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91.
The unusual occurrence of very large cysticerci presenting as tumour-like lesions prompted this search of the pathology records of a south Indian hospital, to find similar cases. The maximum diameter of 187 consecutively diagnosed extraneural cysticerci, was recorded and those cases exceeding the mean by two standard deviations reviewed. Six biopsies showing cysticerci with a maximum diameter ranging from 4 to 11 cm, were identified, and hospital records and all pathological material available, were reexamined. The clinical differential diagnosis included benign and malignant tumours, hydatid cyst and haematoma. All the cysts were confirmed to be cysticerci, but species diagnosis was not possible by examining archival material. In an appropriate geographical setting, large cysticerci should form part of the differential diagnosis of cystic tumour-like lesions. An attemp can then be made, while the specimen is still fresh, to identify the species. 相似文献
92.
Anne‐Marie Lamhonwah Simon E. Olpin Rodney J. Pollitt Christine Vianey‐Saban Priscille Divry Nathalie Guffon Guy T. N. Besley Russell Onizuka Linda J. De Meirleir Ljerka Cvitanovic‐Sojat Ivo Baric Carlo Dionisi‐Vici Ksenija Fumic Miljenka Maradin Ingrid Tein 《American journal of medical genetics. Part A》2002,111(3):271-284
Primary systemic carnitine deficiency or carnitine uptake defect (OMIM 212140) is a potentially lethal, autosomal recessive disorder characterized by progressive infantile‐onset cardiomyopathy, weakness, and recurrent hypoglycemic hypoketotic encephalopathy, which is highly responsive to L ‐carnitine therapy. Molecular analysis of the SLC22A5 (OCTN2) gene, encoding the high‐affinity carnitine transporter, was done in 11 affected individuals by direct nucleotide sequencing of polymerase chain reaction products from all 10 exons. Carnitine uptake (at Km of 5 μM) in cultured skin fibroblasts ranged from 1% to 20% of normal controls. Eleven mutations (delF23, N32S, and one 11‐bp duplication in exon 1; R169W in exon 3; a donor splice mutation [IVS3+1 G > A] in intron 3; frameshift mutations in exons 5 and 6; Y401X in exon 7; T440M, T468R and S470F in exon 8) are described. There was no correlation between residual uptake and severity of clinical presentation, suggesting that the wide phenotypic variability is likely related to exogenous stressors exacerbating carnitine deficiency. Most importantly, strict compliance with carnitine from birth appears to prevent the phenotype. © 2002 Wiley‐Liss, Inc. 相似文献
93.
Vesicular stomatitis virus: mode of transcription. 总被引:44,自引:0,他引:44
94.
Alyce C. Russell Agnieszka Kepka Irena Trbojević-Akmačić Ivo Ugrina Manshu Song Jennie Hui Michael Hunter Simon M. Laws Gordan Lauc Wei Wang 《Immunobiology》2019,224(1):110-115
Background
Increased body fat may be associated with an increased risk of developing an underlying pro-inflammatory state, thus leading to greater risk of developing certain chronic conditions. Immunoglobulin G has the ability to exert both anti- and pro-inflammatory effects, and the N-glycosylation of the fragment crystallisable portion is involved in mediating this process. Body mass index, a rudimentary yet gold standard indication for body fat, has been shown to be associated with agalactosylated immunoglobulin G N-glycans.Aim
We aimed to determine the association between increased body fat and the immunoglobulin G glycosylation features, comparing body mass index to other measures of body fat distribution.Methods
We investigated a sample of 637 community-based 45–69?year olds, with mixed phenotypes, residing in Busselton, Western Australia. Body mass index and the waist-to-hip and waist-to-height ratios were calculated using anthropometry, while dual-energy x-ray absorptiometry was performed to gain an accurate measure of total and area specific body fat. Serum immunoglobulin GN-glycans were analysed by ultra-performance liquid chromatography.Results
Twenty-two N-glycan peaks were found to be associated with at least one of the fat measures. While the previous association of body mass index to agalactosylated immunoglobulin G was replicated, measures of central adiposity explained the most variation in the immunoglobulin G glycome.Conclusion
Central adiposity is associated with an increased pro-inflammatory fraction of immunoglobulin G, suggesting that the android/gynoid ratio or waist-to-height ratio instead be considered when controlling for adiposity in immunoglobulin G glycome biomarker studies. 相似文献95.
Vermeesch JR Melotte C Salden I Riegel M Trifnov V Polityko A Rumyantseva N Naumchik I Starke H Matthijs G Schinzel A Fryns JP Liehr T 《European journal of medical genetics》2005,48(3):319-327
A dysmorphic patient was shown to carry a small supernumerary marker chromosome. Multicolor, centromere-multicolor and regular FISH experiments proved the marker to be an analphoid 12pter derived isochromosome. Microdissection of the marker followed by reverse painting and array CGH analysis showed that the isochromosome contains approximately 6 Mb of 12pter-12p13.31 derived sequence. This is only the second report of a marker with a neocentromere 12pter and the molecular fine mapping of the duplicated region further refines the 12p region defining the Pallister-Killian syndrome phenotype. In addition, we show the feasibility of using microdissected chromosomes or chromosomal fragments to molecularly map the chromosomal breakpoints on array CGH. This technology may aid in the identification of chromosomal translocation breakpoints. 相似文献
96.
Brosens I Gordts S Valkenburg M Puttemans P Campo R Gordts S 《Human reproduction (Oxford, England)》2004,19(8):1689-1692
While the appropriate method for the investigation of female infertility continues to be debated, the timing of the investigation has received less attention. The current approach is time-consuming, and paradoxically may lead to overtreatment as well as undertreatment. Recent findings on fecundity and the conception window in humans have important implications for the timing of the investigation of female infertility. The findings support the view that fertility-oriented intercourse may have a major impact in reducing the time to pregnancy. Procedures for the investigation of female infertility are becoming less invasive and more accurate, while the therapies for infertility are more effective. It is proposed that under appropriate circumstances female infertility should be investigated after 6 months of fertility-oriented intercourse. 相似文献
97.
98.
Sporadic fundic gland polyps: common gastric polyps arising through activating mutations in the beta-catenin gene 总被引:1,自引:0,他引:1 下载免费PDF全文
Abraham SC Nobukawa B Giardiello FM Hamilton SR Wu TT 《The American journal of pathology》2001,158(3):1005-1010
Fundic gland polyps (FGPs) are the most common gastric polyps. FGPs traditionally have been regarded as nondysplastic hamartomatous or hyperplastic lesions, but their pathogenesis remains unclear. We have recently shown that somatic adenomatous polyposis coli (APC) gene alterations are frequently present in FGPs associated with familial adenomatous polyposis (FAP), raising the possibility that mutations of the beta-catenin gene affecting the APC/beta-catenin pathway might be involved in the pathogenesis of sporadic FGPs. We analyzed somatic beta-catenin gene mutations in 57 sporadic FGPs from 40 patients without FAP and in 19 FGPs from 13 FAP patients. Direct DNA sequencing of exon 3 encompassing the glycogen synthase kinase-3beta phosphorylation region for beta-catenin was used with confirmation by HIN:fI restriction endonuclease digestion. The foveolar epithelium and dilated fundic glands of the polyps were separately microdissected and analyzed in 22 of 57 sporadic FGPs. Activating beta-catenin gene mutations were present in 91% (52 of 57) of sporadic FGPs. Both the foveolar epithelium and the dilated fundic gland epithelium comprising the polyps were shown to have the same somatic beta-catenin mutation in 21 of 22 (95%) sporadic FGPs. In contrast, beta-catenin gene mutations were not present in any of the 19 FAP-associated FGPs (P: < 0.000001). The high frequency of beta-catenin mutations in sporadic FGPs indicates that these lesions arise through activating mutations of the beta-catenin gene. Beta-catenin mutations in gastrointestinal tract polyps have previously only been demonstrated in a subset of adenomatous (dysplastic) or neoplastic polyps. Sporadic FGPs are therefore the only lesions of the gastrointestinal tract to demonstrate beta-catenin mutations while lacking dysplastic morphology. 相似文献
99.
Mast cells are traditionally known for mediating allergic reactions. In addition, these cells have been implicated in the
pathogenesis of a variety of clinical conditions such as atopic and contact dermatitis, bullous pemphigoid, fibrotic lung
disease, neurofibromatosis, psoriasis, scleroderma, rheumatoid arthritis, interstitial cystitis, ulcerative colitis, and Crohn’s
disease, but their role in host defense was an enigma until recently. Owing to the strategic location of mast cells at the
host environment interface, their role in bacterial infections has been studied by a number of investigators. Latest reports
show that mast cells have an ability to modulate the host’s innate immune response to infectious agents. This review discusses
the clinical implications of mast cell-bacteria interactions.
Received: 13 August 1997 / Accepted: 7 April 1998 相似文献
100.
Comparative genomic hybridization (CGH) analyses have detected gains of copy number on 13q, especially at 13q31-q32, in cell
lines and primary cases of various types of lymphoma. Since amplification of chromosomal DNA is one of the mechanisms that
can activate tumor-associated genes, and because 13q amplification had been reported in various other types of tumors as well,
we attempted to define by fluorescence in situ hybridization (FISH) a common region at 13q31-q32 in which to explore genes
that might be targets for the amplification events. Although the commonly amplified region we defined was relatively large
(approximately 4 Mb), only one true gene, GPC5, was found there. GPC5 was over-expressed in lymphoma cell lines that had shown amplification, in comparison with those that had not. Our findings
suggest that GPC5 is a likely target for amplification, and that over-expression of this gene may contribute to development and/or progression
of lymphomas and other tumors. 相似文献