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        <title>Folia Neuropathologica 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 'Folia Neuropathologica' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Folia+Neuropathologica&t=Folia+Neuropathologica&s=Search&f=source]]></link>
        <lastBuildDate>Tue, 24 Jan 2012 00:48:21 +0100</lastBuildDate>
        <item>
            <title>Spatial patterns of β-amyloid (Aβ) deposits in familial and sporadic Alzheimer's disease.</title>
            <link>http://www.medworm.com/index.php?rid=5449235&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22101948%26dopt%3DAbstract</link>
            <description>The objective was to determine whether genetic factors influenced the spatial patterns of the A β deposits. A β deposits were distributed either in clusters which were regularly distributed parallel to the pia mater or in larger, non-regularly distributed clusters. There were no significant differences in spatial pattern of the diffuse deposits between patient groups but mean cluster size of the diffuse deposits was larger in FAD compared with SAD. Primitive A β deposits were more frequently distributed in regular clusters and less frequently distributed in large clusters in FAD compared with SAD. Classic A β deposits were more frequently distributed in regularly spaced clusters and less frequently distributed in large clusters in LO-FAD compared with EO-FAD. There were no significant ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5449235</comments>
            <pubDate>Sun, 27 Nov 2011 11:54:03 +0100</pubDate>
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        <item>
            <title>Ultrastructural pathology of cortical capillary pericytes in human traumatic brain oedema.</title>
            <link>http://www.medworm.com/index.php?rid=5449234&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22101949%26dopt%3DAbstract</link>
            <description>Authors: Castejón OJ
    Abstract
    In human traumatic brain oedema pericytes exhibit remarkable oedematous changes, increased vacuolar and vesi-cular transport, transient transpericytal channels, and tubular structures demonstrating pericyte brain barrier dysfunction. They show nuclear invaginations, actin and myosin-like filaments, and coupled interaction with endothelial cells through the macula occludens. Some pericytes display hypertrophic and necrotic changes, and phagocytic capacity. Hypertrophic pericytes induce basement membrane splitting. Degenerated pericytes exhibit lacunar enlargement of endoplasmic reticulum, dense osmiophilic bodies, glycogen granules, vacuolization, oedematous Golgi apparatus, and pleomorphic mitochondria. Certain micropinocytotic vesicles are orientated...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5449234</comments>
            <pubDate>Sun, 27 Nov 2011 11:54:03 +0100</pubDate>
            <guid isPermaLink="false">5449234</guid>        </item>
        <item>
            <title>Ultrastructure of granular osmiophilic material deposits (GOM) in arterioles of CADASIL patients.</title>
            <link>http://www.medworm.com/index.php?rid=5449233&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22101950%26dopt%3DAbstract</link>
            <description>Authors: Lewandowska E, Dziewulska D, Parys M, Pasennik E
    Abstract
    Granular osmiophilic material (GOM) is a pathognomonic feature of CADASIL that may be a consequence of pathological processes triggered by Notch3 mutations. Since knowledge of the effects of CADASIL-associated GOM deposits is important to understand the molecular pathogenesis of this disorder, we performed a thorough ultrastructural analysis of GOM morphology in the skin and muscle arterioles in CADASIL patients. Electron microscopy revealed numerous GOM deposits with different morphology including size, shape and osmiophilic density. Osmiophilic granular material of high density was frequently observed in part of GOM deposits located near vascular smooth muscle cells (VSMC) while a part localized distally from the ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5449233</comments>
            <pubDate>Sun, 27 Nov 2011 11:54:03 +0100</pubDate>
            <guid isPermaLink="false">5449233</guid>        </item>
        <item>
            <title>Histopathological patterns of papillary tumour of the pineal region.</title>
            <link>http://www.medworm.com/index.php?rid=5449232&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22101951%26dopt%3DAbstract</link>
            <description>We present the variability of the histopathological pattern in three cases of PTPR. All cases showed predominant epithelial-like morphology but with various degrees of papillary formation and intensity of cellular pleomorphism. One tumour was highly cystic and exhibited cellular sheets containing vessels covered by several layers of uniform columnar to cuboidal tumour cells. The second tumour showed distinct papillae covered by layers of polymorphous cells with atypical, often hyperchromatic nuclei. Numerous cells displayed foamy, eosinophilic or clear, sometimes vacuolated cytoplasm. The third case consisted of solid cellular areas composed of pseudostratified columnar cells, most often arranged in perivascular pseudorosette formations. The cells lining papillary structures exhibited mark...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5449232</comments>
            <pubDate>Sun, 27 Nov 2011 11:54:03 +0100</pubDate>
            <guid isPermaLink="false">5449232</guid>        </item>
        <item>
            <title>Some markers of neuronal damage in cerebrospinal fluid of multiple sclerosis patients in relapse.</title>
            <link>http://www.medworm.com/index.php?rid=5449231&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22101952%26dopt%3DAbstract</link>
            <description>Authors: Mitosek-Szewczyk K, Gordon-Krajcer W, Flis D, Stelmasiak Z
    Abstract
    In this paper the performance of cerebrospinal fluid (CSF) protein biomarkers important for monitoring damage of brain astrocytes and neurons for MS is reviewed. We estimated neurofilament, tau and phospho-tau proteins, β-APP, Aβ, S-100B and neuron-specific enolase in CSF of MS patients during relapse. We noted elevation of neurofilament, tau and phospho-tau proteins, S-100B, neuron-specific enolase and c-terminal epitopes of β-APP; concomitantly decrease of Aβ was observed. These CSF biomarkers for MS relapse should reflect the central pathoge-nic processes in the brain, i.e., axonal and neuronal degeneration.
    PMID: 22101952 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5449231</comments>
            <pubDate>Sun, 27 Nov 2011 11:54:03 +0100</pubDate>
            <guid isPermaLink="false">5449231</guid>        </item>
        <item>
            <title>Neurolysis of the conducting neuroma-in-continuity in perinatal brachial plexus palsy - evaluation of the results of surgical treatment.</title>
            <link>http://www.medworm.com/index.php?rid=5449230&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22101953%26dopt%3DAbstract</link>
            <description>Conclusions: The choice of microsurgical technique during surgical treatment of perinatal brachial plexus palsies with neuroma-in-continuity should be based on the whole clinical and intraoperative view. The best results after neurolysis should be expected when neuroma-in-continuity is localized in the upper trunk, the injury corresponds to third degree on Sunderland's scale, and during electric stimulation a normal motor response can be obtained.
    PMID: 22101953 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5449230</comments>
            <pubDate>Sun, 27 Nov 2011 11:54:03 +0100</pubDate>
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        <item>
            <title>Long-term consequences of surgical brain injury - characteristics of the neurovascular unit and formation and demise of the glial scar in a rat model.</title>
            <link>http://www.medworm.com/index.php?rid=5449229&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22101954%26dopt%3DAbstract</link>
            <description>Authors: Frontczak-Baniewicz M, Chrapusta SJ, Sulejczak D
    Abstract
    Neurosurgical procedures often involve, as a result of the surgeon approaching the diseased region, unavoidable trauma to the adjacent, non-diseased brain structures. Because of the priority of removing the immediate threats to health or life that underlie such interventions, side effects of surgical brain injuries were not given much attention until recently. The cause-and-effect association of the eventual delayed cognitive and/or neurological deficits is often obscure due to substantial potential of the brain for compensatory changes, long life span in man, and aging-related phenomena. However, animal and human studies have demonstrated that physical insults to the brain can initiate a cascade of changes that res...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5449229</comments>
            <pubDate>Sun, 27 Nov 2011 11:54:03 +0100</pubDate>
            <guid isPermaLink="false">5449229</guid>        </item>
        <item>
            <title>N-nitro-L-arginine methyl ester influence on aluminium toxicity in the brain.</title>
            <link>http://www.medworm.com/index.php?rid=5449228&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22101955%26dopt%3DAbstract</link>
            <description>Authors: Stevanović ID, Jovanović MD, Colić M, Jelenković A, Bokonjić D, Ninković M, Stojanović I
    Abstract
    We investigated the influence of a non-specific nitric oxide synthase (NOS) inhibitor, N-nitro-L-arginine methyl ester (L-NAME), on brain nitrite concentration and acetylcholine esterase activity in AlCl3-treated Wistar rats. Animals were killed 10 min, three hours, three days and 30 days after the treatment and hippocampus and basal forebrain were removed. The biochemical changes observed in neuronal tissues show the involvement of NO in the AlCl3 toxicity and cholinergic neurotransmission, and that L-NAME may have potential neuroprotective effects. Active avoidance learning was significantly impaired after AlCl3 application, while pretreatment with L-NAME prevented th...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5449228</comments>
            <pubDate>Sun, 27 Nov 2011 11:54:03 +0100</pubDate>
            <guid isPermaLink="false">5449228</guid>        </item>
        <item>
            <title>The neuroprotective effect of topiramate on the ultrastructure of pyramidal neurons of the hippocampal CA1 and CA3 sectors in an experimental model of febrile seizures in rats.</title>
            <link>http://www.medworm.com/index.php?rid=5449227&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22101956%26dopt%3DAbstract</link>
            <description>The objective of the current ultrastructural study was to explore the potentiality of the neuroprotective effect of TPM against damage of pyramidal neurons in the hippocampal CA1 and CA3 sectors in an experimental model of febrile seizures (FS) in rats. The FS group exhibited variously pronounced submicroscopic lesions of the neuronal perikarya, including total cell disintegration. Advanced changes induced by hyperthermic stress were manifested by marked degenerative abnormalities, such as substantial swelling of the mitochondria, dilation, degranulation and disintegration of the granular endoplasmic reticulum, and vacuolar changes in the Golgi complex. The most substantially damaged pyramidal neurons showed features of aponecrosis (so-called &quot;dark neurons&quot;), resulting in a marked neuronal...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5449227</comments>
            <pubDate>Sun, 27 Nov 2011 11:54:03 +0100</pubDate>
            <guid isPermaLink="false">5449227</guid>        </item>
        <item>
            <title>Mechanisms related to neuron injury and death in cerebral hypoxic ischaemia.</title>
            <link>http://www.medworm.com/index.php?rid=5146335&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21845535%26dopt%3DAbstract</link>
            <description>Authors: Guo MF, Yu JZ, Ma CG
    Abstract
    Cerebral hypoxic-ischaemic injury is involved in many central nervous system diseases. The mechanisms of neuron injury and death in cerebral hypoxic ischaemia remain unclear. There have been many theories on pathogenesis of neuron injury and death in cerebral hypoxic ischaemia, such as the toxicity of excitatory amino acid, NO, the production of oxygen free radicals, chondriosome injury, complement component, injury of immunological inflammation, matrix metalloproteinase, dopamine, Ca2+ overloading, cell apoptosis and so on. The aim of this review is to describe recent observations regarding the mechanisms of neuron injury and death in cerebral hypoxic ischaemia.
    PMID: 21845535 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5146335</comments>
            <pubDate>Mon, 22 Aug 2011 23:16:03 +0100</pubDate>
            <guid isPermaLink="false">5146335</guid>        </item>
        <item>
            <title>Expression of mutated isocitrate dehydrogenase-1 in gliomas is associated with p53 and EGFR expression.</title>
            <link>http://www.medworm.com/index.php?rid=5146334&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21845536%26dopt%3DAbstract</link>
            <description>Authors: Birner P, Toumangelova-Uzeir K, Natchev S, Guentchev M
    Abstract
    Gliomas are the most common primary brain tumours. Several independent studies have shown that isocitrate dehydrogenase 1 (IDH1) mutation in diffuse gliomas is associated with a more favourable patient outcome. The aim of this study was to evaluate the prognostic relevance of an antibody specifically detecting the R132H point mutation of IDH1 in tissue sections in a large series of human gliomas. Surgical specimens of 220 consecutive patients with infiltrative low and high-grade gliomas were included in this retrospective study. In multivariate analysis, IDH expression did not reach significance (p = 0.122) in regard to prognosis, in contrast to WHO grade and age at time of surgery (p &amp;lt; 0.001, Cox regressio...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5146334</comments>
            <pubDate>Mon, 22 Aug 2011 23:16:03 +0100</pubDate>
            <guid isPermaLink="false">5146334</guid>        </item>
        <item>
            <title>Analysis of the prognostic significance of selected morphological and immunohistochemical markers in ependymomas, with literature review.</title>
            <link>http://www.medworm.com/index.php?rid=5146333&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21845537%26dopt%3DAbstract</link>
            <description>Authors: Zawrocki A, Iżycka-Świeszewska E, Papierz W, Liberski PP, Zakrzewski K, Biernat W
    Abstract
    Aim: Ependymal tumours are relatively uncommon primary neoplasms of the central nervous system. Histological criteria distinguishing ependymoma and anaplastic ependymoma are not clear-cut and other parameters are required to allow more precise prognostication in these tumours. We analysed the histological and immunohistochemical features of these tumours (Ki-67, cyclin D1, EGFR, hTERT, Olig2) and correlated them with the clinical outcome. Material and methods: We analysed 39 patients with grade II ependymoma (30) and anaplastic ependymoma (9). Twenty-eight tumours developed in children and the remaining 11 patients were adults with intracranial and intraspinal tumours. Eighteen pat...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5146333</comments>
            <pubDate>Mon, 22 Aug 2011 23:16:03 +0100</pubDate>
            <guid isPermaLink="false">5146333</guid>        </item>
        <item>
            <title>Radiation-induced lowered neurogenesis associated with shortened latency of inhibitory avoidance memory response.</title>
            <link>http://www.medworm.com/index.php?rid=5146332&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21845538%26dopt%3DAbstract</link>
            <description>In this study, we assessed the effect of single and fractionated cobalt radiation on neurogenesis in the dentate gyrus of the hippocampal formation. The irradiation time for delivering 2 Gy (for fractionated dose radiation) and 10 Gy (for single dose radiation) at maximum depth were respectively 1.98 min and 9.92 min. To study the association with memory function we examined inhibitory avoidance memory using a step-through device. Brains were withdrawn and fixed, and then sections were stained with cresyl violet for neurons. We found that a 10 Gy dose can induce lower neurogenesis in the dentate gyrus of the hippocampus (p &amp;lt; 0.05), in such a way that a fractionated dose (5 fractions of 2 Gy) is more effective than a single dose (one fraction of 10 Gy). Moreover, a fractionated dose coul...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5146332</comments>
            <pubDate>Mon, 22 Aug 2011 23:16:03 +0100</pubDate>
            <guid isPermaLink="false">5146332</guid>        </item>
        <item>
            <title>Astroglia disturbances during development of the central nervous system in fetuses with Down's syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=5146331&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21845539%26dopt%3DAbstract</link>
            <description>Authors: Zdaniuk G, Wierzba-Bobrowicz T, Szpak GM, Stępień T
    Abstract
    Down's syndrome (DS), caused by aneuploidy of chromosome 21, is the most common chromosomal disorder. The most significant symptom of this disorder is mental retardation. Neuropathological changes found in the DS central nervous system (CNS), such as reduced number of neurons, alteration of synapses and synaptic spines or delayed myelination have been widely described. But there are only a few studies of DS-related glia disturbances. A growing number of astroglia new functions have recently been described. In our study we compared the number of astrocytes and radial glial cells in the frontal lobe of DS fetuses at 18-20 weeks of gestation with that observed in age-matched controls. We found a substantially incr...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5146331</comments>
            <pubDate>Mon, 22 Aug 2011 23:16:03 +0100</pubDate>
            <guid isPermaLink="false">5146331</guid>        </item>
        <item>
            <title>Research on alteration of neurons in vagal nuclei in medulla oblongata in newborns with respiratory distress.</title>
            <link>http://www.medworm.com/index.php?rid=5146330&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21845540%26dopt%3DAbstract</link>
            <description>Authors: Islami H, Shabani R, Shabani D, Dacaj R, Manxhuka S, Azemi M, Krasniqi S, Kurtishi I
    Abstract
    Neuronal and axonal degenerative changes in motor vagal neurons (DMNV) and sensory vagal neurons (nTS) in the medulla oblongata in newborns were studied. Material was taken from the autopsies of newborns, live and dead newborns, in different gestational weeks (aborted, immature, premature and mature). 46 cases were studied. Material for research was taken from the medulla oblongata and lung tissue. Serial horizontal incisions were made in the medulla oblongata (± 4 mm), commencing from the obex, where the DMNV and nTS vagal nuclei were explored. Fixed cuttings in buffered formalin (10%) were used for histochemical staining. Serial cuttings were done with a microtome (7 µm). Pulm...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5146330</comments>
            <pubDate>Mon, 22 Aug 2011 23:16:03 +0100</pubDate>
            <guid isPermaLink="false">5146330</guid>        </item>
        <item>
            <title>Expression of 8-oxoguanine DNA glycosylase 1 (OGG1) and the level of p53 and TNF-αlpha proteins in peripheral lymphocytes of patients with Alzheimer's disease.</title>
            <link>http://www.medworm.com/index.php?rid=5146329&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21845541%26dopt%3DAbstract</link>
            <description>Authors: Dezor M, Dorszewska J, Florczak J, Kempisty B, Jaroszewska-Kolecka J, Rozycka A, Polrolniczak A, Bugaj R, Jagodzinski PP, Kozubski W
    Abstract
    The aim of the study was to determine the extent of oxidative DNA damage (levels of 8-oxo2dG) and expression of OGG1 and p53 and TNF-α proteins in lymphocytes of Alzheimer's disease (AD) patients and a control group. The studies were conducted on 41 patients with AD, including 25 women and 16 men aged 34-84 years. The control group included 51 individuals, 20 women and 31 men aged 22-83 years. The level of 8-oxo2dG was determined using HPLC/EC/UV, and the level of OGG1 and p53 and TNF-α proteins was determined with the Western blot method. The results showed that both proteins participating in DNA repair (OGG1, p53) and the inflamm...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5146329</comments>
            <pubDate>Mon, 22 Aug 2011 23:16:03 +0100</pubDate>
            <guid isPermaLink="false">5146329</guid>        </item>
        <item>
            <title>Presence of L-kynurenine aminotransferase III in retinal ganglion cells and corpora amylacea in the human retina and optic nerve.</title>
            <link>http://www.medworm.com/index.php?rid=5146328&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21845542%26dopt%3DAbstract</link>
            <description>Conclusions: Expression of KAT III in CAm in the human retina and optic nerve indicates that this enzyme may be relevant in mechanisms of neurodegeneration leading to CAm formation.
    PMID: 21845542 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5146328</comments>
            <pubDate>Mon, 22 Aug 2011 23:16:03 +0100</pubDate>
            <guid isPermaLink="false">5146328</guid>        </item>
        <item>
            <title>Interleukin 17 receptor in multiple sclerosis patients treated with interferon β-1a.</title>
            <link>http://www.medworm.com/index.php?rid=5146327&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21845543%26dopt%3DAbstract</link>
            <description>Authors: Michałowska-Wender G, Biernacka-Łukanty J, Lasik Z, Jernas L, Wender M
    Abstract
    Interleukin 17 (IL-17) and its receptor IL-17R1 produced by T-helper cells named Th17 are involved in the pathology of autoimmune diseases. In contrast to the at least partially explained role of IL-17 in pathology of multiple sclerosis, the significance of IL-17R in MS is unclear. Therefore we have studied the expression of IL-17R in the stable phase of multiple sclerosis treated by interferon β-1a. The studied material consisted of 20 MS patients with relapsing-remitting form of the disease, and fulfilling the diagnostic McDonald et al. criteria. The patients were treated subcutaneously every second day with 30 mg of interferon β -1a (Betaferon). The interleukin 17 receptor level was meas...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5146327</comments>
            <pubDate>Mon, 22 Aug 2011 23:16:03 +0100</pubDate>
            <guid isPermaLink="false">5146327</guid>        </item>
        <item>
            <title>Rosiglitazone protects the dorsal root ganglion cells and sciatic nerve after crush in rat.</title>
            <link>http://www.medworm.com/index.php?rid=5146326&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21845544%26dopt%3DAbstract</link>
            <description>Authors: Noorafshan A, Shariat K, Karbalay-Doust S, Omidi A
    Abstract
    The aim of this study was to investigate the histological changes in the dorsal root ganglion (DRG) and the sciatic nerve in rats after sciatic nerve crush (SNC) and treatment with rosiglitazone. The rats were divided into four groups, each including seven animals, and underwent the following intervention. Group I: control animals which received carboxy methyl cellulose (0.5 w/v, p.o.). Group II: sham operated animals whose skin of the posterior thigh was opened, closed and the animals received the vehicle (carboxy methyl cellulose). Group III: SNC animals; the animals received the vehicle. Group IV: SNC with rosiglitazone (5 mg/kg body weight/day) dissolved in the vehicle. On the 28th day the fifth lumbar DRG and...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5146326</comments>
            <pubDate>Mon, 22 Aug 2011 23:16:03 +0100</pubDate>
            <guid isPermaLink="false">5146326</guid>        </item>
        <item>
            <title>Amyotrophic lateral sclerosis - looking for pathogenesis and effective therapy.</title>
            <link>http://www.medworm.com/index.php?rid=4676314&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455838%26dopt%3DAbstract</link>
            <description>Authors: Naganska E, Matyja E
    myotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized by loss of motor neurons in the spinal cord, brain stem and motor cortex which dramatically reduces life expectancy. ALS occurs either in familial or, more frequently, in sporadic forms. It finally results in death due to respiratory failure that occurs typically 2-5 years after the disease onset. Although the aetiology of ALS remains largely unclear, its heterogeneity suggests that a combination of various factors, including endogenous and/or environmental ones, may be implicated in progressive motor neuron stress that results in the activation of different cell death pathways. Interactions between genetic, environmental, and age-dependent risk factors have been hy...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4676314</comments>
            <pubDate>Tue, 05 Apr 2011 08:00:05 +0100</pubDate>
            <guid isPermaLink="false">4676314</guid>        </item>
        <item>
            <title>Density and spatial pattern of β-amyloid (Aβ) deposits in corticobasal degeneration.</title>
            <link>http://www.medworm.com/index.php?rid=4676313&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455839%26dopt%3DAbstract</link>
            <description>Authors: Armstrong RA
    Corticobasal degeneration (CBD) is a rare, progressive movement disorder characterized neuropathologically by widespread neuronal and glial pathology including tau-immunoreactive neuronal cytoplasmic inclusions (NCI), oligodendroglial inclusions (GI), and astrocytic plaques (AP). However, β -amyloid (A β) deposits have been observed in the cerebral cortex and/or hippocampus in some cases of CBD. To clarify the role of Aβ deposition in CBD, the densities and spatial patterns of the Aβ deposits were studied in three cases. In two cases, expressing apolipoprotein E (APOE) genotypes 2/3 or 3/3, the densities of the Aβ deposits were similar to those in normal elderly brain. In the remaining case, expressing APOE genotype 3/4, Aβ deposition was observed throughout...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4676313</comments>
            <pubDate>Tue, 05 Apr 2011 08:00:05 +0100</pubDate>
            <guid isPermaLink="false">4676313</guid>        </item>
        <item>
            <title>Effects of haloperidol on striatal neurons: relation to neuronal loss (a stereological study).</title>
            <link>http://www.medworm.com/index.php?rid=4676312&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455840%26dopt%3DAbstract</link>
            <description>Authors: Altunkaynak BZ, Ozbek E, Aydin N, Aydin MD, Altunkaynak ME, Vuraler O, Unal B
    In the present work, we investigated the effect of chronic haloperidol administration on the number of striatal neurons in guinea pigs. For this purpose, adult male guinea pigs were given daily injections of 1, 2 or 3 mg/kg of haloperidol for 6 weeks. After treatment, the animals were anesthetized via brief inhalation of ether, the brains were removed and the corpus striatum was dissected. Then the tissues were processed and semi-thin sections were stained with toluidine blue for stereological and histopathological evaluation. The physical disector was used for measurements of nuclear height and numerical density of striatal neurons and also to evaluate both normal and degenerated neurons within the ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4676312</comments>
            <pubDate>Tue, 05 Apr 2011 08:00:05 +0100</pubDate>
            <guid isPermaLink="false">4676312</guid>        </item>
        <item>
            <title>Epidermal growth factor receptor gene expression in high grade gliomas?</title>
            <link>http://www.medworm.com/index.php?rid=4676311&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455841%26dopt%3DAbstract</link>
            <description>Conclusions: As nearly 1/3 of high grade gliomas do not demonstrate abnormal gene expression levels, EGFR status should be taken into account in any targeted therapy attempt. The significance of EGFR axis-related differences between young and old glioma patients and their impact on the prognosis warrant further study.
    PMID: 21455841 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4676311</comments>
            <pubDate>Tue, 05 Apr 2011 08:00:05 +0100</pubDate>
            <guid isPermaLink="false">4676311</guid>        </item>
        <item>
            <title>Subependymal giant cell astrocytomas with atypical histological features mimicking malignant gliomas.</title>
            <link>http://www.medworm.com/index.php?rid=4676306&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455842%26dopt%3DAbstract</link>
            <description>In this study we report 3 cases of SEGA out of 29 TSC patients, operated on in the Department of Neurosurgery, Children's Memorial Health Institute, from 1990 to 2011 and retrospectively reviewed. These 3 cases exhibited distinct anaplastic features that might mimic malignant glioma. Histologically, the tumours were composed of pleomorphic, gemistocytic, polygonal, ganglion-like or multinucleated cells arranged in sheets or forming perivascular pseudorosettes. Numerous foci of necrosis, microvascular proliferation and high mitotic activity with atypical mito-tic figures were documented. The Ki67 labelling index was about 15-20%. These tumours might be confused with high-grade gliomas and such a misleading diagnosis might result in aggressive radio- or chemotherapy. Despite the common state...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4676306</comments>
            <pubDate>Tue, 05 Apr 2011 08:00:05 +0100</pubDate>
            <guid isPermaLink="false">4676306</guid>        </item>
        <item>
            <title>Differential expression of calbindin D28k, calretinin and parvalbumin in the cerebellum of pups of ethanol-treated female rats.</title>
            <link>http://www.medworm.com/index.php?rid=4676304&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455843%26dopt%3DAbstract</link>
            <description>Authors: Wierzba-Bobrowicz T, Lewandowska E, Stępień T, Szpak GM
    Three calcium-binding proteins (CaBPs), calbindin D28k, calretinin and parvalbumin, were immunohistochemically examined in the cerebellum of ten-day-old rat pups of ethanol-treated dams. Dams were treated with ethanol during pregnancy and/or lactation. In the cerebellar cortex of the pups from control groups, Purkinje cells with their processes and Golgi cells were positive for calbindin D28k, whereas interneurons (Lugaro, Golgi and unipolar brush cells) and sometimes Purkinje cells were positive for calretinin. Parvalbumin immunoreactivity was observed in Golgi and basket cells, stellate cells and in some Purkinje cells. The number of positive cells and staining intensity for calbindin D28k and parvalbumin decreased in...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4676304</comments>
            <pubDate>Tue, 05 Apr 2011 08:00:05 +0100</pubDate>
            <guid isPermaLink="false">4676304</guid>        </item>
        <item>
            <title>Increased reactive oxygen species (ROS) production and low catalase level in fibroblasts of a girl with MEGDEL association (Leigh syndrome, deafness, 3-methylglutaconic aciduria).</title>
            <link>http://www.medworm.com/index.php?rid=4676295&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455844%26dopt%3DAbstract</link>
            <description>Conclusion: (1) the natural history of the disease in the presented patient confirms the existence of previously reported clinical phenotype of MEGDEL (2) antioxidant defence impairment due to abnormal catalase metabolism/transport may characterize an unknown basic defect which led to the development of MEGDEL association.
    PMID: 21455844 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4676295</comments>
            <pubDate>Tue, 05 Apr 2011 08:00:05 +0100</pubDate>
            <guid isPermaLink="false">4676295</guid>        </item>
        <item>
            <title>Are cardiomyocytes able to generate pre-amyloid peptides?</title>
            <link>http://www.medworm.com/index.php?rid=4676289&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455845%26dopt%3DAbstract</link>
            <description>Authors: Fidziańska A, Walczak E, Bekta P, Chojnowska L
    We performed ultrastructural testing of a cardiac biopsy taken from a heart with amyloidosis in which transthyretin mutation and light chain A amyloidosis were excluded. Cardiomyocytes of the affected heart showed accumulation of endosomal-like structures in which soluble amyloid oligomeric conformation was deposited. Intracellular accumulation of β -amyloid as well as phosphorylated tau protein seen in the immunohistochemical study suggest that the heart tissue may generate an amyloidogenic peptide leading to cardiomyocyte destruction and heart dysfunction.
    PMID: 21455845 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4676289</comments>
            <pubDate>Tue, 05 Apr 2011 08:00:05 +0100</pubDate>
            <guid isPermaLink="false">4676289</guid>        </item>
        <item>
            <title>Clinical and neuropathological picture of ethylmalonic aciduria - diagnostic dilemma.</title>
            <link>http://www.medworm.com/index.php?rid=4676285&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455846%26dopt%3DAbstract</link>
            <description>Authors: Jamroz E, Paprocka J, Adamek D, Pytel J, Szczechowska K, Grabska N, Malec M, Głuszkiewicz E, Daab M, Wodołażski A
    Increased ethylmalonic acid (EMA) in urine is a non-specific finding, and is observed in a number of inborn errors of metabolism, as well as in individuals who carry one of two common polymorphisms identified in the SCAD coding region. The authors present an 8-month-old girl with a suspicion of neuroinfection, although the clinical presentation led to diagnosis of ethylmalonic aciduria. From the neuropathological point of view the most remarkable changes were observed in the brain cortex, which was diffusely damaged practically in all regions of the brain. Of note, the most severe destruction was observed in the deepest regions of the sulci. The cortex of the af...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4676285</comments>
            <pubDate>Tue, 05 Apr 2011 08:00:05 +0100</pubDate>
            <guid isPermaLink="false">4676285</guid>        </item>
        <item>
            <title>Brain lesions in tuberous sclerosis complex. Review.</title>
            <link>http://www.medworm.com/index.php?rid=4056044&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20924998%26dopt%3DAbstract</link>
            <description>Authors: Grajkowska W, Kotulska K, Jurkiewicz E, Matyja E
    Tuberous sclerosis complex (TSC) is an autosomal dominant, multisystem disease characterized by the development of multiple hamartomas and benign or rarely malignant neoplasms distributed at various sites throughout the body, especially in the brain, skin, retina, kidney, heart, and lungs. Brain lesions in TSC include: cortical/subcortical glioneuronal tubers, subependymal glial nodules (SENs), and subependymal giant cell astrocytomas (SEGAs). Cortical tubers are characterized by a markedly disorganized cortical lamination with dysplastic aggregates of abnormal glial and neuronal elements, including giant cells. SENs consist of large cells, somewhat similar to the giant cells seen in tubers, accompanied by elongated glial cells....</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4056044</comments>
            <pubDate>Mon, 11 Oct 2010 23:15:03 +0100</pubDate>
            <guid isPermaLink="false">4056044</guid>        </item>
        <item>
            <title>Dispersion of prion protein deposits around blood vessels in variant Creutzfeldt-Jakob disease.</title>
            <link>http://www.medworm.com/index.php?rid=4056043&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20924999%26dopt%3DAbstract</link>
            <description>Authors: Armstrong RA
    In variant Creutzfeldt-Jakob disease (vCJD), a disease linked to bovine spongiform encephalopathy (BSE), florid-type prion protein (PrPsc) deposits are aggregated around the larger diameter (&amp;gt; 10 µm) cerebral microvessels. Clustering of PrPsc deposits around blood vessels may result from blood-borne prions or be a consequence of the cerebral vasculature influencing the development of the florid deposits. To clarify the factors involved, the dispersion of the florid PrPsc deposits was studied around the larger diameter microvessels in the neocortex, hippocampus, and cerebellum of ten cases of vCJD. In the majority of brain regions, florid deposits were clustered around the larger diameter vessels with a mean cluster size of between 50 µm and 628 µm. With the ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4056043</comments>
            <pubDate>Mon, 11 Oct 2010 23:15:03 +0100</pubDate>
            <guid isPermaLink="false">4056043</guid>        </item>
        <item>
            <title>Submicroscopic pathology of human and experimental hydrocephalic cerebral cortex.</title>
            <link>http://www.medworm.com/index.php?rid=4056042&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20925000%26dopt%3DAbstract</link>
            <description>Authors: Castejón OJ
    The ultrastructural pathology of cerebral cortex in human hydrocephalus is reviewed and compared with experimental hydrocephalus. Nerve cells show moderate and severe swelling. The neighboring neuropil exhibits notable enlargement of extracellular space, synaptic plasticity and degeneration, damage of myelinated axons, and myelination delay. The astrocytes display edematous changes and phagocytic activity. Glycogen rich- and glycogen-depleted astrocytes are observed. Some oligodendroglial cells exhibit normal morphology, and other exhibit hydropic changes. The capillary wall shows signs of blood-brain barrier dysfunction. The role of ischemia, oxidative stress, increased calcium concentration, activation of NMDA receptors, and disturbance of ion homeostasis are di...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4056042</comments>
            <pubDate>Mon, 11 Oct 2010 23:15:03 +0100</pubDate>
            <guid isPermaLink="false">4056042</guid>        </item>
        <item>
            <title>Spindle cell oncocytoma of the adenohypophysis - a clinicopathological and ultrastructural study of two cases.</title>
            <link>http://www.medworm.com/index.php?rid=4056041&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20925001%26dopt%3DAbstract</link>
            <description>We report two additional cases of SCO occurring in females aged 63 years (Case 1) and 65 years (Case 2), who presented with pan-hypopituitarism, headache and visual field defect. In both cases, the magnetic resonance imaging showed solid sellar mass of moderate size with suprasellar extension. The clinical and radiological features suggested non-functioning pituitary macroadenomas without evidence of invasive growth. One patient presented with tumour recurrence 3 years after undergoing the previous surgical removal of tumour, which was initially misdiagnosed as schwannoma. The first tumour was removed by transsphenoidal surgery and the second one by frontal craniotomy. Histologically and immunohistochemically, both tumours displayed the features typical for SCO of the pituitary. They were ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4056041</comments>
            <pubDate>Mon, 11 Oct 2010 23:15:03 +0100</pubDate>
            <guid isPermaLink="false">4056041</guid>        </item>
        <item>
            <title>Activation of Akt/mTOR pathway in a patient with atypical teratoid/rhabdoid tumor.</title>
            <link>http://www.medworm.com/index.php?rid=4056040&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20925002%26dopt%3DAbstract</link>
            <description>Authors: Jóźwiak J, Bikowska B, Grajkowska W, Sontowska I, Roszkowski M, Galus R
    A typical teratoid/rhabdoid tumor (AT/RT) is a highly malignant childhood brain tumor. Most AT/RTs are shown to contain chromosome 22 mutation in the region of hSNF5/INI1 gene, whose protein product participates in chromatin remodeling. Although the presence of this mutation is well described, molecular pathways underlying AT/RT development are poorly, if at all, understood. In the current paper we evaluate a case of AT/RT with special consideration of two pathways often implicated in tumor development: protein kinase B (PKB or Akt) and extracellular signal-regulated kinase (Erk). First, we confirmed expression of typical protein pattern being unique for AT/RT, including epithelial membrane antigen, S-10...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4056040</comments>
            <pubDate>Mon, 11 Oct 2010 23:15:03 +0100</pubDate>
            <guid isPermaLink="false">4056040</guid>        </item>
        <item>
            <title>Measurement of glycine in a brain and brain tumors by means of 1H MRS.</title>
            <link>http://www.medworm.com/index.php?rid=4056039&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20925003%26dopt%3DAbstract</link>
            <description>Conclusions: Glycine is found in WHO II grade gliomas as well as in central neurocytomas, but only in a part of a tumor volume. It is necessary to perform 1H MRS of the whole tumor volume to confirm/exclude the presence of glycine. Glycine in a normal brain can not be identified by means of conventional 1H MRS performed by means of 1.5 T or 3.0 T scanners.
    PMID: 20925003 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4056039</comments>
            <pubDate>Mon, 11 Oct 2010 23:15:03 +0100</pubDate>
            <guid isPermaLink="false">4056039</guid>        </item>
        <item>
            <title>Motor endplate remodeling in some cases with congenital myasthenic syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=4056038&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20925004%26dopt%3DAbstract</link>
            <description>Authors: Fidziańska A, Glinka Z
    The architecture of motor endplates in three cases with congenital myasthenic syndrome (CMS) was compared with ultrastructure of the normal control neuromuscular junction (NMJ). The remodeling of postsynaptic region was observed in all three individuals. The most conspicuous abnormalities seen in the slow channel syndrome was the vacuolization and disorganization of secondary synaptic clefts which extended for beyoned the border of NMJ. Degenerated postsynaptic nuclei and junctional sarcoplasm were an additional feature of presented syndromes. The quite different feature of NMJ was observed in the DOK-7 deficient syndrome. The appearance of small, pale terminal axons, poorly developed postsynaptic membrane with the sparse secondary synaptic clefts and d...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4056038</comments>
            <pubDate>Mon, 11 Oct 2010 23:15:03 +0100</pubDate>
            <guid isPermaLink="false">4056038</guid>        </item>
        <item>
            <title>Cerebral amyloid angiopathy as a cause of an extensive brain hemorrhage in adult patient with Down's syndrome - a case report.</title>
            <link>http://www.medworm.com/index.php?rid=4056037&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20925005%26dopt%3DAbstract</link>
            <description>Authors: Mendel T, Bertrand E, Szpak GM, Stępień T, Wierzba-Bobrowicz T
    A case of 54-year old woman who deceased due to consequence of extensive brain hemorrhage is presented. The patient was admitted to our Department of Neurology due to progressive quadriparesis as a complication of the cervical spinal cord compressive myelopathy. On the third day after neurosurgical decompression of the spinal cord sudden worsening of neurological and general condition was observed, finally caused death. An autopsy study revealed an extensive brain lobar hemorrhage and a dorsal-ventral compression of the cervical spinal cord. Alzheimer's disease-type degenerative changes with concomitant CAA were seen in light microscope examination. Extensive foci of demyelination were found especially in dorsal ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4056037</comments>
            <pubDate>Mon, 11 Oct 2010 23:15:03 +0100</pubDate>
            <guid isPermaLink="false">4056037</guid>        </item>
        <item>
            <title>Primary spinal cord melanoma - a case report.</title>
            <link>http://www.medworm.com/index.php?rid=4056036&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20925006%26dopt%3DAbstract</link>
            <description>Authors: Kolasa M, Jesionek-Kupnicka D, Kordek R, Kolasa P
    Authors present a case of a 57-year-old woman with primary spinal cord malignant melanoma. Intramedullary localization of primary melanoma is extremely rare. The patient presented neurological deficits such as lower limbs paresis and sensory loss. MRI examination showed intramedullar tumor located on the Th10 vertebra level. Surgical treatment with total removal of tumor was performed. Histopathological study confirmed melanoma. Subsequent chemotherapy was given. Tumor was successfully treated by neurosurgery; radio- and chemotherapy with disease free follow up of 9 months. Surgical treatment of melanoma in this location is extremely important as it leads to regression of neurological symptoms and improvement of the quality of ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4056036</comments>
            <pubDate>Mon, 11 Oct 2010 23:15:03 +0100</pubDate>
            <guid isPermaLink="false">4056036</guid>        </item>
        <item>
            <title>A spatial pattern analysis of beta-amyloid (Abeta) deposition in the temporal lobe in Alzheimer's disease.</title>
            <link>http://www.medworm.com/index.php?rid=3740881&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20602287%26dopt%3DAbstract</link>
            <description>Authors: Armstrong RA
    To determine the factors influencing the distribution of -amyloid (Abeta) deposits in Alzheimer's disease (AD), the spatial patterns of the diffuse, primitive, and classic A deposits were studied from the superior temporal gyrus (STG) to sector CA4 of the hippocampus in six sporadic cases of the disease. In cortical gyri and in the CA sectors of the hippocampus, the Abeta deposits were distributed either in clusters 200-6400 microm in diameter that were regularly distributed parallel to the tissue boundary or in larger clusters greater than 6400 microm in diameter. In some regions, smaller clusters of Abeta deposits were aggregated into larger 'superclusters'. In many cortical gyri, the density of Abeta deposits was positively correlated with distance below the gy...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3740881</comments>
            <pubDate>Sat, 10 Jul 2010 09:54:03 +0100</pubDate>
            <guid isPermaLink="false">3740881</guid>        </item>
        <item>
            <title>Pituitary adenomas and craniopharyngiomas are CDX2 negative neoplasms.</title>
            <link>http://www.medworm.com/index.php?rid=3740880&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20602288%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: There is no evidence for that CDX2 might play a role in tumourigenesis, invasive growth or tumour recurrence of pituitary adenomas or in tumourigenesis of craniopharyngiomas. But, presence of CDX2 expression might be useful in distinguishing intrasellar metastases from primary tumours of the sellar region.
    PMID: 20602288 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3740880</comments>
            <pubDate>Sat, 10 Jul 2010 09:54:03 +0100</pubDate>
            <guid isPermaLink="false">3740880</guid>        </item>
        <item>
            <title>Differentiation between brain tumor recurrence and radiation injury using perfusion, diffusion-weighted imaging and MR spectroscopy.</title>
            <link>http://www.medworm.com/index.php?rid=3740879&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20602289%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: Among the analyzed advanced neuroimaging methods PWI seems to be most reliable in differentiation between tumor regrowth/recurrence and radiation necrosis. In these results mean rCBV is a better differing factor than max rCBV. Proton MR spectroscopy (1HMRS) and DWI do not differentiate analyzed groups with statistical significance, despite tendency to lower ADC values in recurrence group than in radiation injury one.
    PMID: 20602289 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3740879</comments>
            <pubDate>Sat, 10 Jul 2010 09:54:03 +0100</pubDate>
            <guid isPermaLink="false">3740879</guid>        </item>
        <item>
            <title>Blood-brain barrier breakdown and cerebellar degeneration in the course of experimental neoplastic disease. Are circulating Cytokine-Induced Neutrophil Chemoattractant-1 (CINC-1) and -2alpha(CINC-2alpha) the involved mediators?</title>
            <link>http://www.medworm.com/index.php?rid=3740878&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20602290%26dopt%3DAbstract</link>
            <description>In conclusion, we may state that the development of cerebellar degeneration as an indirect effect of experimental neoplasm can result from blood-brain barrier (BBB) breakdown and possible passage of neurotoxic factors. The decreased serum concentration of CINC-1 as neuroprotective agent and increased CINC-2alpha in late stage of MH may be considered for their contribution to cerebellar degeneration.
    PMID: 20602290 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3740878</comments>
            <pubDate>Sat, 10 Jul 2010 09:54:03 +0100</pubDate>
            <guid isPermaLink="false">3740878</guid>        </item>
        <item>
            <title>Capillary vessel wall in CADASIL angiopathy.</title>
            <link>http://www.medworm.com/index.php?rid=3740877&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20602291%26dopt%3DAbstract</link>
            <description>Authors: Lewandowska E, Szpak GM, Wierzba-Bobrowicz T, Modzelewska J, StepieÅ T, Pasennik E, Schmidt-Sidor B, RafaÅowska J
    The study was aimed at investigating the morphology of capillaries in four skin and muscle biopsy specimens obtained from CADASIL patients. In all cases diagnosis confirmed at the ultrastructural level, and additionally in three cases, the genetic test revealed the Notch3 gene mutations. Using histological and immunohistochemical (IHC) markers for components of capillary vessel wall we showed the reduction and loss of pericytes and and fibrous vessel wall including the thickened basement membrane. The thorough ultrastructural study revealed the presence of widespread GOM deposits in capillary wall, but less numerous than in arterioles. They were located in th...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3740877</comments>
            <pubDate>Sat, 10 Jul 2010 09:54:03 +0100</pubDate>
            <guid isPermaLink="false">3740877</guid>        </item>
        <item>
            <title>Free radical peroxidation products in cerebrospinal fluid and serum of patients with multiple sclerosis after glucocorticoid therapy.</title>
            <link>http://www.medworm.com/index.php?rid=3740876&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20602292%26dopt%3DAbstract</link>
            <description>Authors: Mitosek-Szewczyk K, Gordon-Krajcer W, Walendzik P, Stelmasiak Z
    Multiple sclerosis (MS) patients were found to have elevated thiobarbituric acid reactive material levels, increased soluble sulfhydryl groups and reduced protein sulfhydryl groups in cerebrospinal fluid and serum, and slightly reduced superoxide dismutase in serum, which suggested disease activating free radical peroxidation. Moreover, levels of these varied across methylprednisolone (MP) therapy. We observed significant differences in the levels of peroxidation products between MS patients and controls. These changes were most evident in relapse. After MP therapy, levels of these indicators approached control values, especially in the remission period. Our findings suggest that MP protects against free radical a...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3740876</comments>
            <pubDate>Sat, 10 Jul 2010 09:54:03 +0100</pubDate>
            <guid isPermaLink="false">3740876</guid>        </item>
        <item>
            <title>Architecture of cerebellomedullary cistern structures during foetal period.</title>
            <link>http://www.medworm.com/index.php?rid=3740875&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20602293%26dopt%3DAbstract</link>
            <description>Authors: Kedzia A, Rybaczuk M, Andrzejak R, Kedzia W
    Structures of arachnoid in posterior cranial fossa have been examined during prenatal period. 100 foetuses were examined within IV up to VII month with CRL from 130 mm to 220 mm. Cuts were performed with especially constructed device what enabled ideal cross-section without disturbing of structures of arachnoid of dura mater. Image acquisition was done with the help of digital camera. The very fine structures spanned between posterior cranial fossa and cerebellum and brain stem were made visible. They are characteristics for prenatal period solely. This construction enables light weight elasticity and probably it increases strength as well as stability of circulation. Cross-section of observed structures has geometry of tangent circl...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3740875</comments>
            <pubDate>Sat, 10 Jul 2010 09:54:03 +0100</pubDate>
            <guid isPermaLink="false">3740875</guid>        </item>
        <item>
            <title>Dementia means number of things - the overlap of neurodegeneration with brain iron accumulation (NBIA) and Alzheimer changes: an autopsy case.</title>
            <link>http://www.medworm.com/index.php?rid=3740874&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20602294%26dopt%3DAbstract</link>
            <description>We reported a case of a 77-year-old woman with parkinsonism, dystonia, psychiatric symptoms and progressing dementia misdiagnosed at the age of 51 years as Parkinson's disease. Histopathological examination of the patient's brain performed 26 years after the disease onset revealed numerous axonal spheroids and iron deposits in structures of the nigro-pallido-striatal system that enabled to diagnose neurodegeneration with brain iron accumulation (NBIA) (former Hallervorden-Spatz syndrome), and changes characteristic for Alzheimer's disease (AD). NBIA is a group of rare clinically and genetically heterogeneous diseases of the extrapyramidal system which common feature is abnormal iron storage in the basal ganglia. Disturbed iron metabolism is also one of the hypothetical patho-mechanisms of ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3740874</comments>
            <pubDate>Sat, 10 Jul 2010 09:54:03 +0100</pubDate>
            <guid isPermaLink="false">3740874</guid>        </item>
        <item>
            <title>An unusual case of high cervical spinal cord injury.</title>
            <link>http://www.medworm.com/index.php?rid=3740873&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20602295%26dopt%3DAbstract</link>
            <description>Authors: Velnar T, Smrkolj V, Cerovic O, Pecaric Meglic N, Tauscher G
    Isolated spinal cord injuries can rarely be found in patients with no traumatic radiological abnormalities of the spine. Stenoses of the medullary canal and degeneration of cervical spine are the predisposing factors. A case report of a 68-year-old patient is described, who developed quadriplegia with cardiac arrest due to isolated cervical spinal cord injury while jumping on a trampoline. Compressions of the spinal cord with intramedullary and epidural haemorrhage between vertebrae C3 and C6 were observed with no traumatic radiological abnormalities of the spine skeleton.
    PMID: 20602295 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3740873</comments>
            <pubDate>Sat, 10 Jul 2010 09:54:03 +0100</pubDate>
            <guid isPermaLink="false">3740873</guid>        </item>
        <item>
            <title>Biological clues on neuronal degeneration based on theoretical fits of decay patterns: towards a mathematical neuropathology.</title>
            <link>http://www.medworm.com/index.php?rid=3464060&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20383806%26dopt%3DAbstract</link>
            <description>Authors: Triarhou LC
    The application of the best mathematical fit to quantitative data on cell death over time in models of nervous abiotrophies can yield useful clues as to the cellular properties of degenerative processes. We review data obtained in two neurogenetic models of movement disorders in the laboratory mouse, the 'Purkinje cell degeneration' (pcd) mutant, a model of cerebellar ataxia, and the 'weaver' (wv) mutant, a combined degeneration of multiple systems including the mesostriatal dopaminergic pathway. In the cerebellum of pcd mice, analyses of transsynaptic granule cell death subsequent to the genetically-determined degeneration of Purkinje cells show that granule neuron fallout follows a typical pattern of exponential decay. In the midbrain of weaver mice, regression f...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3464060</comments>
            <pubDate>Tue, 13 Apr 2010 21:10:04 +0100</pubDate>
            <guid isPermaLink="false">3464060</guid>        </item>
        <item>
            <title>Consideration of the ischaemic basis and treatment of Alzheimer's disease.</title>
            <link>http://www.medworm.com/index.php?rid=3464059&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20383807%26dopt%3DAbstract</link>
            <description>Authors: Pluta R, U&amp;#x142;amek M, Jab&amp;#x142;o&amp;#x144;ski M
    Victims of Alzheimer's disease (AD) develop a progressive dementia over years, accompanied by development of neurofibrillary tangles and finally neuronal death, accumulation of amyloid plaques and deposition of amyloid in neuro-vessels. Currently AD is the major form of dementia and the fourth leading cause of death in aged population. The investigation of etiology and therapy of AD, now more than ever, needs an infusion of new concepts. The aims of this review are to analyze knowledge of the influence of ischaemic and amyloid pathology on the final development of AD, especially with regards to the etiology of AD plaques, to develop a consensus on whether ischaemic blood-brain barrier permeability for amyloid peptide or both are...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3464059</comments>
            <pubDate>Tue, 13 Apr 2010 21:10:04 +0100</pubDate>
            <guid isPermaLink="false">3464059</guid>        </item>
        <item>
            <title>Imperfect oligodendrocytic and neuronal differentiation of glioblastoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=3464058&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20383808%26dopt%3DAbstract</link>
            <description>Authors: Wola&amp;#x144;czyk M, Hu&amp;#x142;as-Bigoszewska K, Witusik-Perkowska M, Papierz W, Jask&amp;#xF3;lski D, Liberski PP, Rieske P
    Previously, we have reported that glioblastoma (GBM) cells can be differentiated into cells showing neuronal, glial and non-neural (mesenchymal) phenotypes. Before the differentiation the GBM cells co-expressed GFAP, CD44, Beta III tubulin, MAP2, Vimentin, Nestin and SOX-2, whereas during the exposure to a neural differentiation medium the differentiation process was arrested at the early stages and the GBM cells presented features of four phenotypes: multi-lineage, non-neural (mesenchymal), intermediate of neuronal cells and glial cells. Currently, we decided to check if changes in expression of: TH (tyrosine hydroxylase, marker of catecholaminergic cells) and...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3464058</comments>
            <pubDate>Tue, 13 Apr 2010 21:10:04 +0100</pubDate>
            <guid isPermaLink="false">3464058</guid>        </item>
        <item>
            <title>Neuroprotective effect of erythropoietin in amyotrophic lateral sclerosis (ALS) model in vitro. Ultrastructural study.</title>
            <link>http://www.medworm.com/index.php?rid=3464057&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20383809%26dopt%3DAbstract</link>
            <description>Authors: Naga&amp;#x144;ska E, Taraszewska A, Matyja E, Grieb P, Rafa&amp;#x142;owska J
    Erythropoietin (EPO) is a chemokine hormone that is widely distributed throughout the body including nervous system. For last years its role as cytokine involved in many physiological processes out of the bone marrow has been suggested. Moreover, it plays a very important role in CNS as potential neuroprotective agent. There is much evidence that EPO protects neuronal cells in vitro and in vivo models of brain injury, independently of its erythropoietic action. The aim of this study was to determine the potential neuroprotective effects of erythropoietin on the glutamate-mediated injury of motor neurons (MNs) in vitro. The study was performed on organotypic cultures of the rat lumbar spinal cord subjected t...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3464057</comments>
            <pubDate>Tue, 13 Apr 2010 21:10:04 +0100</pubDate>
            <guid isPermaLink="false">3464057</guid>        </item>
        <item>
            <title>Recombinant forms of myelin antigens expressed on Chinese hamster ovary (CHO) cells as a tool for identification of autoantibodies in serum of multiple sclerosis patients.</title>
            <link>http://www.medworm.com/index.php?rid=3464056&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20383810%26dopt%3DAbstract</link>
            <description>We describe a cell-based assay that specifically identifies serum antibodies directed against three major myelin autoantigens: MBP, PLP and MOG. The method detects antibody binding to recombinant antigens in their native conformation on MBP, PLP and MOG transfected mammalian (hamster ovary) cells. 36 patients with relapsing-remitting MS diagnosed according to criteria of McDonald were recruited. Age 38.2 and duration of the disease 7.1. Serum anti-MBP, anti-PLP and anti-MOG IgG autoantibodies were detected in MS patients and 35 healthy donors by FACS analysis. Compared with healthy controls the titres of IgG autoantibodies directed against membrane-bound recombinant myelin antigens were most significantly increased for PLP, no quite significant for MBP and not significant for MOG. The titr...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3464056</comments>
            <pubDate>Tue, 13 Apr 2010 21:10:04 +0100</pubDate>
            <guid isPermaLink="false">3464056</guid>        </item>
        <item>
            <title>Microscopic and electrophysiological changes on regenerating sciatic nerves of rats treated with simvastatin.</title>
            <link>http://www.medworm.com/index.php?rid=3464055&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20383811%26dopt%3DAbstract</link>
            <description>CONCLUSION: simvastatin was shown to delay regeneration as shown in microscopic studies but still there was no influence on nerve regeneration.
    PMID: 20383811 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3464055</comments>
            <pubDate>Tue, 13 Apr 2010 21:10:04 +0100</pubDate>
            <guid isPermaLink="false">3464055</guid>        </item>
        <item>
            <title>Usefulness of the ultrastructural and immunohistochemical analysis of cardiac biopsy in affected heart.</title>
            <link>http://www.medworm.com/index.php?rid=3464054&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20383812%26dopt%3DAbstract</link>
            <description>Authors: Fidzia&amp;#x144;ska A, Glinka-Lindner Z, Religa G, Walczak E
    In the last few years endomyocardial biopsy becomes a useful diagnostic tool for the investigation of idiopathic dilated cardiomyopathy. The aim of our current study was to try to identify ultrastructural and immunohistochemical specificity of truncated cardiac proteins in affected heart. The focal loss of plasma membrane continuity together with the lack of dystrophin activity in affected myocytes facilitated to find mutation in dystrophin gene. The accumulation of granulofilamentous desmin-positive material in cytoplasm of myocytes was the main indicator of presented mutation in the desmin gene. Nuclear structure remodeling, concomitantly with loss of lamin A/C activity, contributed to identify mutation in lamin A/C g...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3464054</comments>
            <pubDate>Tue, 13 Apr 2010 21:10:04 +0100</pubDate>
            <guid isPermaLink="false">3464054</guid>        </item>
        <item>
            <title>Hyperhomocysteinemia and homozygous MTHFR 677C&gt;T mutation finding in an Alzheimer's disease case with metabolic syndrome diagnosis.</title>
            <link>http://www.medworm.com/index.php?rid=3464053&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20383813%26dopt%3DAbstract</link>
            <description>Authors: Guran S, Kozan S, Bah&amp;#xE7;e M
    
    PMID: 20383813 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3464053</comments>
            <pubDate>Tue, 13 Apr 2010 21:10:04 +0100</pubDate>
            <guid isPermaLink="false">3464053</guid>        </item>
        <item>
            <title>Pathophysiological basis of translational stroke research.</title>
            <link>http://www.medworm.com/index.php?rid=2876642&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19813140%26dopt%3DAbstract</link>
            <description>Authors: Hossmann KA
    The high incidence and the devastating consequences of stroke call for efficient therapies but despite extensive experimental evidence of neuroprotective improvements, most clinical treatments have failed. The poor translational success is attributed to the inappropriate selection of clinically irrelevant animal models, the inappropriate focus on clinically irrelevant injury pathways and the inappropriate estimation of the length of therapeutic windows. To substantiate this conclusion, the pathophysiology of experimental stroke is reviewed. Particular emphasis is placed on the importance of collateral pathways, the penumbra concept and the viability thresholds of ischaemia, the haemodynamic and molecular mechanisms of injury evolution and the effect of secondary co...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2876642</comments>
            <pubDate>Fri, 09 Oct 2009 20:58:03 +0100</pubDate>
            <guid isPermaLink="false">2876642</guid>        </item>
        <item>
            <title>Metastatic tumours of the central nervous system - a pathological approach.</title>
            <link>http://www.medworm.com/index.php?rid=2876641&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19813141%26dopt%3DAbstract</link>
            <description>Authors: Biernat W
    Metastases are the most common tumours of the central nervous system. Histopathological diagnosis remains the most efficient and specific diagnostic procedure that provides the clinician with quick, specific and cost-effective information necessary for the optimal treatment of the patient. Therefore, the pathologist should be acquainted with the potential opportunities to determine the most precise diagnosis in case of metastatic deposits involving the central nervous system.
    PMID: 19813141 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2876641</comments>
            <pubDate>Fri, 09 Oct 2009 20:58:03 +0100</pubDate>
            <guid isPermaLink="false">2876641</guid>        </item>
        <item>
            <title>Inhibition of respiratory processes by overabundance of zinc in neuronal cells.</title>
            <link>http://www.medworm.com/index.php?rid=2876640&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19813142%26dopt%3DAbstract</link>
            <description>Authors: Floria&amp;#x144;czyk B, Trojanowski T
    Studies suggest that excessive amounts of free zinc ions can cause neuron death by interfering with the energy production process. The sites of the cell oxidation activity of zinc are the glycolytic enzymes, the Krebs cycle components and the respiratory chain. Further consequences of reduced access to energy are: increased production of reactive forms of oxygen, decrease of the mitochondrial membrane potential and decreased level of ATP. Also, the toxicity of zinc accelerates the supply of extra amounts of this element to the mitochondria, which results in their increased permeability.
    PMID: 19813142 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2876640</comments>
            <pubDate>Fri, 09 Oct 2009 20:58:03 +0100</pubDate>
            <guid isPermaLink="false">2876640</guid>        </item>
        <item>
            <title>Expression of RCAS1 protein in microglia/macrophages accompanying brain tumours. An immunofluorescence study.</title>
            <link>http://www.medworm.com/index.php?rid=2876639&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19813143%26dopt%3DAbstract</link>
            <description>Authors: Adamek D, Radwa&amp;#x144;ska E, Gajda M
    The expression of protein RCAS1 (receptor-binding cancer antigen expressed on SiSo cells), possibly involved in the mechanisms of evasion of immune surveillance by tumours, has been studied in brain astrocytomas grade III and IV and in metastatic carcinomas to the brain by means of double immunofluorescence with antibodies against RCAS1 and respectively anti-GFAP (astroglia) or CD68 or CD74 (macrophages/microglia). Expression of RCAS1 has been reported in many types of carcinomas and in some normal cells, including bone marrow macrophages. Nakabayashi and coworkers recently reported expression of RCAS1 in gliomas. So far no attention has been paid to expression of RCAS1 in non-neoplastic cellular elements of tumours such as macrophages and ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2876639</comments>
            <pubDate>Fri, 09 Oct 2009 20:58:03 +0100</pubDate>
            <guid isPermaLink="false">2876639</guid>        </item>
        <item>
            <title>Alpha-synuclein inhibits poly (ADP-ribose) polymerase-1 (PARP-1) activity via NO-dependent pathway.</title>
            <link>http://www.medworm.com/index.php?rid=2876638&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19813144%26dopt%3DAbstract</link>
            <description>Authors: Adamczyk A, Ka&amp;#x17A;mierczak A
    alpha-Synuclein (ASN) is a brain-enriched protein that functions as a molecular chaperone and regulator of the synaptic vesicle cycle. However, if ASN is overexpressed and in prefibrillar oligomeric forms it activates free radical formation and has been implicated in neurodegeneration. The nuclear target for the free radical cascade is poly (ADP-ribose) polymerase-1 (PARP-1), a DNA-binding enzyme and transcriptional regulator that decides on cell survival or death. Our previous data indicated that soluble oligomeric form of ASN significantly stimulated nitric oxide synthase (NOS) activity and by oxidative stress leads to mitochondria failure and cell death. The aim of this study was to investigate the effect of ASN on PARP-1 protein level and on...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2876638</comments>
            <pubDate>Fri, 09 Oct 2009 20:58:03 +0100</pubDate>
            <guid isPermaLink="false">2876638</guid>        </item>
        <item>
            <title>Ultrastructural evidence of amyloid beta-induced autophagy in PC12 cells.</title>
            <link>http://www.medworm.com/index.php?rid=2876637&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19813145%26dopt%3DAbstract</link>
            <description>Authors: Pajak B, Songin M, Strosznajder JB, Orzechowski A, Gajkowska B
    Herein we demonstrate that PC12 cells overexpress human amyloid beta precursor protein bearing double Swedish mutation(AbetaPPsw), showing the phenotype characteristic for Alzheimer's disease (AD). Examination of cells at ultrastructural level revealed the intracellular presence of peptide aggregates. Furthermore, autophagy induction was found to be a hallmark of amyloid beta-induced cytotoxicity. Importantly, autophagic vacuoles were co-localized within amyloid beta (Abeta) deposits. This suggests the involvement of autophagy in amyloid beta-elicited cell degeneration.
    PMID: 19813145 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2876637</comments>
            <pubDate>Fri, 09 Oct 2009 20:58:03 +0100</pubDate>
            <guid isPermaLink="false">2876637</guid>        </item>
        <item>
            <title>Kufs' disease: diagnostic difficulties in the examination of extracerebral biopsies.</title>
            <link>http://www.medworm.com/index.php?rid=2876636&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19813146%26dopt%3DAbstract</link>
            <description>We report the case of a 45-year-old woman referred to the Neurological Department with suspicion of Creutzfeldt-Jakob disease (CJD). CJD as well as infectious, autoimmune and some lysosomal diseases were excluded. Since clinical symptoms, i.e. psychotic, auditory and visual hallucinations as well as behavioural disturbances, still suggested metabolic or neurodegenerative disease, a skin and muscle biopsy was performed. On ultrastructural examination the muscle biopsy revealed the subsarcolemmal accumulation of lipofuscin, lipofuscinlike and granular osmiophilic deposits (GRODs). The most unique fingerprint deposits (FP) and curvilinear profiles (CP) for diagnosis of Kufs' disease were located in vascular smooth muscle cells (VSMCs). In these cells lipofuscin-like deposits and GRODs were al...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2876636</comments>
            <pubDate>Fri, 09 Oct 2009 20:58:03 +0100</pubDate>
            <guid isPermaLink="false">2876636</guid>        </item>
        <item>
            <title>Ultrastructural features of astrocytes in the cortex of the hippocampal gyrus and in the neocortex of the temporal lobe in an experimental model of febrile seizures and with the use of topiramate.</title>
            <link>http://www.medworm.com/index.php?rid=2876635&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19813147%26dopt%3DAbstract</link>
            <description>The objective of the current study was ultrastructural assessment of astroglia in specimens of the hippocampal cortex and neocortex of the temporal lobe in our own experimental model of febrile seizures (FS) in rats, as well as the analysis of the influence of a structurally novel broad spectrum anticonvulsant, topiramate (TPM), upon these cells in the CNS regions studied. The current study was inspired by some interesting literature reports on the in vitro investigation into the biological effects of TPM in primary cultures of rat cortical astrocytes and by the lack of data concerning astroglial morphology in vivo in an experimental model with this antiepileptic. In the FS group, the most pronounced changes in the study cell population referred to protoplasmic astroglia and were observed ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2876635</comments>
            <pubDate>Fri, 09 Oct 2009 20:58:03 +0100</pubDate>
            <guid isPermaLink="false">2876635</guid>        </item>
        <item>
            <title>Ganglioglioma associated with alterations of NBN gene. A case report.</title>
            <link>http://www.medworm.com/index.php?rid=2876634&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19813148%26dopt%3DAbstract</link>
            <description>We report a case of a 13-year-old girl with a tumour of the right fronto-parietal region of the brain. The tumour consisted of two components: a well-differentiated astroglial component with Rosenthal fibres and a neoplastic neuronal component. The final histopathology established diagnosis of ganglioglioma WHO grade I. The patient was selected from a group of children with central nervous system (CNS) tumours screened for the most common molecular variants in the NBN gene (exons 5 and 6). Molecular analysis revealed the presence of c.511A&amp;gt;G (p.Ile171Val) substitution on one allele. This is the first patient with ganglioglioma and confirmed mutation in the NBN gene.
    PMID: 19813148 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2876634</comments>
            <pubDate>Fri, 09 Oct 2009 20:58:03 +0100</pubDate>
            <guid isPermaLink="false">2876634</guid>        </item>
        <item>
            <title>Pilocytic astrocytoma as a predominant component of a recurrent complex type DNT.</title>
            <link>http://www.medworm.com/index.php?rid=2876633&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19813149%26dopt%3DAbstract</link>
            <description>We report an unusual case of a 7-year-old girl with a temporal lobe DNT, which recurred four years after subtotal resection of the tumour. In the recurrent lesion we identified pilocytic astrocytoma (PA) as a predominant component of the tumour. Small pieces of the removed tissues also disclosed remnants of DNT. Clinical presentation of the primary tumour consisted of partial simple seizures, while the recurrent tumour manifested with headache and vomiting. Likewise, the radiological appearance of both tumours was different. We conclude that patients with incompletely removed DNT may suffer local recurrence of that tumour. In rare cases development of a secondary, histologically different neoplasm may also occur.
    PMID: 19813149 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2876633</comments>
            <pubDate>Fri, 09 Oct 2009 20:58:03 +0100</pubDate>
            <guid isPermaLink="false">2876633</guid>        </item>
        <item>
            <title>Transmissible mink encephalopathy - review of the etiology of a rare prion disease.</title>
            <link>http://www.medworm.com/index.php?rid=2717025&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19618341%26dopt%3DAbstract</link>
            <description>Authors: Liberski PP, Sikorska B, Guiroy D, Bessen RA
    We review here the history, neuropathology, clinical picture and molecular data on transmissible mink encephalopathy (TME). This obscure disease is of utmost importance as it is plausible that it represents a transmission of hidden bovine spongiform encephalopathy (BSE) to mink in the USA. Of special interest is the similarity of L-type of BSE and TME. Furthermore, experimental molecular studies showed the TME strain-specific in vitro conversion in a cell-free system. In addition, we show here for the first time confocal laser microscopy studies of co-localization of PrPd- amyloid plaques and GFAP-expressing astrocytes.
    PMID: 19618341 [PubMed - indexed for MEDLINE] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2717025</comments>
            <pubDate>Fri, 21 Aug 2009 01:12:02 +0100</pubDate>
            <guid isPermaLink="false">2717025</guid>        </item>
        <item>
            <title>Reflections on a half-century in the field of transmissible spongiform encephalopathy.</title>
            <link>http://www.medworm.com/index.php?rid=2626059&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19618333%26dopt%3DAbstract</link>
            <description>Authors: Brown P
    The subject of transmissible spongiform encephalopathy may properly be said to have begun with the experimental transmission of scrapie by Cuill&amp;#xE9; and Chelle in 1936, although Creutzfeldt and Jakob had described the disease that bears their names in 1920-21. Thirty more years passed before the human disease was also shown to be transmissible, in 1966, and the following half century has seen the field move from classical biology to molecular biology and genetics, and from 'slow virus' to host-encoded 'prion' protein. Because nothing is more important to the research scientist than the process of seeing a problem and devising ways of solving it, and because we live and die by our publications, as much care should be given to these vehicles of our work and reputations...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2626059</comments>
            <pubDate>Wed, 22 Jul 2009 12:40:05 +0100</pubDate>
            <guid isPermaLink="false">2626059</guid>        </item>
        <item>
            <title>Thoughts on mammalian prion strains.</title>
            <link>http://www.medworm.com/index.php?rid=2626058&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19618334%26dopt%3DAbstract</link>
            <description>Authors: Weissmann C
    A plethora of prion strains can be propagated indefinitely in hosts homozygous for the PrP gene. Within the framework of the &quot;protein-only&quot; hypothesis, the strain-specific properties are enciphered in the conformation of the strain-associated PrPSc. Are these conformations codetermined by additional components, whose presence or absence within an infected cell could define the cell's competence to replicate a particular strain? Which cellular components, if any, contribute to the PrPC-to-PrPSc conversion in the cell? Many questions still remain to be answered in the field launched and nurtured by Carlton Gajdusek, to whom this essay is dedicated.
    PMID: 19618334 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2626058</comments>
            <pubDate>Wed, 22 Jul 2009 12:40:05 +0100</pubDate>
            <guid isPermaLink="false">2626058</guid>        </item>
        <item>
            <title>Kuru and D. Carleton Gajdusek: a close encounter.</title>
            <link>http://www.medworm.com/index.php?rid=2626057&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19618335%26dopt%3DAbstract</link>
            <description>Authors: Liberski PP
    Kuru, the first human transmissible spongiform encephalopathy, was transmitted to chimpanzees by D. Carleton Gajdusek (1923-2008). In this review, I briefly summarize the history of this seminal discovery alongside its epidemiology, clinical picture, neuropathology and molecular genetics. The discovery of kuru opened new windows into the realms of human medicine and was instrumental in the later transmission of Creutzfeldt-Jakob disease as well as the prediction that bovine spongiform encephalopathy would be transmitted to humans. It was one of the greatest discoveries in biomedical sciences of the 20th century.
    PMID: 19618335 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2626057</comments>
            <pubDate>Wed, 22 Jul 2009 12:40:05 +0100</pubDate>
            <guid isPermaLink="false">2626057</guid>        </item>
        <item>
            <title>Cannibalism, kuru and anthropology.</title>
            <link>http://www.medworm.com/index.php?rid=2626055&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19618336%26dopt%3DAbstract</link>
            <description>Authors: Lindenbaum S
    This essay discusses the image and practice of cannibalism in a wide range of studies. It also presents the anthropological research on kuru which led to the proposal that cannibalism had enabled transmission of the infectious agent, as well as doubts about the hypothesis, and the assertion by some that cannibalism as a socially approved custom did not exist. The figure of the cannibal as an icon of primitivism took form in the encounter between Europe and the Americas. Cannibalism was to become the prime signifier of &quot;barbarism&quot; for a language of essentialized difference that would harden into the negative racism of the nineteenth century. Anthropological and medical research now challenge the derogatory image of the cannibal as we learn more about the many past ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2626055</comments>
            <pubDate>Wed, 22 Jul 2009 12:40:05 +0100</pubDate>
            <guid isPermaLink="false">2626055</guid>        </item>
        <item>
            <title>A short history of the long and productive search for the cause of subacute sclerosing panencephalitis.</title>
            <link>http://www.medworm.com/index.php?rid=2626054&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19618337%26dopt%3DAbstract</link>
            <description>Authors: Katz M
    This brief historical review recounts the efforts of the discovery of the cause of subacute sclerosing panencephalitis from its initial pathological descriptions, through the identification of measles virus as its pathogen, to the current conceptual framework of its pathogenesis. It is presented as an example of what was once considered an &quot;unconventional&quot; infection, but is now the subject of speculation according to the modern principles of molecular biology.
    PMID: 19618337 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2626054</comments>
            <pubDate>Wed, 22 Jul 2009 12:40:05 +0100</pubDate>
            <guid isPermaLink="false">2626054</guid>        </item>
        <item>
            <title>Contributions of isolated Pacific populations to understanding neurodegenerative diseases.</title>
            <link>http://www.medworm.com/index.php?rid=2626052&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19618338%26dopt%3DAbstract</link>
            <description>Authors: Garruto RM, Yanagihara R
    Isolated human populations have provided a natural experimental laboratory for the ongoing study of human disease. In the mid-20th century a number of high-incidence foci of neurodegenerative diseases were brought to medical attention including kuru, amyotrophic lateral sclerosis, and parkinsonism-dementia. These foci were discovered in Papua New Guinea, West New Guinea, the Kii Peninsula of Japan, and in the Mariana Islands. The study of these diseases in isolated human groups has significantly contributed to our understanding of the cause and mechanisms of pathogenesis of these and related neurodegenerative disorders globally. This paper is dedicated to D. Carleton Gajdusek, a pioneer in the study of neurodegenerative diseases, whose decades of field...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2626052</comments>
            <pubDate>Wed, 22 Jul 2009 12:40:05 +0100</pubDate>
            <guid isPermaLink="false">2626052</guid>        </item>
        <item>
            <title>Viliuisk encephalomyelitis in Eastern Siberia - analysis of 390 cases.</title>
            <link>http://www.medworm.com/index.php?rid=2626051&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19618339%26dopt%3DAbstract</link>
            <description>Authors: Goldfarb LG, Vladimirtsev VA, Platanov FA, Lee HS, McLean CA, Masters CL
    Viliuisk encephalomyelitis (VE) is a unique disease occurring in the Yakut (Sakha) population of Eastern Siberia. VE is always fatal, with some patients dying during the acute encephalitic phase of illness; those surviving the acute phase develop progressive dementia, rigidity and spastic quadriparesis as part of a more prolonged pan-encephalitic syndrome. The disease is characterized neuropathologically by multiple widespread micronecrotic foci with marked inflammatory reactions and subsequent gliosis throughout the cerebral cortex, basal ganglia, cerebellum and brain stem. The acute febrile onset with cerebrospinal fluid pleocytosis and increased protein and neuropathology showing inflammatory reactions...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2626051</comments>
            <pubDate>Wed, 22 Jul 2009 12:40:05 +0100</pubDate>
            <guid isPermaLink="false">2626051</guid>        </item>
        <item>
            <title>HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP): the role of HTLV-I-infected Th1 cells in the pathogenesis, and therapeutic strategy.</title>
            <link>http://www.medworm.com/index.php?rid=2626050&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19618340%26dopt%3DAbstract</link>
            <description>Authors: Nakamura T
    Human T lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a chronic progressive myelopathy characterized by bilateral pyramidal tract involvement with sphincteric disturbances. The primary neuropathological feature of HAM/TSP is chronic myelitis characterized by perivascular cuffing and parenchymal infiltration of lymphocytes. Although the exact cellular and molecular events underlying the induction of chronic inflammation in the spinal cord by HTLV-I are still unclear, a long-standing bystander mechanism, such as the destruction of surrounding nervous tissue by the interaction between HTLV-I-infected CD4+ T cells and HTLV-I-specific cytotoxic T cells in the spinal cord, is probably critical in the immunopathogenesis ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2626050</comments>
            <pubDate>Wed, 22 Jul 2009 12:40:05 +0100</pubDate>
            <guid isPermaLink="false">2626050</guid>        </item>
        <item>
            <title>Transmissible mink encephalopathy - review of the etiology.</title>
            <link>http://www.medworm.com/index.php?rid=2626048&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19618341%26dopt%3DAbstract</link>
            <description>Authors: Liberski PP, Sikorska B, Guiroy D, Bessen RA
    We review here the history, neuropathology, clinical picture and molecular data on transmissible mink encephalopathy (TME). This obscure disease is of utmost importance as it is plausible that it represents a transmission of hidden bovine spongiform encephalopathy (BSE) to mink in the USA. Of special interest is the similarity of L-type of BSE and TME. Furthermore, experimental molecular studies showed the TME strain-specific in vitro conversion in a cell-free system. In addition, we show here for the first time confocal laser microscopy studies of co-localization of PrPd- amyloid plaques and GFAP-expressing astrocytes.
    PMID: 19618341 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2626048</comments>
            <pubDate>Wed, 22 Jul 2009 12:40:05 +0100</pubDate>
            <guid isPermaLink="false">2626048</guid>        </item>
        <item>
            <title>Murine bone marrow stromal cell culture with features of mesenchymal stem cells susceptible to mouse-adapted human TSE agent, Fukuoka-1.</title>
            <link>http://www.medworm.com/index.php?rid=2626045&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19618342%26dopt%3DAbstract</link>
            <description>Authors: Akimov S, Vasilyeva I, Yakovleva O, McKenzie C, Cervenakova L
    Transmission of transmissible spongiform encephalopathies (TSEs)/prion diseases through transplantation of bone marrow (BM) has never been reported in humans. However, the use of fetal bovine serum in current protocols for generating mesenchymal stem cells (MSCs) carries the risk of iatrogenic spread. We developed a cell model from murine BM-derived MSCs and tested its susceptibility to Fukuoka-1 (Fu) strain of TSEs. The adherent cells expressed significant levels of normal prion protein, PrPC, at the time when they became immortalized. The cell culture underwent spontaneous transformation following inoculation with Fu-infected brain homogenate and became persistently infected after reinoculation with Fu agent. Exte...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2626045</comments>
            <pubDate>Wed, 22 Jul 2009 12:40:05 +0100</pubDate>
            <guid isPermaLink="false">2626045</guid>        </item>
        <item>
            <title>Occipital neuralgia: possible failure of surgical treatment - case report.</title>
            <link>http://www.medworm.com/index.php?rid=2538828&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19353436%26dopt%3DAbstract</link>
            <description>Authors: Andrychowski J, Czernicki Z, Netczuk T, Taraszewska A, Dabrowski P, Rakasz L, Budohoski K
    Surgical intervention in severe cases of occipital neuralgia should be considered if pharmacological and local nerve blocking treatment fail. The literature suggests two types of interventions: surgical decompression of the greater occipital nerve (GON) from the entrapment site, as a less invasive approach, and neurotomy of the nerve trunk, which results in ipsilateral sensation deficits in the GON innervated area of the skull. Due to anatomical variations in the division of the GON trunk, typical neurotomy above the line of the trapezius muscle aponeurosis (TMA) may not result in full recovery. The present study discusses a case of a female treated with GON decompression as a result of o...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2538828</comments>
            <pubDate>Sat, 27 Jun 2009 21:26:03 +0100</pubDate>
            <guid isPermaLink="false">2538828</guid>        </item>
        <item>
            <title>Mysteries of CADASIL - the contribution of neuropathology to understanding of the disease.</title>
            <link>http://www.medworm.com/index.php?rid=2315420&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19353429%26dopt%3DAbstract</link>
            <description>We present a review of current concepts regarding CADASIL pathogenesis, clinical picture and diagnosis in which neuropathological examinations played a key role.
    PMID: 19353429 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2315420</comments>
            <pubDate>Thu, 09 Apr 2009 13:50:51 +0100</pubDate>
            <guid isPermaLink="false">2315420</guid>        </item>
        <item>
            <title>Blood-brain barrier ultrastructural alterations in human congenital hydrocephalus and Arnold-Chiari malformation.</title>
            <link>http://www.medworm.com/index.php?rid=2315411&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19353430%26dopt%3DAbstract</link>
            <description>Authors: Castejon OJ
    Cortical biopsies of 13 patients with clinical diagnosis of congenital hydrocephalus, Arnold-Chiari malformation and hydrocephalus, and postmeningitis hydrocephalus were examined by transmission electron microscopy to study the damage of endothelial cells, basement membrane, astrocytic end-feet layer, and perivascular space. Capillaries from the parietal and frontal cortex showed increased vesicular and vacuolar transport, intact endothelial junctions, thin and immature basement membrane, swollen perivascular astrocytic end-feet layer, and enlarged perivascular space. In areas of severe oedema, open endothelial junctions, swollen basement membrane, absent perivascular astrocytic end-feet layer, enlarged perivascular space, and disrupted perivascular neuropil were o...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2315411</comments>
            <pubDate>Thu, 09 Apr 2009 13:50:51 +0100</pubDate>
            <guid isPermaLink="false">2315411</guid>        </item>
        <item>
            <title>Remodelling of skeletal muscle cells in children with SCO2 gene mutation - ultrastructural study.</title>
            <link>http://www.medworm.com/index.php?rid=2315404&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19353431%26dopt%3DAbstract</link>
            <description>Authors: Matyja E, Pronicki M, Kowalski P, Czarnowska E, Taybert J
    Mitochondrial protein coded by the SCO2 gene is involved in the process of assembly of mitochondrial cytochrome c oxidase (COX). Progressive cardiomyopathy, neuropathy and lactic acidosis are presented by infants with SCO2 gene mutations. Only a dozen patients with this gene mutation have been reported in the literature. Muscle ultrastructure is mentioned only in a few case reports. The aim of this study was to search for typical ultrastructural features in 11 skeletal muscle specimens from Polish patients bearing SCO2 gene mutations. Ultrastructural analysis confirms domination of atrophic and degenerative changes, including atrophic muscle fibres of irregular shape with folding of basal lamina and numerous papillary p...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2315404</comments>
            <pubDate>Thu, 09 Apr 2009 13:50:51 +0100</pubDate>
            <guid isPermaLink="false">2315404</guid>        </item>
        <item>
            <title>Increased expression of cell adhesion molecules in inflammatory myopathies: diagnostic utility and pathogenetic insights.</title>
            <link>http://www.medworm.com/index.php?rid=2315396&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19353432%26dopt%3DAbstract</link>
            <description>Conclusions: IMs comprise 6% of all muscle diseases and IBM is not a common IM in India as reported in the Western literature. Our findings support the hypothesis of autoimmune origin of IMs. The difference between expression of these molecules in IMs and controls also has diagnostic implications and these markers should be included along with MHC-1 antigen and membrane attack complex (MAC) in the existing diagnostic armamentarium.
    PMID: 19353432 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2315396</comments>
            <pubDate>Thu, 09 Apr 2009 13:50:51 +0100</pubDate>
            <guid isPermaLink="false">2315396</guid>        </item>
        <item>
            <title>Spectral changes in postoperative MRS in high-grade gliomas and their effect on patient prognosis.</title>
            <link>http://www.medworm.com/index.php?rid=2315390&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19353433%26dopt%3DAbstract</link>
            <description>In conclusion, MRS is a diagnostic tool which, on the basis of direction of changes in the value of metabolite ratios, helps additionally confirm the diagnosis of glioma regrowth. In the case of a visible contrast enhancement area on the postoperative MRI with observed concomitant increase in Cho/NAA ratio and decrease in NAA/Cr ratio between pre- and postoperative MRS examinations, preliminary suspicion should be that of glioma regrowth rather than of remnant tumour after surgery or postradiation lesions.
    PMID: 19353433 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2315390</comments>
            <pubDate>Thu, 09 Apr 2009 13:50:51 +0100</pubDate>
            <guid isPermaLink="false">2315390</guid>        </item>
        <item>
            <title>Unexpected morphological changes within hippocampal structures in a photochemical ring model of cerebral ischaemia.</title>
            <link>http://www.medworm.com/index.php?rid=2315383&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19353434%26dopt%3DAbstract</link>
            <description>Authors: Rafa&amp;#x142;owska J, Gadamski R, Dziewulska D, Zielonka P, Ogonowska W, Lazarewicz JW
    A photochemical ring model of ischaemia was introduced in the middle of the nineteen eighties. Irradiation by a laser or arc lamp followed by intravenous injection of rose bengal resulted in thrombosis of pial and superficial cortical vessels. This ring model imitated focal ischaemic damage in humans. In our experiment twenty-seven Wistar rats of both sexes weighing 250-300 grams were examined. A photochemical ring model based on irradiation of the area of parietal bone 4 mm posteriorly to the bregma and 4 mm laterally from the sagittal suture was applied. A ring-shaped light beam with a wavelength of 510-540 nm with 5 mm diameter was generated by a high pressure discharge lamp at a power of 4...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2315383</comments>
            <pubDate>Thu, 09 Apr 2009 13:50:51 +0100</pubDate>
            <guid isPermaLink="false">2315383</guid>        </item>
        <item>
            <title>Effect of concurrent application of heat, swim stress and repeated dermal application of chlorpyrifos on the hippocampal neurons in mice.</title>
            <link>http://www.medworm.com/index.php?rid=2315376&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19353435%26dopt%3DAbstract</link>
            <description>This study correlates the changes in acetylcholinesterase (AChE) levels and neuronal counts in areas of the hippocampus to consecutive exposure of stress, heat and CPF. Male mice (60 days) were segregated into six groups: one control, one stress control, and four treated groups (n=10). CPF was applied in doses of 1/2 and 1/5 of dermal LD50 (E1 and E2) over the tail of mice under occlusive bandages for 3 weeks. Stress control [(s) C] mice were subjected to swim stress at 38 degrees C (6 mins/day, 3 weeks). (s) E1 and (s) E2 were subjected to swim stress before CPF application. Blood and brain AChE levels were estimated using a spectrofluorometric method (Amplex Red). Pyramidal neurons of the cornu ammonis of the hippocampus under Nissl stain from histological sections were counted per unit ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2315376</comments>
            <pubDate>Thu, 09 Apr 2009 13:50:51 +0100</pubDate>
            <guid isPermaLink="false">2315376</guid>        </item>
        <item>
            <title>Occipital neuralgia: possible failure of surgical treatment.</title>
            <link>http://www.medworm.com/index.php?rid=2315372&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19353436%26dopt%3DAbstract</link>
            <description>Authors: Andrychowski J, Czernicki Z, Netczuk T, Taraszewska A, Dabrowski P, Rakasz L, Budohoski K
    Surgical intervention in severe cases of occipital neuralgia should be considered if pharmacological and local nerve blocking treatment fail. The literature suggests two types of interventions: surgical decompression of the greater occipital nerve (GON) from the entrapment site, as a less invasive approach, and neurotomy of the nerve trunk, which results in ipsilateral sensation deficits in the GON innervated area of the skull. Due to anatomical variations in the division of the GON trunk, typical neurotomy above the line of the trapezius muscle aponeurosis (TMA) may not result in full recovery. The present study discusses a case of a female treated with GON decompression as a result of o...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2315372</comments>
            <pubDate>Thu, 09 Apr 2009 13:50:51 +0100</pubDate>
            <guid isPermaLink="false">2315372</guid>        </item>
        <item>
            <title>Endolymphatic sac tumours and von Hippel-Lindau disease - case report, molecular analysis and histopathological characterization.</title>
            <link>http://www.medworm.com/index.php?rid=2315367&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19353437%26dopt%3DAbstract</link>
            <description>Authors: Krzysztolik K, Cybulski C, Sagan L, Nowacki P, Lubi&amp;#x144;ski J
    Endolymphatic sac tumours (ELST) are aggressive papillary tumours of the temporal bone. The name was finally determined after the endolymphatic sac was determined as the site of their origin. They should be considered in patients with tumours eroding the petrous part of the temporal bone, extending to the cerebellopontine angle or other adjacent structures. These very rare tumours in the general population have much higher prevalence in von Hippel-Lindau disease. Hence molecular analysis of the VHL gene should be performed in patients with ELST and their relatives. The purpose of this study is to present a case report, histopathological characterization of endolymphatic sac tumours, their association with von Hipp...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2315367</comments>
            <pubDate>Thu, 09 Apr 2009 13:50:51 +0100</pubDate>
            <guid isPermaLink="false">2315367</guid>        </item>
        <item>
            <title>Neuroblastoma and opsoclonus-myoclonus-ataxia syndrome--clinical and pathological characteristics.</title>
            <link>http://www.medworm.com/index.php?rid=1865144&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18825593%26dopt%3DAbstract</link>
            <description>CONCLUSION: In some patients the onset of OMA is related to vaccination or infection. Children with OMA and neuroblastoma despite a good oncological prognosis often present permanent neurological and developmental deficits. The inflammatory infiltrations within the tumours are combined, with predominant participation of cytotoxic cells.
    PMID: 18825593 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1865144</comments>
            <pubDate>Fri, 10 Oct 2008 12:32:02 +0100</pubDate>
            <guid isPermaLink="false">1865144</guid>        </item>
        <item>
            <title>Immunohistochemical and ultrastructural changes in the brain in probable adult glycogenosis type IV: adult polyglucosan body disease.</title>
            <link>http://www.medworm.com/index.php?rid=1844147&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18825592%26dopt%3DAbstract</link>
            <description>Authors: Wierzba-Bobrowicz T, Lewandowska E, Stepie&amp;#x144; T, Modzelewska J
    Glycogenosis type IV is caused by a defi ciency of glycogen branching enzyme (alpha-1,4 glucan 6-transglucosylase). Adult polyglucosan body disease (APBD) may represent a neuropathological hallmark of the adult form of this storage disease of the central nervous system. We analysed a case of a 45-year-old unconscious woman who died three days after admission to the hospital. Neuropathological examination revealed massive accumulation of polyglucosan bodies (PBs) in the cortex and white matter of the whole brain. PBs were located in the processes of neurons, astrocytes and microglial cells. The storage material in the cytoplasm of neurons and glial cells was visible as fi ne granules. Ultrastructurally, PBs cons...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1844147</comments>
            <pubDate>Thu, 02 Oct 2008 11:39:27 +0100</pubDate>
            <guid isPermaLink="false">1844147</guid>        </item>
        <item>
            <title>Neuroblastoma and opsoclonus-myoclonus-ataxia syndrome - clinical and pathological characteristics.</title>
            <link>http://www.medworm.com/index.php?rid=1844146&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18825593%26dopt%3DAbstract</link>
            <description>Conclusion: In some patients the onset of OMA is related to vaccination or infection. Children with OMA and neuroblastoma despite a good oncological prognosis often present permanent neurological and developmental defi cits. The infl ammatory infi ltrations within the tumours are combined, with predominant participation of cytotoxic cells.
    PMID: 18825593 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1844146</comments>
            <pubDate>Thu, 02 Oct 2008 11:39:27 +0100</pubDate>
            <guid isPermaLink="false">1844146</guid>        </item>
        <item>
            <title>Asymptomatic and symptomatic glial cysts of the pineal gland.</title>
            <link>http://www.medworm.com/index.php?rid=1844145&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18825594%26dopt%3DAbstract</link>
            <description>Authors: Taraszewska A, Matyja E, Koszewski W, Zaczy&amp;#x144;ski A, Bardadin K, Czernicki Z
    Glial cysts of the pineal gland are benign and mostly asymptomatic incidental lesions found in the brain MRI or at autopsy examinations. In rare cases pineal cysts become symptomatic and require surgical intervention. Symptomatic glial cysts may be clinically and radiologically indistinguishable from cystic neoplasms of the pineal region; therefore, histopathological diagnosis is critical for further prognosis and therapy in operated patients. In this paper we present detailed histopathological characteristics of symptomatic glial cysts in 2 surgical cases and of asymptomatic cysts of the pineal gland found at random in 3 autopsy cases. Both surgical patients, a 19-year-old girl and a 17-year-old ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1844145</comments>
            <pubDate>Thu, 02 Oct 2008 11:39:27 +0100</pubDate>
            <guid isPermaLink="false">1844145</guid>        </item>
        <item>
            <title>Nuclear architecture remodelling in cardiomyocytes with lamin A deficiency.</title>
            <link>http://www.medworm.com/index.php?rid=1844144&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18825595%26dopt%3DAbstract</link>
            <description>Authors: Fidzia&amp;#x144;ska A, Walczak E, Glinka Z, Religa G
    We analysed the architecture of cardiomyocyte nuclei lacking lamin A activity in three patients with dilated cardiomyopathy. The diagnosis was established on the basis of clinical and electrophysiological examinations, chest radiography and electrocardiography. An ultrastructural study of aff ected cardiomyocytes showed dramatic alterations in nuclear distribution and organization aff ecting nuclear shape, lamina structure, chromatin and nuclear interior organization. The most specifi c hallmark of nuclei with lamin A defi ciency was the reorganization of the nuclear interior, the appearance of a various number of mitochondria within the nuclear matrix, and focal or total lack of nuclear membrane.
    PMID: 18825595 [PubMed - i...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1844144</comments>
            <pubDate>Thu, 02 Oct 2008 11:39:27 +0100</pubDate>
            <guid isPermaLink="false">1844144</guid>        </item>
        <item>
            <title>Efficacy of remote ischaemic preconditioning for spinal cord protection against ischaemic injury: association with heat shock protein expression.</title>
            <link>http://www.medworm.com/index.php?rid=1844143&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18825596%26dopt%3DAbstract</link>
            <description>Conclusion: Our results show that production of transient remote ischaemia preconditioning in the lower extremities reduces damage in the spinal cord secondary to ischaemia probably by the increase of HSP.
    PMID: 18825596 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1844143</comments>
            <pubDate>Thu, 02 Oct 2008 11:39:27 +0100</pubDate>
            <guid isPermaLink="false">1844143</guid>        </item>
        <item>
            <title>Apoptotic death of cortical neurons following surgical brain injury.</title>
            <link>http://www.medworm.com/index.php?rid=1844142&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18825597%26dopt%3DAbstract</link>
            <description>Authors: Sulejczak D, Grieb P, Walski M, Frontczak-Baniewicz M
    Unilateral surgical brain injury of the rat is a model of surgery-related brain damage of humans. Our preliminary experiments showed two phenomena within the damaged cortical region of rat brain. Those were: degeneration and death of neurons and massive gliosis. In the present study we aimed to investigate the mechanisms of neuronal death following brain injury and to characterize responses of glial cells to the damage. We analyzed the morphological changes and alterations of immunochemical profile of cells localized in the brain areas adjacent to the lesion. Our data show the massive neuronal death following the lesion. Neurons undergo necrosis and apoptosis, but on the 4th day following the operation apoptosis prevails. A...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1844142</comments>
            <pubDate>Thu, 02 Oct 2008 11:39:27 +0100</pubDate>
            <guid isPermaLink="false">1844142</guid>        </item>
        <item>
            <title>Giant cell ependymoma of the spinal cord and fourth ventricle coexisting with syringomyelia.</title>
            <link>http://www.medworm.com/index.php?rid=1844141&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18825598%26dopt%3DAbstract</link>
            <description>This report presents a case of widespread intramedullary giant cell ependymoma arising from the central canal of the C4 segment of the spinal cord in a 28-year-old man admitted to hospital with tetraplegia and signs of increased intracranial pressure, eight months after surgical spinal cervical decompression without tetraplegia improvement. Magnetic resonance imaging and autopsy revealed a tumour extending from segment C3/C4 of the spinal cord to the lower half of the fourth ventricle with coexisting syringomyelia. This slow-growing ependymoma of low-grade malignancy exhibited unusual morphology as well as degenerative and ischaemic changes. All intramedullary and ventricular tumour segments featured coexistence of two forms of neoplastic cell, classic ependymomal and pleomorphic multinucl...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1844141</comments>
            <pubDate>Thu, 02 Oct 2008 11:39:27 +0100</pubDate>
            <guid isPermaLink="false">1844141</guid>        </item>
        <item>
            <title>Brain and cerebellar hemidysplasia in a case with ipsilateral body dysplasia and suspicion of CHILD syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=1844140&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18825599%26dopt%3DAbstract</link>
            <description>Authors: Schmidt-Sidor B, Obersztyn E, Szyma&amp;#x144;ska K, Wychowski J, Mierzewska H, Wierzba-Bobrowicz T, Stepie&amp;#x144; T
    CHILD syndrome is an acronym for Congenital Hemidysplasia with Ichthyosiform nevus and Limb Defects. This is an X-linked dominant disorder affecting females with early lethality in hemizygous males. The clinical features are congenital hemidysplasia with ichthyosiform erythroderma and ipsilateral hypoplasia of limbs and other parts of the skeleton as well as defects of the brain, heart, kidney and lung. CHILD syndrome is caused by mutations in the NSDHL (steroid dehydrogenase-like protein) gene at Xq28, which affects cholesterol biosynthesis. A female premature newborn with left side body hemidysplasia and ipsilateral defects of the skin, visceral organs and brain i...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1844140</comments>
            <pubDate>Thu, 02 Oct 2008 11:39:27 +0100</pubDate>
            <guid isPermaLink="false">1844140</guid>        </item>
        <item>
            <title>Subependymal plaques in scrapie-affected hamster brains--why are they so different from compact kuru plaques?</title>
            <link>http://www.medworm.com/index.php?rid=1634515&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18368625%26dopt%3DAbstract</link>
            <description>We report here routine thin-section and immunogold electron microscopic studies on diffuse plaques in scrapie-affected hamster brains. These plaques were not discernible by routine HE staining. Ultrastructurally, plaques were recognized as areas of low electron density containing haphazardly-oriented fibrils, but not as stellate compact structures typical of mouse scrapie models; hence we labelled them &quot;loose plaques&quot;. Following immunohistochemistry at the electron microscopy level, fibrils within plaques were heavily decorated with PrP-conjugated gold particles. Loose plaques were located beneath the basal border of the ependymal cells and around blood vessels in the adjacent subependymal neuropil. When dystrophic neurites containing electron-dense inclusion bodies, some of them autophagi...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1634515</comments>
            <pubDate>Fri, 18 Jul 2008 08:59:37 +0100</pubDate>
            <guid isPermaLink="false">1634515</guid>        </item>
        <item>
            <title>Ultrastructure of the blood-brain barrier of the gyrus hippocampal cortex in an experimental model of febrile seizures and with the use of a new generation antiepileptic drug--topiramate.</title>
            <link>http://www.medworm.com/index.php?rid=1634514&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18368628%26dopt%3DAbstract</link>
            <description>Authors: &amp;#x141;otowska JM, Sobaniec-&amp;#x141;otowska ME, Sendrowski K, Sobaniec W, Artemowicz B
    The ultrastructure of the blood-brain barrier (BBB) of the gyrus hippocampal cortex in an experimental model of febrile seizures in rats and the effect of a new generation antiepileptic drug, topiramate, on the morphological status of this barrier were investigated. Advanced changes indicating a substantial increase in BBB permeability were observed in the animals with induced febrile seizures (FS), with approximately 2/3 of capillaries and perivascular astroglial processes being affected. Almost total occlusion of the capillary lumen was frequently seen, caused by damaged endothelial lining and by external pressure from markedly swollen perivascular astrocytic processes. Mitochondrial change...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1634514</comments>
            <pubDate>Fri, 18 Jul 2008 08:59:37 +0100</pubDate>
            <guid isPermaLink="false">1634514</guid>        </item>
        <item>
            <title>Prion diseases: a riddle wrapped in a mystery inside an enigma.</title>
            <link>http://www.medworm.com/index.php?rid=1559977&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18587704%26dopt%3DAbstract</link>
            <description>Authors: Liberski PP
    It is now widely accepted that many structurally diverse proteins can misfold and cause so-called &quot;conformational diseases&quot;, including the most common neurodegenerations, Alzheimer's disease and Parkinson's disease. The conversion of largely a-helical or random coil proteins into cross-b-pleated sheet conformations that form first oligomers and then fibrils underlies these disorders. However, this a- to b-structure transition seems to be a generic propensity of all globular proteins, not only those involved in neurodegenerations, not to mention &quot;prion diseases&quot;. Metaphorically, all these neurodegenerations are &quot;infectious&quot; in the sense that misfolded b-sheeted conformers are formed in a nucleation process in which preformed metastable oligomer acts as a seed (a nuc...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1559977</comments>
            <pubDate>Wed, 02 Jul 2008 08:08:28 +0100</pubDate>
            <guid isPermaLink="false">1559977</guid>        </item>
        <item>
            <title>Implication of active Erk in the classic type of human medulloblastoma.</title>
            <link>http://www.medworm.com/index.php?rid=1559976&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18587705%26dopt%3DAbstract</link>
            <description>Authors: Wlodarski PK, Boszczyk A, Grajkowska W, Roszkowski M, Jozwiak J
    Molecular pathways underlying medulloblastoma (MB), the most common malignant brain tumour in children, are still under scrutiny. The mammalian target of the rapamycin (mTOR) pathway is one of the kinases that was recently found to be implicated in a number of human tumours. Also in the case of MB it is suspected that mTOR dysregulation may play an important role in pathogenesis. Active mTOR leads to translation of several proteins, some of which affect cellular proliferation. On the other hand, Akt/PKB (protein kinase B) and Erk (extracellular signal-regulated kinase, also called mitogen-activated protein kinase, MAPK) are two protein kinases whose hyperactivity leads to a number of downstream effects, including ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1559976</comments>
            <pubDate>Wed, 02 Jul 2008 08:08:28 +0100</pubDate>
            <guid isPermaLink="false">1559976</guid>        </item>
        <item>
            <title>Pathology of skeletal muscle cells in adult-onset glycogenosis type II (Pompe disease): ultrastructural study.</title>
            <link>http://www.medworm.com/index.php?rid=1559975&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18587706%26dopt%3DAbstract</link>
            <description>Authors: Lewandowska E, Wierzba-Bobrowicz T, Rola R, Modzelewska J, Stepie&amp;#x144; T, Lugowska A, Pasennik E, Ryglewicz D
    Ultrastructural analysis of the skeletal muscle in adult-onset Pompe disease revealed lysosomal and cytoplasmic glycogen storage, autophagic vacuoles and abnormal mitochondria. Significant glycogen accumulation within lysosomes causes their rupture and release of glycogen into the cytoplasm. Excess cytoplasmic glycogen could lead to damage of the structure of muscle cells including myofibrils. In consequence, parts of the sarcoplasm and damaged organelles were sequestered within membrane-limited vacuoles. We suppose that massive accumulation of autophagic vacuoles results from the inability of destroyed lysosomes to fuse with vacuoles. Autophagic vacuoles may be a pr...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1559975</comments>
            <pubDate>Wed, 02 Jul 2008 08:08:28 +0100</pubDate>
            <guid isPermaLink="false">1559975</guid>        </item>
        <item>
            <title>Peripheral blood cell immunomarkers in the course of methylprednisolone treatment of multiple sclerosis relapses.</title>
            <link>http://www.medworm.com/index.php?rid=1559974&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18587707%26dopt%3DAbstract</link>
            <description>Authors: Micha&amp;#x142;owska-Wender G, Wender M
    Intravenous methylprednisolone (MP) is the standard method in the treatment of acute relapses in multiple sclerosis (MS) and is believed to affect various immunological processes involved in the pathology of MS, including apoptosis and phagocytosis. Peripheral blood was obtained from 50 patients, with clinically definite MS, fulfilling the revised criteria of McDonald, a day before, after 5 days of MP treatment, and two weeks after conclusion of the treatment. Intravenous administration of 1.0 gamma daily of MP was used to treat the new relapses of the disease. The control group comprised 20 healthy blood donors. The subset of lymphocytes CD3, CD4, CD8, CD16, CD19, CD95 /CD3 and CD95/ CD19 was studied using monoclonal antibodies by flow cyt...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1559974</comments>
            <pubDate>Wed, 02 Jul 2008 08:08:28 +0100</pubDate>
            <guid isPermaLink="false">1559974</guid>        </item>
        <item>
            <title>CDP-choline protects motor neurons against apoptotic changes in a model of chronic glutamate excitotoxicity in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=1559973&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18587708%26dopt%3DAbstract</link>
            <description>Authors: Matyja E, Taraszewska A, Naga&amp;#x144;ska E, Grieb P, Rafa&amp;#x142;owska J
    Cytidine-5-diphosphocholine (CDP-choline, citicoline) is an endogenous nucleoside involved in generation of phospholipids, membrane formation and its repair. It demonstrates beneficial effects in certain central nervous system injury models, including cerebral ischaemia, neurodegenerative disorders and spinal cord injury. Defective neuronal and/or glial glutamate transport is claimed to contribute to progressive loss of motor neurons (MNs) in amyotrophic lateral sclerosis (ALS). Our previous ultrastructural studies, performed on an organotypic tissue culture model of chronic glutamate excitotoxicity, documented a subset of various modes of MN death including necrotic, apoptotic and autophagocytic cell injur...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1559973</comments>
            <pubDate>Wed, 02 Jul 2008 08:08:28 +0100</pubDate>
            <guid isPermaLink="false">1559973</guid>        </item>
        <item>
            <title>Severe hypoxia and multiple infarctions resembling Creutzfeldt-Jakob disease.</title>
            <link>http://www.medworm.com/index.php?rid=1559972&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18587709%26dopt%3DAbstract</link>
            <description>Authors: Mittelbronn M, Capper D, Bader B, Schittenhelm J, Haybaeck J, Weber P, Meyermann R, Kretzschmar HA, Wietholter H
    Although neuropathological examination is still required for the definite diagnosis of Creutzfeldt-Jakob disease (CJD), specialised clinical assessment predicts probable CJD. Here we present a 73-year-old female patient presenting with rapid cognitive decline, visual, acoustic and cerebellar disturbances, ataxia and EEG changes compatible with early CJD stages. MRI revealed hyperintensities within the thalami, hypothalami, corpora mammillaria, the tectum and the cortex. Initial neuropathological examination showed severe cortical and subcortical spongiosis. However, both immunohistochemistry and Western blotting showed no pathological prion protein. Finally, small i...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1559972</comments>
            <pubDate>Wed, 02 Jul 2008 08:08:28 +0100</pubDate>
            <guid isPermaLink="false">1559972</guid>        </item>
        <item>
            <title>Necrobiosis lipoidica and cutaneous anaesthesia: immunohistochemical study of neural fibres.</title>
            <link>http://www.medworm.com/index.php?rid=1559971&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18587710%26dopt%3DAbstract</link>
            <description>Conclusions: The absence of nerve fibres in the central areas of the necrotic foci of NL might explain the anaesthesia which is present in many patients with that disease.
    PMID: 18587710 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1559971</comments>
            <pubDate>Wed, 02 Jul 2008 08:08:28 +0100</pubDate>
            <guid isPermaLink="false">1559971</guid>        </item>
        <item>
            <title>Papillary glioneuronal tumour of the precentral gyrus.</title>
            <link>http://www.medworm.com/index.php?rid=1559970&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18587711%26dopt%3DAbstract</link>
            <description>Authors: Izycka-Swieszewska E, Majewska H, Szurowska E, Mazurkiewicz-Be&amp;#x142;dzi&amp;#x144;ska M, Drozy&amp;#x144;ska E
    The article describes a case of a 15-year old boy after a head contusion with a five-month history of headaches and two seizure episodes. MR imaging revealed a partly solid and partly cystic cortical-subcortical tumour within the precentral gyrus with post-contrast enhancement. The patient underwent gross total resection of the lesion. Histologically the neoplasm was composed of pseudopapillary gliovascular structures surrounded by solid glioneuronal tumour areas. The expression of GFAP and nestin characterized the central parts of the tumour. Moreover the immunolabelling for synaptophysin, neurofilaments, Olig2 and NCAM was present in the peripheral part of the lesion. The ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1559970</comments>
            <pubDate>Wed, 02 Jul 2008 08:08:28 +0100</pubDate>
            <guid isPermaLink="false">1559970</guid>        </item>
        <item>
            <title>Cell death and autophagy in prion diseases (transmissible spongiform encephalopathies).</title>
            <link>http://www.medworm.com/index.php?rid=1334366&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18368623%26dopt%3DAbstract</link>
            <description>Authors: Liberski PP, Brown DR, Sikorska B, Caughey B, Brown P
    Neuronal autophagy, like apoptosis, is one of the mechanisms of programmed cell death. In this review, we summarize current information about autophagy in naturally occurring and experimentally induced scrapie, Creutzfeldt-Jakob disease and Gerstmann-Str&amp;#xE4;ussler-Scheinker syndrome against the broad background of neural degenerations in transmissible spongiform encephalopathies (TSEs). Typically a sequence of events is observed: from a part of the neuronal cytoplasm sequestrated by concentric arrays of double membranes (phagophores); through the enclosure of the cytoplasm and membrane proliferation; to a final transformation of the large area of the cytoplasm into a collection of autophagic vacuoles of different sizes. T...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1334366</comments>
            <pubDate>Fri, 28 Mar 2008 21:30:27 +0100</pubDate>
            <guid isPermaLink="false">1334366</guid>        </item>
        <item>
            <title>Clustering and periodicity of neurofibrillary tangles in the upper and lower cortical laminae in Alzheimer's disease.</title>
            <link>http://www.medworm.com/index.php?rid=1334365&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18368624%26dopt%3DAbstract</link>
            <description>Authors: Armstrong RA
    In Alzheimer's disease (AD), neurofibrillary tangles (NFT) occur within neurons in both the upper and lower cortical laminae. Using a statistical method that estimates the size and spacing of NFT clusters along the cortex parallel to the pia mater, two hypotheses were tested: 1) that the cluster size and distribution of the NFT in gyri of the temporal lobe reflect degeneration of the feedforward (FF) and feedback (FB) cortico-cortical pathways, and 2) that there is a spatial relationship between the clusters of NFT in the upper and lower laminae. In 16 temporal lobe gyri from 10 cases of sporadic AD, NFT were present in both the upper and lower laminae in 11/16 (69%) gyri and in either the upper or lower laminae in 5/16 (31%) gyri. Clustering of the NFT was observ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1334365</comments>
            <pubDate>Fri, 28 Mar 2008 21:30:27 +0100</pubDate>
            <guid isPermaLink="false">1334365</guid>        </item>
        <item>
            <title>Subependymal plaques in scrapie-affected hamster brains - why are they so different from compact kuru plaques?</title>
            <link>http://www.medworm.com/index.php?rid=1334364&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18368625%26dopt%3DAbstract</link>
            <description>We report here routine thin-section and immunogold electron microscopic studies on diffuse plaques in scrapie-affected hamster brains. These plaques were not discernible by routine HE staining. Ultrastructurally, plaques were recognized as areas of low electron density containing haphazardly-oriented fibrils, but not as stellate compact structures typical of mouse scrapie models; hence we labelled them &quot;loose plaques&quot;. Following immunohistochemistry at the electron microscopy level, fibrils within plaques were heavily decorated with PrP-conjugated gold particles. Loose plaques were located beneath the basal border of the ependymal cells and around blood vessels in the adjacent subependymal neuropil. When dystrophic neurites containing electron-dense inclusion bodies, some of them autophagi...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1334364</comments>
            <pubDate>Fri, 28 Mar 2008 21:30:27 +0100</pubDate>
            <guid isPermaLink="false">1334364</guid>        </item>
        <item>
            <title>Expression of tuberin and hamartin in tuberous sclerosis complex-associated and sporadic cortical dysplasia of Taylor's balloon cell type.</title>
            <link>http://www.medworm.com/index.php?rid=1334363&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18368626%26dopt%3DAbstract</link>
            <description>In conclusion, loss of TSC1 and TSC2 products expression in balloon cells of both cortical dysplasia type IIB in TSC-related and sporadic patients suggests that FCD type IIB may represent the focal form of TSC.
    PMID: 18368626 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1334363</comments>
            <pubDate>Fri, 28 Mar 2008 21:30:27 +0100</pubDate>
            <guid isPermaLink="false">1334363</guid>        </item>
        <item>
            <title>The immature endothelial cell in human glioma. Ultrastructural features of blood capillary vessels.</title>
            <link>http://www.medworm.com/index.php?rid=1334362&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18368627%26dopt%3DAbstract</link>
            <description>Authors: Frontczak-Baniewicz M, Czajkowska D, Andrychowski J, Walski M
    New vessel formation is a prerequisite for the growth of a tumour mass. Growing evidence suggests that endothelial progenitor cells circulate in the blood and participate in that process. The purpose of the present study was ultrastructural and electron microscopic immunocytochemical examination of capillary blood vessels in human glioma. The results showed striking morphological changes in these vessels. Our observations indicate that tumours build vessels by cooption of pre-existing vasculature and de novo recruitment of endothelial progenitor cells. Immature endothelial cells characterized by fibrils in the cytoplasm and Flk-1 positive immunoreactivity were observed as small clusters or luminally localized indivi...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1334362</comments>
            <pubDate>Fri, 28 Mar 2008 21:30:27 +0100</pubDate>
            <guid isPermaLink="false">1334362</guid>        </item>
        <item>
            <title>Ultrastructure of the blood-brain barrier of the gyrus hippocampal cortex in an experimental model of febrile seizures and with the use of a new generation antiepileptic drug - topiramate.</title>
            <link>http://www.medworm.com/index.php?rid=1334361&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18368628%26dopt%3DAbstract</link>
            <description>Authors: Lotowska JM, Sobaniec-&amp;#x141;otowska ME, Sendrowski K, Sobaniec W, Artemowicz B
    The ultrastructure of the blood-brain barrier (BBB) of the gyrus hippocampal cortex in an experimental model of febrile seizures in rats and the effect of a new generation antiepileptic drug, topiramate, on the morphological status of this barrier were investigated. Advanced changes indicating a substantial increase in BBB permeability were observed in the animals with induced febrile seizures (FS), with approximately 2/3 of capillaries and perivascular astroglial processes being affected. Almost total occlusion of the capillary lumen was frequently seen, caused by damaged endothelial lining and by external pressure from markedly swollen perivascular astrocytic processes. Mitochondrial changes pred...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1334361</comments>
            <pubDate>Fri, 28 Mar 2008 21:30:27 +0100</pubDate>
            <guid isPermaLink="false">1334361</guid>        </item>
        <item>
            <title>Neuroprotective effects of nicotinamide and 1-methylnicotinamide in acute excitotoxicity in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=1334360&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18368629%26dopt%3DAbstract</link>
            <description>Authors: S&amp;#x142;omka M, Ziemi&amp;#x144;ska E, Sali&amp;#x144;ska E, Lazarewicz JW
    Nicotinamide (NAM), an important cofactor in many metabolic pathways, exhibits at high doses neuroprotective abilities of an unclear mechanism. In the present study we evaluated the unknown protective capability of its immediate metabolite 1-methylnicotinamide (MNA) in comparison to NAM in primary cultures of rat cerebellar granule cells (CGC) submitted to acute excitotoxicity. Neurotoxicity was evaluated with propidium iodide staining 24 h after 30 min exposure to glutamate (GLU) and NMDA. NAM and MNA reduced NMDA toxicity only at 25 mM concentration, while neurotoxicity of 0.5 mM GLU was slightly diminished only by 25 mM NAM. Both compounds at 25 mM reduced GLU-induced 45Ca uptake and dose-dependently inhibit...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1334360</comments>
            <pubDate>Fri, 28 Mar 2008 21:30:27 +0100</pubDate>
            <guid isPermaLink="false">1334360</guid>        </item>
        <item>
            <title>Clinical, biochemical, neuropathological and molecular findings of the first Polish case of adenylosuccinase deficiency.</title>
            <link>http://www.medworm.com/index.php?rid=1334359&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18368630%26dopt%3DAbstract</link>
            <description>We present clinical, biochemical and neuropathological findings of a child affected by a severe form of ADSL deficiency. She had progressive neurological symptoms that started immediately after birth and died at 2.5 months of age. Macroscopically the brain showed signs of moderate atrophy. Histological examination of all grey matter structures showed widespread damage of neurons accompanied by microspongiosis of neuropile. Cerebral white matter showed lack of myelination in the centrum semiovale and diffuse spongiosis of neuropile. Myelination appropriate for the age was visible in posterior limb of internal capsule, in striatum, thalamus and in brain stem structures but diffuse destruction of myelin sheets was seen with severe marked astroglial reaction with signs of destruction of the ce...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1334359</comments>
            <pubDate>Fri, 28 Mar 2008 21:30:27 +0100</pubDate>
            <guid isPermaLink="false">1334359</guid>        </item>
        <item>
            <title>Substance P and its receptors - a potential target for novel medicines in malignant brain tumour therapies (mini-review).</title>
            <link>http://www.medworm.com/index.php?rid=869268&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17849359%26dopt%3DAbstract</link>
            <description>Authors: Lazarczyk M, Matyja E, Lipkowski A
    Tachykinins are excitatory neuropeptides synthesised in neuronal and glial cells of the human central and peripheral nervous system. They participate in both physiological and certain pathological conditions, i.e. synaptic transmission, nociception and neuroimmunomodulation. Tachykinins act as excitatory neurotransmitters and/or neuromodulators and induce DNA synthesis leading to stimulation of cell division and proliferation. Their biological responses are triggered via the well-established tachykinin receptors NK1, NK2 and NK3 that belong to the G protein-coupled receptor family (GPCRs). Substance P is the most important member of the tachykinin family that constitutes the major endogenous ligand for the NK1 receptor type. The presence of f...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=869268</comments>
            <pubDate>Fri, 14 Sep 2007 01:20:03 +0100</pubDate>
            <guid isPermaLink="false">869268</guid>        </item>
        <item>
            <title>Size frequency distributions of abnormal protein deposits in Alzheimer's disease and variant Creutzfeldt-Jakob disease.</title>
            <link>http://www.medworm.com/index.php?rid=869267&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17849360%26dopt%3DAbstract</link>
            <description>Authors: Armstrong RA
    The size frequency distributions of beta-amyloid (Abeta) and prion protein (PrPsc) deposits were studied in Alzheimer's disease (AD) and the variant form of Creutzfeldt-Jakob disease (vCJD) respectively. All size distributions were unimodal and positively skewed. Abeta deposits reached a greater maximum size and their distributions were significantly less skewed than the PrPsc deposits. All distributions were approximately log-normal in shape but only the diffuse PrPsc deposits did not deviate significantly from a log-normal model. There were fewer larger classic Abeta deposits than predicted and the florid PrPsc deposits occupied a more restricted size range than predicted by a log-normal model. Hence, Abeta deposits exhibit greater growth than the corresponding ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=869267</comments>
            <pubDate>Fri, 14 Sep 2007 01:20:03 +0100</pubDate>
            <guid isPermaLink="false">869267</guid>        </item>
        <item>
            <title>Morphological analysis of vascular density in ependymomas.</title>
            <link>http://www.medworm.com/index.php?rid=869266&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17849361%26dopt%3DAbstract</link>
            <description>Authors: Duda-Szyma&amp;#x144;ska J, Papierz W
    Ependymomas generally show slow growth rate and are associated with a long clinical history. In some cases however the biology of these tumours is considered to be unpredictable on the basis of histologic criteria. Density of microvessels was shown to serve in various malignant neoplasms as a prognostic factor that correlates with increased risk of metastasis and overall free survival. Some data suggest that density of blood vessels may be of prognostic value also in patients with neuroepithelial tumours. The aim of this study was to determinate whether that observation can be applied to ependymomas. The materials included 51 ependymomas G2 and G3 according to the WHO classification. Vasculature was visualized immunohistochemically in paraffin...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=869266</comments>
            <pubDate>Fri, 14 Sep 2007 01:20:03 +0100</pubDate>
            <guid isPermaLink="false">869266</guid>        </item>
        <item>
            <title>Advanced reactive astrogliosis associated with hemangioblastoma versus astroglial-vascular neoplasm (&quot;angioglioma&quot;).</title>
            <link>http://www.medworm.com/index.php?rid=869265&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17849362%26dopt%3DAbstract</link>
            <description>Advanced reactive astrogliosis associated with hemangioblastoma versus astroglial-vascular neoplasm (&quot;angioglioma&quot;).
    Folia Neuropathol. 2007;45(3):120-5
    Authors: Matyja E, Grajkowska W, Taraszewska A, Marchel A, Bojarski P, Nauman P
    Hemangioblastomas of the central nervous system are often accompanied by a cyst exhibiting an extensive astroglial reaction. The cyst's wall might be composed of various astroglial elements including reactive pilocytic or gemistocytic and hypertrophic astrocytes. The small tissue samples composed of compact gliotic tissue are sometimes nonrepresentative for primary hemangioblastoma tumour and might be confused with both pilocytic and diffuse infiltrative astrocytoma. Moreover, vascular anomalies of hemangioblastoma-like pattern could be combined wit...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=869265</comments>
            <pubDate>Fri, 14 Sep 2007 01:20:03 +0100</pubDate>
            <guid isPermaLink="false">869265</guid>        </item>
        <item>
            <title>Estimation of prognostic value of CD44 expression in neuroblastic tumours in children.</title>
            <link>http://www.medworm.com/index.php?rid=869264&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17849363%26dopt%3DAbstract</link>
            <description>Authors: Taran K, Kobos J, Sitkiewicz A, Sporny S
    Adversities observed in treatment of children with neoplastic disease based on new diagnostic markers and new prognostic factors. Both of them allow prognosis to be established for a single patient. The aim of our study was to examine the expression of CD44 adhesion molecule in different histologic types in a neuroblastoma group of tumours (35 cases of neuroblastoma from current files and archives) and to estimate the possible prognostic value of CD44 expression by comparison with widely accepted prognostic markers and chosen histoclinical parameters (9 cases of neuroblastoma with follow-up data). We did not find a statistically significant correlation between CD44 expression and histologic type of the tumour. However, we found that all...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=869264</comments>
            <pubDate>Fri, 14 Sep 2007 01:20:03 +0100</pubDate>
            <guid isPermaLink="false">869264</guid>        </item>
        <item>
            <title>Abnormal chaperone-mediated autophagy (CMA).</title>
            <link>http://www.medworm.com/index.php?rid=869263&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17849364%26dopt%3DAbstract</link>
            <description>Authors: Fidzia&amp;#x144;ska A, Walczak E, Walski M
    Ultrastructural analysis of the cardiomyocyte structure in Danon disease reveals dramatic accumulation of abnormal late autophagic vacuoles (AVd) suggestive of primary lysosomal defect. Moreover, the accumulation of AVd in cardiomyocytes is consistent with a decreased rate of autophagic to lysosomal trafficking. These results suggest that the loss of the LAMP-2 protein strongly inhibits uptake of proteins into lysosomes for degeneration. The significant reduction of chaperone-mediated autophagy (CMA) activity in the affected cardiomyocytes induces a dramatic increase in the number and size of AVd and a severe reduction of myocardial contractility.
    PMID: 17849364 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=869263</comments>
            <pubDate>Fri, 14 Sep 2007 01:20:03 +0100</pubDate>
            <guid isPermaLink="false">869263</guid>        </item>
        <item>
            <title>Glioneuronal-mesenchymal tumour with malignant transformation.</title>
            <link>http://www.medworm.com/index.php?rid=869262&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17849365%26dopt%3DAbstract</link>
            <description>We report a case of a 10-year-old girl with a tumour of the right temporoparietal region of the brain. The tumour consisted of three morphologically distinct portions: a well-differentiated one containing a mixture of a ganglioglioma with adipocytic-like cells and focal chondroid metaplasia, a separate island with neurocytic differentiation, and the malignant one, which exhibited an organoid pattern (trabecular and festooned) of primitive neuroectodemal tumour (PNET). We hypothesize that the latter component originated from the multicomponental glioneuronal tumour with mesenchymal differentiation and thus that lesion constituted an unusual example of malignant transformation of low-grade glioneuronal neoplasm.
    PMID: 17849365 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=869262</comments>
            <pubDate>Fri, 14 Sep 2007 01:20:03 +0100</pubDate>
            <guid isPermaLink="false">869262</guid>        </item>
        <item>
            <title>Primary pituitary lymphoma.</title>
            <link>http://www.medworm.com/index.php?rid=869261&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17849366%26dopt%3DAbstract</link>
            <description>We present a 37-year-old male with primary pituitary lymphoma treated in our department. The patient, who had had no previous illnesses, was admitted to the hospital because of bilateral blurred vision. Findings on physical examination were normal except for temporal parts of field of vision deficit. No abnormalities were found in his bilateral ocular movement, facial sensory function or motor function. His blood count and biochemical profile were normal. Basic hormonal studies revealed no symptoms of panhypopituitarism. MRI demonstrated a large intrasellar mass with supra- and parasellar extension. MRS revealed decrease in NAA/tCr proportion and increase in Cho/NAA and Cho/tCr proportions. Endoscopic surgery was performed using the transsphenoidal approach. Histopathological examination d...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=869261</comments>
            <pubDate>Fri, 14 Sep 2007 01:20:03 +0100</pubDate>
            <guid isPermaLink="false">869261</guid>        </item>
        <item>
            <title>Fatal stroke in a young cocaine drug addict: chemical hair analysis and cervical artery examination twenty months after death.</title>
            <link>http://www.medworm.com/index.php?rid=869260&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17849367%26dopt%3DAbstract</link>
            <description>In conclusion, when a vascular accident is suspected or has to be demonstrated, we suggest performing comparative histological examinations of selected artery samples, even several months after death.
    PMID: 17849367 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=869260</comments>
            <pubDate>Fri, 14 Sep 2007 01:20:03 +0100</pubDate>
            <guid isPermaLink="false">869260</guid>        </item>
        <item>
            <title>Nuclear architecture remodelling in envelopathies.</title>
            <link>http://www.medworm.com/index.php?rid=701866&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17594594%26dopt%3DAbstract</link>
            <description>Authors: Fidziańska A, Glinka Z
    We performed ultrastructural studies on nuclear abnormalities in muscle from 8 patients with X-linked and autosomal dominant form of Emery-Dreifuss muscular dystrophy (EDMD) and one case with progeroid syndrome. The diagnosis was based on clinical and molecular findings. We detected various degrees of nuclear architecture remodelling ranging from misshapen shape, nuclear disintegration, nuclear chromatin condensation and decondensation, focal chromatin loss to complete nuclear fragmentation. The most interesting finding was the appearance of tubulofilamentous inclusions inside the nuclear matrix of X-linked EDMD patients. All these nuclear aberrations are considered to be structural indicators of nuclear dysfunction evoked by envelope protein deficiency...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=701866</comments>
            <pubDate>Thu, 28 Jun 2007 16:36:50 +0100</pubDate>
            <guid isPermaLink="false">701866</guid>        </item>
        <item>
            <title>Multi-minicore myopathy: a clinical and histopathological study of 17 cases.</title>
            <link>http://www.medworm.com/index.php?rid=701865&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17594595%26dopt%3DAbstract</link>
            <description>We report on clinical and pathomorphological features of 17 patients diagnosed with multi-minicore myopathy at our department. Clinically, axial and proximal muscle weakness was the predominant distinguishing feature. Dysmorphic features such as high-arched palate and chest deformities were frequent findings. Limitation in cervical spine mobility was found in 4 cases. Most of our cases were slowly progressive but three fatal cases also occurred. Multifocal lack of oxidative activity was found in 16/22 biopsies on LM. Examination on EM enabled the final diagnosis of MmD in all cases. It is of special interest that in 3 patients fulfilling the criteria of pure congenital fibre type disproportion and in 2 cases of centronuclear myopathy, the findings of ultrastructural examination led us to a...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=701865</comments>
            <pubDate>Thu, 28 Jun 2007 16:36:50 +0100</pubDate>
            <guid isPermaLink="false">701865</guid>        </item>
        <item>
            <title>Immunohistochemical identification of kynurenine aminotransferases in corpora amylacea in the human retina and optic nerve.</title>
            <link>http://www.medworm.com/index.php?rid=701864&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17594596%26dopt%3DAbstract</link>
            <description>Conclusions: Presence of kynurenine aminotransferases in CAm in the human retina and optic nerve suggest that both enzymes may be involved in mechanisms of retinal ageing and neurodegeneration leading to CAm formation.
    PMID: 17594596 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=701864</comments>
            <pubDate>Thu, 28 Jun 2007 16:36:50 +0100</pubDate>
            <guid isPermaLink="false">701864</guid>        </item>
        <item>
            <title>Non-functioning pituitary adenoma: immunohistochemical analysis of 85 cases.</title>
            <link>http://www.medworm.com/index.php?rid=701863&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17594597%26dopt%3DAbstract</link>
            <description>Authors: Mahta A, Haghpanah V, Lashkari A, Heshmat R, Larijani B, Tavangar SM
    Pituitary adenomas without clinically active hypersecretion are summarized under the term non-functioning pituitary adenoma (NFPA). Since there are no specific serum markers, the differential diagnosis and treatment imply special difficulties. By using immunohistochemical methods we will have new insight into the nature and pathogenesis of these tumours. Ki-67 is a nuclear antigen detected by the monoclonal antibody MIB-1 and its labelling index (LI) is considered a marker of normal and abnormal cell proliferation. The aim of this study was to investigate the possible role of immunohistochemistry and MIB1-LI determination in NFPAs to predict tumoural behaviour and better management. In this clinicopathologica...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=701863</comments>
            <pubDate>Thu, 28 Jun 2007 16:36:50 +0100</pubDate>
            <guid isPermaLink="false">701863</guid>        </item>
        <item>
            <title>Impact of cytokines on the pathomechanism of diabetic and alcoholic neuropathies.</title>
            <link>http://www.medworm.com/index.php?rid=701862&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17594598%26dopt%3DAbstract</link>
            <description>Authors: Michałowska-Wender G, Adamcewicz G, Wender M
    Diabetic and alcoholic neuropathies are heterogeneous groups with variable lesions of axons or myelin. Their pathogenesis is complex and involves multiple pathways. To elucidate the impact of immunological factors in development of these neuropathies the expression of some cytokines in serum was studied: tumour necrosis factor a (TNF-a), monocyte chemotactic protein-1 (MCP-1) and growth-regulated oncogene alpha (GRO-alpha; CXCL1). 29 patients with type 2 diabetes, 31 with chronic alcohol abuse and 20 healthy controls were included in the study. The type of neuropathy (involvement of axon or myelin) was evaluated by electrophysiological methods (EMG and nerve conduction velocity). The cytokine level was determined by ELISA method. F...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=701862</comments>
            <pubDate>Thu, 28 Jun 2007 16:36:50 +0100</pubDate>
            <guid isPermaLink="false">701862</guid>        </item>
        <item>
            <title>The influence of trkB deficiency on long-term outcome of peripheral nerve injury in mice.</title>
            <link>http://www.medworm.com/index.php?rid=701861&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17594599%26dopt%3DAbstract</link>
            <description>We examined the role of trkB in long-term functional and morphological outcome of peripheral nerve injury. The sciatic nerve was transected in wild-type and heterozygous trkB-deficient mice. The nerve was either left cut or immediately sewn up or the gap injury model was performed. The gap was provided with autologous or cross (obtained from other genetic group) graft. Sciatic nerve function as well as autotomy was assessed during 16-week follow-up. The long-term functional outcome of nerve cut or immediately rejoined did not differ between wild-type and trkB-deficient mice. Gap injury provided with nerve graft resulted in better functional outcome in trkB-deficient mice than wild-type animals. Sixteen weeks after the surgery, the animals were sacrificed and histological evaluations were p...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=701861</comments>
            <pubDate>Thu, 28 Jun 2007 16:36:50 +0100</pubDate>
            <guid isPermaLink="false">701861</guid>        </item>
        <item>
            <title>Rare C-6 vertebral involvement in a child with histiocytosis X: Case report.</title>
            <link>http://www.medworm.com/index.php?rid=701860&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17594600%26dopt%3DAbstract</link>
            <description>Authors: Salehpour F, Tubbs RS, Zarrintan S, Meshkini A, Hadidchi S, Pourfathi H, Azhough R, Fakhrjou A, Goodrich JT, Khaki AA
    The authors present a rare case of C-6 vertebral involvement in a 12-year-old boy with histiocytosis X. The patient presented with limitation in movements of neck and upper extremities. Computed tomography (CT) and magnetic resonance (MRI) imaging were used in the preoperative workup. Surgery was performed via an anterior cervical approach along with stabilization using a fibula strut graft and plate fixation. Pathological assessment showed infiltration of Langerhans cells accompanied by a mixture of many eosinophils, giant cells, neutrophils and foamy cells. The patient went on to make a full recovery with complete resolution of his motor weakness. In an exten...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=701860</comments>
            <pubDate>Thu, 28 Jun 2007 16:36:50 +0100</pubDate>
            <guid isPermaLink="false">701860</guid>        </item>
        <item>
            <title>Clinicopathological considerations on angiogenic potential in neuroblastoma Schwannian stroma - poor tumours.</title>
            <link>http://www.medworm.com/index.php?rid=482410&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17357004%26dopt%3DAbstract</link>
            <description>Authors: Izycka-Swieszewska E, Drozyńska E, Rzepko R, Dembowska B, Grajkowska W, Brozyna A, Perek D, Balcerska A, Jaśkiewicz K
    The aim of the study was to determine microscopic angiogenic parameters of neuroblastoma (NB) Schwannian stroma-poor tumours. Furthermore the associations between vascular parameters and clinicopathological features of tumours and basic prognostic factors were analysed. Examined tissue samples from 62 NB came from 39 untreated and 23 chemotherapy pretreated tumours. The clinicopathological data comprised: patients' age, gender, survival, tumour site and stage, tumour histology and MYCN status.The morphological analysis of the angiogenic potential concentrated on examination of vascular patterns - classical type or pathological angiogenesis with mural microvas...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=482410</comments>
            <pubDate>Mon, 19 Mar 2007 23:15:03 +0100</pubDate>
            <guid isPermaLink="false">482410</guid>        </item>
        <item>
            <title>Lectin binding pattern in meningiomas of various histological subtypes.</title>
            <link>http://www.medworm.com/index.php?rid=482409&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17357005%26dopt%3DAbstract</link>
            <description>Authors: Taraszewska A, Matyja E
    Altered tumour cell glycosylation in relation to cellular heterogeneity in human brain tumours remains relatively unexplored. It has been reported that meningiomas express variability in glycosylation properties; however only limited meningioma subtypes have been studied with lectins histochemistry. The aim of this study was to compare the binding pattern of biotinylated lectins in seven subtypes of histologically benign intracranial meningiomas (meningothelial, transitional, fibroblastic, psammomatous, secretory, microcystic and angiomatous types). The study was performed on biopsy material of 30 cases of meningiomas with different lectins: Peanut agglutinin (PNA), Soybean agglutinin (SBA), Dolichos biflorus agglutinin (DBA), Wheat germ agglutinin (WGA...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=482409</comments>
            <pubDate>Mon, 19 Mar 2007 23:15:03 +0100</pubDate>
            <guid isPermaLink="false">482409</guid>        </item>
        <item>
            <title>Granular cell meningioma. A case report.</title>
            <link>http://www.medworm.com/index.php?rid=482408&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17357006%26dopt%3DAbstract</link>
            <description>We describe a granular cell tumour developing in clear cell meningioma of the falx. Granular and clear cells showed immunoreactivity for vimentin, epithelial membrane antigen and progesterone receptors. This is the first case documenting arachnoid origin of neoplastic granular cells in meningioma.
    PMID: 17357006 [PubMed - as supplied by publisher] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=482408</comments>
            <pubDate>Mon, 19 Mar 2007 23:15:03 +0100</pubDate>
            <guid isPermaLink="false">482408</guid>        </item>
        <item>
            <title>Spinal accessory nerve meningioma in a paediatric patient: Case report.</title>
            <link>http://www.medworm.com/index.php?rid=482407&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17357007%26dopt%3DAbstract</link>
            <description>We present a case of a nine-year-old patient with neurofibromatosis type 2 who had radiologic evidence of spinal cord compression from an upper cervical/foramen magnum lesion. He was asymptomatic from this lesion, but it progressed in size. The tumor was resected and histologic investigation revealed frequent tight whorls and psammoma bodies consistent with meningioma. To the authors' knowledge, this is the first reported spinal accessory nerve meningioma in a pediatric patient.
    PMID: 17357007 [PubMed - as supplied by publisher] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=482407</comments>
            <pubDate>Mon, 19 Mar 2007 23:15:03 +0100</pubDate>
            <guid isPermaLink="false">482407</guid>        </item>
        <item>
            <title>Radiation-induced brachial plexus neuropathy - aetiopathogenesis, risk factors, differential diagnostics, symptoms and treatment.</title>
            <link>http://www.medworm.com/index.php?rid=482406&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17357008%26dopt%3DAbstract</link>
            <description>Authors: Gosk J, Rutowski R, Reichert P, Rabczyński J
    The success of radiation oncology has led to longer patient survival. This provides a greater opportunity for radiation injuries of the peripheral nerves to develop. Brachial plexus neuropathy in cancer patients may result from either tumour recurrence or as a consequence of radiation therapy. Distinguishing between radiation injury and cancer disease recurrence as a cause of brachial plexus dysfunction may be difficult. In this article the most important principles of the differential diagnostics have been presented. Furthermore the aetiopathogenesis of brachial plexus neuropathy after radiotherapy has been discussed as well as main risk factors, symptoms of plexopathy and methods of treatment. It ought to be emphasized that compl...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=482406</comments>
            <pubDate>Mon, 19 Mar 2007 23:15:03 +0100</pubDate>
            <guid isPermaLink="false">482406</guid>        </item>
        <item>
            <title>Brachial plexus injuries after radiotherapy - analysis of 6 cases.</title>
            <link>http://www.medworm.com/index.php?rid=482405&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17357009%26dopt%3DAbstract</link>
            <description>In this study our own experience in treatment of lesions of the brachial plexus after radiotherapy is presented. The clinical material consisted of 6 patients aged from 40 to 64 years with injuries of the brachial plexus after radiotherapy. The analysis of the material comprised: basic disease, duration of radiotherapy, radiated fields, total dose of radiation, onset and character of symptoms, location and severity of injury. 5 women were qualified for surgical treatment. After neurolysis of the brachial plexus a significant improvement was obtained in 2 cases. In one patient remission of pain and sensory recovery was temporary. No improvement was observed in the remaining 2 patients. Lesions of the brachial plexus after radiotherapy are rare but difficult to prevent. The treatment depends...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=482405</comments>
            <pubDate>Mon, 19 Mar 2007 23:15:03 +0100</pubDate>
            <guid isPermaLink="false">482405</guid>        </item>
        <item>
            <title>Idiopathic hypertrophic pachymeningitis - case report and literature review.</title>
            <link>http://www.medworm.com/index.php?rid=482404&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17357010%26dopt%3DAbstract</link>
            <description>We present a case of a 63-year-old woman with cranial variety of that disease. The manifestations of the disease included headaches, paresis of VI, IX, X nerves and cerebellar ataxia. The disease was diagnosed with magnetic resonance imaging (MRI) and histopathological assessment of the pachymeninx biopsy specimen. The MRI revealed significant thickening of the cranial base pachymeninx, compressing the pons and medulla oblongata. MRI examinations could be misinterpreted as extensive meningioma of the skull base. Dura mater biopsy revealed however inflammation with abundant lymphocytic infiltrations. Clinical improvement was obtained after the application of corticosteroids. We noted the subsidence of all symptoms of the disease, as well as radiological improvement, manifested through subst...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=482404</comments>
            <pubDate>Mon, 19 Mar 2007 23:15:03 +0100</pubDate>
            <guid isPermaLink="false">482404</guid>        </item>
        <item>
            <title>Simultaneous lateral and posterior ponticles resulting in the formation of a vertebral artery tunnel of the atlas: Case report and review of the literature.</title>
            <link>http://www.medworm.com/index.php?rid=482403&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17357011%26dopt%3DAbstract</link>
            <description>We present a case of an adult female skeleton noted to harbor both a foramen arcuale and a lateral ponticle that resulted in the formation of a canal for the vertebral artery. The literature regarding these osteological structures is reviewed regarding their presence and potential clinical significance. The simultaneous occurrence of fully developed lateral and posterior ponticuli resulting in encasement of the third part (atlantal segment) of the vertebral artery appears to be very rare. Based on the literature regarding only foramina arcuale and their presence predisposing one to symptomatic entrapment, additional compression, as seen in our specimen, of the vertebral artery by a lateral ponticle could very likely result in stenosis of the vertebral artery.
    PMID: 17357011 [PubMed - a...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=482403</comments>
            <pubDate>Mon, 19 Mar 2007 23:15:03 +0100</pubDate>
            <guid isPermaLink="false">482403</guid>        </item>
        <item>
            <title>Measuring the spatial arrangement patterns of pathological lesions in histological sections of brain tissue.</title>
            <link>http://www.medworm.com/index.php?rid=331060&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17183448%26dopt%3DAbstract</link>
            <description>This article reviews the methods that have been used to study the spatial topography of lesions. These include simple tests of whether the distribution of a lesion departs significantly from random using randomized points or sample fields, and more complex methods that employ grids or transects of contiguous fields and which can detect the intensity of aggregation and the sizes, distribution and spacing of the clusters. The usefulness of these methods in elucidating the pathogenesis of protein aggregates in neurodegenerative disease is discussed.
    PMID: 17183448 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=331060</comments>
            <pubDate>Sat, 23 Dec 2006 11:57:02 +0100</pubDate>
            <guid isPermaLink="false">331060</guid>        </item>
        <item>
            <title>Inhibition of mitochondrial complex II affects dopamine metabolism and decreases its uptake into striatal synaptosomes.</title>
            <link>http://www.medworm.com/index.php?rid=331059&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17183449%26dopt%3DAbstract</link>
            <description>Authors: Cakała M, Drabik J, Kaźmierczak A, Kopczuk D, Adamczyk A
    The mitochondrial toxin, 3-nitropropionic acid (3-NP), is a specific inhibitor of succinate dehydrogenase, complex II in the mitochondrial respiratory chain. The aim of our study was to determine the relationship between inhibition of mitochondrial complex II and dopamine (DA) metabolism and its transport into rat striatal synaptosomes after exposure to 3-NP. The study was carried out using spectrophotometric, radiochemical and HPLC methods. Our data showed that inhibition of succinate dehydrogenase by intraperitoneal (i.p.) injection of 3-NP (cumulated dose 100 mg/kg in 4 days) significantly affected DA metabolism, leading to the accumulation of its metabolites, 3,4-dihydroxylphenylacetic acid (DOPAC) and homovanillic...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=331059</comments>
            <pubDate>Sat, 23 Dec 2006 11:57:02 +0100</pubDate>
            <guid isPermaLink="false">331059</guid>        </item>
        <item>
            <title>Phenotypic diversity resulting from a point mutation.</title>
            <link>http://www.medworm.com/index.php?rid=331058&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17183450%26dopt%3DAbstract</link>
            <description>Authors: Sypecka J, Domańska-Janik K
    Paralytic tremor (pt), a hereditary neurological disorder of rabbits, is a recessive, X-linked point mutation in exon 2 of the plp gene, responsible for substitution of 38 His by Glu in the PLP molecule. Pt genotype is expressed in a range of phenotypes, distinguished by the severity of neurological symptoms. Variable course of the disease, from totally asymptomatic to serious disorder, is observed even within the offspring of one breeding pair. The two most typical phenotypes have been chosen for the studies: one representing mild course of the disease and the other reflecting the most severe course. Since previous developmental studies proved that myelination is not only deficient but also delayed in pt rabbits, the age groups of animals have bee...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=331058</comments>
            <pubDate>Sat, 23 Dec 2006 11:57:02 +0100</pubDate>
            <guid isPermaLink="false">331058</guid>        </item>
        <item>
            <title>TrkB deficiency increases survival and regeneration of spinal motoneurons after axotomy in mice.</title>
            <link>http://www.medworm.com/index.php?rid=331057&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17183451%26dopt%3DAbstract</link>
            <description>Authors: Kotulska K, Larysz-Brysz M, Marcol W, Malinowska I, Matuszek I, Grajkowska W, Lewin-Kowalik J
    Persisting motor function deficit after peripheral nerve injury often results from axotomized motoneuron death. Brain-derived neurotrophic factor (BDNF) and its receptor, trkB, are known to promote peripheral nerve regeneration. However, the requirement of BDNF and trkB for adult motoneuron survival after peripheral nerve injury is not established. We studied the number of surviving and regenerating motoneurons after sciatic nerve transection in wild-type and heterozygous trkB-deficient mice. The nerve was either left cut or immediately sewed up or the gap injury model was performed. The gap was provided with an autologous or cross (obtained from other genetic group) graft. Sixteen we...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=331057</comments>
            <pubDate>Sat, 23 Dec 2006 11:57:02 +0100</pubDate>
            <guid isPermaLink="false">331057</guid>        </item>
        <item>
            <title>Corticobasal degeneration - clinico-pathological considerations.</title>
            <link>http://www.medworm.com/index.php?rid=331056&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17183452%26dopt%3DAbstract</link>
            <description>We report here the first Polish case of pathologically proven CBD. Our patient developed clumsiness of the right hand at age 63 years. During the course of his illness he suffered from progressive asymmetric parkinsonism unresponsive to dopaminergic therapy. Focal dystonia affecting right upper extremity, non-fluent aphasia, dysphagia, supranuclear vertical gaze palsy, imbalance and myoclonus ensued. The patient died of pneumonia at age 71 years. Head magnetic resonance imaging revealed the presence of asymmetric cortical atrophy contralateral to the clinically more affected right side. Median somatosensory evoked potentials performed bilaterally demonstrated significant reduction of cortical evoked potential amplitudes recorded from the left scalp electrodes. Neuropathological examination...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=331056</comments>
            <pubDate>Sat, 23 Dec 2006 11:57:02 +0100</pubDate>
            <guid isPermaLink="false">331056</guid>        </item>
        <item>
            <title>Ultrastructural picture of blood vessels in muscle and skin biopsy in CADASIL.</title>
            <link>http://www.medworm.com/index.php?rid=331055&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17183453%26dopt%3DAbstract</link>
            <description>Authors: Lewandowska E, Leszczyńska A, Wierzba-Bobrowicz T, Skowrońska M, Mierzewska H, Pasennik E, Członkowska A
    CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy) is an inherited systemic vascular disorder affecting mainly the central nervous system. We performed detailed ultrastructural examination of the small vessels in the skin and skeletal muscle of a 51-year-old patient with bilateral cerebral white matter lesions, who had a history of two ischaemic strokes. The arterioles were characterized by degeneration and loss of vascular smooth muscle cells (VSMCs). GOM deposits, varied in size and shape, were located in the neighbourhood of the smooth muscle cells, often within an infolding of the cell membrane. No apparent correlatio...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=331055</comments>
            <pubDate>Sat, 23 Dec 2006 11:57:02 +0100</pubDate>
            <guid isPermaLink="false">331055</guid>        </item>
        <item>
            <title>Cerebellopontine angle tumours: radiologic-pathologic correlation and diagnostic difficulties.</title>
            <link>http://www.medworm.com/index.php?rid=331054&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17183454%26dopt%3DAbstract</link>
            <description>Authors: Izycka-Swieszewska E, Szurowska E, Kloc W, Rzepko R, Dubaniewicz-Wybieralska M, Skorek A, Drozyńska E, Stempniewicz M
    A group of 119 cases of cerebellopontine angle (CPA) tumours was studied looking at the pathological composition, relative incidence of tumour types, their radiological features and the pathological-radiological correlations. Tumours with preoperative radiological diagnosis and verified pathologically were analyzed. Histopathologically the material consisted of 77 schwannomas and 42 non-acoustic tumours. Radiological retrospective evaluation of CT and/or MRI documentation was performed in 84 patients. The tumours were classified according to Koos's staging scale. Diagnostic discrepancies (histopathological vs radiological) according to the clinical stage of CP...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=331054</comments>
            <pubDate>Sat, 23 Dec 2006 11:57:02 +0100</pubDate>
            <guid isPermaLink="false">331054</guid>        </item>
        <item>
            <title>Serial measurements of levels of the chemokines CCL2, CCL3 and CCL5 in serum of patients with acute ischaemic stroke.</title>
            <link>http://www.medworm.com/index.php?rid=331053&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17183455%26dopt%3DAbstract</link>
            <description>Authors: Zaremba J, Ilkowski J, Losy J
    Inflammation, involving cytokine/chemokine expression, occurs after stroke and deteriorates its course with leukocyte-mediated brain infarct progression. Chemokines are cytokines attracting selective leukocyte subsets and subgrouping into the four major subfamilies, CC, CXC, C, and CX3C. The CC subfamily preferentially acts on mononuclears. The study aimed to define serum CCL2, CCL3 and CCL5 levels in stroke patients and their relationship to the extent of disease severity and outcome. 27 ischaemic stroke patients and 20 controls were studied. Blood sampling for the determination of chemokines was performed at days 1, 2 and 3 of stroke, while neurological and functional deficits were estimated, respectively, with the Scandinavian Stroke Scale (SSS...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=331053</comments>
            <pubDate>Sat, 23 Dec 2006 11:57:02 +0100</pubDate>
            <guid isPermaLink="false">331053</guid>        </item>
        <item>
            <title>Hereditary neuropathy with liability to pressure palsy.</title>
            <link>http://www.medworm.com/index.php?rid=331052&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17183456%26dopt%3DAbstract</link>
            <description>Authors: Paprocka J, Kajor M, Jamroz E, Jezela-Stanek A, Seeman P, Marszał E
    Hereditary neuropathy with liability to pressure palsy (HNPP) is an autosomal dominant disease with sensory and motor nerve palsies usually precipitated by trivial trauma or compression. In the majority of cases HNPP is caused by deletion of the peripheral myelin protein 22 gene (PMP22) on chromosome 17p11.2. The authors present a family case with genetically proven HNPP.
    PMID: 17183456 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=331052</comments>
            <pubDate>Sat, 23 Dec 2006 11:57:02 +0100</pubDate>
            <guid isPermaLink="false">331052</guid>        </item>
        <item>
            <title>Malformations of cortical development in children: clinical manifestation, neuroimaging and neuropathology in selected cases.</title>
            <link>http://www.medworm.com/index.php?rid=331051&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17183457%26dopt%3DAbstract</link>
            <description>Authors: Emich-Widera E, Larysz D, Kluczewska E, Larysz P, Adamek D, Mandera M, Marszał E
    Cerebral cortical development can be divided into three steps: cellular proliferation, neuronal migration and organization. Based on known pathologic, genetic and neuroimaging features a classification for malformations of cortical development was proposed by Barkovich in 2001, and updated in 2005. Malformations of cerebral cortex development (MCCD) often demonstrate epileptic seizures and delay in psychomotor development. About 20-40% of children with epilepsy are drug-resistant and there is a large paediatric population requiring epilepsy surgery operations. In our work we performed clinical analysis of 68 children with MCCD treated in our hospital between 2000 and 2006. In our work to consider...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=331051</comments>
            <pubDate>Sat, 23 Dec 2006 11:57:02 +0100</pubDate>
            <guid isPermaLink="false">331051</guid>        </item>
        <item>
            <title>Correlation of neuroradiological, electroencephalographic and clinical findings in cortical dysplasias in children.</title>
            <link>http://www.medworm.com/index.php?rid=331050&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17183458%26dopt%3DAbstract</link>
            <description>Conclusions: There were no correlations between the type of CD and the severity of the clinical picture, especially the level of mental retardation and presence of drug-resistant epilepsy. Different age at epilepsy onset and various responsiveness to antiepileptic drugs in the majority of patients may reflect different dynamics in epileptogenicity of the underlying CD.
    PMID: 17183458 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=331050</comments>
            <pubDate>Sat, 23 Dec 2006 11:57:02 +0100</pubDate>
            <guid isPermaLink="false">331050</guid>        </item>
        <item>
            <title>Cerebral childhood and adolescent X-linked adrenoleukodystrophy. Clinical presentation, neurophysiological, neuroimaging and biochemical investigations.</title>
            <link>http://www.medworm.com/index.php?rid=331049&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17183459%26dopt%3DAbstract</link>
            <description>Authors: Zgorzalewicz-Stachowiak M, Stradomska TJ, Bartkowiak Z, Galas-Zgorzalewicz B
    Clinical, neurophysiological, neuroimaging and biochemical studies were performed in five boys with childhood and adolescent form of cerebral X-ALD, which is a very rare disease in developmental age. In all patients, rapidly progressive spasticity, ataxia and mental deterioration were found. Seizures occurred in four of them. Additionally, visual and hearing impairment were observed in four and three patients respectively. Adrenal insufficiency was also diagnosed in four cases. MR revealed extensive demyelination located mainly symmetrically in the parieto-occipital areas, in one patient in whom asymmetrical lesions in that region were found. All patients had abnormal visual, brainstem and somatosenso...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=331049</comments>
            <pubDate>Sat, 23 Dec 2006 11:57:02 +0100</pubDate>
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            <title>Faulty position of cerebellar cortical neurons as a sequel of disturbed neuronal migration.</title>
            <link>http://www.medworm.com/index.php?rid=331048&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17183460%26dopt%3DAbstract</link>
            <description>Authors: Laure-Kamionowska M, Taraszewska A, Maślińska D, Raczkowska B
    The object of our report is the presentation of the morphological picture of cerebellar cortex malformation as a sequel of disturbed neuronal migration. In the disarranged tissue, cavities with a network of meningeal tissue and embedded pathological vessels were noted. The external granule cells did not form a proper external granule layer, but moved deeper, forming irregular aggregates. Abnormally aggregated external granular cells invaded the cerebellar tissue. Abnormal Purkinje cell positioning and a disarranged molecular layer were observed. The normal layered pattern of the cerebellar cortex was disorganized. The presented cases represent a spectrum of morphological changes which are the consequence of aberra...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=331048</comments>
            <pubDate>Sat, 23 Dec 2006 11:57:02 +0100</pubDate>
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            <title>Maintenance of the rat transgenic model of familial amyotrophic lateral sclerosis expressing human SOD1G93A mutation.</title>
            <link>http://www.medworm.com/index.php?rid=236173&amp;cid=s_33494_32_f&amp;fid=33494&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17039409%26dopt%3DAbstract</link>
            <description>Authors: Herbik MA, Chrapusta SJ, Kowalczyk A, Grieb P
    A colony of transgenic rats expressing the human mutant Cu,Zn superoxide dismutase gene (hSOD1G93A) that is associated with some cases of familial form of amyotrophic lateral sclerosis (ALS) has been maintained in the Animal House of the Polish Academy of Sciences Medical Research Centre since 2003. This transgenic model, generated by Howland et al. (Proc Natl Acad Sci USA 2002; 99: 1604-1609), has been obtained under the material transfer agreement from Wyeth Corporation. The transgenic SOD1G93A (or 'Howland') rats develop neurological and neuropathological symptoms reminiscent of human ALS, i.e. progressive loss of motoneurons leading to paralysis and death. This paper describes maintenance of the transgenic rat colony, and gener...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
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            <pubDate>Mon, 16 Oct 2006 02:01:02 +0100</pubDate>
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