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581.
BACKGROUND: Trypanosoma cruzi, the cause of Chagas' disease, is often transmitted by transfusion in Latin America. Previous studies showed that at least 1 in 1000 eligible blood donors at the Los Angeles County+University of Southern California (LAC+USC) Medical Center Blood Bank had specific antibodies to T. cruzi. In June 1993, serologic screening of prospective allogeneic donors at epidemiologic risk for T. cruzi infection was begun voluntarily. STUDY DESIGN AND METHODS: The risk of T. cruzi infection in all eligible donors was assessed by questionnaire. At-risk donors were screened serologically for antibodies to T. cruzi with an enzyme immunoassay, and confirmatory testing was done with a radioimmunoprecipitation assay. RESULTS: During the 29-month study period 1311 (39.5%) of 3320 donors were judged to be at risk for T. cruzi infection. Seven donors (1/475) were reactive by an enzyme immunoassay, and six of these seven (1/ 553) were positive in a radioimmunoprecipitation assay. All radioimmunoprecipitation assay- positive donors had been born in countries in which Chagas' disease is endemic. One person in this group had received a transfusion in his homeland. CONCLUSION: These results demonstrate that a substantive proportion of eligible blood donors at our institution have antibodies specific for T. cruzi and that a commercially available assay can be used to detect these antibodies. Our data suggest that the risk of transmission of T. cruzi by transfusion could be eliminated by serologic testing limited to persons born in or transfused in countries in which Chagas' disease is endemic.  相似文献   
582.
Until recently, all cephalosporin-induced immune hemolytic anemias appeared to react by a "penicillin-type" drug adsorption mechanism, and hemolysis was extravascular. In 1987 and 1988, the first two cases of cephalosporin-induced immune hemolytic anemia with intravascular hemolysis associated with a so-called immune complex mechanism were reported. This report describes a case of extravascular hemolysis due to a third-generation cephalosporin, cefotaxime, which, to the authors' knowledge, is the first to show in vitro characteristics of both the drug adsorption and the so-called immune complex mechanisms.  相似文献   
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目的评估不同的电极密度对BEAM数据精确性的影响。方法32名年龄50~59岁正常受试者。采用1和4点插值计算方法计算平均平方根功率BEAM。对比16、20、24、28通道记录的BEAM。结果6个脑电频段61%(11/18)的高功率值电极部位不在16通道的记录电极之内。其中73%(8/11)的高功率电极位于中线电极(Fz、Cz、Pz、OZ)。16通道记录时各个频段的功率值明显降低。增加记录电极,BEAM的精确性增加。结论16通道记录的BEAM存在明显的失真,在低密度电极记录的条件下计算BEAM至少20通道。  相似文献   
587.

Objective

To determine if the new, orally active C5a receptor antagonist, the cyclic peptide AcF‐[OPdChaWR], reduces the severity of pathology in a rat model of immune‐mediated monarticular arthritis.

Methods

Arthritis was induced in the right knee of previously sensitized rats by the intraarticular injection of methylated bovine serum albumin. Rats were examined for either 14 days or 28 days, or for 49 days following a second antigen challenge at 28 days. The C5a antagonist (1 or 3 mg/kg/day) and/or ibuprofen (30 mg/kg/day) were administered orally on a daily basis either before or after arthritis induction.

Results

Rats receiving AcF‐[OPdChaWR] had significant reductions in right knee swelling, gait disturbance, lavaged joint cell numbers, and right knee histopathology, as well as in serum levels of tumor necrosis factor α (TNFα) and intraarticular levels of interleukin‐6 and TNFα on day 14. In the 14‐ and 28‐day studies, ibuprofen resulted in a similar reduction in gait abnormalities and intraarticular inflammatory cells compared with the C5a antagonist, but was less effective in reducing knee swelling over the course of the study and had no effect on knee histopathology. Combination therapy with AcF‐[OPdChaWR] and ibuprofen resulted in no greater efficacy than with the C5a antagonist alone. Rats injected twice with the antigen in the 49‐day study displayed the most severe histopathology and this, as well as knee swelling and gait abnormalities, was significantly reduced by repeated treatment with the C5a antagonist.

Conclusion

An agent that inhibits the action of C5a in this model significantly reduced joint pathology, while ibuprofen was not effective. C5a antagonists could therefore have broader therapeutic benefits than nonsteroidal antiinflammatory drugs as antiarthritic agents for rheumatoid arthritis.
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