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        <title>Cellular and Molecular Neurobiology 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 'Cellular and Molecular Neurobiology' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Cellular+and+Molecular+Neurobiology&t=Cellular+and+Molecular+Neurobiology&s=Search&f=source]]></link>
        <lastBuildDate>Tue, 07 Feb 2012 08:48:55 +0100</lastBuildDate>
        <item>
            <title>Protective Effects of Adeno-associated Virus Mediated Brain-derived Neurotrophic Factor Expression on Retinal Ganglion Cells in Diabetic Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5659117&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22297541%26dopt%3DAbstract</link>
            <description>Authors: Gong Y, Chang ZP, Ren RT, Wei SH, Zhou HF, Chen XF, Hou BK, Jin X, Zhang MN
    Abstract
    Adeno-associated virus vector plasmid carrying the expression cassette of brain-derived neurotrophic factor (BDNF), pAAV-BDNF, was constructed and packaged into recombinant adeno-associated virus (rAAV-BDNF). The rAAV-BDNF was intravitreally injected into streptzotocin (STZ)-induced diabetic Sprague-Dawley (SD) Rats. Data showed that over-expression of BDNF could increase alive retinal ganglion cell (RGC) number and improve its function in streptzotocin(STZ)-induced diabetic rats, which might be a new method to treat diabetic neuropathy and retinopathy.
    PMID: 22297541 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5659117</comments>
            <pubDate>Thu, 02 Feb 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Stress, Allostatic Load, Catecholamines, and Other Neurotransmitters in Neurodegenerative Diseases.</title>
            <link>http://www.medworm.com/index.php?rid=5659116&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22297542%26dopt%3DAbstract</link>
            <description>Authors: Goldstein DS
    Abstract
    As populations age, the prevalence of geriatric neurodegenerative diseases will increase. These diseases generally are multifactorial, arising from complex interactions among genes, environment, concurrent morbidities, treatments, and time. This essay provides a concept for the pathogenesis of Lewy body diseases such as Parkinson disease, by considering them in the context of allostasis and allostatic load. Allostasis reflects active, adaptive processes that maintain apparent steady states, via multiple, interacting effectors regulated by homeostatic comparators-&quot;homeostats.&quot; Stress can be defined as a condition or state in which a sensed discrepancy between afferent information and a setpoint for response leads to activation of effectors, reducing th...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5659116</comments>
            <pubDate>Thu, 02 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5659116</guid>        </item>
        <item>
            <title>Hypoxia Inducible Factor-1: Its Potential Role In Cerebral Ischemia.</title>
            <link>http://www.medworm.com/index.php?rid=5659115&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22297543%26dopt%3DAbstract</link>
            <description>Authors: Singh N, Sharma G, Mishra V, Raghubir R
    Abstract
    A divergence in the supply and consumption of oxygen in brain tissue initiates complex cycle of biochemical and molecular events resulting in neuronal death. To overcome such adverse situation, the tissue has to adopt some cellular mechanisms such as induction of various transcription factors, such as hypoxia inducible factor (HIF). It is a transcriptional regulator of oxygen homeostasis and key factor to generate the adaptive responses through upregulation of various target genes involved in the erythropoiesis, angiogenesis as well as glucose metabolism and transport. On the other hand, some studies do suggest that HIF also plays a detrimental role in ischemic reperfusion injury by inducing the pro apoptotic molecules, cyto...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5659115</comments>
            <pubDate>Thu, 02 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5659115</guid>        </item>
        <item>
            <title>Stress Cardiomyopathy: A Syndrome of Catecholamine-Mediated Myocardial Stunning?</title>
            <link>http://www.medworm.com/index.php?rid=5659114&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22297544%26dopt%3DAbstract</link>
            <description>Authors: Wittstein IS
    Abstract
    During the past few years, a novel syndrome of heart failure and transient left ventricular systolic dysfunction precipitated by acute emotional or physical stress has been described. While patients with &quot;stress cardiomyopathy&quot; (SCM) typically present with signs and symptoms that resemble an acute coronary syndrome, it has become clear that this syndrome has unique clinical features that can readily be distinguished from acute infarction. In particular, in contrast to the irreversible myocardial injury seen with infarction, the myocardial dysfunction of SCM is completely reversible and occurs in the absence of plaque rupture and coronary thrombosis. There is increasing evidence that exaggerated sympathetic stimulation may play a pathogenic role in the...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5659114</comments>
            <pubDate>Thu, 02 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5659114</guid>        </item>
        <item>
            <title>Different Temporal Patterns in the Expressions of Bone Morphogenetic Proteins and Noggin During Astroglial Scar Formation After Ischemic Stroke.</title>
            <link>http://www.medworm.com/index.php?rid=5659113&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22297545%26dopt%3DAbstract</link>
            <description>Authors: Shin JA, Kang JL, Lee KE, Park EM
    Abstract
    Bone morphogenetic proteins (BMPs) and their antagonists have roles in scar formation and regeneration after central nervous system injuries. However, temporal changes in their expression during astroglial scar formation in the ischemic brain are unknown. Here, we examined protein levels of BMP2, BMP7, and their antagonist noggin in the ischemic brain up to 4 weeks after experimental stroke in mice. BMP2 and BMP7 levels were increased from 1 to 4 weeks in the ischemic brain, and their expression was associated with astrogliosis. BMP7 expression was more intense and co-localized in reactive astrocytes in the ischemic subcortex at 1 week. Noggin expression began to increase after 2 weeks and was further increased at 4 weeks onl...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5659113</comments>
            <pubDate>Thu, 02 Feb 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Mesenchymal Stromal Cells Rescue Cortical Neurons from Apoptotic Cell Death in an In Vitro Model of Cerebral Ischemia.</title>
            <link>http://www.medworm.com/index.php?rid=5659119&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22290155%26dopt%3DAbstract</link>
            <description>Authors: Scheibe F, Klein O, Klose J, Priller J
    Abstract
    Cell therapy with mesenchymal stromal cells (MSCs) was found to protect neurons from damage after experimental stroke and is currently under investigation in clinical stroke trials. In order to elucidate the mechanisms of MSC-induced neuroprotection, we used the in vitro oxygen-glucose deprivation (OGD) model of cerebral ischemia. Co-culture of primary cortical neurons with MSCs in a transwell co-culture system for 48 h prior to OGD-reduced neuronal cell death by 30-35%. Similar protection from apoptosis was observed with MSC-conditioned media when added 48 h or 30 min prior to OGD, or even after OGD. Western blot analysis revealed increased phosphorylation of STAT3 and Akt in neuronal cultures after treatment with MSC-con...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5659119</comments>
            <pubDate>Wed, 01 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5659119</guid>        </item>
        <item>
            <title>Stress and the Stomach: Corticotropin-Releasing Factor May Protect the Gastric Mucosa in Stress Through Involvement of Glucocorticoids.</title>
            <link>http://www.medworm.com/index.php?rid=5659118&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22290156%26dopt%3DAbstract</link>
            <description>In this study, we investigated whether corticotropin-releasing factor (CRF) may protect the gastric mucosa against stress-induced gastric injury through involvement of glucocorticoids. Intraperitoneal administration of CRF (1.25 μg/kg, 30 min before stress) markedly increased plasma corticosterone level (at 15 and 30 min after the administration) and significantly suppressed the occurrence of gastric erosion induced by 3-h cold-restraint stress (at 10°C) in conscious rats. To test the participation of corticosterone in the gastroprotective effect of exogenous CRF, two approaches were used: pretreatment by the inhibitor of glucocorticoid synthesis, metyrapone (30 mg/kg, i.p.) and the antagonist of glucocorticoid receptors RU-38486 (20 mg/kg, i.p.). Metyrapone injected shortly before ...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5659118</comments>
            <pubDate>Wed, 01 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5659118</guid>        </item>
        <item>
            <title>Neural Regulation of the Stress Response: The Many Faces of Feedback.</title>
            <link>http://www.medworm.com/index.php?rid=5659112&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22302180%26dopt%3DAbstract</link>
            <description>Authors: Myers B, McKlveen JM, Herman JP
    Abstract
    The mammalian stress response is an integrated physiological and psychological reaction to real or perceived adversity. Glucocorticoids (GCs) are an important component of this response, acting to redistribute energy resources to both optimize survival in the face of challenge and restore homeostasis after the immediate threat has subsided. Release of GCs is mediated by the hypothalamo-pituitary-adrenocortical (HPA) axis, driven by a neural signal originating in the paraventricular nucleus (PVN). Stress levels of GCs bind to glucocorticoid receptors (GRs) in multiple body compartments, including brain, and consequently have wide-reaching actions. For this reason, GCs serve a vital function in feedback inhibition of their own secreti...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5659112</comments>
            <pubDate>Wed, 01 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5659112</guid>        </item>
        <item>
            <title>Increased Expression of the Anti-Apoptotic Protein Bcl-xL in the Brain is Associated with Resilience to Stress-Induced Depression-Like Behavior.</title>
            <link>http://www.medworm.com/index.php?rid=5640076&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22278304%26dopt%3DAbstract</link>
            <description>Authors: Dygalo NN, Kalinina TS, Bulygina VV, Shishkina GT
    Abstract
    Clinical observations and the results of animal studies have implicated changes in neuronal survival and plasticity in both the etiology of mood disorders, especially stress-induced depression, and anti-depressant drug action. Stress may predispose individuals toward depression through down-regulation of neurogenesis and an increase in apoptosis in the brain. Substantial individual differences in vulnerability to stress are evident in humans and were found in experimental animals. Recent studies revealed an association between the brain anti-apoptotic protein B cell lymphoma like X, long variant (Bcl-xL) expression and individual differences in behavioral vulnerability to stress. The ability to increase Bcl-xL gene...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5640076</comments>
            <pubDate>Thu, 26 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5640076</guid>        </item>
        <item>
            <title>Changes of Ribosomal Protein S3 Immunoreactivity and Its New Expression in Microglia in the Mice Hippocampus After Lipopolysaccharide Treatment.</title>
            <link>http://www.medworm.com/index.php?rid=5640077&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22274408%26dopt%3DAbstract</link>
            <description>Authors: Lee HY, Park JH, Lee CH, Yan B, Ahn JH, Lee YJ, Park CW, Cho JH, Choi SY, Won MH
    Abstract
    Lipopolysaccharide (LPS) has been used as a reagent for a model of systemic inflammatory response. Ribosomal protein S3 (rpS3) is a multi-functional protein that is involved in transcription, metastasis, DNA repair, and apoptosis. In the present study, we examined the changes of rpS3 immunoreactivity in the mouse hippocampus after systemic administration of 1 mg/kg of LPS. From 6 h after LPS treatment, rpS3 immunoreactivity was decreased in pyramidale cells of the hippocampus proper (CA1-CA3 regions) and in granule cells of the dentate gyrus. At this point in time, rpS3 immunoreactivity began to increase in non-pyramidal cells and non-granule cells. From 1 day after LPS treatment, ...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5640077</comments>
            <pubDate>Wed, 25 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5640077</guid>        </item>
        <item>
            <title>NPY and Stress 30 Years Later: The Peripheral View.</title>
            <link>http://www.medworm.com/index.php?rid=5640079&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22271177%26dopt%3DAbstract</link>
            <description>Authors: Hirsch D, Zukowska Z
    Abstract
    Almost 30 years ago, neuropeptide Y (NPY) was discovered as a sympathetic co-transmitter and one of the most evolutionarily conserved peptides abundantly present all over the body. Soon afterward, NPY's multiple receptors were characterized and cloned, and the peptide's role in stress was first documented. NPY has proven to be pivotal for maintaining many stress responses. Most notably, NPY is known for activating long-lasting vasoconstriction in many vascular beds, including coronary arteries. More recently, NPY was found to play a role in stress-induced accretion of adipose tissue which many times can lead to detrimental metabolic changes. It is however due to its prominent actions in the brain, one of which is its powerful ability to stimu...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5640079</comments>
            <pubDate>Tue, 24 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5640079</guid>        </item>
        <item>
            <title>Single-Cell and Regional Gene Expression Analysis in Alzheimer's Disease.</title>
            <link>http://www.medworm.com/index.php?rid=5640078&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22271178%26dopt%3DAbstract</link>
            <description>Authors: Kwong R, Lupton MK, Janitz M
    Abstract
    The clinical manifestations of Alzheimer's disease (AD) are secondary to the substantial loss of cortical neurons. To be effective, neuroprotective strategies will need to target the primary pathogenic mechanisms of AD prior to cell loss. The differences between neurons are largely determined by their specific repertoire of mRNAs. Thus, transcriptomic analyses that do not assume a priori etiological hypotheses are potentially powerful tools that can be used to understand the pathogenesis of complex diseases, including AD. The human brain comprises thousands of different cell types of both neuronal and non-neuronal origins. Information about individual cell-type-specific gene expression patterns will allow for a better understanding of ...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5640078</comments>
            <pubDate>Sun, 22 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5640078</guid>        </item>
        <item>
            <title>The Molecular Anatomy of Human Hsp60 and its Similarity with that of Bacterial Orthologs and Acetylcholine Receptor Reveal a Potential Pathogenetic Role of Anti-Chaperonin Immunity in Myasthenia Gravis.</title>
            <link>http://www.medworm.com/index.php?rid=5623157&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22258649%26dopt%3DAbstract</link>
            <description>In this study, we demonstrate that Hsp60 proteins from humans and two common pathogens, Chlamydia trachomatis and Chlamydia pneumoniae, share various sequence segments of potentially highly immunogenic epitopes with acetylcholine receptor α1 subunit (AChRα1). The structural data indicate that AChRα1 antibodies, implicated in the pathogenesis of myasthenia gravis, could very well be elicited and/or maintained by self- and/or bacterial Hsp60.
    PMID: 22258649 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5623157</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5623157</guid>        </item>
        <item>
            <title>Transcriptional Regulation of the GLAST/EAAT-1 Gene in Rat and Man.</title>
            <link>http://www.medworm.com/index.php?rid=5623161&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22252783%26dopt%3DAbstract</link>
            <description>Authors: Unger T, Lakowa N, Bette S, Engele J
    Abstract
    Various acute and chronic brain diseases result in disturbed expression of the glial glutamate transporters, GLAST/EAAT-1 and GLT-1/EAAT-2, and subsequent secondary neuronal cell death. The idea that glutamate-induced brain damage can be prevented by restoring glutamate homeostasis in the injured brain, focussed previous efforts on identifying the network controlling astrocytic glutamate transport. Since most of this work was performed with rat astrocytes, we now sought to compare the transcriptional regulation of the GLAST/EAAT-1 gene in rat and man. Reporter gene assay demonstrated that the human GLAST/EAAT-1 promoter comprises the 2.3 kb region immediately flanking the 5'-end of the human GLAST/EAAT-1 gene. Cloning of the p...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5623161</comments>
            <pubDate>Wed, 18 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5623161</guid>        </item>
        <item>
            <title>Mouse Delta Opioid Receptors are Located on Presynaptic Afferents to Hippocampal Pyramidal Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5623160&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22252784%26dopt%3DAbstract</link>
            <description>Authors: Rezaï X, Faget L, Bednarek E, Schwab Y, Kieffer BL, Massotte D
    Abstract
    Delta opioid receptors participate in the control of chronic pain and emotional responses. Recent data have also identified their implication in drug-context associations pointing to a modulatory role on hippocampal activity. We used fluorescent knock-in mice that express a functional delta opioid receptor fused at its carboxy terminus with the green fluorescent protein in place of the native receptor to investigate the receptor neuroanatomical distribution in this structure. Fine mapping of the pyramidal layer was performed in hippocampal acute brain slices and organotypic cultures using fluorescence confocal imaging, co-localization with pre- and postsynaptic markers and correlative light-electron m...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5623160</comments>
            <pubDate>Wed, 18 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5623160</guid>        </item>
        <item>
            <title>The Microtubule-Associated Protein 1A (MAP1A) is an Early Molecular Target of Soluble Aβ-Peptide.</title>
            <link>http://www.medworm.com/index.php?rid=5623159&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22252785%26dopt%3DAbstract</link>
            <description>In conclusion, this study suggests that disruption of MAP1A could be a very early manifestation of Aβ-mediated synaptic dysfunction-one that presages the clinical onset of AD by years. Moreover, our data support the notion of microtubule-stabilizing agents as effective AD drugs.
    PMID: 22252785 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5623159</comments>
            <pubDate>Wed, 18 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5623159</guid>        </item>
        <item>
            <title>Effect of Oxytocin on Neuroblastoma Cell Viability and Growth.</title>
            <link>http://www.medworm.com/index.php?rid=5623158&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22252786%26dopt%3DAbstract</link>
            <description>In conclusion, oxytocin increases growth and viability of neuroblastoma and glioblastoma cells without activation of neurotrophic factors. Oxytocin does not have protective effect in oxidative stress; however, it might be important for neuroprotection to dopaminergic neurons. Its proliferative effect might be important in native cell life, euplastic processes, and tumor progression.
    PMID: 22252786 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5623158</comments>
            <pubDate>Wed, 18 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5623158</guid>        </item>
        <item>
            <title>Flavonoid Baicalein Modulates H(2)O          (2)-Induced Mitogen-Activated Protein Kinases Activation and Cell Death in SK-N-MC Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5602250&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22246135%26dopt%3DAbstract</link>
            <description>Flavonoid Baicalein Modulates H(2)O     (2)-Induced Mitogen-Activated Protein Kinases Activation and Cell Death in SK-N-MC Cells.
    Cell Mol Neurobiol. 2012 Jan 14;
    Authors: Moslehi M, Meshkini A, Yazdanparast R
    Abstract
    It is believed that ROS-induced oxidative stress triggers numerous signaling pathways which are involved in neurodegenerative diseases, including Alzheimer's disease. To find the effective drugs for neurodegenerative diseases, the deep delve into molecular mechanisms underlie these diseases is necessary. In the current study, we investigated the effects of flavonoid baicalein on H(2)O(2)-induced oxidative stress and cell death in SK-N-MC cells. Our results revealed that the treatment of SK-N-MC cells with H(2)O(2) led to a decrease in cell viability through p...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5602250</comments>
            <pubDate>Sat, 14 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5602250</guid>        </item>
        <item>
            <title>Beta3 Adrenoceptors Substitute the Role of M(2) Muscarinic Receptor in Coping with Cold Stress in the Heart: Evidence from M(2)KO Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5578512&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22222438%26dopt%3DAbstract</link>
            <description>Authors: Benes J, Novakova M, Rotkova J, Farar V, Kvetnansky R, Riljak V, Myslivecek J
    Abstract
    We investigated the role of beta3-adrenoceptors (AR) in cold stress (1 or 7 days in cold) in animals lacking main cardioinhibitive receptors-M2 muscarinic receptors (M(2)KO). There was no change in receptor number in the right ventricles. In the left ventricles, there was decrease in binding to all cardiostimulative receptors (beta1-, and beta2-AR) and increase in cardiodepressive receptors (beta3-AR) in unstressed KO in comparison to WT. The cold stress in WT animals resulted in decrease in binding to beta1- and beta2-AR (to 37%/35% after 1 day in cold and to 27%/28% after 7 days in cold) while beta3-AR were increased (to 216% of control) when 7 days cold was applied. MR were reduce...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578512</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578512</guid>        </item>
        <item>
            <title>Tau Protein Phosphorylation in Diverse Brain Areas of Normal and CRH Deficient Mice: Up-Regulation by Stress.</title>
            <link>http://www.medworm.com/index.php?rid=5578511&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22222439%26dopt%3DAbstract</link>
            <description>Authors: Filipcik P, Novak P, Mravec B, Ondicova K, Krajciova G, Novak M, Kvetnansky R
    Abstract
    Tau protein misfolding is a pathological mechanism, which plays a critical role in the etiopathogenesis of neurodegeneration. However, it is not entirely known what kind of stimuli can induce the misfolding. It is believed that physical and emotional stresses belong to such risk factors. Although the influence of stress on the onset and progression of Alzheimer's disease (AD) has already been proposed, the molecular links between stresses and AD are still unknown. We have therefore focused our attention on determination of the influence of acute immobilization stress (IMO) in normal mice and mice deficient in corticotropin-releasing hormone (CRH). Specifically, we have analyzed levels of...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578511</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578511</guid>        </item>
        <item>
            <title>Neuroprotective Effect of Fucoidan on H(2)O          (2)-Induced Apoptosis in PC12 Cells Via Activation of PI3K/Akt Pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5578510&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22222440%26dopt%3DAbstract</link>
            <description>In this study, we investigated the neuroprotective effect of fucoidan on H(2)O(2)-induced apoptosis in PC12 cells and the possible signaling pathways involved. The results showed that fucoidan inhibited the decrease of cell viability, scavenged ROS formation and reduced lactate dehydrogenase release in H(2)O(2)-induced PC12 cells. These changes were associated with an increase in superoxide dismutase and glutathione peroxidase activity, and reduction in malondialdehyde. In addition, fucoidan treatment inhibited apoptosis in H(2)O(2)-induced PC12 cells by increasing the Bcl-2/Bax ratio and decreasing active caspase-3 expression, as well as enhancing Akt phosphorylation (p-Akt). However, the protection of fucoidan on cell survival, p-Akt, the Bcl-2/Bax ratio and caspase-3 activity were aboli...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578510</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578510</guid>        </item>
        <item>
            <title>Protective Effects of Piperine Against Corticosterone-Induced Neurotoxicity in PC12 Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5578513&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22205277%26dopt%3DAbstract</link>
            <description>This study aimed to examine the protective effect of piperine treatment on corticosterone-induced neurotoxicity in cultured rat pheochromocytoma (PC12) cells. The results showed that piperine co-treatment revealed a differential effect on the cytotoxicity of corticosterone and had its maximum inhibitory effect at 1 μM. Piperine (1 μM) co-treatment also significantly decreased intracellular reactive oxygen species level, and enhanced superoxide dismutase activity and total glutathione level in corticosterone-treated PC12 cells. In addition, piperine (1 μM) co-treatment was found to reverse the decreased brain-derived neurotrophic factor (BDNF) mRNA level caused by corticosterone in PC12 cells. The results suggest that piperine exerts a neuroprotective effect on corticosterone-induced ...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578513</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578513</guid>        </item>
        <item>
            <title>Current Therapeutic Strategies to Mitigate the eNOS Dysfunction in Ischaemic Stroke.</title>
            <link>http://www.medworm.com/index.php?rid=5550363&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22198555%26dopt%3DAbstract</link>
            <description>Authors: Srivastava K, Bath PM, Bayraktutan U
    Abstract
    Impairment of endothelial nitric oxide synthase (eNOS) activity is implicated in the pathogenesis of endothelial dysfunction in many diseases including ischaemic stroke. The modulation of eNOS during and/or following ischaemic injury often represents a futile compensatory mechanism due to a significant decrease in nitric oxide (NO) bioavailability coupled with dramatic increases in the levels of reactive oxygen species that further neutralise NO. However, applications of a number of therapeutic agents alone or in combination have been shown to augment eNOS activity under a variety of pathological conditions by potentiating the expression and/or activity of Akt/eNOS/NO pathway components. The list of these therapeutic agents inc...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550363</comments>
            <pubDate>Sun, 25 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550363</guid>        </item>
        <item>
            <title>Intracerebroventricular 4-Methylcatechol (4-MC) Ameliorates Chronic Pain Associated with Depression-Like Behavior via Induction of Brain-Derived Neurotrophic Factor (BDNF).</title>
            <link>http://www.medworm.com/index.php?rid=5550362&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22198556%26dopt%3DAbstract</link>
            <description>Authors: Fukuhara K, Ishikawa K, Yasuda S, Kishishita Y, Kim HK, Kakeda T, Yamamoto M, Norii T, Ishikawa T
    Abstract
    Neuropathic pain concurrent with mood disorder from peripheral nerve injury is a serious clinical problem that significantly affects quality of life. Recent studies have suggested that a lack of brain-derived neurotrophic factor (BDNF) in the limbic system may cause this pain-emotion. BDNF is induced in cultured neurons by 4-methylcatechol (4-MC), but the role of 4-MC-induced BDNF in pain-emotion is poorly understood. Thus, we assessed the possible involvement of BDNF in brain in depression-like behavior during chronic pain following peripheral nerve injury. In addition, we examined whether intracerebroventricular (i.c.v.) 4-MC prevents chronic pain in rats and produc...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550362</comments>
            <pubDate>Sun, 25 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550362</guid>        </item>
        <item>
            <title>Assessing Behavioural Effects of Chronic HPA Axis Activation Using Conditional CRH-Overexpressing Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5550361&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22198557%26dopt%3DAbstract</link>
            <description>In conclusion, the generated mouse lines represent valuable animal models to study the consequences of chronic CRH overproduction and HPA axis activation.
    PMID: 22198557 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550361</comments>
            <pubDate>Sun, 25 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550361</guid>        </item>
        <item>
            <title>Stress Triggered Changes in Expression of Genes for Neurosecretory Granules in Adrenal Medulla.</title>
            <link>http://www.medworm.com/index.php?rid=5550360&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22198558%26dopt%3DAbstract</link>
            <description>Authors: Sabban EL, Tillinger A, Nostramo R, Serova L
    Abstract
    With acute stress, the release of adrenomedullary catecholamines is important for handling the emergency situation. However, when chronic or repeated, stress alters the allostatic load and leads to a hyperadrenergic state, resulting in the development or worsening of a wide range of diseases. To help elucidate the mechanism, we examined the effects of single and repeated immobilization stress on gene expression of components of neurosecretory vesicles in the adrenal medulla. Male Sprague-Dawley rats were exposed to immobilization stress once for 2 h (1× IMO) or daily for six consecutive days (6× IMO). Compared to unstressed controls, 1× IMO elevated gene expression of vesicular monoamine transporter 2 (VMAT2). In re...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550360</comments>
            <pubDate>Sun, 25 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550360</guid>        </item>
        <item>
            <title>Subventricular Zone Under the Neuroinflammatory Stress and Parkinson's Disease.</title>
            <link>http://www.medworm.com/index.php?rid=5535162&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22189676%26dopt%3DAbstract</link>
            <description>Authors: Mori K, Kaneko YS, Nakashima A, Nagasaki H, Nagatsu T, Nagatsu I, Ota A
    Abstract
    This review summarizes the effects of neuroinflammatory stress on the subventricular zone (SVZ), where new neurons are constitutively produced in the adult brain, especially focusing on the relation with Parkinson's disease (PD), because the SVZ is under the control of dopaminergic afferents from the substantia nigra (SN). In Lewy bodies-positive-PD, microglia is known to phagocytoze aggregated α-synuclein, resulting in the release of inflammatory cytokines. The neurogenesis in the SVZ should be affected in PD brain by the neuroinflammatory process. The administration of lipopolysaccaharide is available as an alternative model for microglia-induced loss of dopaminergic neurons and also the im...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535162</comments>
            <pubDate>Thu, 22 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5535162</guid>        </item>
        <item>
            <title>A Modified In vitro Method to Obtain Pure Astrocyte Cultures Induced from Mouse Hippocampal Neural Stem Cells Using Clonal Expansion.</title>
            <link>http://www.medworm.com/index.php?rid=5513690&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22169983%26dopt%3DAbstract</link>
            <description>Authors: Wang W, Shi W, Li H
    Abstract
    The aim of the present study was to produce astrocyte cultures of high purity from mouse hippocampal neural stem cells and to compare their in vitro properties with those isolated from enriched mixed glial cultures prepared from mouse hippocampus, which are commonly contaminated by microglia. We produced primary cultures of newborn mouse hippocampal neural stem cells, which have the potential to differentiate into astrocytes, neurons, and oligodendrocytes. We produced monoclonal neural stem cell colonies by limiting dilution. We induced astrocyte differentiation by plating the colonies on poly-L: -lysine and culturing them in induction medium consisting of minimum essential medium/F12 supplemented with 10% fetal bovine serum and 100 ng/ml cili...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5513690</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5513690</guid>        </item>
        <item>
            <title>Tcf7l2 is Tightly Controlled During Myelin Formation.</title>
            <link>http://www.medworm.com/index.php?rid=5513691&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22160878%26dopt%3DAbstract</link>
            <description>Authors: Fu H, Kesari S, Cai J
    Abstract
    Recent, studies have shown that Tcf7l2, an important transcription factor in Wnt pathway, plays critical roles in oligodendrocyte development. In this article we report a study showing that Tcf7l2 is under tight regulation during myelin formation. We have found that during early development, Tcf7l2 mRNA appears much earlier than the protein, suggesting a regulation at the translational level. We induced demyelination in a mouse model by a dietary toxin, where remyelination followed after a few weeks, and found that Tcf7l2 protein was expressed specifically during the active remyelination phase. Similarly, in human patients with demyelination diseases, Tcf7l2 protein expression was specifically promoted in regions undergoing active remyelinati...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5513691</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5513691</guid>        </item>
        <item>
            <title>Bacopa monnieri Extract Offsets Rotenone-Induced Cytotoxicity in Dopaminergic Cells and Oxidative Impairments in Mice Brain.</title>
            <link>http://www.medworm.com/index.php?rid=5513692&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22160863%26dopt%3DAbstract</link>
            <description>In this study, we tested the hypothesis that BM extract (BME) could offset neurotoxicant-induced oxidative dysfunctions in developing brain in a rotenone (ROT) mouse model. Pretreatment of dopaminergic (N27 cell lines) cells with BME exhibited significant cytoprotective effect as evidenced by the attenuation of ROT-induced oxidative stress and cell death. Further, the neuroprotective efficacy of BME was assessed in prepubertal mice administered ROT (i.p. 1.0 mg/kg b.w./day) for 7 days. BME treatment significantly offset ROT-induced oxidative damage in striatum (St) and other brain regions as evident by the normalized levels of oxidative markers (malondialdehyde, ROS levels, and hydroperoxides) and restoration of depleted GSH levels. Further, BME effectively normalized the protein carbony...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5513692</comments>
            <pubDate>Sat, 10 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5513692</guid>        </item>
        <item>
            <title>Gliosis in the Mice Hippocampus Without Neuronal Death After Systemic Administration of High Dosage of Tetanus Toxin.</title>
            <link>http://www.medworm.com/index.php?rid=5513693&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22138813%26dopt%3DAbstract</link>
            <description>In conclusion, these results indicate that the systemic administration of 100 ng/kg TeT induced a distinctive microglia changes in the mouse hippocampus without any neuronal death/damage.
    PMID: 22138813 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5513693</comments>
            <pubDate>Sat, 03 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5513693</guid>        </item>
        <item>
            <title>Nemo-like Kinase (NLK) Involves in Neuronal Apoptosis after Traumatic Brain Injury.</title>
            <link>http://www.medworm.com/index.php?rid=5513695&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22127415%26dopt%3DAbstract</link>
            <description>Authors: Li Z, Cui G, Wang J, Yu Z, Zhao L, Lv Z
    Abstract
    Traumatic brain injury (TBI) consists of two phases: an immediate phase in which damage is caused as a direct result of the mechanical impact: and a late phase of altered biochemical events that results in delayed tissue damage and is therefore amenable to therapeutic treatment. Because the molecular mechanisms of delayed post-traumatic neuronal cell death are still poorly understood, we investigated whether nemo-like kinase (NLK), an evolutionarily conserved serine/threonine kinase involved in neuronal apoptosis following TBI. In the model of TBI, western blot analysis, double immunofluorescent staining and immunohistochemistry were used to analyze the role of NLK in the process. The results showed a significant down-regula...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5513695</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5513695</guid>        </item>
        <item>
            <title>SorLA in Glia: Shared Subcellular Distribution Patterns with Caveolin-1.</title>
            <link>http://www.medworm.com/index.php?rid=5513694&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22127416%26dopt%3DAbstract</link>
            <description>Authors: Salgado IK, Serrano M, García JO, Martínez NA, Maldonado HM, Báez-Pagán CA, Lasalde-Dominicci JA, Silva WI
    Abstract
    SorLA is an established sorting and trafficking protein in neurons with demonstrated relevance to Alzheimer's disease (AD). It shares these roles with the caveolins, markers of membrane rafts microdomains. To further our knowledge on sorLA's expression and traffic, we studied sorLA expression in various cultured glia and its relation to caveolin-1 (cav-1), a caveolar microdomain marker. RT-PCR and immunoblots demonstrated sorLA expression in rat C6 glioma, primary cultures of rat astrocytes (PCRA), and human astrocytoma 1321N1 cells. PCRA were determined to express the highest levels of sorLA's message. Induction of differentiation of C6 cells into an ast...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5513694</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5513694</guid>        </item>
        <item>
            <title>Neuronal NOS Inhibitor and Conventional Antidepressant Drugs Attenuate Stress-induced Fos Expression in Overlapping Brain Regions.</title>
            <link>http://www.medworm.com/index.php?rid=5513696&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22120186%26dopt%3DAbstract</link>
            <description>Authors: Silva M, Aguiar DC, Diniz CR, Guimarães FS, Joca SR
    Abstract
    Recent evidence indicates that the administration of inhibitors of neuronal nitric oxide synthase (nNOS) induces antidepressant-like effects in animal models such as the forced swimming test (FST). However, the neural circuits involved in these effects are not yet known. Therefore, this study investigated the expression of Fos protein, a marker of neuronal activity, in the brain of rats submitted to FST and treated with the preferential nNOS inhibitor, 7-nitroindazole (7-NI), or with classical antidepressant drugs (Venlafaxine and Fluoxetine). Male Wistar rats were submitted to a forced swimming pretest (PT) and, immediately after, started receiving a sequence of three ip injections (0, 5, and 23 h after PT) of...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5513696</comments>
            <pubDate>Sun, 27 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5513696</guid>        </item>
        <item>
            <title>Relevance of Stress and Female Sex Hormones for Emotion and Cognition.</title>
            <link>http://www.medworm.com/index.php?rid=5513697&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22113371%26dopt%3DAbstract</link>
            <description>Authors: Ter Horst JP, de Kloet ER, Schächinger H, Oitzl MS
    Abstract
    There are clear sex differences in incidence and onset of stress-related and other psychiatric disorders in humans. Yet, rodent models for psychiatric disorders are predominantly based on male animals. The strongest argument for not using female rodents is their estrous cycle and the fluctuating sex hormones per phase which multiplies the number of animals to be tested. Here, we will discuss studies focused on sex differences in emotionality and cognitive abilities in experimental conditions with and without stress. First, female sex hormones such as estrogens and progesterone affect emotions and cognition, contributing to sex differences in behavior. Second, females respond differently to stress than males which...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5513697</comments>
            <pubDate>Thu, 24 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5513697</guid>        </item>
        <item>
            <title>Sulfated Polysaccharide Isolated from the Sea Cucumber Stichopus japonicus Promotes Neurosphere Migration and Differentiation via Up-regulation of N-Cadherin.</title>
            <link>http://www.medworm.com/index.php?rid=5513698&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22109513%26dopt%3DAbstract</link>
            <description>In this report, the sulfated polysaccharide (SJP) from the body wall of the sea cucumber Stichopus japonicas was extracted and tested for its capacity to affect migration and differentiation of neural stem/progenitor cells. SJP is an intensely sulfated polysaccharide with a molecular weight of 1.79 × 10(5) Da that is capable of promoting neurosphere attachment and migration in a dose-dependent manner. Moreover, SJP effectively maintains cell viability even after being deprived of mitogens. Our current results demonstrate that neurosphere are differentiated into neuronal and glial cells when exposed to SJP. These effects were accompanied by an up-regulation of the adhesion molecule, N-cadherin. In addition, we observed that blocking of PI3K activity inhibited N-cadherin-mediated activit...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5513698</comments>
            <pubDate>Wed, 23 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5513698</guid>        </item>
        <item>
            <title>Synergistic Effects of Bone Mesenchymal Stem Cells and Chondroitinase ABC on Nerve Regeneration After Acellular Nerve Allograft in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5513699&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22095068%26dopt%3DAbstract</link>
            <description>This study aimed to evaluate whether combination therapy of bone marrow stromal cells (BMSCs) transplantation and chondroitinase ABC (ChABC) treatment further enhances axonal regeneration and functional recovery after acellular nerve allograft repair of the sciatic nerve gap in rats. Eight Sprague-Dawley rats were used as nerve donors, and 32 Wistar rats were randomly divided into four groups: Group I: acellular rat sciatic nerve (ARSN) group; Group II: ChABC treatment; Group III: BMSCs transplantation; and Group IV: ChABC treatment and BMSCs transplantation. The results showed that compared with ARSN control group, BMSC transplantation promoted axonal regeneration, the secretion of neural trophic factors NGF, BDNF and axon angiogenesis in nerve graft. ChABC treatment degraded chondroitin ...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5513699</comments>
            <pubDate>Fri, 18 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5513699</guid>        </item>
        <item>
            <title>Epinephrine: A Short- and Long-Term Regulator of Stress and Development of Illness : A Potential New Role for Epinephrine in Stress.</title>
            <link>http://www.medworm.com/index.php?rid=5421282&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22090159%26dopt%3DAbstract</link>
            <description>Authors: Wong DL, Tai TC, Wong-Faull DC, Claycomb R, Meloni EG, Myers KM, Carlezon WA, Kvetnansky R
    Abstract
    Epinephrine (Epi), which initiates short-term responses to cope with stress, is, in part, stress-regulated via genetic control of its biosynthetic enzyme, phenylethanolamine N-methyltransferase (PNMT). In rats, immobilization (IMMO) stress activates the PNMT gene in the adrenal medulla via Egr-1 and Sp1 induction. Yet, elevated Epi induced by acute and chronic stress is associated with stress induced, chronic illnesses of cardiovascular, immune, cancerous, and behavioral etiologies. Major sources of Epi include the adrenal medulla and brainstem. Although catecholamines do not cross the blood-brain barrier, circulating Epi from the adrenal medulla may communicate with the cen...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5421282</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5421282</guid>        </item>
        <item>
            <title>Correlations Between Cholinesterase Activity and Cognitive Scores in Post-Ischemic Rats and Patients with Vascular Dementia.</title>
            <link>http://www.medworm.com/index.php?rid=5421281&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22090160%26dopt%3DAbstract</link>
            <description>Authors: Xiao Y, Guan ZZ, Wu CX, Li Y, Kuang SX, Pei JJ
    Abstract
    The biochemical changes such as the activities of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) were investigated in rats with global cerebral ischemia and in vascular dementia (VaD) subjects in this study. The AChE activity showed a significant decrease in plasma and a significant increase in the hippocampus but not in the cerebral cortices in the post-ischemic rats as compared to the controls. The learning abilities and spatial memory were impaired in the post-ischemic rats as compared to controls. Furthermore, the AChE activity in plasma was significantly reduced in VaD subjects as compared to normal control subjects. The BuChE activity did not show any change in both post-ischemic rats and VaD pati...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5421281</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5421281</guid>        </item>
        <item>
            <title>Gene Expression Profile of THP-1 Monocytes Following Knockdown of DAP12, A Causative Gene for Nasu-Hakola Disease.</title>
            <link>http://www.medworm.com/index.php?rid=5421283&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22080356%26dopt%3DAbstract</link>
            <description>Authors: Satoh JI, Shimamura Y, Tabunoki H
    Abstract
    Nasu-Hakola disease (NHD), also designated polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy, is a rare autosomal recessive disorder characterized by progressive presenile dementia and formation of multifocal bone cysts, caused by a loss-of-function mutation of DAP12 or TREM2. TREM2 and DAP12 constitute a receptor/adaptor complex expressed on osteoclasts, dendritic cells, macrophages, monocytes, and microglia. At present, the precise molecular mechanisms underlying development of leukoencephalopathy and bone cysts in NHD remain largely unknown. We established THP-1 human monocyte clones that stably express small interfering RNA targeting DAP12 for serving as a cellular model of NHD. Genome-wide transcrip...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5421283</comments>
            <pubDate>Sat, 12 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5421283</guid>        </item>
        <item>
            <title>EGCG Ameliorates the Suppression of Long-Term Potentiation Induced by Ischemia at the Schaffer Collateral-CA1 Synapse in the Rat.</title>
            <link>http://www.medworm.com/index.php?rid=5421284&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22076575%26dopt%3DAbstract</link>
            <description>Authors: Ding J, Fu G, Zhao Y, Cheng Z, Chen Y, Zhao B, He W, Guo LJ
    Abstract
    The function of Epigallocatechin gallate (EGCG), a main component of green tea, has been widely investigated, amelioration of synaptic transmission and neuroprotective effects against ischemia-induced brain damage among others. However, the mechanism underlying is still unveiled. We investigated the effects of EGCG on high frequency stimulation-induced long-term potentiation (LTP) in the Schaffer collateral-CA1 synapse with or without cerebral ischemia injury induced by middle cerebral artery occlusion (MCAO) in vivo to examine the possible relations between EGCG and synaptic transmission. Application of EGCG modulated synaptic transmission and produced a dose-dependent improvement of the induction of LTP...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5421284</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5421284</guid>        </item>
        <item>
            <title>Protective Effect of Isorhynchophylline Against β-Amyloid-Induced Neurotoxicity in PC12 Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5380016&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22042506%26dopt%3DAbstract</link>
            <description>Authors: Xian YF, Lin ZX, Mao QQ, Ip SP, Su ZR, Lai XP
    Abstract
    Beta-amyloid peptide (Aβ), a major protein component of senile plaques, has been considered as a critical cause in the pathogenesis of Alzheimer's disease (AD). Modulation of the Aβ-induced neurotoxicity has emerged as a possible therapeutic approach to ameliorate the onset and progression of AD. The present study aimed to evaluate the protective effect of isorhynchophylline, an oxindole alkaloid isolated from a Chinese herb Uncaria rhynchophylla, on Aβ-induced neurotoxicity in cultured rat pheochromocytoma (PC12) cells. The results showed that pretreatment with isorhynchophylline significantly elevated cell viability, decreased the levels of intracellular reactive oxygen species and malondialdehyde, increased the l...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5380016</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5380016</guid>        </item>
        <item>
            <title>Increase of CGRP-Containing Nerve Fibers in the Rat Periodontal Ligament After Luxation.</title>
            <link>http://www.medworm.com/index.php?rid=5380017&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22038237%26dopt%3DAbstract</link>
            <description>Authors: Nagayama T, Seiryu M, Deguchi T, Kano M, Suzuki T, Takano-Yamamoto T, Ichikawa H
    Abstract
    The distribution of calcitonin gene-related peptide (CGRP) was examined in the periodontal ligament (PDL) after experimental luxation injury of the rat first molar tooth. The luxational injury increased the number of CGRP-immunoreactive (IR) nerve fibers. At 3-7 days, numerous CGRP-IR nerve fibers appeared throughout the injured PDL. These nerve fibers terminated as free nerve endings within resorption cavities. Immunohistochemistry for receptor activity modifying protein 1 (RAMP1) also demonstrated that the subunit of CGRP receptor was expressed by periodontal cells adjacent to the alveolar bone in the intact and injured PDL. RAMP1-IR cells were divided into two types; small cells w...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5380017</comments>
            <pubDate>Sun, 30 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5380017</guid>        </item>
        <item>
            <title>Immunocytochemical Localization of TASK-3 Channels in Rat Motor Neurons.</title>
            <link>http://www.medworm.com/index.php?rid=5380018&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22011781%26dopt%3DAbstract</link>
            <description>Authors: Marinc C, Prüss H, Derst C, Veh RW
    Abstract
    Motor neurons are large cholinergic neurons located in the brain stem and spinal cord. In recent years, a functional role for TASK channels in cellular excitability and vulnerability to anesthetics of motor neurons has been described. Using a polyclonal monospecific antibody against the tandem pore domain K(+) channel (K2P channel) TWIK-related acid-sensitive K(+) channel (TASK-3), we analyzed the expression of the TASK-3 protein in motor systems of the rat CNS. Immunocytochemical staining showed strong TASK-3 expression in motor neurons of the facial, trigeminal, ambiguus, and hypoglossal nuclei. Oculomotor nuclei (including trochlear and abducens nucleus) were also strongly positive for TASK-3. The parasympathetic Edinger-West...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5380018</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5380018</guid>        </item>
        <item>
            <title>3-Methylcrotonylglycine Disrupts Mitochondrial Energy Homeostasis and Inhibits Synaptic Na(+),K          (+)-ATPase Activity in Brain of Young Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5329183&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21993987%26dopt%3DAbstract</link>
            <description>3-Methylcrotonylglycine Disrupts Mitochondrial Energy Homeostasis and Inhibits Synaptic Na(+),K     (+)-ATPase Activity in Brain of Young Rats.
    Cell Mol Neurobiol. 2011 Oct 13;
    Authors: Moura AP, Ribeiro CA, Zanatta A, Busanello EN, Tonin AM, Wajner M
    Abstract
    Deficiency of 3-methylcrotonyl-CoA carboxylase activity is an inherited metabolic disease biochemically characterized by accumulation and high urinary excretion of 3-methylcrotonylglycine (3MCG), and also of 3-hydroisovalerate in lesser amounts. Affected patients usually have neurologic dysfunction, brain abnormalities and cardiomyopathy, whose pathogenesis is still unknown. The present study investigated the in vitro effects of 3MCG on important parameters of energy metabolism, including CO(2) production from labeled...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5329183</comments>
            <pubDate>Thu, 13 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5329183</guid>        </item>
        <item>
            <title>Gossypin Induces G2/M Arrest in Human Malignant Glioma U251 Cells by the Activation of Chk1/Cdc25C Pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5329184&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21984341%26dopt%3DAbstract</link>
            <description>Authors: Shi L, Chen J, Wang YY, Sun G, Liu JN, Zhang JX, Yan W, Qian CF, Liu N, Fu Z, You YP, Zeng Y
    Abstract
    Gossypin is a flavone that was originally isolated from Hibiscus           vitifolius and has traditionally been used for the treatment of diabetes, jaundice, and inflammation. Recently, gossypin was found to have potent anticancer properties; however, its effect on human gliomas still remain unknown. To investigate the potential anticancer effects of gossypin on malignant gliomas and analyze the associated molecular mechanisms, we treated human glioma U251 cells with gossypin. Our study showed that the treatment of U251 cells with gossypin inhibited cell proliferation in a dose- and time-dependent manner and was observed to be minimally toxic to normal human astrocytes. G...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5329184</comments>
            <pubDate>Sun, 09 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5329184</guid>        </item>
        <item>
            <title>Donepezil in a Narrow Concentration Range Augments Control and Impaired by Beta-Amyloid Peptide Hippocampal LTP in NMDAR-Independent Manner.</title>
            <link>http://www.medworm.com/index.php?rid=5297775&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21968642%26dopt%3DAbstract</link>
            <description>Authors: Kapai NA, Bukanova JV, Solntseva EI, Skrebitsky VG
    Abstract
    Acetylcholinesterase (AChE) inhibitor donepezil is widely used for the treatment of Alzheimer's disease (AD). The mechanisms of therapeutic effects of the drug are not well understood. The ability of donepezil to reverse a known pathogenic effect of β-amyloid peptide (Abeta), namely, the impairment of hippocampal long-term potentiation (LTP), was not studied yet. The goal of the present study was to study the influence of donepezil in 0.1-10 μM concentrations on control and Abeta-impaired hippocampal LTP. Possible involvement of N-methyl-D: -aspartate receptors (NMDARs) into mechanisms of donepezil action was also studied. LTP of population spike (PS) was studied in the CA1 region of rat hippocampal slices. Cha...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5297775</comments>
            <pubDate>Tue, 04 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5297775</guid>        </item>
        <item>
            <title>Cutaneous Magnetic Stimulation Reduces Rat Chronic Pain via Activation of the Supra-Spinal Descending Pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5297774&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21968643%26dopt%3DAbstract</link>
            <description>Authors: Shiiba SJ, Yamamoto S, Sasaki H, Nishi M, Ishikawa K, Yasuda S, Tokuda N, Nakanishi O, Ishikawa T
    Abstract
    Recent studies have demonstrated that magnetic stimulation (MS) can induce cellular responses such as Ca(2+) influx into the cultured neurons and glia, leading to increased intracellular phosphorylation. We have demonstrated previously that MS reduces rat neuropathic pain associated with the prevention of neuronal degeneration. Thus, we aimed to elucidate the actions of MS in relation to modulation of spinal neuron-glia and the descending inhibitory system in chronic pain. The male SD rats intrathecally implanted with catheters were subjected to sciatic nerve ligation (CCI). MS is a low power apparatus characterized by two different frequencies, 2 KHz and 83 MHz. Ra...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5297774</comments>
            <pubDate>Tue, 04 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5297774</guid>        </item>
        <item>
            <title>Existence of Tenascin-C Isoforms in Rat that Contain the Alternatively Spliced AD1 Domain are Developmentally Regulated During Hippocampal Development.</title>
            <link>http://www.medworm.com/index.php?rid=5297773&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21968644%26dopt%3DAbstract</link>
            <description>In this report, we show that seven alternatively spliced FNIII domains exist in rat and describe the differential expression pattern of the additional domain AD1 during embryonic and postnatal rat brain development. The AD1 domain of rat is homologous to the ones described in human and chick proteins but does not exist in mouse. Its expression can be located to the developing rat hippocampus and the lining of the lateral ventricle, regions where the TN-C protein may affect the behavior of stem and progenitor cells. During hippocampal development AD1 and the other alternatively spliced domains are differentially expressed as shown by RT-PCRs, immunocytochemistry and in situ hybridizations.
    PMID: 21968644 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5297773</comments>
            <pubDate>Tue, 04 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5297773</guid>        </item>
        <item>
            <title>Akt as a victim, villain and potential hero in Parkinson's disease pathophysiology and treatment.</title>
            <link>http://www.medworm.com/index.php?rid=5281286&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21547489%26dopt%3DAbstract</link>
            <description>Authors: Greene LA, Levy O, Malagelada C
    Abstract
    There are two major purposes of this essay. The first is to summarize existing evidence that irrespective of the initiating causes, neuron death and degeneration in Parkinson's disease (PD) are due to the common feature of failure of signaling by Akt, a kinase involved in neuron survival and maintenance of synaptic contacts. The second is to consider possible means by which such a failure of Akt signaling might be benignly prevented or reversed in neurons affected by PD, so as to treat PD symptoms, block disease progression, and potentially, promote recovery.
    PMID: 21547489 [PubMed - in process] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5281286</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5281286</guid>        </item>
        <item>
            <title>Expression analysis of prestin and selected transcription factors in newborn rats.</title>
            <link>http://www.medworm.com/index.php?rid=5281285&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21614551%26dopt%3DAbstract</link>
            <description>Authors: Gross J, Angerstein M, Fuchs J, Stute K, Mazurek B
    Abstract
    Transcription factors (TFs) have a central role to play in regulating gene expression. To analyze the co-expression patterns of selected TFs with the motor protein prestin of the outer hair cells, we applied an real-time PCR approach combining several kinds of information: (i) expression changes during postnatal development, (ii) expression changes by exposure of organotypic cultures of the organ of Corti to factors which significantly affect prestin expression [thyroid hormone (T4), retinoic acid (RA), butyric acid (BA), increased KCl concentration] and (iii) changes along the apical-basal gradient. We found that the mRNA levels of the TF Brn-3c (Pou4f3), a member of the POU family, are significantly associated w...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5281285</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5281285</guid>        </item>
        <item>
            <title>Neuroprotective effects of 2-cyclopropylimino-3-methyl-1,3-thiazoline hydrochloride against oxidative stress.</title>
            <link>http://www.medworm.com/index.php?rid=5281284&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21618048%26dopt%3DAbstract</link>
            <description>In this study, we report the effects of 2-cyclopropylimino-3-methyl-1,3-thiazoline hydrochloride on primary cultured cortical astrocytes after exposure to hydrogen peroxide (H(2)O(2)). Pretreatment of cells with 2-cyclopropylimino-3-methyl-1,3-thiazoline hydrochloride prior to H(2)O(2) exposure attenuated the H(2)O(2)-induced reductions in cell survival and superoxide dismutase, catalase, glutathione, and glutathione peroxidase activities. It also reduced H(2)O(2)-induced increases in reactive oxygen species levels, malondialdehyde content, and production of nitric oxide. These effects were all concentration-dependent. Our results suggest that 2-cyclopropylimino-3-methyl-1,3-thiazoline hydrochloride protects against oxidative stress.
    PMID: 21618048 [PubMed - in process] (Source: Cellul...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5281284</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5281284</guid>        </item>
        <item>
            <title>Nitric oxide contributes to hypoxia-reoxygenation-induced p-glycoprotein expression in rat brain endothelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=5281283&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21618049%26dopt%3DAbstract</link>
            <description>Authors: Robertson SJ, Mokgokong R, Kania KD, Guedj AS, Hladky SB, Barrand MA
    Abstract
    Ischemia-reperfusion leads to increased levels at the blood-brain barrier of the multidrug efflux transporter, P-glycoprotein that provides protection to the brain by limiting access of unwanted substances. This is coincident with the production of nitric oxide. This present study using immortalized rat brain endothelial cells (GPNTs) examines whether following hypoxia-reoxygenation, nitric oxide contributes to the alterations in P-glycoprotein levels. After 6 h of hypoxia, both nitric oxide and reactive oxygen species, detected intracellularly using fluorescent monitoring dyes, were produced in the subsequent reoxygenation phase coincident with increased P-glycoprotein. The evidence that nitric...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5281283</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5281283</guid>        </item>
        <item>
            <title>Transplantation of predifferentiated adipose-derived stromal cells for the treatment of spinal cord injury.</title>
            <link>http://www.medworm.com/index.php?rid=5281282&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21630007%26dopt%3DAbstract</link>
            <description>Authors: Arboleda D, Forostyak S, Jendelova P, Marekova D, Amemori T, Pivonkova H, Masinova K, Sykova E
    Abstract
    Adipose-derived stromal cells (ASCs) are an alternative source of stem cells for cell-based therapies of neurological disorders such as spinal cord injury (SCI). In the present study, we predifferentiated ASCs (pASCs) and compared their behavior with naïve ASCs in vitro and after transplantation into rats with a balloon-induced compression lesion. ASCs were predifferentiated into spheres before transplantation, then pASCs or ASCs were injected intraspinally 1 week after SCI. The cells' fate and the rats' functional outcome were assessed using behavioral, histological, and electrophysiological methods. Immunohistological analysis of pASCs in vitro revealed the expressio...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5281282</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5281282</guid>        </item>
        <item>
            <title>A Role for Hypothalamic AMP-Activated Protein Kinase in the Mediation of Hyperphagia and Weight Gain Induced by Chronic Treatment with Olanzapine in Female Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5281281&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21681559%26dopt%3DAbstract</link>
            <description>Authors: Sejima E, Yamauchi A, Nishioku T, Koga M, Nakagama K, Dohgu S, Futagami K, Kataoka Y
    Abstract
    Olanzapine is known to be advantageous with respect to outcome and drug compliance in patients with schizophrenia. However, olanzapine has adverse effects, including a higher incidence of weight gain and metabolic disturbances, when compared with those of other antipsychotic agents. The mechanisms underlying these adverse events remain obscure. Female rats were orally administered olanzapine (2 mg/kg) or vehicle once a day for 2 weeks to ascertain if hypothalamic AMP-activated protein kinase (AMPK) mediates olanzapine-induced weight gain and hyperphagia. Body weight and food intake in each rat were evaluated every day and every two days, respectively. After the termination of dr...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5281281</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5281281</guid>        </item>
        <item>
            <title>Opioid Receptor Trafficking and Signaling: What Happens After Opioid Receptor Activation?</title>
            <link>http://www.medworm.com/index.php?rid=5281280&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21947865%26dopt%3DAbstract</link>
            <description>Authors: Bian JM, Wu N, Su RB, Li J
    Abstract
    Prolonged opioid treatment leads to a comprehensive cellular adaptation mediated by opioid receptors, a basis to understand the development of opioid tolerance and dependence. However, the molecular mechanisms underlying opioid-induced cellular adaptation remain obscure. Recent advances in opioid receptor trafficking and signaling in cells have extensively increased our insight into the network of intracellular signal integration. This review focuses on those important intracellular biochemical processes that play critical roles in the development of opioid tolerance and dependence after opioid receptor activation, and tries to explain what happens after opioid receptor activation, and how the cellular adaptation develops from cell membr...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5281280</comments>
            <pubDate>Sun, 25 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5281280</guid>        </item>
        <item>
            <title>Death Receptor 5 and Neuroproliferation.</title>
            <link>http://www.medworm.com/index.php?rid=5247215&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21938487%26dopt%3DAbstract</link>
            <description>We report on the distribution of DR5 expression in mouse hippocampus, cerebellum, and rostral migratory stream (RMS) of olfactory bulb from embryonic (E) day 16 (E16) to postnatal (P) day (P180). At E16, DR5-positive cells were distributed widely in embryonic hippocampus with strong immunostaining in the developing dentate gyrus. In newborn hippocampus, DR5-positive cells were predominantly located in proliferative zones, such as dentate gyrus, subventricular zone, and RMS. After postnatal day 7 (P7), the number of DR5-positive cells decreased, and cells with intense fluorescence were primarily restricted to the subgranular layer (SGL), although the granular cell layer showed weak fluorescence. After P30, only few DR5-positive cells were found in SGL, and mature granule cells were negative...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247215</comments>
            <pubDate>Thu, 22 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247215</guid>        </item>
        <item>
            <title>Angiotensin II AT(1) Receptor Blockers Ameliorate Inflammatory Stress: A Beneficial Effect for the Treatment of Brain Disorders.</title>
            <link>http://www.medworm.com/index.php?rid=5247214&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21938488%26dopt%3DAbstract</link>
            <description>Authors: Saavedra JM
    Abstract
    Excessive allostatic load as a consequence of deregulated brain inflammation participates in the development and progression of multiple brain diseases, including but not limited to mood and neurodegenerative disorders. Inhibition of the peripheral and brain Renin-Angiotensin System by systemic administration of Angiotensin II AT(1) receptor blockers (ARBs) ameliorates inflammatory stress associated with hypertension, cold-restraint, and bacterial endotoxin administration. The mechanisms involved include: (a) decreased inflammatory factor production in peripheral organs and their release to the circulation; (b) reduced progression of peripherally induced inflammatory cascades in the cerebral vasculature and brain parenchyma; and (c) direct anti-inflamm...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247214</comments>
            <pubDate>Thu, 22 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247214</guid>        </item>
        <item>
            <title>Elk-1 Interacts with Dynein upon Serum Stimulation but Independent of Serine 383 Phosphorylation.</title>
            <link>http://www.medworm.com/index.php?rid=5247216&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21935709%26dopt%3DAbstract</link>
            <description>Authors: Demir O, Ari O, Kurnaz IA
    Abstract
    Elk-1 belongs to the Ternary Complex Factor (TCF) subfamily of the ETS (from E26 viral oncogene) domain superfamily of transcription factors, and has been known as a regulator of mitogen-induced immediate early gene transcription upon Mitogen Activated Protein Kinase (MAPK) activation. Elk-1 has been previously shown to interact with neuronal microtubules, and here we show that P-S383-Elk-1, in addition to co-localizing with motor proteins kinesin, Eg5 and Mitotik Kinesin-Like Protein (MKLP) at the mitotic spindles, it physically interacts with dynein in a serum induction-dependent but Ser383 phosphorylation-independent manner.
    PMID: 21935709 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247216</comments>
            <pubDate>Wed, 21 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247216</guid>        </item>
        <item>
            <title>The Promoter Hypermethylation Status of GATA6, MGMT, and FHIT in Glioblastoma.</title>
            <link>http://www.medworm.com/index.php?rid=5247217&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21928112%26dopt%3DAbstract</link>
            <description>In conclusion, our study demonstrates that promoter hypermethylation of MGMT is a common event in GBMs, whereas GATA6 is epigenetically affected in GBMs. Furthermore, inactivation of FHIT by epigenetic mechanisms in GBM may not be associated with brain tumorigenesis.
    PMID: 21928112 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247217</comments>
            <pubDate>Sun, 18 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247217</guid>        </item>
        <item>
            <title>Neuroprotective Effect of Crocin on Acrylamide-induced Cytotoxicity in PC12 cells.</title>
            <link>http://www.medworm.com/index.php?rid=5219205&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21901509%26dopt%3DAbstract</link>
            <description>In conclusion, our results indicated that pretreatment with crocin protected cells from ACR-induced apoptosis partly by inhibition of intracellular ROS production.
    PMID: 21901509 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5219205</comments>
            <pubDate>Wed, 07 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5219205</guid>        </item>
        <item>
            <title>Aging-Associated Modulation in the Expression of Pax6 in Mouse Brain.</title>
            <link>http://www.medworm.com/index.php?rid=5219204&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21901510%26dopt%3DAbstract</link>
            <description>Authors: Tripathi R, Mishra R
    Abstract
    Symptoms like mental retardation, depression, and anxiety have been observed during aging. Almost similar phenotypes have been evident in patients having haploinsufficiency or mutations in Pax6, a transcriptional regulator. Since Pax6 regulates axon guidance, differentiation of neurons from glia, and neuronal migration, it has been considered as a marker of newly generated neurons. The immunohistochemical analysis of Pax6 positive cells and expression pattern of Pax6 in olfactory lobe, hippocampus, and cerebellum of aging mouse brain have been investigated. The number of Pax6 positive cells and level of Pax6 were reduced progressively in olfactory lobe, cerebellum, and hippocampus from postnatal day-zero (P0) to old age mice. Pax6 positive cel...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5219204</comments>
            <pubDate>Wed, 07 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5219204</guid>        </item>
        <item>
            <title>SNAP-25 Contains Non-Acylated Thiol Pairs that can Form Intrachain Disulfide Bonds: Possible Sites for Redox Modulation of Neurotransmission.</title>
            <link>http://www.medworm.com/index.php?rid=5141572&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21850520%26dopt%3DAbstract</link>
            <description>Authors: Foley TD, Clark AR, Stredny ES, Wierbowski BM
    Abstract
    Intrachain disulfide bond formation among the cysteine thiols of SNAP-25, a component of the SNARE protein complex required for neurotransmitter release, has been hypothesized to link oxidative stress and inhibition of synaptic transmission. However, neither the availability in vivo of SNAP-25 thiols, which are known targets of S-palmitoylation, nor the tendency of these thiols to form intrachain disulfide bonds is known. We have examined, in rat brain extracts, both the availability of closely spaced, or vicinal, thiol pairs in SNAP-25 and the propensity of these dithiols toward disulfide bond formation using a method improved by us recently that exploits the high chemoselectivity of phenylarsine oxide (PAO) for vicin...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141572</comments>
            <pubDate>Wed, 17 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141572</guid>        </item>
        <item>
            <title>Functional Gene Expression Analysis of Tissue-Specific Isoforms of Mef2c.</title>
            <link>http://www.medworm.com/index.php?rid=5141573&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21842419%26dopt%3DAbstract</link>
            <description>In this study, differences in the transcriptional activities of each tissue-specific isoform of Mef2c in neuronal cells were examined. Using an MEF2-responsive reporter, exon β-dependent transactivation was found in neuronal cells, as well as in other cell lines previously described. Microarray analysis was used to examine the transcriptional activities of each Mef2c isoform and to assess differences in endogenous gene expression induced by the different isoforms. The results showed significant gene expression changes due to overexpression of Mef2c isoforms in both an isoforms-dependent and -independent manner.
    PMID: 21842419 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141573</comments>
            <pubDate>Sat, 13 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141573</guid>        </item>
        <item>
            <title>The Interaction of Amyloid β and the Receptor for Advanced Glycation Endproducts Induces Matrix Metalloproteinase-2 Expression in Brain Endothelial Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5141574&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21837459%26dopt%3DAbstract</link>
            <description>This study offers new insights into neuroinflammation in the progression of AD.
    PMID: 21837459 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141574</comments>
            <pubDate>Thu, 11 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141574</guid>        </item>
        <item>
            <title>Recovery of CNS Pathway Innervating the Sciatic Nerve Following Transplantation of Human Neural Stem Cells in Rat Spinal Cord Injury.</title>
            <link>http://www.medworm.com/index.php?rid=5141575&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21833549%26dopt%3DAbstract</link>
            <description>Authors: Lee KB, Choi JH, Byun K, Chung KH, Ahn JH, Jeong GB, Hwang IK, Kim S, Won MH, Lee B
    Abstract
    Stem cell research has been attained a greater attention in most fields of medicine due to its potential for many incurable diseases through replacing or helping the regeneration of damaged cells or tissues. Here, we demonstrated the functional recovery and structural connection of the central nervous system pathway innervating the sciatic nerve after total transection of the spinal cord followed by the transplantation of human neural stem cells (hNSC) in the injured rat spinal cord site. The limb function of hNSC-treated group recovered dramatically compared with that in the sham group by Basso-Beattie-Bresnahan (BBB) scores. Transplanted hNSC differentiated into astrocytes and ne...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141575</comments>
            <pubDate>Wed, 10 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141575</guid>        </item>
        <item>
            <title>The Possible Roles of Brain Pericytes in Brain Ischemia and Stroke.</title>
            <link>http://www.medworm.com/index.php?rid=5141576&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21830084%26dopt%3DAbstract</link>
            <description>Authors: Kamouchi M, Ago T, Kuroda J, Kitazono T
    Abstract
    Brain pericytes regulate a variety of functions, such as microcirculation, angiogenesis, and the blood brain barrier in the brain. Recent studies have also shown that they are pluripotent in a manner similar to mesenchymal stem cells. Since, brain pericytes actively control these functions, these cells probably play an important role not only during brain ischemia, but also in the post-stroke period.
    PMID: 21830084 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141576</comments>
            <pubDate>Tue, 09 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141576</guid>        </item>
        <item>
            <title>Activation of ERK1/2 and PI3K/Akt by IGF-1 on GAP-43 Expression in DRG Neurons with Excitotoxicity Induced by Glutamate In Vitro.</title>
            <link>http://www.medworm.com/index.php?rid=5141577&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21822733%26dopt%3DAbstract</link>
            <description>In this study, embryonic 15-day-old rat DRG explants were cultured for 48 h and then exposed to IGF-1, Glu, Glu + IGF-1, Glu + IGF-1 + PD98059, Glu + IGF-1 + LY294002, Glu + IGF-1 + PD98059 + LY294002 for additional 12 h. The DRG explants were continuously exposed to growth media as control. The levels of GAP-43 mRNA were detected by real time-PCR analysis. The protein levels of GAP-43, phosphorylated ERK1/2, phosphorylated Akt, total ERK1/2, and total Akt were detected by Western blot assay. GAP-43 expression in situ was determined by immunofluorescent labeling. Apoptotic cell death was monitored by Hoechst 33342 staining. IGF-1 alone increased GAP-43 and its mRNA levels in the absence of Glu. The decreased GAP-43 and its mRNA levels caused by Glu could be partially reve...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141577</comments>
            <pubDate>Fri, 05 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141577</guid>        </item>
        <item>
            <title>Ginsenoside Rd Protects Neurons Against Glutamate-Induced Excitotoxicity by Inhibiting Ca(2+) Influx.</title>
            <link>http://www.medworm.com/index.php?rid=5103888&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21811848%26dopt%3DAbstract</link>
            <description>In this study, we treated glutamate-injured cultured rat hippocampal neurons with different concentrations of GSRd, and then examined the changes in neuronal apoptosis and intracellular free Ca(2+) concentration. Our MTT assay showed that GSRd significantly increased the survival of neurons injured by glutamate in a dose-dependent manner. Consistently, TUNEL and Caspase-3 staining showed that GSRd attenuated glutamate-induced cell death. Furthermore, calcium imaging assay revealed that GSRd significantly attenuated the glutamate-induced increase of intracellular free Ca(2+) and also inhibited NMDA-triggered Ca(2+) influx. Thus, the present study demonstrates that GSRd protects the cultured hippocampal neurons against glutamate-induced excitotoxicity, and that this neuroprotective effect ma...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103888</comments>
            <pubDate>Tue, 02 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103888</guid>        </item>
        <item>
            <title>Progranulin Genetic Screening in Frontotemporal Lobar Degeneration Patients From Central Italy.</title>
            <link>http://www.medworm.com/index.php?rid=5103889&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21800185%26dopt%3DAbstract</link>
            <description>Authors: Bagnoli S, Piaceri I, Tedde A, Piacentini S, Nannucci S, Bracco L, Sorbi S, Nacmias B
    Recently, mutations in the progranulin gene (GRN) were reported to account for the vast majority of Frontotemporal lobar Degeneration (FTLD) and a growing number of reports describe the implication of this gene in the development of the FTLD pathology with a significant variation in clinical features. To better clarify the contribution of GRN mutations to Italian FTLD, we screened 381 subjects: 171 cases and 210 healthy subjects, all from Central Italy, particularly of Tuscan origins. GRN gene was analyzed using High Resolution Melting Analysis and automated Genetic Analyzer. Human Progranulin ELISA Kit was employed to determine the plasma progranulin levels. The screening showed a total of s...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103889</comments>
            <pubDate>Thu, 28 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103889</guid>        </item>
        <item>
            <title>Decreased Cholinergic Receptor Expression in the Striatum: Motor Function Deficit in Hypoglycemic and Diabetic Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5103890&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21796364%26dopt%3DAbstract</link>
            <description>This study evaluated the effect of insulin-induced hypoglycemia and STZ-induced diabetes on striatal cholinergic receptors and enzyme expression and on motor function. Cholinergic enzymes: AChE and ChAT gene expression, radioreceptor binding assay and immunohistochemistry of muscarinic M1, M3 receptors and α7nAChR were carried out. Motor performance on grid walk test was analysed. AChE and ChAT expression significantly downregulated in hypoglycemic and diabetic rats. Total muscarinic and Muscarinic M3 receptor binding decreased in hypoglycemic rats compared to diabetic rats whereas muscarinic M1 receptor binding increased in hypoglycemic rats compared to diabetic rats. Real-time PCR analysis and confocal imaging of muscarinic M1, M3 receptors confirmed the changes in muscarinic receptor b...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103890</comments>
            <pubDate>Wed, 27 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103890</guid>        </item>
        <item>
            <title>The Striatum and Pain Modulation.</title>
            <link>http://www.medworm.com/index.php?rid=5103891&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21789630%26dopt%3DAbstract</link>
            <description>Authors: Barceló AC, Filippini B, Pazo JH
    The aim of this review was to give a general aspect of the sensorial function of the striatum related to pain modulation, which was intensively studied in our laboratory. We analyse the effect of electrical and chemical stimulation of the striatum on the orofacial pain, especially that produced by tooth pulp stimulation of the lower incisors. We demonstrated specific sites within the nucleus which electrical or chemical stimulation produced inhibition of the nociceptive jaw opening reflex. This analgesic action of the striatum was mediated by activation of its dopamine D(2) receptors and transmitted through the indirect pathways of the basal ganglia and the medullary dorsal reticular nucleus (RVM) to the sensorial nuclei of the trigeminal nerv...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103891</comments>
            <pubDate>Mon, 25 Jul 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Ischaemia-Induced Protein Ubiquitinylation is Differentially Accompanied with Heat-Shock Protein 70 Expression After Naïve and Preconditioned Ischaemia.</title>
            <link>http://www.medworm.com/index.php?rid=5103892&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21789629%26dopt%3DAbstract</link>
            <description>Authors: Racay P
    The aim of this study was to investigate the effect of transient global brain ischaemia, both naïve and preconditioned, on accumulation of ubiquitinylated proteins and induction of stress/chaperone proteins specific to cytoplasm and endoplasmic reticulum. In addition, possible correlation between stress response and ischaemia/induced translocation of p53 to mitochondria was investigated. Rats were subjected to 15-min forebrain ischaemia followed by 1, 3, 24 and 72 h of reperfusion. Transient cerebral ischaemia induced a massive increase in protein ubiquitinylation in the hippocampus as well as in both cerebral and cerebellar cortex. Enhanced ubiquitinylation of proteins was paralleled with transcriptional activation of hsp70.1 gene but not hsp70.3 gene. However, HSP7...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103892</comments>
            <pubDate>Fri, 22 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103892</guid>        </item>
        <item>
            <title>Regional Distribution and Cell Type-Specific Subcellular Localization of Prothymosin Alpha in Brain.</title>
            <link>http://www.medworm.com/index.php?rid=5057994&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21750924%26dopt%3DAbstract</link>
            <description>In this study, our immunohistochemical analysis demonstrated that ProTα is expressed ubiquitously throughout adult brain with difference in the intensity of region-specific protein reactivity. Interestingly, the highest ProTα signals were observed in the brain regions relevant to neurogenesis, such as sub-ventricular zone, granular cell layer of dentate gyrus, as well as granule cell layer of olfactory bulb. Strong immunoreactivity was also found in habenula, ependymal cells lining the dorsal third and fourth ventricle, and in neurons in the Purkinje cell layer of cerebellum. We showed that ProTα was strictly localized in the nuclei of neurons, while it was found in the cytosolic space of astroglial and microglial processes and cell body in the adult brain. To clarify the phenomenon und...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5057994</comments>
            <pubDate>Tue, 12 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5057994</guid>        </item>
        <item>
            <title>Ethanolic Extract of Fructus Alpinia oxyphylla Protects Against 6-Hydroxydopamine-Induced Damage of PC12 Cells In Vitro and Dopaminergic Neurons in Zebrafish.</title>
            <link>http://www.medworm.com/index.php?rid=5057995&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21744117%26dopt%3DAbstract</link>
            <description>Authors: Zhang ZJ, Cheang LC, Wang MW, Li GH, Chu IK, Lin ZX, Lee SM
    In an attempt to understand the neuroprotective effect of Fructus Alpinia oxyphylla (AOE) and to elucidate its underlying mechanism of action, the ethanolic extract of AOE was investigated using zebrafish and PC12 cell models. AOE prevented and restored 6-hydroxydopamine (6-OHDA)-induced dopaminergic (DA) neuron degeneration and attenuated a deficit of locomotor activity in a zebrafish (Danio rerio) model of Parkinson's disease (PD). Treatment with AOE increased the viability of 6-OHDA-treated PC12 cells in vitro in a dose-dependent manner by attenuating cellular apoptosis. However, protocatechuic acid (PCA) and chrysin, two known polyphenol components of AOE, could not reproduce the neuroprotective activity of AOE in...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5057995</comments>
            <pubDate>Fri, 08 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5057995</guid>        </item>
        <item>
            <title>Orexin A in Cortical Cultures: Expression and Effect on Synaptogenesis During Development.</title>
            <link>http://www.medworm.com/index.php?rid=5057997&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21739363%26dopt%3DAbstract</link>
            <description>Authors: Stoyanova II, Rutten WL, le Feber J
    Orexin A (OXA) is an excitatory hypothalamic neurotransmitter and ligand for Orexin Receptor-1 (OR1), isolated from a small group of hypothalamic neurons. OXA orchestrates different brain functions, and at the cognitive level some of the effects of insufficiency of OXA are well-known, for example in Parkinson's disease. It is widely assumed that deteriorated cognitive processes are related to impaired network connectivity. However, little is known about the effects of OXA in network connectivity and synaptogenesis. Therefore, to obtain insight into this problem we designed experiments with two groups of networks of dissociated cortical neurons: one group incubated in a plain medium and another chronically treated with OXA. After 1, 2, 3 or 4...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5057997</comments>
            <pubDate>Thu, 07 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5057997</guid>        </item>
        <item>
            <title>Unique Induction of CA1 LTP Components After Intake of Theanine, an Amino Acid in Tea Leaves and its Effect on Stress Response.</title>
            <link>http://www.medworm.com/index.php?rid=5057996&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21739364%26dopt%3DAbstract</link>
            <description>This study was undertaken to evaluate the effect of theanine intake on long-term potentiation (LTP) induction at hippocampal CA1 synapses and exposure to acute stress. Young rats were fed water containing 0.3% theanine after birth. Key findings: Serum corticosterone level was markedly decreased by theanine intake. Because this decrease can modify synaptic plasticity, the effect of theanine intake was examined focused on CA1 LTP induction. CA1 LTP induced by a 100-Hz tetanus for 1 s was almost the same extent in hippocampal slices from theanine-administered rats, whereas that induced by a 200-Hz tetanus for 1 s was significantly attenuated. 2-Amino-5-phosphonovalerate (APV), an N-methyl-D: -aspartate (NMDA) receptor antagonist, significantly attenuated CA1 LTP induced by a 200-Hz tetanus ...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5057996</comments>
            <pubDate>Thu, 07 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5057996</guid>        </item>
        <item>
            <title>Time-Course of Changes in Phosphorylated CREB in Neuroblasts and BDNF in the Mouse Dentate Gyrus at Early Postnatal Stages.</title>
            <link>http://www.medworm.com/index.php?rid=4865917&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21607831%26dopt%3DAbstract</link>
            <description>In this study, we observed changes of phosphorylated CREB (pCREB) immunoreactivity and its protein levels as well as brain-derived neurotrophic factor (BDNF) levels in the hippocampal dentate gyrus at postnatal (P) 1, 7, 14, and 21 in mice. In addition, we also investigated pCREB expression in doublecortin (DCX, a marker for neuronal progenitors) immunoreactive neuroblasts at P21. pCREB immunoreaction at P1 was detected in most of cells in the dentate gyrus, thereafter pCREB immunoreactivity was decreased in all the layers of the dentate gyrus with time, however, strong pCREB immunoreactivity was shown in cells confined to the subgranular zone of the dentate gyrus at P21. In this group, many pCREB immunoreactive cells were co-localized with DCX immunoreactive neuroblasts. In addition, pCRE...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4865917</comments>
            <pubDate>Fri, 27 May 2011 03:00:06 +0100</pubDate>
            <guid isPermaLink="false">4865917</guid>        </item>
        <item>
            <title>Facilitated Neurogenesis in the Developing Hippocampus After Intake of Theanine, an Amino Acid in Tea Leaves, and Object Recognition Memory.</title>
            <link>http://www.medworm.com/index.php?rid=4865918&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21604187%26dopt%3DAbstract</link>
            <description>This study indicates that 0.3% theanine administration facilitates neurogenesis in the developing hippocampus followed by enhanced recognition memory. Theanine intake may be of benefit to the postnatal development of hippocampal function.
    PMID: 21604187 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4865918</comments>
            <pubDate>Sat, 21 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4865918</guid>        </item>
        <item>
            <title>Expression Profile and Role of EphrinA1 Ligand After Spinal Cord Injury.</title>
            <link>http://www.medworm.com/index.php?rid=4865919&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21603973%26dopt%3DAbstract</link>
            <description>This study suggests that ephrinA1 ligands play a role in the pathophysiology of SCI.
    PMID: 21603973 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4865919</comments>
            <pubDate>Fri, 20 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4865919</guid>        </item>
        <item>
            <title>p65/RelA-Ser529 NF-κB Subunit Phosphorylation Induces Autophagic Astroglial Death (Clasmatodendrosis) Following Status Epilepticus.</title>
            <link>http://www.medworm.com/index.php?rid=4865921&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21598036%26dopt%3DAbstract</link>
            <description>This study was designed to elucidate whether clasmatodendrosis may be one of the autophagy-related degeneration of astrocytes. In this study, clasmatodendritic astrocytes were observed only in the stratum radiatum in the CA1 region. Vacuoles in clasmatodendritic astrocytes showed LAMP-1 immunoreactivity. In addition, both LC3-II and Beclin-1 expression were detected in most of clasmatodendritic astrocytes as well as a few non-vacuolized astrocytes. Clasmatodendritic astrocytes also showed p65/RelA-Ser529 phosphorylation in the nuclei. The neutralization of TNF-α by sTNFp55R infusion reduced clasmatodendritic astrocytes with nuclear p65/RelA-Ser529 phosphorylation. Therefore, these findings suggest that clasmatodendrosis may be autophagic astroglial death in response to epileptic seizures ...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4865921</comments>
            <pubDate>Thu, 19 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4865921</guid>        </item>
        <item>
            <title>Inhibition of Morphine-Induced cAMP Overshoot: A Cell-Based Assay Model in a High-Throughput Format.</title>
            <link>http://www.medworm.com/index.php?rid=4865920&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21598037%26dopt%3DAbstract</link>
            <description>Authors: Xia M, Guo V, Huang R, Shahane SA, Austin CP, Nirenberg M, Sharma SK
    Opiates are not only potent analgesics but also drugs of abuse mainly because they produce euphoria. Chronic use of opiates results in the development of tolerance and dependence. Dr Marshall Nirenberg's group at the National Institutes of Health (NIH) was the first to use a cellular model system of Neuroblastoma × Glioma hybrid cells (NG108-15) to study morphine addiction. They showed that opiates affect adenylyl cyclase (AC) by two opposing mechanisms mediated by the opiate receptor. Although the cellular mechanisms that cause addiction are not yet completely understood, the most observed correlative biochemical adaptation is the upregulation of AC. This model also provides the opportunity to look for comp...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4865920</comments>
            <pubDate>Thu, 19 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4865920</guid>        </item>
        <item>
            <title>Responses to Apical and Basolateral Application of Glutamate in Mouse Fungiform Taste Cells with Action Potentials.</title>
            <link>http://www.medworm.com/index.php?rid=4865922&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21573975%26dopt%3DAbstract</link>
            <description>Authors: Niki M, Takai S, Kusuhara Y, Ninomiya Y, Yoshida R
    In taste bud cells, glutamate may elicit two types of responses, as an umami tastant and as a neurotransmitter. Glutamate applied to apical membrane of taste cells would elicit taste responses whereas glutamate applied to basolateral membrane may act as a neurotransmitter. Using restricted stimulation to apical or basolateral membrane of taste cells, we examined responses of taste cells to glutamate stimulation, separately. Apical application of monosodium glutamate (MSG, 0.3 M) increased firing frequency in some of mouse fungiform taste cells that evoked action potentials. These cells were tested with other basic taste compounds, NaCl (salty), saccharin (sweet), HCl (sour), and quinine (bitter). MSG-sensitive taste cells cou...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4865922</comments>
            <pubDate>Sat, 14 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4865922</guid>        </item>
        <item>
            <title>The Relationship Between Src-Suppressed C Kinase Substrate and β-1,4 Galactosyltransferase-I in the Process of Lipopolysaccharide-Induced TNF-α Secretion in Rat Primary Astrocytes.</title>
            <link>http://www.medworm.com/index.php?rid=4865924&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21573722%26dopt%3DAbstract</link>
            <description>Authors: Shao B, Li C, Yang H, Shen A, Wu X, Yuan Q, Wu X, Kang L, Liu Z, Zhang G, Lu X, Cheng C
    Src-suppressed C kinase substrate (SSeCKS), a protein kinase C substrate, is a major lipopolysaccharide (LPS) response protein. In addition, β-1,4 Galactosyltransferase-I (β-1,4-GalT-I) also plays an important role in the inflammation reactions of nervous system. It was reported that both SSeCKS and β-1,4-GalT-I were involved in the LPS-induced tumor necrosis factor-alpha (TNF-α) expression in rat primary astrocytes. However, the functional interaction between SSeCKS and β-1,4-GalT-I in the LPS-induced TNF-α secretion remains unclear. Therefore, in this study, using the inflammation model of astrocytes treated by LPS in vitro, we found that the changed expressions of SSeCKS and β-1,4...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4865924</comments>
            <pubDate>Fri, 13 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4865924</guid>        </item>
        <item>
            <title>Plasminogen Activator Promotes Recovery Following Spinal Cord Injury.</title>
            <link>http://www.medworm.com/index.php?rid=4865923&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21573723%26dopt%3DAbstract</link>
            <description>Authors: Seeds N, Mikesell S, Vest R, Bugge T, Schaller K, Minor K
    Plasminogen activators play an important role in synaptic plasticity associated with the crossed phrenic phenomenon (CPP) and recovery of respiratory function after spinal cord injury. A genetic approach using knockout mice lacking various genes in the plasminogen activator/plasmin system has shown that induction of urokinase plasminogen activator (uPA) is required during the first hour after a C2-hemisection for the acquisition of the CPP response. The uPA knockout mice do not show the structural remodeling of phrenic motor neuron synapses characteristic of the CPP response. As shown here uPA acts in a cell signaling manner via binding to its receptor uPAR rather than as a protease, since uPAR knockout mice or knock-in...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4865923</comments>
            <pubDate>Fri, 13 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4865923</guid>        </item>
        <item>
            <title>Upregulation of Peroxiredeoxin III in the Hippocampus of Acute Immobilization Stress Model Rats and the Foxo3a-Dependent Expression in PC12 Cells.</title>
            <link>http://www.medworm.com/index.php?rid=4865925&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21562855%26dopt%3DAbstract</link>
            <description>This study investigated whether acute stress altered the expression pattern of peroxiredoxin (Prx) III, which is an antioxidant enzyme that controls cytokine-induced peroxide levels. Prx III immunoreactivity was upregulated in the pyramidal neurons of the hippocampus and in the motor neurons of the spinal cord in an acute immobilization stress (AIS) model. In addition, we tested whether the transcription factor Foxo3a was necessary for the expression of Prx III. The depletion of Foxo3a led to a marked reduction of Prx III and a compensatory enhancement of mitochondrial superoxide dismutase (Mn-SOD) in PC12 cells. The results of this study suggest that Foxo3a mediates the neuronal levels of expression of Prx III and the levels of expression of Mn-SOD in mitochondria. These mechanisms may pl...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4865925</comments>
            <pubDate>Wed, 11 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4865925</guid>        </item>
        <item>
            <title>BIT/SHPS-1 Promotes Antiapoptotic Effect of BDNF on Low Potassium-Induced Cell Death of Cultured Cerebellar Granule Neurons.</title>
            <link>http://www.medworm.com/index.php?rid=4813370&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21553247%26dopt%3DAbstract</link>
            <description>Authors: Koshimizu H, Suzuki S, Araki T, Yamada M, Kojima M, Hatanaka H
    Brain immunoglobulin-like molecule with tyrosine-based activation motifs/SHP substrate 1 (BIT/SHPS-1) is a neuronal adhesion molecule that is highly expressed in cerebellar granule neurons (CGNs); however its function in CGNs remains unclear. Our previous studies indicated that BIT/SHPS-1 is able to modulate the antiapoptotic effect of brain-derived neurotrophic factor (BDNF) on CNS neurons by cell type-specific mechanisms. In this article, we have studied the role of BIT/SHPS-1 in the antiapoptotic function of BDNF on low potassium (LK)-induced cell death of cultured CGNs which is an in vitro model system of neuronal apoptosis during brain development. Cultured rat CGNs were transduced with wild-type rat BIT/SHPS-...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4813370</comments>
            <pubDate>Sat, 07 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4813370</guid>        </item>
        <item>
            <title>Brain Tumor Microvesicles: Insights into Intercellular Communication in the Nervous System.</title>
            <link>http://www.medworm.com/index.php?rid=4813366&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21553248%26dopt%3DAbstract</link>
            <description>Authors: van der Vos KE, Balaj L, Skog J, Breakefield XO
    Brain tumors are heterogeneous tumors composed of differentiated tumor cells that resemble various neural cells and a small number of multipotent cancer stem cells. These tumors modify normal cells in their environment to promote tumor growth, invasion and metastases by various ways. Recent publications show that glioblastoma cells release microvesicles that contain a select subset of cellular proteins and RNAs. These microvesicles are avidly taken up by normal cells in cell culture and can change the translational profile of these cells through delivery of tumor-derived mRNAs, which are translated into functional proteins. In addition to mRNA and proteins, microvesicles have been shown to contain microRNAs, non-coding RNAs and D...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4813366</comments>
            <pubDate>Sat, 07 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4813366</guid>        </item>
        <item>
            <title>Differential Display RT-PCR Reveals Genes Associated with Lithium-Induced Neuritogenesis in SK-N-MC Cells.</title>
            <link>http://www.medworm.com/index.php?rid=4813371&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21547488%26dopt%3DAbstract</link>
            <description>Authors: Italia J, Mukhopadhyaya R, Rajadhyaksha MS
    Lithium is shown to be neurotrophic and protective against variety of environmental stresses both in vitro as well as in vivo. In view of the wider clinical applications, it is necessary to examine alterations in levels of expression of genes affected by lithium. Lithium induces neuritogenesis in human neuroblastoma cell line SK-N-MC. Our aim was to elucidate genes involved in lithium-induced neuritogenesis using SK-N-MC cells. The differential display reverse transcriptase polymerase chain reaction (DD-RT-PCR) technique was used to study gene expression profiles in SK-N-MC cells undergoing lithium-induced neuritogenesis. Differential expression of genes in control and lithium (2.5 mM, 24 h)-treated cells was compared by display of ...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4813371</comments>
            <pubDate>Thu, 05 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4813371</guid>        </item>
        <item>
            <title>The Neurobiology of Erythropoietin.</title>
            <link>http://www.medworm.com/index.php?rid=4813380&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21538117%26dopt%3DAbstract</link>
            <description>Authors: Sytkowski AJ
    
    PMID: 21538117 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4813380</comments>
            <pubDate>Mon, 02 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4813380</guid>        </item>
        <item>
            <title>Aβ Oligomer-Induced Synapse Degeneration in Alzheimer's Disease.</title>
            <link>http://www.medworm.com/index.php?rid=4813373&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21538118%26dopt%3DAbstract</link>
            <description>Authors: Wilcox KC, Lacor PN, Pitt J, Klein WL
    Aβ oligomers cause a collection of molecular events associated with memory loss in Alzheimer's disease, centering on disrupting the maintenance of synapse structure and function. In this brief review of the synaptotoxic effects of Aβ oligomers, we focus on the neuronal properties governing oligomer targeting and toxicity-especially with respect to binding sites and mechanisms of binding. We also discuss ways in which mechanistic insights from other diseases offer clues in the pursuit of the molecular basis of Alzheimer's disease.
    PMID: 21538118 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4813373</comments>
            <pubDate>Mon, 02 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4813373</guid>        </item>
        <item>
            <title>Role of Acetylcholinesterase on the Structure and Function of Cholinergic Synapses: Insights Gained from Studies on Knockout Mice.</title>
            <link>http://www.medworm.com/index.php?rid=4813372&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21538119%26dopt%3DAbstract</link>
            <description>Authors: Adler M, Sweeney RE, Hamilton TA, Lockridge O, Duysen EG, Purcell AL, Deshpande SS
    Electrophysiological and ultrastructural studies were performed on phrenic nerve-hemidiaphragm preparations isolated from wild-type and acetylcholinesterase (AChE) knockout (KO) mice to determine the compensatory mechanisms manifested by the neuromuscular junction to excess acetylcholine (ACh). The diaphragm was selected since it is the primary muscle of respiration, and it must adapt to allow for survival of the organism in the absence of AChE. Nerve-elicited muscle contractions, miniature endplate potentials (MEPPs) and evoked endplate potentials (EPPs) were recorded by conventional electrophysiological techniques from phrenic nerve-hemidiaphragm preparations isolated from 1.5- to 2-month-old ...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4813372</comments>
            <pubDate>Mon, 02 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4813372</guid>        </item>
        <item>
            <title>The Non-Psychoactive Plant Cannabinoid, Cannabidiol Affects Cholesterol Metabolism-Related Genes in Microglial Cells.</title>
            <link>http://www.medworm.com/index.php?rid=4813382&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21533611%26dopt%3DAbstract</link>
            <description>We report that CBD significantly upregulated the mRNAs of the enzymes sterol-O-acyl transferase (Soat2), which synthesizes cholesteryl esters, and of sterol 27-hydroxylase (Cyp27a1). In addition, CBD increased the mRNA of the lipid droplet-associated protein, perilipin2 (Plin2). Moreover, we found that pretreatment of the cells with the cholesterol chelating agent, methyl-β-cyclodextrin (MBCD), reversed the CBD-induced increase in Soat2 mRNA but not in Plin2 mRNA. Incubation with AEA increased the level of Plin2, but not of Soat2 mRNA. Furthermore, MBCD treatment did not affect the reduction by CBD of the LPS-induced release of the proinflammatory cytokine IL-1β. CBD treatment modulates cholesterol homeostasis in microglial cells, and pretreatment with MBCD reverses this effect without i...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4813382</comments>
            <pubDate>Fri, 29 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4813382</guid>        </item>
        <item>
            <title>Effect of Cavtratin, a Caveolin-1 Scaffolding Domain Peptide, on Oligodendroglial Signaling Cascades.</title>
            <link>http://www.medworm.com/index.php?rid=4759186&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21523467%26dopt%3DAbstract</link>
            <description>In this study, we used a caveolin-1 scaffolding domain (CSD) peptide (cavtratin) of which an inhibitory effect on growth factor receptors was reported. Our data showed that cavtratin suppresses the NGF-induced phosphorylation of TrkA as well as the activation of MAPK in porcine oligodendrocytes significantly.
    PMID: 21523467 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4759186</comments>
            <pubDate>Tue, 26 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4759186</guid>        </item>
        <item>
            <title>Non-phosphorylated FTY720 Induces Apoptosis of Human Microglia by Activating SREBP2.</title>
            <link>http://www.medworm.com/index.php?rid=4759187&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21519925%26dopt%3DAbstract</link>
            <description>Authors: Yoshino T, Tabunoki H, Sugiyama S, Ishii K, Kim SU, Satoh JI
    A synthetic analog of sphingosine named FTY720 (Fingolimod), phosphorylated by sphingosine kinase-2, interacts with sphingosine-1-phosphate (S1P) receptors expressed on various cells. FTY720 suppresses the disease activity of multiple sclerosis (MS) chiefly by inhibiting S1P-dependent egress of autoreactive T lymphocytes from secondary lymphoid organs, and possibly by exerting anti-inflammatory and neuroprotective effects directly on brain cells. However, at present, biological effects of FTY720 on human microglia are largely unknown. We studied FTY720-mediated apoptosis of a human microglia cell line HMO6. The exposure of HMO6 cells to non-phosphorylated FTY720 (FTY720-non-P) induced apoptosis in a dose-dependent ma...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4759187</comments>
            <pubDate>Mon, 25 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4759187</guid>        </item>
        <item>
            <title>Effects of a Brain-Engraftable Microglial Cell Line Expressing Anti-Prion scFv Antibodies on Survival Times of Mice Infected with Scrapie Prions.</title>
            <link>http://www.medworm.com/index.php?rid=4759190&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21516351%26dopt%3DAbstract</link>
            <description>Authors: Fujita K, Yamaguchi Y, Mori T, Muramatsu N, Miyamoto T, Yano M, Miyata H, Ootsuyama A, Sawada M, Matsuda H, Kaji R, Sakaguchi S
    We first verified that a single chain Fv fragment against prion protein (anti-PrP scFv) was secreted by HEK293T cells and prevented prion replication in infected cells. We then stably expressed anti-PrP scFv in brain-engraftable murine microglial cells and intracerebrally injected these cells into mice before or after infection with prions. Interestingly, the injection before or at an early time point after infection attenuated the infection marginally but significantly prolonged survival times of the mice. These suggest that the ex vivo gene transfer of anti-PrP scFvs using brain-engraftable cells could be a possible immunotherapeutic approach agains...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4759190</comments>
            <pubDate>Fri, 22 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4759190</guid>        </item>
        <item>
            <title>Oxidative Stress in Phenylketonuria: What is the Evidence?</title>
            <link>http://www.medworm.com/index.php?rid=4759189&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21516352%26dopt%3DAbstract</link>
            <description>This article addresses some of the recent developments obtained from animal studies and from phenylketonuric patients indicating that oxidative stress may represent an important element in the pathophysiology of PKU. Several studies have shown that enzymatic and non-enzymatic antioxidant defenses are decreased in plasma and erythrocytes of PKU patients, which may be due to an increased free radical generation or secondary to the deprivation of micronutrients which are essential for these defenses. Indeed, markers of lipid, protein, and DNA oxidative damage have been reported in PKU patients, implying that reactive species production is increased in this disorder. A considerable set of data from in vitro and in vivo animal studies have shown that phenylalanine and/or its metabolites elicit ...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4759189</comments>
            <pubDate>Fri, 22 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4759189</guid>        </item>
        <item>
            <title>γ-Secretase-Regulated Mechanisms Similar to Notch Signaling May Play a Role in Signaling Events, Including APP Signaling, Which Leads to Alzheimer's Disease.</title>
            <link>http://www.medworm.com/index.php?rid=4759188&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21516353%26dopt%3DAbstract</link>
            <description>Authors: Nakayama K, Nagase H, Koh CS, Ohkawara T
    Although γ-secretase was first identified as a protease that cleaves amyloid precursor protein (APP) within the transmembrane domain, thus producing Aβ peptides that are thought to be pathogenic in Alzheimer's disease (AD), its physiological functions have not been fully elucidated. In the canonical Notch signaling pathway, intramembrane cleavage by γ-secretase serves to release an intracellular domain of Notch that shows activity in the nucleus through binding to transcription factors. Many type 1 transmembrane proteins, including Notch, Delta, and APP, have recently been shown to be substrates for γ-secretase, and their intracellular domains are released from the cell membrane following cleavage by γ-secretase. The common enzyme ...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4759188</comments>
            <pubDate>Fri, 22 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4759188</guid>        </item>
        <item>
            <title>BanI/D13S141/D13S175 Represents a Novel Informative Haplotype at the GJB2 Gene Region in the Iranian Population.</title>
            <link>http://www.medworm.com/index.php?rid=4759192&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21484343%26dopt%3DAbstract</link>
            <description>In this study, genotyping and analysis of the haplotype frequency of three markers, including BanI, D13S141, and D13S175, at the GJB2 region were investigated. The haplotype frequency was estimated using PHASE program. The input data contained two alleles (+ and -) for BanI, four alleles for D13S141, and seven alleles for D13S175. Among the 42 possible haplotypes examined, four haplotypes showed relatively high frequencies (≥5%). Therefore, a combination of BanI/D13S141/D13S175 could be suggested as an informative haplotype for possible carrier detection and prenatal diagnosis of NSHL in the Iranian population.
    PMID: 21484343 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4759192</comments>
            <pubDate>Mon, 11 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4759192</guid>        </item>
        <item>
            <title>Intraperitoneal Aminoguanidine Improves Sciatic Nerve Ischemia-Reperfusion Injury in Male Sprague-Dawley Rats.</title>
            <link>http://www.medworm.com/index.php?rid=4759191&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21484344%26dopt%3DAbstract</link>
            <description>In conclusion, our findings suggest that post-ischemic administration of AG exhibits protective effect against sciatic nerve I/R injury.
    PMID: 21484344 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4759191</comments>
            <pubDate>Mon, 11 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4759191</guid>        </item>
        <item>
            <title>Conditional Tet-Regulated Over-Expression of Hoxa2 in CG4 Cells Increases Their Proliferation and Delays Their Differentiation into Oligodendrocyte-like Cells Expressing Myelin Basic Protein.</title>
            <link>http://www.medworm.com/index.php?rid=4759193&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21479584%26dopt%3DAbstract</link>
            <description>Authors: Wang M, Doucette JR, Nazarali AJ
    Hoxa2 gene was reported to be expressed by oligodendrocytes (OLs) and down-regulated at the terminal differentiation stage during oligodendrogenesis in mice (Nicolay et al. 2004b). To further investigate the role of Hoxa2 in oligodendroglial development, a tetracycline regulated controllable expression system was utilized to establish a stable cell line (CG4-SHoxa2 [sense Hoxa2]), where the expression level of Hoxa2 gene could be up-regulated. The impact of Hoxa2 over-expression on the proliferation and differentiation of CG4-SHoxa2 cells was investigated. Up-regulation of Hoxa2 increased the proliferation of CG4-SHoxa2 cells. The mRNA levels of PDGFαR (platelet-derived growth factor [PDGF] alpha receptor), which is expressed by OL progenitor ...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4759193</comments>
            <pubDate>Fri, 08 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4759193</guid>        </item>
        <item>
            <title>Appearance of Nuclear-sorted Caspase-12 Fragments in Cerebral Cortical and Hippocampal Neurons in Rats Damaged by Autologous Blood Clot Embolic Brain Infarctions.</title>
            <link>http://www.medworm.com/index.php?rid=4759194&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21476018%26dopt%3DAbstract</link>
            <description>Authors: Shimoke K, Matsuki Y, Fukunaga K, Matsumura Y, Fujita E, Sugihara K, Nobuhara M, Maruoka H, Ikeuchi T, Kudo M
    Following endoplasmic reticulum (ER) stress, cerebral infarctions have been reported to involve an apoptotic process, including the activation of the caspase cascade. To confirm whether fragmented caspase-12, which is activated by cleavage and is detectable during ER stress, is also involved in embolic cerebral infarctions in rats, we adopted an autologous blood clot model for the analysis of cerebral infarctions. We performed experiments in rats with brain infarctions, which are closely related to embolic cerebral infarctions. We utilized a homologous blood clot, i.e., natural materials, to form the infarct area. Our findings reveal that caspase-12 is fragmented when ...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4759194</comments>
            <pubDate>Thu, 07 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4759194</guid>        </item>
        <item>
            <title>Guggulipid and Nimesulide Differentially Regulated Inflammatory Genes mRNA Expressions via Inhibition of NF-kB and CHOP Activation in LPS-Stimulated Rat Astrocytoma Cells, C6.</title>
            <link>http://www.medworm.com/index.php?rid=4759195&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21461920%26dopt%3DAbstract</link>
            <description>In conclusion, our findings elucidated the molecular mechanism of neuroinflammation in response to LPS and its modulation by guggulipid and nimesulide in rat astrocytoma cells (C6), which suggest the use of these drugs in the treatment of neuroinflammation-associated disorders.
    PMID: 21461920 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4759195</comments>
            <pubDate>Sat, 02 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4759195</guid>        </item>
        <item>
            <title>Modeling Pathogenesis of Huntington's Disease with Inducible Neuroprogenitor Cells.</title>
            <link>http://www.medworm.com/index.php?rid=4759196&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21452052%26dopt%3DAbstract</link>
            <description>Authors: Dong G, Ferguson JM, Duling AJ, Nicholas RG, Zhang D, Rezvani K, Fang S, Monteiro MJ, Li S, Li XJ, Wang H
    Huntington's disease (HD) is caused by an abnormal expansion of CAG trinucleotide repeats encoding polyglutamine (polyQ) in the first exon of the huntingtin (htt) gene. Despite considerable efforts, the pathogenesis of HD remains largely unclear due to a paucity of models that can reliably reproduce the pathological characteristics of HD. Here, we report a neuronal cell model of HD using the previously established tetracycline regulated rat neuroprogenitor cell line, HC2S2. Stable expression of enhanced green fluorescence protein tagged htt exon 1 (referred to as 28Q and 74Q, respectively) in the HC2S2 cells did not affect rapid neuronal differentiation. However, compared ...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4759196</comments>
            <pubDate>Wed, 30 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4759196</guid>        </item>
        <item>
            <title>Codes and Circuits.</title>
            <link>http://www.medworm.com/index.php?rid=4759197&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21448809%26dopt%3DAbstract</link>
            <description>Authors: Nelson PG
    Marshall Nirenberg will always be remembered for deciphering the genetic code by which DNA and RNA sequences specify the amino acid sequence in proteins. His switch to neurobiology in the 1960s was driven, in part, by an interest in the possibility of a neural code specifying the development and functioning of the neural circuits that underlie brain function. Neural cell adhesion or recognition molecules would probably be involved in such circuit formation, and this review briefly examines one set of such molecules. The specific binding between presynaptic neurexins and postsynaptic neuroligins could constitute one aspect of the code underlying the formation of specific synaptic circuits.
    PMID: 21448809 [PubMed - as supplied by publisher] (Source: Cellular and Mo...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4759197</comments>
            <pubDate>Mon, 28 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4759197</guid>        </item>
        <item>
            <title>The Blood-Brain Barrier Permeability of Geissoschizine Methyl Ether in Uncaria Hook, a Galenical Constituent of the Traditional Japanese Medicine Yokukansan.</title>
            <link>http://www.medworm.com/index.php?rid=4649155&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21442303%26dopt%3DAbstract</link>
            <description>In this study, we investigated the BBB permeability of seven Uncaria hook alkaloids (GM, isocorynoxeine, isorhynchophylline, hirsuteine, hirsutine, rhynchophylline, and corynoxeine) using in vivo and in vitro methods. In the in vivo experiment, seven alkaloids in the plasma and brain of rats orally administered with yokukansan were measured by liquid chromatography-mass spectroscopy/mass spectrometric multiple reaction monitoring assay. In the in vitro experiment, the BBB permeability of seven alkaloids were examined using the BBB model composed of co-culture of endothelial cells, pericytes, and astrocytes. In the in vivo study, six components containing GM but not isocorynoxeine were detected in the plasma, and three (GM, hirsuteine, and corynoxeine) of components were detected in the bra...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4649155</comments>
            <pubDate>Sat, 26 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4649155</guid>        </item>
        <item>
            <title>Targeting Neurons of Rat Nucleus Tractus Solitarii with the Gene Transfer Vector Adeno-Associated Virus Type 2 to Up-Regulate Neuronal Nitric Oxide Synthase.</title>
            <link>http://www.medworm.com/index.php?rid=4649156&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21431420%26dopt%3DAbstract</link>
            <description>In this study, we first tested the hypothesis that AAV serotype 2 (AAV2) selectively transfects neurons but not glial cells in the nucleus tractus solitarii (NTS) by examining expression of the reporter gene, enhanced green fluorescent protein (eGFP), in the rat NTS after unilateral microinjection of AAV2eGFP into NTS. Expression of eGFP was observed in 1-2 cells in the NTS 1 day after injection. The number of transduced cells and the intensity of eGFP fluorescence increased from day 1 to day 28 and decreased on day 60. The majority (92.9 ± 7.0%) of eGFP expressing NTS cells contained immunoreactivity for the neuronal marker, protein gene product 9.5, but not that for the glial marker, glial fibrillary acidic protein. We observed eGFP expressing neurons and fibers in the nodose ganglia...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4649156</comments>
            <pubDate>Wed, 23 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4649156</guid>        </item>
        <item>
            <title>Experimental Evidence that Methylmalonic Acid Provokes Oxidative Damage and Compromises Antioxidant Defenses in Nerve Terminal and Striatum of Young Rats.</title>
            <link>http://www.medworm.com/index.php?rid=4649157&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21424830%26dopt%3DAbstract</link>
            <description>Authors: Fernandes CG, Borges CG, Seminotti B, Amaral AU, Knebel LA, Eichler P, de Oliveira AB, Leipnitz G, Wajner M
    Methylmalonic acidemia and propionic acidemia are organic acidemias biochemically characterized by predominant tissue accumulation of methylmalonic acid (MMA) and propionic acid (PA), respectively. Affected patients present predominantly neurological symptoms, whose pathogenesis is not yet fully established. In the present study we investigated the in vitro effects of MMA and PA on important parameters of lipid and protein oxidative damage and on the production of reactive species in synaptosomes from cerebrum of developing rats. Synaptosomes correspond to nerve terminals that have been used to investigate toxic properties of compounds on neuronal cells. The in vivo ef...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4649157</comments>
            <pubDate>Tue, 22 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4649157</guid>        </item>
        <item>
            <title>In Vitro Differentiation of Mouse Embryonic Stem Cells into Neurons of the Dorsal Forebrain.</title>
            <link>http://www.medworm.com/index.php?rid=4649158&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21424551%26dopt%3DAbstract</link>
            <description>Authors: Jing Y, Machon O, Hampl A, Dvorak P, Xing Y, Krauss S
    Pluripotent embryonic stem cells (ESCs) are able to differentiate into all cell types in the organism including cortical neurons. To follow the dynamic generation of progenitors of the dorsal forebrain in vitro, we generated ESCs from D6-GFP mice in which GFP marks neocortical progenitors and neurons after embryonic day (E) 10.5. We used several cell culture protocols for differentiation of ESCs into progenitors and neurons of the dorsal forebrain. In cell culture, GFP-positive cells were induced under differentiation conditions in quickly formed embryoid bodies (qEBs) after 10-12 day incubation. Activation of Wnt signaling during ESC differentiation further stimulated generation of D6-GFP-positive cortical cells. In contr...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4649158</comments>
            <pubDate>Sun, 20 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4649158</guid>        </item>
        <item>
            <title>Regional Changes in Gene Expression after Limbic Kindling.</title>
            <link>http://www.medworm.com/index.php?rid=4649160&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21424270%26dopt%3DAbstract</link>
            <description>Authors: Corcoran ME, Kroes RA, Burgdorf JS, Moskal JR
    Repeated electrical stimulation results in development of seizures and a permanent increase in seizure susceptibility (kindling). The permanence of kindling suggests that chronic changes in gene expression are involved. Kindling at different sites produces specific effects on interictal behaviors such as spatial cognition and anxiety, suggesting that causal changes in gene expression might be restricted to the stimulated site. We employed focused microarray analysis to characterize changes in gene expression associated with amygdaloid and hippocampal kindling. Male Long-Evans rats received 1 s trains of electrical stimulation to either the amygdala or hippocampus once daily until five generalized seizures had been kindled. Yoked c...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4649160</comments>
            <pubDate>Sat, 19 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4649160</guid>        </item>
        <item>
            <title>Notes from Abroad on the Deciphering of Biology's Rosetta Stone.</title>
            <link>http://www.medworm.com/index.php?rid=4649159&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21424271%26dopt%3DAbstract</link>
            <description>Authors: Clark BF
    
    PMID: 21424271 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4649159</comments>
            <pubDate>Sat, 19 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4649159</guid>        </item>
        <item>
            <title>Functional Identification of Cell Phenotypes Differentiating from Mice Retinal Neurospheres Using Single Cell Calcium Imaging.</title>
            <link>http://www.medworm.com/index.php?rid=4649163&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21409522%26dopt%3DAbstract</link>
            <description>Authors: De Melo Reis RA, Schitine CS, Kofalvi A, Grade S, Cortes L, Gardino PF, Malva JO, de Mello FG
    Degeneration of neural retina causes vision impairment and can lead to blindness. Neural stem and progenitor cells might be used as a tool directed to regenerative medicine of the retina. Here, we describe a novel platform for cell phenotype-specific drug discovery and screening of proneurogenic factors, able to boost differentiation of neural retinal progenitor cells. By using single cell calcium imaging (SCCI) and a rational-based stimulation protocol, a diversity of cells emerging from differentiated retinal neurosphere cultures were identified. Exposure of retinal progenitor cultures to KCl or to α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA) stimulated Ca(2+) transien...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4649163</comments>
            <pubDate>Thu, 17 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4649163</guid>        </item>
        <item>
            <title>Polymorphisms in the DLG3 Gene is not Associated with Non-Syndromic Mental Retardation in the Chinese Han Population of Qin-Ba Mountain.</title>
            <link>http://www.medworm.com/index.php?rid=4582624&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21369957%26dopt%3DAbstract</link>
            <description>In conclusion, the results of this study indicated that DLG3 did not associate with NSMR in Chinese Han population; however, further studies are needed.
    PMID: 21369957 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4582624</comments>
            <pubDate>Thu, 03 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4582624</guid>        </item>
        <item>
            <title>Time Course of Postnatal Distribution of Doublecortin Immunoreactive Developing/Maturing Neurons in the Somatosensory Cortex and Hippocampal CA1 Region of C57BL/6 Mice.</title>
            <link>http://www.medworm.com/index.php?rid=4582625&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21360195%26dopt%3DAbstract</link>
            <description>In this study, we observed neuroblast differentiation in the somatosensory cortex (SSC) and hippocampal CA1 region (CA1), which is vulnerable to oxidative stress, of the mouse at various early postnatal days (P) 1, 7, 14, and 21 using doublecortin (DCX, a marker for neuroblasts). Cresyl violet and NeuN (Neuronal Nuclei) staining showed development of layers as well as neurons in the SSC and CA1. At P1, DCX-positive neuroblasts expressed strong DCX immunoreactivity in both the SSC and CA1. Thereafter, DCX immunoreactivity was decreased with time. At P7, many DCX-immunoreactive neuroblasts were well detected in the SSC and CA1. At P14, some DCX-positive neuroblasts were found in the SSC and CA1: The immunoreactivity was weak. At P21, DCX immunoreactivity was hardly found in cells in the SSC ...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4582625</comments>
            <pubDate>Tue, 01 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4582625</guid>        </item>
        <item>
            <title>Electrophysiological and Structural Aspects in the Frontal Cortex After the Bee (Apis mellifera) Venom Experimental Treatment.</title>
            <link>http://www.medworm.com/index.php?rid=4582626&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21359542%26dopt%3DAbstract</link>
            <description>Authors: Florea A, Puică C, Vinţan M, Benga I, Crăciun C
    The aim of this study is to evaluate the bioelectrical and structural-functional changes in frontal cortex after the bee venom (BV) experimental treatments simulating both an acute envenomation and a subchronic BV therapy. Wistar rats were subcutaneously injected once with three different BV doses: 700 μg/kg (T(1) group), 2100 μg/kg (T(3) group), and 62 mg/kg (sublethal dose-in T(SL) group), and repeated for 30 days with the lowest dose (700 μg/kg-in T(S) group). BV effects were assessed by electrophysiological, histological, histochemical, and ultrastructural methods. Single BV doses produced discharges of negative and biphasic sharp waves, and epileptiform spike-wave complexes. The increasing frequency of these eleme...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4582626</comments>
            <pubDate>Sat, 26 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4582626</guid>        </item>
        <item>
            <title>Ect2, an Ortholog of Drosophila's Pebble, Negatively Regulates Neurite Outgrowth in Neuroblastoma × Glioma Hybrid NG108-15 Cells.</title>
            <link>http://www.medworm.com/index.php?rid=4530384&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21350944%26dopt%3DAbstract</link>
            <description>Authors: Tsuji T, Higashida C, Yoshida Y, Islam MS, Dohmoto M, Koizumi K, Higashida H
    To identify genes required for brain development, we previously performed in vivo RNA interference (RNAi) screening in Drosophila embryos. We identified pebble as a gene that disrupts development of the Drosophila nervous system. Although pebble has been shown to be involved in neuronal development of Drosophila in several screens, the involvement of Ect2, a mammalian ortholog of pebble, in mammalian neuronal development has not been addressed. To examine the role of Ect2 in neuronal differentiation, we performed Ect2 RNAi in the mouse neuroblastoma × rat glioma NG108-15 cell line. Depletion of Ect2 resulted in an increased proportion of binucleate cells and morphological differentiation of NG108-1...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4530384</comments>
            <pubDate>Fri, 25 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4530384</guid>        </item>
        <item>
            <title>The Mental Retardation Associated Protein, srGAP3 Negatively Regulates VPA-Induced Neuronal Differentiation of Neuro2A Cells.</title>
            <link>http://www.medworm.com/index.php?rid=4530383&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21350945%26dopt%3DAbstract</link>
            <description>Authors: Chen K, Mi YJ, Ma Y, Fu HL, Jin WL
    The Slit-Robo GTPase-activating proteins (srGAPs) are important multifunctional adaptor proteins involved in various aspects of neuronal development, including axon guidance, neuronal migration, neurite outgrowth, dendritic morphology and synaptic plasticity. Among them, srGAP3, also named MEGAP (Mental disorder-associated GTPase-activating protein), plays a putative role in severe mental retardation. SrGAP3 expression in ventricular zones of neurogenesis indicates its involvement in early stage of neuronal development and differentiation. Here, we show that overexpression of srGAP3 inhibits VPA (valproic acid)-induced neurite initiation and neuronal differentiation in Neuro2A neuroblastoma cells, whereas knockdown of srGAP3 facilitates the n...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4530383</comments>
            <pubDate>Fri, 25 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4530383</guid>        </item>
        <item>
            <title>Effect of Valproate, Lamotrigine and Levetiracetam on Excitability and Firing Properties of CA1 Neurons in Rat Brain Slices.</title>
            <link>http://www.medworm.com/index.php?rid=4530385&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21336651%26dopt%3DAbstract</link>
            <description>Authors: Englund M, Hyllienmark L, Brismar T
    The purpose of this study was to analyze the rapid effects of the antiepileptic drugs valproate, lamotrigine, and levetiracetam on excitability and firing properties of hippocampal neurons. The drug effects on resting potential, action potential, and repetitive firing properties were studied in whole-cell current-clamp recordings of CA1 neurons in rat brain slices. Lamotrigine changed action potential rising slope by -24 ± 38 V/s (mean ± SD), peak amplitude by -6.8 ± 5.0 mV, and maximum firing frequency by -60 ± 13%. Lamotrigine thereto increased the voltage threshold by 4.3 ± 4.2 mV and augmented the action potential attenuation during repetitive firing. All effects were significant (P &amp;lt; 0.01 to P &amp;lt; 0.0002) compa...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4530385</comments>
            <pubDate>Sat, 19 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4530385</guid>        </item>
        <item>
            <title>Effects of 6(5H)-phenanthridinone, an Inhibitor of Poly(ADP-ribose)Polymerase-1 Activity (PARP-1), on Locomotor Networks of the Rat Isolated Spinal Cord.</title>
            <link>http://www.medworm.com/index.php?rid=4530388&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21331624%26dopt%3DAbstract</link>
            <description>This article investigated whether PHE could actually preserve the function of locomotor networks in vitro from excitotoxicity. Bath-applied PHE (after a 60 min kainate application) failed to recover locomotor network function 24 h later. When the PHE administration was advanced by 30 min (during the administration of kainate), locomotor function could still not be recovered, while basic network rhythmicity persisted. Histochemical analysis showed that, even if the number of surviving neurons was improved with this protocol, it had failed to reach the threshold of minimal network membership necessary for expressing locomotor patterns. These results suggest that PARP-1 hyperactivity was a rapid onset mechanism of neuronal loss after an excitotoxic challenge and that more selective and fas...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4530388</comments>
            <pubDate>Fri, 18 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4530388</guid>        </item>
        <item>
            <title>Rapid Differentiation of Human Embryonal Carcinoma Stem Cells (NT2) into Neurons for Neurite Outgrowth Analysis.</title>
            <link>http://www.medworm.com/index.php?rid=4530387&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21331625%26dopt%3DAbstract</link>
            <description>Authors: Tegenge MA, Roloff F, Bicker G
    Human neurons derived from stem cells can be employed as in vitro models to predict the potential of neurochemicals affecting neurodevelopmental cellular processes including proliferation, migration, and differentiation. Here, we developed a model of differentiating human neurons from well characterized human embryonal carcinoma stem cells (NT2). NT2 cells were induced to differentiate into neuronal phenotypes after 2 weeks of treatment with retinoic acid in aggregate culture. Nestin positive progenitor cells migrate out of NT2 aggregates and differentiate into βIII-tubulin expressing neuronal cells. Culturing the NT2 cells for an additional 7-14 days resulted in increased percentage of βIII-tubulin expressing cells, elaborating a long neurit...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4530387</comments>
            <pubDate>Fri, 18 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4530387</guid>        </item>
        <item>
            <title>Adenosine 5'-Triphosphate-Sensitive Potassium Channel Activator Induces the Up-Regulation of Caveolin-1 Expression in a Rat Brain Tumor Model.</title>
            <link>http://www.medworm.com/index.php?rid=4530386&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21331626%26dopt%3DAbstract</link>
            <description>This study was performed to determine whether minoxidil sulfate (MS), a selective Adenosine 5'-triphosphate-sensitive potassium channel (K (ATP) channel) activator, has an effect on the expression of caveolin-1 in the rat's brain tumor tissue. Using a rat brain glioma (C6) model, we found that the expression of caveolin-1 protein at tumor sites was greatly increased after intracarotid infusion of MS at a dose of 30 μg/kg/min for 15, 30, and 60 min via Western blot analysis. And the peak value of the caveolin-1 expression was observed in rats with glioma after 15 min of MS perfusion, which was significantly attenuated by reactive oxygen species (ROS) scavenger (N-2-mercaptopropionyl glycine, MPG). In addition, MPG also significantly inhibited the increase of blood-brain tumor barrier (B...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4530386</comments>
            <pubDate>Fri, 18 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4530386</guid>        </item>
        <item>
            <title>Effects of Estradiol and IGF-1 on the Sodium Calcium Exchanger in Rat Cultured Cortical Neurons.</title>
            <link>http://www.medworm.com/index.php?rid=4474519&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21311966%26dopt%3DAbstract</link>
            <description>Authors: Sánchez JC, López-Zapata DF, Francis L, De Los Reyes L
    The Na(+)/Ca(2+) exchanger (NCX) is an important bidirectional transporter of calcium in neurons and has been shown to be involved in neuroprotection. Calcium can activate a number of cascades that can result in apoptosis and cell death, and NCX is a key factor in regulating the cytoplasmic concentration of this ion. 17-β-estradiol and insulin-like growth factor 1 (IGF-1) are known neuroprotective hormones with interacting mechanisms and effects on intracellular calcium; however, their relationship with the NCX has not been explored. In this article, the effects of these two hormones on neuronal NCX were tested using the whole-cell patch clamp technique on rat primary culture neurons. Both 17-β-estradiol and IGF-1 prod...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4474519</comments>
            <pubDate>Fri, 11 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4474519</guid>        </item>
        <item>
            <title>Lower Frequency of Antidepressant Use in Patients on Renin-Angiotensin-Aldosterone System Modifying Medications.</title>
            <link>http://www.medworm.com/index.php?rid=4474520&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21301954%26dopt%3DAbstract</link>
            <description>Authors: Nasr SJ, Crayton JW, Agarwal B, Wendt B, Kora R
    Both hypertension and depression are common disorders which may both involve components of the hypothalamic-pituitary-adrenal axis system and the Renin-Angiotensin-Aldosterone System (RAAS). These observations, coupled with growing evidence that RAAS-active drugs may have anti-depressant properties prompted us to study the frequency of anti-depressant medication usage in the patients receiving RAAS-active agents. A chart review was performed on 378 patients who were seen during a 3-month period in a primary care clinic and who were diagnosed with hypertension. Demographic information and data on the rates of co-administration of antihypertensive and anti-depressant medications was collected. Overall, 23.7% of the sample was on an...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4474520</comments>
            <pubDate>Tue, 08 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4474520</guid>        </item>
        <item>
            <title>Elevated S100B and Neuron Specific Enolase Levels in Patients with Migraine-without Aura: Evidence for Neurodegeneration?</title>
            <link>http://www.medworm.com/index.php?rid=4474521&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21293918%26dopt%3DAbstract</link>
            <description>In this study, in order to investigate a possible neuronal and/or glial damage at the cellular level in migraine, we measured and compared serum levels of S100B which is a protein marker of glial damage or activation, and neuron specific enolase (NSE) which is a marker of neuronal damage, in migraine patients and control subjects. Serum levels of S100B and NSE were measured in blood samples from 41 patients with migraine-without aura taken during a migraine attack (ictal) and in the attack-free period between migraine attacks (interictal) and 35 age- and sex-matched controls. Patients with migraine-without aura had significantly higher ictal serum levels of S100B and NSE (P &amp;lt; 0.05, for both) than control subjects; whereas in the interictal phase, there was a significant increment only...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4474521</comments>
            <pubDate>Fri, 04 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4474521</guid>        </item>
        <item>
            <title>Generation of TrkA/TrkB Chimeric Receptor Constructs Reveals Molecular Mechanisms Underlying BDNF-Induced Dendritic Outgrowth in Hippocampal Neurons.</title>
            <link>http://www.medworm.com/index.php?rid=4474522&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21279681%26dopt%3DAbstract</link>
            <description>Authors: Sato Y, Suzuki S, Kitabatake M, Hara T, Kojima M
    Neurotrophins (NTs) regulate neuronal survival, differentiation, and synaptic plasticity through tropomyosin receptor kinases (Trks). The molecular mechanisms underlying these functions, however, have remained incompletely understood. In the present study, we first showed that brain-derived neurotrophic factor (BDNF) increased both the number of primary dendrites and dendritic complexity in cultured hippocampal neurons. Since hippocampal neurons predominantly express the BDNF receptor TrkB, but not the nerve growth factor (NGF) receptor Trk, we generated DNA constructs encoding the extracellular domain of TrkA fused with the transmembrane and intracellular domain of TrkB and introduced these constructs into cultured hippocampal ...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4474522</comments>
            <pubDate>Sun, 30 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4474522</guid>        </item>
        <item>
            <title>Latanoprost Promotes Neurite Outgrowth in Differentiated RGC-5 Cells via the PI3K-Akt-mTOR Signaling Pathway.</title>
            <link>http://www.medworm.com/index.php?rid=4474523&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21279434%26dopt%3DAbstract</link>
            <description>This study presents novel in vitro evidence that latanoprost could promote neurite outgrowth through an FP receptor-mediated modulation of the PI3K-Akt-mTOR signaling pathway. This finding may provide insight into a better understanding of a new mechanism of latanoprost for glaucoma therapy and into the physiological-modulating activities of prostaglandins.
    PMID: 21279434 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4474523</comments>
            <pubDate>Sat, 29 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4474523</guid>        </item>
        <item>
            <title>IGF-1 Participates Differently in Regulation of Severing Activity of Katanin and Spastin.</title>
            <link>http://www.medworm.com/index.php?rid=4474525&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21274617%26dopt%3DAbstract</link>
            <description>This study indicated that IGF-1 participates differently in the regulation of spastin and p60-katanin in terms of neuronal branching.
    PMID: 21274617 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4474525</comments>
            <pubDate>Fri, 28 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4474525</guid>        </item>
        <item>
            <title>Baclofen and Adenosine Inhibition of Synaptic Transmission at CA3-CA1 Synapses Display Differential Sensitivity to K(+) Channel Blockade.</title>
            <link>http://www.medworm.com/index.php?rid=4474524&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21274618%26dopt%3DAbstract</link>
            <description>Authors: Skov J, Andreasen M, Hablitz JJ, Nedergaard S
    The metabotropic GABA(B) and adenosine A(1) receptors mediate presynaptic inhibition through regulation of voltage-dependent Ca(2+) channels, whereas K(+) channel regulation is believed to have no role at the CA3-CA1 synapse. We show here that the inhibitory effect of baclofen (20 μM) and adenosine (300 μM) on field EPSPs are differentially sensitive to Cs(+) (3.5 mM) and Ba(2+) (200 μM), but not 4-aminopyridine (100 μM). Barium had no effect on paired-pulse facilitation (PPF) in itself, but gave significant reduction (14 ± 5%) when applied in the presence of baclofen, but not adenosine, suggesting that the effect is presynaptic and selective on the GABA(B) receptor-mediated response. The effect of Ba(2+) on PPF was not...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4474524</comments>
            <pubDate>Fri, 28 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4474524</guid>        </item>
        <item>
            <title>Role of the Autonomic Nervous System in Rat Liver Regeneration.</title>
            <link>http://www.medworm.com/index.php?rid=4411775&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21264506%26dopt%3DAbstract</link>
            <description>Authors: Xu C, Zhang X, Wang G, Chang C, Zhang L, Cheng Q, Lu A
    To study the regulatory role of autonomic nervous system in rat regenerating liver, surgical operations of rat partial hepatectomy (PH) and its operation control (OC), sympathectomy combining partial hepatectomy (SPH), vagotomy combining partial hepatectomy (VPH), and total liver denervation combining partial hepatectomy (TDPH) were performed, then expression profiles of regenerating livers at 2 h after operation were detected using Rat Genome 230 2.0 array. It was shown that the expressions of 97 genes in OC, 230 genes in PH, 253 genes in SPH, 187 genes in VPH, and 177 genes in TDPH were significantly changed in biology. The relevance analysis showed that in SPH, genes involved in stimulus response, immunity response, am...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4411775</comments>
            <pubDate>Tue, 25 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4411775</guid>        </item>
        <item>
            <title>Lercanidipine Rescues Hippocampus Pyramidal Neurons from Mild Ischemia-Induced Delayed Neuronal Death in SHRSP.</title>
            <link>http://www.medworm.com/index.php?rid=4411778&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21259046%26dopt%3DAbstract</link>
            <description>This study was designed to compare the effects of the antihypertensive drugs lercanidipine, nicardipine, lisinopril, valsartan, and hydralazine on occlusion-induced DND in SHRSPs. Drugs were administered for 2 weeks, from 15 to 17 weeks of age. 0.1% Nicardipine and 0.01 or 0.03% lercanidipine were administered in the SP diet (about 61.3, 5.7, and 18.8 mg/kg/day, respectively), and the remaining drugs were administered at 10 mg/kg/day using the mini-osmotic pump. The animals were operated on at 16 weeks of age, and DND was analyzed by histological examination 1 week later. Systolic blood pressure was measured at 15, 16, and 17 weeks of age. For chronic treatment, Calcium-channel blockers were administered from 8 to 17 weeks of age. All antihypertensive drugs significantly lowered sy...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4411778</comments>
            <pubDate>Sun, 23 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4411778</guid>        </item>
        <item>
            <title>Expressions of Forkhead Class Box O 3a on Crushed Rat Sciatic Nerves and Differentiated Primary Schwann cells.</title>
            <link>http://www.medworm.com/index.php?rid=4411777&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21259047%26dopt%3DAbstract</link>
            <description>Authors: Wang Q, Wang Y, Zhou Z, Lu X, Cao Y, Liu Y, Yan M, He F, Pan X, Qian X, Ji Y, Yang H
    Forkhead box-containing protein, class O 3 a (FOXO3a), an Akt downstream target, plays an important role in peripheral nervous system. FOXO3a shares the ability to be inhibited and translocated from the nucleus on phosphorylation by proteins such as Akt/PKB in the PI3K signaling pathway. To elucidate the expression and possible function of FOXO3a in lesion and repair, we performed an acute sciatic nerve crush model and studied differential expressions of FOXO3a. We observed that expressions of FOXO3a in Schwann cells (SCs) of the peripheral nervous system and cAMP-induced differentiation were dynamically regulated. Western blot analysis showed FOXO3a level significantly decreased post injury. ...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4411777</comments>
            <pubDate>Sun, 23 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4411777</guid>        </item>
        <item>
            <title>Electrical Stimulation Promotes BDNF Expression in Spinal Cord Neurons Through Ca(2+)- and Erk-Dependent Signaling Pathways.</title>
            <link>http://www.medworm.com/index.php?rid=4411776&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21259048%26dopt%3DAbstract</link>
            <description>Authors: Wenjin W, Wenchao L, Hao Z, Feng L, Yan W, Wodong S, Xianqun F, Wenlong D
    Brief electrical stimulation has been shown to be effective in promoting neuronal regeneration following peripheral nerve injury. These effects are thought to be mediated largely by the upregulation of the expression of brain-derived neurotrophic factor (BDNF) in spinal cord neurons. However, the molecular mechanisms by which electrical stimulation can promote BDNF expression are not known. The mechanism involved in BDNF expression after electrical stimulation was explored in this study. Immunohistochemistry and Western blotting were used to test BDNF expression. Confocal microscopy was utilized to study intracellular Ca(2+) volume. Immunohistochemistry and Western blotting confirmed that brief electrica...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4411776</comments>
            <pubDate>Sun, 23 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4411776</guid>        </item>
        <item>
            <title>Tailless-like (TLX) Protein Promotes Neuronal Differentiation of Dermal Multipotent Stem Cells and Benefits Spinal Cord Injury in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=4411779&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21258860%26dopt%3DAbstract</link>
            <description>In conclusion, TLX promotes the proliferation and neuronal differentiation of DMSCs and thus, may serve as a promising therapy for SCI in the clinic.
    PMID: 21258860 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4411779</comments>
            <pubDate>Sat, 22 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4411779</guid>        </item>
        <item>
            <title>Modulation of LPA Receptor Expression in the Human Brain Following Neurotrauma.</title>
            <link>http://www.medworm.com/index.php?rid=4411782&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21234797%26dopt%3DAbstract</link>
            <description>Authors: Frugier T, Crombie D, Conquest A, Tjhong F, Taylor C, Kulkarni T, McLean C, Pébay A
    Lysophosphatidic acid (LPA) is involved in physiological and pathological states, including in neural development and inflammation. We assessed the expression pattern of the LPA receptors 1-3 and of LPA-producing enzyme autotaxin in post-mortem human brain tissue, both in normal individuals and in individuals who died following traumatic brain injury. We found that LPA receptors and autotaxin are weakly expressed in the normal control adult brain. Quantitative PCR for the LPA receptors and autotaxin mRNA showed an increase of LPAR(2) and a decrease of autotaxin mRNA expression in the cortex following brain injury. Immunohistochemical analysis showed that LPAR(1) colocalized with astrocytes and...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4411782</comments>
            <pubDate>Sat, 15 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4411782</guid>        </item>
        <item>
            <title>SMN Deficiency Reduces Cellular Ability to Form Stress Granules, Sensitizing Cells to Stress.</title>
            <link>http://www.medworm.com/index.php?rid=4411781&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21234798%26dopt%3DAbstract</link>
            <description>Authors: Zou T, Yang X, Pan D, Huang J, Sahin M, Zhou J
    Spinal Muscular Atrophy (SMA) is a neurodegenerative disease that is caused by deletion of the SMN (Survival of Motor Neuron) gene. The SMN protein is essential for cell survival and co-localized with TIA-1/R and G3BP, two characteristic markers of stress granules (SGs). To further study the SMN function in stress granules and in response to stress, we generated stable cell lines with SMN knockdown. Our data indicate that suppression of SMN drastically reduces cellular ability to form stress granules in response to stress treatment. In addition, we show that SMN deficiency sensitizes cells to sodium arsenite and H(2)O(2), two well-known stress inducers, leading to cell death at a much lower concentration of inducers in SMN knockdo...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4411781</comments>
            <pubDate>Sat, 15 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4411781</guid>        </item>
        <item>
            <title>No Observable Relationship Between the 12 Genes of Nervous System and Reasoning Skill in a Young Chinese Han Population.</title>
            <link>http://www.medworm.com/index.php?rid=4411780&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21234799%26dopt%3DAbstract</link>
            <description>This study suggests that some of the functional variations in BDNF, COMT, DBH, DRD ( 2 ), DRD ( 3 ), MAOA, 5-HT ( 2A ), 5-HT ( 6 ), GRM ( 1 ), and GRIN2B have no observable effects on the certain reasoning skills in a young healthy Chinese Han population.
    PMID: 21234799 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4411780</comments>
            <pubDate>Sat, 15 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4411780</guid>        </item>
        <item>
            <title>Masseteric Nerve Injury Increases Expression of Brain-Derived Neurotrophic Factor in Microglia Within the Rat Mesencephalic Trigeminal Tract Nucleus.</title>
            <link>http://www.medworm.com/index.php?rid=4343853&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21225335%26dopt%3DAbstract</link>
            <description>Authors: Ichikawa H, Sato T, Kano M, Suzuki T, Matsuo S, Kanetaka H, Shimizu Y
    The distribution of brain-derived neurotrophic factor was examined in the rat mesencephalic trigeminal tract nucleus after transection and crush of the masseteric nerve. In the intact mesencephalic trigeminal tract nucleus, brain-derived neurotrophic factor was detected in small cells with fine processes. These cells and processes were occasionally located adjacent to tyrosine kinase B receptor-immunoreactive sensory neurons. The transection and crush of the masseteric nerve increased expression of brain-derived neurotrophic factor in the nucleus. The number and size of brain-derived neurotrophic factor-immunoreactive cells and processes were dramatically elevated by the nerve injury. As a result, the densit...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4343853</comments>
            <pubDate>Wed, 12 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4343853</guid>        </item>
        <item>
            <title>SNAI1 is Involved in the Proliferation and Migration of Glioblastoma Cells.</title>
            <link>http://www.medworm.com/index.php?rid=4343852&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21225336%26dopt%3DAbstract</link>
            <description>Authors: Han SP, Kim JH, Han ME, Sim HE, Kim KS, Yoon S, Baek SY, Kim BS, Oh SO
    Glioblastoma is the most common type of astrocytoma in the brain. Due to its high invasiveness and chemoresistance, patients with advanced stage of glioblastoma have a poor prognosis. SNAI1, an important regulator of epithelial-mesenchymal transition, has been associated with metastasis in various carcinoma cells. However, its roles in glioblastoma cells have been poorly characterized. To examine roles of SNAI1 in glioblastoma cells, we knockdowned SNAI1 expression using siRNA. SNAI1 siRNA increased the expression level of E-cadherin and decreased that of vimentin. In the water-soluble tetrazolium salt (WST-1) assay, SNAI1 siRNA inhibited the proliferation of U87-MG and GBM05 glioblastoma cells. Moreover, i...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4343852</comments>
            <pubDate>Wed, 12 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4343852</guid>        </item>
        <item>
            <title>The Effects of Tag-1 on the Maturation of Mouse Cerebellar Granule Neurons.</title>
            <link>http://www.medworm.com/index.php?rid=4343859&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21191645%26dopt%3DAbstract</link>
            <description>Authors: Wang W, Karagogeos D, Kilpatrick DL
    The cell adhesion molecule Tag-1 is highly expressed in immature cerebellar granule neurons (CGNs) during axonogenesis and is down-regulated prior to onset of radial migration. However, its precise role(s) during development of mammalian CGNs has been unclear. Here we studied the effects of anti-Tag-1 function blocking antibodies on the development of mouse CGNs in primary cell culture and in situ. Interfering antibodies inhibited axon formation by mouse CGNs in both cell cultures and in cerebellar slices. Effects on axon extension in cell cultures were observed under conditions of homotypic cell-cell contact, consistent with inhibition of cell adhesion activity. Further, when used as a substratum Tag-1 protein strongly stimulated neurite ou...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4343859</comments>
            <pubDate>Thu, 30 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4343859</guid>        </item>
        <item>
            <title>Comparison of Phosphorylated Extracellular Signal-Regulated Kinase 1/2 Immunoreactivity in the Hippocampal Ca1 Region Induced by Transient Cerebral Ischemia Between Adult and Aged Gerbils.</title>
            <link>http://www.medworm.com/index.php?rid=4343857&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21191646%26dopt%3DAbstract</link>
            <description>In this study, the authors examined the difference of phosphorylated extracellular signal-regulated kinase 1/2 (pERK1/2) in the hippocampal CA1 region (CA1) between adult and aged gerbils after 5 min of transient cerebral ischemia. Delayed neuronal death in the CA1 of the aged group was much slower than that in the adult group after ischemia/reperfusion (I/R). pERK1/2 immunoreaction was observed in the CA1 region of the sham-operated adult gerbil. pERK1/2 immunoreactivity and protein levels in the ischemic CA1 region of the adult group were markedly increased 4 days after I/R, and then reduced up to 10 days after I/R. In contrast, pERK1/2 immunoreaction was hardly detected in the CA1 region of sham-operated aged gerbils, and the immunoreactivity increased from 1 day after the ischemic ...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4343857</comments>
            <pubDate>Thu, 30 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4343857</guid>        </item>
        <item>
            <title>Evidence that L: -Carnitine and Selenium Supplementation Reduces Oxidative Stress in Phenylketonuric Patients.</title>
            <link>http://www.medworm.com/index.php?rid=4343855&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21191647%26dopt%3DAbstract</link>
            <description>In conclusion, our results suggest that supplementation of L: -carnitine and selenium is important for PKU patients since it could help to correct the oxidative stress process which possibly contributes, at least in part, to the neurological symptoms found in phenylketonuric patients.
    PMID: 21191647 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Neurobiology)</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4343855</comments>
            <pubDate>Thu, 30 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4343855</guid>        </item>
        <item>
            <title>Effect of the PARP-1 Inhibitor PJ 34 on Excitotoxic Damage Evoked by Kainate on Rat Spinal Cord Organotypic Slices.</title>
            <link>http://www.medworm.com/index.php?rid=4343860&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21190076%26dopt%3DAbstract</link>
            <description>Authors: Mazzone GL, Nistri A
    Excitotoxicity triggered by over-activation of glutamate receptors is thought to be an early mechanism of extensive neuronal death with consequent loss of function following lesion of spinal networks. One important process responsible for excitotoxic death is 'parthanatos' caused by hyperactivation of poly(ADP-ribose) polymerase (PARP) enzyme 1. Using rat organotypic spinal slices as in vitro models, the present study enquired if 2-(dimethylamino)-N-(5,6-dihydro-6-oxophenanthridin-2yl)acetamide (PJ 34), a pharmacological inhibitor of PARP-1, could counteract the excitotoxic damage evoked by transient application (1 h) of kainate, a potent analogue of glutamate. Kainate induced dose-dependent (1 μM threshold) neuronal loss (without damage to astrocytes) ...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4343860</comments>
            <pubDate>Wed, 29 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4343860</guid>        </item>
        <item>
            <title>Protective Effects of Flavonoid Extract from Apocynum venetum Leaves Against Corticosterone-Induced Neurotoxicity in PC12 Cells.</title>
            <link>http://www.medworm.com/index.php?rid=4279026&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21170580%26dopt%3DAbstract</link>
            <description>Authors: Zheng M, Liu C, Pan F, Shi D, Ma F, Zhang Y, Zhang Y
    Depression is a major psychiatric disorder affecting nearly 21% of the world population and imposes a substantial health burden on society. Although significant progress has been made in depression research, the common molecular mechanism of antidepressants is still far from clearly understood. The neuroprotective effect of antidepressants has been proposed as a possible mechanism. Although Apocynum venetum (AV) L. (Apocynaceae) was previously shown to produce an antidepressant-like effect in the tail suspension test, the mechanisms underlying such antidepressant-like effect are yet to be understood. In this work, we studied the neuroprotective effect of AV leaf flavonoid extract in corticosterone-induced neurotoxicity, usin...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4279026</comments>
            <pubDate>Sat, 18 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4279026</guid>        </item>
        <item>
            <title>Beneficial Effects of Folic Acid on Enhancement of Memory and Antioxidant Status in Aged Rat Brain.</title>
            <link>http://www.medworm.com/index.php?rid=4279025&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21170581%26dopt%3DAbstract</link>
            <description>This study was carried out on 6-, 11-, and 16-month-old rats, which received folic acid at a dose of 5 mg/kg body weight/day for a period of 8 weeks. Respective control groups of the same age groups were also taken. At the end of the treatment duration, behavioral studies were performed and later the animals were killed for various biochemical and histological investigations. Results indicated significant improvement in memory as assessed by active avoidance, passive avoidance, and plus maze tests in the folic acid supplemented aged animals. Significant improvement was also seen in the cellular protective mechanisms where by the activity of superoxide dismutase and catalase enzymes increased in folic acid supplemented group and so was the glutathione content. Increased lipid peroxidation...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4279025</comments>
            <pubDate>Sat, 18 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4279025</guid>        </item>
        <item>
            <title>Fibrinogen Depleting Agent Batroxobin has a Beneficial Effect on Experimental Autoimmune Encephalomyelitis.</title>
            <link>http://www.medworm.com/index.php?rid=4279027&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21165693%26dopt%3DAbstract</link>
            <description>Authors: Yang Y, Tian SJ, Wu L, Huang DH, Wu WP
    Multiple sclerosis (MS) was characterized with widespread demyelination and axonal loss of central nervous system (CNS). Fibrinogen (fibrin) deposition was considered as one of the pathogenesis of MS. Therefore, we explored the effects of fibrinogen depleting agent batroxobin in experimental autoimmune encephalomyelitis (EAE) mice model. Our study showed that prevention and suppression with batroxobin significantly ameliorated clinical severity of EAE, reduced inflammatory cells infiltration, and demyelination, and suppressed the activation of astrocytes and macrophages comprising the CD11b(+) population. Batroxobin treatment leads to reduced expression of p-Akt and increased expression of MBP as compared to control. In addition, batroxob...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4279027</comments>
            <pubDate>Fri, 17 Dec 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>Optimal Location and Time for Neural Stem Cell Transplantation into Transected Rat Spinal Cord.</title>
            <link>http://www.medworm.com/index.php?rid=4279028&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21161579%26dopt%3DAbstract</link>
            <description>This study investigated the effect and fate of NSC engrafted into spinal cords at different locations and time points following T(9) spinal cord transection. Engrafted NSC could survive and migrate in host spinal cords. Significant improvement in hindlimb locomotor functions associated with NSC survival was found in rats receiving NSC transplantation in the spinal cords rostral to the transection site at the subacute stage (7 days post operation), compared with those caudal to the transection site at the acute stage (at the time of injury). At 4 weeks post operation, CD68 immunohistochemical staining confirmed that macrophages were less in rostrally transplanted sites and in subacute groups than seen in caudal and acute transplanted rats. The present findings indicated that NSC transplan...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4279028</comments>
            <pubDate>Tue, 14 Dec 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>The Change of the Spinal Cord Ischemia-Reperfusion Injury in Mitochondrial Passway and the Effect of the Ginkgo biloba Extract's Preconditioning Intervention.</title>
            <link>http://www.medworm.com/index.php?rid=4279029&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21153434%26dopt%3DAbstract</link>
            <description>Authors: Cheng B, Wang W, Lin L, Li F, Wang X
    In order to explore whether the apoptosis in ischemia-reperfusion injury could be affected by Ginkgo biloba extract (GBE) and the free radical scavenger GBE could suppress this affection. Rabbits were randomly divided into sham group, ischemia group, ischemia-reperfusion group (1, 6, 24, 48 h), the drug group (1, 6, 24, 48 h). Measure the rate of apoptosis by flow cytometry, the caspase 9 and apoptosis-inducing factor (AIF) in the cytoplasm and serum by ELISA. Compared with the sham group and ischemia group, the reperfusion group increased the rate of apoptosis, the caspase 9 and AIF in serum have a peak at 24 h after reperfusion, in the cytoplasm the peak at 6 h.GBE inhibit performance has the systemic and local aspects. The apoptosis ...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4279029</comments>
            <pubDate>Fri, 10 Dec 2010 00:00:00 +0100</pubDate>
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            <title>Decreased Glucagon-Like Peptide-1 Receptor Immunoreactivity in the Dentate Granule Cell Layer from Adult in the Gerbil Hippocampus.</title>
            <link>http://www.medworm.com/index.php?rid=4279031&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21152969%26dopt%3DAbstract</link>
            <description>In this study, we investigated age-related changes in glucagon-like peptide-1 receptor (GLP-1R) immunoreactivity and its protein levels in the gerbil hippocampus during normal aging. In the postnatal month 3 (PM 3) group, GLP-1R immunoreaction was well observed in neurons, especially pyramidal and non-pyramidal cells in the hippocampus proper, and granule and polymorphic cells in the dentate gyrus. In the hippocampus proper, GLP-1R immunoreactivity in neurons was maintained until PM 24. In the dentate gyrus, however, GLP-1R immunoreactivity in granule cells, not polymorphic cells, was hardly detected from PM 6. Western blot analysis also showed that age-dependent change patterns in GLP-1R protein levels in the gerbil hippocampus were similar to the immunohistochemical changes. These result...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4279031</comments>
            <pubDate>Thu, 09 Dec 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>Gonadal Steroids do not Affect Apolipoprotein E Expression in Aging Mouse Cerebral Cortex.</title>
            <link>http://www.medworm.com/index.php?rid=4279030&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21152970%26dopt%3DAbstract</link>
            <description>Authors: Singh S, Thakur MK
    The allelic variant of apolipoprotein (Apo) E4 is a known risk factor for the development of most common late onset form of Alzheimer's disease (AD). As aging is associated with reduced circulating level of gonadal steroid hormones, hormone replacement therapies have been used for the possible treatment of AD. Both estrogen and testosterone have beneficial effects on brain due to interaction with apoE, but the underlying mechanism is still not clear. In this article, we report the effects of gonadectomy and hormone supplementation on apoE protein level in male and female mouse cerebral cortex during normal aging. We could not get any effect of gonadectomy and estradiol or testosterone treatment in adult and old mice of either sex. This suggests that during n...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4279030</comments>
            <pubDate>Thu, 09 Dec 2010 00:00:00 +0100</pubDate>
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            <title>In Vitro and In Vivo Magnetic Resonance Tracking of Sinerem-Labeled Human Umbilical Mesenchymal Stromal Cell-Derived Schwann Cells.</title>
            <link>http://www.medworm.com/index.php?rid=4221298&amp;cid=s_37768_171_f&amp;fid=37768&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21120599%26dopt%3DAbstract</link>
            <description>In this study, we induce HUMSCs into Schwann-like cells in terms of morphology, phenotype, and function by an improved protocol basing on our previous studies. Furthermore, HUMSCs-derived SCs are labeled efficiently in vitro with ultrasmall superparamagnetic iron oxide contrast agent (USPIO) Sinerem and poly-L: -lysine (PLL) without affecting morphology, cell cycle, proliferation, and differentiation ability of the labeled cells between the concentration of 200 to 800 μg/ml. Importantly, when grafted into the intact cerebral cortex and striatum, the survival and migration of these Sinerem-labeled cells were observed using MRI. Our study suggest the effective concentration field for Sinerem use in tracking transdifferentiated HUMSCs, and Sinerem labeling transdifferentiated HUMSCs is feas...</description>
            <author>Cellular and Molecular Neurobiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4221298</comments>
            <pubDate>Wed, 01 Dec 2010 00:00:00 +0100</pubDate>
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