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排序方式: 共有668条查询结果,搜索用时 187 毫秒
1.
Sonoelasticity imaging of prostate cancer: in vitro results 总被引:2,自引:0,他引:2
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3.
Screening for early ovarian cancer 总被引:5,自引:0,他引:5
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5.
The vascularity of 49 renal masses (26 malignant and 23 benign lesions) was investigated with duplex Doppler ultrasound. Doppler signals obtained at the margins of renal masses were defined as "tumor signals" when the Doppler-shifted frequency of the lesion exceeded the frequency shift in the ipsilateral main renal artery. These exceeded 2.5 kHz with a 3-MHz insonating frequency. Among the 26 renal masses that subsequently proved to be malignant, tumor signals were obtained in 15 of 18 (83%) untreated renal cell carcinomas, in three of four Wilms tumors, and in two patients with metastases to the kidney, but not in the one patient with lymphoma. None of the 23 benign renal masses demonstrated tumor signals. Tumor vascularity in malignant lesions gives rise to abnormal, high-velocity, Doppler-shifted signals that can help in the differential diagnosis of renal masses. 相似文献
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7.
Effect of IL-5, glucocorticoid, and Fas ligation on Bcl-2 homologue expression and caspase activation in circulating human eosinophils 总被引:6,自引:0,他引:6
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Zangrilli J Robertson N Shetty A Wu J Hastie A Fish JE Litwack G Peters SP 《Clinical and experimental immunology》2000,120(1):12-21
IL-5 is a potent eosinophil viability-enhancing factor that has been strongly implicated in the pathogenesis of IgE-mediated inflammation in vivo. Recently published data have suggested that IL-5 (and related cytokines) may act by altering the expression of the anti-apoptotic regulator Bcl-2 or its homologues, but this is controversial. The behaviour of the recently described pro-apoptotic cysteine proteases (caspases) in eosinophils after IL-5 treatment has not been explored. We examined the effect of IL-5 on the expression of four major Bcl-2 homologues, as well as on the expression/activation of key members of the caspase cell death cascade in cultured circulating human eosinophils. The effect of relevant inducers of eosinophil apoptosis (glucocorticoid and Fas ligation) on these regulatory proteins was also examined. We observed baseline expression of the anti-apoptotic Mcl-1 and pro-apoptotic Bax proteins in immunoblots of eosinophil lysates, but not Bcl-x, Bcl-2. IL-5 treatment had the effect of maintaining this basal level of expression over time without altering the balance of Bcl-2 homologues. The (upstream) caspase 8 and (downstream) caspase 3 proenzymes were detected in eosinophils at baseline, and were processed during spontaneous and stimulated eosinophil death. IL-5 completely blocked caspase processing in spontaneous and dexamethasone-induced cell death, and significantly slowed processing during Fas ligation. Our data do not support the theory that IL-5 acts by altering the balance of anti-apoptotic and pro-apoptotic Bcl-2 homologues, but suggest that it may act by regulating activation of the caspase cell death cascade. 相似文献
8.
Detection of reactive oxygen species (ROS) and apoptosis in human fragmented embryos 总被引:8,自引:2,他引:8
Yang HW; Hwang KJ; Kwon HC; Kim HS; Choi KW; Oh KS 《Human reproduction (Oxford, England)》1998,13(4):998-1002
In human in-vitro fertilization (IVF)-embryo transfer, the in-vitro culture
environment differs from in-vivo conditions in that the oxygen
concentration is higher, and in such conditions the mouse embryos show a
higher concentration of reactive oxygen species (ROS) in simple culture
media. ROS are believed to cause damage to cell membranes and DNA
fragmentation in somatic cells. This study was conducted to ascertain the
level of H2O2 concentration within embryos and the morphological features
of cell damage induced by H2O2. A total of 62 human oocytes and embryos (31
fragmented, 15 non-fragmented embryos, 16 unfertilized oocytes) was
obtained from the IVF-embryo transfer programme. The relative intensity of
H2O2 concentrations within embryos was measured using
2',7'-dichlorodihydrofluorescein diacetate by Quanti cell 500 fluorescence
imaging and DNA fragmentation was observed with transmission electron
microscopy and an in-situ apoptosis detection kit. The H2O2 concentrations
were significantly higher in fragmented embryos (72.21 +/- 9.62, mean +/-
SEM) compared to non-fragmented embryos (31.30 +/- 3.50, P < 0.05) and
unfertilized oocytes (30.75 +/- 2.67, P < 0.05). Apoptosis was observed
only in fragmented embryos, and was absent in non-fragmented embryos.
Electron microscopic findings confirmed apoptotic bodies and cytoplasmic
condensation in the fragmented blastomeres. We conclude that there is a
direct relationship between increased H2O2 concentration and apoptosis, and
that further studies should be undertaken to confirm these findings.
相似文献
9.
WT1 is a key regulator of podocyte function: reduced expression levels cause crescentic glomerulonephritis and mesangial sclerosis 总被引:15,自引:0,他引:15
Guo JK Menke AL Gubler MC Clarke AR Harrison D Hammes A Hastie ND Schedl A 《Human molecular genetics》2002,11(6):651-659
Glomerular disease is one of the most common causes of end-stage renal failure. Increasing evidence suggests that these glomerulopathies are frequently caused by primary lesions in the renal podocytes. One of the major consequences of podocyte lesions is the accumulation of mesangial matrix in the glomerular basement membrane, a process called glomerulosclerosis. Mesangial sclerosis is one of the most consistent findings in Denys-Drash patients and can be caused by dominant mutations in the Wilms' tumor 1 gene (WT1). The underlying mechanism, however, is poorly understood. WT1 is expressed in the podocytes throughout life, but its function in this cell type is unknown. Combining Wt1-knockout and inducible yeast artificial chromosome transgenic mouse models, we demonstrate that reduced expression levels of WT1 result in either crescentic glomerulonephritis or mesangial sclerosis depending on the gene dosage. Strikingly, the two podocyte-specific genes nphs1 and podocalyxin are dramatically downregulated in mice with decreased levels of Wt1, suggesting that these two genes act downstream of Wt1. Taken together, our data provide genetic evidence that reduced levels of Wt1 are responsible for the pathogenesis of two distinct renal diseases and offer a molecular explanation for the increased occurrence of glomerulosclerosis in patients with WAGR syndrome. 相似文献