Clinicopathologic features and prednisone therapeutic effect of 50 cases of proliferative sclerosing IgA nephropathy

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.     

宫颈合并阴道高级别上皮内病变的诊断与处理

目的 总结宫颈合并阴道上皮内病变诊断与处理的临床经验.方法 对1例宫颈冷刀锥切(cold knifeconization,CKC)术后反复新柏氏液基细胞学技术(thinprep cytologic test,TCT)异常患者进行多次阴道镜下宫颈及阴道壁活检,发现高级别上皮内病变,对此患者诊断过程和治疗方法进行总结分析.结果 本例54岁女性,因高级别宫颈上皮内病变行CKC手术,术后仍提示反复TCT异常,高危型人乳头瘤病毒(high-risk humanpapilomavirus,HR-HPV)持续感染,阴道镜活检发现宫颈合并阴道高级别上皮内病变,阴道病变广泛延伸至阴道上1/3,随行腹腔镜下筋膜外全子宫切除术+双附件切除术+部分阴道切除术,术后发现仍有阴道高级别上皮内病变残留,故继续补充阴道腔内放疗.结论 对于宫颈上皮内病变患者,建议常规行阴道镜下阴道壁全面检查,对可疑病变部分活检,尤其高级别宫颈上皮内病变患者.对于宫颈合并阴道高级别上皮内病变患者,尽量行全子宫切除时同时切除阴道病变,减少阴道上皮内病变残留.     

对侧皮质锁定技术治疗股骨远端骨折的研究近况

传统锁定螺钉装置存在刚度较高、近钢板侧应力集中的缺陷。近年来,因为传统锁定螺钉装置治疗股骨远端骨折愈合率较低,对侧皮质锁定技术（FCL）逐渐受到重视。其能降低传统锁定螺钉装置80%的固定强度,且保留锁定螺钉装置整体固定强度,提供弹性固定和骨折断端的平行微动,骨折端的骨痂生长较多、对称。在治疗骨折的理论上,FCL有新突破。在动物实验和初步临床应用中,可以使传统锁定螺钉装置治疗股骨远端骨折的愈合率提高。

     

划痕损伤对大鼠大脑皮层微血管内皮细胞NF-κB表达及继发性死亡的影响

目的  通过体外培养SD大鼠大脑皮层微血管内皮细胞并制作划痕损伤模型,观察划痕损伤对脑微血管内皮细胞NF-κB表达及其自噬、凋亡和坏死的影响。方法  体外培养SD大鼠大脑皮层微血管内皮细胞并制作划痕损伤模型,应用NF-κB抑制剂吡咯醛二硫氨基甲酸（PDTC）干预划痕损伤脑微血管内皮细胞。随机分为对照组、单纯损伤组、损伤+抑制组,在不同时间点（损伤后1、6、12、24及48 h）分别应用免疫荧光细胞化学法测定磷酸化NF-κB p65蛋白的表达,Annexin V/PI染色法检测凋亡、坏死,Western blot检测自噬蛋白LC3Ⅱ表达情况。对照组为无划痕损伤的脑微血管内皮细胞。结果  脑微血管内皮细胞划痕损伤后NF-κB蛋白表达于伤后1 h开始表达增强,于24 h达高峰,与对照组比较差异有统计学意义（P <0.05）。凋亡、坏死及自噬各指标均随时间推移有不同程度升高,与对照组比较差异有统计学意义（P <0.05）。而经PDTC处理后上述变化均受不同程度的抑制,与单纯损伤组相比差异有统计学意义（P <0.05）。结论  划痕损伤后可激活脑微血管内皮细胞NF-κB表达,同时可引起脑微血管内皮细胞的自噬、凋亡和坏死。

     

双环钢丝捆扎技术联合关节置换对转子间骨折患者快速康复的临床观察

目的  探讨交叉双环钢丝捆扎技术联合关节置换术治疗高龄股骨转子间粉碎骨折的临床疗效。方法选取本院2013～2014年行人工关节置换结合钢丝捆扎治疗转子间骨折（Evans-Jensen分型：Ⅲ型、Ⅵ型）病例进行回顾性分析,其中15例采用双环钢丝捆扎加人工关节置换术,19例采用普通环形钢丝捆扎加人工关节置换术。两组分别比较住院时间、首次行走时间、术前术后记录每日睡眠时间、每日饮食量、精神状态、髋关节Harris评分、血红蛋白、白蛋白、电解质、是否有关节脱位、呼吸及泌尿系统炎症等疾病,并进行对比分析。结果  采用交叉双环钢丝捆扎组与采用普通钢丝捆扎组比较,前者术后下床时间、住院天数及术后首月髋关节Harris评分优于后者（P <0.05）,两者血液指标出院前后无明显差异（P >0.05）,但前者恢复速度较后者更快（P <0.05）,两组术后第3个月、第6个月及1年髋关节Harris功能评分差异无统计学意义（P >0.05）。结论  交叉双环钢丝捆扎加人工关节置换术能促进患者术后快速康复,减少住院时间,提高患髋近期功能,在患者术后快速恢复方面有积极作用。

     

Activation of ASK1 during reperfusion of ischemic spinal cord

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.