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Koch Hüsselrath Dinkler Gaubatz Zinn Gaübatz Schmidt Uhlmann Kahlstorf Bernhardt Pendl Rust Pauschardt A. Hermann Müller Vaternahm Koch Hüsselrath 《Journal of molecular medicine (Berlin, Germany)》1939,18(7):256-259
Ohne Zusammenfassung 相似文献
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Elevated amounts of platelet-associated serum proteins (PASP) can be detected in idiopathic thrombocytopenic purpura (ITP) and are considered to be of patho-aetiological importance especially in the case of acute ITP, that commonly follows acute febrile illnesses. Using a micro-enzyme-linked immunoassay we examined PASP (IgG, IgM, and C3) in 120 paediatric patients with acute fever caused by viral (n = 45), bacterial (n = 48), or non-detectable agents (n = 27) and compared those values to the levels of PASP of an own paediatric control group (n = 21). Two of the patients presented mild temporary thrombocytopenia without clinical signs in the course of their infectious disease. While having normal platelet counts, the majority of our patients (69.2%) however, showed increased levels of PASP (IgG, IgM, C3; single or combined). Significant differences of PASP levels by discrimination of viral and bacterial diseases could not be demonstrated. Elevated platelet-associated complement was of special interest, because - in the absence of low platelet counts due to platelet-specific antibodies - it must be regarded as an indicator for immune complexes (IC) binding to thrombocyte surface IgG Fc-receptors. Thus we suggest that platelets play a considerable role in the elimination of circulating IC. 相似文献
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Ross JL Bellus G Scott CI Abboudi J Grigelioniene G Zinn AR 《American journal of medical genetics. Part A》2003,(1):61-65
We studied two children with combined genetic skeletal disorders. Both had Leri-Weill dyschondrosteosis (LWD); one also had achondroplasia and the other had hypochondroplasia. Both had severe short stature and evidence of rhizomelia and mesomelia as well as other phenotypic features of their individual genetic disorders. Achondroplasia was due to the G380R FGF3R mutation and hypochondroplasia to a N540K mutation in the same gene. The patient with hypochondroplasia had a heterozygous SHOX deletion; no SHOX mutation was identified in the child with achondroplasia. The phenotypes of combined LWD and achondroplasia or hypochondroplasia appeared to be less than additive, suggesting that SHOX and FGFR3 act on overlapping pathways of bone growth and development. 相似文献