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J Neurol Sci. 2000 Oct 1;179(S 1-2):70-5.
Estrogen receptor gene polymorphism in Japanese patients with multiple sclerosis.

Niino M, Kikuchi S, Fukazawa T, Yabe I, Tashiro K.

Department of Neurology, Hokkaido University Graduate School of Medicine, Kita-15 Nishi-7, Kita-ku, 060-8638, Sapporo, Japan. niined.hokudai.ac.jp

Estrogen has been reported to have immunosuppressive functions, and to inhibit the progression of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). Since estrogen shows its biological effects via estrogen receptors (ER), we investigate the possible role of ER genes (ERG) in the pathogenesis of MS. PvuII and XbaI polymorphisms in ERG were detected by PCR-RFLP from the DNA of 79 conventional MS patients and 73 healthy controls. The [P] allele in the profiles in PvuII was significantly more prevalent in MS patients than in the controls (P<0.0005). In the study of XbaI polymorphism, the onset age of MS patients with the Xx genotype was earlier than that of the xx genotype group (mean age+/-S.D.; 22.60+/-8.04, and 27.49+/-9.14, respectively) (P<0.05) by ANOVA followed by Fisher's PLSD. Although the Xx genotype group tended to earlier onset age than the XX genotype group (29.60+/-11.10), this difference did not reach. On the basis of these results, PvuII polymorphism might be associated with susceptibility to MS, and XbaI polymorphism with onset age of MS. ERG polymorphism should be further studied in other populations to improve strategies for treatment of MS.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11054488&dopt=Abstract

J Neurol Sci. 2000 Oct 1;179(S 1-2):92-102.
Peripheral neuropathy associated with hereditary and sporadic inclusion body myositis: confirmation by electron microscopy and morphometry.

Hermanns B, Molnar M, Schroder JM.

Institut fur Neuropathologie, Universitatsklinikum der Rheinisch-Westfalischen Technischen Hochschule Aachen, Pauwelsstrasse 30, D-52074, Aachen, Germany.

Inclusion body myositis (IBM) is a disabling myopathy affecting proximal and distal muscle groups. The involvement of peripheral nerves in IBM is still a controversial matter. In a previous morphometric study at the light microscopic level only, we described a peripheral neuropathy in sural nerve biopsies of eight patients with sporadic IBM (s-IBM). Here we present a larger series of 14 cases in which a combined muscle and nerve biopsy was available for additional electron microscopic investigation. In two of the new cases, the IBM had a hereditary background (h-IBM). The presence of neuropathy was confirmed in all 14 cases studied. Morphometry using an optic-electronic, digital evaluation system showed large variation of severity presumably due to age and coincidal factors such as diabetes mellitus or lymphoma. Ultrastructural analysis revealed a variety of changes considered to be non-specific. Signs of axonal damage predominated. In addition, there were numerous changes in Schwann cells and myelin sheaths. Neither inflammatory changes nor tubulofilamentous inclusions were detectable in the sural nerves. Peripheral neuropathy, although occasionally without apparent clinical manifestation, appears to be a common and aggravating feature in IBM; its pathogenesis, however, remains elusive.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11054491&dopt=Abstract

Int J Cardiol. 2000 Aug;75(1):23-33; discussion 33-5.
Inflammatory cells, apoptosis and Chlamydia pneumoniae infection in atherosclerosis.

Matturri L, Cazzullo A, Turconi P, Roncoroni L, Grana D, Milei J.

Institute of Pathology, University of Milan, Milan, Italy.

Chlamydia pneumoniae (CP), chromosomal alterations and apoptosis were suggested as contributing factors in the pathogenesis of atherosclerosis. Early (EP) and unstable plaques (UP) were studied in order to assess infiltrate composition, the apoptotic index, chromosome 7 stability and to investigate the concurrent presence of CP in EP and UP. Paraffin embedded sections of three iliac arteries and four aortas from young donors (EP), and four coronaries and nine carotid arteries (UP) were used. Aside from histological techniques, immunophenotypification for macrophages, T and B cells, smooth muscle and endothelial cells; FISH and DNA nick end labeling were performed. The amplifications with PCR for CP infection were negative in all specimens. In the EP, a focal myointimal thickening with foam cells and scarce smooth muscle cells was observed. Macrophages were most frequent in the intima (10.8%) while T and B cells were found in 2.3 and 1.5%. In the UP a thin cap covering a lipid-rich core with widespread vascularization and with severe luminal obstruction was observed. Macrophages were increased (21%), and T (1.5%) and B cells (3.5%) in the caps and inner areas of the lipid cores. At these sites, the FISH showed trisomy and tetrasomy of chromosome 7 and apoptosis was very frequent (10-30%). Macrophages in intimal lesions is one of the most prominent, consistent and permanent features in EP, and an elevated apoptotic index and chromosome 7 instability might contribute to evolution from stable to complicated plaques, while CP seems to play no role. However, further studies are needed with more cases to confirm this last observation.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11054502&dopt=Abstract

Cancer Lett. 2003 Apr 25;193(2):217-23.
Expression of the inhibitor of apoptosis protein survivin in benign meningiomas.

Das A, Tan WL, Smith DR.

Department of Neurology, National Neuroscience Institute, 11, Jalan Tan Tock Seng 308433, Singapore.

Survivin is a recently characterised inhibitor of apoptosis protein that has been implicated in the pathogenesis of several types of solid organ cancer. This study sought to describe the expression of survivin in a cohort of 90 benign meningiomas, together with the pattern of expression of other genes involved in the apoptotic process, namely bax and bcl2. Survivin expression was noted in 94% (85/90) of samples and was not correlated with the expression of either bax or bcl2 or with clinicopathological factors.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12706880&dopt=Abstract

Gene. 2000 Oct 3;256(1-2):35-42.
dfh is a Drosophila homolog of the Friedreich's ataxia disease gene.

Canizares J, Blanca JM, Navarro JA, Monros E, Palau F, Molto MD.

Departament de Genetica, Facultat de Ciencies Biologiques, Universitat de Valencia, 46100, Burjassot, Spain.

A putative Drosophila homolog of the Friedreich's ataxia disease gene (FRDA) has been cloned and characterized; it has been named Drosophila frataxin homolog (dfh). It is located at 8C/D position on X chromosome and is spread over 1kb, a much smaller genomic region than the human gene. Its genomic organization is simple, with a single intron dividing the coding region into two exons. The predicted encoded product has 190 amino acids, being considered a frataxin-like protein on the basis of the sequence and secondary structure conservation when compared with human frataxin and related proteins from other eukaryotes. The closest match between the Drosophila and the human proteins involved a stretch of 38 amino acids at C-terminus, encoded by dfh exon 2, and exons 4 and 5a of the FRDA gene, respectively. This highly conserved region is very likely to form a functional domain with a beta sheet structure flanked by alpha-helices where the sequence is less conserved. A signal peptide for mitochondrial import has also been predicted in the Drosophila frataxin-like protein, suggesting its mitochondrial localization, as occurs for human frataxin and other frataxin-like proteins described in eukaryotes. The Drosophila gene is expressed throughout the development of this organism, with a peak of expression in 6-12h embryos, and showing a spatial ubiquitous pattern from 4h embryos to the last embryonic stage examined. The isolation of dfh will soon make available specific dfh mutants that help in understanding the pathogenesis of FRDA.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11054533&dopt=Abstract

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