the number in the aged DG was 40.6 ± 1.8% of that in the adult DG. Thereafter, the number decreased with time. After ischemic damage, ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578320</comments>
            <pubDate>Wed, 04 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578320</guid>        </item>
        <item>
            <title>Induction of Tyrosine Hydroxylase Gene Expression by Glucocorticoids in the Perinatal Rat Brain is Age-Dependent.</title>
            <link>http://www.medworm.com/index.php?rid=5578322&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22212880%26dopt%3DAbstract</link>
            <description>Authors: Kalinina TS, Shishkina GT, Dygalo NN
    Abstract
    Brain noradrenergic system has been implicated in early-life stress effects on adult physiology and behavior; however, the mechanisms for this relationship are not clear. Here we tested the hypothesis that stress hormones, glucocorticoids, may affect noradrenergic system activity by modulating gene expression and function of tyrosine hydroxylase (TH), the key enzyme for catecholamine synthesis, in the rat brain during perinatal life. We have shown that TH mRNA levels and enzyme activity increase in the fetal rat brainstem during the last days of pregnancy. Administration of hydrocortisone or dexamethasone to female rats on day 20 of pregnancy significantly increased TH mRNA levels (real-time PCR) and enzyme activity (DOPA accum...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578322</comments>
            <pubDate>Tue, 03 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578322</guid>        </item>
        <item>
            <title>Effect of Chronic Administration of the Vinyl Chalcogenide 3-Methyl-1-phenyl-2-(phenylseleno)oct-2-en-1-one on Oxidative Stress in Different Brain Areas of Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5578321&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22212881%26dopt%3DAbstract</link>
            <description>This study aims to investigate the effect of the chronic treatment with the vinyl chalcogenide 3-methyl-1-phenyl-2-(phenylseleno)oct-2-en-1-one on some parameters of oxidative stress in the brain of rats. Animals received the vinyl chalcogenide (125, 250 or 500 μg/kg body weight) intraperitoneally once a day during 30 days. The cerebral cortex, the hippocampus, and the cerebellum were dissected and homogenized in KCl. Afterward, thiobarbituric acid reactive substances (TBARS), carbonyl, sulfhydryl, catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities were measured in the brain. Results showed that the organoselenium enhanced TBARS in the cerebral cortex of rats but the compound was not able to change carbonyl levels. Furthermore, the organoselenium redu...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578321</comments>
            <pubDate>Tue, 03 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578321</guid>        </item>
        <item>
            <title>Brain Serum Amyloid P Levels are Reduced in Individuals that Lack Dementia While Having Alzheimer's Disease Neuropathology.</title>
            <link>http://www.medworm.com/index.php?rid=5578323&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22205573%26dopt%3DAbstract</link>
            <description>Authors: Crawford JR, Bjorklund NL, Taglialatela G, Gomer RH
    Abstract
    The neuropathological signs of Alzheimer's disease (AD) include beta amyloid plaques and neurofibrillary tangles. There is a significant population of individuals that have these key hallmarks but show no signs of cognitive impairment, termed non-demented with AD neuropathology (NDAN). The protective mechanism allowing these individuals to escape dementia is unknown. Serum amyloid P (SAP) is a serum protein associated with wound repair that is elevated in the brains of Alzheimer's patients and binds to amyloid plaques. Using immunoblotting and immunohistochemistry, we evaluated SAP levels in postmortem samples of hippocampus and frontal cortex in age-matched controls, AD, and NDAN individuals. AD individuals had ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578323</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578323</guid>        </item>
        <item>
            <title>The Interaction Between Intrathecal Administration of Low Doses of Palmitoylethanolamide and AM251 in Formalin-Induced Pain Related Behavior and Spinal Cord IL1-β Expression in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5550231&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22201038%26dopt%3DAbstract</link>
            <description>The objective of the present study was to evaluate the possible role of spinal CB1 and GPR55 receptors on antinociceptive activity of PEA in formalin test as well as in the spinal expression of IL1-β in rat. Intrathecal (i.t.) administration of PEA (1, 10 μg) significantly decreased both pain-related scores in formalin test and IL1-β expression in rat spinal cord. Pretreatment of rats with low doses of CB1 receptor antagonist/GPR55 receptor agonist AM251 (10, 100 ng; i.t.), did not attenuated the effect of PEA, yet even significantly increased the effect of PEA on IL1-β expression in rat spinal cord. Interestingly, i.t. administration of low doses of AM251 per se significantly decreased both pain related behavior and spinal IL1-β expression in formalin test. These findings suggest t...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550231</comments>
            <pubDate>Tue, 27 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550231</guid>        </item>
        <item>
            <title>Role of Secondary Mediators in Caffeine-Mediated Neuroprotection in Maneb- and Paraquat-Induced Parkinson's Disease Phenotype in the Mouse.</title>
            <link>http://www.medworm.com/index.php?rid=5550230&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22201039%26dopt%3DAbstract</link>
            <description>Authors: Yadav S, Gupta SP, Srivastava G, Srivastava PK, Singh MP
    Abstract
    Maneb and paraquat are known to induce Parkinson's disease (PD) phenotype, however, caffeine offers neuroprotection. Nitric oxide (NO) acts an important mediator in PD phenotype and tyrosine kinase (TK), nuclear factor kappa B (NF-kB), p38 mitogen activated protein kinase (p38 MAPK) are known to regulate its production. The present study aimed to elucidate the role of caffeine in the regulation of NO production and microglial activation and their subsequent contribution in dopaminergic neuroprotection. The animals were treated with caffeine and/or maneb and paraquat along with controls. In a few sets of experiments, the animals were also treated with aminoguanidine, an inhibitor of inducible NO synthase, pyr...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550230</comments>
            <pubDate>Tue, 27 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550230</guid>        </item>
        <item>
            <title>Amelioration of Age Associated Neuroinflammation on Long Term Bacosides Treatment.</title>
            <link>http://www.medworm.com/index.php?rid=5550232&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22198697%26dopt%3DAbstract</link>
            <description>Authors: Rastogi M, Ojha RP, Devi BP, Aggarwal A, Agrawal A, Dubey GP
    Abstract
    Bacopa monnieri (L.) is a revered medicinal plant of traditional Indian system of medicine effective against cognitive impairment in ageing and SDAT. In our previous study, long term administration of bacosides was found to exhibit remarkable anti ageing effect, ameliorate age associated neurochemical and neurobehavioral deficits and prevent hippocampal neuronal degeneration in middle aged and aged rat brain cortex. In continuation to the previous study, the present study aims to investigate the neuroprotective effect of bacosides against age related chronic neuroinflammation in Wistar rat brain on 3 months treatment. Recently, neuroinflammation has gained considerable interest in age associated neurode...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550232</comments>
            <pubDate>Sun, 25 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550232</guid>        </item>
        <item>
            <title>Trans Fatty Acids Enhanced Beta-Amyloid Induced Oxidative Stress in Nerve Growth Factor Differentiated PC12 Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5550233&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22198657%26dopt%3DAbstract</link>
            <description>Authors: Tsai SJ, Liu WH, Yin MC
    Abstract
    The effects of trans fatty acids, elaidic acid (trans-9, C18:1) and linoelaidic acid (trans-9, trans-12 C18:2), at 20 or 40 μM in nerve growth factor differentiated PC12 cells with or without beta-amyloid peptide (Aβ) were examined. Elaidic acid treatment alone did not affect cell viability and oxidative injury associated markers (P &amp;gt; 0.05). However, co-treatments of elaidic acid and Aβ led to more reduction in mitochondrial membrane potential (MMP) and Na(+)-K(+)-ATPase activity, and more increase in DNA fragmentation and 8-hydroxydeoxyguanosine (8-OHdG) production than Aβ treatment alone (P &amp;lt; 0.05). Linoelaidic acid alone exhibited apoptotic and oxidative effects in cells via decreasing MMP and Na(+)-K(+)-ATPase activity, i...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550233</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550233</guid>        </item>
        <item>
            <title>Acute Restraint-Mediated Increases in Glutamate Levels in the Rat Brain: An In Vivo (1)H-MRS Study at 4.7 T.</title>
            <link>http://www.medworm.com/index.php?rid=5534852&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22187117%26dopt%3DAbstract</link>
            <description>Authors: Kim SY, Jang EJ, Hong KS, Lee C, Lee DW, Choi CB, Lee H, Choe BY
    Abstract
    It is well known that a variety of stressors induces a significant alteration in various putative neurotransmitters in the mammalian CNS. However, relatively little attention has been paid on the alteration of central glutamate neurotransmission, which is a major excitatory neurotransmitter in the brain. The present study aimed to determine whether acute restraint stress induces the changes in neurotransmitter level, especially glutamate, in rat brain and to examine whether 1-h recovery time after the termination of stress can revert to its pre-stress state. In vivo (1)H-NMR spectra were acquired from the cerebral cortex and hippocampus (control: N = 10, stress: N = 10, stress + 1 h rest: N =...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5534852</comments>
            <pubDate>Thu, 22 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5534852</guid>        </item>
        <item>
            <title>Evaluation of the Antipsychotic Potential of Panax quinquefolium in Ketamine Induced Experimental Psychosis Model in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5534851&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22189635%26dopt%3DAbstract</link>
            <description>Authors: Chatterjee M, Singh S, Kumari R, Verma AK, Palit G
    Abstract
    The search for novel pharmacotherapy from medicinal plants for psychiatric illnesses has progressed significantly from the past few decades and their therapeutic potential has been assessed in a variety of animal models. The aim of our study was to screen one such plant, Panax quinquefolium (PQ), with significant neuroactive properties for its antipsychotic potential. A graded dose study with PQ at 12.5-200 mg/kg, p. o. showed differential effects against the ketamine induced hyperactivity in the Digiscan animal activity monitor. Nevertheless at 100 mg/kg, p.o., PQ blocked ketamine induced memory impairment in the passive avoidance paradigm. In the chronic studies, PQ reduced the ketamine induced enhanced immobi...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5534851</comments>
            <pubDate>Thu, 22 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5534851</guid>        </item>
        <item>
            <title>Tenuigenin Promotes Proliferation and Differentiation of Hippocampal Neural Stem Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5534853&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22179853%26dopt%3DAbstract</link>
            <description>Authors: Chen Y, Huang X, Chen W, Wang N, Li L
    Abstract
    The present study was to investigate the influence of tenuigenin, an active ingredient of Polygala tenuifolia Willd, on the proliferation and differentiation of hippocampal neural stem cells in vitro. Tenuigenin was added to a neurosphere culture and neurosphere growth was measured using MTT assay. The influence of tenuigenin on the proliferation of neural progenitors was examined by Clone forming assay and BrdU detection. In addition, the differentiation of neural stem cells was compared using immunocytochemistry for β III-tubulin and GFAP. The results showed that addition of tenuigenin to the neural stem cell medium increased the number of newly formed neurospheres. More neurons were also obtained when tenuigenin was added ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5534853</comments>
            <pubDate>Sun, 18 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5534853</guid>        </item>
        <item>
            <title>Preconditioning with a Novel Metallopharmaceutical NO Donor in Anesthetized Rats Subjected to Brain Ischemia/Reperfusion.</title>
            <link>http://www.medworm.com/index.php?rid=5513536&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22160748%26dopt%3DAbstract</link>
            <description>In conclusion, Rut-bpy improved the total brain infarction area and hippocampal neuronal viability in part by inhibiting NF-κB signaling and helped to stabilize the blood pressure during the transition from ischemia to reperfusion.
    PMID: 22160748 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5513536</comments>
            <pubDate>Sat, 10 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5513536</guid>        </item>
        <item>
            <title>Increased Placental Growth Factor in Cerebrospinal Fluid of Patients with Epilepsy.</title>
            <link>http://www.medworm.com/index.php?rid=5513535&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22160787%26dopt%3DAbstract</link>
            <description>In this study, we assessed concentrations of PIGF in cerebrospinal fluid (CSF) of 60 epileptic patients and 24 non-seizure subjects using sandwich enzyme-linked immunosorbent assays. Epileptic patients in general had higher concentration of CSF-PIGF than controls (7.95 ± 0.88 ng/l vs. 5.87 ± 0.79 ng/l, P &amp;lt; 0.01). CSF-PIGF level in secondary epileptic patients (8.59 ± 1.26 ng/l) was higher than that in idiopathic epileptic patients (7.62 ± 0.20 ng/l) (P &amp;lt; 0.05). In idiopathic epilepsy, CSF-PIGF level in patients with high seizure frequency was higher than those in patients with low seizure frequency and seizure-free in recent 3 years (7.78 ± 0.23 ng/l vs. 7.49 ± 0.09 ng/l and 7.59 ± 0.10 ng/l, P &amp;lt; 0.05). Concentration of CSF-PIGF in patients with ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5513535</comments>
            <pubDate>Thu, 08 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5513535</guid>        </item>
        <item>
            <title>Depolarization-Induced Release of Amino Acids From the Vestibular Nuclear Complex.</title>
            <link>http://www.medworm.com/index.php?rid=5513537&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22147284%26dopt%3DAbstract</link>
            <description>Authors: Godfrey DA, Sun Y, Frisch C, Godfrey MA, Rubin AM
    Abstract
    There is evidence from immunohistochemistry, quantitative microchemistry, and pharmacology for several amino acids as neurotransmitters in the vestibular nuclear complex (VNC), including glutamate, γ-aminobutyrate (GABA), and glycine. However, evidence from measurements of release has been limited. The purpose of this study was to measure depolarization-stimulated calcium-dependent release of amino acids from the VNC in brain slices. Coronal slices containing predominantly the VNC were prepared from rats and perfused with artificial cerebrospinal fluid (ACSF) in an interface chamber. Fluid was collected from the chamber just downstream from the VNC using a microsiphon. Depolarization was induced by 50 mM potassiu...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5513537</comments>
            <pubDate>Wed, 07 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5513537</guid>        </item>
        <item>
            <title>Malondialdehyde, Bcl-2, Superoxide Dismutase and Glutathione Peroxidase may Mediate the Association of Sonic Hedgehog Protein and Oxidative Stress in Autism.</title>
            <link>http://www.medworm.com/index.php?rid=5513539&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22143957%26dopt%3DAbstract</link>
            <description>Authors: Ghanizadeh A
    Abstract
    Sonic hedgehog signaling and brain-derived neurotrophic factor play a neuro-protective role against oxidative stress in autism. Sonic hedgehog also increases Bcl-2 expression and the activities of superoxide dismutase and glutathione peroxidase. The level or activity of Bcl-2, brain-derived neurotrophic factor, and the activities of superoxide dismutase and glutathione peroxidase are decreased in autism. Sonic hedgehog also decreases the production of malondialdehyde that its level is high in autism. Therefore, it is supposed that sonic hedgehog may be associated with oxidative stress in autism through other pathways too.
    PMID: 22143957 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5513539</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5513539</guid>        </item>
        <item>
            <title>Sesaminol Glucosides Protect β-Amyloid Induced Apoptotic Cell Death by Regulating Redox System in SK-N-SH Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5513538&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22147283%26dopt%3DAbstract</link>
            <description>Authors: Um MY, Ahn JY, Kim MK, Ha TY
    Abstract
    We have investigated the neuroprotective effect of sesaminol glucosides (SG) in SK-N-SH cells. SG prevented apoptotic cell death induced by Aβ(25-35). In parallel, SK-N-SH cells exposed to Aβ(25-35) underwent oxidative stress as shown by the elevated level of intracellular ROS, lipid peroxidation, and 8-hydroxy-2'-deoxyguanosine (8-OHdG) formation, which were effectively suppressed by SG treatment. Furthermore, SG reversed the activities of catalase and glutathione peroxidase, and restored intracellular GSH levels in Aβ(25-35) challenged SK-N-SH cells. In addition, SG inhibited not only Aβ(25-35)-induced apoptotic features including cleavage of poly(ADP-ribose) polymerase, activation of caspase-3, and activation of caspase-9, but a...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5513538</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5513538</guid>        </item>
        <item>
            <title>Reversal of Postischemic Hypoperfusion by Tempol: Endothelial Signal Transduction Mechanism.</title>
            <link>http://www.medworm.com/index.php?rid=5513540&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22139482%26dopt%3DAbstract</link>
            <description>This report entails in vivo and in vitro studies concerned with free radical species involved in brain ischemia. The participation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in the early manifestation of cerebral ischemia/reperfusion was investigated in gerbils exposed to transient global ischemia using 4-OH-2,2,6,6-Tetramethylpiperidine-1-oxyl (TPL), a well-known antioxidant. TPL treatment reversed cerebral postischemic hypoperfusion and tissue edema in these animals. The findings are consistent with ROS/RNS participation in tissue injury and the reduction of cerebromicrovascular blood flow (CBF) during postischemic recirculation. The activation/deactivation of signal transduction pathway by oxidation/antioxidation [i.e., using hydrogen peroxide (H(2)O(2))/TPL] w...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5513540</comments>
            <pubDate>Sat, 03 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5513540</guid>        </item>
        <item>
            <title>Stress Proteins and Glial Cell Functions During Chronic Aluminium Exposures: Protective Role of Curcumin.</title>
            <link>http://www.medworm.com/index.php?rid=5475354&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22130689%26dopt%3DAbstract</link>
            <description>Authors: Sood PK, Nahar U, Nehru B
    Abstract
    Involved in the ongoing debate is the speculation that aluminium is somehow toxic for neurons. Glial cells cope up to protect neurons from this toxic insult by maintaining the glutathione homeostasis. Of late newer and newer roles of glial cells have been depicted. The present work looks into the other regulatory mechanisms that show the glial cells response to pro-oxidant effects of aluminium exposure. In the present investigation we have evaluated the inflammatory responses of the glial cells as well as HSP70-induction during aluminium exposure. Further, the protective role of curcumin is also evaluated. Aluminium was administered by oral gavage at a dose level of 100 mg/kg b.wt/day for a period of 8 weeks. Curcumin was administered i...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5475354</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5475354</guid>        </item>
        <item>
            <title>Mechanism of Action of Nitrogen Pressure in Controlling Striatal Dopamine Level of Freely Moving Rats is Changed by Recurrent Exposures to Nitrogen Narcosis.</title>
            <link>http://www.medworm.com/index.php?rid=5475356&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22127756%26dopt%3DAbstract</link>
            <description>Authors: Lavoute C, Weiss M, Risso JJ, Rostain JC
    Abstract
    In rats, a single exposure to 3 MPa nitrogen induces change in motor processes, a sedative action and a decrease in dopamine release in the striatum. These changes due to a narcotic effect of nitrogen have been attributed to a decrease in glutamatergic control and the facilitation of GABAergic neurotransmission involving NMDA and GABA(A) receptors, respectively. After repeated exposure to nitrogen narcosis, a second exposure to 3 MPa increased dopamine levels suggesting a change in the control of the dopaminergic pathway. We investigated the role of the nigral NMDA and GABA(A) receptors in changes in the striatal dopamine levels. Dopamine-sensitive electrodes were implanted into the striatum under general anesthesia, toge...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5475356</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5475356</guid>        </item>
        <item>
            <title>Protective Role of Quercetin on PCBs-Induced Oxidative Stress and Apoptosis in Hippocampus of Adult Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5475355&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22127757%26dopt%3DAbstract</link>
            <description>Authors: Selvakumar K, Bavithra S, Suganthi M, Benson CS, Elumalai P, Arunkumar R, Krishnamoorthy G, Venkataraman P, Arunakaran J
    Abstract
    Polychlorinated biphenyls (PCBs) exposure produces neurodegeneration and induces oxidative stress. Neuroprotective role of quercetin, on PCBs induced apoptosis in hippocampus has not yet been studied. The present study is focused to see whether quercetin supplementation precludes against PCBs induced oxidative stress and hippocampal apoptosis. The results have shown that quercetin at 50 mg/kg bwt/30 days has protected oxidative stress in hippocampus of adult male rats. Quercetin, a free radical scavenger decreased the levels of oxidative stress markers in the hippocampus of simultaneous PCB+quercetin treated rats. The pro-apoptotic and anti-ap...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5475355</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5475355</guid>        </item>
        <item>
            <title>Pathobiochemical Effect of Acylated Steryl-β-Glucoside on Aggregation and Cytotoxicity of α-Synuclein.</title>
            <link>http://www.medworm.com/index.php?rid=5475357&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22124781%26dopt%3DAbstract</link>
            <description>This study demonstrated that ASG directly enhances aggregation and cytotoxicity of α-synuclein, which are often observed in patients with ALS/PDC. These results, using assays that replicate cytoplasmic conditions, are consistent with the molecular mechanism that cytotoxicity is caused by intracellular α-synuclein fibril formation in neuronal cells.
    PMID: 22124781 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5475357</comments>
            <pubDate>Tue, 29 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5475357</guid>        </item>
        <item>
            <title>CDK11(p58) Promotes Rat Astrocyte Inflammatory Response via Activating p38 and JNK Pathways Induced by Lipopolysaccharide.</title>
            <link>http://www.medworm.com/index.php?rid=5475359&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22120654%26dopt%3DAbstract</link>
            <description>This study delineates that CDK11(p58) may be a significant regulatory factor for host defenses in central nervous system (CNS) inflammation.
    PMID: 22120654 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5475359</comments>
            <pubDate>Sun, 27 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5475359</guid>        </item>
        <item>
            <title>Letter from the Editor-in-Chief.</title>
            <link>http://www.medworm.com/index.php?rid=5475358&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22120655%26dopt%3DAbstract</link>
            <description>Authors: 
    PMID: 22120655 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5475358</comments>
            <pubDate>Sun, 27 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5475358</guid>        </item>
        <item>
            <title>Possible Involvement of Oxidative Stress and Inflammatory Mediators in the Protective Effects of the Early Preconditioning Window Against Transient Global Ischemia in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5475360&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22113727%26dopt%3DAbstract</link>
            <description>Authors: Nassar NN, Abdelsalam RM, Abdel-Rahman AA, Abdallah DM
    Abstract
    Ischemic preconditioning (IPC), comprising exposure to sub-lethal short term ischemic events, has been shown to exert adaptive responses in many organs including the brain, thus guarding against exacerbations of ischemia reperfusion (IR). However, the mechanisms involved in the early phase of such a protection remain elusive; hence, the present study aimed to investigate the modulatory effect of preconditioning against IR induced injury on infarct size, free radicals, inflammatory/anti-inflammatory markers, caspase-3 and heat shock protein (HSP)70 in the rat hippocampus. To this end, male Wistar rats were divided into 3 groups, (1) sham operated (SO) control; (2) IPC, animals were subject to 3 episodes of isch...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5475360</comments>
            <pubDate>Thu, 24 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5475360</guid>        </item>
        <item>
            <title>Long-Lasting Effects of Maternal Separation on an Animal Model of Post-Traumatic Stress Disorder: Effects on Memory and Hippocampal Oxidative Stress.</title>
            <link>http://www.medworm.com/index.php?rid=5475361&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22108759%26dopt%3DAbstract</link>
            <description>In conclusion, periodic maternal separation may increase the susceptibility to the effects of a stressor applied in adulthood on performance in the water maze. Increased DNA breaks in hippocampus was induced by both, maternal separation and exposure to shock.
    PMID: 22108759 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5475361</comments>
            <pubDate>Wed, 23 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5475361</guid>        </item>
        <item>
            <title>Tricyclodecan-9-yl-Xanthogenate (D609) Mechanism of Actions: A Mini-Review of Literature.</title>
            <link>http://www.medworm.com/index.php?rid=5475365&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22101393%26dopt%3DAbstract</link>
            <description>Authors: Adibhatla RM, Hatcher JF, Gusain A
    Abstract
    Tricyclodecan-9-yl-xanthogenate (D609) is known for its antiviral and antitumor properties. D609 actions are widely attributed to inhibiting phosphatidylcholine (PC)-specific phospholipase C (PC-PLC). D609 also inhibits sphingomyelin synthase (SMS). PC-PLC and/or SMS inhibition will affect lipid second messengers 1,2-diacylglycerol (DAG) and/or ceramide. Evidence indicates either PC-PLC and/or SMS inhibition affected the cell cycle and arrested proliferation, and stimulated differentiation in various in vitro and in vivo studies. Xanthogenate compounds are also potent antioxidants and D609 reduced Aß-induced toxicity, attributed to its antioxidant properties. Zn(2+) is necessary for PC-PLC enzymatic activity; inhibition by D609 ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5475365</comments>
            <pubDate>Tue, 22 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5475365</guid>        </item>
        <item>
            <title>Brain-Derived Neurotrophic Factor in Post-Partum Depressive Mothers.</title>
            <link>http://www.medworm.com/index.php?rid=5475362&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22102172%26dopt%3DAbstract</link>
            <description>Authors: Gazal M, Motta LS, Wiener CD, Fernandes JC, Quevedo LA, Jansen K, Pinheiro KA, Giovenardi M, Souza DO, Azevedo da Silva R, Pinheiro RT, Portela LV, Oses JP
    Abstract
    Postpartum depression (PPD) is the most common psychiatric complication observed in women after they give birth. Some women are particularly sensitive to hormonal changes, starting in early menarche, thus increasing their vulnerability to psychological stressing agents that are triggered by environmental and physiological factors throughout their lives. Decreased serum brain-derived neurotrophic factor (BDNF) levels have been associated to different neuropsychiatric conditions and BDNF has been considered as a candidate marker for such dysfunctions. The goal of this study was to compare the levels of BDNF betwe...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5475362</comments>
            <pubDate>Sun, 20 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5475362</guid>        </item>
        <item>
            <title>Cryptotanshinione Inhibits β-Amyloid Aggregation and Protects Damage from β-Amyloid in SH-SY5Y Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5475364&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22102154%26dopt%3DAbstract</link>
            <description>In this study, we demonstrated that CTS can inhibit Aβ42 spontaneous aggregation using thioflavin T fluorescence assay and transmission electron microscopy. Furthermore, we investigated the effects of CTS on Aβ-induced oxidative cell death in cultured SH-SY5Y cells. MTT and lactate dehydrogenase assays showed that CTS reduced the cytotoxicity induced by Aβ42. CTS also dramatically reduced Aβ42-induced cellular apoptosis and increased level of reactive oxygen species in these cells. Our study suggests that CTS may be useful in the inhibition or prevention of AD development and progression.
    PMID: 22102154 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5475364</comments>
            <pubDate>Sat, 19 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5475364</guid>        </item>
        <item>
            <title>Expression of PirB Protein in Intact and Injured Optic Nerve and Retina of Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5475363&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22102155%26dopt%3DAbstract</link>
            <description>Authors: Cai X, Yuan R, Hu Z, Chen C, Yu J, Zheng Z, Ye J
    Abstract
    The aim of this study was to investigate the expression of PirB protein in intact mice ON (optic nerve) and retina, and to evaluate its change after ON injury. The mouse ON crush model was established. The immunohistochemistry and western blot were used to detect PirB expression. We discovered PirB signals were located as beaded arrangement along the ON long axis in intact ON, disordered in injured ON, and distributed mainly in ganglion cell layer in intact and injured retina. Both PirB expression in injured ON and retina were significantly increased at 1-day post injury (1-dpi), nearly peaked at 7-dpi, but thereafter there was no significant change of them till at least 28-dpi. We concluded the expression of PirB w...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5475363</comments>
            <pubDate>Sat, 19 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5475363</guid>        </item>
        <item>
            <title>Neuroprotective Effect of Sesame Seed Oil in 6-Hydroxydopamine Induced Neurotoxicity in Mice Model: Cellular, Biochemical and Neurochemical Evidence.</title>
            <link>http://www.medworm.com/index.php?rid=5420947&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22089932%26dopt%3DAbstract</link>
            <description>Authors: Ahmad S, Khan MB, Hoda MN, Bhatia K, Haque R, Fazili IS, Jamal A, Khan JS, Katare DP
    Abstract
    Natural antioxidants have shown a remarkable reduction in oxidative stress due to excess formation of reactive oxygen species by enhancing antioxidant mechanism in the neurodegenerative disorders. Sesame seed oil (SO) is one of the most important edible oil in India as well as in Asian countries and has potent antioxidant properties thus the present study evaluated the neuroprotective effect of SO by using 6-Hydroxydopamine (6-OHDA)-induced Parkinson's disease model in mice. The mice were fed an SO mix diet for 15 days and then 6-OHDA was injected into the right striatum of mice brain. Three weeks after 6-OHDA infusion, mice were sacrificed and the striatum was removed. The neuro...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5420947</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5420947</guid>        </item>
        <item>
            <title>Interactions of Amyloid β Peptide 1-40 and Cerebrosterol.</title>
            <link>http://www.medworm.com/index.php?rid=5420946&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22089933%26dopt%3DAbstract</link>
            <description>In this study, stereospecificity in the interactions of natural 24(S)hydroxycholesterol (cerebrosterol) or synthetic 24(R)hydroxycholesterol with soluble fragment 1-40 was evaluated by means of an in vitro test based on increased vulnerability of the hemicholinium-3 sensitive high-affinity choline uptake system in rat hippocampal cholesterol-depleted synaptosomes to the actions of amyloid β; computational simulations were also performed. Our results suggest that: (1) 24(S)hydroxycholesterol interacts with L: -peptide 1-40 but not with the reverse L: -peptide 40-1, (2) 24(R)hydroxycholesterol does not interact with L: -peptide 1-40 or reverse 40-1, and (3) both enantiomers can probably interact with D: -peptide 1-40. Therefore, the binding of 24(S)hydroxycholesterol is not fully stereospec...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5420946</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5420946</guid>        </item>
        <item>
            <title>Striatal GABA Receptor Alterations in Hypoxic Neonatal Rats: Role of Glucose, Oxygen and Epinephrine Treatment.</title>
            <link>http://www.medworm.com/index.php?rid=5420945&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22089934%26dopt%3DAbstract</link>
            <description>Authors: Anju TR, Binoy J, Anitha M, Paulose CS
    Abstract
    Hypoxia in neonates disrupts the oxygen flow to the brain, essentially starving the brain and preventing it from performing vital biochemical processes important for central nervous system development. Hypoxia results in a permanent brain damage by gene and receptor level alterations mediated through neurotransmitters. The present study evaluated GABA, GABAA, GABAB receptor functions and gene expression changes in glutamate decarboxylase in the corpus striatum of hypoxic neonatal rats and the treatment groups with glucose, oxygen and epinephrine. Since GABA is the principal neurotransmitter involved in hypoxic ventilatory decline, the alterations in its level under hypoxic stress points to an important aspect of respiratory c...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5420945</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5420945</guid>        </item>
        <item>
            <title>Peripheral Assessment of the Genes AQP4, PBP and TH in Patients with Parkinson's Disease.</title>
            <link>http://www.medworm.com/index.php?rid=5420949&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22083667%26dopt%3DAbstract</link>
            <description>The objective of the current study was to assess mRNA expressional changes of AQP4, TH and PBP in blood samples of control and patients with PD. The study included 30 healthy controls and 90 PD patients subjected to treatment through the entire period of the study. RNA isolation was carried out using blood samples of the subjects recruited in the study and used for RT-PCR analysis of AQP4, TH as well as PBP. The mRNA expressions of AQP4 and TH were found to be reduced whereas that of PBP was found to be elevated when compared with those of healthy control samples. The statistically analysed data were presented which could be helpful for appreciation of PD pathology reflecting in the blood samples of PD population.
    PMID: 22083667 [PubMed - as supplied by publisher] (Source: Neurochemica...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5420949</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5420949</guid>        </item>
        <item>
            <title>The Role of the Golgi-Resident SPCA Ca(2+)/Mn          (2+) Pump in Ionic Homeostasis and Neural Function.</title>
            <link>http://www.medworm.com/index.php?rid=5420948&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22083668%26dopt%3DAbstract</link>
            <description>The Role of the Golgi-Resident SPCA Ca(2+)/Mn     (2+) Pump in Ionic Homeostasis and Neural Function.
    Neurochem Res. 2011 Nov 15;
    Authors: He W, Hu Z
    Abstract
    Recent evidence highlights the functional importance of the Golgi apparatus (GA) in neurological diseases. The functions of the mammalian GA, in addition to the processing and transport of cargo, also include ionic homeostasis. Besides Ca(2+)-release channels which serves GA as an agonist-sensitive intracellular Ca(2+) store, and Ca(2+)-binding proteins, the GA contains Ca(2+)-uptake mechanisms consisting of the well-known sarco-endoplasmic reticulum Ca(2+)-transport ATPases and the much less characterized secretory-pathway Ca(2+)-transport ATPases (SPCA). SPCA can transport both Ca(2+) and Mn(2+) into the Golgi lumen...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5420948</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5420948</guid>        </item>
        <item>
            <title>Regulation of [(3)H]D-Aspartate Release by the 5-F(2t)-Isoprostane and Its 5-Epimer in Isolated Bovine Retina.</title>
            <link>http://www.medworm.com/index.php?rid=5420950&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22081406%26dopt%3DAbstract</link>
            <description>Authors: Jamil J, Wright A, Harrison N, Kegey E, Flowers AF, Flyod NJ, Kotera C, Guy A, Galano JM, Durand T, Njie-Mbye YF, Ohia SE, Opere CA
    Abstract
    We have evidence that 15-F(2)-isoprostanes (15-F(2)-IsoPs) regulate excitatory neurotransmitter release in ocular tissues. Although 5-F(2)-IsoPs are abundantly produced in mammals, their pharmacological actions on neurotransmitter release remain unknown. In the present study, we compared the effect of the 5-F(2)-IsoP epimer pair, 5-F(2t)-IsoP (C5-OH in β-position) and 5-epi-5-F(2t)-IsoP (C5-OH in α-position), on K(+)-evoked [(3)H]D-aspartate release in isolated bovine retina. We further examined the role of prostanoid receptors on the inhibitory action of 5-epi-5-F(2t)-IsoP on [(3)H]D-aspartate overflow. Isolated bovine retina were ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5420950</comments>
            <pubDate>Sun, 13 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5420950</guid>        </item>
        <item>
            <title>Intermittent Hypobaric Hypoxia Preconditioning Induced Brain Ischemic Tolerance by Up-Regulating Glial Glutamate Transporter-1 in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5420954&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22076500%26dopt%3DAbstract</link>
            <description>Authors: Gong SJ, Chen LY, Zhang M, Gong JX, Ma YX, Zhang JM, Wang YJ, Hu YY, Sun XC, Li WB, Zhang Y
    Abstract
    Several studies showed that the up-regulation of glial glutamate transporter-1 (GLT-1) participates in the acquisition of brain ischemic tolerance induced by cerebral ischemic preconditioning or ceftriaxone pretreatment in rats. To explore whether GLT-1 plays a role in the acquisition of brain ischemic tolerance induced by intermittent hypobaric hypoxia (IH) preconditioning (mimicking 5,000 m high-altitude, 6 h per day, once daily for 28 days), immunohistochemistry and western blot were used to observe the changes in the expression of GLT-1 protein in hippocampal CA1 subfield during the induction of brain ischemic tolerance by IH preconditioning, and the effect of dihydr...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5420954</comments>
            <pubDate>Sat, 12 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5420954</guid>        </item>
        <item>
            <title>Epicatechin Inhibits Human Plasma Lipid Peroxidation Caused by Haloperidol In Vitro.</title>
            <link>http://www.medworm.com/index.php?rid=5420953&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22076501%26dopt%3DAbstract</link>
            <description>In conclusion, the presented results indicate that epicatechin-the major polyphenolic component of green tea reduced significantly human plasma lipid peroxidation caused by haloperidol. Moreover, epicatechin was found to be a more effective antioxidant, than the solution of pure resveratrol or quercetin.
    PMID: 22076501 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5420953</comments>
            <pubDate>Sat, 12 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5420953</guid>        </item>
        <item>
            <title>FoxO3a Changes in Pyramidal Neurons and Expresses in Non-Pyramidal Neurons and Astrocytes in the Gerbil Hippocampal CA1 Region After Transient Cerebral Ischemia.</title>
            <link>http://www.medworm.com/index.php?rid=5420952&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22076502%26dopt%3DAbstract</link>
            <description>Authors: Yoo KY, Kwon SH, Lee CH, Yan B, Park JH, Ahn JH, Choi JH, Ohk TG, Cho JH, Won MH
    Abstract
    The forkhead box O (FoxO) proteins regulate processes ranging from cell longevity to cell apoptosis and function as transcription factors. FoxO3a is expressed throughout the brain including the hippocampus. In the present study, we investigated the changes in FoxO3a immunoreactivity and its protein levels in the gerbil hippocampal CA1 region after 5 min of transient global cerebral ischemia. FoxO3a immunoreactivity and protein levels in the ischemic CA1 region, which is very vulnerable to ischemic damage, were slightly decreased from 3 h after ischemia-reperfusion (I-R) and maintained until 12 h after I-R. One and 2 days after I-R, FoxO3a immunoreactivity and protein levels were s...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5420952</comments>
            <pubDate>Sat, 12 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5420952</guid>        </item>
        <item>
            <title>Allopregnanolone Potentiates the Glutamate-Mediated Seizures Induced by 4-Aminopyridine in Rat Hippocampus in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=5420951&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22081320%26dopt%3DAbstract</link>
            <description>Authors: Salazar P, Tapia R
    Abstract
    Excitatory and inhibitory neurotransmission in the central nervous system can be modulated by neurosteroids. We previously found that in rat hippocampal slices allopregnanolone (3α-hydroxy-5α-pregnan-20-one), a positive GABA(A) receptor modulator, suppresses the epileptic discharges induced by 4-aminopyridine (4-AP), a convulsant K(+) channel blocker that stimulates glutamate release. Here, we tested the action of allopregnanolone on the epileptogenic and excitotoxic effects of the intrahippocampal administration of 4-AP in vivo. Drugs were perfused by a microdialysis cannula-electrode in the dorsal hippocampus and the EEG was recorded. Extracellular levels of aspartate, glutamate and GABA were analyzed by HPLC in the microdialysis fractions, ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5420951</comments>
            <pubDate>Sat, 12 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5420951</guid>        </item>
        <item>
            <title>SCH58261 the Selective Adenosine A(2A) Receptor Blocker Modulates Ischemia Reperfusion Injury Following Bilateral Carotid Occlusion: Role of Inflammatory Mediators.</title>
            <link>http://www.medworm.com/index.php?rid=5420955&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22071908%26dopt%3DAbstract</link>
            <description>Authors: Mohamed RA, Agha AM, Nassar NN
    Abstract
    In the present study, the effects of SCH58261, a selective adenosine A(2A) receptor antagonist that crosses the blood brain barrier (BBB) and 8-(4-sulfophenyl) theophylline (8-SPT), a non-selective adenosine receptor antagonist that acts peripherally, were investigated on cerebral ischemia reperfusion injury (IR). Male Wistar rats (200 - 250 g) were divided into four groups: (1) sham-operated (SO), IR pretreated with either (2) vehicle (DMSO); (3) SCH58261 (0.01 mg/kg); (4) 8-SPT (2.5 mg/kg). Animals were anesthetized and submitted to occlusion of both carotid arteries for 45 min. All treatments were administered intraperitoneally (i.p.) post carotid occlusion prior to exposure to a 24 h reperfusion period. Ischemic rats showed ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5420955</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5420955</guid>        </item>
        <item>
            <title>Specific Alterations of the HtrA2/HAX-1 Ratio in the Penumbra Upon Focal Cerebral Ischemia in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5420956&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22057932%26dopt%3DAbstract</link>
            <description>In this study, we performed focal cerebral ischemia in mice and investigated principally the dynamic changes of HAX-1 expression and other apoptotic agents such as HtrA2, AIF and caspase-3. Western blot and immunohistochemistry analysis revealed that HAX-1 was expressed at very low levels under normal conditions. Focal cerebral ischemia significantly decreased cytosolic accumulation of HAX-1, induced an upregulation of HtrA2, an upregulation of AIF and activation of caspase-3. Taken together, these results suggested that HAX-1 is probably involved in the pathophysiology of cell death induced by focal ischemia.
    PMID: 22057932 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5420956</comments>
            <pubDate>Sun, 06 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5420956</guid>        </item>
        <item>
            <title>Association Between Na(+),K          (+)-ATPase Activity and the Vulnerability/Resilience to Mood Disorders induced by Early Life Experience.</title>
            <link>http://www.medworm.com/index.php?rid=5280328&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21695394%26dopt%3DAbstract</link>
            <description>The objective of this study was to evaluate the interaction between early experience and vulnerability to chronic variable stress in adulthood, analyzing emotional, metabolic and neurochemical aspects related to depression. Pups were (1) handled (10 min/day) or (2) left undisturbed from day 1 to 10 after birth. When the animals reached adulthood, the groups were subdivided and the rats were submitted or not to CVS, which consisted of daily exposure to different stressors for 40 days, followed by a period of behavioral tasks, biochemical (plasma corticosterone and insulin sensitivity) and neurochemical (Na(+),K(+)-ATPase activity in hippocampus, amygdala and parietal cortex) measurements. Neonatally-handled rats demonstrated shorter immobility times in the forced swimming test, independen...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5280328</comments>
            <pubDate>Tue, 04 Oct 2011 04:32:46 +0100</pubDate>
            <guid isPermaLink="false">5280328</guid>        </item>
        <item>
            <title>The Phosphatidyl Inositol 3 Kinase-Glycogen Synthase Kinase 3β Pathway Mediates Bilobalide-Induced Reduction in Amyloid β-Peptide.</title>
            <link>http://www.medworm.com/index.php?rid=5280331&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21952928%26dopt%3DAbstract</link>
            <description>Authors: Shi C, Zheng DD, Wu FM, Liu J, Xu J
    Abstract
    Bilobalide (BB), a sesquiterpenoid extract of Ginkgo biloba leaves, has been demonstrated to have neuroprotective effects. The neuroprotective mechanisms were suggested to be associated with modulation of intracellular signaling cascades such as the phosphatidyl inositol 3-kinase (PI3K) pathway. Since some members of intracellular signalling pathways such as PI3K have been demonstrated to be involved in amyloid precursor protein (APP) processing, the present study investigated whether BB has an influence on the β-secretase-mediated APP cleavage via PI3K-dependent pathway. Using HT22 cells and SAMP8 mice (a senescence-accelerated strain of mice), this study showed that BB treatment reduced generation of two β-secretase cleavage...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5280331</comments>
            <pubDate>Wed, 28 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5280331</guid>        </item>
        <item>
            <title>ConBr, a Lectin from Canavalia brasiliensis Seeds, Protects Against Quinolinic Acid-Induced Seizures in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5280336&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21948344%26dopt%3DAbstract</link>
            <description>In this study, we investigated the neuroprotective effects of ConBr against quinolinic acid (QA), a well-known NMDA agonist that produces severe neurotoxicity when administered in vivo. ConBr (10 μg/site) administered via intracerebroventricular (i.c.v.) showed a neuroprotective activity against seizures induced by QA (36.8 nmol/site; i.c.v.) when administered 15 min prior to QA, with a percentage of protection around 50%. ConBr was also able to significantly decrease the severity of the seizures but without changes in the latency of the first convulsion or the duration of the seizures. This effect was dependent on the structural integrity of the ConBr protein and its binding capacity to oligosaccharides residues. ConA, a lectin with high similarity to ConBr, did not reverse the QA-ind...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5280336</comments>
            <pubDate>Tue, 27 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5280336</guid>        </item>
        <item>
            <title>Evidence that Hyperprolinemia Alters Glutamatergic Homeostasis in Rat Brain: Neuroprotector Effect of Guanosine.</title>
            <link>http://www.medworm.com/index.php?rid=5247127&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21935728%26dopt%3DAbstract</link>
            <description>This study investigated the effects of acute and chronic hyperprolinemia on glutamate uptake, as well as some mechanisms underlying the proline effects on glutamatergic system in rat cerebral cortex. The protective role of guanosine on effects mediated by proline was also evaluated. Results showed that acute and chronic hyperprolinemia reduced glutamate uptake, Na(+), K(+)-ATPase activity, ATP levels and increased lipoperoxidation. GLAST and GLT-1 immunocontent were increased in acute, but not in chronic hyperprolinemic rats. Our data suggest that the effects of proline on glutamate uptake may be mediated by lipid peroxidation and disruption of Na(+), K(+)-ATPase activity, but not by decreasing in glutamate transporters. This probably induces excitotoxicity and subsequent energy deficit. G...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247127</comments>
            <pubDate>Wed, 21 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247127</guid>        </item>
        <item>
            <title>Glutamate Decarboxylase and GABA Aminotransferase Levels in Different Regions of Rat Brain on the Onset of Leptazol Induced Convulsions.</title>
            <link>http://www.medworm.com/index.php?rid=5247126&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21935729%26dopt%3DAbstract</link>
            <description>Authors: Nasreen Z, Jameel T, Hasan A, Parveen N, Sadasivudu B
    Abstract
    The activities of Glutamate decarboxylase (GAD) and Gamma aminobutyric acid (GABA) were studied in three regions of rat brain in heightened neuronal activity resulting in convulsions by Leptazol. These enzymes were studied in preconvulsive, convulsive and post convulsive phases. The activity of GAD decreases significantly in the preconvulsive phase in all the three regions of brain followed by a significant increase during the convulsive and post convulsive phase in cerebral cortex and cerebellum. The activity of GABA-T decreases maximal during the preconvulsive phase followed by convulsive phase. The activity of this enzyme tended to increase to control values when the postconvulsive phase was reached. Therefo...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247126</comments>
            <pubDate>Wed, 21 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247126</guid>        </item>
        <item>
            <title>An In Vitro Paradigm for Diabetic Cerebral Oedema and its Therapy: A Critical Role for Taurine and Water Channels.</title>
            <link>http://www.medworm.com/index.php?rid=5247125&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21935730%26dopt%3DAbstract</link>
            <description>Authors: Koves IH, Russo VC, Higgins S, Mishra A, Pitt J, Cameron FJ, Werther GA
    Abstract
    The pathophysiology of cerebral oedema (CE) in diabetic ketoacidosis (DKA) remains enigmatic. We investigated the role of the idiogenic osmol taurine and aquaporin channels in an in vitro model, the SH-SY5Y neuroblastoma cell line, by sequentially mimicking DKA-like hyperglycemia/hypertonicity and hypotonic fluid therapy. Exposure to DKA-like hyperosmolarity led to shrinkage, while hypotonic fluid exposure led to cell swelling and impaired viability. Low sodium compensated in part for elevated glucose, pointing to a critical role for overall osmolality. Taurine, was synthesized and retained intracellularly during DKA-like hypertonicity, and released during hypotonicity, in part mitigating neur...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247125</comments>
            <pubDate>Wed, 21 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247125</guid>        </item>
        <item>
            <title>Humanin Protects Cortical Neurons from Ischemia and Reperfusion Injury by the Increased Activity of Superoxide Dismutase.</title>
            <link>http://www.medworm.com/index.php?rid=5247124&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21935731%26dopt%3DAbstract</link>
            <description>Authors: Zhao ST, Huang XT, Zhang C, Ke Y
    Abstract
    The neuroprotective effects of superoxide dismutase (SOD) against hypoxia/reperfusion (I/R) injury and of humanin (HN) against toxicity by familial amyotrophic lateral sclerosis (ALS)-related mutant SOD led us to hypothesize that HN might have a role to increase the activity of SOD, which might be involved in the protective effects of HN on neuron against Alzheimer's disease-unrelated neurotoxicities. In the present study, we found that 4 h ischemia and 24 h reperfusion induced a significant increase in lactate dehydrogenase (LDH) release, malondialdehyde (MDA) formation and the number of karyopyknotic nuclei (4',6-diamidino-2-phenylindole dihydrochloride nuclear dyeing) and a decrease in the number of Calcein-AM-positive living ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247124</comments>
            <pubDate>Wed, 21 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247124</guid>        </item>
        <item>
            <title>Differential Effect of Nimodipine in Attenuating Iron-Induced Toxicity in Brain- and Blood-Brain Barrier-Associated Cell Types.</title>
            <link>http://www.medworm.com/index.php?rid=5247123&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21935732%26dopt%3DAbstract</link>
            <description>Authors: Lockman JA, Geldenhuys WJ, Bohn KA, Desilva SF, Allen DD, Van der Schyf CJ
    Abstract
    Metal homeostasis is increasingly being evaluated as a therapeutic target in stroke and neurodegenerative diseases. Metal dysregulation has been shown to lead to protein aggregation, plaque formation and neuronal death. In 2007, we first reported that voltage-gated calcium channels act as a facile conduit for the entry of free ferrous (Fe(2+)) ions into neurons. Herein, we evaluate differential iron toxicity to central nervous system cells and assess the ability of the typical L-type voltage-gated calcium channel blocker nimodipine to attenuate iron-induced toxicity. The data demonstrate that iron sulfate induces a dose-dependent decrease in cell viability in rat brain endothelial cells (RB...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247123</comments>
            <pubDate>Wed, 21 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247123</guid>        </item>
        <item>
            <title>L-Type Calcium Channel Mediates Anticonvulsant Effect of Cannabinoids in Acute and Chronic Murine Models of Seizure.</title>
            <link>http://www.medworm.com/index.php?rid=5247128&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21928146%26dopt%3DAbstract</link>
            <description>In this study, the effects of cannabinoid compounds and L-type Ca(2+) channels blockers, either alone or in combination were investigated using acute model of pentylenetetrazole (PTZ)-induced seizure in mice and chronic model electrical kindling of amygdala in rats. Pretreatment of mice with both cannabinoid CB1 receptor agonist arachidonyl-2'-chloroethylamide (ACEA) and endocannabinoid degradating enzyme inhibitor cyclohexylcarbamic acid 3'-carbamoyl-biphenyl-3-yl ester (URB597) produced a protective effect against PTZ-induced seizure. Administration of various doses of the two L-type Ca(2+) channel blockers verapamil and diltiazem did not alter PTZ-induced seizure threshold. However, co-administration of verapamil and either ACEA or URB597 attenuated the protective effect of cannabinoid ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247128</comments>
            <pubDate>Sun, 18 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247128</guid>        </item>
        <item>
            <title>Effects of Cu,Zn-Superoxide Dismutase on Cell Proliferation and Neuroblast Differentiation in the Mouse Dentate Gyrus.</title>
            <link>http://www.medworm.com/index.php?rid=5247130&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21927927%26dopt%3DAbstract</link>
            <description>In this study, we observed the effects of Cu,Zn-superoxide dismutase (SOD1) on lipid peroxidation, cell proliferation, and neuroblast differentiation in the mouse dentate gyrus using malondialdehyde (MDA), Ki67, and doublecortin (DCX), respectively. We constructed an expression vector, PEP-1, fused PEP-1 with SOD1, and generated PEP-1-SOD1 fusion protein. We administered PEP-1 and 100 or 500 μg PEP-1-SOD1 intraperitoneally once a day for 3 weeks and sacrificed at 30 min after the last administrations. PEP-1 administration did not change the MDA levels compared to those in the vehicle-treated group, while PEP-1-SOD1 treatment significantly reduced MDA levels compared to the vehicle-treated group. In the PEP-1-treated group, the number of Ki67-positive nuclei was similar to that in the v...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247130</comments>
            <pubDate>Sat, 17 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247130</guid>        </item>
        <item>
            <title>Alternatively Spliced Three Novel Transcripts of gria1 in the Cerebellum and Cortex of Mouse Brain.</title>
            <link>http://www.medworm.com/index.php?rid=5247129&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21927928%26dopt%3DAbstract</link>
            <description>Authors: Azim S, Banday AR, Tabish M
    Abstract
    Glutamate receptor type 1 (GluR1) subunit of α-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptors plays an important role in the expression of long-term potentiation and memory formation. GluR1 is encoded by gria1 gene containing 16 exons and 15 introns in mouse. Previous studies have reported two alternatively spliced variants of this subunit. These flip and flop variants differ enormously in their properties as well as expression. In our studies, we report the presence of three new transcripts of this gene present in the cerebellum and cortex of mouse brain produced by alternative splicing at 5' end. Four new exons are reported; N1 is located in 5' untranslated region, N2 is located in the 1st intronic region while N3 and N4 a...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247129</comments>
            <pubDate>Sat, 17 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247129</guid>        </item>
        <item>
            <title>Moderate Grade Hyperammonemia Induced Concordant Activation of Antioxidant Enzymes is Associated with Prevention of Oxidative Stress in the Brain Slices.</title>
            <link>http://www.medworm.com/index.php?rid=5231154&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21922254%26dopt%3DAbstract</link>
            <description>This article describes profiles of all the antioxidant enzymes Vis a Vis status of oxidative stress/damage in the brain slices exposed to 0.1-1 mM ammonia, reported to exist in the brain of animals with chronic liver failure and in liver cirrhotic patients. Superoxide dismutase catalyzes the first step of antioxidant mechanism and, with concerted activity of catalase, neutralizes [Formula: see text] produced in the cells. Both these enzymes remained unchanged up to 0.2-0.3 mM ammonia, however, with significant increments (P &amp;lt; 0.01-0.001) in the brain slices exposed to 0.5-1 mM ammonia. This was consistent with the similar pattern of production of reactive oxygen species in the brain slices. However, level of lipid peroxidation remained unchanged throughout the ammonia treatment. Sy...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5231154</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5231154</guid>        </item>
        <item>
            <title>Increased β-Catenin/Tcf Signaling in Pilocytic Astrocytomas: A Comparative Study to Distinguish Pilocytic Astrocytomas from Low-Grade Diffuse Astrocytomas.</title>
            <link>http://www.medworm.com/index.php?rid=5231153&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21922255%26dopt%3DAbstract</link>
            <description>In this study, we investigated the Wnt/β-catenin/Tcf pathway in pilocytic astrocytomas and compared with diffuse astrocytomas. We observed the differential expression of β-catenin, Tcf4, Lef1 and c-Myc in astrocytomas particularly higher levels were observed in pilocytic astrocytomas and GBM while very little expression was documented in grade II tumors. Further, immunohistochemical analysis revealed the strong positivity of β-catenin, Tcf4, Lef1 and c-Myc in pilocytic astrocytomas than that of grade II tumors and also exhibited the strong positivity in vascular endothelial cells of pilocytic astrocytomas and GBM. Hence, Wnt/β-catenin/Tcf signaling pathway is differentially expressed in astrocytomas, activation of this pathway might be helpful in separating pilocytic astrocytomas from ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5231153</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5231153</guid>        </item>
        <item>
            <title>The Cannabinoid WIN 55212-2 Mitigates Apoptosis and Mitochondrial Dysfunction After Hypoxia Ischemia.</title>
            <link>http://www.medworm.com/index.php?rid=5219062&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21909954%26dopt%3DAbstract</link>
            <description>Authors: Alonso-Alconada D, Alvarez A, Alvarez FJ, Martínez-Orgado JA, Hilario E
    Abstract
    Perinatal hypoxia-ischemia has significant mortality and morbidity due to there is still no specific treatment as a consequence of the complexities of hypoxic-ischemic pathophysiology. The aim of this work was to evaluate the effects of the cannabinoid agonist WIN 55212-2 on apoptotic cell death and mitochondrial dysfunction after perinatal asphyxia in fetal lambs. Animals were assigned to: one SHAM group and two hypoxic-ischemic groups that received a dose of 0.01 μg/kg WIN 55,212-2 (HI + WIN) or not (HI + VEH) after 60 min of partial occlusion of the umbilical cord, and sacrificed 3 h later. Different brain regions were separated for morphological studies, and the same territories w...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5219062</comments>
            <pubDate>Sun, 11 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5219062</guid>        </item>
        <item>
            <title>BDNF-, IGF-1- and GDNF-Secreting Human Neural Progenitor Cells Rescue Amyloid β-Induced Toxicity in Cultured Rat Septal Neurons.</title>
            <link>http://www.medworm.com/index.php?rid=5219061&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21909955%26dopt%3DAbstract</link>
            <description>In this study, septal neurons were prepared from septal nucleus of embryonic (day 16-17) rat brain and treated with monomeric, oligomeric or fibrillar Aβ(1-42) peptide. Oligomeric Aβ(1-42), (10 μM) was the most potent at sublethal dose. Septal neuron cultures treated with BDNF, IGF-1 or GDNF or co-cultured with genetically modified human neural progenitor cells (hNPCs) secreting these neurotrophic factors (but not allowing contact between the two cell types), were protected from oligomeric Aβ(1-42) peptide-induced cell death, and these trophic factors enhanced cholinergic functions by increasing ChAT expression level. These results indicate the potential of employing transplanted hNPCs for treatment of AD.
    PMID: 21909955 [PubMed - as supplied by publisher] (Source: Neurochemical R...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5219061</comments>
            <pubDate>Sun, 11 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5219061</guid>        </item>
        <item>
            <title>Maternal Depression Model: Long-Lasting Effects on the Mother Following Separation from Pups.</title>
            <link>http://www.medworm.com/index.php?rid=5219060&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21909956%26dopt%3DAbstract</link>
            <description>This study was carried out to ascertain the effects of maternal separation (3 h per day) of mothers from their pups in the neonatal period in rats, which has been suggested to induce a depressive-like state, would have long lasting effects on different parameters including hippocampal Na(+), K(+)-ATPase activity, NO production, free radical production and antioxidant enzymes activities in dams. Fourty-eight Wistar rats were divided into 3 groups: control, brief separation (10 min) and long separation (3 h). The neonatal interventions were done on postpartum days 1-10. At 35 days post-partum the dams were killed and the hippocampal Na(+), K(+)-ATPase activity were measured, as well as the activity of the antioxidant enzymes catalase, glutathione peroxidase, superoxide dismutase, free ra...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5219060</comments>
            <pubDate>Sun, 11 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5219060</guid>        </item>
        <item>
            <title>Alterations in the Expression of the Anti-Apoptotic Factor HAX-1 upon Seizures-Induced Hippocampal Injury in the Neonatal Rat Brain.</title>
            <link>http://www.medworm.com/index.php?rid=5219059&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21909957%26dopt%3DAbstract</link>
            <description>In this study, we performed a status epilepticus in rats and investigated the dynamic changes of HAX-1 expression, HtrA2 distribution and caspase-3 activation in the hippocampus. Western blot and immunohistochemistry analysis revealed that HAX-1 was expressed at very low levels in the hippocampus. Status epilepticus in the immature brain significantly induced increased cytosolic accumulation of HAX-1 in a biphasic manner, induced an upregulation of HtrA2 and enhanced caspase-3 activity in the selectively vulnerable hippocampal CA1-subfield. Taken together, these results suggested that HAX-1 is probably involved in the pathophysiology of cell death induced by epilepsy.
    PMID: 21909957 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5219059</comments>
            <pubDate>Sun, 11 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5219059</guid>        </item>
        <item>
            <title>Protection by DHA of Early Hippocampal Changes in Diabetes: Possible Role of CREB and NF-κB.</title>
            <link>http://www.medworm.com/index.php?rid=5219058&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21909958%26dopt%3DAbstract</link>
            <description>In this study, we try to address the mechanisms of diabetes induced damage and whether docosahexaenoic acid (DHA) could attenuate the degenerative changes in diabetic hippocampus in a rodent model of diabetes. Diabetes was induced in rats by an intraperitoneal injection of streptozotocin. Animals were divided into the following experimental groups: control rats; control animals treated with DHA; untreated diabetic rats; diabetic rats treated with insulin; diabetic rats treated with DHA; diabetic rats treated with insulin and DHA. At the end of week 12, rats were killed and one of the hemispheres was cryosectioned and the other was dissected and hippocampi homogenized. The number of bromodeoxyuridine positive cells in the hippocampus of diabetic rats was decreased, and the latency time to f...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5219058</comments>
            <pubDate>Sun, 11 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5219058</guid>        </item>
        <item>
            <title>Neural Stem Cells Over-Expressing Brain-Derived Neurotrophic Factor (BDNF) Stimulate Synaptic Protein Expression and Promote Functional Recovery Following Transplantation in Rat Model of Traumatic Brain Injury.</title>
            <link>http://www.medworm.com/index.php?rid=5219063&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21901549%26dopt%3DAbstract</link>
            <description>In this study, we used neural stem cells (NSCs) genetically modified to encode BDNF gene (BDNF/NSCs) and naive NSCs transplantation and found that BDNF/NSCs significantly improved neurological motor function following traumatic brain injury (TBI) on selected behavioral tests. Our data clearly demonstrate that the transplantation of BDNF/NSCs causes overexpression of BDNF in the brains of TBI rats. The number of surviving engrafted cells and the proportion of engrafted cells with a neuronal phenotype were significantly greater in BDNF/NSCs than in naive NSCs-transplanted rats. The expression of pre- and post-synaptic proteins and a regeneration-associated gene in the BDNF/NSCs-transplanted rats was significantly increased compared to that in NSCs-transplanted rats, especially at the early s...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5219063</comments>
            <pubDate>Wed, 07 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5219063</guid>        </item>
        <item>
            <title>Nitric Oxide Implicates c-Fos Expression in the Cuneate Nucleus Following Electrical Stimulation of the Transected Median Nerve.</title>
            <link>http://www.medworm.com/index.php?rid=5219065&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21892689%26dopt%3DAbstract</link>
            <description>In this study, we investigated whether nitric oxide (NO) modulated injury-induced neuropeptide Y (NPY) releasing and c-Fos expression in the cuneate nucleus (CN) after median nerve transection (MNT). We first examined the temporal changes of neuronal nitric oxide synthase (nNOS) expression in the dorsal root ganglion (DRG) and CN after MNT. Following MNT, the amounts of nNOS-like immunoreactive (nNOS-LI) neurons in the DRG and CN significantly increased as compared with those of the sham-operated rats. Furthermore, 4 weeks after MNT, the increases of nNOS-LI neurons in the DRG and CN were attenuated by pre-emptive lidocaine treatment in a dose-dependent manner. Finally, 4 weeks after MNT, pre-stimulation administration of L-NAME (N (ω)-Nitro-L: -arginine methyl ester) or 7-NI (7-nitroin...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5219065</comments>
            <pubDate>Sat, 03 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5219065</guid>        </item>
        <item>
            <title>Inhibition of Neuron-Specific CREB Dephosphorylation is Involved in Propofol and Ketamine-Induced Neuroprotection Against Cerebral Ischemic Injuries of Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5219064&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21892690%26dopt%3DAbstract</link>
            <description>Authors: Shu L, Li T, Han S, Ji F, Pan C, Zhang B, Li J
    Abstract
    Propofol and ketamine may provide certain degree of neuroprotection, but the underlying mechanism remains unclear to date. The cAMP response element-binding protein (CREB) was proposed that its phosphorylation at Ser133 (P-CREB) constituted a convergence point involved in neuroprotection. The purpose of this study was to determine whether different dosages of propofol and ketamine could provide neuroprotection against permanent middle cerebral artery occlusion (MCAO)-induced ischemic injuries and the involvement of P-CREB. Eighty adult male BALB/c mice that underwent 6 h MCAO were randomly divided into eight groups: Sham-operation; MCAO + saline; MCAO + 25, 50, 100 mg/kg propofol; and MCAO + 25, 50, 100 mg/kg...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5219064</comments>
            <pubDate>Sat, 03 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5219064</guid>        </item>
        <item>
            <title>PEP-1-Frataxin Significantly Increases Cell Proliferation and Neuroblast Differentiation by Reducing Lipid Peroxidation in the Mouse Dentate Gyrus.</title>
            <link>http://www.medworm.com/index.php?rid=5192974&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21882036%26dopt%3DAbstract</link>
            <description>In this study, we observed the effects of frataxin on cell proliferation and neuroblast differentiation in the mouse hippocampal dentate gyrus. For this, we constructed an expression vector, PEP-1, that was fused with frataxin to create a PEP-1-frataxin fusion protein that easily penetrated frataxin into the blood-brain barrier. Three mg/kg PEP-1-frataxin was intraperitoneally administered to mice once a day for 2 weeks. The administration of PEP-1 alone did not result in any significant changes in the number of Ki67-positive cells and doublecortin (DCX)-immunoreactive neuroblasts in the mouse dentate gyrus. However, the administration of PEP-1-frataxin significantly increased the number of Ki67-positive cells and DCX-immunoreactive neuroblasts in the mouse dentate gyrus. In addition, PEP...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5192974</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5192974</guid>        </item>
        <item>
            <title>Thioacetamide-Induced Fulminant Hepatic Failure Induces Cerebral Mitochondrial Dysfunction by Altering the Electron Transport Chain Complexes.</title>
            <link>http://www.medworm.com/index.php?rid=5192975&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21879353%26dopt%3DAbstract</link>
            <description>Authors: Chadipiralla K, Reddanna P, Chinta RM, Reddy PV
    Abstract
    Fulminant hepatic failure (FHF) is an acute form of hepatic encephalopathy resulting from severe inflammatory or necrotic liver damage without any previously established liver damage. This develops as a complication due to viral infections, and drug abuse. FHF also occurs in acute disorders like Reye's syndrome. Although the exact mechanisms in the etiology of FHF are not understood, elevated levels of brain ammonia have been consistently reported. Such increased ammonia levels are suggested to alter neurotransmission signals and impair cerebral energy metabolism due to mitochondrial dysfunctions. In the present study we have examined the role of cerebral electron transport chain complexes, including complex I, II, I...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5192975</comments>
            <pubDate>Tue, 30 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5192975</guid>        </item>
        <item>
            <title>Comparison of Transdifferentiated and Untransdifferentiated Human Umbilical Mesenchymal Stem Cells in Rats after Traumatic Brain Injury.</title>
            <link>http://www.medworm.com/index.php?rid=5192976&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21877237%26dopt%3DAbstract</link>
            <description>Authors: Hong SQ, Zhang HT, You J, Zhang MY, Cai YQ, Jiang XD, Xu RX
    Abstract
    Transdifferentiated and untransdifferentiated mesenchymal stem cells (MSCs) have shown therapeutic benefits in central nervous system (CNS) injury. However, it is unclear which would be more appropriate for transplantation. To address this question, we transplanted untransdifferentiated human umbilical mesenchymal stem cells (HUMSCs) and transdifferentiated HUMSCs (HUMSC-derived neurospheres, HUMSC-NSs) into a rat model of traumatic brain injury. Cognitive function, cell survival and differentiation, brain tissue morphology and neurotrophin expression were compared between groups. Significant improvements in cognitive function and brain tissue morphology were seen in the HUMSCs group compared with HUMSC-N...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5192976</comments>
            <pubDate>Mon, 29 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5192976</guid>        </item>
        <item>
            <title>Effect of Phenolic Compounds Against Aβ Aggregation and Aβ-Induced Toxicity in Transgenic C. elegans.</title>
            <link>http://www.medworm.com/index.php?rid=5157382&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21858698%26dopt%3DAbstract</link>
            <description>Authors: Jagota S, Rajadas J
    Abstract
    Substantial evidence suggests that the aggregation of amyloid-β (Aβ) peptide into fibrillar structures that is rich in β-sheets is implicated as the cause of Alzheimer's disease. Therefore, an attractive therapeutic strategy is to prevent or alter Aβ aggregation. Phenolic compounds are natural substances that are composed of one or more aromatic phenolic rings and present in wine, tea, fruits, vegetables and a wide variety of plants. In this work, we investigated the effects of ferulic acid, morin, quercetin and gossypol against Aβ aggregation. From the ThT and turbidity assays, it is observed that in addition to the fibril aggregate, another type of aggregate is formed in the presence of morin, quercetin, and gossypol. On the other hand, ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157382</comments>
            <pubDate>Sat, 20 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157382</guid>        </item>
        <item>
            <title>Hydrolysis of Substance P in the Presence of the Osteosarcoma Cell Line SaOS-2: Release of Free Amino Acids.</title>
            <link>http://www.medworm.com/index.php?rid=5157381&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21858699%26dopt%3DAbstract</link>
            <description>Authors: Cavazza A, Marini M, Roda LG, Tarantino U, Valenti A
    Abstract
    The possible hydrolysis of substance P (Arg-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gly-Leu-Met) in presence of the osteoblastic cell line SaOS-2 was measured by capillary electrophoresis coupled to mass detection. The results obtained indicate that a very rapid disappearance of the intact undecapeptide was associated to a slower appearance of seven of its eight component amino acids. These results can be interpreted as indicating that an extremely fast hydrolysis of substance P by endopeptidases, which released peptidic by-products, was followed by a noticeably slower secondary degradation which released free amino acids. In decreasing quantitative importance, these phenomena appear to originate by the hydrolysis of the Pr...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157381</comments>
            <pubDate>Sat, 20 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157381</guid>        </item>
        <item>
            <title>Distribution of TRPC6 in the Cerebrospinal Fluid-Contacting Nucleus of Rat Brain Parenchyma and its Expression in Morphine Dependence and Withdrawal.</title>
            <link>http://www.medworm.com/index.php?rid=5157383&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21858483%26dopt%3DAbstract</link>
            <description>Authors: Wu TT, Zhao ZJ, Xu C, Zhang LC
    Abstract
    To investigate the role of cerebrospinal fluid contacting nucleus (CSF-CN) and the changes of TRPC6 expression in morphine dependence and withdrawal. Male Sprague-Dawley rats (250 ± 50 g) were randomly divided into four groups: the normal group (N); the saline group (S); the morphine dependence group (D); the morphine withdrawal group (W). All animals in each group were tested the morphine withdrawal-like behavioral signs by total withdrawal scores. Double-labeled immunofluorescent technique and laser scanning confocal microscopy were used to identify the expression of TRPC6 in CSF-CN. TRPC6 labeled neurons were found in CSF-CN and the number of CB-HRP/TRPC6 double labeled neurons in CSF-CN significantly increased. TRPC6 existed i...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157383</comments>
            <pubDate>Fri, 19 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157383</guid>        </item>
        <item>
            <title>Resveratrol Pretreatment Attenuates Cerebral Ischemic Injury by Upregulating Expression of Transcription Factor Nrf2 and HO-1 in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5141466&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21850487%26dopt%3DAbstract</link>
            <description>Authors: Ren J, Fan C, Chen N, Huang J, Yang Q
    Abstract
    Oxidative stress damage plays a vital role in cerebral ischemia/reperfusion (I/R) pathogenesis. The nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway can be activated by pharmacological and dietary means to attenuate cellular oxidative stress. Resveratrol, a plant-derived polyphenolic compound, has antioxidant property. Recent studies have demonstrated that resveratrol has protective effects against cerebral I/R injury. However, little is known about its mechanism. Hence, this study identified the neuroprotective effect of resveratrol pretreatment and elucidate the Nrf2/ARE signaling mechanism after focal cerebral I/R injury in rats. Adult male Sprague-Dawley rats were rand...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141466</comments>
            <pubDate>Wed, 17 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141466</guid>        </item>
        <item>
            <title>The Hypothalamic Proline-Rich Polypeptide-1 (Galarmin) and its Analogue d-15 are the Inhibitors of Protein Tyrosine Kinase Activity at Cyclophosphamide-Induced Lymphocytopenia.</title>
            <link>http://www.medworm.com/index.php?rid=5141467&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21842394%26dopt%3DAbstract</link>
            <description>Authors: Kirakosova AS, Abrahamyan SS, Tumasyan NV, Davtyan TK, Khachatryan AR, Galoyan AA
    PMID: 21842394 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141467</comments>
            <pubDate>Sat, 13 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141467</guid>        </item>
        <item>
            <title>Long-term Effects of Recurrent Neonatal Seizures on Neurobehavioral Function and Related Gene Expression and Its Intervention by Inhibitor of Cathepsin B.</title>
            <link>http://www.medworm.com/index.php?rid=5141473&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21842268%26dopt%3DAbstract</link>
            <description>We examined the expression pattern of autophagy-related genes at acute phase after the last seizures using western blot method, and evaluated behavioral deficits during postnatal day 28 (P28) to P35. The results showed improved neurological scores and learning ability in CBI-treated rats compared with the nontreated control. Flurothyl-induced increases in the ratio of LC3-II/LC3-I, Beclin-1 and Cathepsin-B were blocked by pre-treatment with CBI at 1.5, 3, 6 and 24 h after the last seizures in hippocampus and cerebral cortex by western blot analysis. Meanwhile, CBI also reversed flurothyl-induced down-regulation of Bcl-2 protein levels. Furthermore, in the long-term time point of 35 days (P35), PRG-1 mRNA and protein level in hippocampus and cerebral cortex of recurrent seizure group were...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141473</comments>
            <pubDate>Fri, 12 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141473</guid>        </item>
        <item>
            <title>Profile of Nucleotide Catabolism and Ectonucleotidase Expression from the Hippocampi of Neonatal Rats After Caffeine Exposure.</title>
            <link>http://www.medworm.com/index.php?rid=5141472&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21842269%26dopt%3DAbstract</link>
            <description>Authors: Da Silva RS, Richetti SK, Tonial EM, Bogo MR, Bonan CD
    Abstract
    Nucleotides and nucleosides play an important role in neurodevelopment acting through specific receptors. Ectonucleotidases are the major enzymes involved in controlling the availability of purinergic receptors ligands. ATP is co-released with several neurotransmitters and is the most important source of extracellular adenosine by catabolism exerted by ectonucleotidases. The main ectonucleotidases are named NTPDases (1-8) and 5'-nucleotidase. Adenosine is a powerful modulator of neurotransmitter release. Caffeine blocks adenosine receptor activity as well as adenosine-mediated neuromodulation. Considering the susceptibility of the immature brain to caffeine and the need for correct purinergic signaling during ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141472</comments>
            <pubDate>Fri, 12 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141472</guid>        </item>
        <item>
            <title>Increased Phosphorylation of Tau and Synaptic Protein Loss in the Aged Transgenic Mice Expressing Familiar Alzheimer's Disease-Linked Presenilin 1 Mutation.</title>
            <link>http://www.medworm.com/index.php?rid=5141471&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21842270%26dopt%3DAbstract</link>
            <description>In this study, we further examined the in vivo effects of PS-1 mutation on tau and synapse protein markers. The data showed that the phosphorylation of tau at Ser396, Ser404, Thr231 and Tau-1 (Ser198/199/202) epitopes was significantly increased in hippocampus of the aged (twenty-one and a half-month-old) transgenic mice expressing PS-1 (L235P) compared to that of the age-matched wild-type littermates (WTs). Concurrently, a significant decrease in the phosphorylation of glycogen synthase kinase (GSK)-3β at Ser9 was observed. The above changes were not observed in the young transgenic mice (6-8 months old). No significant changes in the levels of cyclin-dependent kinase (CDK)-5, its co-activator p35, and phosphorylation of protein phosphatase (PP)-2A catalytic subunit at Tyrosine 307 (Y30...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141471</comments>
            <pubDate>Fri, 12 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141471</guid>        </item>
        <item>
            <title>Retinal Metabolic Changes in an Experimental Model of Optic Nerve Transection by Ex Vivo (1)H Magnetic Resonance Spectroscopy.</title>
            <link>http://www.medworm.com/index.php?rid=5141470&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21842271%26dopt%3DAbstract</link>
            <description>This study aims to investigate the retinal metabolic processes in a rat axotomy model. Retinal metabolic changes in optic nerve transection (ONT) rat model were analyzed by (1)H magnetic resonance spectroscopy ((1)H-MRS). Retinal ganglion cells (RGCs) densities were assessed from retinal whole mounts. The retina was stained immunohistochemically with glial fibrillary acidic protein (GFAP). The results showed that the retina in ONT rats had significantly decreased concentrations of γ-aminobutyric acid (GABA), N-acetylaspartate (NAA), taurine (Tau), creatine (Cr) and increased concentrations of alanine (Ala) compared with control. Examination of glutamate (Glu), glutamine (Gln) and Glx (Glu + Gln) concentrations disclosed no significant differences. The mean density of RGCs reduced from 2...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141470</comments>
            <pubDate>Fri, 12 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141470</guid>        </item>
        <item>
            <title>Time-Course Alterations of Toll-Like Receptor 4 and NF-κB p65, and Their Co-Expression in the Gerbil Hippocampal CA1 Region After Transient Cerebral Ischemia.</title>
            <link>http://www.medworm.com/index.php?rid=5141469&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21842272%26dopt%3DAbstract</link>
            <description>Authors: Yoo KY, Yoo DY, Hwang IK, Park JH, Lee CH, Choi JH, Kwon SH, Her S, Lee YL, Won MH
    Abstract
    Innate immune system is very important to modulate the host defense against a large variety of pathogens. Toll-like receptors (TLRs) play a key role in controlling innate immune response. Among TLRs, TLR4 is a specific receptor for lipopolysaccharide and associated with the release of pro-inflammatory cytokines. In the present study, we investigated ischemia-related changes of TLR4 immunoreactivity and its protein level, and nuclear factor κB (NF-κB) p65 immunoreactivity regarding inflammatory responses in the hippocampal CA1 region after 5 min of transient cerebral ischemia to identify the correlation between transient ischemia and inflammation. In the sham-operated group, TLR4 ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141469</comments>
            <pubDate>Fri, 12 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141469</guid>        </item>
        <item>
            <title>Neuroprotective Potential of Biphalin, Multireceptor Opioid Peptide, Against Excitotoxic Injury in Hippocampal Organotypic Culture.</title>
            <link>http://www.medworm.com/index.php?rid=5141468&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21842273%26dopt%3DAbstract</link>
            <description>Authors: Kawalec M, Kowalczyk JE, Beresewicz M, Lipkowski AW, Zablocka B
    Abstract
    Biphalin is a dimeric opioid peptide that exhibits affinity for three types of opioid receptors (MOP, DOP and KOP). Biphalin is undergoing intensive preclinical study. It was recognized that activation of δ-opioid receptor elicits neuroprotection against brain hypoxia and ischemia. We compare the effect of biphalin and morphine and the inhibition of opioid receptors by naltrexone on survival of neurons in rat organotypic hippocampal cultures challenged with NMDA. Findings: (1) 0.025-0.1 μM biphalin reduces NMDA-induced neuronal damage; (2) biphalin neuroprotection is abolished by naltrexone; (3) reduced number of dead cells is shown even if biphalin is applied with delay after NMDA challenge.
    P...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141468</comments>
            <pubDate>Fri, 12 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141468</guid>        </item>
        <item>
            <title>Role of Signal Transducer and Activator of Transcription-3 in Up-Regulation of GFAP After Epilepsy.</title>
            <link>http://www.medworm.com/index.php?rid=5141479&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21833841%26dopt%3DAbstract</link>
            <description>In this study, we measured p-STAT3 and GFAP expression during the epileptic process using immunohistochemistry, Western blotting and immunofluorescence. Both p-STAT3 and GFAP expression were highly expressed in the rat hippocampus during different phases of the epileptic process. The augmentation of GFAP expression was inhibited by AG490, a janus kinase 2 (JAK2, an upstream gene of STAT3) inhibitor. The coexpression of p-STAT3 and GFAP was detected in the epileptic rat hippocampus and temporal neocortex of patients. These findings indicate that epilepsy involves the activation of STAT3 that up-regulates the expression of GFAP, which may play an important role in epileptogenesis.
    PMID: 21833841 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141479</comments>
            <pubDate>Wed, 10 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141479</guid>        </item>
        <item>
            <title>Carnosic Acid, a Rosemary Phenolic Compound, Induces Apoptosis Through Reactive Oxygen Species-Mediated p38 Activation in Human Neuroblastoma IMR-32 Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5141478&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21833842%26dopt%3DAbstract</link>
            <description>In conclusion, ROS-mediated p38 MAPK activation plays a critical role in CA-induced apoptosis in IMR-32 cells.
    PMID: 21833842 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141478</comments>
            <pubDate>Wed, 10 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141478</guid>        </item>
        <item>
            <title>Na(+)/HCO(3) (-) Cotransporter Immunoreactivity Changes in Neurons and Expresses in Astrocytes in the Gerbil Hippocampal CA1 Region After Ischemia/Reperfusion.</title>
            <link>http://www.medworm.com/index.php?rid=5141477&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21833843%26dopt%3DAbstract</link>
            <description>We examined the alterations of NBC immunoreactivity and its protein levels in the hippocampal CA1 region after transient cerebral ischemia in gerbils. In the sham-operated group, moderate NBC immunoreactivity was detected in CA1 pyramidal neurons, and, 12 h after I/R, the immunoreactivity in the pyramidal neurons was markedly increased over controls. Three days after I/R, NBC immunoreactivity nearly disappeared in the CA1 pyramidal neurons. However, NBC immunoreactivity was detected in the non-pyramidal neurons of the ischemic CA1 region at 3 days after I/R. From double immunofluorescence study with glial markers, NBC immunoreactivity was detected in astrocytes, not in microglia, at 4 days after I/R. NBC protein level in the CA1 region was significantly increased at 12 h post-ischemia ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141477</comments>
            <pubDate>Wed, 10 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141477</guid>        </item>
        <item>
            <title>Depletion of Nrf2 Enhances Inflammation Induced by Oxyhemoglobin in Cultured Mice Astrocytes.</title>
            <link>http://www.medworm.com/index.php?rid=5141476&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21833844%26dopt%3DAbstract</link>
            <description>Authors: Pan H, Wang H, Zhu L, Mao L, Qiao L, Su X
    Abstract
    Nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element pathway has been proved to be the key regulator in reducing inflammatory damage, which is involved in subarachnoid hemorrhage (SAH). Here, in a traditional in vitro SAH model, we investigated the effect of Nrf2 depletion on pro-inflammatory cytokines production. Primary cultured astrocytes from Nrf2 wild type (WT) or knockout (KO) mouse were exposed or not exposed to oxyhemoglobin (OxyHb). Then the DNA-binding activity of transcription factor nuclear factor-κB (NF-κB) was detected by EMSA. The expression of TNF-α, IL-1β, IL-6 and MMP9 were evaluated. The activity of MMP9 was measured by Gelatin zymography. After exposure to OxyHb, NF-κB wa...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141476</comments>
            <pubDate>Wed, 10 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141476</guid>        </item>
        <item>
            <title>Downregulation of Hippocampal GABA after Hypoxia-Induced Seizures in Neonatal Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5141475&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21833845%26dopt%3DAbstract</link>
            <description>This study aims to determine the expression of Gamma-aminobutyric acid (GABA) following hypoxia in neonatal rats and explore how it may increase susceptibility to epilepsy later in life. A modified model of neonatal hypoxia-induced epileptic susceptibility was simulated by 17 min of hypoxia (5% O(2) and 95% N(2)) in postnatal day (P) 10 rats. Hippocampal glutamate decarboxylase (GAD) and parvalbumin (PV) during the development with or without hypoxia were examined using immunohistochemistry. No detectable neuronal loss was observed in the hippocampus either immediately or 14 days after hypoxia. During the development GAD- and PV-immunoreactivity increased substantially during P 11-13 and reached mature expression in the control rats, and decreased significantly at different time points e...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141475</comments>
            <pubDate>Wed, 10 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141475</guid>        </item>
        <item>
            <title>NAD(+) Treatment Induces Delayed Autophagy in Neuro2a Cells Partially by Increasing Oxidative Stress.</title>
            <link>http://www.medworm.com/index.php?rid=5141474&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21833846%26dopt%3DAbstract</link>
            <description>In this study, we reported that treatment of NAD(+) induces delayed autophagy in Neuro2a cells. Moreover, the effects of NAD(+) on the autophagy in the cells appear to be, at least partially, mediated by oxidative stress. However, nicotinamide, a degradation product of NAD(+), does not affect the autophagy. Our experiments have further indicated that the NAD(+)-induced autophagy contributes to the NAD(+)-induced decrease in the survival of these cells. In summary, our study has provided the first evidence that NAD(+) treatment induces autophagy in cancer cells such as Neuro2a cells, which contributes to the NAD(+)-induced decrease in cancer cell survival.
    PMID: 21833846 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141474</comments>
            <pubDate>Wed, 10 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141474</guid>        </item>
        <item>
            <title>[+]-Huperzine A Protects Against Soman Toxicity in Guinea Pigs.</title>
            <link>http://www.medworm.com/index.php?rid=5141482&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21822920%26dopt%3DAbstract</link>
            <description>In this study, we evaluated the efficacy of [+]-Huperzine A for protection against soman toxicity in guinea pigs. Pretreatments with [+]-Huperzine A, i.m., significantly increased the survival rate in a dose-dependent manner against 1.2× LD(50) soman exposures. Behavioral signs of soman toxicity were significantly reduced in 20 and 40 mg/kg [+]-Huperzine A treated animals at 4 and 24 h compared to vehicle and PB controls. Electroencephalogram (EEG) power spectral analysis showed that [+]-Huperzine A significantly reduces soman-induced seizure compared to PB. [+]-Huperzine A (40 mg/kg) preserved higher blood and brain AChE activity compared to PB in soman exposed animals. These data suggest that [+]-Huperzine A protects against soman toxicity stronger than PB and warrant further develo...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141482</comments>
            <pubDate>Sat, 06 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141482</guid>        </item>
        <item>
            <title>Antioxidants Prevent Memory Deficits Provoked by Chronic Variable Stress in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5141481&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21822921%26dopt%3DAbstract</link>
            <description>Authors: Tagliari B, Scherer EB, Machado FR, Ferreira AG, Dalmaz C, Wyse AT
    Abstract
    Learning and memory deficits occur in depression and other stress related disorders. Although the pathogenesis of cognitive impairment after stress has not been fully elucidated, factors such as oxidative stress and neurotrophins are thought to play possible roles. Here we investigated the effect of treatment with vitamin E (40 mg/kg) and vitamin C (100 mg/kg) on the effects elicited by chronic variable stress on rat performance in Morris water maze. Brain-derived neurotrophic factor (BDNF) immunocontent was also evaluated in hippocampus of rats. Sixty-day old Wistar rats were submitted to different stressors for 40 days (stressed group). Half of stressed group received administration of vitamin...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141481</comments>
            <pubDate>Sat, 06 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141481</guid>        </item>
        <item>
            <title>Soluble NgR Fusion Protein Modulates the Proliferation of Neural Progenitor Cells via the Notch Pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5141480&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21822922%26dopt%3DAbstract</link>
            <description>Authors: Li X, Su H, Fu QL, Guo J, Lee DH, So KF, Wu W
    Abstract
    NogoA, myelin-associated glycoprotein (MAG) and oligodendrocyte myelin glycoprotein are CNS myelin molecules that bind to the neuronal Nogo-66 receptor (NgR) and inhibit axon growth. The NgR antagonist, soluble NgR1-Fc protein (sNgR-Fc), facilitates axon regeneration by neutralizing the inhibitory effects of myelin proteins in experimental models of CNS injury. Here we aim to investigate the effect of sNgR-Fc on the proliferation of neural progenitor cells (NPCs). The hippocampus cells of embryonic rats were isolated and cultured in vitro. The expression of nestin, βIII-Tubulin, GFAP and Nogo-A on these cells was observed using immunocytochemistry. In order to investigate the effect on proliferation of NPCs, sNgR-Fc, ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141480</comments>
            <pubDate>Sat, 06 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141480</guid>        </item>
        <item>
            <title>Reduced Cell Proliferation and Neuroblast Differentiation in the Dentate Gyrus of High Fat Diet-Fed Mice are Ameliorated by Metformin and Glimepiride Treatment.</title>
            <link>http://www.medworm.com/index.php?rid=5103576&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21818657%26dopt%3DAbstract</link>
            <description>Authors: Yoo DY, Kim W, Nam SM, Yoo KY, Lee CH, Choi JH, Won MH, Hwang IK, Yoon YS
    We investigated the effects of a high-fat diet (HFD) and the subsequent treatment of metformin (met) and glimepiride (glim), which are widely prescribed for type 2 diabetes, on cell proliferation and neuroblast differentiation using Ki67 and doublecortin (DCX) immunohistochemistry, respectively. Animals were fed low-fat diet (LFD) or HFD for 8 weeks. After 5 weeks of the HFD treatment, met alone or met + glim was administered orally once a day for 3 weeks. Body weight and food intake were much higher in the HFD + vehicle-treated group than the LFD-treated group. The administration of met or met + glim to the HFD-treated group resulted in a decrease in weight gain and food intake. Ki67-immunoreac...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103576</comments>
            <pubDate>Thu, 04 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103576</guid>        </item>
        <item>
            <title>Dopamine Content in the Striatum and Expression Changes of Bad and Bcl-2 in Elderly Rats with Abnormal Behavior.</title>
            <link>http://www.medworm.com/index.php?rid=5103575&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21818658%26dopt%3DAbstract</link>
            <description>Authors: Yu ZQ, Liu MY, Ren QX, Xiong Y, Xu JH, Xiao CH, Gao DS
    To determine the dopamine (DA) content in the striatum and the expression changes of the apoptosis-associated proteins Bad and Bcl-2 in the substantia nigra compacta (SNc) in elderly rats with abnormal behavior. Fifty three Sprague-Dawley rats were divided into three groups: adult, age-motorplus (normal behavior) and aged-motorminus (abnormal behavior) using the hanger test. The DA content in the striatum and the expression of tyrosine hydroxylase (TH), Bad and Bcl-2 in the SNc were measured by HPLC/MS (high performance liquid chromatogram-mass spectra) and Western Blot. (1) The results from the hanger test demonstrated that the scores and latency of aged-motorminus group were lower than the age-motorplus group. (2) Result...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103575</comments>
            <pubDate>Thu, 04 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103575</guid>        </item>
        <item>
            <title>The Effects of Single and Repeated Exposure to 2.45 GHz Radiofrequency Fields on c-Fos Protein Expression in the Paraventricular Nucleus of Rat Hypothalamus.</title>
            <link>http://www.medworm.com/index.php?rid=5103574&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21818659%26dopt%3DAbstract</link>
            <description>This study investigated the effects of microwave radiation on the PVN of the hypothalamus, extracted from rat brains. Expression of c-Fos was used to study the pattern of cellular activation in rats exposed once or repeatedly (ten times in 2 weeks) to 2.45 GHz radiation in a GTEM cell. The power intensities used were 3 and 12 W and the Finite Difference Time Domain calculation was used to determine the specific absorption rate (SAR). High SAR triggered an increase of the c-Fos marker 90 min or 24 h after radiation, and low SAR resulted in c-Fos counts higher than in control rats after 24 h. Repeated irradiation at 3 W increased cellular activation of PVN by more than 100% compared to animals subjected to acute irradiation and to repeated non-radiated repeated session control animals...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103574</comments>
            <pubDate>Thu, 04 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103574</guid>        </item>
        <item>
            <title>Expression of Matrix Metalloproteinase-9, Type IV Collagen and Vascular Endothelial Growth Factor in Adamantinous Craniopharyngioma.</title>
            <link>http://www.medworm.com/index.php?rid=5103577&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21814723%26dopt%3DAbstract</link>
            <description>Authors: Xia Z, Liu W, Li S, Jia G, Zhang Y, Li C, Ma Z, Tian J, Gong J
    To explore the expression of matrix metalloproteinase 9 (MMP-9), type IV collagen (Col IV) and vascular endothelial growth factor (VEGF) in adamantinomatous craniopharyngioma (ACP) and analyze the correlation between the level of these markers and adamantimous craniopharyngiomas recurrence. Expressions of MMP-9, Col IV and VEGF were tested by immunohistochemistry (IHC) in 40 cases of ACP, including 24 cases of primary group and 16 cases of recurred group. The expression level of MMP-9 and VEGF in recurred group were significantly higher than primary group (93.7% vs. 41.7%, P &amp;lt; 0.05, 87.5% vs. 45.8%, P &amp;lt; 0.05, respectively). The expression of Col IV in the recurred group was significant different from the ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103577</comments>
            <pubDate>Wed, 03 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103577</guid>        </item>
        <item>
            <title>Postnatal Nitric Oxide Inhibition Modifies Neurotensin Effect on ATPase Activity.</title>
            <link>http://www.medworm.com/index.php?rid=5103578&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21800170%26dopt%3DAbstract</link>
            <description>Authors: López Ordieres MG, Alvarez-Juliá A, Kemmling A, Rodríguez de Lores Arnaiz G
    We have previously showed that peptide neurotensin inhibits neuronal Na(+), K(+)-ATPase activity, an effect which involves high affinity neurotensin receptor. Nitric oxide (NO) acts as a neurotransmitter or as a neuromodulator when it is synthesized by neuronal nitric oxide synthase. Neurotensin effect on Na(+), K(+)-ATPase activity was evaluated in cortical synaptosomal membranes isolated from rats injected at 3, 4 and 5 postnatal days with saline (control) or N (ω)-nitro-L: -arginine methyl esther (L-NAME), a nitric oxide synthase inhibitor. Assays were carried out at two stages: juvenile (35 days) and adult (56 days) ages. In an open field task, results recorded in juvenile rats markedly diffe...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103578</comments>
            <pubDate>Thu, 28 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103578</guid>        </item>
        <item>
            <title>Physical Exercise Reverses Cognitive Impairment in Rats Subjected to Experimental Hyperprolinemia.</title>
            <link>http://www.medworm.com/index.php?rid=5103581&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21792675%26dopt%3DAbstract</link>
            <description>This study investigated whether physical exercise would reverse proline-induced performance deficits in water maze tasks, as well as its effects on brain-derived neurotrophic factor (BDNF) immunocontent and brain acetylcholinesterase (AChE) activity in Wistar rats. Proline administration followed partial time (6th-29th day of life) or full time (6th-60th day of life) protocols. Treadmill exercise was performed from 30th to 60th day of life, when behavioral testing was started. After that, animals were sacrificed for BDNF and AChE determination. Results show that proline impairs cognitive performance, decreases BDNF in cerebral cortex and hippocampus and increases AChE activity in hippocampus. All reported effects were prevented by exercise. These results suggest that cognitive, spatial lea...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103581</comments>
            <pubDate>Tue, 26 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103581</guid>        </item>
        <item>
            <title>Hyperacute Detection of Neurofilament Heavy Chain in Serum Following Stroke: A Transient Sign.</title>
            <link>http://www.medworm.com/index.php?rid=5103580&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21792676%26dopt%3DAbstract</link>
            <description>Authors: Sellner J, Patel A, Dassan P, Brown MM, Petzold A
    Serological biomarkers which enable quick and reliable diagnosis or measurement of the extent of irreversible brain injury early in the course of stroke are eagerly awaited. Neurofilaments (Nf) are a group of proteins integrated into the scaffolding of the neuronal and axonal cytoskeleton and an established biomarker of neuro-axonal damage. The Nf heavy chain (NfH(SMI35)) was assessed together with brain-specific astroglial proteins GFAP and S100B in hyperacute stroke (6 and 24 h from symptom onset) and daily for up to 6 days. Twenty-two patients with suspected stroke (median NIHSS 8) were recruited in a prospective observational study. Evidence for an ischaemic or haemorrhagic lesion on neuroimaging was found in 18 (ischaemi...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103580</comments>
            <pubDate>Tue, 26 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103580</guid>        </item>
        <item>
            <title>Activation of Adenosine A2(A) Receptor Up-Regulates BDNF Expression in Rat Primary Cortical Neurons.</title>
            <link>http://www.medworm.com/index.php?rid=5103579&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21792677%26dopt%3DAbstract</link>
            <description>In this study, we investigated the possibility that the activation of A2(A) receptor modulates BDNF production in rat primary cortical neuron. CGS21680, an adenosine A2(A) receptor agonist, induced BDNF expression and release. An antagonist against A2(A) receptor, ZM241385, prevented CGS21680-induced increase in BDNF production. A2(A) receptor stimulation induced the activation of Akt-GSK-3β signaling pathway and the blockade of the signaling pathway with specific inhibitors abolished the increase in BDNF production, possibly via modulation of ERK1/2-CREB pathway. The physiological roles of A2(A) receptor-induced BDNF production was demonstrated by the protection of neurons from the excitotoxicity and increased neurite extension as well as synapse formation from immature and mature neuron...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103579</comments>
            <pubDate>Tue, 26 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103579</guid>        </item>
        <item>
            <title>Valproic Acid Induced Differentiation and Potentiated Efficacy of Taxol and Nanotaxol for Controlling Growth of Human Glioblastoma LN18 and T98G Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5103583&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21786169%26dopt%3DAbstract</link>
            <description>We examined the efficacy of combination of valproic acid (VPA) and taxol (TX) or nanotaxol (NTX) in human glioblastoma LN18 and T98G cell lines. Cell differentiation was manifested in changes in morphological features and biochemical markers. Cell growth was controlled with down regulation of vascular endothelial growth factor (VEGF), epidermal growth factor receptor (EGFR), nuclear factor-kappa B (NF-κB), phospho-Akt (p-Akt), and multi-drug resistance (MDR) marker, indicating suppression of angiogenic, survival, and multi-drug resistance pathways. Cell cycle analysis showed that combination therapy (VPA and TX or NTX) increased the apoptotic sub G1 population and apoptosis was further confirmed by Annexin V-FITC/PI binding assay and scanning electron microscopy. Combination therapy cause...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103583</comments>
            <pubDate>Sat, 23 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103583</guid>        </item>
        <item>
            <title>Gelsolin in Cerebrospinal Fluid as a Potential Biomarker of Epilepsy.</title>
            <link>http://www.medworm.com/index.php?rid=5103582&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21786170%26dopt%3DAbstract</link>
            <description>In this study we found that lumbar CSF-gelsolin concentrations markedly decreased in epileptic patients by enzyme linked immunosorbent assay. In order to help judge the result, we determined gelsolin expression in temporal lobe tissues of patients with temporal lobe epilepsy using double-label immunofluorescence to location and using western blot to quantitation. Then we observed that gelsolin was co-expressed with microtubule-associated protein-2 in axons and cytoplasms of neurons and gelsolin protein level was also down-regulated in temporal lobe tissues of epileptic patients. Our findings suggested that CSF-gelsolin level might reflect the alteration of gelsolin in brain tissue of epileptic patients and CSF-gelsolin seems to be a potential biomarker for epilepsy.
    PMID: 21786170 [Pub...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103582</comments>
            <pubDate>Sat, 23 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103582</guid>        </item>
        <item>
            <title>Differentiation and Neuro-Protective Properties of Immortalized Human Tooth Germ Stem Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5103585&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21785835%26dopt%3DAbstract</link>
            <description>This study evaluated the expression of stem cell markers, surface antigens, differentiation capacity, and karyotype of hTGSCs that have been immortalized by human telomerase reverse transcriptase (hTERT) or simian vacuolating virus 40 (SV40) large T antigen. These undying cells were also evaluated for their neuro-protective potential using an in vitro SH-SY5Y neuro-blastoma model treated with hydrogen-peroxide or doxo-rubicin. Although hTGSC-SV40 showed abnormal karyotypes, our results suggest that hTGSC-hTERT preserve their MSC characteristics, differentiation capacity and normal karyotype, and they also possess high proliferation rate and neuro-protective effects even at great passage numbers. These peculiars indicate that hTGSC-hTERT could be used as a viable model for studying adipo-, ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103585</comments>
            <pubDate>Thu, 21 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103585</guid>        </item>
        <item>
            <title>Quinoprotein Adducts Accumulate in the Substantia Nigra of Aged Rats and Correlate with Dopamine-Induced Toxicity in SH-SY5Y Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5103584&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21785836%26dopt%3DAbstract</link>
            <description>Authors: Wang N, Wang Y, Yu G, Yuan C, Ma J
    Parkinson's disease (PD) is an age-dependent neurodegenerative disorder characterized by dopaminergic neuron loss in substantia nigra. Previous studies have implicated a role of dopamine oxidation in PD. Dopamine oxidation leads to the formation of dopamine quinone, which generates reactive oxygen species and covalently modifies cysteinyl proteins to form quinoprotein adduct. We compared quinoprotein adduct formation and lipid peroxidation in different brain regions of young and old rats. We found a prominent age-dependent accumulation of quinoprotein adducts in the substantia nigra, while no significant change of lipid peroxidation was detected in any brain regions of 2- to 15-month old rats. To determine whether quinoprotein adduct formatio...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103584</comments>
            <pubDate>Thu, 21 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103584</guid>        </item>
        <item>
            <title>Effects of Zingerone [4-(4-Hydroxy-3-Methoxyphenyl)-2-Butanone] and Eugenol [2-Methoxy-4-(2-Propenyl)Phenol] on the Pathological Progress in the 6-Hydroxydopamine-Induced Parkinson's Disease Mouse Model.</title>
            <link>http://www.medworm.com/index.php?rid=5056842&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21769642%26dopt%3DAbstract</link>
            <description>Authors: Kabuto H, Yamanushi TT
    Parkinson's disease (PD) is characterized by progressive degeneration of dopaminergic neurons in the nigrostriatal system and dopamine (DA) depletion in the striatum. The most popular therapeutic medicine for treating PD, 3-(3,4-Dihydroxyphenyl)-L: -alanine (L-DOPA), has adverse effects, such as dyskinesia and disease acceleration. As superoxide (·O(2) (-)) and hydroxyl radical (·OH) have been implicated in the pathogenesis of PD, free radical scavenging and antioxidants have attracted attention as agents to prevent disease progression. Rodents injected with 6-hydroxydopamine (6-OHDA) intracerebroventricularly are considered to be a good animal model of PD. Zingerone and eugenol, essential oils extracted from ginger and cloves, are known to have free r...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5056842</comments>
            <pubDate>Mon, 18 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5056842</guid>        </item>
        <item>
            <title>Neuroprotective Effect of Salvia sahendica is Mediated by Restoration of Mitochondrial Function and Inhibition of Endoplasmic Reticulum Stress.</title>
            <link>http://www.medworm.com/index.php?rid=5056841&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21769643%26dopt%3DAbstract</link>
            <description>Authors: Shaerzadeh F, Alamdary SZ, Esmaeili MA, Sarvestani NN, Khodagholi F
    Herein, we investigated the protective effect of Salvia sahendica against H(2)O(2)-induced cell death in rat pheochromocytoma (PC12) cells. Our data show that S. sahendica blocks apoptosis pathway by inhibition of cytochrome c release from mitochondria and leakage of calcium from endoplasmic reticulum. It also activates/inactivates two members of Bcl-2 family, Bax and Bcl-2. Bax inhibition and Bcl-2 activation suppress release of cytochrome c from mitochondria that prevents cleavage of caspase-3. Besides S. sahendica suppresses ER stress via attenuation of intracellular levels of calcium. Suppression of ER stress decreased calpain activation and subsequently cleavage of caspase-12. Altogether, these results in...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5056841</comments>
            <pubDate>Fri, 15 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5056841</guid>        </item>
        <item>
            <title>The Neuroprotective Effect of Curcumin and Nigella sativa Oil Against Oxidative Stress in the Pilocarpine Model of Epilepsy: A Comparison with Valproate.</title>
            <link>http://www.medworm.com/index.php?rid=5056843&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21751034%26dopt%3DAbstract</link>
            <description>This study reflects the promising anticonvulsant and potent antioxidant effects of curcumin and NSO in reducing oxidative stress, excitability and the induction of seizures in epileptic animals and improving some of the adverse effects of antiepileptic drugs.
    PMID: 21751034 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5056843</comments>
            <pubDate>Tue, 12 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5056843</guid>        </item>
        <item>
            <title>A Theory and a Model to Understand Glioblastoma Development Both in the Bulk and in the Microinfiltrated Brain Parenchyma.</title>
            <link>http://www.medworm.com/index.php?rid=5056846&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21739256%26dopt%3DAbstract</link>
            <description>Authors: Brognaro E
    The prognosis of patients affected by glioblastoma remains dismal despite many efforts have been devoted worldwide in research and therapeutic strategies. Reasons of our failure include the fact that the patient harboring a glioblastoma always has two problems inside the brain, the bulk tumor and the parenchyma microinfiltrated; the other reason is that the tumor is able to grow dynamically adapting to the mutated conditions of its growth microenvironment. This paper tries to give an interpretation to the dynamic process of the tumor growth, from the beginning to the end of its natural history, dividing it in three phases, one pre-hypoxia and two post-hypoxia, and these are then correlated with the types of cancer stem cells (CSCs) involved. Furthermore, the paper p...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5056846</comments>
            <pubDate>Thu, 07 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5056846</guid>        </item>
        <item>
            <title>Endogenous Hydrogen Sulfide is Involved in Asymmetric Dimethylarginine-induced Protection Against Neurotoxicity of 1-Methyl-4-phenyl-pyridinium Ion.</title>
            <link>http://www.medworm.com/index.php?rid=5056845&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21748658%26dopt%3DAbstract</link>
            <description>This study is to assess the potential role of endogenous H(2)S in the neuroprotection of ADMA against MPP(+)-induced toxicity in PC12 cells. We showed that ADMA prevented MPP(+)-induced inhibition of endogenous H(2)S generation through inhibiting the down-regulation of cystathionine-β-synthetase (CBS, the major enzyme responsible for endogenous H(2)S generation in PC12 cells) expression and activity elicited by MPP(+). ADMA obviously attenuated MPP(+)-triggered accumulation of intracellular ROS, dissipation of mitochondrial membrane potential (MMP), release of cytochrome c (Cyt-c), and downregulation of Bcl-2 protein expression in PC12 cells. Inhibition of CBS activity by amino-oxyacetate and CBS silencing with a short hairpin RNA vector targeting rat CBS gene reversed the protective acti...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5056845</comments>
            <pubDate>Wed, 06 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5056845</guid>        </item>
        <item>
            <title>p53- and Bax-Mediated Apoptosis in Injured Rat Spinal Cord.</title>
            <link>http://www.medworm.com/index.php?rid=5056844&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21748659%26dopt%3DAbstract</link>
            <description>Authors: Kotipatruni RR, Dasari VR, Veeravalli KK, Dinh DH, Fassett D, Rao JS
    Spinal cord injury (SCI) induces a series of endogenous biochemical changes that lead to secondary degeneration, including apoptosis. p53-mediated mitochondrial apoptosis is likely to be an important mechanism of cell death in spinal cord injury. However, the signaling cascades that are activated before DNA fragmentation have not yet been determined. DNA damage-induced, p53-activated neuronal cell death has already been identified in several neurodegenerative diseases. To determine DNA damage-induced, p53-mediated apoptosis in spinal cord injury, we performed RT-PCR microarray and analyzed 84 DNA damaging and apoptotic genes. Genes involved in DNA damage and apoptosis were upregulated whereas anti-apoptotic g...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5056844</comments>
            <pubDate>Wed, 06 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5056844</guid>        </item>
        <item>
            <title>An Active Fraction of Achyranthes bidentata Polypeptides Prevents Apoptosis Induced by Serum Deprivation in SH-SY5Y Cells Through Activation of PI3K/Akt/Gsk3β Pathways.</title>
            <link>http://www.medworm.com/index.php?rid=5008943&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21735136%26dopt%3DAbstract</link>
            <description>This study aimed to investigate the possible therapeutic potential of ABPP-E4. Assessments of cell viability and apoptosis indicated that ABPP-E4 pretreatment, in a concentration-dependent manner, antagonized the cell viability loss and cell apoptosis of cultured SH-SY5Y cells deprived of serum. ABPP-E4 pretreatment also resulted in increase of Bcl-2/Bax ratio and inhibition of caspase-3 activation in the cells on exposure to serum deprivation. Signaling pathway analysis indicated that ABPP-E4 treatment stimulated the activation of Akt/Gsk3β signaling in cultured SH-SY5Y cells, and anti-apoptotic effects of ABPP-E4 could be blocked by chemical inhibition of PI3K. Taken together, all the results suggest that ABPP-E4 might exert protective effects against serum deprivation-induced neuronal ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5008943</comments>
            <pubDate>Wed, 06 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5008943</guid>        </item>
        <item>
            <title>Attenuation of 1-(m-Chlorophenyl)-Biguanide Induced Hippocampus-Dependent Memory Impairment by a Standardised Extract of Bacopa monniera (BESEB CDRI-08).</title>
            <link>http://www.medworm.com/index.php?rid=5008942&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21735137%26dopt%3DAbstract</link>
            <description>Authors: Emmanuvel Rajan K, Singh HK, Parkavi A, Charles PD
    Bacopa monniera is a well-known medhya-rasayana (memory enhancing and rejuvenating) plant in Indian traditional medical system of Ayurveda. The effect of a standardized extract of Bacopa monniera (BESEB CDRI-08) on serotonergic receptors and its influence on other neurotransmitters during hippocampal-dependent learning was evaluated in the present study. Wistar rat pups received a single dose of BESEB CDRI-08 during postnatal days 15-29 showed higher latency during hippocampal-dependent learning accompanied with enhanced 5HT(3A) receptor expression, serotonin and acetylcholine levels in hippocampus. Furthermore, 5HT(3A) receptor agonist 1-(m-chlorophenyl)-biguanide (mCPBG) impaired learning in the passive avoidance task follow...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5008942</comments>
            <pubDate>Wed, 06 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5008942</guid>        </item>
        <item>
            <title>Changes in TWIK-related Acid Sensitive K(+)-1 and -3 Channel Expressions from Neurons to Glia in the Hippocampus of Temporal Lobe Epilepsy Patients and Experimental Animal Model.</title>
            <link>http://www.medworm.com/index.php?rid=5008944&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21710317%26dopt%3DAbstract</link>
            <description>Authors: Kim JE, Yeo SI, Ryu HJ, Chung CK, Kim MJ, Kang TC
    In the present study, we analyzed expressions of tandem of P domains in a Weak Inwardly rectifying K(+) channel (TWIK)-related Acid-Sensitive K(+) (TASK) channel-1 and -3 in the hippocampus of patients with temporal lobe epilepsy (TLE) and in rat model. In the control human subjects, TASK-1, and -3 immunoreactivity was observed in pyramidal neurons and dentate granule cells. In TLE patients, TASK-1 and -3 immunoreactivity was rarely observed in neurons. However, TASK-1 immunoreactivity was observed in astrocytes, and TASK-3 immunoreactivity was detected in both astrocytes and microglia. In the rat hippocampus, TASK-1 immunoreactivity was observed in astrocytes within normal and epileptic hippocampus. The alterations in TASK-3 i...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5008944</comments>
            <pubDate>Mon, 27 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5008944</guid>        </item>
        <item>
            <title>Ceruloplasmin Protects Against Rotenone-Induced Oxidative Stress and Neurotoxicity.</title>
            <link>http://www.medworm.com/index.php?rid=5008947&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21706374%26dopt%3DAbstract</link>
            <description>Authors: Hineno A, Kaneko K, Yoshida K, Ikeda SI
    To clarify the neuroprotective property of ceruloplasmin and the pathogenesis of aceruloplasminemia, we generated ceruloplasmin-deficient (CP (-/-)) mice on the C57BL/10 genetic background and further treated them with a mitochondrial complex I inhibitor, rotenone. There was no iron accumulation in the brains of CP (-/-) mice at least up to 60 weeks of age. Without rotenone treatment, CP (-/-) mice showed slight motor dysfunction compared with CP (+/+) mice, but there were no detectable differences in the levels of oxidative stress markers between these two groups. A low dose of rotenone did not affect the mitochondrial complex I activity in our mice, however, it caused a significant change in motor behavior, neuropathology, or the leve...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5008947</comments>
            <pubDate>Sat, 25 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5008947</guid>        </item>
        <item>
            <title>Expression of Cholinergic, Insulin, Vitamin D Receptors and GLUT 3 in the Brainstem of Streptozotocin Induced Diabetic Rats: Effect of Treatment with Vitamin D(3).</title>
            <link>http://www.medworm.com/index.php?rid=5008946&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21706375%26dopt%3DAbstract</link>
            <description>This study provides an evidence that diabetes can alter the expression of cholinergic, insulin, Vitamin D receptors and GLUT 3 in brainstem. We found that Vitamin D(3) treatment could modulate the Vitamin D receptors and plays a pivotal role in maintaining the glucose transport and expressional level of cholinergic receptors in the brainstem of diabetic rats. Thus, our results suggest a therapeutic role of Vitamin D(3) in managing neurological disorders associated with diabetes.
    PMID: 21706375 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5008946</comments>
            <pubDate>Sat, 25 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5008946</guid>        </item>
        <item>
            <title>Plasma Ceruloplasmin Ferroxidase Activity Correlates with the Nigral Sonographic Area in Parkinson's Disease Patients: A Pilot Study.</title>
            <link>http://www.medworm.com/index.php?rid=5008945&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21706376%26dopt%3DAbstract</link>
            <description>Authors: Martínez-Hernández R, Montes S, Higuera-Calleja J, Yescas P, Boll MC, Diaz-Ruiz A, Rios C
    Increased area of the substantia nigra (SN) associated to iron deposition has been proposed as a specific marker for Parkinson's disease (PD). Echogenicity, assessed by transcranial sonography (TCS), has been used to measure such an iron deposition. On the other hand, ferroxidase activity is known to play a role in brain iron metabolism and thus could be involved in increased SN echogenicity of PD patients. The present study was conducted to search for a possible correlation between both markers: TCS of SN and plasma ferroxidase activity. Twenty-one PD patients and 13 healthy volunteers (HV) were included. Mean SN sonographic areas were 0.31 cm(2) for PD patients and 0.12 cm(2) for HV...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5008945</comments>
            <pubDate>Sat, 25 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5008945</guid>        </item>
        <item>
            <title>Protective Effects of Walnut Extract Against Amyloid Beta Peptide-Induced Cell Death and Oxidative Stress in PC12 Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5008948&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21706234%26dopt%3DAbstract</link>
            <description>Authors: Muthaiyah B, Essa MM, Chauhan V, Chauhan A
    Amyloid beta-protein (Aβ) is the major component of senile plaques and cerebrovascular amyloid deposits in individuals with Alzheimer's disease. Aβ is known to increase free radical production in neuronal cells, leading to oxidative stress and cell death. Recently, considerable attention has been focused on dietary antioxidants that are able to scavenge reactive oxygen species (ROS), thereby offering protection against oxidative stress. Walnuts are rich in components that have anti-oxidant and anti-inflammatory properties. The inhibition of in vitro fibrillization of synthetic Aβ, and solubilization of preformed fibrillar Aβ by walnut extract was previously reported. The present study was designed to investigate whether walnut ext...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5008948</comments>
            <pubDate>Fri, 24 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5008948</guid>        </item>
        <item>
            <title>Comparison of Neurosphere-like Cell Clusters Derived from Dental Follicle Precursor Cells and Retinal Müller Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5008949&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21698470%26dopt%3DAbstract</link>
            <description>In conclusion spheres from different types of cells have highly similar proteomes. These proteomes probably show essential cellular processes in neurosphere-like cell clusters.
    PMID: 21698470 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5008949</comments>
            <pubDate>Wed, 22 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5008949</guid>        </item>
        <item>
            <title>Acupuncture Alleviates the Affective Dimension of Pain in a Rat Model of Inflammatory Hyperalgesia.</title>
            <link>http://www.medworm.com/index.php?rid=4961343&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21695393%26dopt%3DAbstract</link>
            <description>Authors: Zhang Y, Meng X, Li A, Xin J, Berman BM, Lao L, Tan M, Ren K, Zhang RX
    Although studies demonstrate that electroacupuncture (EA) alleviates the sensory dimension of pain, they have not addressed EA's effect on the affective dimension. An inflammatory pain rat model, produced by a complete Freund adjuvant (CFA) injection into the hind paw, was combined with a conditioned place avoidance test to determine EA's effects and its underpinning mechanism on the affective dimension of pain. CFA-injected rats showed place aversion, i.e. the affective dimension of pain, by spending less time in a pain-paired compartment after conditioning than before, while saline-injected rats did not. CFA rats given EA treatment at GB30 before a post-conditioning test showed no aversion to the pain-pai...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4961343</comments>
            <pubDate>Tue, 21 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4961343</guid>        </item>
        <item>
            <title>Association Between Na(+),K (+)-ATPase Activity and the Vulnerability/Resilience to Mood Disorders induced by Early Life Experience.</title>
            <link>http://www.medworm.com/index.php?rid=4961342&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21695394%26dopt%3DAbstract</link>
            <description>The objective of this study was to evaluate the interaction between early experience and vulnerability to chronic variable stress in adulthood, analyzing emotional, metabolic and neurochemical aspects related to depression. Pups were (1) handled (10 min/day) or (2) left undisturbed from day 1 to 10 after birth. When the animals reached adulthood, the groups were subdivided and the rats were submitted or not to CVS, which consisted of daily exposure to different stressors for 40 days, followed by a period of behavioral tasks, biochemical (plasma corticosterone and insulin sensitivity) and neurochemical (Na(+),K(+)-ATPase activity in hippocampus, amygdala and parietal cortex) measurements. Neonatally-handled rats demonstrated shorter immobility times in the forced swimming test, independen...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4961342</comments>
            <pubDate>Tue, 21 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4961342</guid>        </item>
        <item>
            <title>Neuroprotective Effects of 3α-Acetoxyeudesma-1,4(15),11(13)-trien-12,6α-olide Against Dopamine-Induced Apoptosis in the Human Neuroblastoma SH-SY5Y Cell Line.</title>
            <link>http://www.medworm.com/index.php?rid=4961345&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21688047%26dopt%3DAbstract</link>
            <description>We examined the inhibitory effects of 3α-acetoxyeudesma-1,4(15),11(13)-trien-12,6α-olide (AETO), purified from the leaves of Laurus nobilis L., on DA-induced apoptosis and α-synuclein (α-syn) formation in dopaminergic SH-SY5Y cells. AETO decreased the active form of caspase-3 and the levels of p53, which were accompanied by increased levels of Bcl-2 in a dose-dependent manner. Flow cytometric and Western blot analysis showed that AETO significantly inhibited DA-induced apoptosis along with suppression of intracellular tyrosinase activity, ROS generation, quinoprotein, and α-syn formation (P &amp;lt; 0.01). These results indicate that AETO inhibited DA-induced apoptosis, which is closely related to the suppression of intracellular tyrosinase activity and the formation of α-syn, ROS, and...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4961345</comments>
            <pubDate>Fri, 17 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4961345</guid>        </item>
        <item>
            <title>Distribution and Time-Course of 4-Hydroxynonenal, Heat Shock Protein 110/105 Family Members and Cyclooxygenase-2 Expression in the Hippocampus of Rat During Trimethyltin-Induced Neurodegeneration.</title>
            <link>http://www.medworm.com/index.php?rid=4961344&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21688048%26dopt%3DAbstract</link>
            <description>Authors: Corvino V, Marchese E, Zarkovic N, Zarkovic K, Cindric M, Waeg G, Michetti F, Geloso MC
    Trimethyltin (TMT), an organotin compound considered a useful tool to obtain an experimental model of neurodegeneration, exhibits neurotoxicant effects selectively localised in the limbic system and especially in the hippocampus, which are different in the rat and in mice. In the rat hippocampus, we investigated the expression of aldehyde 4-hydroxynonenal, a major bioactive marker of membrane lipid peroxidation, heat shock protein (HSP) 110/105 family members, markers of oxidative stress, and the neuroinflammatory marker cyclooxygenase-2 after TMT-intoxication at various time points after treatment. Our data show that TMT-induced neurodegeneration in the rat hippocampus is associated specif...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4961344</comments>
            <pubDate>Fri, 17 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4961344</guid>        </item>
        <item>
            <title>Effect of Baicalin on Matrix Metalloproteinase-9 Expression and Blood-Brain Barrier Permeability Following Focal Cerebral Ischemia in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=4961346&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21678122%26dopt%3DAbstract</link>
            <description>Authors: Tu XK, Yang WZ, Liang RS, Shi SS, Chen JP, Chen CM, Wang CH, Xie HS, Chen Y, Ouyang LQ
    Focal cerebral ischemia results in an increased expression of matrix metalloproteinase-9 (MMP-9), which induces vasogenic brain edema via disrupting the blood-brain barrier (BBB) integrity. Recent studies from our laboratory showed that baicalin reduces ischemic brain damage by inhibiting inflammatory reaction and neuronal apoptosis in a rat model of focal cerebral ischemia. In the present study, we first explored the effect of baicalin on the neuronal damage, brain edema and BBB permeability, then further investigated its potential mechanisms. Sprague-Dawley rats underwent permanent middle cerebral artery occlusion (MCAO). Baicalin was administrated by intraperitoneally injected twice at 2 ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4961346</comments>
            <pubDate>Thu, 16 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4961346</guid>        </item>
        <item>
            <title>Identification of Novel α-Synuclein Isoforms in Human Brain Tissue by using an Online NanoLC-ESI-FTICR-MS Method.</title>
            <link>http://www.medworm.com/index.php?rid=4961348&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21674238%26dopt%3DAbstract</link>
            <description>Authors: Ohrfelt A, Zetterberg H, Andersson K, Persson R, Secic D, Brinkmalm G, Wallin A, Mulugeta E, Francis PT, Vanmechelen E, Aarsland D, Ballard C, Blennow K, Westman-Brinkmalm A
    Parkinson's disease (PD) and Dementia with Lewy bodies (DLB) are neurodegenerative diseases that are characterized by intra-neuronal inclusions of Lewy bodies in distinct brain regions. These inclusions consist mainly of aggregated α-synuclein (α-syn) protein. The present study used immunoprecipitation combined with nanoflow liquid chromatography (LC) coupled to high resolution electrospray ionization Fourier transform ion cyclotron resonance tandem mass spectrometry (ESI-FTICR-MS/MS) to determine known and novel isoforms of α-syn in brain tissue homogenates. N-terminally acetylated full-length α-syn (...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4961348</comments>
            <pubDate>Wed, 15 Jun 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Sphingosylphosphorylcholine Attenuated β-Amyloid Production by Reducing BACE1 Expression and Catalysis in PC12 Cells.</title>
            <link>http://www.medworm.com/index.php?rid=4961349&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21674237%26dopt%3DAbstract</link>
            <description>Authors: Yi H, Lee SJ, Lee J, Myung CS, Park WK, Lim HJ, Lee GH, Kong JY, Cho H
    Abnormal accumulation of β-amyloid (Aβ) is the main characteristic of Alzheimer's disease (AD) brain and Aβ peptides are generated from proteolytic cleavages of amyloid precursor protein (APP) by β-site APP-converting enzyme 1 (BACE1) and presenilin 1 (PS1). Sphingosylphosphorylcholine (SPC), a choline-containing sphingolipid, showed suppressive effect on Aβ production in PC12 cells which stably express Swedish mutant of amyloid precursor protein (APPsw). SPC (&amp;gt;3 μM) significantly lowered the accumulation of Aβ40/42 and the expression of BACE1. However, the transcriptions of other APP processing enzymes like ADAM10 and PS1 were not affected by the SPC addition. Meanwhile, phosphocholine (PC) or o...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4961349</comments>
            <pubDate>Tue, 14 Jun 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Effects of Taurine on Nitric Oxide and 3-Nitrotyrosine Levels in Spleen During Endotoxemia.</title>
            <link>http://www.medworm.com/index.php?rid=4961347&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21674239%26dopt%3DAbstract</link>
            <description>In conclusion, taurine may act as an antioxidant during endotoxemia, and as a prooxidant in healthy subjects at this dose.
    PMID: 21674239 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4961347</comments>
            <pubDate>Tue, 14 Jun 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Cytolytic Effects and Apoptosis Induction of Newcastle Disease Virus Strain AF2240 on Anaplastic Astrocytoma Brain Tumor Cell Line.</title>
            <link>http://www.medworm.com/index.php?rid=4961351&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21671106%26dopt%3DAbstract</link>
            <description>Authors: Ali R, Alabsi AM, Ali AM, Ideris A, Omar AR, Yusoff K, Saif-Ali R
    Newcastle disease virus (NDV) is a member of genus Avulavirus within the family Paramyxoviridae. Interest of using NDV as an anticancer agent has arisen from its ability to kill tumor cells with limited toxicity to normal cells. In this investigation, the cytotolytic properties of NDV strain AF2240 were evaluated on brain tumor cell line, anaplastic astrocytoma (U-87MG), by using MTT assay. Cytological observations were studied using fluorescence microscopy and transmission electron microscopy to show the apoptogenic features of NDV on U-87MG. DNA laddering in agarose gel electrophoresis and terminal deoxyribonucleotide transferase-mediated dUTP-X nick end-labeling staining assay confirmed that the mode of cell ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4961351</comments>
            <pubDate>Mon, 13 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4961351</guid>        </item>
        <item>
            <title>Differential Pharmacological Actions of Methadone and Buprenorphine in Human Embryonic Kidney 293 Cells Coexpressing Human μ-Opioid and Opioid Receptor-Like 1 Receptors.</title>
            <link>http://www.medworm.com/index.php?rid=4961350&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21671107%26dopt%3DAbstract</link>
            <description>In this study, we compared their effects on adenylate cyclase (AC) activity in human embryonic kidney (HEK) 293 cells stably overexpressing human μ-opioid receptor (MOR) and nociceptin/opioid receptor-like 1 receptor (ORL1) simultaneously. After acute exposure, methadone inhibited AC activity; however, buprenorphine induced compromised AC inhibition. When naloxone was introduced after 30 min incubation with methadone, the AC activity was enhanced. This was not observed in the case of buprenorphine. Enhancement of the AC activity was more significant when the incubation lasted for 4 h, and prolonged exposure to buprenorphine elevated the AC activity as well. The removal of methadone and buprenorphine by washing also obtained similar AC superactivation as that revealed by naloxone challen...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4961350</comments>
            <pubDate>Mon, 13 Jun 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Extract from Terminalia chebula Seeds Protect Against Experimental Ischemic Neuronal Damage Via Maintaining SODs and BDNF Levels.</title>
            <link>http://www.medworm.com/index.php?rid=4961353&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21667226%26dopt%3DAbstract</link>
            <description>Authors: Park JH, Joo HS, Yoo KY, Shin BN, Kim IH, Lee CH, Choi JH, Byun K, Lee B, Lim SS, Kim MJ, Won MH
    The fruit of Terminalia chebula Retz has been used as a traditional medicine in Asia and contains tannic acid, chebulagic acid, chebulinic acid and corilagin. Extract from T. chebula seeds (TCE) has various biological functions. We observed the neuroprotective effects of TCE against ischemic damage in the hippocampal C1 region (CA1) of the gerbil that had received oral administrations of TCE (100 mg/kg) once a day for 7 days before the induction of transient cerebral ischemia. In the TCE-treated ischemia group, neuronal neuclei (a marker for neurons)-positive neurons were distinctively abundant (62% of the sham group) in the CA1 4 days after ischemia-reperfusion (I-R) compared t...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4961353</comments>
            <pubDate>Sat, 11 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4961353</guid>        </item>
        <item>
            <title>Neuroprotection by Ulinastatin in Experimental Autoimmune Encephalomyelitis.</title>
            <link>http://www.medworm.com/index.php?rid=4961352&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21667278%26dopt%3DAbstract</link>
            <description>Authors: Shu Y, Yang Y, Qiu W, Lu Z, Li Y, Bao J, Feng M, Hu X
    Ulinastatin has previously been used as a drug for patients with acute inflammatory disorders. The goal of the present study was to investigate the protective effects of ulinastatin on myelin sheaths and oligodendrocytes in experimental autoimmune encephalomyelitis (EAE), and to explore the possible underlying mechanism. Mice were divided into an ulinastatin treatment group, a normal saline treatment group, and a normal control group. EAE was induced in the mice with and without ulinastatin treatment. Demyelination was evaluated, as was the number of oligodendrocytes. The ulinastatin treatment group had a significantly lower clinical score, demyelinating score, and large numbers of oligodendrocytes compared with the group w...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4961352</comments>
            <pubDate>Sat, 11 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4961352</guid>        </item>
        <item>
            <title>Determination of Oxidative Glucose Metabolism In Vivo in the Young Rat Brain Using Localized Direct-Detected (13)C NMR Spectroscopy.</title>
            <link>http://www.medworm.com/index.php?rid=4961355&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21660589%26dopt%3DAbstract</link>
            <description>Authors: Ennis K, Deelchand DK, Tkac I, Henry PG, Rao R
    Determination of oxidative metabolism in the brain using in vivo (13)C NMR spectroscopy ((13)C MRS) typically requires repeated blood sampling throughout the study to measure blood glucose concentration and fractional enrichment (input function). However, drawing blood from small animals, such as young rats, placed deep inside the magnet is technically difficult due to their small total blood volume. In the present study, a custom-built animal holder enabled temporary removal of the animal from the magnet for blood collection, followed by accurate repositioning in the exact presampling position without degradation of B(0) shimming. (13)C label incorporation into glutamate C4 and C3 positions during a 120 min [1,6-(13)C(2)] glucos...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4961355</comments>
            <pubDate>Thu, 09 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4961355</guid>        </item>
        <item>
            <title>Risperidone in Ultra Low Dose Protects Against Stress in the Rodent Cold Restraint Model by Modulating Stress Pathways.</title>
            <link>http://www.medworm.com/index.php?rid=4961354&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21660590%26dopt%3DAbstract</link>
            <description>Authors: Krishnamurthy S, Garabadu D, Reddy NR, Joy KP
    The present investigation evaluates the anti-stress activity of risperidone (RIS) in the cold restraint stress (CRS) model and related stress pathways. Rats were pretreated with RIS (0.1 and 1.0 mg/kg) for 21 days before subjecting to CRS. Ultra low dose of RIS (ULD; 0.1 mg/kg) in contrast to higher dose (1.0 mg/kg) significantly reduced stress in terms of ulcer index. ULD also reversed stress-induced increase in plasma corticosterone and norepinephrine levels used as markers for the function of hypothalamo-pituitary-adrenal (HPA) axis and sympathetic nervous system (SNS) respectively. ULD caused dose and brain region (hippocampus, prefrontal cortex and striatum) specific changes to stress-induced perturbations of serotonin, do...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4961354</comments>
            <pubDate>Thu, 09 Jun 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Doxycycline Attenuates Peripheral Inflammation in Rat Experimental Autoimmune Neuritis.</title>
            <link>http://www.medworm.com/index.php?rid=4961356&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21656035%26dopt%3DAbstract</link>
            <description>Authors: Yi C, Zhang Z, Wang W, Zug C, Schluesener HJ, Zhang Z
    Experimental autoimmune neuritis (EAN) is a T cell-mediated autoimmune inflammatory demyelinating disease of the peripheral nervous system and widely-used animal model of human inflammatory demyelinating polyradiculoneuropathies. Doxycycline is a well-known antibiotic and has been reported to have neuroprotective and anti-inflammatory effects. Here we investigated the effects of doxycycline on rat EAN. Therapeutic treatment with doxycycline (40 mg/kg body weight daily from the Day 9 to Day 14 post immunization) significantly attenuated the severity of EAN, decreased inflammatory infiltration of macrophages, B- and T-cells and demyelination in sciatic nerves of EAN rats. Pro-inflammatory molecules including matrixmetallopro...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4961356</comments>
            <pubDate>Tue, 07 Jun 2011 23:00:00 +0100</pubDate>
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