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To date, 33 human platelet alloantigens (HPAs) have been identified on six functionally important platelet glycoprotein (GP) complexes and have been implicated in alloimmune platelet disorders including foetal and neonatal alloimmune thrombocytopenia (FNAIT), posttransfusion purpura (PTP) and multitransfusion platelet refractoriness (MPR). The greatest number of recognized HPA (20 of 33) resides on the GPIIb/IIIa complex, which serves as the receptor for ligands important in mediating haemostasis and inflammation. These include HPA‐1a, the most commonly implicated HPA in FNAIT and PTP in Caucasian populations. Other platelet GP complexes, GPIb/V/IX, GPIa/IIa and CD109, express the remaining 13 HPAs. Of the recognized HPAs, 12 occur as six serologically and genetically defined biallelic ‘systems’ where the –a form designates the higher frequency allele and the –b form, the lower. Twenty‐one other HPAs are low‐frequency or rare antigens for which postulated higher frequency –a alleles have not yet been identified as antibody specificities. In addition to the HPA markers, platelets also express ABO and human leucocyte antigen (HLA) antigens; antibodies directed at the former are occasionally important in FNAIT, and to the latter, in MPR.  相似文献   

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Pro – rebuttal     
《Liver international》2009,29(5):640-640
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Objective Influenza‐associated myositis (IAM), characterized by severe lower‐extremity myalgia and reluctance to walk, is a complication of influenza among children. We investigated IAM in Nebraska during six influenza seasons, 2001–2007. Methods During 2006–2007, we requested reports of severe influenza illness among persons aged <18 years and investigated medical records to identify and confirm IAM cases defined as severe myalgia with elevated serum creatinine kinase level in a patient aged <18 years, occurring within 7 days of laboratory confirmed influenza illness onset. Statewide hospital discharge data (HDD) were reviewed to identify retrospectively confirmed IAM cases during 2006–2007 and five previous seasons, by using surveillance data to define periods of influenza activity. Statewide IAM incidence was estimated for 2001–2002 through 2006–2007. Results During 2006–2007, a total of 13 IAM cases were confirmed by enhanced surveillance. Median age was 6 years (range, 4–11 years). Influenza diagnosis was established by viral isolation from six patients (one influenza A and five influenza B) and rapid diagnostic tests for seven. Twelve (92%) patients, including one who died, were hospitalized for a median of 3 days (range, 1–4 days). Review of HDD identified 12 retrospectively confirmed IAM cases during 2006–2007, including four not reported through enhanced surveillance, and only one during five previous seasons (2003–2004). The HDD‐derived, retrospectively confirmed statewide IAM incidence estimates/1 00 000 population aged <18 years were 2·693 and 0·225 during 2006–2007 and 2003–2004, respectively. Conclusion An IAM epidemic occurred in Nebraska during the 2006–2007 influenza season.  相似文献   

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Glutamic acid decarboxylase (GAD) enzymes catalyse the formation of gamma-aminobuturic acid (GABA), which is a major transmittor in the central nervous system but also exerts functions in peripheral organs. Recent molecular analyses have revealed surprising new roles for the GAD isoforms in human diseases of autoimmune character including neurological disorders and insulin-dependent diabetes. In the 1995 Frontiers in Medicine Symposium, the coauthors of this review discussed the genetics, cell biology, molecular immunology and the role of GAD as autoantigens in human autoimmunity. Studies on disease diagnosis, prediction, and prognosis have revealed unique patterns of reactivities in both cellular and humoral immune responses. Further work will be needed to establish whether the GAD molecules can be used to treat autoimmune diseases.  相似文献   

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