急性白血病合并静脉血栓栓塞症临床分析

目的分析急性白血病合并静脉血栓栓塞症的临床治疗。方法我院2008年1月-2012年1月收治确诊为急性白血病且并发静脉血栓栓塞症的患者18例,对其临床资料进行分析。结果所有患者栓塞肢体肿胀处均消失,消失时间为6-13d,患者均无出血倾向。结论治疗急性白血病患者时需预防血栓栓塞的发生,对于已发生血栓栓塞的患者,可给予肝素及抗凝剂进行治疗,效果确切安全。     

再生障碍性贫血外周血Th17和CD4~+ CD25~+ Treg细胞表达情况研究

本研究旨在探讨成人再生障碍性贫血(aplastic anemia,AA)外周血Th17和CD4+CD25+调节性T细胞(Treg)表达情况。45例初发AA患者分为轻型AA(n=25)和重型AA(n=25)两组,15例正常人作为对照。应用流式细胞术检测AA患者外周血中Th17和CD4+CD25+Treg的比例,ELISA检测血清及刺激后外周血单个核细胞(PBMNC)上清液中的白介素(IL-17)、γ干扰素(IFN-γ)及肿瘤坏死因子-α(TNF-α)水平,并与正常对照组比较。结果表明:重型AA(SAA)组外周血Th17细胞比例,血清中IL-17及IFN-γ表达高于轻型AA(MAA)和正常人组,而重型AA组外周血CD4+CD25+Foxp3+Treg细胞比例降低。与轻型AA和正常对照相比,重型AA患者单个核细胞培养后上清液中IL-17及IFN-γ表达水平显著增加。AA患者血红蛋白计数与Th17细胞及血清IL-17表达呈负相关,与CD4+CD25+Treg表达成正相关。结论:重型AA患者外周血Th17细胞应答增强,而CD4+CD25+Treg细胞缺乏,贫血的严重程度与外周血Th17/Treg免疫应答失衡密切相关。     

microRNA在急性胰腺炎中的研究进展

目的总结microRNA在急性胰腺炎中的研究进展。方法通过阅读近几年国内外的相关文献,对近年来microRNA在急性胰腺炎中的研究进展进行归纳总结。结果近几年的研究发现,microRNA可以作为急性胰腺炎的生物标志物,以预测并且判定急性胰腺炎的发生、发展、并发症发生等,还可以调控急性胰腺炎的程序性细胞死亡,在调控急性胰腺炎的炎症发展、并发症发生等中都发挥着重要作用,并且可以作为急性胰腺炎的治疗靶点。结论 microRNA在急性胰腺炎的发生和发展中扮演着十分重要的角色,研究microRNA在急性胰腺炎中的机制对于急性胰腺炎的治疗、预防等有一定的帮助。     

近10年“大承气汤”相关研究知识图谱分析

目的通过可视化知识图谱方式,整体分析近10年经方"大承气汤"的研究概况及趋势。方法以"大承气汤"为主题词,检索2009年1月1日至2019年2月1日中国知网(CNKI)数据库中相关文献,通过CiteSpace软件对纳入的数据分别以作者、研究机构及关键词为节点进行分析,并对其出现频次进行统计。结果共纳入数据1 275条,发现了以唐文富为代表的主要研究人员及团队,研究机构以华西医院及天津中医药大学为主,肠梗阻、急性胰腺炎和急性肺损伤是与大承气汤最为相关的疾病。结论在近10年的"大承气汤"学术文献中,研究领域涉及临床、药理学、炮制等多个学科,其有效成分在治疗疾病中的机制研究仍是主要方向。     

甲状腺全切除术治疗良性甲状腺疾病128例临床疗效

目的：探讨甲状腺全切除术治疗甲状腺良性疾病的疗效及术后并发症的预防。方法：回顾性分析128例行甲状腺全切除术的甲状腺良性疾病病人的临床资料,其中首次手术者98例,再次手术者30例。分析总结该128例病人的术后并发症。结果：128例病人术后均未发生永久性甲状旁腺功能低下和永久性喉返神经损伤。首次甲状腺全切除组术后暂时性喉返神经损伤和暂时性甲状旁腺功能低下的发生率均为1．02％,再次手术组的发生率明显增高,分别为10．00％和13．33％,两组比较,Fisher精确概率P分别为0．040、0．011。两组暂时性喉上神经损伤发生率均很低,无明显差别。结论：对符合指征的良性甲状腺疾病,甲状腺全切除术是一合适的治疗选择。熟悉甲状腺解剖和精细手术操作,可有效预防并发症发生。     

高脂血症性重症急性胰腺炎病因及发病机制研究概况

高脂血症能够诱发和加重重症急性胰腺炎的胰腺损伤,一直是临床研究的焦点,其发病机制尚未完全阐明.在众多学说中,游离脂肪酸的毒性作用、胰蛋白酶原活化加速、胰腺微循环障碍一直是占主导地位的理论.近年来,关于肠道细菌移位、胰腺腺泡内钙超载等理论也受到了关注和重视.本文将对高脂血症性重症急性胰腺炎的病因及发病机制的研究概况进行概述.     

水通道蛋白1在急性坏死性胰腺炎大鼠胰腺组织的表达及其意义

Objective To study the expression of aquaporin 1 ( AQP1 ) in pancreas and its pathogenic role in rats with experimental acute necrotizing pancreatitis (ANP). Methods Forty-eight male Sprague-Dawley rats were randomly divided into two groups : control group ( n = 24 ) and ANP group ( n = 24). Six rats in each group were sacrificed at 3,6,12 and 18 h after induction of experimental models. Quantity of ascites and levels of serum amylases were measured at each time point. Serum AQPI was determined by ELISA. Pathological changes of pancreatic tissues were examined. Capillary permeability in pancreatic tissues was tested by Evans Blue (EB) extravasation method. AQPI expression in pancreatic tissues was detected by immunohistochemieal staining, Western blot and fluorescence quantitative polymerase chain reaction (FQ-PCR). Results (1) Serum amylase level at 3,6,12, and 18 h in control group was (1308±759) ,(1077±508), (1325±761),(1328±762) U/L,and that in ANP group was (9102± 2199), (8799±1634), (9398±1473), (9484±862) U/L respectively. The concentration of EB in pancreatic tissues at each time point in control group was (205.61±32.99), (141.46±27.18 ), (96.94± 26.79), (61.43±24.82) mg/L, and that in ANP group was ( 273.59±23.47 ), ( 253.51±31.68 ), (221.15±73.68 ), (185.28±42.35) ,respectively. There was significandy difference between two groups. Serum AQP1 level in control group at each point was ( 74.08±11.80), (78.49±9.06 ), (75.77± 7.37 ), ( 72.75±13.87 ) mg/L, and that in AN P group was (73.29±9.61 ), ( 62.85±7.28 ), (62.07± 4.39 ), (46.33±11.91 ) mg/L, respectively ( P < 0.01 ). ( 2 ) Protein expression of AQPI in pancreatic tissues detected by immunohistochemical staining in control group at each time point was 114.13±7.92, 122.39±7.99,145.98±6.48,113.98±6.48, and that in ANP group was 80.07±14.89,110.54± 4.45,103.77±10.48,99.18±6.95;Protein expression of AQP1 in pancreatic tissues detected by Western blot in control group at each time point was 1.19±0.33,1.02±0.25,0.90±0.33,1.06±0.20,and that in ANP group was 0.83±0.11,0.96±0.21,0. 58±0.28,0.72±0.14, respectively ( P < 0.05 ). ( 3 ) The mRNA level of AQP1 gene expressed in pancreas in control group at each time point was 0.91±0.22,1.01±0.83,0.48±0.23,0.61±0.51,and that in ANP group was 2.13±0.63,2.02±1.40, 2.07±0.86,2.49±2.47,respectively (P<0.01).Condusion The expression of AQP1 wasdown-reg-ulated in pancreas in rats with ANP,which might could play an important role in the pathogenesis of capil-lary leak syndrome.     

水通道蛋白1在急性坏死性胰腺炎大鼠胰腺组织的表达及其意义

Objective To study the expression of aquaporin 1 ( AQP1 ) in pancreas and its pathogenic role in rats with experimental acute necrotizing pancreatitis (ANP). Methods Forty-eight male Sprague-Dawley rats were randomly divided into two groups : control group ( n = 24 ) and ANP group ( n = 24). Six rats in each group were sacrificed at 3,6,12 and 18 h after induction of experimental models. Quantity of ascites and levels of serum amylases were measured at each time point. Serum AQPI was determined by ELISA. Pathological changes of pancreatic tissues were examined. Capillary permeability in pancreatic tissues was tested by Evans Blue (EB) extravasation method. AQPI expression in pancreatic tissues was detected by immunohistochemieal staining, Western blot and fluorescence quantitative polymerase chain reaction (FQ-PCR). Results (1) Serum amylase level at 3,6,12, and 18 h in control group was (1308±759) ,(1077±508), (1325±761),(1328±762) U/L,and that in ANP group was (9102± 2199), (8799±1634), (9398±1473), (9484±862) U/L respectively. The concentration of EB in pancreatic tissues at each time point in control group was (205.61±32.99), (141.46±27.18 ), (96.94± 26.79), (61.43±24.82) mg/L, and that in ANP group was ( 273.59±23.47 ), ( 253.51±31.68 ), (221.15±73.68 ), (185.28±42.35) ,respectively. There was significandy difference between two groups. Serum AQP1 level in control group at each point was ( 74.08±11.80), (78.49±9.06 ), (75.77± 7.37 ), ( 72.75±13.87 ) mg/L, and that in AN P group was (73.29±9.61 ), ( 62.85±7.28 ), (62.07± 4.39 ), (46.33±11.91 ) mg/L, respectively ( P < 0.01 ). ( 2 ) Protein expression of AQPI in pancreatic tissues detected by immunohistochemical staining in control group at each time point was 114.13±7.92, 122.39±7.99,145.98±6.48,113.98±6.48, and that in ANP group was 80.07±14.89,110.54± 4.45,103.77±10.48,99.18±6.95;Protein expression of AQP1 in pancreatic tissues detected by Western blot in control group at each time point was 1.19±0.33,1.02±0.25,0.90±0.33,1.06±0.20,and that in ANP group was 0.83±0.11,0.96±0.21,0. 58±0.28,0.72±0.14, respectively ( P < 0.05 ). ( 3 ) The mRNA level of AQP1 gene expressed in pancreas in control group at each time point was 0.91±0.22,1.01±0.83,0.48±0.23,0.61±0.51,and that in ANP group was 2.13±0.63,2.02±1.40, 2.07±0.86,2.49±2.47,respectively (P<0.01).Condusion The expression of AQP1 wasdown-reg-ulated in pancreas in rats with ANP,which might could play an important role in the pathogenesis of capil-lary leak syndrome.     

盐酸氟桂利嗪的临床应用进展

盐酸氟桂利嗪(Flunarizine)为非竞争性双苯哌嗪类钙通道抑制剂[1],可以抑制ca2 内流,从而使血管扩张,尤其对脑血管有选择性作用,在临床上主要用于脑血管灌注不足的疾病。随着临床应用的增加,其应用领域不断扩大。     

水通道蛋白1在急性坏死性胰腺炎大鼠胰腺组织的表达及其意义

Objective To study the expression of aquaporin 1 ( AQP1 ) in pancreas and its pathogenic role in rats with experimental acute necrotizing pancreatitis (ANP). Methods Forty-eight male Sprague-Dawley rats were randomly divided into two groups : control group ( n = 24 ) and ANP group ( n = 24). Six rats in each group were sacrificed at 3,6,12 and 18 h after induction of experimental models. Quantity of ascites and levels of serum amylases were measured at each time point. Serum AQPI was determined by ELISA. Pathological changes of pancreatic tissues were examined. Capillary permeability in pancreatic tissues was tested by Evans Blue (EB) extravasation method. AQPI expression in pancreatic tissues was detected by immunohistochemieal staining, Western blot and fluorescence quantitative polymerase chain reaction (FQ-PCR). Results (1) Serum amylase level at 3,6,12, and 18 h in control group was (1308±759) ,(1077±508), (1325±761),(1328±762) U/L,and that in ANP group was (9102± 2199), (8799±1634), (9398±1473), (9484±862) U/L respectively. The concentration of EB in pancreatic tissues at each time point in control group was (205.61±32.99), (141.46±27.18 ), (96.94± 26.79), (61.43±24.82) mg/L, and that in ANP group was ( 273.59±23.47 ), ( 253.51±31.68 ), (221.15±73.68 ), (185.28±42.35) ,respectively. There was significandy difference between two groups. Serum AQP1 level in control group at each point was ( 74.08±11.80), (78.49±9.06 ), (75.77± 7.37 ), ( 72.75±13.87 ) mg/L, and that in AN P group was (73.29±9.61 ), ( 62.85±7.28 ), (62.07± 4.39 ), (46.33±11.91 ) mg/L, respectively ( P < 0.01 ). ( 2 ) Protein expression of AQPI in pancreatic tissues detected by immunohistochemical staining in control group at each time point was 114.13±7.92, 122.39±7.99,145.98±6.48,113.98±6.48, and that in ANP group was 80.07±14.89,110.54± 4.45,103.77±10.48,99.18±6.95;Protein expression of AQP1 in pancreatic tissues detected by Western blot in control group at each time point was 1.19±0.33,1.02±0.25,0.90±0.33,1.06±0.20,and that in ANP group was 0.83±0.11,0.96±0.21,0. 58±0.28,0.72±0.14, respectively ( P < 0.05 ). ( 3 ) The mRNA level of AQP1 gene expressed in pancreas in control group at each time point was 0.91±0.22,1.01±0.83,0.48±0.23,0.61±0.51,and that in ANP group was 2.13±0.63,2.02±1.40, 2.07±0.86,2.49±2.47,respectively (P<0.01).Condusion The expression of AQP1 wasdown-reg-ulated in pancreas in rats with ANP,which might could play an important role in the pathogenesis of capil-lary leak syndrome.