孕鼠与非孕鼠重症急性胰腺炎多器官损伤的对比

目的 观察孕鼠和非孕鼠重症急性胰腺炎(SAP)各器官的功能和组织病理变化.方法 SD孕鼠分为孕鼠组和孕鼠SAP组,非孕雌鼠分为SO组和SAP组,分别设立3、6、12 h时间点,各时间点8只.检测血清淀粉酶(AMY)、肝功能酶学指标[丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)]、肾功能[肌酐(Cr)、尿素氮(BUN)],观察胰腺、肝脏、肾脏、肺和心脏组织病理变化.结果 孕鼠SAP组AMY和胰腺组织病理评分在3、6h显著高于SAP组(P＜0.05),肝、肾功能在3、6、12 h均高于SAP组[3 h ALT (128.38 ±.24.92)比(99.75±16.27) U/L,AST(261.25 ± 64.98)比(194.50±49.00) U/L,Cr (52.38 ±8.99)比(41.88±7.28)μmol/L,BUN(8.63±1.24)比(7.11±1.29) mmol/L,P ＜0.05],肝脏和肾脏组织病理评分(6h肝脏2.13±.0.44比1.56±0.49,肾脏5.25 ±1.28比3.88±1.13),在6、12h,肺脏组织病理评分在12h显著高于SAP组(5.00±0.85比3.75±0.49,P＜0.05).结论 孕鼠较非孕鼠胰腺炎发病要急且病情进展更快,并发多器官损伤时间更早且损伤程度更重.     

肠源性内毒素与Treg在重症急性胰腺炎肝损伤中的作用

目的 探讨肠源性内毒素(ET)及CD4+ CD25+调节性T细胞(Treg)在重症急性胰腺炎(SAP)肝损伤中的作用.方法 雄性Wistar大鼠60只,随机分成假手术组(SO组)和SAP组.逆行性胰胆管注射牛磺胆酸钠造模.分别于术后3、6、12 h留取标本,检测血淀粉酶及丙氨酸转氨酶水平,鲎试剂法测血浆内毒素含量,流式细胞术测外周血Treg百分数,肝脏及胰腺行病理组织学观察,免疫组化法测肝脏组织Foxp3表达,并对以上指标进行相关性分析.结果 病理组织学观察及丙氨酸转氨酶水平证实,SAP组肝脏出现病理性形态改变.与SO组相比,SAP各组Treg百分数显著升高(SAP组3、6、12h分别为:2.26％±0.32％、2.36％±0.48％、2.80％±0.35％),差异有统计学意义(P＜0.01).SAP各组ET水平与SO组相比,差异有统计学意义(P＜0.01),与12 h(0.85±0.11)相比,3 h(0.74±0.11)和6 h(0.78±0.07)差异无统计学意义(P＞0.05).SAP各组肝脏Foxp3蛋白表达明显上调,Treg的表达与ET呈正相关(r=0.89,P＜0.01).结论 SAP可致肝损伤,ET与Treg细胞在SAP肝损伤中可能发挥重要作用.     

大黄素对重症急性胰腺炎大鼠核因子-кB的影响

目的 观察大黄素对重症急性胰腺炎(SAP)大鼠核因子-кB(NF-кB)的影响,探讨大黄素治疗SAP的作用机制.方法 胰胆管逆行注射牛磺胆酸钠建立大鼠SAP模型.将雄性Wistar大鼠随机分为SAP模型组、大黄素干预组(E1组)及正常对照组(Sham组).观测各组不同时间点(注射牛磺胆酸钠后3、6、12 h)血清淀粉酶、肿瘤坏死因子(TNF)-α和白细胞介素(IL)-6的含量,胰腺病理组织学评分,免疫组织化学方法 检测各组胰腺组织的核因子(NF)-кB的表达.结果 与SAP组比较,EI组各时间点(3、6、12 h)的病理学评分(13.41±2.14比18.42±3.14比15.89±1.98)、血清淀粉酶(U/L)(3634.2±247.8比4758.5±305.2比4687.8±345.8)、TNF-α(g/L)(2.24±0.47比2.87±0.87比2.76 ±0.82)和IL-6(g/L)(2.14±0.34比2.83±0.44比2.71±0.37)明显降低(P＜0.05),NFKB p65阳性表达率(0.31±0.06比0.44±0.09比0.33±0.08)下降(P＜0.05).各时间点SAP大鼠胰腺组织NF-κB p65的阳性率随血清TNF-α及IL-6含量变化.结论 大黄素可能通过胰腺组织NF-κB而调控血清炎症因子含量,以降低SAP大鼠血淀粉酶,发挥治疗作用.     

羟乙基淀粉对重症急性胰腺炎大鼠肝脏水通道蛋白-1表达及肝脏损伤的影响

目的 研究羟乙基淀粉130/0.4(万汶)对重症急性胰腺炎大鼠肝脏水通道蛋白-1(AQP-1)表达及肝脏损伤的影响.方法 将雄性SD大鼠48只按完全随机法分为假手术组(sham operation group,Sham组)、重症急性胰腺炎组(severe acute pancreatitis,SAP组)、羟乙基淀粉治疗组(HES组),每组分6 h、24 h两个时间点,每个时间点8只.以5%牛磺脱氧胆酸钠逆行胰胆管注射建立SAP模型.各组于造模后6 h、24 h处死大鼠,检测血淀粉酶(AMY),谷丙转氨酶(ALT),谷草转氨酶(AST),肝脏含水量,HE染色观察胰腺、肝脏组织病理,酶联免疫吸附(ELISA)方法检测血清TNF-α水平,RT-PCR检测肝组织AQP-1mRNA,免疫组化检测肝组织AQP-1蛋白.结果 各时间点SAP组与假手术组比较,血淀粉酶、ALT、AST、肝脏含水量、血清TNF-α水平、AQP-1mRNA及AQP-1蛋白均显著上调(P＜0.05);HES组与SAP组比较,血淀粉酶、ALT、AST、肝脏含水量、血清TNF-α水平、AQP-1mRNA及AQP-1蛋白均显著下调(P＜0.05).6 h时间点,Sham组、SAP组和HES组AQP-1mRNA表达量分别为(0.402±0.023)mmol/L、(0.811±0.032)mmol/L和(0.595±0.015)mmol/L,3组间差异有统计学意义(P＜0.05);24 h时间点,各组AQP-1mRNA表达量分别为(0.412±0.017)mmol/L、(0.823±0.029)mmol/L和(0.607±0.021)mmol/L,3组间差异有统计学意义(P＜0.05).6 h时间点,Sham组、SAP组和HES组AQP-1蛋白表达分别为(2.07±0.25)、(6.90±0.38)和(4.48±0.29),3组间差异有统计学意义(P＜0.05);24 h时间点,各组AQP-1蛋白表达分别为(2.32±0.31)、(7.04±0.32)和(4.56±0.25),3组间差异有统计学意义(P＜0.05).胰腺、肝脏组织病理HES组较SAP组明显改善.结论 HES130/0.4可一定程度改善重症急性胰腺炎的肝脏损伤,减轻毛细血管渗漏,AQP-1在重症急性胰腺炎肝脏损伤导致的毛细血管渗漏中起一定作用.

Abstract：

Objective To investigate the effect of hydroxyethyl starch (HES 130/0. 4) on the expression of aquaporin 1 (AQP-1) and liver injury in rats with severe acute pancreatitis(SAP).Methods Forty-eight male SD rats were randomly divided into three groups: Sham, SAP, and HES;each group was divided into 6 hour and 24 hour timepoints, with 8 in each subgroup. An SAP model was induced by injecting 5% sodium taurodeoxycholate into the biliary pancreatic duct. AMY, ALT,AST and water content in the liver were measured and TNF-a was examined by ELISA, and the expression of liver AQP-1mRNA was determined by RT-PCR, and the expression of liver AQP-Ⅰ protein was evaluated by immunohistochemical methods. Results Compared with the Sham group, the level of AMY, ALT, AST, TNF-a, water content, AQP-1mRNA and AQP-1 protein increased significantly in the SAP group (P＜0.05). Compared with the SAP group, the level of AMY, ALT, AST,TNF-a, water content, AQP-1mRNA and AQP-1 protein decreased significantly in the HES group (P＜0.05). At 6 hours, the expressions of liver AQP-1mRNA were (0. 402 ± 0. 023), (0. 811 ±0. 032) and (0. 595 ± 0. 015) in the Sham, SAP, and HES groups, respectively; at 24 hours, they were(0. 412 ± 0. 017), ( 0. 823 ± 0. 029) and (0. 607 ± 0. 021 ), with significant differences between each group (P＜0. 05). At 6 hours, the expressions of liver AQP-1 proteins were (2.07±0.25),(6.90±0.38)and (4.48±0.29) in the Sham, SAP and HES groups, respectively;at 24 hours, they were (2. 32±0. 31 ), (7. 04 ± 0. 32) and (4. 56 ± 0. 35), with significant differences between each group (P＜0. 05). Compared with the SAP group, the pathology of the pancreas and liver ameliorated significantly in the HES group. Conclusions Hydroxyethyl starch 130/0.4 may ameliorate liver injury of severe acute pancreatitis and alleviate the capillary leak. AQP-1 may play a role in the capillary leak caused by the liver injury of severe acute pancreatitis.     

参麦注射液对重症急性胰腺炎大鼠细胞间黏附分子-1的影响

目的 观察参麦注射液对重症急性胰腺炎(SAP)大鼠模型血中可溶性细胞间黏附分子-1(sICAM-1)水平及胰腺组织中1CAM-1 mRNA的影响.方法 将108只成年雄性SD大鼠随机分为3组:对照组(A组)、SAP模型组(B组)及参麦治疗组(C组);其中B组及C组再分为4、8、16、24h4个亚组,各个亚组及A组各12只.对各组大鼠血清中sICAM-1水平及胰腺组织中ICAM-1mRNA水平进行比较.结果 B组各时间点大鼠血清sICAM-1浓度较A组均显著升高(128.07±15.86比87.31±13.16、142.33±22.61比98.82±11.39、187.45±17.39比129.51±15.61、176.18±19.36比123.57±17.03)(P＜0.05);C组各时间点大鼠血清sICAM-1浓度较B组均显著降低(92.55±8.09比128.07±15.86、105.28±14.29比142.33±22.61、142.36±18.25比187.45±17.39、131.32±21.83比176.18±19.36)(P＜0.05);B组各时间点大鼠胰腺组织内ICAM-1 mRNA表达水平较A组均显著升高(0.97±0.12比0.52±0.11、1.08±0.18比0.61±0.13、1.32±0.18比0.82±0.14、1.23±0.09比0.74±0.13)(P＜0.05);C组各时间点大鼠胰腺组织内ICAM-1 mRNA表达水平较B组均显著降低(0.59±0.13比0.97±0.12、0.68±0.09比1.08±0.18、0.96±0.20比1.32±0.18、0.88±0.09比1.23±0.09)(P＜0.05).结论 参麦注射液通过下调SAP大鼠ICAM-1 mRNA及ICAM-1的表达,起到改善SAP大鼠微循环、保护SAP大鼠的作用.     

丙酮酸乙酯对重症急性胰腺炎大鼠血清高迁移率蛋白-1水平的影响及意义

目的　探讨重症急性胰腺炎 (SAP)大鼠血清高迁移率蛋白 1(HMGB1)水平的变化规律 ,以及丙酮酸乙酯 (EP)对其水平的影响和意义。方法　采用胰管逆行灌注人工胆汁的方法复制大鼠SAP模型。随机分为正常对照组 (N组 ,n =8)、重症急性胰腺炎组 (SAP组 ,n =80 )、EP治疗组 (Treat组 ,n =3 2 )。Treat组建模 12h开始使用EP治疗。酶联免疫吸附试验检测各组动物血清肿瘤坏死因子 α(TNF α)、白细胞介素 1β(IL 1β)水平。Westernblot法检测血清HMGB1水平。另设实验组研究EP对SAP大鼠生存时间的影响。结果　SAP组大鼠血清TNF α和IL 1β水平在建模 3～ 6h达高峰 ,12h即大幅下降。SAP组大鼠血清HMGB1水平在建模后 12h明显升高 ,至 2 4和 48h仍维持在较高水平 [(161.4± 2 2 .8) μg/L和(98.7± 15 .8) μg/L]。Treat组血清HMGB1水平在建模 2 4、48h [(95 .3± 3 0 .1) μg/L和(4 2 .2± 2 1.5 ) μg/L]明显低于SAP组(P <0 .0 5 )。而血清TNF α和IL 1β水平与SAP组比较差异无显著性。Kaplan Meier分析显示 ,EP治疗组动物生存时间 (71± 6)h明显高于SAP组 (4 6± 4)h (P <0 .0 0 0 1)。结论　HMGB1作为晚期炎症因子参与了SAP的全身炎症反应。延迟的EP治疗仍能降低SAP大鼠血清HMGB1水平 ,延长动物生存时间。     

银杏苦内酯B对重症急性胰腺炎胰腺组织病理变化的影响

目的 通过银杏苦内酯B(BN52021)对血小板活化因子(PAF)的拮抗作用,探讨BN52021治疗重症急性胰腺炎(SAP)的疗效.方法 Wistar大鼠180只按随机数字表法分为对照组(60只)、SAP组(60只)、BN52021组(60只),每组按不同时相点(1、2、3、6、12、24 h)分为6小组,分别监测血清淀粉酶的变化,用RT-PCR和Western blot法分别监测胰腺组织PAF受体mRNA和蛋白表达的变化,同时对胰腺组织进行病理学观察.多组比较采用单因素方差分析.结果 血清淀粉酶和病理学结果显示SAP制模成功,BN52021组血清淀粉酶在3、6、24 h[(4185 ±148)U/L,(3785 ±124)U/L,(1360 ±161)U/L]较SAP组[(4799 ±107)U/L,(4920±140)U/L,(2283±127)U/L]显著降低,病理学评分在3、6、12 h(5.95 ±0.19,5.55 ±0.36,6.72 ±0.30)较SAP组(8.85±0.39,9.15±0.55,10.10±0.65)显著降低;PAF受体mRNA及蛋白检测结果显示,SAP组和BN52021组早期逐渐上升(0.49±0.09～0.71±0.14,0.43±0.06～1.69±0.06),在3 h达到高峰,3组比较差异有统计学意义(F=4.58.6.24,P<0.05).结论 PAF受体在SAP大鼠胰腺组织中表达是动态变化的,PAF受体参与了SAP病情的发生、发展;BN52021可降低SAP血清淀粉酶和改善胰腺组织病理变化,发挥了一定的治疗作用,但对胰腺组织PAF受体的表达无显著影响.     

血管内皮生长因子对关节软骨细胞诱导型一氧化氮合酶的影响

目的 观察血管内皮生长因子(VEGF)对体外培养的关节软骨细胞诱导型一氧化氮合酶(iNOS)表达的影响。方法 体外培养SD乳鼠关节软骨细胞,用白细胞介素(IL)-1β诱导的方法建立骨关节炎(OA)体外模型,实验分为4组,每组加入不同处理因素进行干预,A组:(正常对照组)不加任何处理因素;B组:10 μg/L VEGF;C组:10 μg/L IL-1β;D组:10 μg/L VEGF+ 10 μg/LIL-1β。采用实时荧光定量PCR( Real Time PCR)检测iNOS mRNA的表达,采用蛋白免疫印迹法( Western blot)检测iNOS蛋白的表达。结果 iNOS mRNA的表达:A组iNOS mRNA无表达,B组(9.64±1.64)、C组(17.27±2.01)及D组(28.93±6.63),3组的iNOS mRNA表达量显著升高,进一步组间比较,D组软骨细胞iNOS的mRNA表达水平明显高于B组(P＜0.01)及C组(P＜0.05),C组软骨细胞iNOS的mRNA表达水平高于B组(P＜0.05)。iNOS蛋白的表达:A组iNOS蛋白无表达,B组(0.44±0.12)、C组(0.74±0.07)及D组(1.38±0.38),3组的iNOS蛋白表达量显著升高,进一步组间比较,D组软骨细胞iNOS的蛋白表达水平明显高于B组(P＜0.01)及C组(P＜0.05),C组软骨细胞iNOS的mRNA表达水平高于B组(P＜0.01)。结论 在OA的发病过程中,VEGF可能通过上调软骨细胞iNOS的表达发挥重要作用。     

RNA干扰Kupffer细胞肿瘤坏死因子-α减轻大鼠肝脏缺血再灌注损伤

目的 观察RNA干扰肝脏Kupffer细胞肿瘤坏死因子-α(TNF-α)对大鼠肝脏缺血再灌注损伤的保护作用.方法 构建针对大鼠TNF-α基因的短发夹状RNA(shRNA)真核表达载体.肝脏缺血再灌注损伤前48 h经门静脉注射磷酸盐缓冲液(PBS)、空载体或TNF-α shRNA.实验随机分为4组,假手术组、PBS组、空载体组和shRNA组.阻断大鼠70%入肝血流40 min,再灌注6 h检测血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、肝脏Kupffer细胞TNF-α mRNA、血清TNF-α、肝组织中丙二醛(MDA)以及超氧化物岐化酶(SOD)含量.结果 与PBS组和空载体组比较,shRNA组再灌注6 h后血清ALT和AST水平显著降低(P＜0.05),Kupffer细胞TNF-α mRNA水平、血清TNF-α水平(56.6±6.7 pg/ml比87.8±8.7 pg/ml和96.5±7.3 pg/ml,P＜0.05)、肝组织中MDA含量(93.4±13.3 nmol/mg比133.5±12.4 nmo1/mg和136.7±13.6 nmol/mg,P＜0.05)显著降低,SOD活性显著升高(22.4±4.6 U/mg比12.2±3.1 U/mg和11.4±2.9 U/mg,P＜0.05).结论 RNA干扰Kupffer细胞TNF-α基因的表达可以减轻大鼠肝脏缺血再灌注损伤.     

急性胰腺炎大鼠肾脏中聚腺苷二磷酸核糖聚合酶-1mRNA的表达及意义

目的 探讨聚腺苷二磷酸核糖聚合酶-1(poly ADP-ribose polymerase-1,PARP-1)mRNA在重症急性胰腺炎(severe acute pancreatitis,SAP)大鼠肾脏中的表达及意义.方法 48只Wistar大鼠按随机数字表法分为SAP组和假手术组(SO)组,分别于造模术后1、3、6及12 h测定血清肌酐,观察胰腺和肾脏组织病理变化,并以RT-PCR法检测PARP-1 mRNA在肾脏中的表达水平.结果 SAP组大鼠术后血清肌酐逐渐升高,于3、6及12 h明显高于SO组(P＜0.05).SAP组大鼠术后胰腺出现腺体破坏、腺泡坏死、出血、炎性细胞浸润等病理损害,且呈进行性加重;SO组各时相胰腺组织基本正常.SAP组大鼠术后出现肾小管上皮细胞变性、坏死、肾小球瘀血、缺血等改变,并随时间延长逐渐加重,其损伤程度在3、6及12 h明显较SO组严重(P＜0.05).SO组大鼠肾脏组织仅表达少量PARP-1 mRNA,而SAP组大鼠随病程延长肾脏组织中PARP-1 mRNA表达逐渐增加,自3 h时起明显高于SO组(P＜0.01).结论 在SAP发病过程中,PARP-1 mRNA的表达在肾脏组织中逐渐增加,PARP-1可能参与了SAP相关肾损伤过程.     

2015年乳腺癌辅助化疗进展

【摘要】〓乳腺癌是危害我国女性健康的头号杀手,尽管近年来辅助化疗的研究进展突飞猛进,但临床中仍有不少问题未能明确,如辅助化疗的合适人群、化疗的开始时间、蒽环及紫杉类的地位和用法、强化维持治疗的作用、疗效及预后的生物标志物等。本文结合乳腺癌辅助化疗在临床上的常见问题和2015年各大乳腺癌会议阐述乳腺癌辅助化疗的最新进展。     

Alterations in T-Cell Subset Frequency in Peripheral Blood in Obesity

Background: Obesity affects the regulation of immune and inflammatory responses. This study characterizes differences in peripheral blood lymphocyte phenotype in obese humans. Methods: Frequencies of lymphocyte subsets among peripheral blood mononuclear cells were compared between 10 obese (BMI ≥35) and 10 lean subjects, as determined by antibodies directed against cluster differentiation (CD) markers. Results: Obese patients demonstrated an increased frequency of CD3+CD4+ T-cells (mean difference 12%, P=0.004), a decreased frequency of CD3+CD8+ T-cells (mean difference 9.4%, P=0.016) and an increased frequency of CD3+CD8+CD95+ T-cells (mean difference 13.3%, P=0.032). No other differences among T-cell or monocyte subsets were noted. Conclusions: Obesity is associated with alterations in frequencies of peripheral CD4+ and CD8+ T-cells and aberrations in the expression of CD95 among CD8+ T-cells. These data suggest both CD4+ and CD8+ T-cell compartments, as well as the regulation of CD95 expression on CD8+ T-cells, as targets for further study into obesity's effects on the immune system.     

西宁地区烧伤病人动脉血气分析观察

对高海拔地区的27例烧伤病人动脉血气变化进行了分析和观察。结果证明:无论是存活病人还是死亡病人伤后均存在有低氧血症问题。并且在死亡病人和烧伤合并吸入性损伤病人其低氧血症的发生早于单纯烧伤病人。提示:吸入性损伤病人应立即行气管切开术以保障氧气供给,单纯烧伤病人可常规吸氧以维持正常血 PaO_2,ARDS 均发生在合并吸入性损伤的病人,高频喷射通气技术对纠正低氧血症有一定效果。     

Controversies in Fistula in Ano

Managing a complex fistula in ano can be a daunting task for most surgeons; largely due to the two major dreaded complications—recurrence & fecal incontinence. It is important to understand the anatomy of the anal sphincters & the aetiopathological process of the disease to provide better patient care. There are quite a few controversies associated with fistula in ano & its management, which compound the difficulty in treating fistula in ano. This article attempts to clear some of those major controversies.     

β-半乳糖苷酶在体内外成骨细胞中的表达

目的 研究β—半乳糖苷酶(β—gal)在成骨细胞中的表达状况，为阐明MorquioB综合征的发病机制提供依据。方法 裸鼠各器官和骨组织标本行X-gal染色检测。抽取羊和人骨髓行骨髓基质细胞(BMSCs)培养，分为4组：I：Adv-hBMP-2转染组；Ⅱ：Adv—β—gal转染组；Ⅲ：未转染组；Ⅳ：地塞米松诱导组。分别行X-gal染色和RT-PCR检测β—gal的表达。结果 裸鼠骺板两侧、骨膜内面及松质骨的成骨细胞和破骨细胞可见多量β—gal的表达。未转染BMSCs组有少量β—gal的表达，其他3组细胞的β—gal表达增高。结论成骨细胞和破骨细胞可表达多量β—gal，该两种细胞的β—gal缺乏可能是MorquioB综合征骨骼异常的直接原因。     

Smoking-Attributable mortality in Spain in 2016

IntroductionSmoking-attributable mortality (SAM) is a valuable indicator that can be used to characterize the course and health burden of the smoking epidemic. The aim of this paper was to estimate SAM in Spain in 2016 in the population aged 35 and over, using the best available evidence.MethodsA smoking prevalence-dependent analysis based on the estimation of population-attributable fractions was performed. Smoking prevalence (never, former, and current smokers) was calculated from a combination of the Spanish Health Survey (2016) and the European Health Survey (2014); the relative risk of death among current and former smokers was taken from the follow-up of various cohorts; and mortality rates were obtained from National Center for Statistics data. SAM estimates are presented globally, and by sex, age groups, and major disease categories: cancer, cardiometabolic diseases and respiratory diseases.ResultsIn 2016, 56,124 deaths were attributed to tobacco consumption, 84% in men (47,000), and 50% in the population aged over 74 (27,795). Overall, 50% of SAM was due to cancer (28,281), 65% of which was lung cancer. One in 4 attributable deaths (13,849) occurred before the age of 65.ConclusionsOne in 7 deaths in Spain in 2016 were attributable to smoking. This estimation of SAM clearly highlights the great impact of smoking on mortality in Spain, mainly due to lung cancer and chronic obstructive pulmonary disease.     

MicroRNAs in hepatic pathophysiology in diabetes

MicroRNAs(miRNAs or miRs) are small approximately 22 nucleotide RNA species that are believed to regulate diverse metabolic and physiological processes.In the recent past,several reports have surfaced that demonstrate the role of miRNAs in various biological processes and numerous disease states.For a disease as complex as diabetes,the emergence of miRNAs as key regulators leading to the disease phenotype has added a novel dimension to the area of diabetes research.On the other hand,the liver,a metabolic hub,contributes in a major way towards maintaining normal glucose levels in the body as it can both stimulate and inhibit hepatic glucose output.This equilibrium is frequently disturbed in diabetes and hence,the liver assumes special significance considering the correlation between altered hepatic physiology and diabetes.While the understanding of the mechanisms behind this altered hepatic behavior is not yet completely understood,recent reports on the status and role of miRNAs in the diabetic liver have further added to the complexities of the knowledge of hepatic pathophysiology in diabetes.Here,we bring together the various miRNAs that play a role in the altered hepatic behavior during diabetes.     

Fluid-phase transcytosis in the primate epididymis in vitro and in vivo

Ligated tubules from the corpus epididymidis of men and monkeys were incubated in medium containing horseradish peroxidase (HRP) as a marker for fluid-phase endocytosis. HRP was localized by light and electron microscopy after 0, 15, 30 and 60 min of incubation. Movement between the cells was prevented by tight junctions, but bypass of this barrier was apparently achieved by an intracellular vesicular mechanism leading to a time-dependent appearance of HRP in the lumen. Uptake of HRP into basal cells and capture by the lysosomal apparatus of principal cells were also observed. HRP-filled vesicles also appeared in the basal, mid and apical cytoplasm of epithelial cells in the caput 1 h after injection of the tracer into the epididymal circulation of the monkey, suggesting that this pathway also operates in vivo.