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        <title>Neurochemical Research via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Neurochemical Research' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Neurochemical+Research&t=Neurochemical+Research&s=Search&f=source]]></link>
        <lastBuildDate>Sat, 20 Mar 2010 16:33:18 +0100</lastBuildDate>
        <item>
            <title>Effects of N-acetylcysteine/deferoxamine, taurine and RC-3095 on respiratory chain complexes and creatine kinase activities in rat brain after sepsis.</title>
            <link>http://www.medworm.com/index.php?rid=3381573&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20238483%26dopt%3DAbstract</link>
            <description>Authors: Cassol OJ, Rezin GT, Petronilho FC, Scaini G, Gon&amp;#xE7;alves CL, Ferreira GK, Roesler R, Schwartsmann G, Dal-Pizzol F, Streck EL
    The pathogenesis of sepsis is characterized by an overwhelming systemic inflammatory response that can lead to multiple organ failure. Considering that we have recently demonstrated that mitochondrial respiratory chain and creatine kinase (CK) are altered in the brain of rats after cecal ligation and perforation (CLP) and that a combination of N-acetylcysteine/deferoxamine (NAC/DFX), taurine and RC-3095 were shown to be an effective treatment of sepsis, we investigated whether the alterations of these enzymes may be reversed by these drugs. The results demonstrated that CLP inhibited complexes I and II, and that all the treatments were able to revers...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3381573</comments>
            <pubDate>Fri, 19 Mar 2010 16:48:18 +0100</pubDate>
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        <item>
            <title>Sex steroids inhibit osmotic swelling of retinal glial cells.</title>
            <link>http://www.medworm.com/index.php?rid=3381572&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20238484%26dopt%3DAbstract</link>
            <description>Authors: Neumann F, Wurm A, Linnertz R, Pannicke T, Iandiev I, Wiedemann P, Reichenbach A, Bringmann A
    Osmotic swelling of glial cells may contribute to the development of retinal edema. We investigated whether sex steroids inhibit the swelling of glial somata in acutely isolated retinal slices and glial cells of the rat. Superfusion of retinal slices or cells from control animals with a hypoosmolar solution did not induce glial swelling, whereas glial swelling was observed in slices of postischemic and diabetic retinas. Progesterone, testosterone, estriol, and 17beta-estradiol prevented glial swelling with half-maximal effects at approximately 0.3, 0.6, 6, and 20 microM, respectively. The effect of progesterone was apparently mediated by transactivation of metabotropic glutamate recep...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3381572</comments>
            <pubDate>Fri, 19 Mar 2010 16:48:14 +0100</pubDate>
            <guid isPermaLink="false">3381572</guid>        </item>
        <item>
            <title>Anti-inflammatory Activity of Salvianolic Acid B in Microglia Contributes to its Neuroprotective Effect.</title>
            <link>http://www.medworm.com/index.php?rid=3381574&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20238162%26dopt%3DAbstract</link>
            <description>In conclusion, these data demonstrate that anti-inflammatory activity of Sal B in microglia contributes to its neuroprotective effect and suggest that it may be useful for preventing microglia-mediated neuroinflammation.
    PMID: 20238162 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3381574</comments>
            <pubDate>Thu, 18 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3381574</guid>        </item>
        <item>
            <title>Tyrosine Phosphorylation of Apoptotic Proteins During Hyperoxia in Mitochondria of the Cerebral Cortex of Newborn Piglets.</title>
            <link>http://www.medworm.com/index.php?rid=3355083&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20213344%26dopt%3DAbstract</link>
            <description>Authors: Mudduluru M, Zubrow AB, Ashraf QM, Delivoria-Papadopoulos M, Mishra OP
    The present study tests the hypothesis that hyperoxia results in increased tyrosine phosphorylation of apoptotic proteins Bcl-2, Bcl-xl, Bax &amp; Bad in the mitochondrial fraction of the cerebral cortex of newborn piglets. Twelve newborn piglets were divided into normoxic [Nx, n = 6], exposed to a FiO(2) of 0.21 for 1 h and hyperoxic [Hyx, n = 6], exposed to FiO(2) of 1.0 for 1 h. PaO(2) in Hyx group was maintained at 400 mmHg while the Nx group was kept at 80 to100 mmHg. The density (O.D.x mm(2)) of phosphorylated Bcl2 protein on westernblot was 19.3 +/- 3.6 in Nx and 41.5 +/- 18.3 in Hyx, (P &amp;lt; 0.05). The density of phosphorylated Bcl-xl protein density was 26.9 +/- 7.0 in Nx and 47.9 +/- 2.5 in Hyx, (...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3355083</comments>
            <pubDate>Tue, 09 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3355083</guid>        </item>
        <item>
            <title>Flavonoids and Astrocytes Crosstalking: Implications for Brain Development and Pathology.</title>
            <link>http://www.medworm.com/index.php?rid=3355082&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20213345%26dopt%3DAbstract</link>
            <description>Authors: Nones J, Stipursky J, Costa SL, Gomes FC
    Flavonoids are naturally occurring polyphenolic compounds that are present in a variety of fruits, vegetables, cereals, tea, and wine, and are the most abundant antioxidants in the human diet. Evidence suggests that these phytochemicals might have an impact on brain pathology and aging; however, neither their mechanisms of action nor their cell targets are completely known. In the mature mammalian brain, astroglia constitute nearly half of the total cells, providing structural, metabolic, and trophic support for neurons. During the past few years, increasing knowledge of these cells has indicated that astrocytes are pivotal characters in neurodegenerative diseases and brain injury. Most of the physiological benefits of flavonoids are ge...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3355082</comments>
            <pubDate>Tue, 09 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3355082</guid>        </item>
        <item>
            <title>Light-Induced Tyrosine Phosphorylation of Rod Outer Segment Membrane Proteins Regulate the Translocation, Membrane Binding and Activation of Type II alpha Phosphatidylinositol-5-Phosphate 4-Kinase.</title>
            <link>http://www.medworm.com/index.php?rid=3337061&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20204506%26dopt%3DAbstract</link>
            <description>Authors: Huang Z, Anderson RE, Cao W, Wiechmann AF, Rajala RV
    Type II phosphatidylinositol 5-phosphate 4-kinase (PIPKIIalpha) catalyzes the synthesis of phosphatidylinositol-4,5-bisphosphate (PI-4,5-P(2)), an essential lipid second messenger that may be involved in the regulation of phototransduction, neuroprotection, and morphogenesis in the vertebrate retina. Here we report that in rodent and transgenic frogs, the light-mediated activity and membrane binding of PIPKIIalpha in rod outer segments (ROS) is dependent on tyrosine phosphorylation of ROS proteins. The greater type II alpha PIP kinase activity in the light-adapted ROS membrane results from light-driven translocation of PIPKIIalpha from the rod inner segment to ROS, and subsequent binding to the ROS membrane, thus improving a...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3337061</comments>
            <pubDate>Fri, 05 Mar 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>Expression of the Hippocampal NMDA Receptor GluN1 Subunit and Its Splicing Isoforms in Schizophrenia: Postmortem Study.</title>
            <link>http://www.medworm.com/index.php?rid=3337058&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20204507%26dopt%3DAbstract</link>
            <description>Authors: Vrajov&amp;#xE1; M, S&amp;#x165;astn&amp;#xFD; F, Hor&amp;#xE1;&amp;#x10D;ek J, Lochman J, Ser&amp;#xFD; O, Pekov&amp;#xE1; S, Klaschka J, H&amp;#xF6;schl C
    There is accumulating evidence that disturbances in N-methyl-D: -aspartate receptor (NMDA-R) functioning are associated with the pathogenesis of schizophrenia. To assess actual changes in the expression of the GluN1 subunit and its isoforms, we measured absolute differences in the levels of mRNA/protein for panGluN1 (eight isoforms altogether) as well as the mRNA individual isoforms in the postmortem left/right hippocampus of patients with schizophrenia in comparison with non-psychiatric subjects. There were no significant differences in the panGluN1 subunit mRNA expression, but the absolute left/right differences were much more pronounced in the patient...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3337058</comments>
            <pubDate>Fri, 05 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3337058</guid>        </item>
        <item>
            <title>Erratum to: Protective Effects of Acetyl-L: -Carnitine on Cisplatin Cytotoxicity and Oxidative Stress in Neuroblastoma.</title>
            <link>http://www.medworm.com/index.php?rid=3337062&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20191382%26dopt%3DAbstract</link>
            <description>Authors: Altun ZS, G&amp;#xFC;ne&amp;#x15F; D, Akta&amp;#x15F; S, Erbayraktar Z, Olgun N
    
    PMID: 20191382 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3337062</comments>
            <pubDate>Sat, 27 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3337062</guid>        </item>
        <item>
            <title>Transient Receptor Potential Vanilloid-1 (TRPV1) and Ankyrin-1 (TRPA1) Participate in Visceral Hyperalgesia in Chronic Water Avoidance Stress Rat Model.</title>
            <link>http://www.medworm.com/index.php?rid=3312263&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20182791%26dopt%3DAbstract</link>
            <description>Authors: Yu YB, Yang J, Zuo XL, Gao LJ, Wang P, Li YQ
    Stressfull life events have powerful influences on visceral perception of certain IBS patients. In the present study, we aimed to examine the involvement of TRPV1 and TRPA1 in the stress-induced visceral hyperalgesia. Rats were exposed to 1-h water avoidance stress (WAS) daily for 10 consecutive days. The abdominal withdrawal reflex (AWR) to colorectal distension was assessed at the end of the 10-day period. Western-blotting analysis was applied to investigate the alterations of TRPV1 and TRPA1 in the colonic afferent dorsal root ganglia (DRG). Compared with control rats, the WAS-treated rats demonstrated a significant increase in the AWR with the pressure &amp;gt;/=40 mm Hg (P &amp;lt; 0.05). Meanwhile, in the WAS-treated rats, western-blo...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3312263</comments>
            <pubDate>Thu, 25 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3312263</guid>        </item>
        <item>
            <title>Stimulation of Prostaglandin EP2 Receptors on RGC-5 Cells in Culture Blunts the Negative Effect of Serum Withdrawal.</title>
            <link>http://www.medworm.com/index.php?rid=3312265&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20180018%26dopt%3DAbstract</link>
            <description>Authors: Kang KD, Andrade da Costa BL, Osborne NN
    Reduced neurotrophic support is one possible cause for retinal ganglion cells dying in glaucoma. Experiments were designed to investigate the effect of EP2 receptor agonist butaprost on transformed retinal ganglion (RGC-5) cells where reduced neurotrophic support was simulated by serum withdrawal. Cultures were analysed for cell viability, flow cytometry, reactive oxygen species and apoptosis. Western blot and immunohistochemistry were used to provide information for the occurrence of PGE(2) receptor-types. We demonstrated the existence of all four types of PGE(2) receptors in RGC-5 cells and exposure of cultures to butaprost resulted in an elevation of cAMP. Serum deprivation induced RGC-5 cell death was significantly attenuated by but...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3312265</comments>
            <pubDate>Wed, 24 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3312265</guid>        </item>
        <item>
            <title>Inhibition of ATP-Induced Ca(2+) Influx by Corticosterone in Dorsal Root Ganglion Neurons.</title>
            <link>http://www.medworm.com/index.php?rid=3312264&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20180019%26dopt%3DAbstract</link>
            <description>Authors: Liu X, Zeng J, Zhao Y, Xiao Z, Fang C, Ruan H
    In addition to the classic genomic effects, it is well known that glucocorticoids also have rapid, nongenomic effects on neurons. In the present study, the effect of corticosterone (CORT) on ATP-induced Ca(2+) mobilization in cultured dorsal root ganglion (DRG) neurons were detected with confocal laser scanning microscopy using fluo-4/AM as a calcium fluorescent indicator that could monitor real-time alterations of intracellular calcium concentration ([Ca(2+)]i). ATP, an algesic agent, caused [Ca(2+)]i increase in DRG neurons by activation of P2X receptor. Pretreatment with CORT (1 nM-1 muM for 5 min) inhibited ATP-induced [Ca(2+)]i increase in DRG neurons. The rapid inhibition of ATP-induced Ca(2+) response by CORT was concentrati...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3312264</comments>
            <pubDate>Wed, 24 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3312264</guid>        </item>
        <item>
            <title>Effect of Combination Treatment of Rapamycin and Isoflavones on mTOR Pathway in Human Glioblastoma (U87) Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3303340&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20177775%26dopt%3DAbstract</link>
            <description>In this study we investigated the effect of combination treatment of rapamycin with isoflavones such as genistein and biochanin A on mTOR pathway and activation of Akt and eIF4E in human glioblastoma (U87) cells. Our results show that combination treatment of rapamycin with isoflavones, especially biochanin A at 50 muM, decreased the phosphorylation of Akt and eIF4E proteins and rendered U87 cells more sensitive to rapamycin treatment when compared to cells treated with rapamycin alone. These results suggest the importance of combining chemopreventive with chemotherapeutic agents in order to increase the efficacy of chemotherapeutic drugs.
    PMID: 20177775 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3303340</comments>
            <pubDate>Tue, 23 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3303340</guid>        </item>
        <item>
            <title>Urokinase-Type Plasminogen Activator Induces BV-2 Microglial Cell Migration Through Activation of Matrix Metalloproteinase-9.</title>
            <link>http://www.medworm.com/index.php?rid=3303339&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20177776%26dopt%3DAbstract</link>
            <description>In this study, we investigated the effect of urokinase-type plasminogen activator (uPA) on the BV-2 microglial cell migration. At resting state, BV-2 microglial cells secreted uPA and the release of uPA was increased by ATP, a chemoattractant released from injured neuron. The migration of BV-2 cell was significantly induced by uPA and inhibited by uPA inhibitors. In this condition, uPA increased the activity of matrix metalloproteinase (MMP-9) and the inhibition of MMP activity with pharmacological inhibitors against either uPA (amiloride) or MMP (phenanthrolene and SB-3CT) effectively prevented BV2 cell migration. Interestingly, the level of MMP-9 protein and mRNA in the cell were not changed by uPA. These results suggest that the increase of MMP-9 activity by uPA is regulated at the post...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3303339</comments>
            <pubDate>Tue, 23 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3303339</guid>        </item>
        <item>
            <title>The Fat-1 Mouse has Brain Docosahexaenoic Acid Levels Achievable Through Fish Oil Feeding.</title>
            <link>http://www.medworm.com/index.php?rid=3303338&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20177777%26dopt%3DAbstract</link>
            <description>In conclusion, brain levels of DHA in the fat-1 mouse can be obtained by and were not further augmented with fish oil feeding.
    PMID: 20177777 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3303338</comments>
            <pubDate>Tue, 23 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3303338</guid>        </item>
        <item>
            <title>Molecular Profiling of a 6-Hydroxydopamine Model of Parkinson's Disease.</title>
            <link>http://www.medworm.com/index.php?rid=3291503&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20169470%26dopt%3DAbstract</link>
            <description>Authors: Na SJ, Dilella AG, Lis EV, Jones K, Levine DM, Stone DJ, Hess JF
    Convection enhanced delivery of 6-hydroxydopamine (6-OHDA) to the rat striatum results in a model of Parkinson's disease. An important feature of this unilateral model is the progressive loss of dopaminergic (DA) neurons over the course of several weeks. To improve the understanding of this model, gene expression changes in the substantia nigra, which contains the DA neuron cell bodies, and the striatum, which contains the DA neuron synaptic terminals, were examined using DNA microarrays. Samples were collected and behavior was analyzed from vehicle and toxin treated animals at 3 days, 1 week, 2 weeks and 4 weeks following 6-OHDA treatment. Tissue DA content was determined and samples from animals which exhibited...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3291503</comments>
            <pubDate>Fri, 19 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3291503</guid>        </item>
        <item>
            <title>Regulation of AMPA Receptor Trafficking by O-Glycosylation.</title>
            <link>http://www.medworm.com/index.php?rid=3285759&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20165912%26dopt%3DAbstract</link>
            <description>Authors: Kanno T, Yaguchi T, Nagata T, Mukasa T, Nishizaki T
    The present study investigated the role of O-linked beta-N-acetylglucosamine (O-GlcNAc) glycosylation (O-GlcNAcylation) in AMPA receptor trafficking. Alloxan, an inhibitor of O-GlcNAc transferase, potentiated responses of AMPA receptors composed of the GluR1 subunit expressed in Xenopus oocytes. No potentiating effect of alloxan was obtained with mutant GluR1 (S831A) receptor lacking CaMKII phosphorylation site. Alloxan facilitated basal synaptic transmission to approximately 120% of basal levels and enhanced Schaffer collateral-CA1 long-term potentiation (LTP) in rat hippocampal slices, especially in the late phase of the LTP. Alloxan stimulated translocation of the GluR1 and GluR2 subunit from the cytosol towards the plasma...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3285759</comments>
            <pubDate>Thu, 18 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3285759</guid>        </item>
        <item>
            <title>Leucine-Rich Glioma Inactivated 3 Induces Neurite Outgrowth Through Akt and Focal Adhesion Kinase.</title>
            <link>http://www.medworm.com/index.php?rid=3285760&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20162351%26dopt%3DAbstract</link>
            <description>Authors: Park WJ, Lim YY, Kwon NS, Baek KJ, Kim DS, Yun HY
    Leucine-rich glioma inactivated 3 (LGI3) is a secreted protein that belongs to LGI/epitempin family. LGI3 is highly expressed in brain in a transcriptionally and developmentally regulated manner. Here we found that LGI3 induced neurite outgrowth in Neuro-2a cells and dorsal root ganglia explants. LGI3 treatment or overexpression increased neurite outgrowth and knockdown of LGI3 by siRNA had opposite effect. LGI3 treatment increased phosphorylation of Akt and a 125-kDa protein. Immunoprecipitation identified the 125-kDa protein as focal adhesion kinase (FAK). LGI3 overexpression increased phospho-Akt, phospho-FAK and FAK protein. Inhibition of Akt activation by PI3 kinase inhibitor attenuated LGI3-induced FAK phosphorylation and...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3285760</comments>
            <pubDate>Wed, 17 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3285760</guid>        </item>
        <item>
            <title>Cornel Iridoid Glycoside Inhibits Inflammation and Apoptosis in Brains of Rats with Focal Cerebral Ischemia.</title>
            <link>http://www.medworm.com/index.php?rid=3280237&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20155318%26dopt%3DAbstract</link>
            <description>Authors: Ya BL, Li CY, Zhang L, Wang W, Li L
    The capacity of cornel iridoid glycoside (CIG) to suppress the manifestations of ischemic stroke was investigated. CIG was administered to rats by the intragastric route once daily for 7 days. Focal cerebral ischemia was induced by 2 h of middle cerebral artery occlusion followed by 24 h of reperfusion. In non-treated rats large infarct areas were observed within 24 h of reperfusion. Examination of the ischemic cerebral cortex revealed microglia and astrocyte activation, increased interleukin-1beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) concentrations, increased DNA fragmentation in the ischemia penumbra, elevated Bax expression, increased caspase-3 cleavage, and decreased Bcl-2 expression. Pretreatment with CIG decreased th...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3280237</comments>
            <pubDate>Sat, 13 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3280237</guid>        </item>
        <item>
            <title>Withdrawal from Fixed-Dose Injection of Methamphetamine Decreases Cerebral Levels of 3-Methoxy-4-hydroxyphenylglycol and Induces the Expression of Anxiety-Related Behavior in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=3270038&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20148307%26dopt%3DAbstract</link>
            <description>Authors: Kitanaka N, Kitanaka J, Tatsuta T, Tanaka KI, Watabe K, Nishiyama N, Morita Y, Takemura M
    A variety of drug treatment regimens have been proposed to model the dysphoric state observed during methamphetamine (METH) withdrawal in rats, but little has been established in experiments using mice. In male ICR mice, a fixed-dose injection regimen of METH (1.0 or 2.5 mg/kg, i.p., twice daily for 10 consecutive days) induced a significant decrease in the time spent in open arms in an elevated plus maze after 5 days of drug abstinence. Under an escalating-dose injection regimen (0.2-2.0 mg/kg, i.p., 3 times daily for 4 days, total: 15 mg/kg/animal) or continuous subcutaneous administration with osmotic mini-pumps (15 or 76 mg/kg of METH for 2 weeks), no significant behavioral change was...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3270038</comments>
            <pubDate>Thu, 11 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3270038</guid>        </item>
        <item>
            <title>High Affinity Carnitine Transporters from OCTN Family in Neural Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3263306&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20143157%26dopt%3DAbstract</link>
            <description>Authors: Januszewicz E, Bekisz M, Mozrzymas JW, Na&amp;#x142;&amp;#x119;cz KA
    Neurons are known to accumulate L: -carnitine-a compound necessary for transfer of acyl moieties through biological membranes, apart from very low beta-oxidation of fatty acids in adult brain. Present study demonstrates expression of octn2 and octn3 genes coding high affinity carnitine transporters, as well as presence of both proteins in neurons obtained from suckling and adult rats, and also in mouse transformed neural cells. Measurements of carnitine transport show activity of both transporters in neural cells, pointing to their importance in physiological processes other than beta-oxidation.
    PMID: 20143157 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3263306</comments>
            <pubDate>Tue, 09 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3263306</guid>        </item>
        <item>
            <title>Transportable and Non-transportable Inhibitors of L: -glutamate Uptake Produce Astrocytic Stellation and Increase EAAT2 Cell Surface Expression.</title>
            <link>http://www.medworm.com/index.php?rid=3263305&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20143158%26dopt%3DAbstract</link>
            <description>Authors: Lau CL, Beart PM, O'Shea RD
    Astrocytic excitatory amino acid transporters (EAATs) regulate excitatory transmission and limit excitotoxicity. Evidence for a functional interface between EAATs and glial fibrillary acidic protein (GFAP) relevant to astrocytic morphology led to investigations of actions of transportable (D: -Aspartate (D: -Asp) and (2S,3S,4R)-2-(carboxycyclopropyl)glycine (L: -CCG-III)) and non-transportable (DL: -threo-beta-benzyloxyaspartate (DL: -TBOA)) inhibitors of Glu uptake in murine astrocytes. D: -Asp (1 mM), L: -CCG-III (0.5 mM) and DL: -TBOA (0.5 mM) produced time-dependent (24-72 h) reductions in (3)[H]D: -Asp uptake (approximately 30-70%) with little or no gliotoxicity. All drugs induced a profound change in phenotype from cobblestone to stellate morp...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3263305</comments>
            <pubDate>Tue, 09 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3263305</guid>        </item>
        <item>
            <title>A Milk-Based Wolfberry Preparation Prevents Prenatal Stress-Induced Cognitive Impairment of Offspring Rats, and Inhibits Oxidative Damage and Mitochondrial Dysfunction In Vitro.</title>
            <link>http://www.medworm.com/index.php?rid=3244944&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20131093%26dopt%3DAbstract</link>
            <description>Authors: Feng Z, Jia H, Li X, Bai Z, Liu Z, Sun L, Zhu Z, Bucheli P, Ball&amp;#xE8;vre O, Wang J, Liu J
    Lycium barbarum (Fructus Lycii, Wolfberry, or Gouqi) belongs to the Solanaceae. The red-colored fruits of L. barbarum have been used for a long time as an ingredient in Chinese cuisine and brewing, and also in traditional Chinese herbal medicine for improving health. However, its effects on cognitive function have not been well studied. In the present study, prevention of a milk-based wolfberry preparation (WP) on cognitive dysfunction was tested in a prenatal stress model with rats and the antioxidant mechanism was tested by in vitro experiments. We found that prenatal stress caused a significant decrease in cognitive function (Morris water maze test) in female offspring. Pretreatment o...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3244944</comments>
            <pubDate>Fri, 05 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3244944</guid>        </item>
        <item>
            <title>Developing Brain as an Endocrine Organ: A Paradoxical Reality.</title>
            <link>http://www.medworm.com/index.php?rid=3244942&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20135220%26dopt%3DAbstract</link>
            <description>Authors: Ugrumov MV
    The maintaining of homeostasis in the organism in response to a variable environment is provided by the highly hierarchic neuroendocrine-immune system. The crucial component of this system is the hypothalamus providing the endocrine regulation of key peripheral organs, and the adenohypophysis. In this case, neuron-derived signaling molecules (SM) are delivered to the blood vessels in hypothalamic &quot;neurohaemal organs&quot; lacking the blood-brain barrier (BBB), the posterior lobe of the pituitary and the median eminence. The release of SM to the blood vessels in most other brain regions is prohibited by BBB. According to the conventional concept, the development of the neuroendocrine system in ontogenesis begins with the &quot;maturation&quot; of peripheral endocrine glands which f...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3244942</comments>
            <pubDate>Fri, 05 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3244942</guid>        </item>
        <item>
            <title>Erratum to: Recombinant DNA Vaccine Against Inhibition of Neurite Outgrowth Promotes Functional Recovery Associated with Endogeous NGF Expression in Spinal Cord Hemisected Adult Rats.</title>
            <link>http://www.medworm.com/index.php?rid=3244943&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20131094%26dopt%3DAbstract</link>
            <description>Authors: Zhang Y, Hao CG, Hu LQ, Dong J, Wei P, Xu D, Xiao ZC, Wang TH
    
    PMID: 20131094 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3244943</comments>
            <pubDate>Thu, 04 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3244943</guid>        </item>
        <item>
            <title>Increased Plasma Levels of Brain Derived Neurotrophic Factor (BDNF) in Patients with Fibromyalgia.</title>
            <link>http://www.medworm.com/index.php?rid=3231924&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20119637%26dopt%3DAbstract</link>
            <description>Authors: Haas L, Portela LV, B&amp;#xF6;hmer AE, Oses JP, Lara DR
    Brain-derived neurotrophic factor (BDNF) is involved in neuronal survival and synaptic plasticity of the central and peripheral nervous system. BDNF appears to modulate nociceptive sensory inputs and pain hypersensitivity and has been studied in pathological situations, including chronic pain conditions and major depression. Increased serum BDNF levels have been recently reported in fibromyalgia (FM). In the present study, we assessed plasma BDNF levels in patients with FM and controls. Plasma BDNF was measured from 30 female patients with FM and 30 healthy age- and gender-matched volunteers using an enzyme immunoassay. FM patients showed higher levels of BDNF (FM = 167.1 +/- 171.2 pg/mL) when compared with the control group...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3231924</comments>
            <pubDate>Sat, 30 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3231924</guid>        </item>
        <item>
            <title>Neurturin Effects on Nigrostriatal Dopamine Release and Content: Comparison with GDNF.</title>
            <link>http://www.medworm.com/index.php?rid=3231923&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20119638%26dopt%3DAbstract</link>
            <description>Authors: Cass WA, Peters LE
    Neurturin (NTN) is a member of the glial cell line-derived neurotrophic factor (GDNF) family; and, while GDNF has been shown to increase dopamine (DA) release in normal animals, the ability of NTN to alter DA release has not been previously reported. The purpose of the present study was to determine if NTN could alter striatal DA release, and to compare the effects of NTN to GDNF. Male Fischer-344 rats were given a single injection of vehicle or 5 mug NTN or GDNF into the right substantia nigra. Three weeks later microdialysis experiments were conducted to assess striatal DA release. Basal extracellular levels of striatal DA were not affected by either NTN or GDNF. However, both NTN and GDNF led to increases in amphetamine-evoked overflow of DA from the ipsi...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3231923</comments>
            <pubDate>Sat, 30 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3231923</guid>        </item>
        <item>
            <title>On a New Strategy of Preventive Oncology.</title>
            <link>http://www.medworm.com/index.php?rid=3231922&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20119639%26dopt%3DAbstract</link>
            <description>Authors: Mkrtchyan LN
    The etiology of cancer is much wider than separately taken causal agent and rests against the most complicated interrelation and mutuality of many external and internal influences. Our researches with use of fluorescing antibodies to AFP, CEA and Ca-19-9 have shown that they are intensively besieged on a surface of cultivated malignant cells. It is the basic mechanism of tolerance and immunological escape, which is similar to pregnancy when &amp;lt;&amp;lt;the maximal immunological most favored status&quot; to developing fetus (semiallogenic transplant) is provided. The earliest revealing of first cancer cells, before steady community of cells and tumor angiogenesis were formed, has particular importance in the fight against cancer. The necessity of the specific completion of ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3231922</comments>
            <pubDate>Sat, 30 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3231922</guid>        </item>
        <item>
            <title>A Pressurized Nitrogen Counterbalance to Cortical Glutamatergic Pathway Stimulation.</title>
            <link>http://www.medworm.com/index.php?rid=3225096&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20111995%26dopt%3DAbstract</link>
            <description>In conclusion, the function of the corticostriatal pathway is affected by nitrogen under pressure. This suggests that the nitrogen-induced break point seems to be located at the glutamatergic striatopetal neurons.
    PMID: 20111995 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3225096</comments>
            <pubDate>Fri, 29 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3225096</guid>        </item>
        <item>
            <title>Alternative Complement Pathway in Schizophrenia.</title>
            <link>http://www.medworm.com/index.php?rid=3213220&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20101522%26dopt%3DAbstract</link>
            <description>Authors: Boyajyan A, Khoyetsyan A, Chavushyan A
    In the present study, we evaluated functional activity of the alternative pathway of complement in schizophrenia by measuring the alternative pathway hemolytic activity (AH50) of complement as well as hemolytic activity of the complement C3 component (C3H50) in the blood of patients with schizophrenia and healthy subjects. To assess the influence of neuroleptic treatment on measured parameters, both drug-free and medicated patients were examined. In addition, correlation analysis between AH50 and C3H50 has been performed. The results of the present study clearly demonstrate upregulation of the alternative complement cascade in schizophrenia and activator effect of neuroleptics on complement alternative pathway. Based upon the results obta...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3213220</comments>
            <pubDate>Tue, 26 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3213220</guid>        </item>
        <item>
            <title>Linoleic Acid Derivative DCP-LA Protects Neurons from Oxidative Stress-Induced Apoptosis by Inhibiting Caspase-3/-9 Activation.</title>
            <link>http://www.medworm.com/index.php?rid=3213221&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20099079%26dopt%3DAbstract</link>
            <description>Authors: Yaguchi T, Fujikawa H, Nishizaki T
    The present study aimed at understanding the effect of the linoleic acid derivative 8-[2-(2-pentyl-cyclopropylmethyl)-cyclopropyl]-octanoic acid (DCP-LA) on oxidative stress-induced neuronal death. Sodium nitroprusside (SNP; 1 mM) reduced viability of cultured rat cerebral cortical neurons to 50% of basal levels, but DCP-LA significantly prevented the SNP effect in a concentration (1-100 nM)-dependent manner. In addition, DCP-LA (100 nM) rescued neurons from SNP-induced degradation. SNP (1 mM) activated caspase-3 and -9 in cultured rat cerebral cortical neurons, but DCP-LA (100 nM) abolished the caspase activation. For a mouse model of middle cerebral artery occlusion, oral administration with DCP-LA (1 mg/kg) significantly diminished degrade...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3213221</comments>
            <pubDate>Sat, 23 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3213221</guid>        </item>
        <item>
            <title>The Physical Chemistry of Brain and Neural Cell Membranes: An Overview.</title>
            <link>http://www.medworm.com/index.php?rid=3201198&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20094775%26dopt%3DAbstract</link>
            <description>Authors: Robertson DS
    The formation of cell membranes through the physical-chemical interaction of two hydrophilic colloidal fluids is applied to the formation of the membranes of brain and neural cells. Also described is the membrane mechanism of transfer of ions and compounds necessary for brain and neural cell functions into the cerebrospinal fluid through the blood-brain barrier. Changes in the cerebrospinal fluid giving rise to degradation of brain and neural cells and the formation of precipitates within the brain are considered. Monitoring of electrolyte changes in metabolic fluids is shown to be a possible method of predicting the onset of degenerate brain conditions.
    PMID: 20094775 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3201198</comments>
            <pubDate>Fri, 22 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3201198</guid>        </item>
        <item>
            <title>Proline-Rich Hypothalamic Polypeptide Has Opposite Effects on the Proliferation of Human Normal Bone Marrow Stromal Cells and Human Giant-cell Tumour Stromal Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3195431&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20087764%26dopt%3DAbstract</link>
            <description>Authors: Chailakhyan RK, Gerasimov YV, Chailakhyan MR
    In the present study we carried out experiments in vitro and in vivo and investigated the effect of proline-rich polypeptide (PRP) on the proliferation and effectiveness of colony formation of MMSCs in vitro. Various routes and doses of PRP administration to rats increased the number of MMSCs in bone marrow and spleen. Our research revealed opposite effects of PRP on the proliferation of bone marrow stromal cells obtained from normal humans and stromal cells isolated from a human giant-cell tumour.
    PMID: 20087764 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3195431</comments>
            <pubDate>Wed, 20 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3195431</guid>        </item>
        <item>
            <title>Cynomorium songaricum Extracts Functionally Modulate Transporters of gamma-Aminobutyric Acid and Monoamine.</title>
            <link>http://www.medworm.com/index.php?rid=3189466&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20084455%26dopt%3DAbstract</link>
            <description>Authors: Zhao G, Wang J, Qin GW, Guo LH
    Cynomorium songaricum Rupr. (SY) is a central nervous system-oriented herb material that has actions of anti-dementia, anti-epilepsy, and anti-stress. It is unclear whether SY would be biologically active in functionally regulating neurotransmitter transporters. Here, we assessed these potential actions using Chinese hamster ovary cells expressing gamma-aminobutyric acid (GABA) transporter (GAT-1), dopamine transporter (DAT), norepinephrine transporter (NET), or serotonin transporter (SERT) (i.e. G1, D8, N1, or S6 cells, respectively). It was shown that SY extracts, such as SYw, SYa, SYp, SYc, SYe, and SYb (SY water, ethanol, petroleum ether, chloroform, ethyl acetate, and n-butyl alcohol extract, respectively) increased dopamine/norepinephrine (...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3189466</comments>
            <pubDate>Tue, 19 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3189466</guid>        </item>
        <item>
            <title>Acute Restraint Stress Enhances Calcium Mobilization and Glutamate Exocytosis in Cerebrocortical Synaptosomes from Mice.</title>
            <link>http://www.medworm.com/index.php?rid=3172668&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20069359%26dopt%3DAbstract</link>
            <description>Authors: Satoh E, Shimeki S
    Acute stress is known to enhance the memory of events that are potentially threatening to the organisms. Glutamate, the most abundant excitatory neurotransmitter in the mammalian central nervous system, plays a critical role in learning and memory formation and calcium (Ca(2+)) plays an essential role in transmitter release from nerve terminals (synaptosomes). In the present study, we investigated the effects of acute restraint stress on cytosolic free Ca(2+) concentration ([Ca(2+)](i)) and glutamate release in cerebrocortical synaptosomes from mice. Acute restraint stress caused a significant increase in resting [Ca(2+)](i) and significantly enhanced the ability of the depolarizing agents K(+) and 4-aminopyridine (4-AP) to increase [Ca(2+)](i). It also brou...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3172668</comments>
            <pubDate>Wed, 13 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3172668</guid>        </item>
        <item>
            <title>Metformin Normalizes Type 2 Diabetes-Induced Decrease in Cell Proliferation and Neuroblast Differentiation in the Rat Dentate Gyrus.</title>
            <link>http://www.medworm.com/index.php?rid=3172667&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20069360%26dopt%3DAbstract</link>
            <description>In this study, we observed the effects of metformin, one of the most widely prescribed drugs for the treatment of type 2 diabetes, on cell proliferation and neuroblast differentiation in the subgranular zone of the hippocampal dentate gyrus (SZDG) in Zucker diabetic fatty (ZDF) rats, which are a model for type 2 diabetes. For this, metformin was administered orally once a day to 14-week-old ZDF rats for 2 weeks and the animals were sacrificed at 16 weeks of age. During this period, blood glucose levels were higher in the vehicle-treated ZDF rats than in the Zucker lean control (ZLC) rats. Metformin treatment significantly decreased the blood glucose levels from 15.5 weeks of age. In the SZDG, Ki67 (a marker for cell proliferation)- and doublecortin (DCX, a marker for differentiated neurobl...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3172667</comments>
            <pubDate>Wed, 13 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3172667</guid>        </item>
        <item>
            <title>Temperature Dependence of the Sodium Pump is Altered in the Cerebral Cortex of CCK(2) Receptor-Deficient Mice.</title>
            <link>http://www.medworm.com/index.php?rid=3154469&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20058075%26dopt%3DAbstract</link>
            <description>In this study we compared temperature dependence of the Na(+),K(+)-ATPase in the fronto-parietal cortex of CCK(2) receptor-deficient (homo- and heterozygous) and normal (wild-type) mice. The Arrhenius plot for Na(+),K(+)-ATPase from wild-type brain is non-linear with a breakpoint at 20.3 +/- 0.4 degrees C. In case of the brain cell membrane of CCK(2) receptor-deficient mice (homo- and heterozygous) the breakpoint on Arrhenius plot was detected at 26.0 +/- 1.1 degrees C and 25.4 +/- 0.4 degrees C, respectively. The shift of the breakpoint on the Arrhenius plot established in CCK(2) receptor-deficiency as well as in case of some other pathological conditions confirms that such kind of alteration in the Na(+),K(+)-ATPase temperature dependence is likely related to the homeostatic adjustment o...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3154469</comments>
            <pubDate>Fri, 08 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3154469</guid>        </item>
        <item>
            <title>Modulation of Carbohydrate Metabolism During N-Methyl N-Nitrosourea Induced Neurotoxicity in Mice: Role of Curcumin.</title>
            <link>http://www.medworm.com/index.php?rid=3154470&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20054649%26dopt%3DAbstract</link>
            <description>Authors: Singla N, Dhawan DK
    The present study was carried out to elucidate the effectiveness of curcumin in mitigating the adverse effects caused by N-Methyl N-Nitrosourea (MNU) on mouse cerebellum and cerebrum. Male laca mice received either intravenous MNU treatment at a dose of 10 mg/kg bw in sterile double distilled water, curcumin alone 60 mg/kg bw in drinking water, or combined MNU and curcumin treatment on alternate days for a period of 2 months. The effects of different treatments were studied on carbohydrate metabolizing enzymes viz: hexokinase, glucose-6-phosphatase (G6P), glucose-6-isomerase (G6I), lactate dehydrogenase (LDH), succinate dehydrogenase (SDH) and glycogen levels. Curcumin supplementation to MNU treated mice was able to reduce significantly the activities of th...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3154470</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3154470</guid>        </item>
        <item>
            <title>Tau Phosphorylation and Cleavage in Ethanol-Induced Neurodegeneration in the Developing Mouse Brain.</title>
            <link>http://www.medworm.com/index.php?rid=3149397&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20049527%26dopt%3DAbstract</link>
            <description>Authors: Saito M, Chakraborty G, Mao RF, Paik SM, Vadasz C, Saito M
    Previous studies indicated that ethanol-induced neurodegeneration in postnatal day 7 (P7) mice, widely used as a model for the fetal alcohol spectrum disorders, was accompanied by glycogen synthase kinase-3beta (GSK-3beta) and caspase-3 activation. Presently, we examined whether tau, a microtubule associated protein, is modified by GSK-3beta and caspase-3 in ethanol-treated P7 mouse forebrains. We found that ethanol increased phosphorylated tau recognized by the paired helical filament (PHF)-1 antibody and by the antibody against tau phosphorylated at Ser199. Ethanol also generated tau fragments recognized by an antibody against caspase-cleaved tau (C-tau). C-tau was localized in neurons bearing activated caspase-3 and...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3149397</comments>
            <pubDate>Tue, 05 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3149397</guid>        </item>
        <item>
            <title>Human Serotonin Transporter Expression During Megakaryocytic Differentiation of MEG-01 Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3135935&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20041293%26dopt%3DAbstract</link>
            <description>In this study, we used cell cultures of platelet precursors as models of investigation on mechanisms of SERT regulation: SERT expression was appraised during megakaryocytic differentiation of human megakaryoblastic MEG-01 cells. Cells were cultured for 8 days with 10(-7)M 4-beta-12-tetradecanoylphorbol-13-acetate (beta-TPA) in the presence of 10% fetal bovine serum (FBS) and SERT was assessed by real time PCR, immunofluorescence microscopy, Western blot and [(3)H]5-HT re-uptake. Results revealed that SERT is present in control-untreated MEG-01 cells. beta-TPA-differentiating MEG-01 cells showed a redistribution of SERT fluorescence, diffuse to cell bodies and blebs along with a 3-fold SERT mRNA increase and a moderate raise in SERT protein (1.5/1.4-fold) by immunoblot and re-uptake assays....</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3135935</comments>
            <pubDate>Wed, 30 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3135935</guid>        </item>
        <item>
            <title>In Vivo Neuroprotective Effects of Peripheral Kynurenine on Acute Neurotoxicity Induced by Glutamate in Rat Cerebral Cortex.</title>
            <link>http://www.medworm.com/index.php?rid=3122779&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20035383%26dopt%3DAbstract</link>
            <description>Authors: Kumar A, Nagesh Babu G
    N-methyl-D-aspartate (NMDA) receptors play a crucial role in Glutamate (L: -Glu) neurotoxicity. To evaluate the effects of astrocyte-derived tryptophan metabolite kynurenic acid (KYNA), on L: -Glu neurotoxicity, adult male rats were pretreated with Kynurenine (KYN) which is a precursor of KYNA, at a dose of 30 mg or 300 mg/kg bw i.p., 2 h before stereotactic L: -Glu bolus (1mumole/1 mul) administration in cerebral cortex. Results showed that acute L: -Glu increased reactive oxygen species, rate of lipid peroxidation, calcium, nitric oxide and neuroinflammatory markers viz. TNF-alpha, IFN-gamma levels and decreased key antioxidant parameters such as SOD, catalase, total glutathione and glutathione reductase along with mitochondrial membrane potential. Whi...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3122779</comments>
            <pubDate>Fri, 25 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3122779</guid>        </item>
        <item>
            <title>Synemin Isoforms in Astroglial and Neuronal Cells from Human Central Nervous System.</title>
            <link>http://www.medworm.com/index.php?rid=3115535&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20024673%26dopt%3DAbstract</link>
            <description>Authors: Izmiryan A, Peltekian E, Paulin D, Li Z, Xue Z
    The intermediate filament (IF) synemin gene encodes three IF proteins (H 180, M 150, L 41 kDa) with overlapping distributions. Synemin M was present early with vimentin and nestin. Synemin H was found later in the nervous system and mesodermic derivatives concomitantly with angiogenesis and the migration of neural crest cells. Synemin L appeared later in neurons. A series of in vitro cell cultures were done to identify the linkage between synemin isoforms and specific cell types of the central nervous system (CNS). The neurons and glia from the brains of humans and rats were cultured and double immunostaining done with antibodies against the H/M or L synemin isoforms and neural cell types (betaIII-tubulin or NeuN) or astrocyte int...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3115535</comments>
            <pubDate>Sat, 19 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3115535</guid>        </item>
        <item>
            <title>Hypothalamic Proline Rich Polypeptide Regulates Hematopoiesis.</title>
            <link>http://www.medworm.com/index.php?rid=3105665&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20020325%26dopt%3DAbstract</link>
            <description>Authors: Bezirganyan KB, Davtyan TK, Galoyan AA
    The AGAPEPAEPAQPGVY proline-rich polypeptide (PRP-1) was isolated from neurosecretory granules of the bovine neurohypophysis; it is produced by N. supraopticus and N. paraventricularis. It has been shown that PRP-1 has many potentially beneficial biological effects including immunoregulatory, hematopoietic, antimicrobial and anti-neurodegenerative properties. Here we demonstrated that PRP-1 administration influence on redistribution of monocytes, granulocytes and lymphocytes between bone marrow (BM) and peripheral blood and promotes the influx of granulocytes and monocytes/macrophages from BM into peripheral blood and accumulation of immature granulocyte and monocyte in BM and delayed the maturation of T cells in BM. PRP-1 increased colon...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105665</comments>
            <pubDate>Fri, 18 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105665</guid>        </item>
        <item>
            <title>Brain Arachidonic Acid Cascade Enzymes are Upregulated in a Rat Model of Unilateral Parkinson Disease.</title>
            <link>http://www.medworm.com/index.php?rid=3076046&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19997776%26dopt%3DAbstract</link>
            <description>Authors: Lee HJ, Bazinet RP, Rapoport SI, Bhattacharjee AK
    Arachidonic acid (AA) signaling is upregulated in the caudate-putamen and frontal cortex of unilaterally 6-hydroxydopamine (6-OHDA) lesioned rats, a model for asymmetrical Parkinson disease. AA signaling can be coupled to D(2)-like receptor initiated AA hydrolysis from phospholipids by cytosolic phospholipase A(2) (cPLA(2)) and subsequent metabolism by cyclooxygenase (COX)-2. In unilaterally 6-OHDA- and sham-lesioned rats, we measured brain expression of cPLA(2), other PLA(2) enzymes, and COX-2. Activity and protein levels of cPLA(2) were significantly higher as was COX-2-protein in caudate-putamen, frontal cortex and remaining brain on the lesioned compared to intact side of the 6-OHDA lesioned rats, and compared to sham brain...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3076046</comments>
            <pubDate>Tue, 08 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3076046</guid>        </item>
        <item>
            <title>Hemorphins Act as Homeostatic Agents in Response to Endotoxin-Induced Stress.</title>
            <link>http://www.medworm.com/index.php?rid=3067735&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19967445%26dopt%3DAbstract</link>
            <description>Authors: Barkhudaryan N, Zakaryan H, Sarukhanyan F, Gabrielyan A, Dosch D, Kellermann J, Lottspeich F
    The effect of synthetic LVV-hemorphin-7 and hemorphin-7 on hypothalamo-pituitary-adrenocortical axis activity in response to endotoxin-induced stress was studied. The intraperitoneal (ip) endotoxin (lipopolysaccaride, LPS) (0.5 mg/kg) administration in combination with hemorphin (1 mg/kg) induce significant decrease in plasma corticosterone and modest decrease in plasma levels of tumor necrosis factor-alpha (TNFalpha) in compare with elevated levels of both corticosterone and TNFalpha in plasma of rats received LPS administration alone. Increased activity of calcineurin in both plasma and brain of rats received ip administration of LPS, was recovered under LPS + hemorphin treatment. In...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3067735</comments>
            <pubDate>Sat, 05 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3067735</guid>        </item>
        <item>
            <title>Comparison of the Efficiencies of Three Neural Induction Protocols in Human Adipose Stromal Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3061759&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19960248%26dopt%3DAbstract</link>
            <description>Authors: Qian DX, Zhang HT, Ma X, Jiang XD, Xu RX
    The aim of this study was to compare the neural differentiation potential and the expression of neurotrophic factors (NTFs) in differentiated adipose-derived stem cells (ADSCs) using three established induction protocols, serum free (Protocol 1), chemical reagents (Protocol 2), and spontaneous (Protocol 3) protocols. Protocol 1 produced the highest percentage of mature neural-like cells (MAP2ab(+)). Protocol 2 showed the highest percentage of immature neural-like cells (beta-tubulin III(+)), but the neural-like state was transient and reversible. Protocol 3 caused ADSCs to differentiate spontaneously into immature neural-like cells, but not into mature neural cell types. The neural-like cells produced by Protocol 1 lived the longest in ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3061759</comments>
            <pubDate>Fri, 04 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3061759</guid>        </item>
        <item>
            <title>Tyrosine Kinase Inhibitor AG126 Reduces 7-Ketocholesterol-Induced Cell Death by Suppressing Mitochondria-Mediated Apoptotic Process.</title>
            <link>http://www.medworm.com/index.php?rid=3057470&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19957203%26dopt%3DAbstract</link>
            <description>Authors: Kim YJ, Lee CS
    The preventive effect of tyrosine kinase inhibitor AG126 against the 7-ketocholesterol toxicity was investigated in relation to the mitochondria-mediated cell death process. 7-Ketocholesterol induced the nuclear damage, the mitochondrial membrane permeability changes, the formation of reactive oxygen species and the depletion of GSH, which leads to cell death in differentiated PC12 cells. Tyrphostin AG126 significantly attenuated the 7-ketocholesterol-induced decrease in cytosolic Bid and Bcl-2 levels, increase in cytosolic pro-apoptotic Bax levels, mitochondrial membrane potential loss, cytochrome c release and subsequent caspase-3 activation. The inhibitory effect of tyrphostin AG126 may be supported by the inhibitory effect on another oxysterol 25-hydroxychol...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057470</comments>
            <pubDate>Thu, 03 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3057470</guid>        </item>
        <item>
            <title>Proline-rich Polypeptide-1 Protects the Cells In Vitro from Genotoxic Effects of Mitomycin C.</title>
            <link>http://www.medworm.com/index.php?rid=3049304&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19949858%26dopt%3DAbstract</link>
            <description>Authors: Aroutiounian RM, Hovhannisyan GG, Gasparyan GH, Margaryan KS, Aroutiounian DN, Sarkissyan NK, Galoyan AA
    A new proline-rich polypeptide (PRP-1) has been earlier shown to possess a broad spectrum of biological activities and seems to be a potential medicine. The potential genotoxic properties of PRP-1 and protective effect of PRP-1 against genotoxic action of Mitomycin C (MMC) were analyzed in details in the present work. DNA and chromosome damages were studied in KCL-22 cell line of human myeloid leukemia by the Comet assay and micronucleus induction test, respectively. The results suggest that DNA damages are, at least partly, transient and reparable. PRP-1 at the doses 0.5-2.0 mug/ml does not possess genotoxic activity. Moreover, this peptide expresses both preventive and th...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3049304</comments>
            <pubDate>Tue, 01 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3049304</guid>        </item>
        <item>
            <title>Nicotine Reduces the Cytotoxic Effect of Glycated Proteins on Microglial Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3041735&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19946744%26dopt%3DAbstract</link>
            <description>In this study the effect of nicotine on protein glycation and structural alterations of the glycated protein were investigated. Bovine serum albumin, as a model protein, was glycated by glucose in the presence or absence of nicotine and structural changes in the protein together with the effect of glycated proteins on the activation of microglia via receptor of AGE were studied. Nicotine not only could not prevent glycation, but even increased protein glycation. However, proteins glycated in the presence of nicotine did not form beta-structures. In the absence of this secondary structure glycated proteins cannot bind to the receptor of AGE on microglia. Here we showed that glycated proteins prepared in the presence of nicotine could not activate microglial cells.
    PMID: 19946744 [PubMed...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3041735</comments>
            <pubDate>Sat, 28 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3041735</guid>        </item>
        <item>
            <title>mRNA Expression of Proteins Involved in Iron Homeostasis in Brain Regions is Altered by Age and by Iron Overloading in the Neonatal Period.</title>
            <link>http://www.medworm.com/index.php?rid=3037138&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19943190%26dopt%3DAbstract</link>
            <description>Authors: Dornelles AS, Garcia VA, de Lima MN, Vedana G, Alcalde LA, Bogo MR, Schr&amp;#xF6;der N
    Abnormally high levels of iron are observed in the brain of patients suffering from neurodegenerative disorders. The mechanisms involved in iron accumulation in neurodegenerative disorders remain poorly understood. In the present study we investigated the effects of aging and neonatal iron overload on the mRNA expression of proteins critically involved in controlling iron homeostasis. Wistar rat pups received a single daily dose of vehicle or iron (10 mg/kg of b.w. of Fe(2+)), at postnatal days 12-14. The expression of Transferrin Receptor (TfR), H-Ferritin, and IRP2 were analyzed by a semi-quantitative reverse transcriptase polymerase chain reaction assay in cortex, hippocampus and striatum of...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3037138</comments>
            <pubDate>Fri, 27 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3037138</guid>        </item>
        <item>
            <title>Changes in Extracellular Kynurenic Acid Concentrations in Rat Prefrontal Cortex After D: -Kynurenine Infusion: An In vivo Microdialysis Study.</title>
            <link>http://www.medworm.com/index.php?rid=3034124&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19941066%26dopt%3DAbstract</link>
            <description>Authors: Ogaya T, Song Z, Ishii K, Fukushima T
    Using a microdialysis technique, we continuously infused D: -kynurenine (KYN) (0, 50, and 100 muM) into the prefrontal cortices (PFCs) of male Sprague-Dawley rats. We then used column-switching high-performance liquid chromatography to assess the alterations in the concentration of kynurenic acid (KYNA)-an antagonist of N-methyl-D: -aspartate and alpha7 nicotinic acetylcholine receptors-in the extracellular fluid in the PFC. Local infusion of D: -KYN into the PFC remarkably increased the extracellular KYNA concentration, indicating that D: -KYN is metabolized to KYNA in the PFC. The D: -KYN-induced increase in KYNA levels was significantly attenuated by the co-administration of 3-methylpyrazole-5-carboxylic acid (AS057278)-a specific inhib...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3034124</comments>
            <pubDate>Thu, 26 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3034124</guid>        </item>
        <item>
            <title>Apoptosis-Associated Tyrosine Kinase and Neuronal Cell Death.</title>
            <link>http://www.medworm.com/index.php?rid=3034123&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19941067%26dopt%3DAbstract</link>
            <description>Authors: Hughes JP, Ward DR, Facci L, Richardson JC, Skaper SD
    Apoptosis-associated tyrosine kinase (AATYK) is up-regulated by phosphorylation in cultured cerebellar granule neurons (CGN) undergoing apoptosis upon switch to low KCl-containing medium. However, the underlying signaling pathways remain to be fully characterized. When CGN at culture day 7 were switched from 25 mM KCl (K25) to 5 mM (K5) medium, AATYK band migration on SDS-PAGE shifted to a more slowly migrating position expected for the hyperphosphorylated protein. The apoptosis-inducing agent C(2)-ceramide also caused a mobility shift of the AATYK protein. Exposing CGN (K25) to L-type voltage-dependent Ca(2+) channel antagonists shifted the AATYK band to the K5-induced position, while the Ca(2+) channel activator FPL-64176...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3034123</comments>
            <pubDate>Thu, 26 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3034123</guid>        </item>
        <item>
            <title>The Effects of Alpha-Tocopherol on Hippocampal Oxidative Stress Prior to in Pilocarpine-Induced Seizures.</title>
            <link>http://www.medworm.com/index.php?rid=3034122&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19941068%26dopt%3DAbstract</link>
            <description>The objective of the present study was to evaluate the neuroprotective effects of alpha-tocopherol (TP) in rats, against oxidative stress caused by pilocarpine-induced seizures. 30 min prior to behavioral observation, Wistar rats were treated with, 0.9% saline (i.p., control group), TP (200 mg/kg, i.p., TP group), pilocarpine (400 mg/kg, i.p., P400 group), or the combination of TP (200 mg/kg, i.p.) and pilocarpine (400 mg/kg, i.p.). After the treatments all groups were observed for 6 h. The enzymatic activities, lipid peroxidation and nitrite concentrations were measured using speccitrophotometric methods and these data were assayed. In P400 group mice there was a significant increase in lipid peroxidation and nitrite levels. However, no alteration was observed in superoxide dismutase (SOD...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3034122</comments>
            <pubDate>Thu, 26 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3034122</guid>        </item>
        <item>
            <title>HIV-1 Integrase and Virus and Cell DNAs: Complex Formation and Perturbation by Inhibitors of Integration.</title>
            <link>http://www.medworm.com/index.php?rid=3034125&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19937113%26dopt%3DAbstract</link>
            <description>Authors: Hobaika Z, Zargarian L, Maroun RG, Mauffret O, Burke TR, Fermandjian S
    HIV-1 integrase (IN) catalyzes integration of viral DNA into cell DNA through 3'-processing of viral DNA and strand transfer reactions. To learn on binding of IN to DNAs and IN inhibition we applied spectroscopy (circular dichroism, fluorescence) in a simplified model consisting in a peptide analogue (K156) of alpha4 helix involved in recognition of viral and cell DNA; an oligonucleotide corresponding to the U5' LTR DNA end; and an inhibitor (TB11) of the diketo acid (DKA) family. Results extrapolated to IN show that: the enzyme binds viral DNA with high affinity and specificity, but cell DNA with low affinity and specificity; the affinity of TB11 for IN is high enough to impair the binding of IN to cell DN...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3034125</comments>
            <pubDate>Tue, 24 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3034125</guid>        </item>
        <item>
            <title>Altered Regulation of CD200 Receptor in Monocyte-Derived Macrophages from Individuals with Parkinson's Disease.</title>
            <link>http://www.medworm.com/index.php?rid=3009312&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19924532%26dopt%3DAbstract</link>
            <description>Authors: Luo XG, Zhang JJ, Zhang CD, Liu R, Zheng L, Wang XJ, Chen SD, Ding JQ
    Microglia are the representative myeloid cells in the brain, and their over-activation plays an important role in the pathogenesis of Parkinson's disease (PD). Microglia activation is believed to be regulated by the CD200-CD200R signaling. As the peripheral counterpart of microglia, monocyte-derived macrophages (MDMs) share the same progenitor and antigen markers, and they have similar biological behaviors and mirror microglial function in the brain. Here, we studied CD200R expression and its regulation in MDMs from 32 PD cases, 27 age-matched old controls, and 28 young controls. We found that the basal CD200R expression is similar in MDMs from young control, old control and PD patients. However, the inducti...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3009312</comments>
            <pubDate>Thu, 19 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3009312</guid>        </item>
        <item>
            <title>Sex Steroids Inhibit Osmotic Swelling of Retinal Glial Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3009311&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19924533%26dopt%3DAbstract</link>
            <description>Authors: Neumann F, Wurm A, Linnertz R, Pannicke T, Iandiev I, Wiedemann P, Reichenbach A, Bringmann A
    Osmotic swelling of glial cells may contribute to the development of retinal edema. We investigated whether sex steroids inhibit the swelling of glial somata in acutely isolated retinal slices and glial cells of the rat. Superfusion of retinal slices or cells from control animals with a hypoosmolar solution did not induce glial swelling, whereas glial swelling was observed in slices of postischemic and diabetic retinas. Progesterone, testosterone, estriol, and 17ss-estradiol prevented glial swelling with half-maximal effects at approximately 0.3, 0.6, 6, and 20 muM, respectively. The effect of progesterone was apparently mediated by transactivation of metabotropic glutamate receptors,...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3009311</comments>
            <pubDate>Thu, 19 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3009311</guid>        </item>
        <item>
            <title>Strain Difference in the Up-Regulation of FGF-2 Protein Following a Neurotoxic Lesion of the Nigrostriatal Pathway.</title>
            <link>http://www.medworm.com/index.php?rid=3009314&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19921430%26dopt%3DAbstract</link>
            <description>In this study we examined protein content of basic fibroblast growth factor (FGF-2) in tissue samples taken from the ventral midbrain and striatum at two different time points following a neurotoxic lesion of the nigrostriatal pathway in two different rat strains, the outbred Sprague-Dawley (SD) and inbred F344 x Brown Norway F1 hybrid (F344BNF(1)). Despite both rat strains having comparable lesions of the nigrostriatal pathway, we observed a difference in the temporal up-regulation of FGF-2 in ventral midbrain samples taken from the side ipsilateral to the lesion. Basic FGF was significantly up-regulated in ventral midbrain in SD rats 1 week post-lesion while we did not observe an up-regulation of FGF-2 in the lesioned ventral midbrain of F344BNF(1) at this same time point. However, both ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3009314</comments>
            <pubDate>Wed, 18 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3009314</guid>        </item>
        <item>
            <title>Cardioactive Protein-Hormonal Complexes of Brain and Heart.</title>
            <link>http://www.medworm.com/index.php?rid=3009313&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19921431%26dopt%3DAbstract</link>
            <description>Authors: Srapionyan RM, Galoyan AA
    New cardioactive protein-hormone complexes (PHC) are identified in magnocellular nuclei of hypothalamus. It was proved that they are specific for nervous tissues and are involved in the regulation of metabolic processes of brain and visceral organs, including the heart. PHC dissociate into high-molecular forms which are new specific glycoproteins and the low-molecular cardioactive neurohormones. Results of our own studies on the functional activities of PHC as well as cardioactive peptides in the precardiac and auricular regions of the heart with respect to the parameters of haemostasis system are reviewed.
    PMID: 19921431 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3009313</comments>
            <pubDate>Wed, 18 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3009313</guid>        </item>
        <item>
            <title>Synergy of IL-23 and Th17 Cytokines: New Light on Inflammatory Bowel Disease.</title>
            <link>http://www.medworm.com/index.php?rid=3003427&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19915978%26dopt%3DAbstract</link>
            <description>Authors: Shen W, Durum SK
    Inflammatory bowel diseases (IBDs), including Crohn's disease and ulcerative colitis, involve an interplay between host genetics and environmental factors including intestinal microbiota. Animal models of IBD have indicated that chronic inflammation can result from over-production of inflammatory responses or deficiencies in key negative regulatory pathways. Recent research advances in both T-helper 1 (Th1) and T-helper 17 (Th17) effect responses have offered new insights on the induction and regulation of mucosal immunity which is linked to the development of IBD. Th17 cytokines, such as IL-17 and IL-22, in combination with IL-23, play crucial roles in intestinal protection and homeostasis. IL-23 is expressed in gut mucosa and tends to orchestrate T-cell-inde...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3003427</comments>
            <pubDate>Sat, 14 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3003427</guid>        </item>
        <item>
            <title>Effects of N-Acetylcysteine/Deferoxamine, Taurine and RC-3095 on Respiratory Chain Complexes and Creatine Kinase Activities in Rat Brain After Sepsis.</title>
            <link>http://www.medworm.com/index.php?rid=3003429&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19911272%26dopt%3DAbstract</link>
            <description>Authors: Cassol OJ, Rezin GT, Petronilho FC, Scaini G, Gon&amp;#xE7;alves CL, Ferreira GK, Roesler R, Schwartsmann G, Dal-Pizzol F, Streck EL
    The pathogenesis of sepsis is characterized by an overwhelming systemic inflammatory response that can lead to multiple organ failure. Considering that we have recently demonstrated that mitochondrial respiratory chain and creatine kinase (CK) are altered in the brain of rats after cecal ligation and perforation (CLP) and that a combination of N-acetylcysteine/deferoxamine (NAC/DFX), taurine and RC-3095 were shown to be an effective treatment of sepsis, we investigated whether the alterations of these enzymes may be reversed by these drugs. The results demonstrated that CLP inhibited complexes I and II, and that all the treatments were able to revers...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3003429</comments>
            <pubDate>Fri, 13 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3003429</guid>        </item>
        <item>
            <title>Lead Affects Apoptosis and Related Gene XIAP and Smac Expression in the Hippocampus of Developing Rats.</title>
            <link>http://www.medworm.com/index.php?rid=3003428&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19911273%26dopt%3DAbstract</link>
            <description>Authors: Liu J, Han D, Li Y, Zheng L, Gu C, Piao Z, Au WW, Xu X, Huo X
    Lead (Pb) exposure poses devastating effects on central nervous system development of children. To replicate aspects of this neurotoxicity, we examined the effect of lead on the expression of apoptosis and of apoptosis-related genes, XIAP (X chromosome-linked inhibitor of apoptosis protein) and Smac (second mitochondrial activator of caspase), in the hippocampus of developing rats. A total of 48 rats (30-day old) were randomly divided into four groups for intragastrical perfusion of lead acetate [Pb(Ac)(2)]: untreated, low (2 mg/kg/d), medium (20 mg/kg/d), and high (200 mg/kg/d) dose groups. Pb content was determined in blood, and the apoptosis indexes and XIAP and Smac gene expression were analyzed in the hippocamp...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3003428</comments>
            <pubDate>Fri, 13 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3003428</guid>        </item>
        <item>
            <title>Editors List From 1976 To 2009.</title>
            <link>http://www.medworm.com/index.php?rid=2985547&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19904604%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 19904604 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2985547</comments>
            <pubDate>Wed, 11 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2985547</guid>        </item>
        <item>
            <title>Fatty Acid Composition of Frontal, Temporal and Parietal Neocortex in the Normal Human Brain and in Alzheimer's Disease.</title>
            <link>http://www.medworm.com/index.php?rid=2985546&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19904605%26dopt%3DAbstract</link>
            <description>Authors: Fraser T, Tayler H, Love S
    Dietary omega3-polyunsaturated fatty acids are thought to influence the risk of Alzheimer's disease (AD), and supplemental docosahexaenoic acid (DHA; 22:6n-3) has been reported to reduce neurodegeneration in mouse models of AD. We have analysed the fatty acid composition of frontal, temporal and parietal neocortex in 58 normal and 114 AD brains. Significant reductions were found for stearic acid (18:0) in frontal and temporal cortex and arachidonic acid (20:4n-6) in temporal cortex in AD, and increases in oleic acid in frontal and temporal cortex (18:1n-9) and palmitic acid (16:0) in parietal cortex. DHA level varied more in AD than controls but the mean values were not significantly different. Fatty acid composition was not related to APOE genotype,...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2985546</comments>
            <pubDate>Wed, 11 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2985546</guid>        </item>
        <item>
            <title>Effect of Hydrogen Sulfide on Cyclic AMP Production in Isolated Bovine and Porcine Neural Retinae.</title>
            <link>http://www.medworm.com/index.php?rid=2978214&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19898983%26dopt%3DAbstract</link>
            <description>Authors: Njie-Mbye YF, Bongmba OY, Onyema CC, Chitnis A, Kulkarni M, Opere CA, Leday AM, Ohia SE
    Hydrogen sulfide (H(2)S) has been reported to exert pharmacological effects on neural and non-neural tissues from several mammalian species. In the present study, we examined the role of the intracellular messenger, cyclic AMP in retinal response to H(2)S donors, sodium hydrosulfide (NaHS) and sodium sulfide (Na(2)S) in cows and pigs. Isolated bovine and porcine neural retinae were incubated in oxygenated Krebs buffer solution prior to exposure to varying concentrations of NaHS, Na(2)S or the diterpene activator of adenylate cyclase, forskolin. After incubation at different time intervals, tissue homogenates were prepared for cyclic AMP assay using a well established methodology. In isolate...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2978214</comments>
            <pubDate>Sun, 08 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2978214</guid>        </item>
        <item>
            <title>Intrastriatal Transplantation of GDNF-engineered BMSCs and its neuroprotection in Lactacystin-induced Parkinsonian Rat Model.</title>
            <link>http://www.medworm.com/index.php?rid=2972312&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19894114%26dopt%3DAbstract</link>
            <description>Authors: Wu J, Yu W, Chen Y, Su Y, Ding Z, Ren H, Jiang Y, Wang J
    The potential value of glial cell line-derived neurotrophic factor (GDNF) in treating Parkinson's disease (PD) remains controversial. In order to evaluate the therapeutic effect of GDNF-engineered bone marrow stromal cells (BMSCs) in parkinsonian rat model, GDNF-BMSCs and LacZ-BMSCs were transplanted into striatum and followed by Lactacystin lesioning at median forebrain bundles 1 week later. We observed that the intrastriatal transplantation of GDNF-BMSCs could significantly rescue the dopaminergic neurons from lactacystin-induced neurotoxicity with regard to behavioral recovery, tyrosine hydroxylase level in nigra and striatum, and striatal dopamine level. We interpret the outcomes that intrastriatal transplantation of...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2972312</comments>
            <pubDate>Fri, 06 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2972312</guid>        </item>
        <item>
            <title>Brain-Derived Neurotrophic Factor Inhibits Phenylalanine-Induced Neuronal Apoptosis by Preventing RhoA Pathway Activation.</title>
            <link>http://www.medworm.com/index.php?rid=2972313&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19890711%26dopt%3DAbstract</link>
            <description>In this study, we reported that brain-derived growth factor (BDNF) protected neurons from phenylalanine-induced apoptosis and inhibition of Trk receptor by K252a or downregulation of TrkB abrogated the effect of BDNF. We further demonstrated that phenylalanine-induced RhoA activation and myosin light chain phosphorylation were inhibited by pretreatment with BDNF, while phenylalanine activates the mitochondria-mediated apoptosis through the RhoA/Rho-associated kinase pathway. Thus our studies indicate that the protective effect of BDNF against phenylalanine-induced neuronal apoptosis is probably mediated by suppression of RhoA signaling pathway via TrkB receptor. Taken together, these findings suggest a potential neuroprotective action of BDNF in prevention and treatment of PKU brain injury...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2972313</comments>
            <pubDate>Thu, 05 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2972313</guid>        </item>
        <item>
            <title>Neuroprotective and Neurological Properties of Melissa officinalis.</title>
            <link>http://www.medworm.com/index.php?rid=2805125&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19760174%26dopt%3DAbstract</link>
            <description>Authors: L&amp;#xF3;pez V, Mart&amp;#xED;n S, G&amp;#xF3;mez-Serranillos MP, Carretero ME, J&amp;#xE4;ger AK, Calvo MI
    Melissa officinalis has traditionally been used due to its effects on nervous system. Both methanolic and aqueous extracts were tested for protective effects on the PC12 cell line, free radical scavenging properties and neurological activities (inhibition of MAO-A and acetylcholinesterase enzymes and affinity to the GABA(A)-benzodiazepine receptor). The results suggest that the plant has a significant (P &amp;lt; 0.05) protective effect on hydrogen peroxide induced toxicity in PC12 cells. The radical scavenging properties were also investigated in cells and in cell free systems, where this plant was shown to be a good free radical scavenger. The MAO-A bioassay was also performed to detect...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2805125</comments>
            <pubDate>Fri, 18 Sep 2009 13:54:08 +0100</pubDate>
            <guid isPermaLink="false">2805125</guid>        </item>
        <item>
            <title>Regulation of [(3)h] d: -aspartate release from Mammalian isolated retinae by hydrogen sulfide.</title>
            <link>http://www.medworm.com/index.php?rid=2805124&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19760175%26dopt%3DAbstract</link>
            <description>Authors: Opere CA, Monjok EM, Kulkarni KH, Njie YF, Ohia SE
    Hydrogen sulfide (H(2)S), can produce pharmacological effects on neural and non-neural tissues from several mammalian species. The present study investigates the pharmacological action of H(2)S, (using sodium hydrosulfide, NaHS, and/or sodium sulfide, Na(2)S as donors) on amino acid neurotransmission (using [(3)H] D: -aspartate as a marker for glutamate) from isolated, superfused bovine and porcine retinae. Isolated neural retinae were incubated in Krebs solution containing [(3)H] D: -aspartate at 37 degrees C. Release of [(3)H] D: -aspartate was elicited by high potassium (K(+) 50 mM) pulse. Both NaHS and Na(2)S donors caused an inhibition of K(+)-evoked [(3)H] D: -aspartate release from isolated bovine retinae without affect...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2805124</comments>
            <pubDate>Fri, 18 Sep 2009 13:54:05 +0100</pubDate>
            <guid isPermaLink="false">2805124</guid>        </item>
        <item>
            <title>BACE and gamma-Secretase Characterization and Their Sorting as Therapeutic Targets to Reduce Amyloidogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=2805126&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19760173%26dopt%3DAbstract</link>
            <description>Authors: Marks N, Berg MJ
    Secretases are named for enzymes processing amyloid precursor protein (APP), a prototypic type-1 membrane protein. This led directly to discovery of novel Aspartyl proteases (beta-secretases or BACE), a tetramer complex gamma-secretase (gamma-SC) containing presenilins, nicastrin, aph-1 and pen-2, and a new role for metalloprotease(s) of the ADAM family as a alpha-secretases. Recent advances in defining pathways that mediate endosomal-lysosomal-autophagic-exosomal trafficking now provide targets for new drugs to attenuate abnormal production of fibril forming products characteristic of AD. A key to success includes not only characterization of relevant secretases but mechanisms for sorting and transport of key metabolites to abnormal vesicles or sites for asse...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2805126</comments>
            <pubDate>Wed, 16 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2805126</guid>        </item>
        <item>
            <title>The Extracellular Matrix Protein SC1/Hevin Localizes to Multivesicular Bodies in Bergmann Glial Fibers in the Adult Rat Cerebellum.</title>
            <link>http://www.medworm.com/index.php?rid=2805131&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19757034%26dopt%3DAbstract</link>
            <description>Authors: Lively S, Brown IR
    SC1 is an extracellular matrix molecule prominent in the mammalian brain. In the cerebellum, SC1 localizes to Bergmann glial cells and perisynaptic glial processes that envelop synapses in the molecular layer. In the present study, confocal microscopy revealed a punctate distribution of SC1 along Bergmann glial fibers that colocalized with the intermediate filament GFAP when fibers were viewed in cross-section. Immunoelectron microscopy showed that the punctate SC1 pattern corresponded to the localization of SC1 in multivesicular bodies situated within Bergmann glial fibers. The pattern of SC1 localization was not disrupted following hyperthermia or pilocarpine-induced status epilepticus. The present study suggests that SC1 protein may reach its destination ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2805131</comments>
            <pubDate>Tue, 15 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2805131</guid>        </item>
        <item>
            <title>Promotion of Lipid and Protein Oxidative Damage in Rat Brain by Ethylmalonic Acid.</title>
            <link>http://www.medworm.com/index.php?rid=2805130&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19757035%26dopt%3DAbstract</link>
            <description>Authors: Schuck PF, Busanello EN, Moura AP, Tonin AM, Grings M, Ritter L, Vargas CR, da Costa Ferreira G, Wajner M
    High concentrations of ethylmalonic acid are found in tissues and biological fluids of patients affected by ethylmalonic encephalopathy, deficiency of short-chain acyl-CoA dehydrogenase activity and other illnesses characterized by developmental delay and neuromuscular symptoms. The pathophysiological mechanisms responsible for the brain damage in these patients are virtually unknown. Therefore, in the present work we investigated the in vitro effect of EMA on oxidative stress parameters in rat cerebral cortex. EMA significantly increased chemiluminescence and thiobarbituric acid-reactive species levels (lipoperoxidation), as well as carbonyl content and oxidation of sulfh...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2805130</comments>
            <pubDate>Tue, 15 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2805130</guid>        </item>
        <item>
            <title>Cocaine Induces Alterations in Mitochondrial Membrane Potential and Dual Cell Cycle Arrest in Rat C6 Astroglioma Cells.</title>
            <link>http://www.medworm.com/index.php?rid=2805129&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19757036%26dopt%3DAbstract</link>
            <description>Authors: Badisa RB, Darling-Reed SF, Goodman CB
    Investigations with astroglial cells carry more prominence in drug abuse studies. However, due to earlier perception that astroglial cells were only passive bystanders in neural signal transmission, not many investigations were conducted on the toxicity of various abused drugs, like cocaine. The present study was aimed to discern the effect of cocaine on rat astroglioma cells and analyzed qualitatively for morphological features as well as vacuolation by phase contrast microscope, quantitatively for cytotoxicity, mitochondrial membrane potential by rhodamine- 123 fluorometric assay, and cell cycle analysis by flow cytometry. Based on population cell doubling time studies, glial cells were grown in 10% FBS in RPMI 1640 medium and treated w...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2805129</comments>
            <pubDate>Tue, 15 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2805129</guid>        </item>
        <item>
            <title>Scopolamine Induced Amnesia is Reversed by Bacopa monniera Through Participation of Kinase-CREB Pathway.</title>
            <link>http://www.medworm.com/index.php?rid=2805128&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19757037%26dopt%3DAbstract</link>
            <description>Authors: Saraf MK, Anand A, Prabhakar S
    Scopolamine, an anticholinergic drug, is reported to produce amnesia by interference of long term potentiation and has been used for discerning the efficacy of various antiamnesic drugs. The intoxication with anticholinergics and benzodiazepines tend to produce neurodegeneration which cause memory deficits. Our earlier reports have shown the antiamnesic drug, B. monniera to be capable of alleviating diazepam induced memory deficits. We have now tested how scopolamine affects downstream signaling molecules of long term potentiation and if B. monniera can also modulate the scopolamine induced amnesia. We used Morris water maze scale to test the amnesic effect of scopolamine and its reversal by B. monniera. Rota-rod test was used to screen muscle co...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2805128</comments>
            <pubDate>Tue, 15 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2805128</guid>        </item>
        <item>
            <title>SSeCKS is a Suppressor in Schwann Cell Differentiation and Myelination.</title>
            <link>http://www.medworm.com/index.php?rid=2805127&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19757038%26dopt%3DAbstract</link>
            <description>Authors: Ji Y, Tao T, Cheng C, Yang H, Wang Y, Yang J, Liu H, He X, Wang H, Shen A
    Src-suppressed protein kinase C substrate (SSeCKS) plays an important role in the differentiation process. In regeneration of sciatic nerve injury, expression of SSeCKS decreases, mainly in Schwann cells. However, the function of SSeCKS in Schwann cells differentiation remains unclear. We observed that SSeCKS was decreased in differentiated Schwann cells. In long-term SSeCKS-reduced Schwann cells, cell morphology changed and myelin gene expression induced by cAMP was accelerated. Myelination was also enhanced in SSeCKS-suppressed Schwann cells co-culture with dorsal root ganglion (DRG). In addition, we found suppression of SSeCKS expression promoted Akt serine 473 phosphorylation in cAMP-treated Schwann ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2805127</comments>
            <pubDate>Tue, 15 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2805127</guid>        </item>
        <item>
            <title>An Improved Phenylarsine Oxide-Affinity Method Identifies Triose Phosphate Isomerase as a Candidate Redox Receptor Protein.</title>
            <link>http://www.medworm.com/index.php?rid=2767931&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19731017%26dopt%3DAbstract</link>
            <description>Authors: Foley TD, Stredny CM, Coppa TM, Gubbiotti MA
    Reversible oxidation on proteins of vicinal thiols to form intraprotein disulfides is believed to be an important means by which redox sensitivity is conferred on cellular signaling and metabolism. Affinity chromatography using immobilized phenylarsine oxide (PAO), which binds preferentially to vicinal thiols over monothiols, has been used in very limited studies to isolate the fraction of cellular proteins that exhibit reversible oxidation of vicinal thiols to presumed disulfide bonds. A challenge to the use of PAO-affinity chromatography for isolation of readily oxidizable vicinal thiol proteins (VTPs) has been the lack of a disulfide reducing agent that reverses oxidation of the PAO-binding protein thiols and maintains these in t...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2767931</comments>
            <pubDate>Wed, 02 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2767931</guid>        </item>
        <item>
            <title>Phosphorylation Changes of CaMKII, ERK1/2, PKB/Akt Kinases and CREB Activation During Early Long-Term Potentiation at Schaffer Collateral-CA1 Mouse Hippocampal Synapses.</title>
            <link>http://www.medworm.com/index.php?rid=2767930&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19731018%26dopt%3DAbstract</link>
            <description>Authors: Racaniello M, Cardinale A, Mollinari C, D'Antuono M, De Chiara G, Tancredi V, Merlo D
    Protein phosphorylation is the main signaling system known to trigger synaptic changes underlying long-term potentiation (LTP). The timing of these phosphorylations plays an essential role to maintain the potentiated state of synapses. However, in mice a simultaneous analysis of phosphorylated proteins during early-LTP (E-LTP) has not been thoroughly carried out. Here we described phosphorylation changes of alphaCaMKII, ERK1/2, PKB/Akt and CREB at different times after E-LTP induced at Schaffer collateral/commissural fiber-CA1 synapses by 1 s 100 Hz tetanic stimulation in mouse hippocampal slices. We found that phosphorylation levels of all the molecules examined rapidly increased after tetan...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2767930</comments>
            <pubDate>Wed, 02 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2767930</guid>        </item>
        <item>
            <title>Behavioural and Histological Effects of Preconditioning with Lipopolysaccharide in Epileptic Rats.</title>
            <link>http://www.medworm.com/index.php?rid=2767932&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19728087%26dopt%3DAbstract</link>
            <description>Authors: Dmowska M, Cybulska R, Schoenborn R, Piersiak T, Jaworska-Adamu J, Gawron A
    Sublethal stress stimuli such as systemic endotoxin treatment can induce tolerance of the brain to subsequent ischemic stress, which results in a decreased infarct size. Based on this evidence, we hypothesized that lipopolysaccharide (LPS)-induced preconditioning could protect hippocampal neurons in epileptic rats. To test this hypothesis, the anticonvulsant effect of a low dose of LPS against seizures elicited by pilocarpine hydrochloride was measured. Using the pilocarpine model of temporal lobe epilepsy and LPS-preconditioning, we also investigated hippocampal pathology in the rat brain. Based on the behavioural observations conducted, it can be assumed that the preconditioning procedure used may de...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2767932</comments>
            <pubDate>Fri, 28 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2767932</guid>        </item>
        <item>
            <title>Postnatal Expression of GAD67.</title>
            <link>http://www.medworm.com/index.php?rid=2730657&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19701789%26dopt%3DAbstract</link>
            <description>Authors: Turner CP, Ware E, Stowe R, Debenedetto D, Walburg C, Lee A, Swanson J, Lambert A, Lyle M, Desai P, Liu C
    N-methyl-D: -aspartate receptor blockade promotes apoptosis at postnatal day 7 (P7) and is linked to loss of glutamic acid decarboxylase 67 (GAD67) expression in older animals. To more fully appreciate this relationship we must first understand how GAD67 is regulated postnatally. Thus, the brains of P7, P14 and P21 rats were examined for expression of GAD67 protein and we found that levels of this GABAergic marker increased steadily with age, such that by P21 there was as much as a 6-fold increase compared to P7 animals and a 1.5- to 2-fold increase compared to P14 animals, depending on the region sampled. At P7, GAD67 was almost exclusively detected in puncta, with very f...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2730657</comments>
            <pubDate>Sat, 22 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2730657</guid>        </item>
        <item>
            <title>The Effects of Polyphenols on Survival and Locomotor Activity in Drosophila melanogaster Exposed to Iron and Paraquat.</title>
            <link>http://www.medworm.com/index.php?rid=2730656&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19701790%26dopt%3DAbstract</link>
            <description>Authors: Jimenez-Del-Rio M, Guzman-Martinez C, Velez-Pardo C
    Parkinson's disease (PD) is a common progressive neurodegenerative disorder, for which at present no causal treatment is available. On the understanding that the causes of PD are mainly oxidative stress and mitochondrial dysfunction, antioxidants and other drugs are expected to be used. In the present study, we demonstrated for the first time that pure polyphenols such as gallic acid, ferulic acid, caffeic acid, coumaric acid, propyl gallate, epicatechin, epigallocatechin, and epigallocatechin gallate protect, rescue and, most importantly, restore the impaired movement activity (i.e., climbing capability) induced by paraquat in Drosophila melanogaster, a valid model of PD. We also showed for the first time that high concentra...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2730656</comments>
            <pubDate>Sat, 22 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2730656</guid>        </item>
        <item>
            <title>GABA and Homovanillic Acid in the Plasma of Schizophrenic and Bipolar I Patients.</title>
            <link>http://www.medworm.com/index.php?rid=2730658&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19701707%26dopt%3DAbstract</link>
            <description>Authors: Arr&amp;#xFA;e A, D&amp;#xE1;vila R, Zum&amp;#xE1;rraga M, Basterreche N, Gonz&amp;#xE1;lez-Torres MA, Goienetxea B, Zamalloa MI, Anguiano JB, Guim&amp;#xF3;n J
    We have determined the plasma (p) concentration of gamma-aminobutyric acid (GABA) and the dopamine metabolite homovanillic acid (HVA), and the pHVA/pGABA ratio in schizophrenic and bipolar patients. The research was undertaken in a geographic area with an ethnically homogeneous population. The HVA plasma concentrations were significantly elevated in the schizophrenic patients compared to the bipolar patients. The levels of pGABA was significantly lower in the two groups of patients compared to the control group, while the pHVA/pGABA ratio was significantly greater in the both groups of patients compared to the controls. As the levels of p...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2730658</comments>
            <pubDate>Fri, 21 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2730658</guid>        </item>
        <item>
            <title>Neurotoxic Effects of Methamphetamine.</title>
            <link>http://www.medworm.com/index.php?rid=2725447&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19697126%26dopt%3DAbstract</link>
            <description>This study was undertaken to gain greater mechanistic understanding of the toxicity induced by methamphetamine. We evaluated the effect of methamphetamine on the generation of reactive oxygen species, mitochondrial monoamine oxidase, complex I &amp; IV activities. Behavioral analysis evaluated the effect on catalepsy, akinesia and swim score. Neurotransmitter levels were evaluated using high pressure liquid chromatography (HPLC) electrochemical detection (ECD). Results showed that methamphetamine caused significant generation of reactive oxygen species and decreased complex I activity in the mitochondria leading to dopamine depletion in the striatum.
    PMID: 19697126 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2725447</comments>
            <pubDate>Thu, 20 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2725447</guid>        </item>
        <item>
            <title>Telomerase Deficiency Affects Normal Brain Functions in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=2713445&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19685288%26dopt%3DAbstract</link>
            <description>Authors: Lee J, Jo YS, Sung YH, Hwang IK, Kim H, Kim SY, Yi SS, Choi JS, Sun W, Seong JK, Lee HW
    Telomerase maintains telomere structures and chromosome stability, and it is essential for preserving the characteristics of stem and progenitor cells. In the brain, the hippocampus and the olfactory bulbs are continuously supplied with neural stem and progenitor cells that are required for adult neurogenesis throughout the life. Therefore, we examined whether telomerase plays important roles in maintaining normal brain functions in vivo. Telomerase reverse transcriptase (TERT) expression was observed in the hippocampus, the olfactory bulbs, and the cerebellum, but the telomerase RNA component (TERC) was not detected in hippocampus and olfactory bulbs. Interestingly, TERT-deficient mice exh...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2713445</comments>
            <pubDate>Fri, 14 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2713445</guid>        </item>
        <item>
            <title>Combination Treatment with Resveratrol and Sulforaphane Induces Apoptosis in Human U251 Glioma Cells.</title>
            <link>http://www.medworm.com/index.php?rid=2713444&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19685289%26dopt%3DAbstract</link>
            <description>Authors: Jiang H, Shang X, Wu H, Huang G, Wang Y, Al-Holou S, Gautam SC, Chopp M
    Resveratrol is a naturally occurring polyphenolic compound highly enriched in grapes, peanuts, red wine, and a variety of food sources. Sulforaphane belongs to the family of isothiocyanates and is highly enriched in cruciferous vegetables. Our previous study showed that resveratrol, when used at high concentrations, inhibited cell proliferation, caused the cell cycle arrest and induced apoptotic cell death in glioma cells. In the current study, we tested the effect of combination treatment with resveratrol and sulforaphane, when both were used at low concentrations, on cell proliferation, migration and death in human U251 glioma cells. Our study shows that combination treatment with resveratrol and sulfora...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2713444</comments>
            <pubDate>Fri, 14 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2713444</guid>        </item>
        <item>
            <title>Oxidative Mechanisms of Brain Dysfunction During Sepsis.</title>
            <link>http://www.medworm.com/index.php?rid=2703990&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19680806%26dopt%3DAbstract</link>
            <description>Authors: Dal-Pizzol F, Ritter C, Cassol-Jr OJ, Rezin GT, Petronilho F, Zugno AI, Quevedo J, Streck EL
    Oxidative stress has drawn a lot of attention in the past few decades, since it has been reported to participate in the mechanism of many diseases. Therefore, it seemed to be a good rationale to aim oxidative stress on therapeutic research. Sepsis is a complex systemic syndrome characterized by an imbalance between pro- and anti-inflammatory responses to a pathogen; its pathophysiology is a dynamic process which involves components of the immune system, the coagulation pathway, parenchymal cells, and the endocrine and metabolic pathways. It is well characterized that oxidative stress plays a crucial role in sepsis development, but the relation between central nervous system dysfunction...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2703990</comments>
            <pubDate>Thu, 13 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2703990</guid>        </item>
        <item>
            <title>Effects of Hydroxysafflor Yellow A in the Attenuation of MPTP Neurotoxicity in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=2703989&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19680807%26dopt%3DAbstract</link>
            <description>Authors: Han B, Zhao H
    Parkinson's disease (PD) is a progressive neurodegenerative disorder whose etiology is not understood. The 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mouse model is widely used for studying PD. The present study was undertaken to investigate the effect of hydroxysafflor yellow A (HSYA) on MPTP-induced neurotoxicity in mice. Pretreatment with HSYA at a dose of 2, 8 mg/kg for a week was followed by intraperitoneal injection with MPTP (30 mg/kg) for five consecutive days. Next, the subsequent behavior, biochemical index and immunohistochemical manifestations in mice were determined. Behavioral testing showed that MPTP-treated mice exhibited motor deficits but HSYA at dose of 8 mg/kg prevented the appearance of motor abnormalities. Treatment with HSY...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2703989</comments>
            <pubDate>Wed, 12 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2703989</guid>        </item>
        <item>
            <title>Lipoic Acid Increases Hippocampal Choline Acetyltransferase and Acetylcholinesterase Activities and Improvement Memory in Epileptic Rats.</title>
            <link>http://www.medworm.com/index.php?rid=2692239&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19669875%26dopt%3DAbstract</link>
            <description>Authors: de Freitas RM
    In the present study we investigated the effect of seizures on rat performance in the Morris water maze task, as well as on choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities in rat hippocampus. Wistar rats were treated with 0.9% saline (i.p., control group), lipoic acid (20 mg/kg, i.p., LA group), pilocarpine (400 mg/kg, i.p., pilocarpine group), and the association of LA (20 mg/kg, i.p.) plus pilocarpine (400 mg/kg, i.p.), 30 min before of administration of LA (LA plus pilocarpine group). After the treatments all groups were observed for 1 h. The effect of lipoic acid administration was observed on reference and working spatial memory of seized rats. The ChAT and AChE activities were measured using spectrophotometric methods and the res...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2692239</comments>
            <pubDate>Mon, 10 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2692239</guid>        </item>
        <item>
            <title>Expression of Adenomatous Polyposis Coli Protein in Reactive Astrocytes in Hippocampus of Kainic Acid-Induced Rat.</title>
            <link>http://www.medworm.com/index.php?rid=2675454&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19655246%26dopt%3DAbstract</link>
            <description>In this study, we evaluated the expression of APC and its association with beta-catenin signaling pathway, following the induction of an excitotoxic lesion by kainic acid (KA) injection, which cause pyramidal cell degeneration. APC was predominantly present in oligodendrocytes in the normal brain, but was specifically associated with activated astrocytes in the KA-treated brain. Our quantitative analysis revealed that APC significantly increased from 1 day post lesion (PI), reached peak values at 3 days PI, and decreased thereafter. The phospho-GSK3beta levels also showed similar spatiotemporal patterns while beta-catenin expression was reduced at 1 and then increasingly returned to normal levels at 3, 7 days PI. For the first time, our data demonstrate the injury-induced astrocytic change...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2675454</comments>
            <pubDate>Tue, 04 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2675454</guid>        </item>
        <item>
            <title>Genome-Wide Microarray Analysis of the Differential Neuroprotective Effects of Antioxidants in Neuroblastoma Cells Overexpressing the Familial Parkinson's Disease alpha-Synuclein A53T Mutation.</title>
            <link>http://www.medworm.com/index.php?rid=2668693&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19649707%26dopt%3DAbstract</link>
            <description>Authors: Ma L, Cao TT, Kandpal G, Warren L, Fred Hess J, Seabrook GR, Ray WJ
    In Parkinson's disease substantia nigra neurons degenerate likely due to oxidative damage interacting with genetic risk factors. Here, SH-SY5Y cells expressing wild-type or A53T alpha-synuclein had increased sensitivity to methyl-4-phenylpyridinium iodide (MPP(+)), which induces mitochondrial dysfunction, and 6-hydroxydopamine (6-OHDA), which causes oxidative stress. Edaravone protected only against MPP(+), and EGCG ((-)-epigallocatechin-3-O-gallate) protected only against 6-OHDA. Thus genomic responses to MPP(+) and 6-OHDA in the presence of these antioxidants were analyzed using microarrays. Pathway analysis indicated that MPP(+) activated p53 (P &amp;lt; 0.001) while 6-OHDA induced the Nrf2 antioxidative stress...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2668693</comments>
            <pubDate>Sat, 01 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2668693</guid>        </item>
        <item>
            <title>Age-dependent increase in desmosterol restores DRM formation and membrane-related functions in cholesterol-free DHCR24(-/-) mice. Neurochemical Research (34, 1167-82).</title>
            <link>http://www.medworm.com/index.php?rid=2525453&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19475506%26dopt%3DAbstract</link>
            <description>Authors: Kuehnle K, Ledesma MD, Kalvodova L, Smith AE, Crameri A, Skaanes-Brunner F, Thelen KM, Kulic L, L&amp;#xFC;tjohann D, Heppner FL, Nitsch RM, Mohajeri MH
    
    PMID: 19475506 [PubMed - in process] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525453</comments>
            <pubDate>Sat, 27 Jun 2009 11:08:51 +0100</pubDate>
            <guid isPermaLink="false">2525453</guid>        </item>
        <item>
            <title>Intermittent Hypercapnic Hypoxia Induced Protein Changes in the Piglet Hippocampus Identified by MALDI-TOF-MS.</title>
            <link>http://www.medworm.com/index.php?rid=2525424&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19548086%26dopt%3DAbstract</link>
            <description>Authors: Tang S, Machaalani R, Kashem MA, Matsumoto I, Waters KA
    Intermittent hypercapnic hypoxia (IHH) induces protein changes in the brainstem, but its effects on the hippocampus have not yet been studied. Using a proteomics-based approach, we tested the hypothesis that IHH up-regulates apoptotic promoters and down-regulates apoptotic inhibitors in the developing hippocampus. Male piglets aged 13-14 days were assigned to control (n = 6) or IHH (n = 5) groups. Using two-dimensional polyacrylamide gel electrophoresis, matrix-assisted laser desorption/ionisation-time of flight-mass spectrometry (MALDI-TOF-MS), a total of 26 protein spots were differentially expressed in IHH compared to control group. Thirteen of these (6 up-regulated, 7 down-regulated) were identified including 14-3-3th...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525424</comments>
            <pubDate>Mon, 22 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525424</guid>        </item>
        <item>
            <title>Decrease of Tau Hyperphosphorylation by 17beta Estradiol Requires Sphingosine Kinase in a Glutamate Toxicity Model.</title>
            <link>http://www.medworm.com/index.php?rid=2525425&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19543831%26dopt%3DAbstract</link>
            <description>Authors: Lopez-Tob&amp;#xF3;n A, Cepeda-Prado E, Cardona-G&amp;#xF3;mez GP
    Several studies have linked estrogens with sphingosine kinase (SphK) activity, enzyme responsible of sphingosine-1-phosphate synthesis (S-1P), however their possible interaction in the nervous system is not documented yet. In the present study, we developed a glutamate toxicity model in SH-SY5Y cells to evaluate the possible effect of the inhibition of SphK activity on the protective capability of 17beta-estradiol (E2). Glutamate induced cytoskeletal actin changes associated to cytotoxic stress, significant increase of apoptotic-like nuclear fragmentation, Tau hyperphosphorylation and increase of p25/p35 cleavage. These effects were prevented by E2 pre-treatment during 24 h. Although the inhibition of SphK did not block...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525425</comments>
            <pubDate>Thu, 18 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525425</guid>        </item>
        <item>
            <title>Effects of Ketamine on the Balance of Ions Ca(2+), Mg (2+), Cu (2+) and Zn (2+) in the Ischemia-reperfusion Affected Spinal Cord Tissues in Rabbits.</title>
            <link>http://www.medworm.com/index.php?rid=2525427&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19529985%26dopt%3DAbstract</link>
            <description>Authors: Yu QJ, Zhou QS, Huang HB, Wan YL, Tian SF, Duan DM
    To test the effects of ketamine on metal ion balance in the spinal cord tissues after ischemic reperfusion (I/R), 24 white adult Japanese rabbits were randomly assigned to sham operation group, I/R group or ketamine-treated I/R group. Spinal cord injuries in I/R group and ketamine-treated I/R group were induced by aortic occlusions. Rabbits in ketamine-treated I/R group were intravenously infused 10 mg/kg ketamine twice: once at 10 min before aortic clamping and once at the onset of reperfusion. Post-operative neurological functions and concentrations of ions Ca(2+), Mg(2+), Cu(2+) and Zn(2+) in the spinal cord were assessed. Compared with the sham operation group, rabbits in the I/R group showed significantly worsened neurolo...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525427</comments>
            <pubDate>Mon, 15 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525427</guid>        </item>
        <item>
            <title>Neurite Outgrowth is Dependent on the Association of c-Src and Lipid Rafts.</title>
            <link>http://www.medworm.com/index.php?rid=2525426&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19529986%26dopt%3DAbstract</link>
            <description>Authors: Zhao H, Cao X, Wu G, Loh HH, Law PY
    Regulation of neurite outgrowth is an important aspect not only for proper development of the nervous system but also for tissue regeneration after nerve injury and the treatment of neuropathological conditions. Here, we report that neurite outgrowth in cortical neuron and neuro 2A (N2A) cell was dependent on intact lipid rafts, as well as the enhanced localization of c-Src in the lipid rafts. Src inhibition or lipid rafts disruption could specifically block c-Src phosphorylation profile, pY416 Src increase and pY529 Src decrease, they also resulted in pY529 Src and c-terminal Src kinase (Csk) partition out of lipid rafts. Thus, we concluded that c-Src signal cascades within the lipid rafts is crucial for efficient neurite outgrowth.
    PMI...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525426</comments>
            <pubDate>Mon, 15 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525426</guid>        </item>
        <item>
            <title>Role of Selenium on Calcium Signaling and Oxidative Stress-induced Molecular Pathways in Epilepsy.</title>
            <link>http://www.medworm.com/index.php?rid=2525429&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19513830%26dopt%3DAbstract</link>
            <description>In conclusion, there is convincing evidence for the proposed crucial role of selenium and deficiency of GSH-Px enzyme activity in epilepsy pathogenesis. Blood GSH-Px activities could be a reliable indicator of selenium deficiency in patients with epilepsy.
    PMID: 19513830 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525429</comments>
            <pubDate>Tue, 09 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525429</guid>        </item>
        <item>
            <title>Role of Prostanoid Production and Receptors in the Regulation of Retinal Endogenous Amino Acid Neurotransmitters by 8-Isoprostaglandin E(2), Ex Vivo.</title>
            <link>http://www.medworm.com/index.php?rid=2525428&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19513831%26dopt%3DAbstract</link>
            <description>Authors: Zhao M, Destache CJ, Ohia SE, Opere CA
    The role of enzymes and receptors of the prostanoid pathway in the inhibitory effect of 8-isoprostaglandin E(2) (8-isoPGE(2)) on endogenous amino acid neurotransmitter levels was examined, ex vivo. Freshly isolated bovine eyeballs were injected intravitreally with IsoPs, incubated in Krebs buffer for 30 min and retina prepared for HPLC-ECD detection of amino acids. 8-isoPGE(2) attenuated retinal glutamate and its metabolite, glutamine and glycine in a concentration-dependent manner. The non-selective cyclooxygenase (COX)-inhibitor, flurbiprofen, COX-2 selective inhibitor, NS-398 and thromboxane (Tx) synthase inhibitor, furegrelate had no effect on both basal amino acid levels and the inhibitory effects of 8-isoPGE(2) (1-100 muM) on the re...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525428</comments>
            <pubDate>Tue, 09 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525428</guid>        </item>
        <item>
            <title>Targeting BuChE-inflammatory Pathway by SK0506 to Manage Type 2 Diabetes and Alzheimer Disease.</title>
            <link>http://www.medworm.com/index.php?rid=2525430&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19504347%26dopt%3DAbstract</link>
            <description>In conclusion, current study has opened new potential avenues towards research for management of T2DM and AD by Chinese herbal extracts, &quot;SK0506&quot;.
    PMID: 19504347 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525430</comments>
            <pubDate>Sat, 06 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525430</guid>        </item>
        <item>
            <title>Design and Assessment of a Potent Sodium Channel Blocking Derivative of Mexiletine for Minimizing Experimental Neuropathic Pain in Several Rat Models.</title>
            <link>http://www.medworm.com/index.php?rid=2525431&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19504185%26dopt%3DAbstract</link>
            <description>Authors: Weston RM, Subasinghe KR, Staikopoulos V, Jarrott B
    Physical or chemical damage to peripheral nerves can result in neuropathic pain which is not easily alleviated by conventional analgesic drugs. Substantial evidence has demonstrated that voltage-gated Na(+) channels in the membrane of damaged nerves play a key role in the establishment and maintenance of pathological neuronal excitability not only of these peripheral nerves but also in the second- and third-order neurons in the pain pathway to the cerebral cortex. Na(+) channel blocking drugs have been used in treating neuropathic pain with limited success mainly because of a preponderance of side-effects. We have developed an analogue of mexiletine which is approximately 80 times more potent than mexiletine in competing with...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525431</comments>
            <pubDate>Fri, 05 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525431</guid>        </item>
        <item>
            <title>Detecting Protein-Protein Interactions in Living Cells: Development of a Bioluminescence Resonance Energy Transfer Assay to Evaluate the PSD-95/NMDA Receptor Interaction.</title>
            <link>http://www.medworm.com/index.php?rid=2525444&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19495967%26dopt%3DAbstract</link>
            <description>Authors: Gottschalk M, Bach A, Hansen JL, Krogsgaard-Larsen P, Kristensen AS, Str&amp;#xF8;mgaard K
    The PDZ domain mediated interaction between the NMDA receptor and its intracellular scaffolding protein, PSD-95, is a potential target for treatment of ischemic brain diseases. We have recently developed a number of peptide analogues with improved affinity for the PDZ domains of PSD-95 compared to the endogenous C-terminal peptide of the NMDA receptor, as evaluated by a cell-free protein-protein interaction assay. However, it is important to address both membrane permeability and effect in living cells. Therefore a bioluminescence resonance energy transfer (BRET) assay was established, where the C-terminal of the NMDA receptor and PDZ2 of PSD-95 were fused to green fluorescent protein (GFP) ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525444</comments>
            <pubDate>Wed, 03 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525444</guid>        </item>
        <item>
            <title>Effect of Ageing and Ischemia on Enzymatic Activities Linked to Krebs' Cycle, Electron Transfer Chain, Glutamate and Aminoacids Metabolism of Free and Intrasynaptic Mitochondria of Cerebral Cortex.</title>
            <link>http://www.medworm.com/index.php?rid=2525434&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19495970%26dopt%3DAbstract</link>
            <description>Authors: Villa RF, Gorini A, Hoyer S
    The effect of ageing and the relationships between the catalytic properties of enzymes linked to Krebs' cycle, electron transfer chain, glutamate and aminoacid metabolism of cerebral cortex, a functional area very sensitive to both age and ischemia, were studied on mitochondria of adult and aged rats, after complete ischemia of 15 minutes duration. The maximum rate (V (max)) of the following enzyme activities: citrate synthase, malate dehydrogenase, succinate dehydrogenase for Krebs' cycle; NADH-cytochrome c reductase as total (integrated activity of Complex I-III), rotenone sensitive (Complex I) and cytochrome oxidase (Complex IV) for electron transfer chain; glutamate dehydrogenase, glutamate-oxaloacetate- and glutamate-pyruvate transaminases for ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525434</comments>
            <pubDate>Wed, 03 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525434</guid>        </item>
        <item>
            <title>Rotenone Induces Cell Death of Cholinergic Neurons in an Organotypic Co-Culture Brain Slice Model.</title>
            <link>http://www.medworm.com/index.php?rid=2525433&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19495971%26dopt%3DAbstract</link>
            <description>Authors: Ullrich C, Humpel C
    In Alzheimer and Parkinson's disease cell death of cholinergic and dopaminergic neurons are characteristic hallmarks, respectively. It is well established that rotenone, an inhibitor of complex I of the electron transport chain, induces cell death of dopaminergic neurons, however, not much is known on the effects of rotenone on cholinergic neurons. The aim of the present study was to evaluate the effects of rotenone on cholinergic neurons in an organotypic in vitro brain co-slice model. When co-cultures were treated with 10 muM rotenone for 24 h a significantly decreased number of cholinergic neurons was found in the basal nucleus of Meynert but not in the dorsal striatum. This cell death exhibited apoptotic DAPI-positive malformed nuclei and enhanced TUNEL...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525433</comments>
            <pubDate>Wed, 03 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525433</guid>        </item>
        <item>
            <title>Age-related Changes in the Insulin Receptor beta in the Gerbil Hippocampus.</title>
            <link>http://www.medworm.com/index.php?rid=2525432&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19495972%26dopt%3DAbstract</link>
            <description>In this study, we observed age-related changes in the insulin receptor beta immunoreactivity and its protein levels in the hippocampus of gerbils of various ages in order to identify the correlation between the insulin receptor beta and aging processes in the hippocampus. Insulin receptor beta immunoreactivity was mainly detected in the molecular and polymorphic layers of the dentate gyrus, and in mossy fibers, Schaffer collaterals, alveus and stratum lacunosum-moleculare of the hippocampus proper (CA1-3) of gerbils at postnatal month 1 (PM 1). Insulin receptor beta immunoreactivity decreased with age in all of these structures, except for the alveus. Reduction of the insulin receptor beta immunoreactivity was prominent in the molecular layer of the dentate gyrus at PM 6 and in the stratum...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525432</comments>
            <pubDate>Wed, 03 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525432</guid>        </item>
        <item>
            <title>Rottlerin Inhibits (Na(+), K (+))-ATPase Activity in Brain Tissue and Alters D: -Aspartate Dependent Redistribution of Glutamate Transporter GLAST in Cultured Astrocytes.</title>
            <link>http://www.medworm.com/index.php?rid=2525443&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19495968%26dopt%3DAbstract</link>
            <description>Authors: Nguyen KT, Shin JW, Rae C, Nanitsos EK, Acosta GB, Pow DV, Buljan V, Bennett MR, Else PL, Balcar VJ
    The naturally occurring toxin rottlerin has been used by other laboratories as a specific inhibitor of protein kinase C-delta (PKC-delta) to obtain evidence that the activity-dependent distribution of glutamate transporter GLAST is regulated by PKC-delta mediated phosphorylation. Using immunofluorescence labelling for GLAST and deconvolution microscopy we have observed that D: -aspartate-induced redistribution of GLAST towards the plasma membranes of cultured astrocytes was abolished by rottlerin. In brain tissue in vitro, rottlerin reduced apparent activity of (Na(+), K(+))-dependent ATPase (Na(+), K(+)-ATPase) and increased oxygen consumption in accordance with its known activ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525443</comments>
            <pubDate>Tue, 02 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525443</guid>        </item>
        <item>
            <title>Free Radical Generation by Neurons in Rat Model of Japanese Encephalitis.</title>
            <link>http://www.medworm.com/index.php?rid=2525441&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19495969%26dopt%3DAbstract</link>
            <description>Authors: Srivastava R, Kalita J, Khan MY, Misra UK
    Increased generation of free radicals resulting in brain injury is a feature of many viral infections. The present study has been undertaken to evaluate the level of free radicals in Japanese encephalitis. Twelve days old Wistar rats were inoculated intracerebrally with 3 x 10(6) pfu of JE virus and were sacrificed on 3, 6, 10, and 20 days post inoculation (dpi). The neuronal levels of reactive oxygen species (ROS), nitric oxide (NO), peroxinitrite (OONO(-)), necrotic and apoptotic cell population were estimated by flow cytometry. Hematoxylin-eosin staining was also performed. Maximum level of neuronal ROS and OONO(-) was observed on 6 dpi; however, NO levels peaked on 10 dpi. Free radical generation significantly declined on 20 dpi as...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525441</comments>
            <pubDate>Tue, 02 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525441</guid>        </item>
        <item>
            <title>Systemic Oxidative Stress Associated with the Neurological Diseases of Aging.</title>
            <link>http://www.medworm.com/index.php?rid=2525449&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19488852%26dopt%3DAbstract</link>
            <description>Authors: Serra JA, Dom&amp;#xED;nguez RO, Marschoff ER, Guareschi EM, Famulari AL, Boveris A
    Markers of oxidative stress were measured in blood samples of 338 subjects (965 observations): Alzheimer's, vascular dementia, diabetes (type II) superimposed to dementias, Parkinson's disease and controls. Patients showed increased thiobarbituric acid reactive substances (+21%; P &amp;lt; 0.05), copper-zinc superoxide dismutase (+64%; P &amp;lt; 0.001) and decreased antioxidant capacity (-28%; P &amp;lt; 0.001); pairs of variables resulted linearly related across groups (P &amp;lt; 0.001). Catalase and glutathione peroxidase, involved in discrimination between diseases, resulted non-significant. When diabetes is superimposed with dementias, changes resulted less marked but significant. Also, superoxide dismutase ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525449</comments>
            <pubDate>Mon, 01 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525449</guid>        </item>
        <item>
            <title>Diazoxide Reverses the Enhanced Expression of K(ATP) Subunits in Cholinergic Neurons Caused by Exposure to Abeta(1-42).</title>
            <link>http://www.medworm.com/index.php?rid=2525448&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19488853%26dopt%3DAbstract</link>
            <description>Authors: Ma G, Gao J, Fu Q, Jiang L, Wang R, Zhang Y, Liu K
    The ATP-sensitive potassium channel (K(ATP)) play a crucial role in coupling metabolic energy to the cell membrane potential, beta-amyloid peptide (Abeta) neurotoxicity has been associated with cellular oxidative stress and metabolic impairment. Whether there is an interaction between K(ATP) and Abeta or not? The expression of K(ATP) subunits was to be investigated after the cultured primary rat basal forebrain cholinergic neurons being exposed to Abeta(1-42). The subunits of K(ATP): Kir6.1, Kir6.2, SUR1 and SUR2 expressing change was observed by double Immunofluorescence and immunoblotting in cultured cholinergic neurons from different groups: treatment with Abeta(1-42) (group Abeta(1-42)), pretreatment with diazoxide and the...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525448</comments>
            <pubDate>Mon, 01 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525448</guid>        </item>
        <item>
            <title>Hydrogen Sulfide Attenuates Neuronal Injury Induced by Vascular Dementia Via Inhibiting Apoptosis in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=2525447&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19488854%26dopt%3DAbstract</link>
            <description>Authors: Zhang LM, Jiang CX, Liu DW
    Hydrogen sulfide (H(2)S) is a gaseous messenger and serves as an important neuromodulator in the central nervous system. The current study was undertaken to investigate whether H(2)S attenuates the neuronal injury induced by vascular dementia (VD). Rats were subjected to bilateral common carotid artery and vertebral artery occlusion for 5 min three times in an interval of 5 min to induce VD. An H(2)S donor, sodium hydrosulfide (NaHS) or an inhibitor of cystathionine-beta-synthase, hydroxylamine (HA) was administered intraperitoneally. The number of neurons in the hippocampus was determined by hematoxylin and eosin staining, and the performance of learning and memory was tested by the Morris water maze. H(2)S content in plasma was evaluated. Apoptosis...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525447</comments>
            <pubDate>Mon, 01 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525447</guid>        </item>
        <item>
            <title>GABA Analogues Derived from 4-Aminocyclopent-1-enecarboxylic Acid.</title>
            <link>http://www.medworm.com/index.php?rid=2525446&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19488855%26dopt%3DAbstract</link>
            <description>This study has shown that GABA analogues derived by thiol addition to 4-aminocyclopent-1-enecarboxylic acid display interesting antagonist activity at the alpha(1)beta(2)gamma(2L) GABA(A) receptor.
    PMID: 19488855 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525446</comments>
            <pubDate>Mon, 01 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525446</guid>        </item>
        <item>
            <title>Alterations in Membrane Potential in Mitochondria Isolated from Brain Subregions During Focal Cerebral Ischemia and Early Reperfusion: Evaluation Using Flow Cytometry.</title>
            <link>http://www.medworm.com/index.php?rid=2525445&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19488856%26dopt%3DAbstract</link>
            <description>Authors: Lee DR, Helps SC, Macardle PJ, Nilsson M, Sims NR
    Mitochondria isolated from brain tissue following middle cerebral artery occlusion or during early reperfusion were tested for their ability to generate a membrane potential under standard conditions in vitro. Membrane potential was evaluated based on rhodamine 123 fluorescence in the mitochondria as detected using flow cytometry. Compared with equivalent samples from the contralateral hemisphere, the geometric mean fluorescence was significantly lower in mitochondria prepared from the striatum and perifocal tissue in the cortex at 3 h ischemia. During reperfusion, this property was decreased in mitochondria from tissue in the striatum and cortex that had been part of severely ischemic core tissue during the arterial occlusion....</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525445</comments>
            <pubDate>Mon, 01 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525445</guid>        </item>
        <item>
            <title>Antitumorigenic Effect of Brain Proline Rich Polypeptide-1 in Human Chondrosarcoma.</title>
            <link>http://www.medworm.com/index.php?rid=2525450&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19484491%26dopt%3DAbstract</link>
            <description>Authors: Galoian K, Scully S, McNamara G, Flynn P, Galoyan A
    Proline rich polypeptide (PRP-1) produced by neurosecretory cells of the hypothalamus is one of the fragments of neurophysin-vasopressin-associated glycoprotein. The primary structure of the neuropeptide PRP-1 isolated from neurosecretory granules of bovine neurohypophysis. We investigated PRP-1 action on chondrosarcoma, the second most common malignancy in bone, which primarily affects the cartilage cells. This deadly disease does not have any effective treatment. Earlier we demonstrated MYC oncogene inactivating effect by 1 mug/ml concentration brain PRP-1 In the present study we observed reduced viable sarcoma JJ012 cell numbers in comparison with control (89% growth inhibition) when treated with low concentrations of PRP-...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525450</comments>
            <pubDate>Sat, 30 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525450</guid>        </item>
        <item>
            <title>Graham Johnston: Bringing Success to Neuroscience Through Medicinal Chemistry.</title>
            <link>http://www.medworm.com/index.php?rid=2525451&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19484383%26dopt%3DAbstract</link>
            <description>Authors: Beart PM, Balcar VJ
    
    PMID: 19484383 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525451</comments>
            <pubDate>Fri, 29 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525451</guid>        </item>
        <item>
            <title>Evidence Group I mGluR Drugs Modulate the Activation Profile of Lipopolysaccharide-Exposed Microglia in Culture.</title>
            <link>http://www.medworm.com/index.php?rid=2525452&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19479374%26dopt%3DAbstract</link>
            <description>This study aimed to investigate the effects of group I mGluR selective ligands, (S)-3,5-dihydroxyphenylglycine ((S)-3,5-DHPG) and (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA), in lipopolysaccharide (LPS; 50 ng/ml)-activated rat microglial cultures. (S)-3,5-DHPG (150 muM) significantly reduced (approximately 20-60%) the LPS-mediated production of nitrite (NO(2) (-)), tumour necrosis factor alpha (TNF-alpha), and L: -glutamate (Glu) at 24 and 72 h. Image analysis revealed increases in both cell area and number, with larger amoeboid microglia (with retracted processes) formed following 2 h LPS exposure. This cellular population was absent after addition of (S)-3,5-DHPG, an effect antagonised by AIDA, and a concomitant reduction in cell area was also found. Taken together, these biochemical ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525452</comments>
            <pubDate>Thu, 28 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525452</guid>        </item>
        <item>
            <title>Effect of Intranigral Injection of GDNF and EGF on the Survival and Possible Differentiation Fate of Progenitors and Immature Neurons in 6-OHDA-Lesioned Rats.</title>
            <link>http://www.medworm.com/index.php?rid=2525454&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19472051%26dopt%3DAbstract</link>
            <description>Authors: Yu ZQ, Zha JH, Liu HM, Ding YX, Wang YQ, Wang HJ, Gao DS
    We investigated the survival and the possible differentiation fate of the progenitors and immature neurons in the pars compacta of the substantia nigra (SNc) by intranigral injection of a glial cell line-derived neurotropic factor (GDNF) or glial cell line-derived neurotropic factor plus epidermal growth factor (EGF + GDNF) in 6-hydroxydopamine (6-OHDA)-lesioned rats. First, we performed behavioral tests by postural asymmetry and forelimb akinesia on the rats injected with 6-OHDA in striatum at day 7, and selected the qualified model according to the results. Then, intranigral GDNF or EGF + GDNF treatment was administered in the qualified PD model rats. On day 21, behavioral tests were performed with these rats; and then...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525454</comments>
            <pubDate>Tue, 26 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525454</guid>        </item>
        <item>
            <title>An Improved Method to Obtain a Soluble Nuclear Fraction from Embryonic Brain Tissue.</title>
            <link>http://www.medworm.com/index.php?rid=2525481&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19462231%26dopt%3DAbstract</link>
            <description>In conclusion, the procedure presently described appears to be reliable and convenient for obtaining a pure soluble nuclear fraction from a discrete amount of embryonic brain tissue.
    PMID: 19462231 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525481</comments>
            <pubDate>Thu, 21 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525481</guid>        </item>
        <item>
            <title>Cografted Wharton's Jelly Cells-derived Neurospheres and BDNF Promote Functional Recovery After Rat Spinal Cord Transection.</title>
            <link>http://www.medworm.com/index.php?rid=2525480&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19462232%26dopt%3DAbstract</link>
            <description>Authors: Zhang L, Zhang HT, Hong SQ, Ma X, Jiang XD, Xu RX
    An animal model of transected spinal cord injury (SCI) was used to test the hypothesis that cografted human umbilical mesenchymal stem cells-derived neurospheres (HUMSC-NSs) and BDNF can promote morphologic and functional recoveries of injured spinal cord. In vitro, HUMSC-NSs terminally differentiated into higher percentages of cells expressing neuronal markers: beta-tubulin III and MAP2ab by the supplement with BDNF. Following grafted into injured spinal cord, very few grafted cells survived in the HUMSC-NSs + BDNF-treated (&amp;lt;3%) and HUMSC-NSs-treated (&amp;lt;1%) groups. The survived cells were differentiated into various cells, which were confirmed by double staining of BrdU and neural or glia markers. In comparison, more graf...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525480</comments>
            <pubDate>Thu, 21 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525480</guid>        </item>
        <item>
            <title>Different Mechanisms of NMDA-Mediated Protection Against Neuronal Apoptosis: A Stimuli-Dependent Effect.</title>
            <link>http://www.medworm.com/index.php?rid=2525479&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19462233%26dopt%3DAbstract</link>
            <description>Authors: Jantas D, Lason W
    The mechanisms of protective effect of N-methyl-D-aspartate (NMDA) receptor stimulation on apoptosis of neurons at their early stage of development are poorly understood. In the present study, we investigated the effects of NMDA on staurosporine (St)- and low-potassium (LP)-evoked apoptotic cell death in primary cerebellar granule cell (CGC) cultures at 7 days in vitro (DIV). We found that NMDA (200 muM) attenuated the St (0.5 muM)- and LP (5 mM KCl)-induced neuronal cell death in 7 but not 12 DIV CGC as confirmed by LDH release and MTT reduction assays. Moreover, NMDA attenuated St-and LP-evoked DNA fragmentation and cytosolic apoptosis inducing factor (AIF) protein level but not caspase-3 activation induced by both pro-apoptotic factors. Neuroprotective eff...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525479</comments>
            <pubDate>Thu, 21 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525479</guid>        </item>
        <item>
            <title>Effects of Electro-Acupuncture on IGF-I Expression in Spared Dorsal Root Ganglia and Associated Spinal Dorsal Horn in Cats Subjected to Adjacent Dorsal Root Ganglionectomies.</title>
            <link>http://www.medworm.com/index.php?rid=2525455&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19462234%26dopt%3DAbstract</link>
            <description>Authors: Dai P, Wang ZJ, Sun WW, Pang JX, You C, Wang TH
    The effects of electro-acupuncture (EA) on insulin-like growth factor-I (IGF-I) expression in the spared dorsal root ganglia (DRG) and associated spinal dorsal horns were explored in cats subjected to unilateral removal of L(1)-L(5) and L(7)-S(2) DRG, sparing the L(6) DRG. Immunohistochemistry revealed the presence of IGF-I immunoreactive products in the L(6) DRG neurons and some neurons and glial cells in the spinal cord. Western blot demonstrated that the level of IGF-I was significantly up-regulated both in the spared DRG and the dorsal horns of L(3) and L(6) cord segments at both 7 and 14 days post operation following EA. The present findings demonstrated the association between neuroplasticity and IGF-I expression, suggestin...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525455</comments>
            <pubDate>Thu, 21 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525455</guid>        </item>
        <item>
            <title>Neuroprotection Against Transient Focal Cerebral Ischemia and Oxygen-Glucose Deprivation by Interference with GluR6-PSD95 Protein Interaction.</title>
            <link>http://www.medworm.com/index.php?rid=2525483&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19449206%26dopt%3DAbstract</link>
            <description>Authors: Yu CZ, Li C, Pei DS, Zong YY, Shi Q, Wen XR, Guan QH, Hang D, Hou XY, Zhang GY
    Previous studies have shown that KA receptor subunit GluR6 mediated c-Jun N-terminal protein kinase (JNK) signaling is involved in global ischemia injury. Our present study indicates that focal ischemic brain insult on rat middle cerebral artery occlusion (MACo) model enhances the assembly of the GluR6-PSD95-MLK3 module and facilitates the phosphorylation of JNK. Most importantly, a peptide containing the TAT protein transduction sequence, Tat-GluR6-9c, can perturb the assembly of the GluR6-PSD95-MLK3 signaling module and suppress the activation of MLK3, MKK7/4 and JNK. As result, the inhibition of JNK activation caused by Tat-GluR6-9c diminishes the phosphorylation of the transcription factor c-Jun...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525483</comments>
            <pubDate>Sun, 17 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525483</guid>        </item>
        <item>
            <title>The Low Affinity Dopamine Binding Site on Tyrosine Hydroxylase: The Role of the N-Terminus and In Situ Regulation of Enzyme Activity.</title>
            <link>http://www.medworm.com/index.php?rid=2525485&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19448984%26dopt%3DAbstract</link>
            <description>Authors: Gordon SL, Webb JK, Shehadeh J, Dunkley PR, Dickson PW
    Tyrosine hydroxylase (TH), the rate-limiting enzyme in catecholamine biosynthesis, is inhibited in vitro by catecholamines binding to two distinct sites on the enzyme. The N-terminal regulatory domain of TH contributes to dopamine binding to the high affinity site of the enzyme. We prepared an N-terminal deletion mutant of TH to examine the role of the N-terminal domain in dopamine binding to the low affinity site. Deletion of the N-terminus of TH removes the high affinity dopamine binding site, but does not affect dopamine binding to the low affinity site. The role of the low affinity site in situ was examined by incubating PC12 cells with L-DOPA to increase the cytosolic catecholamine concentration. This resulted in an i...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525485</comments>
            <pubDate>Fri, 15 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525485</guid>        </item>
        <item>
            <title>Regional and Temporal Changes in Proteomic Profile after Middle Cerebral Artery Occlusion with or without Reperfusion in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=2525493&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19444605%26dopt%3DAbstract</link>
            <description>Authors: Yao H, Nakahara T, Nakagawa N, Hashimoto K, Kuroki T
    Although DNA microarray studies showed up-regulation of various genes, failures of translation of many genes are expected to occur under ischemic conditions even in the penumbra with mild reduction in cerebral blood flow. We applied surface enhanced laser desorption/ionization-time of flight mass spectrometry (SELDI-TOF-MS) technology to study proteomic profile at 6, 12, and 24 h after photothrombotic middle cerebral artery (MCA) occlusion with or without YAG laser-induced reperfusion in adult male spontaneously hypertensive rats. Of the 43 protein peaks that differed from the sham-operation group with a criterion (no overlap of peak intensities between the two groups), 36 peaks (84%) were down-regulated, and seven were up-r...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525493</comments>
            <pubDate>Thu, 14 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525493</guid>        </item>
        <item>
            <title>Neuroprotective Effects of Withania somnifera Dunal.: A Possible Mechanism.</title>
            <link>http://www.medworm.com/index.php?rid=2525491&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19444606%26dopt%3DAbstract</link>
            <description>Authors: Bhatnagar M, Sharma D, Salvi M
    Present study was carried out to understand the possible mechanism of neuroprotective action of the root extract of Withania somnifera Dunal (WS). The study is focused on WS mediated inhibition of nitric oxide production, which is known to mediate neurodegeneration during stress. Adult mice (28 +/- 5 g) were exposed to restraint stress for 30 days. Activity of NADPH diaphorase (NADPH-d) and factors (Acetylcholine, serotonin and corticosterone), which regulates NADPH-d activity were studied. Treatment with WS extract for 30 days during stress, significantly reversed the stress induced NADPH-d activation. Observations suggest that inhibition of NADPH-d by WS is not a direct effect of extract on NADPH-d, instead it inhibits via suppressing corticost...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525491</comments>
            <pubDate>Thu, 14 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525491</guid>        </item>
        <item>
            <title>Modulation of alpha-Synuclein Aggregation by Dopamine: A Review.</title>
            <link>http://www.medworm.com/index.php?rid=2525489&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19444607%26dopt%3DAbstract</link>
            <description>Authors: Leong SL, Cappai R, Barnham KJ, Pham CL
    Parkinson's disease (PD) is a progressive neurodegenerative disorder that is characterized by (1) the selective loss of dopaminergic neurons in the substantia nigra and (2) the deposition of misfolded alpha-synuclein (alpha-syn) as amyloid fibrils in the intracellular Lewy bodies in various region of the brain. Current thinking suggests that an interaction between alpha-syn and dopamine (DA) leads to the selective death of neuronal cells and the accumulation of misfolded alpha-syn. However, the exact mechanism by which this occurs is not fully defined. DA oxidation could play a key role is the pathogenesis of PD by causing oxidative stress, mitochondria dysfunction and impairment of protein metabolism. Here, we review the literature on t...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525489</comments>
            <pubDate>Thu, 14 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525489</guid>        </item>
        <item>
            <title>Modulation of Glutamate and Glycine Transporters by Niflumic, Flufenamic and Mefenamic Acids.</title>
            <link>http://www.medworm.com/index.php?rid=2525487&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19444608%26dopt%3DAbstract</link>
            <description>Authors: Habjan S, Vandenberg RJ
    Three fenamates-niflumic, flufenamic and mefenamic acids-were tested for effects on substrate-induced currents of glutamate and glycine transporters (EAAT1, EAAT2, GLYT1b and GLYT2a) expressed in Xenopus laevis oocytes. All fenamates inhibited EAAT1 currents; 100 muM flufenamic acid produced the most inhibition, decreasing the I (max) by 53 +/- 4% (P &amp;lt; 0.001). EAAT2 currents were less sensitive, but 100 muM flufenamic acid inhibited the I (max) by 34 +/- 5% (P = 0.006). All fenamates inhibited GLYT1b currents; 100 muM flufenamic acid produced the most inhibition, decreasing the I (max) by 61 +/- 1% (P &amp;lt; 0.001). At 100 muM, effects on the GLYT2a I (max) were mixed: 13 +/- 2% inhibition by flufenamic acid (P = 0.002), 30 +/- 6% enhancement by niflum...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525487</comments>
            <pubDate>Thu, 14 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525487</guid>        </item>
        <item>
            <title>The Value of the Serum Neurofilament Protein Heavy Chain as a Biomarker for Peri-operative Brain Injury After Carotid Endarterectomy.</title>
            <link>http://www.medworm.com/index.php?rid=2525497&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19430903%26dopt%3DAbstract</link>
            <description>Authors: Sellner J, Petzold A, Sadikovic S, Esposito L, Weber MS, Heider P, Eckstein HH, Hemmer B, Poppert H
    This prospective study examined the value of serum neurofilament protein levels for detecting peri-operative brain damage following carotid endarterectomy. An ELISA was used for quantification of neurofilament protein heavy chain (NfH(SMI35)) levels from patients undergoing endarterectomy for symptomatic (n = 17) and asymptomatic high-grade internal carotid artery stenosis (n = 30). All patients underwent diffusion-weighted brain imaging before and after the procedure. NfH(SMI35) levels were significantly higher in patients with a symptomatic carotid artery stenosis (0.131 ng/ml) if compared to asymptomatic patients (0.055 ng/ml, P = 0.01). However, serum NfH(SMI35) levels were ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525497</comments>
            <pubDate>Fri, 08 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525497</guid>        </item>
        <item>
            <title>Distribution of Glutamate Transporter GLAST in Membranes of Cultured Astrocytes in the Presence of Glutamate Transport Substrates and ATP.</title>
            <link>http://www.medworm.com/index.php?rid=2525495&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19440835%26dopt%3DAbstract</link>
            <description>Authors: Shin JW, Nguyen KT, Pow DV, Knight T, Buljan V, Bennett MR, Balcar VJ
    Neurotransmitter L: -glutamate released at central synapses is taken up and &quot;recycled&quot; by astrocytes using glutamate transporter molecules such as GLAST and GLT. Glutamate transport is essential for prevention of glutamate neurotoxicity, it is a key regulator of neurotransmitter metabolism and may contribute to mechanisms through which neurons and glia communicate with each other. Using immunocytochemistry and image analysis we have found that extracellular D: -aspartate (a typical substrate for glutamate transport) can cause redistribution of GLAST from cytoplasm to the cell membrane. The process appears to involve phosphorylation/dephosphorylation and requires intact cytoskeleton. Glutamate transport ligan...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525495</comments>
            <pubDate>Thu, 07 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525495</guid>        </item>
        <item>
            <title>Developmental Profiles of Lipogenic Enzymes and Their Regulators in the Neonatal Mouse Brain.</title>
            <link>http://www.medworm.com/index.php?rid=2525501&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19418221%26dopt%3DAbstract</link>
            <description>Authors: Saito M, Chakraborty G, Mao RF, Vadasz C, Saito M
    It has been shown that lipogenic enzymes, such as fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC), are highly expressed in the rodent brain during the early neonatal period and decline thereafter. However, cellular localization of these enzymes is unknown. Presently, we examined developmental changes in the levels and cellular localization of FAS and ACC, and their putative regulators, sterol-regulatory element-binding protein (SREBP)-1 and AMP-activated protein kinase (AMPK) in the mouse brain. Levels of these proteins including phosphorylated forms of ACC and AMPK decreased between postnatal day 4 (P4) and P19. Immunohistochemical studies indicated that FAS, ACC, AMPK, and SREBP-1 were expressed in neurons at P7, w...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525501</comments>
            <pubDate>Tue, 05 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525501</guid>        </item>
        <item>
            <title>Neurochemistry Underlying Relapse to Opiate Seeking Behaviour.</title>
            <link>http://www.medworm.com/index.php?rid=2525499&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19418222%26dopt%3DAbstract</link>
            <description>Authors: Brown RM, Lawrence AJ
    Relapse is a major clinical problem and remains a major challenge in the treatment of addictions. A goal of current research is to gain a greater understanding of the neurochemistry underlying relapse to opiate use. Factors which trigger relapse in humans such as stress, exposure to opiates and/or drug-associated cues, can also trigger opiate-seeking in animals. This review will overview preclinical studies relating to the neurochemistry of opiate-seeking with a focus on studies published from 2005 to present.
    PMID: 19418222 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525499</comments>
            <pubDate>Tue, 05 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525499</guid>        </item>
        <item>
            <title>Regulation of CaMKII In vivo: The Importance of Targeting and the Intracellular Microenvironment.</title>
            <link>http://www.medworm.com/index.php?rid=2525505&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19415486%26dopt%3DAbstract</link>
            <description>Authors: Skelding KA, Rostas JA
    CaMKII (calcium/calmodulin-stimulated protein kinase II) is a multifunctional protein kinase that regulates normal neuronal function. CaMKII is regulated by multi-site phosphorylation, which can alter enzyme activity, and targeting to cellular microdomains through interactions with binding proteins. These proteins integrate CaMKII into multiple signalling pathways, which lead to varied functional outcomes following CaMKII phosphorylation, depending on the identity and location of the binding partner. A new phosphorylation site on CaMKII (Thr253) has been identified in vivo. Thr253 phosphorylation controls CaMKII purely by targeting, does not effect enzyme activity, and occurs in response to physiological and pathological stimuli in vivo, but only in CaMK...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525505</comments>
            <pubDate>Mon, 04 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525505</guid>        </item>
        <item>
            <title>Astrocytes and Interneurons in Memory Processing in the Chick Hippocampus: Roles for G-Coupled Protein Receptors, GABA(B) and mGluR1.</title>
            <link>http://www.medworm.com/index.php?rid=2525504&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19415487%26dopt%3DAbstract</link>
            <description>Authors: Gibbs ME, Bowser DN
    Glutamate and GABA acting at mGluR1 and GABA(B) receptors, respectively, have roles in memory processing in the hippocampus up to 35 min after bead discrimination learning in the young chick. Activation of mGluR1 receptors is important at 2.5 and 30 min after training, but modulation of these receptors between these two times has no effect on memory. This timing is similar to the action of glutamate on NMDA receptors. The GABA(B) antagonist, phaclofen, and the inhibitor of astrocytic oxidative metabolism, fluoroacetate, inhibited memory when injected between 2.5 and 30 min. Paradoxically, a high dose of the GABA(B) agonist, baclofen, also inhibited memory, but a low dose promoted memory consolidation-an effect possibly caused by too much information and los...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525504</comments>
            <pubDate>Mon, 04 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525504</guid>        </item>
        <item>
            <title>Melatonin Ameliorates Cerebral Vasospasm After Experimental Subarachnoidal Haemorrhage Correcting Imbalance of Nitric Oxide Levels in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=2525503&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19415488%26dopt%3DAbstract</link>
            <description>In conclusion, melatonin administration ameliorated cerebral vasospasm by increasing serum NO level and decreasing the brain the levels of arginase and oxidative stress. It is therefore possible that increased brain arginase activity after SAH may also have a significant role in the pathogenesis of vasospasm by limiting the availability of arginine for NO production.
    PMID: 19415488 [PubMed - as supplied by publisher] (Source: Neurochemical Research)</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525503</comments>
            <pubDate>Mon, 04 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525503</guid>        </item>
        <item>
            <title>Cruciferous Nutraceutical 3H-1,2-dithiole-3-thione Protects Human Primary Astrocytes Against Neurocytotoxicity Elicited by MPTP, MPP(+), 6-OHDA, HNE and Acrolein.</title>
            <link>http://www.medworm.com/index.php?rid=2525506&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19408115%26dopt%3DAbstract</link>
            <description>In this study, we show that incubation of human primary astrocytes with micromolar concentrations (5-100 muM) of D3T for 24 h resulted in significant increases in the levels of reduced glutathione (GSH), glutathione reductase (GR), and the phase 2 enzyme NAD(P)H:quinone oxidoreductase 1 (NQO1). D3T treatment also caused time-dependent increases in mRNA expression of the gamma-glutamylcysteine ligase catalytic subunit (GCLC), GR, and of NQO1 in these cells. Pretreatment of astrocytes with D3T was found to afford remarkable protection against the neurocytotoxicity elicited by MPTP, MPP(+), 6-OHDA, HNE and acrolein. Taken together, this study demonstrates for the first time that in human astrocytes, the cruciferous nutraceutical D3T potently induces the cellular GSH system and the phase 2 enz...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525506</comments>
            <pubDate>Thu, 30 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525506</guid>        </item>
        <item>
            <title>New Insights into Mechanisms of gamma-Diketone-Induced Axonopathy.</title>
            <link>http://www.medworm.com/index.php?rid=2525508&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19404740%26dopt%3DAbstract</link>
            <description>Authors: Tshala-Katumbay D, Desjardins P, Sabri M, Butterworth R, Spencer P
    We analyzed the impact of axonopathy-inducing agents 1,2-diacetylbenzene (1,2-DAB) and 2,5-hexanedione (2,5-HD) on membrane-bound protein disulfide isomerase (mPDI) versus soluble PDI (sPDI), or PDI-family member thioredoxin (THX), and asked whether changes in PDI/THX were associated with production of oxidative/nitrosative species in the Sprague-Dawley rat. We show that 1,2-DAB and 2,5-HD lower the abundance of sPDI and THX. However, the protein expression of mPDI is increased in 1,2-DAB axonopathy and neuroproteins became more S-nitrosylated. The abundance of heme oxygenase-1 (HO-1) and isoforms of nitric oxide synthase (neuronal, endothelial, and inducible NOS) remained unchanged suggesting that S-nitrosylat...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525508</comments>
            <pubDate>Tue, 28 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525508</guid>        </item>
        <item>
            <title>Metabolic Effects of Blocking Lactate Transport in Brain Cortical Tissue Slices Using an Inhibitor Specific to MCT1 and MCT2.</title>
            <link>http://www.medworm.com/index.php?rid=2525507&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19404741%26dopt%3DAbstract</link>
            <description>Authors: Rae C, Nasrallah FA, Br&amp;#xF6;er S
    A novel inhibitor of lactate transport, AR-C122982, was used to study the effect of inhibiting the monocarboxylate transporters MCT1 and MCT2 on cortical brain slice metabolism. We studied metabolism of L: -[3-(13)C]lactate, and D: -[1-(13)C]glucose under a range of conditions. Experiments using L: -[3-(13)C]lactate showed that the inhibitor AR-C122982 altered exchange of lactate. Under depolarizing conditions, net flux of label from D: -[1-(13)C]glucose was barely altered by 10 or 100 nM AR-C122982. In the presence of AMPA or glutamate there were increases in net flux of label and metabolic pool sizes. These data suggest lactate may supply compartments in the brain not usually directly accessed by glucose. In general, it would appear that mov...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525507</comments>
            <pubDate>Tue, 28 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525507</guid>        </item>
        <item>
            <title>The Human G93A-Superoxide Dismutase-1 Mutation, Mitochondrial Glutathione and Apoptotic Cell Death.</title>
            <link>http://www.medworm.com/index.php?rid=2525509&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19399611%26dopt%3DAbstract</link>
            <description>Authors: Muyderman H, Hutson PG, Matusica D, Rogers ML, Rush RA
    Mutations in Cu/Zn superoxide dismutase are a cause of motor neuron death in about 20% of cases of familial amyotrophic lateral sclerosis (ALS). Although the molecular mechanism of which these mutations induce motor neuron cell death is to a large extent unknown, there is significant evidence that effects on mitochondrial function and development of oxidative stress make a major contribution to the selective death of motor neurons in this disease. In this overview article we review the current understanding of mutant SOD1-mediated motor neuron degeneration in ALS with focus on oxidative damage and mitochondrial dysfunction. We also present novel information on the role of mitochondrial glutathione for the survival of NSC-3...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525509</comments>
            <pubDate>Mon, 27 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525509</guid>        </item>
        <item>
            <title>Acupuncture at Both ST25 and ST37 Improves the Pain Threshold of Chronic Visceral Hypersensitivity Rats.</title>
            <link>http://www.medworm.com/index.php?rid=2525512&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19387829%26dopt%3DAbstract</link>
            <description>Authors: Liu HR, Wang XM, Zhou EH, Shi Y, Li N, Yuan LS, Wu HG
    Previous studies demonstrated the efficacy of electro-acupuncture (EA) in relieving chronic visceral hypersensitivity (CVH) in IBS rats. However, ST25 which is a key acupoint for patients with IBS has not been reported in these experiments. Eight CVH rats were treated by EA at both ST25 and ST37 for 20 min, once daily for seven consecutive days, model rats (n = 8) and normal rats (n = 8) as controls. After the first EA treatment, the abdominal withdrawal reflex scores were investigated to evaluate the pain threshold. After seven EA treatments, the concentrations of 5-hydroxytryptamine (5-HT), 5-HT3 receptor (5-HT3R) and 5-HT4 receptor (5-HT4R) in colon tissue were assayed quantitatively by enzyme-linked immunosorbent assay....</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525512</comments>
            <pubDate>Wed, 22 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525512</guid>        </item>
        <item>
            <title>The Flavonoid Glycosides, Myricitrin, Gossypin and Naringin Exert Anxiolytic Action in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=2525511&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19387830%26dopt%3DAbstract</link>
            <description>This study assessed the potential anxiolytic effect of three flavonoid glycosides, myrcitrin, naringin and gossypin, in the elevated plus maze test (EPM). Myricitrin (1 mg/kg) was effective on the EPM showing a clear anxiolytic effect with no signs of sedation. However, higher doses showed possible sedative and myorelaxation effects. Gossypin and naringin both shared a similar profile, with low doses (1 mg/kg) inducing a robust anxiolytic effect which diminished with increasing doses of the flavonoids. Higher doses of these two flavonoids showed a dramatic increase in the open arm exploration accompanied by a decrease in locomotor activity. Hence, naringin (30 mg/kg) and gossypin (30 mg/kg) induce both anxiolytic and sedative effects. These results suggest that flavonoid glycosides have th...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525511</comments>
            <pubDate>Wed, 22 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525511</guid>        </item>
        <item>
            <title>Guanidino Acids Act as rho1 GABA(C) Receptor Antagonists.</title>
            <link>http://www.medworm.com/index.php?rid=2525510&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19387831%26dopt%3DAbstract</link>
            <description>Authors: Chebib M, Gavande N, Wong KY, Park A, Premoli I, Mewett KN, Allan RD, Duke RK, Johnston GA, Hanrahan JR
    GABA(C) receptors play a role in myopia, memory-related disorders and circadian rhythms signifying a need to develop potent and selective agents for this class of receptors. Guanidino analogs related to glycine, beta-alanine and taurine were evaluated at human rho(1)GABA(C) receptors expressed in Xenopus oocytes using 2-electrode voltage clamp methods. Of the 12 analogs tested, 8 analogs were active as antagonists and the remaining were inactive. (S)-2-Guanidinopropionic acid (IC(50) = 2.2 muM) and guanidinoacetic acid (IC(50) = 5.4 muM; K (B) = 7.75 muM [pK (B) = 5.11 +/- 0.06]) were the most potent being competitive antagonists at this receptor. In contrast, the beta-alani...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525510</comments>
            <pubDate>Wed, 22 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525510</guid>        </item>
        <item>
            <title>The Potential Role of Nitric Oxide Synthase in Survival and Regeneration of Magnocellular Neurons of Hypothalamo-Neurohypophyseal System.</title>
            <link>http://www.medworm.com/index.php?rid=2525513&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19381805%26dopt%3DAbstract</link>
            <description>Authors: Yuan Q, Scott DE, So KF, Lin Z, Wu W
    Previous investigations from this laboratory have demonstrated that hypophysectomy induces up-regulation of neuronal nitric oxide synthase (nNOS) in magnocellular neurons of the mammalian hypothalamo-neurohypophyseal system (HNS). Accompanied by this upregulation of nNOS, both neuronal regeneration and degeneration are also observed in this system following hypophysectomy. The specific aim of this study was to determine the potential role of nNOS upregulation in neuronal survival and regeneration after hypophysectomy in the adult Sprague-Dawley (SD) rat by using a competitive nitric oxide synthase blocker, N(G)-nitrol-L: -arginine methyl ester (L: -NAME). We found that L: -NAME treatment effectively blocked the regeneration of magnocellular...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525513</comments>
            <pubDate>Mon, 20 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525513</guid>        </item>
        <item>
            <title>Pore Structure of the Cys-loop Ligand-gated Ion Channels.</title>
            <link>http://www.medworm.com/index.php?rid=2525514&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19381804%26dopt%3DAbstract</link>
            <description>Authors: Absalom NL, Schofield PR, Lewis TM
    The Cys-loop receptor family of ligand-gated ion channels (LGICs) play a key role in synaptic transmission in the central nervous system of animals. Recent advances have led to the elucidation of two crystal structures of related prokaryotic LGICs and the electron micrograph derived structure of the acetylcholine receptor from Torpedo marmorata. Here, we review the structural and biochemical data that form our understanding of the structure of the channel pore. We introduce original data from the glycine receptor using the substituted-cysteine accessibility technique and show that while the helical structure of the segment that surrounds the channel pore is generally agreed, the location of the channel gate, the pore diameter and the structur...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525514</comments>
            <pubDate>Sat, 18 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525514</guid>        </item>
        <item>
            <title>Norepinephrine Homogeneously Inhibits alpha-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate- (AMPAR-) Mediated Currents in All Layers of the Temporal Cortex of the Rat.</title>
            <link>http://www.medworm.com/index.php?rid=2525515&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19357950%26dopt%3DAbstract</link>
            <description>Authors: Dinh L, Nguyen T, Salgado H, Atzori M
    The primary auditory cortex is subject to the modulation of numerous neurotransmitters including norepinephrine (NE), which has been shown to decrease cellular excitability by yet unclear mechanisms. We investigated the possibility that NE directly affects excitatory glutamatergic synapses. We found that bath applications of NE (20 muM) decreased glutamatergic excitatory post-synaptic currents (EPSCs) in all cortical layers. Changes in the kinetics of synaptic EPSCs, invariance of pair pulse ratio and of the coefficient-of-variation, together with the decrease of responses to pressure-application of AMPA (500 muM), indicated the postsynaptic nature of the adrenergic effect. Pharmacological experiments suggested that the NE-induced depressi...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525515</comments>
            <pubDate>Wed, 08 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525515</guid>        </item>
        <item>
            <title>Effects of Bone Marrow Stromal Cell-conditioned Medium on Primary Cultures of Peripheral Nerve Tissues and Cells.</title>
            <link>http://www.medworm.com/index.php?rid=2525516&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19350389%26dopt%3DAbstract</link>
            <description>In this study, rat dorsal root ganglion (DRG) explants, rat DRG neurons, and rat Schwann cells (SCs) were treated with monkey MSC-conditioned medium, respectively, and then subjected to MTT assay, Bromodeoxyuridine/Hoechst 33342 double staining, flow cytometry, immunohistochemistry, real-time quantitative PCR, and Western blot analysis, respectively. The results showed that MSC-conditioned medium enhanced axon growth and neurogenesis in cultured DRG explants, augmented cell survival of and expression of NF and GAP-43 by cultured DRG neurons, promoted cell survival and proliferation of cultured SCs, and increased the expression of NGF, BDNF, and bFGF in cultured SCs. We also found that mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (Erk) 1/2 pathway was involv...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525516</comments>
            <pubDate>Mon, 06 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525516</guid>        </item>
        <item>
            <title>Intramembranous Fragment of Amyloid-beta: A Potential Immunogen for Alzheimer's Disease Immunotherapy.</title>
            <link>http://www.medworm.com/index.php?rid=2525518&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19347579%26dopt%3DAbstract</link>
            <description>This study was aimed to investigate alternative approaches for a safer vaccine to treat AD. We used intramembranous fragment of amyloid-beta (IF-Abeta) to immunize Kunming mice for up to 2.5 months and then evaluated the immunization efficacy and potential adverse effects. Immunization of mice with IF-Abeta plus Freund's adjuvant resulted in moderate levels of Abeta antibodies (IgG), and the anti-sera were able to neutralize Abeta1-42-neurotoxicity in cultured primary cortical neurons. IF-Abeta itself did not show neurotoxicity, and immunization with IF-Abeta did not cause behavioral deficits in Morris water maze or any abnormalities by histological examinations of major organs including the brain. We conclude that vaccination with IF-Abeta may be a potentially safe and effective treatment...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525518</comments>
            <pubDate>Fri, 03 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525518</guid>        </item>
        <item>
            <title>The Role of Intracellular Glutathione in Inorganic Mercury-Induced Toxicity in Neuroblastoma Cells.</title>
            <link>http://www.medworm.com/index.php?rid=2525517&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19347580%26dopt%3DAbstract</link>
            <description>Authors: Becker A, Soliman KF
    It is well known that antioxidants containing sulfhydryl (-SH) groups are protective against the toxic effects of mercury. The current study was designed to elucidate the mechanism(s) of the cytoprotective effects of glutathione (GSH) and N-acetylcysteine (NAC) against the toxicity of inorganic mercury (HgCl(2)) in neuroblastoma cells (N-2A). The obtained results demonstrated the protective effects of these compounds in a dose dependant manner up to 95 and 74% cell viability, respectively as compared to the control of HgCl(2) of 10%. The administration of buthionine sulfoximine (BSO), an inhibitor of GSH synthesis, increased the toxicity of HgCl(2) in a dose dependent manner. Moreover, BSO treatment attenuated the levels of the cellular free -SH concentrat...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525517</comments>
            <pubDate>Fri, 03 Apr 2009 23:00:00 +0100</pubDate>
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        <item>
            <title>Release of Endogenous Amino Acids from the Hippocampus and Brain Stem from Developing and Adult Mice in Ischemia.</title>
            <link>http://www.medworm.com/index.php?rid=2525519&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19343493%26dopt%3DAbstract</link>
            <description>Authors: Oja SS, Saransaari P
    The release of neurotransmitters and modulators has been studied mostly using labeled preloaded compounds. For several reasons, however, the estimated release may not reliably reflect the release of endogenous compounds. The basal and K(+)-evoked release of the neuroactive endogenous amino acids GABA, glycine, taurine, L: -glutamate and L: -aspartate was now studied in slices from the hippocampus and brain stem from 7-day-old and 3-month-old mice under control and ischemic conditions. The release of synaptically not active L: -glutamine, L: -alanine, L: -threonine and L: -serine was assessed for comparison. The estimates for the hippocampus and brainstem were markedly different and also different in developing and adult mice. GABA release was much greater ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2525519</comments>
            <pubDate>Thu, 02 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2525519</guid>        </item>
        <item>
            <title>Dysregulation of Calcium Homeostasis in Alzheimer's Disease.</title>
            <link>http://www.medworm.com/index.php?rid=2300744&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19337829%26dopt%3DAbstract</link>
            <description>Authors: Small DH
    The accumulation of oligomeric species of beta-amyloid protein in the brain is considered to be a key factor that causes Alzheimer's disease (AD). However, despite many years of research, the mechanism of neurotoxicity in AD remains obscure. Recent evidence strongly supports the theory that Ca(2+) dysregulation is involved in AD. Amyloid proteins have been found to induce Ca(2+) influx into neurons, and studies on transgenic mice suggest that this Ca(2+) influx may alter neuronal excitability. The identification of a risk factor gene for AD that may be involved in the regulation of Ca(2+) homeostasis and recent findings which suggest that presenilins may be involved in the regulation of intracellular Ca(2+) stores provide converging lines of evidence that support the ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2300744</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
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        <item>
            <title>Recombinant DNA Vaccine Against Inhibition of Neurite Outgrowth Promotes Functional Recovery Associated with Endogeous NGF Expression in Spinal Cord Hemisected Adult Rats.</title>
            <link>http://www.medworm.com/index.php?rid=2300743&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19337830%26dopt%3DAbstract</link>
            <description>Authors: Zhang Y, Hao CG, Hu LQ, Dong J, Wei P, Xu D, Xiao ZC, Wang TH
    Axonal regeneration across the site of spinal cord lesion is often aborted in adult mammalian species. The use of DNA vaccine to nullify the inhibitory molecules has been shown to be effective in promoting axonal regeneration in injured spinal cord. The possible molecular mechanisms, however, remain to be elucidated. The present study showed that the administration of recombinant DNA vaccine encoding multiple domains, Nogo-66, Nogo-N, TnR, and MAG, significantly improved hindlimb locomotor functions in rats subjected to ablation of the dorsal halves of the cord. Western blot analysis demonstrated that nerve growth factor (NGF) levels in the spinal cord of immunized rats were significantly upregulated than those of c...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2300743</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
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        <item>
            <title>Activation of NMDA Receptor is Associated with Up-regulation of COX-2 Expression in the Spinal Dorsal Horn during Nociceptive Inputs in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=2300742&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19337831%26dopt%3DAbstract</link>
            <description>Authors: Li SQ, Xing YL, Chen WN, Yue SL, Li L, Li WB
    Cyclooxygenases-2 (COX-2) in the spinal dorsal horn is up-regulated and plays an important role in pain and hyperalgesia induced by nociceptive stimulation. The mechanisms involved in the up-regulation of spinal COX-2 during nociceptive stimulation are yet not well understood. Because the important role of NMDA and its receptor in transmission of nociceptive information in the spinal cord, activation of the spinal NMDA receptor might contribute to the up-regulation of spinal COX-2 expression. The present study was undertaken to demonstrate the above hypothesis by observing changes of COX-2 expression in the spinal dorsal horn in rats subjected to formalin test and intrathecal administration of NMDA, a selective NMDA receptor agonist...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2300742</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
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        <item>
            <title>Differential Expression of Small Heat Shock Protein 27 (Hsp27) in Ataxia telangiectasia Brains.</title>
            <link>http://www.medworm.com/index.php?rid=2300746&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19322656%26dopt%3DAbstract</link>
            <description>Authors: Chen W, Kuizon S, Chiou BL, Bolton DC, Pullarkat RK, Junaid MA
    Ataxia telangiectasia (A-T) is a progressive neurodegenerative disorder caused by disruption of the gene, ataxia telangiectasia mutated (ATM). Present study was aimed at identifying proteins that are present in abnormal levels in A-T brain that may identify alternative targets for therapeutic interventions. Proteomic and Western blot analysis have shown massive expression of the small heat shock protein 27 (Hsp27) in frontal cortices of A-T brains compared to negligible levels in controls. The expression of other stress proteins, Hsp70, alphaB-crystallin, and prohibitin remained unchanged in the A-T and control brains. Significant decreases in reactive oxygen species, protein carbonyl groups and lipid peroxidation ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2300746</comments>
            <pubDate>Thu, 26 Mar 2009 04:00:00 +0100</pubDate>
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        <item>
            <title>Intracerebroventricular Administration of Ouabain to Rats Changes the Expression of NMDA Receptor Subunits in Cerebral Cortex and Hippocampus.</title>
            <link>http://www.medworm.com/index.php?rid=2300745&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19322657%26dopt%3DAbstract</link>
            <description>Authors: Bersier MG, Rodr&amp;#xED;guez de Lores Arnaiz G
    Ouabain exerts neurotoxic action and activates the population of NMDA receptors. Herein the effect of ouabain on the expression of NMDA subunits was evaluated. Adult Wistar rats were administered intracerebroventricularly with 0.1, 10 and 100 nmol ouabain or saline solution (control). Two days later, membranes of cerebral cortex and hippocampus were isolated. Western blots with antibodies for the NMDA receptor subunits: NR1; NR2A; NR2B; NR2C and NR2D were carried out. In cerebral cortex, NR2D subunit increased 30% with 10 nmol ouabain dose. With 100 nmol ouabain, NR1 and NR2D subunits enhanced 40 and 20%, respectively. In hippocampus, with the dose of 0.1 nmol ouabain, NR1 subunit enhanced roughly 50% whereas NR2B subunit decreased ...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2300745</comments>
            <pubDate>Thu, 26 Mar 2009 04:00:00 +0100</pubDate>
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        <item>
            <title>Are Astrocytes the Missing Link Between Lack of Brain Aspartoacylase Activity and the Spongiform Leukodystrophy in Canavan Disease?</title>
            <link>http://www.medworm.com/index.php?rid=2300748&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19319678%26dopt%3DAbstract</link>
            <description>Authors: Baslow MH, Guilfoyle DN
    Canavan disease (CD) is a genetic degenerative brain disorder associated with mutations of the gene encoding aspartoacylase (ASPA). In humans, the CD syndrome is marked by early onset, hydrocephalus, macroencephaly, psychomotor retardation, and spongiform myelin sheath vacuolization with progressive leukodystrophy. Metabolic hallmarks of the disease include elevated N-acetylaspartate (NAA) levels in brain, plasma and CSF, along with daily excretion of large amounts of NAA and its anabolic metabolite, N-acetylaspartylglutamate (NAAG). Of the observed neuropathies, the most important appears to be the extensive demyelination that interferes with normal neuronal signaling. However, finding the links between the lacks of ASPA activity in oligodendrocytes, t...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2300748</comments>
            <pubDate>Wed, 25 Mar 2009 04:00:00 +0100</pubDate>
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        <item>
            <title>Neuronal Expression of Splice Variants of &quot;Glial&quot; Glutamate Transporters in Brains Afflicted by Alzheimer's Disease: Unmasking an Intrinsic Neuronal Property.</title>
            <link>http://www.medworm.com/index.php?rid=2300747&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19319679%26dopt%3DAbstract</link>
            <description>This study analysed the expression of exon-skipping forms of the three predominant excitatory amino acid (glutamate) transporters (EAATs1-3) in brains afflicted with AD. We demonstrate by immunocytochemistry in temporal cortex, the expression of these proteins particularly in limited subsets of neurons, some of which appeared to be dys-morphic. Whilst the neuronal expression of the &quot;glial&quot; glutamate transporters EAAT1 and EAAT2 is frequently considered to represent the abnormal and ectopic expression of such transporters, we suggest this may be a misinterpretation, since neurons such as cortical pyramidal cells normally express abundant mRNA for these EAATs (but little if any EAAT protein expression). We hypothesize instead that distressed neurons in the AD brain can turn on the translatio...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2300747</comments>
            <pubDate>Wed, 25 Mar 2009 04:00:00 +0100</pubDate>
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        <item>
            <title>Dietary Enrichment with Medium Chain Triglycerides (AC-1203) Elevates Polyunsaturated Fatty Acids in the Parietal Cortex of Aged Dogs: Implications for Treating Age-Related Cognitive Decline.</title>
            <link>http://www.medworm.com/index.php?rid=2285263&amp;cid=s_37701_168_f&amp;fid=37701&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19301124%26dopt%3DAbstract</link>
            <description>Authors: Taha AY, Henderson ST, Burnham WM
    Dogs demonstrate an age-related cognitive decline, which may be related to a decrease in the concentration of omega-3 polyunsaturated fatty acids (n-3 PUFA) in the brain. Medium chain triglycerides (MCT) increase fatty acid oxidation, and it has been suggested that this may raise brain n-3 PUFA levels by increasing mobilization of n-3 PUFA from adipose tissue to the brain. The goal of the present study was to determine whether dietary MCT would raise n-3 PUFA concentrations in the brains of aged dogs. Eight Beagle dogs were randomized to a control diet (n = 4) or an MCT (AC-1203) enriched diet (n = 4) for 2 months. The animals were then euthanized and the parietal cortex was removed for phospholipid, cholesterol and fatty acid determinations b...</description>
            <author>Neurochemical Research</author>
            <type>journals</type>
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            <pubDate>Fri, 20 Mar 2009 04:00:00 +0100</pubDate>
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