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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, 08 Dec 2009 14:54:02 +0100</lastBuildDate>
        <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>
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            <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>
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            <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>
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        <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>
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            <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>
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            <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>
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            <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>
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        <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>
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        <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>
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        <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>
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            <pubDate>Wed, 22 Jul 2009 12:40:05 +0100</pubDate>
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        <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>
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        <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>
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        <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>
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            <pubDate>Wed, 22 Jul 2009 12:40:05 +0100</pubDate>
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            <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>
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            <pubDate>Wed, 22 Jul 2009 12:40:05 +0100</pubDate>
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        <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>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 with true neoplastic glial proliferation. Such association of glioma with certain types of vascular anomalies has been designated as angioglioma. In the current stu...</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>
            <guid isPermaLink="false">331049</guid>        </item>
        <item>
            <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>
            <guid isPermaLink="false">331048</guid>        </item>
        <item>
            <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>
        <comments>http://www.medworm.com/rss/comments.php?id=236173</comments>
            <pubDate>Mon, 16 Oct 2006 02:01:02 +0100</pubDate>
            <guid isPermaLink="false">236173</guid>        </item>
        <item>
            <title>Morphological changes and selective loss of motoneurons in the lumbar part of the spinal cord in a rat model of familial amyotrophic lateral sclerosis (fALS).</title>
            <link>http://www.medworm.com/index.php?rid=236172&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%3D17039410%26dopt%3DAbstract</link>
            <description>Authors: Gadomski R, Chrapusta SJ, Wojda R, Grieb P
    Morphological alterations and the course of changes in motoneuron counts were studied by light microscopy (cresyl violet staining) in the L2/L3 region of the spinal cord of hemizygotic transgenic rats carrying the amyotrophic lateral sclerosis-associated mutant human gene for Cu,Zn superoxide dismutase (hSOD1G93A) and of their non-transgenic littermates. In 60-day old transgenic rats, a few ischaemic-looking alpha-motoneurons and occasional vacuolization and accumulation of tigroid in some of the cells were apparent. On day 93 of life more distinct cellular pathology was found in transgenic rats, including moderate gliosis, neuronophagy of alpha-motoneurons, and occasional neuronophagy of gamma-motoneurons. In 120-day-old transgenic r...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=236172</comments>
            <pubDate>Mon, 16 Oct 2006 02:01:02 +0100</pubDate>
            <guid isPermaLink="false">236172</guid>        </item>
        <item>
            <title>Progression of morphological changes within CNS in a transgenic rat model of familial amyotrophic lateral sclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=236171&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%3D17039411%26dopt%3DAbstract</link>
            <description>Conclusions: 1) In the subclinical stage of the disease the pathological process within the CNS takes place already on the 60th day of age and its intensity increases with age. 2) Morphological changes are not limited to motor neuronal cells. Various structures of the CNS are damaged. 3) Weak astroglial reaction probably depends on pathological accumulation of ubiquitin and tau protein in cytoplasm. 4) Astroglial cells are probably also a &quot;target&quot; for pathogenic factors in the rat model of fALS.
    PMID: 17039411 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=236171</comments>
            <pubDate>Mon, 16 Oct 2006 02:01:02 +0100</pubDate>
            <guid isPermaLink="false">236171</guid>        </item>
        <item>
            <title>Ultrastructural changes in lumbar spinal cord in transgenic SOD1G93A rats.</title>
            <link>http://www.medworm.com/index.php?rid=236170&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%3D17039412%26dopt%3DAbstract</link>
            <description>Authors: Fidziańska A, Gadomski R, Rafałowska J, Chrzanowska H, Grieb P
    The purpose of this study was to determine structural changes which trigger the onset and progression of amyotrophic lateral sclerosis in rats expressing a human SOD1 transgene with mutation G93A. Lumbar spinal cord of affected rats in early and late presymptomatic (PM, 60 and 93 days of age) and symptomatic (S, 120 days of age) stage of the disease were analyzed ultrastructurally. At 60 days the structure of lumbar spinal cord as well as alpha motoneurons type S and F appeared normal; however, careful examination revealed that approximately 15% of axons were filled with mitochondria that were abnormal in number, size and morphology. Grossly swollen mitochondria with disrupted cristae were a prominent feature in ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=236170</comments>
            <pubDate>Mon, 16 Oct 2006 02:01:02 +0100</pubDate>
            <guid isPermaLink="false">236170</guid>        </item>
        <item>
            <title>Astroglial alterations in amyotrophic lateral sclerosis (ALS) model of slow glutamate excitotoxicity in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=236169&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%3D17039413%26dopt%3DAbstract</link>
            <description>This study was performed to determine the ultrastructural characteristics of astroglial changes concomitant with motor neuron (MN) degeneration in a model of slow excitotoxicity in vitro. The study was performed on organotypic cultures of rat lumbar spinal cord subjected to the glutamate uptake blockers threohydroxyaspartate (THA) and L-trans-pyrrolidine-2,4-dicarboxylate (PDC). The chronic inhibition of glutamate transport by THA and PDC resulted in slow degeneration of the rat's MNs accompanied by distinct glial changes predominantly involving protoplasmic astrocytes. The presence of irregular vacuoles and vesicles in the astroglial cells was frequently observed. Occasionally the astrocytes exhibited proliferation and accumulation of abnormal profiles of smooth endoplasmic reticulum. In ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=236169</comments>
            <pubDate>Mon, 16 Oct 2006 02:01:02 +0100</pubDate>
            <guid isPermaLink="false">236169</guid>        </item>
        <item>
            <title>Auto-antibodies against proteins of spinal cord cells in cerebrospinal fluid of patients with amyotrophic lateral sclerosis (ALS).</title>
            <link>http://www.medworm.com/index.php?rid=236168&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%3D17039414%26dopt%3DAbstract</link>
            <description>We report here our investigations of auto-antibodies against proteins of spinal cord cells in the cerebrospinal fluid (CSF) and serum of ALS patients. The results were correlated with the severity of disease course. The subjects were 57 ALS patients (29 severe, 28 mild) and 10 normal controls. The major finding in CSF was the presence of antibodies against a 70 kD protein in the majority of ALS patients. This protein was identified as neurofilament 68. The second protein of high reactivity and frequency of appearance was a 82 kD protein, which was identified as a-actinin. Less reactive and less frequent were antibodies directed against 55 kD and 40 kD proteins. They were immunologically defined to be related to desmin and actin, resp. The difference between the reactivity of anti-neurofila...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=236168</comments>
            <pubDate>Mon, 16 Oct 2006 02:01:02 +0100</pubDate>
            <guid isPermaLink="false">236168</guid>        </item>
        <item>
            <title>Does the ganglion of Ribes exist?</title>
            <link>http://www.medworm.com/index.php?rid=236167&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%3D17039415%26dopt%3DAbstract</link>
            <description>Authors: Tubbs RS, Kelly DR, Shoja MM, Khaki AA, Loukas M, Humphrey R, Chua GD, Lott R, Salter EG, Oakes WJ
    Some have included the ganglion of Ribes (Francois Ribes, 1765-1845), lying on the anterior communicating artery, as the most superior ganglion of the sympathetic nervous system. To verify the presence of this structure, the anterior communicating artery was harvested from 40 fresh adult cadavers and histological analysis and immunochemistry performed. Grossly and with magnification, no ganglion-like structures were found in or around the anterior communicating artery in any specimen. However, scattered neuronal cell bodies were found in the adventitia of the anterior communicating artery with histological immunochemical analysis. Based on the lack of vasoactive intestinal peptid...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=236167</comments>
            <pubDate>Mon, 16 Oct 2006 02:01:02 +0100</pubDate>
            <guid isPermaLink="false">236167</guid>        </item>
        <item>
            <title>The brain immune response in human prion diseases.Microglial activation and microglial disease. I. Sporadic Creutzfeldt-Jakob disease.</title>
            <link>http://www.medworm.com/index.php?rid=236166&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%3D17039416%26dopt%3DAbstract</link>
            <description>Authors: Szpak GM, Lewandowska E, Lechowicz W, Wierzba-Bobrowicz T, Kulczycki J, Bertrand E, Pasennik E, Dymecki J
    A study of microglial activation and its contribution to the CNS immune response was performed on the brain autopsy material of 40 patients with definite sporadic Creutzfeldt-Jakob disease (sCJD). Spatial patterns of microglial activation and prion protein disease-associated (PrPd) deposition were compared in cerebellar and cerebral cortices using immunohistochemical (IHC) activation markers. Morphological phenotype forms of microglial cells in activation stages were assessed immunohistochemically (IHC). The immune inflammatory response dominated by microglia was found to be a characteristic feature in CJD. Differences in the intensity and patterns of microglial activation...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=236166</comments>
            <pubDate>Mon, 16 Oct 2006 02:01:02 +0100</pubDate>
            <guid isPermaLink="false">236166</guid>        </item>
        <item>
            <title>Activation of Akt and Erk pathways in medulloblastoma.</title>
            <link>http://www.medworm.com/index.php?rid=236165&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%3D17039417%26dopt%3DAbstract</link>
            <description>Authors: Włodarski P, Grajkowska W, Lojek M, Rainko K, Jóźwiak J
    Medulloblastoma (MB) is the most common malignant brain tumour in children. Its aetiology is unknown, although several signalling pathways controlling cell proliferation are thought to participate in the progress of the neoplasm. Mutations of the genes encoding proteins participating in the pathways triggered by embryonic growth factors like Sonic hedgehog (Shh) or WNT are often found in MB. Another model of MB development is overexpression or mutation of several types of growth factor receptors, including IGF-IR, EGF-R and PDGFR, that have the ability to activate cellular kinases responsible for promoting cell proliferation. In order to test this hypothesis, in the current paper we tested the activation of two kinases...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=236165</comments>
            <pubDate>Mon, 16 Oct 2006 02:01:02 +0100</pubDate>
            <guid isPermaLink="false">236165</guid>        </item>
        <item>
            <title>The role of trkB receptor in the formation of post-traumatic neuroma.</title>
            <link>http://www.medworm.com/index.php?rid=236164&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%3D17039418%26dopt%3DAbstract</link>
            <description>Authors: Kotulska K, Larysz-Brysz M, Marcol W, Grajkowska W, Jóźwiak S, Lewin-Kowalik J
    The outcome of peripheral nerve injury is often impaired by post-traumatic neuroma developing at the injury site. Neuroma is usually accompanied by neuropathic pain, which is usually resistant to most analgesics and presents a serious clinical problem. The mechanisms underlying post-traumatic neuroma remain unclear, but they are likely associated with regeneration processes. Brain-derived neurotrophic factor (BDNF) and its receptor, trkB, are strongly implicated in axonal regeneration after injury. The aim of this work was to examine the role of trkB in post-traumatic neuroma formation. The sciatic nerve was transected in wild-type and heterozygous trkB-deficient mice. The nerve was either left cu...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=236164</comments>
            <pubDate>Mon, 16 Oct 2006 02:01:02 +0100</pubDate>
            <guid isPermaLink="false">236164</guid>        </item>
        <item>
            <title>Plaques and tangles and the pathogenesis of Alzheimer's disease.</title>
            <link>http://www.medworm.com/index.php?rid=185137&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%3D16565925%26dopt%3DAbstract</link>
            <description>Authors: Armstrong RA
    Since the earliest descriptions, senile plaques (SP) and neurofibrillary tangles (NFT) have been regarded as the pathological hallmarks of Alzheimer's disease (AD). Consequently, studies of the morphology, distribution, and molecular composition of SP and NFT have played an important role in developing theories as to the pathogenesis of AD; the most important being the 'Amyloid Cascade Hypothesis (ACH)'. Nevertheless, the significance of SP and NFT to the pathogenesis of AD remains controversial. This review examines three questions: 1) is there a relationship between the lesions and the degree of clinical dementia, 2) is the pathogenesis of the NFT linked to that of the SP, and 3) what is the relationship of SP and NFT to the pathogenesis of AD? These questions a...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185137</comments>
            <pubDate>Mon, 11 Sep 2006 14:12:05 +0100</pubDate>
            <guid isPermaLink="false">185137</guid>        </item>
        <item>
            <title>No association between the brain-derived neurotrophic factor 196 G&gt;A or 270 C&gt;T polymorphisms and Alzheimer's or Parkinson's disease.</title>
            <link>http://www.medworm.com/index.php?rid=185136&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%3D16565926%26dopt%3DAbstract</link>
            <description>In conclusion, it seems that the BDNF gene does not contribute significantly to the risk of AD or PD in Finnish patients.
    PMID: 16565926 [PubMed - indexed for MEDLINE] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185136</comments>
            <pubDate>Mon, 11 Sep 2006 14:12:05 +0100</pubDate>
            <guid isPermaLink="false">185136</guid>        </item>
        <item>
            <title>Involvement of immature endothelial cells in vascular alterations in Alzheimer's disease.</title>
            <link>http://www.medworm.com/index.php?rid=185135&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%3D16565927%26dopt%3DAbstract</link>
            <description>Authors: Frontczak-Baniewicz M, Andrychowski J, Czernicki Z, Walski M
    The aim of the present study was to investigate ultrastructural features of cerebral capillaries and the pattern of new vessel formation in a patient with Alzheimer's disease (AD). Recent neuropathological studies have demonstrated that patients with AD have cerebrovascular pathology. Using electron microscopy, we showed that alterations of the capillaries are a common finding both in vascular disease and in AD, suggesting that vascular factors may also play a role in the pathogenesis of AD. We also found regionally increased capillary density, and in many sections immature endothelial cells lying on the preexisting endothelium were present in the lumen of capillaries. These cells might thus contribute to the patholo...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185135</comments>
            <pubDate>Mon, 11 Sep 2006 14:12:05 +0100</pubDate>
            <guid isPermaLink="false">185135</guid>        </item>
        <item>
            <title>Teratoma or enterogenous cyst? The histopathological and clinical dilemma in co-existing occult neural tube dysraphism.</title>
            <link>http://www.medworm.com/index.php?rid=185134&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%3D16565928%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: (1) Enterogenous cyst often co-exists with other dysraphic features; (2) Clinical signs of an enterogenous cyst are non-typical and depend on location of the lesion. The presence of secreting gastric mucosa may lead to chemical myelitis; (3) Severity of the postoperative neurological deficit is due to the developmental nature of the lesion and common vascular supply; (4) Late results of treatment are satisfactory, provided the lesion is excised radically; (5) Enterogenous cyst may be diagnosed in the case of a tumor composed of tissues originating from 1, 2 or 3 embryonic layers coexisting with dysraphic stigmata, congenital vertebral abnormalities or a mediastinal tumor of the same type. Types II and III of enterogenous cyst were historically diagnosed as &quot;adult teratoma&quot;.
  ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185134</comments>
            <pubDate>Mon, 11 Sep 2006 14:12:05 +0100</pubDate>
            <guid isPermaLink="false">185134</guid>        </item>
        <item>
            <title>Chordoid meningiomas of a different histopathological pattern: a report of two cases.</title>
            <link>http://www.medworm.com/index.php?rid=185133&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%3D16565929%26dopt%3DAbstract</link>
            <description>We report two cases of chordoid meningiomas in adult patients without manifestation of Castleman's syndrome. One tumour was almost totally composed of chordoma-like areas whereas the second one exhibited the unique combination of chordoma- and chondroma-like pattern. This is the first description of chordoid meningioma combined with extensive cartilaginous metaplasia. Both tumours exhibited histological evidence of infiltrative growth, accompanied by a relatively high proliferative index within structures of chordoid appearance. The designation of the chordoid component in meningioma is very important as this subtype of meningioma exhibits a more aggressive biological behaviour and higher risk of recurrence.
    PMID: 16565929 [PubMed - indexed for MEDLINE] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185133</comments>
            <pubDate>Mon, 11 Sep 2006 14:12:05 +0100</pubDate>
            <guid isPermaLink="false">185133</guid>        </item>
        <item>
            <title>The interaction between lung cancer metastases to the brain and their surroundings.</title>
            <link>http://www.medworm.com/index.php?rid=185132&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%3D16565930%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: a dispersed mode of infiltration by sqclc metastases to the brain causes precise detection of the macroscopic border between the metastatic tumour and the nervous tissue to be much more difficult than in sclc, which is sharply demarcated from the surroundings. The poor prognosis in sqclc metastases to the brain may, among other, depend on metastatic remnants in the form of dispersed neoplastic cells within the seemingly uninvolved nervous tissue, not removed during neurosurgical procedures.
    PMID: 16565930 [PubMed - indexed for MEDLINE] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185132</comments>
            <pubDate>Mon, 11 Sep 2006 14:12:05 +0100</pubDate>
            <guid isPermaLink="false">185132</guid>        </item>
        <item>
            <title>The effect of propofol on astro- and microglial reactivity in the course of experimental intracerebral haemorrhage in rats.</title>
            <link>http://www.medworm.com/index.php?rid=185131&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%3D16565931%26dopt%3DAbstract</link>
            <description>Authors: Karwacki Z, Kowiański P, Dziewiatowski J, Domaradzka-Pytel B, Ludkiewicz B, Wójcik S, Narkiewicz O, Moryś J
    The glial cells play an important role in pathophysiology of the intracerebral haemorrhage (ICH). Thus the attempt at evaluating the possible influence of the propofol on the reactivity of astro- and microglial cells in the course of ICH was performed. 50 rats were divided into two groups depending on the applied anaesthesia. All animals were generally anaesthetized with fentanyl, dehydrobenzperidol and midazolam. No additional agents were given to the animals of the control group (group I). In the experimental group (group II), the animals received additionally intraperitoneally propofol in a dose of 50 mg/kg every thirty minutes. ICH was produced through infusion of...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185131</comments>
            <pubDate>Mon, 11 Sep 2006 14:12:05 +0100</pubDate>
            <guid isPermaLink="false">185131</guid>        </item>
        <item>
            <title>Interleukin-12 in acute ischemic stroke patients.</title>
            <link>http://www.medworm.com/index.php?rid=185130&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%3D16565932%26dopt%3DAbstract</link>
            <description>Authors: Zaremba J, Losy J
    Cytokines are important mediators of stroke-induced immunological/inflammatory reaction which contributes to brain infarct progression as well as to the disease severity and outcome. The aim of the study was to evaluate the levels of the proinflammatory and immunomodulatory cytokine interleukin-12 (IL-12) in serum of acute ischemic stroke patients, and to investigate the relation between these levels and demographic, laboratory, neuroimaging, and clinical data. The study comprised 23 first-ever ischemic stroke patients and 15 age- and sex-matched controls. Blood sampling for the determination of IL-12 and such peripheral markers of inflammation as erythrocyte sedimentation rate (ESR) and leukocyte count, together with cranial CT were performed within 24 h of ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185130</comments>
            <pubDate>Mon, 11 Sep 2006 14:12:05 +0100</pubDate>
            <guid isPermaLink="false">185130</guid>        </item>
        <item>
            <title>Mononuclear subsets in the peripheral blood of multiple sclerosis patients in relation to results of brain gadolinium- enhancing imaging.</title>
            <link>http://www.medworm.com/index.php?rid=185129&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%3D16565933%26dopt%3DAbstract</link>
            <description>CONCLUSION: An appropriate regulation of the Th /T helper/ cells seems to be critical in the control and prevention of diverse states of the disease. In the course of an acute process, gadolinium positive imaging as well as immunological events, represented by mononuclear subsets in the peripheral blood may proceed and change very quickly, whereas gadolinium negative findings reflecting a stabilization of processes, are changing more slowly and therefore may be detected more easily in peripheral blood cell counts.
    PMID: 16565933 [PubMed - indexed for MEDLINE] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185129</comments>
            <pubDate>Mon, 11 Sep 2006 14:12:05 +0100</pubDate>
            <guid isPermaLink="false">185129</guid>        </item>
        <item>
            <title>The cerebral form of toxocarosis in a seven-year-old patient.</title>
            <link>http://www.medworm.com/index.php?rid=185128&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%3D16565934%26dopt%3DAbstract</link>
            <description>We present a seven-year-old patient who developed a cerebral form of toxocarosis. She demonstrated focal neurological symptoms (epilepsy) confirmed by neuro-imaging and histopathological examinations. A positive test for toxocarosis essentially completed the other outcomes. On the basis of the clinical picture and the conducted tests a diagnosis of a cerebral form of toxocarosis was established. Mebendazole was applied in treatment.
    PMID: 16565934 [PubMed - indexed for MEDLINE] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185128</comments>
            <pubDate>Mon, 11 Sep 2006 14:12:05 +0100</pubDate>
            <guid isPermaLink="false">185128</guid>        </item>
        <item>
            <title>Abstracts from the 1st Conference of Polish-German Cooperation Program in Neuroscience ordered by the Federal Ministry of Education and Research and the Polish Ministry of Education and Science. April 21-22, 2006. Warsaw, Poland.</title>
            <link>http://www.medworm.com/index.php?rid=185127&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%3D16565935%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 16565935 [PubMed - indexed for MEDLINE] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185127</comments>
            <pubDate>Mon, 11 Sep 2006 14:12:05 +0100</pubDate>
            <guid isPermaLink="false">185127</guid>        </item>
        <item>
            <title>Variant CJD (vCJD) and bovine spongiform encephalopathy (BSE): 10 and 20 years on: part 1.</title>
            <link>http://www.medworm.com/index.php?rid=185126&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%3D16823691%26dopt%3DAbstract</link>
            <description>Authors: Bradley R, Collee JG, Liberski PP
    From 1986 more than 184,000 cattle in the UK and islands (of which &amp;gt;1,880 have been detected by active surveillance using rapid tests) and approaching 5,500 elsewhere have been confirmed with BSE. The original 1988 ban on the use of ruminant-derived protein in ruminant feed has been upgraded and now prohibits the use of any processed animal protein in feed for any farmed food animal. As a result of rigorous enforcement this reinforced ban is now regarded as fully effective from 1 Aug. 1996. Reasons are given for the substantial slippage that occurred initially and for the small but diminishing number of cases that have occurred in cattle born after 1 Aug. 1996. The 1989 offal ban, initially introduced to protect public health, has likewise ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185126</comments>
            <pubDate>Mon, 11 Sep 2006 14:12:05 +0100</pubDate>
            <guid isPermaLink="false">185126</guid>        </item>
        <item>
            <title>Variant CJD (vCJD) and bovine spongiform encephalopathy (BSE): 10 and 20 years on: part 2.</title>
            <link>http://www.medworm.com/index.php?rid=185125&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%3D16823692%26dopt%3DAbstract</link>
            <description>Authors: Collee JG, Bradley R, Liberski PP
    Up until February 2006, variant CJD (vCJD), the human disease associated with transmission of BSE from cattle, has been confirmed in 160 patients resident in the UK and 28 elsewhere, some of whom have never visited the UK. Cases have been reported in France (16 cases), Ireland (3), USA (2), Canada, Italy, Japan, The Netherlands, Portugal, Saudi Arabia and Spain (1 each). The presumed main period of hazard for ingestion of the BSE agent in bovine products in the UK is 1984-89, or perhaps up to 1995-6 but at a reduced level. Debated incubation periods for vCJD are discussed, with special reference to the wide, but currently reducing, range of predicted further primary cases in the UK. The primary disease seems to be preferentially acquired by, a...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185125</comments>
            <pubDate>Mon, 11 Sep 2006 14:12:05 +0100</pubDate>
            <guid isPermaLink="false">185125</guid>        </item>
        <item>
            <title>Immunohistochemical expression of progesterone and estrogen receptors in meningiomas.</title>
            <link>http://www.medworm.com/index.php?rid=185124&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%3D16823693%26dopt%3DAbstract</link>
            <description>In this study we present results of investigations of progesterone and estrogen receptors in most frequent, WHO grade I histological types of meningiomas (meningothelial, fibrous, and transitional) and in atypical--WHO grade II variant of these tumors. Samples from 64 tumors were examined. The cohort consisted of 46 WHO grade I (21 transitional, 13 fibrous and 12 meningothelial histologic variants) and of 18 atypical meningiomas. Apart from immunohistochemical examination of progesterone and estrogen receptors, MIB 1 labeling index was estimated. Positive immunoreaction for progesterone receptors was found in 100% meningothelial, 95% transitional, 46% fibrous and 78% atypical variant of meningiomas. Intensity of immunoreaction was stronger in grade I than in grade II tumors. Immunoexpressi...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185124</comments>
            <pubDate>Mon, 11 Sep 2006 14:12:05 +0100</pubDate>
            <guid isPermaLink="false">185124</guid>        </item>
        <item>
            <title>Could lipid CH2/CH3 analysis by in vivo 1H MRS help in differentiation of tumor recurrence and post-radiation effects?</title>
            <link>http://www.medworm.com/index.php?rid=185123&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%3D16823694%26dopt%3DAbstract</link>
            <description>CONCLUSION: The analysis of the lipid CH2/CH3 ratio may be useful in differentiation of the tumor recurrence from radiation response. The Lip signals observed in normally appearing brain tissue after radiotherapy could originate from the change of metabolism of irradiated cells.
    PMID: 16823694 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185123</comments>
            <pubDate>Mon, 11 Sep 2006 14:12:05 +0100</pubDate>
            <guid isPermaLink="false">185123</guid>        </item>
        <item>
            <title>Apoptotic neuronal changes enhanced by zinc chelator--TPEN in organotypic rat hippocampal cultures exposed to anoxia.</title>
            <link>http://www.medworm.com/index.php?rid=185122&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%3D16823695%26dopt%3DAbstract</link>
            <description>This study was undertaken to determine the effect of zinc chelating agent--TPEN on neuronal morphological changes in organotypic hippocampal culture and its effect on post-anoxic changes in this model. The study evidenced that exposition to 15 microM of TPEN induced various stages of apoptotic changes in hippocampal pyramidal neurons and enhanced the anoxia-induced neuronal apoptosis in this model. These results confirmed the hypothesis that manipulations of intracellular pool of zinc by zinc-chelating agents may be a cause of both induction and prevention of apoptotic cell death in various pathological conditions.
    PMID: 16823695 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185122</comments>
            <pubDate>Mon, 11 Sep 2006 14:12:05 +0100</pubDate>
            <guid isPermaLink="false">185122</guid>        </item>
        <item>
            <title>Changes of cytoskeletal proteins in ischaemic brain under cardiac arrest and reperfusion conditions.</title>
            <link>http://www.medworm.com/index.php?rid=185121&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%3D16823696%26dopt%3DAbstract</link>
            <description>In conclusion, our results show a temporal pattern of changes in calpain proteolytic activity and protein expression in the applied model of brain ischaemia caused by cardiac arrest and reperfusion. In these conditions calpain-mediated degradation of cytoskeleton may be involved in the disturbances in synaptic vesicles transport and hence to the changes in neurotransmission.
    PMID: 16823696 [PubMed - in process] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185121</comments>
            <pubDate>Mon, 11 Sep 2006 14:12:05 +0100</pubDate>
            <guid isPermaLink="false">185121</guid>        </item>
        <item>
            <title>Multiple mononeuropathy due to vasculitis associated with anticardiolipin antibodies: a case report.</title>
            <link>http://www.medworm.com/index.php?rid=185120&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%3D16823697%26dopt%3DAbstract</link>
            <description>This report illustrates a case of peripheral nerve vasculitis associated with elevated anticardiolipin antibodies. A 49-year-old female with a history of seven spontaneous abortions initially complained of pain and numbness in her right calf that later spread to the left foot and ankle. Over the next few months, she developed a Raynaud phenomenon and livedo reticularis. Clinical examination revealed signs of multiple mononeuropathy. Right sural nerve biopsy performed two months after the beginning of the disease revealed active necrotizing arteritis of the epineural arteries with transmural inflammatory infiltrate and thrombosis. Vasculitis is a rare finding in sural nerve biopsies, usually in patients with systemic vasculitis or autoimmune connective tissue diseases. However, vasculitis r...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185120</comments>
            <pubDate>Mon, 11 Sep 2006 14:12:05 +0100</pubDate>
            <guid isPermaLink="false">185120</guid>        </item>
        <item>
            <title>Leukoencephalopathy with vanishing white matter due to homozygous EIF2B2 gene mutation. First Polish cases.</title>
            <link>http://www.medworm.com/index.php?rid=185119&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%3D16823698%26dopt%3DAbstract</link>
            <description>We present three sisters, 18, 11 and 8 years old, with the early to late childhood phenotype. The first signs of the disease were gait disturbances at 4, 2 and 6 years of age, respectively. Neurological examination showed mild tremor of hands and head, truncal ataxia, dysarthria, and hypotonia, after several years followed by spasticity. The course of the disease was slowly progressive. Intellectual abilities are relatively spared. The MRI showed diffusely abnormal white matter of the cerebral hemispheres. The FLAIR images revealed rarefaction of the affected white matter with some stripe-like structures, suggesting the presence of remaining tissue strands. The abnormalities were most pronounced with the middle sister, who had the earliest onset of the disease. A homozygous point mutation ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185119</comments>
            <pubDate>Mon, 11 Sep 2006 14:12:05 +0100</pubDate>
            <guid isPermaLink="false">185119</guid>        </item>
        <item>
            <title>The brain immune response in human prion diseases. Microglial activation and microglial disease. I. Sporadic Creutzfeldt-Jakob disease.</title>
            <link>http://www.medworm.com/index.php?rid=454210&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%3D17039416%26dopt%3DAbstract</link>
            <description>Authors: Szpak GM, Lewandowska E, Lechowicz W, Wierzba-Bobrowicz T, Kulczycki J, Bertrand E, Pasennik E, Dymecki J
    A study of microglial activation and its contribution to the CNS immune response was performed on the brain autopsy material of 40 patients with definite sporadic Creutzfeldt-Jakob disease (sCJD). Spatial patterns of microglial activation and prion protein disease-associated (PrPd) deposition were compared in cerebellar and cerebral cortices using immunohistochemical (IHC) activation markers. Morphological phenotype forms of microglial cells in activation stages were assessed immunohistochemically (IHC). The immune inflammatory response dominated by microglia was found to be a characteristic feature in CJD. Differences in the intensity and patterns of microglial activation...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=454210</comments>
            <pubDate>Sun, 01 Jan 2006 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">454210</guid>        </item>
        <item>
            <title>A quantitative analysis of optic nerve axons in elderly control subjects and patients with Alzheimer's disease.</title>
            <link>http://www.medworm.com/index.php?rid=185178&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%3D15827884%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: The data suggest that image analysis provides an accurate and reproducible method of quantifying axons in the optic nerve. In addition, the data suggest that axons are lost throughout the optic nerve with a specific loss of the smaller-sized axons. Loss of the smaller axons may explain the deficits in color vision observed in a significant proportion of patients with AD.
    PMID: 15827884 [PubMed - indexed for MEDLINE] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185178</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185178</guid>        </item>
        <item>
            <title>The mode of spinal motor neurons degeneration in a model of slow glutamate excitotoxicity in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=185177&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%3D15827885%26dopt%3DAbstract</link>
            <description>Authors: Matyja E, Nagańska E, Taraszewska A, Rafałowska J
    The defective glial and/or neuronal glutamate transport may, in chronic neurotoxicity, contribute to several neurodegenerative diseases including amyotrophic lateral sclerosis (ALS)--a progressive neurodegenerative disorder of lower and upper motor neurons (MNs). To determine the detailed ultrastructural characteristics of excitotoxic motor neurons neurodegeneration we used a model of slow excitotoxicity in vitro based on selective inhibition of glutamate uptake. The study was performed on organotypic cultures of the rat lumbar spinal cord subjected to various concentrations of glutamate uptake blockers: threohydroxyaspartate (THA) and L-trans-pyrrolidine-2, 4-dicarboxylate (PDC). The chronic inhibition of glutamate transport...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185177</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185177</guid>        </item>
        <item>
            <title>The antiphospholipid syndrome in pregnant rabbits and their offspring. Neuropathological aspects.</title>
            <link>http://www.medworm.com/index.php?rid=185176&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%3D15827886%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: 1. The antiphospholipid syndrome in pregnant rabbits results in serological markers of the syndrome in their offspring. 2. The central nervous system of fetuses delivered from pregnant rabbits with the antiphospholipid syndrome remains intact despite the serological markers of the syndrome in fetus circulation. 3. The miscarriages in pregnant rabbits with the antiphospholipid syndrome depend rather on placental pathology related to the syndrome than on the syndrome per se transmitted from adult females to fetal circulation.
    PMID: 15827886 [PubMed - indexed for MEDLINE] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185176</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185176</guid>        </item>
        <item>
            <title>Expression of apoptosis-related proteins in model of anoxia in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=185175&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%3D15827887%26dopt%3DAbstract</link>
            <description>We examined the expression of proteins related to programmed cell death in hippocampal neurons in vitro, exposed to pure anoxia or pretreated with apoptosis modulating agents: zinc and zinc chelator - TPEN. The results evidenced the noticeable differences in the expression of pro- and anti-apoptotic proteins in particular experiments. In the cultures exposed to pure anoxia, a significant increase of p53 and BAX immunoreactivity, associated with the decreased level of BCL-2 and BCL-X immunopositive cells was observed, related to the activation of apoptotic process. Hippocampal cultures pretreated with ZnCl2 before anoxia showed decreased immunoreactivity for p53 and BAX, connected with BCL-2 overexpression, whereas the cultures exposed to zinc chelating agent - TPEN or TPEN connected with a...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185175</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185175</guid>        </item>
        <item>
            <title>The neuroprotective function of vascular endothelial growth factor (VEGF).</title>
            <link>http://www.medworm.com/index.php?rid=185174&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%3D15827888%26dopt%3DAbstract</link>
            <description>Authors: Góra-Kupilas K, Jośko J
    The vascular endothelial growth factor (VEGF) is known mainly as the potent angiogenic and vascular permeability-enhancing factor. Both processes are very effective in hypoxia. The latest studies show that VEGF has neurotrophic and neuroprotective as well as angiogenic properties. It exerts neuroprotective actions directly through the inhibition of programmed cell death (PCD), or apoptosis and the stimulation of neurogenesis. VEGF is also a mediator of multiple processes including angiogenesis, enhancing blood brain barrier permeability for glucose, antioxidants activation, which indirectly result in neuroprotection. VEGF prevents neurons from death under critical conditions such as hypoxia, glucose deprivation through binding to the specific receptor...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185174</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185174</guid>        </item>
        <item>
            <title>Brain abscess as the first clinical manifestation of multiple pulmonary arteriovenous malformations in a patient with hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber disease).</title>
            <link>http://www.medworm.com/index.php?rid=185173&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%3D15827889%26dopt%3DAbstract</link>
            <description>In this report we described a case of a cerebral abscess that developed in presence of asymptomatic pulmonary arteriovenous malformations (PAVMs) in a 53-year-old woman with hereditary hemorrhagic telangiectasia (HHT). The brain abscess was aspirated with good clinical result and the arteriovenous fistulae qualified for transcatheter embolotherapy. Each patient suspected to suffer from HHT should be diagnosed for the presence of visceral vascular malformations. Most of them are found in the lungs, liver and brain. Early diagnosis and treatment of PAVM prevent the occurrence of severe neurological complications such as brain stroke or brain abscess. Cases of a cerebral abscess in adults of unexplained etiology should raise the suspicion of an asymptomatic PAVM.
    PMID: 15827889 [PubMed - ...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185173</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185173</guid>        </item>
        <item>
            <title>Recurrent cerebral infarcts as the first manifestation of infection with the HIV virus.</title>
            <link>http://www.medworm.com/index.php?rid=185172&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%3D15827890%26dopt%3DAbstract</link>
            <description>We present a case of a 40-year-old patient, hospitalized three times in our department because of recurrent ischemic strokes. Diagnostic tests revealed a high titre of anticardiolipin antibodies and the early stage of HIV infection. Recurrent ischemic strokes were the first manifestation of HIV infection in this patient.
    PMID: 15827890 [PubMed - indexed for MEDLINE] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185172</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185172</guid>        </item>
        <item>
            <title>Proteinaceous intracellular inclusions in neurodegenerative disorders.</title>
            <link>http://www.medworm.com/index.php?rid=185171&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%3D16012906%26dopt%3DAbstract</link>
            <description>Authors: Dziewulska D, Rafałowska J
    Neurodegenerative disorders are characterized by accumulation of &quot;toxic&quot;, pathologic proteins in brain cells. Mutations in genes coding these proteins result in conformational disturbances of the protein structure and their accumulation and aggregation manifesting at the level of light microscope as various intracellular inclusions. This paper is an attempt of approach cellular mechanisms underlying neurodegenerative disorders with special attention to mechanisms of protein elimination.
    PMID: 16012906 [PubMed - indexed for MEDLINE] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185171</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185171</guid>        </item>
        <item>
            <title>Molecular genetics studies in Polish Charcot-Marie-Tooth families.</title>
            <link>http://www.medworm.com/index.php?rid=185170&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%3D16012907%26dopt%3DAbstract</link>
            <description>Authors: Kochański A
    Charcot-Marie-Tooth (CMT) disorders are the extremely heterogeneous group of diseases of the peripheral nervous system in humans with a prevalence of 1: 2500. Up to date mutations in 30 genes have been reported in various CMT forms. In numerous CMT types only locus is known and some CMT forms were shown not to be linked with any known locus. Genetic studies in CMT disorders cover a wide spectrum of problems ranging from identification of novel mutations through studies of pathogenic nature of mutations to genotype-phenotype correlations. The aim of this study was to present the main directions of genetic analysis performed in Polish families with CMT disease.
    PMID: 16012907 [PubMed - indexed for MEDLINE] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185170</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185170</guid>        </item>
        <item>
            <title>Does apoptosis occur in amyotrophic lateral sclerosis? TUNEL experience from human amyotrophic lateral sclerosis (ALS) tissues.</title>
            <link>http://www.medworm.com/index.php?rid=185169&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%3D16012908%26dopt%3DAbstract</link>
            <description>Authors: Tomik B, Adamek D, Pierzchalski P, Banares S, Duda A, Partyka D, Pawlik W, Kałuza J, Krajewski S, Szczudlik A
    The role that apoptosis plays in the pathogenesis of amyotrophic lateral sclerosis (ALS) is still unclear. From our autopsy samples, we have undertaken an effort to verify if apoptosis in ALS really occurs or if can at least be detected. The study was performed using TUNEL method for screening the apoptotic changes in the autopsy samples from 8 ALS cases compared with 16 control cases. No features of apoptosis (DNA cleavages) were noted in any of the investigated regions of the central nervous system in ALS cases as well as in controls. These preliminary results seem to support the reports, which deny the role of apoptosis in human ALS. The following investigations us...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185169</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185169</guid>        </item>
        <item>
            <title>Quantitative analysis of activated microglia, ramified and damage of processes in the frontal and temporal lobes of chronic schizophrenics.</title>
            <link>http://www.medworm.com/index.php?rid=185168&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%3D16012909%26dopt%3DAbstract</link>
            <description>Authors: Wierzba-Bobrowicz T, Lewandowska E, Lechowicz W, Stepień T, Pasennik E
    Under pathological conditions, microglial cells undergo activation, which is manifested by the expression of histocompatibility locus antigens class II (HLA II) on their surface as well as by proliferation and varied morphological forms. In schizophrenia, characterised by an essential role played by immunological mechanisms, quantitative analysis of activated microglia -- with well-developed ramification (RM), degenerative traits and damaged processes (from their shortening to their complete lack) (DM) -- may contribute to better understanding of schizophrenia etiopathogenesis. Quantitative analysis was performed on slices derived from the frontal and temporal lobes of 9 brains of schizophrenics and 6 cont...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185168</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185168</guid>        </item>
        <item>
            <title>Distribution of metallothioneins in the brain neoplastic cells.</title>
            <link>http://www.medworm.com/index.php?rid=185167&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%3D16012910%26dopt%3DAbstract</link>
            <description>Authors: Floriańczyk B, Osuchowski J, Kaczmarczyk R, Starosławska E, Trojanowski T
    Metallothioneins (MT) are common proteins in animal tissues. These proteins take part in the homeostasis of the ions of the metals which are necessary for the proper metabolism of the organism (zinc, copper), biosynthesis regulation and zincprotein activity (for example the activity of the zinc-dependant transcription factors) and they also take part in the detoxication of the tissue from toxic metals. Apart from these, they also protect the tissue from reactive oxygen species, radiation, electrophilic pharmacological agents used in the cancer therapy and the mutagens. The aim of this work was to obtain cellular sub-fractions of brain tumors and to separate these proteins by SDS-polyacrylamide gel elec...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185167</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185167</guid>        </item>
        <item>
            <title>CXCL1 (GRO-alpha) chemokine in acute ischaemic stroke patients.</title>
            <link>http://www.medworm.com/index.php?rid=185166&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%3D16012911%26dopt%3DAbstract</link>
            <description>Authors: Losy J, Zaremba J, Skrobański P
    The inflammation accompanies and exacerbates cerebral ischaemia. The infiltrated leucocytes are thought to contribute to tissue injury in stroke patients. GRO-alpha (CXCL1) is a potent neutrophil chemoattractant which may play an important role in pathophysiology of stroke. 23 ischaemic stroke patients and 15 controls have been studied. CSF and blood sampling together with cranial CT were performed within first 24 hours of stroke. CXCL1 levels were determined by ELISA, and volume of stroke-related brain CT hypodense areas was calculated. Stroke patients displayed significantly higher CSF CXCL1 level than controls (65.6+/-22.3 vs 43.8+/-2.3 pg/ml; p&amp;lt;0.01). Serum CXCL1 levels in stroke patients did not differ from controls. CSF CXCL1 level cor...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185166</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185166</guid>        </item>
        <item>
            <title>The protective action of alpha-tocopherol on the white matter lipids during moderate hypoxia in rats.</title>
            <link>http://www.medworm.com/index.php?rid=185165&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%3D16012912%26dopt%3DAbstract</link>
            <description>Authors: Kapelusiak-Pielok M, Adamczewska-Goncarzewicz Z, Dorszewska J, Grochowalska A
    Hypoxia and ischemia acting on the brain cause alterations of the level of lipids and sterols. Famile 3.0-3.5-month-old rats were used for the experiment. They were given alpha-tocopherol in the dose of 11.43 mg/kg of body weight through seven days, then underwent hypoxia (7% of oxygen in the breathing mixture) and myelin was isolated in four times after experiment: 4, 24 hours, 14 days and 2 months after experiment. Three lipids groups were isolated that are neutral lipids, galactolipids and phospholipids. They were quantitatively analyzed with spectrophotocolorimetry. The obtained results indicate that vitamin E administration to animals does not cause significant changes of brain lipids levels. Ho...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185165</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185165</guid>        </item>
        <item>
            <title>Minimal changes of TNF-alpha and MCP-1 expression in blood serum of rats subjected to experimental cardiac arrest.</title>
            <link>http://www.medworm.com/index.php?rid=185164&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%3D16012913%26dopt%3DAbstract</link>
            <description>Conclusion: The obtained results indicate that proinflammatory cytokines do not play a key role in the development of delayed neurodegeneration after cardiac arrest. Thus it is not so much the immunological reaction, but a neuroexcitatory mechanism that plays a decisive role in the delayed neuronal death.
    PMID: 16012913 [PubMed - indexed for MEDLINE] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185164</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185164</guid>        </item>
        <item>
            <title>Paraneoplastic encephalomyelitis/sensory motor peripheral neuropathy - an autopsy case study.</title>
            <link>http://www.medworm.com/index.php?rid=185163&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%3D16012914%26dopt%3DAbstract</link>
            <description>We present an autopsy case study of anti-Hu paraneoplastic encephalomyelitis/sensory-motor neuropathy, which confirms an inflammatory paraneoplastic destruction of sensory neuron cell bodies in the dorsal root ganglia and lower motor neurons in the spinal cord, as a cause of clinically rapidly progressive peripheral sensory-motor neuropathy.
    PMID: 16012914 [PubMed - indexed for MEDLINE] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185163</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185163</guid>        </item>
        <item>
            <title>Paraganglioma of the lumbar spinal canal -- case report.</title>
            <link>http://www.medworm.com/index.php?rid=185162&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%3D16012915%26dopt%3DAbstract</link>
            <description>We present the case of a 46-year-old female with a lumbar spine paraganglioma. The patient complained of a right-sided lumboischialgia. Preoperative MRI revealed an intradural tumour at the vertebra L3 level, located in the midline, 7 mm in diameter. The tumour was totally removed by laminectomy. Histopathological examination showed nests of chief cells (zellballen), surrounded by reticulin fibres. Immunohistochemistry showed a positive reaction for chromogranin A, neuronal specific protein, synaptophysin and cytokeratin in the chief cells. The sustentacular cells displayed immunopositivity for S-100 protein, single cells were also positive for GFAP. We found no proliferative activity in the tumour cells (Ki-67 index = 0%). In the two years follow-up the patient remains without clinical or...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185162</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185162</guid>        </item>
        <item>
            <title>Epidermal growth factor receptor in glioblastoma.</title>
            <link>http://www.medworm.com/index.php?rid=185161&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%3D16245205%26dopt%3DAbstract</link>
            <description>Authors: Zawrocki A, Biernat W
    We compiled the current state of knowledge about the epidermal growth factor receptor (EGFR) in glioblastoma. Glioblastoma is one of the most common primary brain tumours and has an unfavourable prognosis despite aggressive treatment. These factors stimulate new research trials and a recent area of interest of neuro-oncologists is EGFR. This molecule is frequently altered in glioblastoma and constitutes the potential target for therapy. We decided to review the literature on biological structure of that molecule, its biological activity and the role in GBL with potential targeting it in the future neuro-oncological practice.
    PMID: 16245205 [PubMed - indexed for MEDLINE] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185161</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185161</guid>        </item>
        <item>
            <title>Is there a spatial association between senile plaques and neurofibrillary tangles in Alzheimer's disease?</title>
            <link>http://www.medworm.com/index.php?rid=185160&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%3D16245206%26dopt%3DAbstract</link>
            <description>CONCLUSION: There was little evidence that SP and NFT were spatially associated except in brain areas with high densities of lesions. The data support the hypothesis that SP and NFT are distributed relatively independently in the cerebral cortex and hippocampus and therefore, could be distinct phenomena in AD.
    PMID: 16245206 [PubMed - indexed for MEDLINE] (Source: Folia Neuropathologica)</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185160</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185160</guid>        </item>
        <item>
            <title>Alzheimer's disease related peptides affected cholinergic receptor mediated poly(ADP-ribose) polymerase activity in the hippocampus.</title>
            <link>http://www.medworm.com/index.php?rid=185159&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%3D16245207%26dopt%3DAbstract</link>
            <description>In this study the effect of Abeta 25-35 (25 microM) and non-Abeta component of Alzheimer's disease amyloid (NAC, 10 microM) on mChR-dependent signaling to PARP-1 was determined. PARP-1 activity was estimated radiochemically using egzogenous substrate adenine[14C]NAD. The results showed that the non hydrolysable agonist of mChR, carbachol (1 mM) together with GTP(g)S (100 microM) stimulated PARP-1 activity in the hippocampus by about 100%. TMB-8, inhibitor of IP3 receptor decreased PARP-1 activation evoked by carbachol/GTP(g)S. Stimulation of mChR did not lead to free radicals generation but activate PARP-1 through IP3/Ca2+ regulated processes. This cholinergic receptor dependent PARP-1 activation was abolished by Abeta and NAC peptide. These toxic peptides themselves significantly stimulat...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185159</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185159</guid>        </item>
        <item>
            <title>The analysis of the intra-surgical view of the obstetric brachial plexus palsy.</title>
            <link>http://www.medworm.com/index.php?rid=185158&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%3D16245208%26dopt%3DAbstract</link>
            <description>In this study the intra-surgical view and the applied microsurgical techniques were analysed. The clinical material consisted of 49 children with the obstetric brachial plexus palsy treated operatively, on which the following changes were found intra-surgically: compression of the brachial plexus in 21 cases and injuries with discontinuity of the elements of the brachial plexus in 28 cases. The following surgical procedures were performed: neurolysis - 31 cases, direct neurorrhaphy - 7 cases, 2 - 4 sural nerve grafting from 2 to 3 cm - 4 cases, extra-anatomical extra-plexual reconstruction - 6 cases, extra-anatomical intra-plexual reconstruction - 1 case. In all cases the intra-surgical view motivated the operative intervention. The most important problem in treatment of the obstetric brac...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185158</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185158</guid>        </item>
        <item>
            <title>The lower extremity nerve injuries - own experience in surgical treatment.</title>
            <link>http://www.medworm.com/index.php?rid=185157&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%3D16245209%26dopt%3DAbstract</link>
            <description>In this study, results of the surgical treatment of the lower extremity nerve injuries have been presented. The clinical material consisted of 270 patients (192 males, 78 females aged from 3 months to 74 years) with injuries of the common peroneal nerve - 125, sciatic nerve - 93, common peroneal and tibial nerve - 21, tibial nerve - 17, femoral nerve - 10, others - 4. The following surgical procedures were performed: external neurolysis - 164, internal neurolysis - 27, reconstruction with sural nerve grafting - 63, direct neurorrhaphy - 12, neurotisation - 3, supplementary tenomioplasty - 23. Evaluation of the results with the use of BMRC scale (M0-M5) and Highet scale (S0-S4) included the group of 120 patients. After the surgical treatment a significant improvement was found in 63.3%. The...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185157</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185157</guid>        </item>
        <item>
            <title>CCL2 (MCP-1) and CCL5 (RANTES) levels in the peripheral blood of multiple sclerosis patients treated with Glatiramer Acetate (Copaxone).</title>
            <link>http://www.medworm.com/index.php?rid=185156&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%3D16245210%26dopt%3DAbstract</link>
            <description>Authors: Losy J, Michałowska-Wender G, Kurdyńska A, Wender M
    The MCP-1 and RANTES levels were measured in 20 multiple sclerosis patients before and after 1 year daily treatment with 20 mg of subcutaneously applied glatiramer acetate. The level of MCP-1 in serum from multiple sclerosis patients was lower than in control subjects. After one year of therapy with glatiramer acetate, the level of MCP-1 was almost identical with that at the starting point. The concentration of RANTES in MS, both before and after therapy, did not differ from the control subjects. The results emphasise the marked difference between the influence of glatiramer acetate and IFNbeta-1a on the expression of the studied cytokine. Glatiramer acetate therapy in multiple sclerosis is not so much an effective as a pro...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185156</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">185156</guid>        </item>
        <item>
            <title>Inhibition of poly(ADP-ribose) polymerase activity protects hippocampal cells against morphological and ultrastructural alteration evoked by ischemia-reperfusion injury.</title>
            <link>http://www.medworm.com/index.php?rid=185155&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%3D16245211%26dopt%3DAbstract</link>
            <description>In this study we investigated the effect of PARP inhibitor, 3-aminobenzamide (3-AB) on intracellular organelles alteration. Gerbils were submitted to 3 and 10 min transient global ischemia followed by recirculation and survival for 1 till 7 days. The histological and electron microscopic examination indicated a pronounced protective effect of 3-AB on the swelling of astrocytes and neurons 1 day after 3 and 10 min ischemic insult. It decreased also the swelling of pericytes. 3-AB decreases evoked by ischemia swelling of mitochondria and Golgi apparatus. The significant ameliorating effect of 3-AB was also observed on the 7th day of reperfusion after 3 min ischemia and was also visible on the 1st day after 10 min ischemia. However, 7 days after prolonged 10 min ischemia almost all neurons in...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=185155</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
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            <title>Ultrastructural study of cerebellar dentate nucleus astrocytes in chronic experimental model with valproate.</title>
            <link>http://www.medworm.com/index.php?rid=185154&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%3D16245212%26dopt%3DAbstract</link>
            <description>Authors: Sobaniec-Łotowska ME, Lotowska JM
    The current study focuses on the morphogenesis of changes in the cerebellum dentate nucleus in the course of experimental valproate encephalopathy. Valproate - a broad spectrum antiepileptic and antipsychotic drug - chronically used in rats, intragastrically, once daily at a dose of 200 mg/kg b. w. for 1, 3, 6, 9 and 12 months, induced pronounced ultrastructural changes in the population of glial cells and nerve cells of the dentate nucleus of the cerebellum in the last two phases of the experiment. Astrocytic and neuronal lesions coexisted with a considerable damage to the elements of the blood-brain barrier of the cerebellar structure examined. The changes affected mainly the population of protoplasmic astrocytes lying loosely in a neuropil...</description>
            <author>Folia Neuropathologica</author>
            <type>journals</type>
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            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
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