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排序方式: 共有593条查询结果,搜索用时 8 毫秒
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Normal and diseased isolated lungs: high-resolution CT 总被引:8,自引:0,他引:8
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Picotamide inhibition of excess in vitro thromboxane B2 release by colorectal mucosa in inflammatory bowel disease. 总被引:1,自引:0,他引:1
Collins CE Benson MJ Burnham WR Rampton DS 《Alimentary pharmacology & therapeutics》1996,10(3):315-320
BACKGROUND: Inflammatory bowel disease is associated with increased mucosal release of eicosanoids. Among these, thromboxane A2 has been proposed as a possible inflammatory mediator; its suppression may be a useful therapeutic option. METHODS: Using a tissue incubation technique, we compared release of immunoreactive thromboxane B2 by colonic biopsies from patients with ulcerative colitis, Crohn's disease and controls, and assessed the inhibitory effect of picotamide, a thromboxane synthesis inhibitor-receptor antagonist, which has been widely used in Italy for management of ischaemic heart and cerebrovascular disease. RESULTS: Increased amounts of thromboxane B2 were released from biopsies from patients with active ulcerative colitis (median 238 pg/20 min/mg wet weight (interquartile range 147- 325), n = 12) and active Crohn's disease (252 (174-450), 6) compared with those from patients with quiescent ulcerative colitis (95 (61- 140), 12) or Crohn's disease (105 (57-201), 13), or controls (136 (64- 206), 8). Incubation with picotamide at concentrations between 100 microM and 1 mM reduced thromboxane B2 release (IC50 890 microM). CONCLUSION: Since increased thromboxane A2 production may have pathogenetic importance, thromboxane synthesis inhibitor-receptor antagonists such as picotamide merit therapeutic trial in the management of inflammatory bowel disease. 相似文献
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Preferential recognition of human myocardial antigens by T lymphocytes from rheumatic heart disease patients. 总被引:2,自引:0,他引:2
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M El-Demellawy R El-Ridi N I Guirguis M Abdel Alim A Kotby M Kotb 《Infection and immunity》1997,65(6):2197-2205
Acute rheumatic fever (ARF) and rheumatic heart disease (RHD) are autoimmune sequelae of upper respiratory infections with group A streptococci (GAS). To gain a better understanding of the pathogenesis of these diseases, we examined the in vitro proliferative responses of peripheral blood mononuclear cells (PBMC) from RHD patients to human myocardial proteins in a T-cell Western assay. A number of myocardial proteins fractionated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis were recognized by PBMC from both patients and controls. However, PBMC from a significant percentage of RHD patients (40%) responded to a discrete band of myocardial proteins migrating with an apparent molecular mass of 50 to 54 kDa while none of the control subject PBMC responded to this protein band (P < or = 0.0001). To further investigate the link between infections with GAS and autoimmune carditis, we studied the proliferative responses of PBMC from patients and controls to myocardial proteins before and after in vitro stimulation of the cells with opsonized GAS isolated from ARF patients. Priming of PBMC with rheumatogenic GAS caused the percentage of RHD patients responding to the 50- to 54-kDa myocardial proteins to increase from 43 to 90% (P < or = 0.0284). By contrast, PBMC from control subjects failed to recognize the 50- to 54-kDa myocardial proteins even after stimulation with the opsonized streptococci (P < or = 0.0001). The assay sensitivity was increased from 40 to 90% after priming of a patient's cells with opsonized GAS, but the positive predictive value was 100% in both unprimed and primed cultures. Antibodies generated to partially purified 50- to 54-kDa myocardial proteins did not cross-react with either streptococcal homogenates, purified M protein, myosin, laminin, or vimentin, suggesting a lack of cross-reactivity at the humoral level. This study suggests that the 50- to 54-kDa myocardial proteins contain a putative antigen that is preferentially recognized by T cells from RHD patients and demonstrates that exposure to streptococcal antigens enhances the ability of patients to recognize these proteins. 相似文献
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Hydrosalpinges adversely affect markers of endometrial receptivity 总被引:22,自引:10,他引:22
Meyer WR; Castelbaum AJ; Somkuti S; Sagoskin AW; Doyle M; Harris JE; Lessey BA 《Human reproduction (Oxford, England)》1997,12(7):1393-1398
While in-vitro fertilization (IVF) was initially developed in women with
tubal factor infertility, recent clinical studies have suggested that the
presence of hydrosalpinges lowers implantation and pregnancy rates. We
postulated that these hydrosalpinges cause impaired endometrial
receptivity. A total of 103 women with hydrosalpinges were prospectively
evaluated, and compared with 55 infertile and 44 fertile controls. All
women had endometrial biopsies during the window of implantation, analysed
by conventional histological criteria, and also stained for three integrin
markers of endometrial receptivity (alpha1beta1, alpha4beta1 and alpha
vbeta3). Women with hydrosalpinges (cases) expressed significantly less of
the alpha vbeta3 integrin compared with controls. There was no difference
in expression of alpha1beta1 or alpha4beta1 among groups. A significantly
greater number of cases had out of phase histology and missing alpha vbeta3
(type I defects) and absent integrin expression despite normal histological
maturation (type II) defects, compared with controls. Of 20 women with
impaired endometrial receptivity who were also biopsied after hydrosalpinx
surgery, 70% demonstrated increased alpha vbeta3 expression. Seventy-seven
percent of type I and 57% of type II defects were corrected
postoperatively. Using markers of endometrial receptivity, this study
demonstrates that inflammatory hydrosalpinges have an adverse effect on
endometrial receptivity, which in some cases may be overcome by surgical
treatment of the hydrosalpinx.
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