Objective To analyze the clinicopathologic features of proliferative sclerosing IgA nephropathy and the efficacy of prednisone therapy. Methods A retrospective analysis was conducted, enrolling 50 patients with biopsy-proven primary proliferative sclerosing IgA nephropathy who were admitted in the Hospital from January 2005 to June 2015 - 26 males and 24 females, mean age (36.8±10.4) years. Clinicopathologic features and prednisone therapeutic effect were analyzed. Results The clinical manifestations of 50 cases were nephritis syndrome with varying degrees of renal insufficiency, including 32 cases (64.0%) with hypertension, 15 cases (30.0%) with microscopic hematuria. Renal biopsy showed the incidence of glomerular global sclerosis was 17.0%-47.2%, tubular atrophy/ interstitial fibrosis outstanding (T0 50%, T1 32%, T2 18%). After prednisone treatment, compared with sustained remission group and relapse group, invalid patients had higher incidence of hypertension (P<0.05), relatively lower Hb (P<0.01) and serum albumin, more significant renal dysfunction (P<0.01), more severe glomerular global sclerosis, segmental sclerosis, tubular atrophy/interstitial fibrosis, while the lower interstitial inflammatory cell infiltration. During the follow-up, which lasted from 6 to 132 months (median 27.3 months), the effective rate of treatment was 74.0% after sufficient prednisone or half dose prednisone therapy. Repeated recurrence rate was 32.0%. At the end of the follow-up period, 13(26.0%) patients entered the stage of uremia. Conclusions Application of glucocorticoids in the treatment of proliferative sclerosing IgA nephropathy can protect renal function and delay the progression of renal impairment. The efficacy of glucocorticoids therapy is significantly associated with the presence or absence of hypertension, the degree of renal function impairment, and the severity of the onset of renal pathology. 相似文献
Apoptosis signal-regulating kinase 1 (ASK1) is a mitogen-activated protein kinase kinase kinase (MAPKKK), which plays a pivotal role in cell apoptosis. To determine the mechanism of ASK1 induction during reperfusion of ischemic spinal tissue, we used a model of rabbit spinal cord ischemia and reperfusion. To assess the role of ASK1 in spinal cord ischemia-reperfusion injuries, we examined alterations in spinal tissue morphology, protein-protein interactions, and activation of key members of the ASK1-mediated signaling pathway. Changes in spinal cord morphology were observed with hematoxylin and eosin (H&E) staining and electron microscopy. The phosphorylation levels of ASK1, JNK, and p38 were assessed by immunoblotting proteins from animals that received 30 min of ischemia followed by 1 or 24h of reperfusion. We observed increased phosphorylation of ASK1, JNK, and p38 after reperfusing ischemic spinal cords. Immunohistochemical studies were performed to determine the cellular localization of phosphorylated ASK1 (pASK1) and 14-3-3. Following reperfusion for 24h, we observed increased cytoplasmic localization of pASK1 and decreased cytoplasmic localization of 14-3-3. Immunoprecipitation analyses suggested that 14-3-3 dissociates from ASK1 during reperfusion of ischemic spinal cords. These results indicate that activation of ASK1 may play an important role in the apoptotic signaling mechanisms that occur in reperfused spinal cord injuries. 相似文献
Visual evoked potentials (VEPs) are time-varying signals typically buried in relatively large background noise known as the electroencephalogram (EEG). In this paper, an adaptive noise cancellation with neural network-based fuzzy inference system (NNFIS) was used and the NNFIS was carefully designed to model the VEP signal. It is assumed that VEP responses can be modelled by NNFIS with the centres of its membership functions evenly distributed over time. The weights of NNFIS are adaptively determined by minimizing the variance of the error signal using the least mean squares (LMS) algorithm. As the NNFIS is dynamic to any change of VEP, the non-stationary characteristics of VEP can be tracked. Thus, this method should be able to track the VEP. Four sets of simulated data indicate that the proposed method is appropriate to estimate VEP. A total of 150 trials are processed to demonstrate the superior performance of the proposed method. 相似文献