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Constant Feature (constant + feature)
Selected AbstractsComparative analysis of NK cell subset distribution in normal and lymphoproliferative disease of granular lymphocyte conditionsEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 10 2004Véronique Pascal Abstract We have characterized the heterogeneity of human blood NK cell subsets defined by expression of KIR, lectin like receptors and NK cell differentiation markers within a cohort of 51 healthy Caucasian individuals. High inter-individual variability in cell surface expression of most NK cell markers is observed. Range values defining NK cell subsets in healthy donors were further used as references to characterize 14 patients with NK-type lymphoproliferative disease of granular lymphocytes (NK-LDGL). Alterations of the KIR repertoire were noted in all NK-LDGL patients. NK cell expansions were classified as oligoclonal KIR+ or as non-detectable KIR (ndKIR) using anti-KIR2DL1/2DS1, anti-KIR2DL2/2DL3/2DS2, anti-KIR3DL1 and anti-KIR2DS4 monoclonal antibodies. A major reduction in the size of the CD56bright NK cell subset was a constant feature of NK-LDGL. Altered distribution of CD94+, CD161+, and CD162R+ NK cell subsets was also observed in NK-LDGL patients. Considering the potential role of NK cells in eliminating tumors or virus-infected cells, the reference values defined in this study should be valuable to characterize both quantitative and qualitative alterations of the NK cell repertoire in pathological conditions and to monitor NK cell reconstitution following hematopoietic transplantation. [source] Type V Osteogenesis Imperfecta: A New Form of Brittle Bone Disease,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 9 2000Francis H. Glorieux Abstract Osteogenesis imperfecta (OI) is commonly subdivided into four clinical types. Among these, OI type IV clearly represents a heterogeneous group of disorders. Here we describe 7 OI patients (3 girls), who would typically be classified as having OI type IV but who can be distinguished from other type IV patients. We propose to call this disease entity OI type V. These children had a history of moderate to severe increased fragility of long bones and vertebral bodies. Four patients had experienced at least one episode of hyperplastic callus formation. The family history was positive for OI in 3 patients, with an autosomal dominant pattern of inheritance. All type V patients had limitations in the range of pronation/supination in one or both forearms, associated with a radiologically apparent calcification of the interosseous membrane. Three patients had anterior dislocation of the radial head. A radiodense metaphyseal band immediately adjacent to the growth plate was a constant feature in growing patients. Lumbar spine bone mineral density was low and similar to age-matched patients with OI type IV. None of the type V patients presented blue sclerae or dentinogenesis imperfecta, but ligamentous laxity was similar to that in patients with OI type IV. Levels of biochemical markers of bone metabolism generally were within the reference range, but serum alkaline phosphatase and urinary collagen type I N-telopeptide excretion increased markedly during periods of active hyperplastic callus formation. Qualitative histology of iliac biopsy specimens showed that lamellae were arranged in an irregular fashion or had a meshlike appearance. Quantitative histomorphometry revealed decreased amounts of cortical and cancellous bone, like in OI type IV. However, in contrast to OI type IV, parameters that reflect remodeling activation on cancellous bone were mostly normal in OI type V, while parameters reflecting bone formation processes in individual remodeling sites were clearly decreased. Mutation screening of the coding regions and exon/intron boundaries of both collagen type I genes did not reveal any mutations affecting glycine codons or splice sites. In conclusion, OI type V is a new form of autosomal dominant OI, which does not appear to be associated with collagen type I mutations. The genetic defect underlying this disease remains to be elucidated. [source] The Guinea Fowl Spleen at Embryonic and Post-Hatch PeriodsANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 3 2006B. I. Onyeanusi Summary The spleen of the guinea fowl was bean-shaped but without a dented hilus. It is supplied by three short arteries that came from the ventral surface, two on the cranial end and one at the caudal end of the organ. The whole organ had a thin but tough capsule covering the outer surface except at the point of entry of the blood vessels. By day 18 of incubation, the spleen had a thin but well-defined capsule and internal to this been complete network of sinusoids filled with erythrocytes, lymphocytes and granulocytes. By day 19, dark and light staining zones, which could be termed red and white pulps, had appeared. By day 20, the granulocytes with a lot of granules within their cytoplasm, had become the biggest-sized cells in the spleen. At day 21, arteries and veins were noticed clearly in the spleen and many lymphocytes, few granulocytes and reticular cells surrounded these. Red pulp with its sinusoids was now distinct. A giant cell containing three nuclei was seen within the red pulp. At day 1 post-hatch, the capsule was at its greatest thickness so far and muscle cells were seen at the inner most part of the capsule. Granulocytes that had been a constant feature suddenly disappeared. At day 5, the small lymphocytes had dominated the large and medium-sized ones. By 2 weeks, the red and white pulps were virtually equal in distribution but by 3 weeks, the red pulp was convincingly greater. By 7 weeks, plasma cells had appeared in the peripheral splenic cords. Monocytes were observed in the sinusoids. Two germinal centres were identified for the first time in week 13 post-hatch. [source] Angiotensin I-converting enzyme and potential substrates in human testis and testicular tumoursAPMIS, Issue 1 2003Review article The angiotensin I-converting enzyme (ACE, kininase II, CD143) shows a broad specificity for various oligopeptides. Besides the well-known conversion of angiotensin I to II, ACE degrades efficiently kinins and the tetrapeptide AcSDKP (goralatide) and thus equally participates in the renin-angiotensin system, the kallikrein-kinin system, and the regulation of stem cell proliferation. In the mammalian testis, ACE occurs in two isoforms. The testicular isoform (tACE) is exclusively expressed during spermatogenesis and is generally thought to represent the germ cell-specific isozyme. However, we have previously demonstrated that, in addition to tACE, the somatic isoform (sACE) is also present in human germ cells. Similar to other oncofoetal markers, sACE exhibits a transient expression during foetal germ cell development and appears to be a constant feature of intratubular germ cell neoplasm, the so-called carcinoma-in-situ (CIS) and, in particular, of classic seminoma. This demands the existence of specific paracrine functions during male germ cell differentiation and development of male germ cell tumours, which are mediated by either of the two ACE isoforms. Considering the complexity of current data about ACE, a logical connection is required between () the precise localisation of ACE isoforms, (I) the local access to potential substrates and (II) functional data obtained by knockout mice models. The present article summarises the current knowledge about ACE and its potential substrates with special emphasis on the differentiation-restricted ACE expression during human spermatogenesis and prespermatogenesis, the latter being closely linked to the pathogenesis of human germ cell tumours. [source] A central role of eNOS in the protective effect of wine against metabolic syndromeCELL BIOCHEMISTRY AND FUNCTION, Issue 4 2006Federico Leighton Abstract The positive health effects derived from moderate wine consumption are pleiotropic. They appear as improvements in cardiovascular risk factors such as plasma lipids, haemostatic mechanisms, endothelial function and antioxidant defences. The active principles would be ethanol and mainly polyphenols. Results from our and other laboratories support the unifying hypothesis that the improvements in risk factors after red wine consumption are mediated by endothelial nitric oxide synthase (eNOS). Many genes are involved, but the participation of eNOS would be a constant feature. The metabolic syndrome is a cluster of metabolic risk factors associated with high risk of cardiovascular disease (CVD). The National Cholesterol Education Programmmes Adult Treatment Panel III (NCEPATP III) clinical definition of the metabolic syndrome requires the presence of at least three risk factors, from among abdominal obesity, high plasma triacylglycerols, low plasma HDL, high blood pressure and high fasting plasma glucose. The molecular mechanisms responsible for the metabolic syndrome are not known. Since metabolic syndrome apparently affects 10,30% of the population in the world, research on its pathogenesis and control is needed. The recent finding that eNOS knockout mice present a cluster of cardiovascular risk factors comparable to those of the metabolic syndrome suggests that defects in eNOS function may cause human metabolic syndrome. These mice are hypertensive, insulin resistant and dyslipidemic. Further support for a pathogenic role of eNOS comes from the finding in humans that eNOS polymorphisms associate with insulin resistance and diabetes, with hypertension, with inflammatory and oxidative stress markers and with albuminuria. So, the data sustain the hypothesis that eNOS enhancement should reduce metabolic syndrome incidence and its consequences. Therefore red wine, since it enhances eNOS function, should be considered as a potential tool for the control of metabolic syndrome. This hypothesis is supported by epidemiological observations and needs experimental validation in human intervention studies. Copyright © 2005 John Wiley & Sons, Ltd. [source] Clinical evidence that hyperinsulinaemia independent of gonadotropins stimulates ovarian growthCLINICAL ENDOCRINOLOGY, Issue 1 2005Carla Musso Summary Objective, Ovarian enlargement is a constant feature of syndromes of extreme insulin resistance. The objective of this study is to show the role of insulin on ovarian growth in the presence of low gonadotropin levels. Patients, Seven young patients with syndromes of extreme insulin resistance (five with lipodystrophy, one with Type B syndrome and one with Rabson,Mendenhall syndrome) were studied. Measurements, Baseline LH concentrations and luteinizing hormone releasing hormone (LHRH) tests were performed. Total testosterone, insulin and C-peptide values were measured. Pelvic ultrasounds were performed. Results, Four patients were prepubertal (age range 7,10 years old) and had prepubertal gonadotropin levels, and 2 of the 4 who were tested did not respond to LHRH (NIH 10 and RM-PAL). Three patients were Tanner stage 4 (age range 13,17 years old) and had low gonadotropins that did not respond to LHRH stimulation test. All seven patients had marked hyperinsulinaemia and 6 of 7 had at least one enlarged ovary. Testosterone values were increased in 4 of 7 patients. Conclusion, This represents the first example of the pathologic role of insulin to stimulate ovarian growth with low circulating gonadotropins. Thus, while ovarian growth and steroidogenesis are normally stimulated by gonadotropins at puberty, hyperinsulinaemia stimulates pathologic growth of the ovary and an androgenic steroid profile that is active at all ages. We suggest that these patients constitute a model to separate the effect of insulin from gonadotropin in stimulating ovarian growth and/or steroidogenesis. [source] | |||||||||||||