葡萄糖转运蛋白4及其下游信号分子在高糖刺激下肾小球系膜细胞中的作用

目的 探讨高糖和胰岛素对肾小球系膜细胞（GMC）葡萄糖转运蛋白4（GLUT4）和Cbl相关蛋白（CAP）的mRNA表达及细胞骨架纤维状肌动蛋白F-actin 的影响,探讨糖尿病肾病发生发展中GLUT4 及其下游分子F-actin和CAP的重要作用。 方法 将细胞分为8组：正常对照组、生理浓度胰岛素（10－9 mol/L）组、低浓度胰岛素（10－8 mol/L）组、高浓度胰岛素（10－6 mol/L）组、高糖（30 mmol/L）组、甘露醇组（25 mmol/L甘露醇＋5 mmol/L葡萄糖）、高糖加高浓度胰岛素组、高糖加生理浓度胰岛素组。采用RT-PCR法和免疫组化法,观察不同情况下GMC中GLUT4蛋白和mRNA以及CAP mRNA 的表达及其变化。Rhodamine-phalloidin染色和激光共聚焦显微镜观察F-actin形态及荧光强度。 结果 正常对照组GMC中GLUT4蛋白和mRNA以及CAP mRNA有一定表达,而生理浓度胰岛素组与正常对照组差异均无统计学意义。高糖组GLUT4蛋白（P < 0.01)和mRNA（P < 0.05）以及CAP mRNA（P < 0.01)表达均显著减少,F-actin解聚增加（P < 0.01）;而甘露醇组以上各指标与对照组差异均无统计学意义。低浓度胰岛素组和高浓度胰岛素组GLUT4 mRNA表达分别为生理浓度胰岛素组的2.06倍和2.66倍,GLUT4蛋白表达分别为对照组的1.93倍和2.83倍,CAP mRNA表达分别为对照组的1.91倍和2.15倍,F-actin荧光强度分别为对照组的1.296倍及1.224倍,均呈一定的浓度依赖性。高糖加高浓度胰岛素组GLUT4 mRNA表达为高糖组的2.15倍（P < 0.05）,GLUT4蛋白表达为高糖组的2.08倍（P < 0.01）,CAP mRNA表达为高糖组的2.14倍（P < 0.01）,F-actin荧光强度为高糖组的1.838倍（P < 0.01）。GLUT4 mRNA与CAP mRNA呈正相关（r = 0.905,P = 0.002）;GLUT4与F-actin呈正相关（r = 0.929,P = 0.001）。 结论 （1）正常GMC中GLUT4 mRNA与蛋白、CAP mRNA有一定表达。（2）高糖可抑制GLUT4的蛋白和mRNA以及CAP mRNA表达,促进F-actin解聚。（3）胰岛素能部分拮抗高糖导致系膜细胞中GLUT4的蛋白和mRNA以及CAP mRNA表达的下调作用。（4）GLUT4、CAP和F-actin是糖尿病肾病发生发展的重要影响因子之一。     

高糖和胰岛素对肾小球系膜细胞葡萄糖转运蛋白4表达及易位的影响

目的 观察高糖和胰岛素对体外培养的肾小球系膜细胞（GMC）葡萄糖转运蛋白4（GLUT4）的影响以及胰岛素引起GLUT4易位的情况，探讨GLUT4在糖尿病肾病(DN)发生发展机制中的作用。 方法 将体外培养的鼠1097系膜细胞分为8组：对照组、生理浓度胰岛素组（10^-9 mol/L）、低浓度胰岛素组（10^-8 mol/L）、高浓度胰岛素组（10^-6 mol/L）、高糖组（30 mmol/L）、甘露醇组、高糖加高浓度胰岛素组和高糖加生理浓度胰岛素组。RT-PCR检测GLUT4 mRNA表达；共聚焦显微镜观察各组GLUT4蛋白表达，以及胰岛素引起GMC GLUT4易位的剂量-时间效应。 结果 胰岛素可增加GLUT4的表达，高糖使GLUT4表达明显下降。胰岛素可引起系膜细胞GLUT4易位。低浓度胰岛素组、高浓度胰岛素组细胞GLUT4均在加入胰岛素15 min后达到最大易位，且以后的45 min胞膜上的GLUT4的荧光强度与15 min时差异无统计学意义（P > 0.05）。 结论 不同浓度的胰岛素均可刺激系膜细胞GLUT4易位，且过程是相似的。高糖明显抑制GLUT4在系膜细胞上的表达。胰岛素可部分拮抗高糖导致的GLUT4下调，且呈剂量依赖性。     

Cbl相关蛋白在高糖刺激下肾小球系膜细胞中的作用

目的：探讨高糖对肾小球系膜细胞（GMC）Cbl相关蛋白（CAP）mRNA表达的影响,以及糖尿病肾病发生发展中葡萄糖转运蛋白4（GLUT4）的下游信号分子CAP的重要作用。方法：系膜细胞株分为8组,正常对照组,生理浓度胰岛素组（10^-9mol／L）,低浓度胰岛素组（10^-9mol／L）,高浓度胰岛素组（10^-6mol／L）,高糖组（30mmol／L）,甘露醇组,高糖加高浓度胰岛素组,高糖加生理浓度胰岛素组。采用RT—PCR法,观察高糖刺激与不同浓度胰岛素作用下,系膜细胞中CAPmRNA的表达及其变化。结果：正常对照组系膜细胞中（CAPmRNA有一定表达。高糖组CAPmRNA表达明显下降;低浓度胰岛素组和高浓度胰岛素组分别为对照组的1．91倍和2．15倍（P〈0．01）;高糖加入高浓度胰岛素组CAPmRNA表达为单纯高糖组的2．14倍（P〈0．01）。结论：（1）正常系膜细胞中CAPmRNA有一定表达;（2）高糖可抑制CAPmRNA表达;（3）胰岛素能部分拮抗高糖导致系膜细胞中CAPmRNA表达的下调作用;（4）CAP在糖尿病肾病发生发展过程中是其重要因子之一。     

高糖对大鼠肾系膜细胞泛素及泛素化蛋白表达的影响

目的 探讨高糖对大鼠肾系膜细胞泛素及泛素化蛋白表达的影响。 方法 将大鼠HBZY-1肾系膜细胞进行体外培养,高糖作为刺激因子,分别设正常对照组(5.6 mmol/L葡萄糖)、高糖组（10、20、30 mmol/L葡萄糖）、甘露醇组。刺激12、24、48 h后,分别用实时定量PCR法和Western印迹法检测各组系膜细胞泛素mRNA和泛素化蛋白的表达。 结果 泛素化蛋白多以大分子蛋白为主。与正常对照组比较,30 mmol/L葡萄糖刺激24 h和48 h后泛素化蛋白的表达分别增加36％和52％（均P ＜ 0.01）;20 mmol/L和30 mmol/L葡萄糖作用48 h泛素化蛋白的表达分别增加31％和52％（均P ＜ 0.01）;高糖作用24、48 h,泛素mRNA的表达显著增加（均P ＜ 0.05）。 结论 高糖呈时间浓度依赖性地促进大鼠肾系膜细胞泛素mRNA及泛素化蛋白的表达,增加泛素蛋白酶体途径活性。     

高糖刺激肾小球系膜细胞葡萄糖转运蛋白4及p21的表达及其意义

目的探讨早期糖尿病肾病(DN)肾小球系膜细胞(GMC)中葡萄糖转运蛋白(GLUT)4、p21mRNA表达变化及其与GMC肥大的关系。方法大鼠1097系膜细胞株分为高糖组、甘露醇组、不同浓度胰岛素组、高糖加不同浓度胰岛素组、正常对照组。用RT-PCR法检测各组GLUT4mRNA、p21mRNA的表达。流式细胞仪测各组GMC体积大小。结果正常对照组GMC有一定GLUT4mRNA、p21mRNA表达。高糖组GLUT4mRNA表达明显下降,p21mRNA表达明显增加。胰岛素刺激GMCGLUT4mRNA表达存在浓度依赖关系。p21mRNA表达越高,细胞前向角度散射光(FSC)越强,GMC体积越大。结论高糖刺激导致GMC肥大,GMC的p21mRNA表达上调和GLUT4mRNA表达下调与DN早期GMC肥大-肾小球肥大有关。     

中药复方含药血清对体外培养的肾小球系膜细胞的作用

目的:观察糖基化终末产物(AGEs)对大鼠肾小球系膜细胞ROS、RAGE mRNA和结缔组织生长因子(CTGF)表达的影响,以及中药复方(由太子参、生黄芪、白术、川连、泽兰、丹参、全瓜蒌5 g等组成)的干预作用。方法:原代培养大鼠肾小球系膜细胞,细胞在DMEM/F12培养液中培养传代(37℃,5%CO2),取5~8代细胞用于实验。随机分为正常糖浓度组(含5.5 mmol/L)、高糖浓度组(30 mmol/L)、AGE-BSA组、中药复方+高糖组、中药复方+AGE-BSA组。分别于培养12、24、48 h时用0.25%胰蛋白酶消化液消化并收集细胞,采用CCK-8法检测细胞增殖,RT-PCR法检测细胞RAGE mRNA、CTGF mRNA的表达,流式细胞仪检测细胞内ROS表达。结果:高糖作用24 h和48 h的系膜细胞增殖显著高于正常组(P0.05),AGE-BSA组12 h、24 h和48 h的细胞增殖均有明显增加(P0.05),中药复方加高糖组较高糖组细胞增殖显著降低(P0.05);中药复方加AGE-BSA组较AGE-BSA组细胞增殖也有明显下降(P0.05)。高糖组和AGE-BSA组作用12 h、24 h和48 h的系膜细胞ROS表达均明显升高(P0.05);中药复方加高糖组作用12 h、24 h、48 h较高糖组细胞ROS表达均有下降(P0.05)。高糖组和AGE-BSA组作用12 h、24 h和48 h的系膜细胞CTGF mRNA表达均明显升高(P0.05),中药复方加高糖组作用48 h较高糖组细胞CTGF mRNA表达均有下降(P0.05)。中药复方加AGE-BSA组作用48 h较AGE-BSA组细胞CTGF mRNA也有明显下降(P0.05)。高糖组和AGE-BSA组作用12 h、24 h和48 h的系膜细胞RAGE mRNA表达均明显升高(P0.05);中药复方加高糖组作用12 h、24 h、48 h较高糖组细胞RAGE mRNA表达均有下降(P0.05);中药复方加AGE-BSA组作用48 h较AGE-BSA组细胞RAGE mRNA也有明显下降(P0.05)。结论:AGEs可能部分通过诱导细胞内ROS,促进肾小球系膜细胞表达CTGF,从而引起肾小球系膜基质增生,最终导致肾小球硬化,而中药复方可能通过调节AGEs-RAGE介导的氧化应激过程,从而阻止肾小球纤维化的发展进程。     

罗格列酮抑制环孢素诱导的大鼠肾脏成纤维细胞基质金属蛋白酶9和金属蛋白酶1组织抑制剂表达

目的 观察罗格列酮(RGZ)对环孢素A(CsA)作用下大鼠肾脏成纤维细胞(NRK)过氧化物酶体增生物激活受体γ(PPARγ)和基质金属蛋白酶-9(MMP-9)表达的影响,探讨罗格列酮对环孢素A肾毒性保护作用的分子机制.方法 构建、筛选和扩增PPARγ基因的siRNA载体,并将载体转染至体外培养的NRK细胞.体外培养NRK细胞,随机分组.(1)对照组:不加处理;(2)RGZ组:加RGZ( 10 μmol/L);(3)CsA组:加CsA( 1.0 mg/L);(4)CsA+RGZ 组:同时加CsA( 1.0 mg/L)及RGZ(10 μmol/L);(5)CsA+RGZ+siRNA组:质粒pRNAT- U6.2/LentiPPARγ-236转染NRK细胞,然后同时加入CsA( 1.0 mg/L)及RGZ(10 μmol/L).培养24 h后,用实时荧光定量和RT-PCR法检测各组细胞中PPARγ、MMP-9、金属蛋白酶1组织抑制剂(TIMP-1) mRNA表达,用Western印迹法检测纤连蛋白(FN)的蛋白表达.结果 CsA明显上调PPARγ、MMP-9和TIMP-1 mRNA的表达(均P＜0.05);RGZ与CsA合用后,PPARγ、MMP-9和TIMP-1 mRNA表达下降(均P＜0.05);应用PPARγ siRNA后,与RGZ+ CsA组相比,PPARγ mRNA表达显著下降(P＜0.05),MMP-9 mRNA和TIMP-1 mRNA表达有所增加(均P＜ 0.05).CsA明显上调FN蛋白表达(P＜0.05);RGZ与CsA合用后,FN蛋白表达下降(P＜0.05);应用含PPARγ siRNA后,FN蛋白表达有所增加(P＜0.05).结论 罗格列酮可以显著减轻CsA诱导NRK细胞分泌的FN蛋白及MMP-9、TIMP-1 mRNA的表达,构建的siRNA质粒转染NRK细胞,能够有效地阻断NRK中PPARγ mRNA的表达,部分阻断罗格列酮对CsA毒性的改善作用.     

活性维生素D_3对高糖环境下小鼠足细胞巢蛋白表达的影响

目的:探讨活性维生素D3是否与高糖环境下小鼠足细胞巢蛋白(nestin)的表达调控有关。方法:采用体外培养永生化小鼠足细胞,将分化成熟的足细胞分为正常糖(糖5 mmol/L)组、高糖(糖25 mmol/L)组、甘露醇对照组、高糖+活性维生素D3(10-7,10-8,10-9mol/L)组,应用Western blot及RT-PCR半定量检测nestin蛋白水平及其mRNA水平的表达情况。结果:高糖+活性维生素D3组较高糖组小鼠足细胞nestin蛋白水平及其mRNA水平表达均增高(P0.05)。结论:活性维生素D3能上调高糖环境下nestin mRNA和蛋白水平的表达而发挥保护作用。     

高糖通过转化生长因子β信号诱导肾小球内皮细胞向肌成纤维细胞转分化

目的 探讨高糖(HG)能否通过转化生长因子β(TGF-β)途径诱导大鼠肾小球内皮细胞向肌成纤维细胞转分化(EndMT).方法 体外培养大鼠肾小球内皮细胞(GEnC),分为正常对照组(NG,5.5 mmol/L)、高糖组(HG,15、30 mmol/L)、TGF-β抑制剂组(HG+LY36,30 mmol/L葡萄糖+10 μmol/L LY364947)以及高渗对照组(M,5.5 mmol/L葡萄糖+25.5 mmol/L甘露醇)和溶剂对照组(D,5.5 mmol/L葡萄糖+1 ml/LDMSO).采用Western印迹法检测各组细胞内皮细胞标志物claudin5和肌成纤维细胞标志物α-SMA表达变化;实时定量PCR法检测细胞TGF-β1和TGF-β2 mRNA表达改变;免疫荧光法观察细胞形态学变化以及血管内皮细胞标志物VE-cadherin和肌成纤维细胞标志物α-SMA的表达.结果 与NG组比较,HG组claudin5蛋白的表达量随葡萄糖浓度增加而降低(P＜0.05),α-SMA蛋白表达量随葡萄糖浓度增加而升高(P＜0.05),TGF-β1和TGF-β2 mRNA表达均升高(P＜0.05).与HG组比较,TGF-β抑制剂组claudin5蛋白表达量升高(P＜0.05),α-SMA蛋白表达降低(P＜0.05).高渗对照组和溶剂对照组改变差异无统计学意义.激光共聚焦免疫荧光结果显示,高糖处理可引起细胞形态由卵圆形向梭形改变,VE-cadherin表达减少,α-SMA表达增加;TGF-β抑制剂组细胞形态无明显改变.与HG组比较,TGF-β抑制剂组VE-cadherin表达增加,α-SMA表达降低(P＜0.05).结论 高糖诱导大鼠肾小球内皮细胞TGF-β表达增加及内皮细胞-肌成纤维细胞转分化.抑制TGF-β可抑制高糖引起的转分化,提示TGF-β参与了高糖引起的肾小球内皮细胞转分化过程.     

骨化三醇对高糖诱导的肾小管上皮细胞肾素高表达的影响

目的探讨骨化三醇对高糖状态下肾小管上皮细胞肾素表达的影响及其机制。方法按随机数字表法将24只6~8周龄Wistar大鼠随机分为对照组、糖尿病组、骨化三醇组(0.03μg·kg~(-1)·d~(-1)),各组8只。16周后处死各组大鼠,检测尿蛋白、尿肌酐、内生肌酐清除率(endogenous creatinine clearance rate,CCr),并应用实时荧光定量法(real time-polymerase chain reaction,RT-PCR)和蛋白印迹法(Western blot)检测肾脏组织肾素及磷酸化细胞外信号调节激酶(phosphorylated extracellularsignal-regulated kinase,p-ERK)/细胞外信号调节激酶(extracellularsignal-regulated kinase,ERK)表达情况。NRK-52E细胞分组:①正常对照组;②高糖组(糖浓度为25 mmol/L,不同时间点);③高糖+骨化三醇(10~8 mol/L、10~9 mol/L、10~10 mol/L)组;④高糖+ERK抑制剂(FR18020410~5 mol/L)组。RT-PCR法检测肾素mRNA表达,Western印记法检测肾素蛋白、p-ERK/ERK蛋白表达。结果与对照组比较,糖尿病组大鼠尿β2微球蛋白(β2-microglobulin,β2-MG)、尿白蛋白/尿肌酐升高(P0.05),CCr降低(P0.05);与糖尿病组比较,骨化三醇组大鼠尿β2-MG、尿白蛋白/肌酐降低(P0.05),CCr升高(P0.05)。与对照组比较,糖尿病组大鼠肾组织肾素、p-ERK/总ERK表达均明显升高,骨化三醇能显著减轻糖尿病大鼠上述蛋白的高表达(P0.05)。高糖可诱导NRK-52E细胞ERK蛋白磷酸化(P0.05),诱导肾素mRNA及蛋白表达上调,并呈时间依赖性(P0.05)。骨化三醇可浓度依赖性地降低高糖诱导的NRK-52E细胞ERK蛋白磷酸化及肾素mRNA、蛋白的高表达(P0.05)。ERK抑制剂能部分抑制高糖诱导的肾素蛋白高表达(P0.05)。结论骨化三醇降低糖尿病大鼠蛋白尿,具有肾脏保护作用,其机制可能与抑制ERK通路降低高糖诱导的肾素高表达有关。     

Histochemical and contractile properties of striated muscles of urethra and levator ani of dogs and sheep

AIMS: To understand their possible importance in long- and short-term control of continence, some properties of the striated muscles of the urethra and pelvic floor (levator ani) of dogs and sheep were investigated, especially fiber types and contractile characteristics. MATERIALS AND METHODS: Striated muscles of urethra and levator ani of 29 male and 6 female dogs and 11 male and 6 female sheep were removed and cut into strips. Some strips were frozen and stained for ATPase at pH 9.4 and 4.3 for fiber typing; others were set up in an organ bath to study contractile responses to nerve stimulation. RESULTS: All muscles contained both type I (slow) and type II fibers, ranging from 97% type II in female greyhound urethra to 60% in female sheep levator ani. For each muscle, there were fewer type II muscles in sheep than in dog. The diameters of the urethral fibers were about 60% of the levator ani in dogs and 34% in sheep. Contraction of the urethral muscle was faster than for levator ani and declined to about 80% of the peak, 500 msec after the beginning of stimulation at 20 Hz. The levator ani contraction rose to a steady level as long as stimulation continued. CONCLUSIONS: Both the levator ani and urethral striated muscles contain slow and fast fiber types. The levator ani muscles are capable of sustained contraction with rapid onset which will produce long-term closure of the urethra. The circular urethral muscle contraction was faster but less well maintained.     

Incorporation and release of85Sr and14C-proline-hydroxyproline in mineral and collagen of bone and incisor teeth of growing rats

The extent to which exchange and reutilization processes of mineral tracers affect skeletal mineral accretion and resorption measurements was evaluated by comparing the rates of appearance and disappearance of⁸⁵Sr and¹⁴C-proline-hydroxyproline in bones and teeth in growing rats for 12 days following simultaneous parenteral injection of these tracers. Expressions for the relative rates of collagen synthesis and breakdown, which unlike mineral metabolism are considered not to be complicated by exchange phenomena, were based on¹⁴C-proline conversion to¹⁴C-hydroxyproline; the specific activity of the latter was determined. Both the mineral and the collagen specific activities reflected the rates and patterns of growth of the samples assayed; rapid growth and a short interval of time between formation and resorption of tissue in themetaphyseal bone which contains the cartilagineous growth plate, slow growth and an interval of time between formation and resorption of tissue indiaphyseal bone and incisor teeth which is longer than the 12 days of the experiment. However, in metaphyseal bone the specific activity collagen/mineral ratio dropped by one half during the 4–12 day interval in contrast to diaphyseal bone and incisor teeth in which no change in this ratio was observed during this period of time. The data indicate that collagen in the metaphyseal growth zone is removed by resorption before it has become fully mineralized, and that exchange is a relatively unimportant factor in the long term kinetics of bone mineral.

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Zusammenfassung Das Ausmaß, bis zu welchem Austausch- und Wiederverwendungsprozesse der mineralen Tracer die Messungen des mineralen Skelett-Auf- und Abbaues beeinflussen können, wurde ausgewertet; zu diesem Zweck wurde die Geschwindigkeit des Auftretens und Verschwindens von⁸⁵Sr und von¹⁴C-Prolin-Hydroxyprolin in Knochen und Zähnen von wachsenden Ratten während der 12 auf die simultane parenterale Injektion dieser Tracer folgenden Tage verglichen.Der Ausdruck für die relative Geschwindigkeit des Kollagen-Auf- und Abbaues, bei welchem im Gegensatz zum Mineralmetabolismus kein Mitwirken des Austauschphänomens vermutet wird, basiert auf der Umwandlung von¹⁴C-Prolin zu¹⁴C-Hydroxyprolin; die spezifische Aktivität des letzteren wurde bestimmt.Aus der spezifischen Aktivität des Minerals sowie jener des Kollagens konnten die Geschwindigkeit und die Art des Wachstums der untersuchten Proben ersehen werden, d.h.schnelles Wachstum und ein kurzes Zeitintervall zwischen Bildung und Resorption des Gewebes imKnochen der Metaphyse, die auch die knorpelige Wachstumsplatte enthält, und andererseitslangsames Wachstum und längeres Zeitintervall (länger als die 12 Tage des Experimentes) zwischen Bildung und Resorption des Gewebes imKnochen der Diaphyse und in den Schneidezähnen. Immerhin fiel die spezifische Aktivität des Kollagen/Mineral-Anteils im Knochen der Metaphyse während dem 4–12tägigen Zeitintervall auf die Hälfte, im Gegensatz zum Knochen der Diaphyse und der Schneidezähne, bei welchen während dieser Zeitspanne kein Unterschied in diesem Verhältnis beobachtet wurde.Diese Ergebnisse zeigen, daß Kollagen in der Wachstumszone der Metaphyse durch Resorption verschwindet, bevor es ganz mineralisiert ist, und daß der Austausch ein relativ unwichtiger Faktor in der Kinetik auf lange Sicht des Knochenminerals ist.

     

Instrumented ligamentotaxis and stabilization of compression and burst fractures of dorsolumbar and mid-lumbar spines

Background:

Controversy continues regarding the best treatment for compression and burst fractures. The axial distraction reduction utilizing the technique employing the long straight rod or curved short rod without derotation to reduce fracture are practised together with short segment posterolateral fusion (PLF). Effects of the early postoperative mobilization without posterolateral fusion on reduction maintenance and fracture consolidation were not evaluated so far. The present prospective study is designed to assess the effectiveness of i) reduction and restoration of sagittal alignment, ii) no posterolateral fusion on the reduced, fractured vertebral body and injured disc, iii) fracture consolidation and iv) the fate of the unfused cephalad and caudal injured motion segments of the fractured vertebra.

Materials and Methods:

The study includes 15 Denis burst and two Denis type D compression fractures between T₁₂ and L₃. The lordotic distraction technique was used for ligamentotaxis utilizing the contoured short rods and pedicle screw fixator. Three vertebrae including the fractured one were fixed. The patients after surgery were braced for ten weeks with activity restriction for 2-4 weeks. The patients were evaluated for change in vertebral body height, sagittal curve, reduction of retropulsion, improvement in neural deficit. The unfused motion segments, residual postoperative pain and bone and metal failure were also evaluated.

Results:

The preoperative and postreduction percentile vertebral heights at, zero (immediate postoperative), at three, six and 12 months followup were 62.4, 94.8, 94.6, 94.5 and 94.5%, respectively. The percentages of the intracanal fragment retropulsion at preoperative, and postoperative at zero, 3, 6 and 12 months followup were 59.0, 36.2,, 36.0, 32.3, and 13.6% respectively.The preoperative and postreduction percentile loss of the canal dimension and at zero, three, six and 12 months were 52.1, 45.0, 44.0, 41.0 and 29% respectively suggesting that the under-reduced fragment was being resorbed gradually by a remodeling process. The mean initial kyphosis of 33° became mean 2° immediately after reduction and mean 3° at the final followup. The fractured vertebral bodies consolidated in an average period of ten weeks (range 8-14 weeks). The restored disc heights were relatively well maintained throughout the observation period. All paraparetic patients recovered neurologically. There were no postoperative complications.

Conclusion:

Instrument-aided ligamentotaxis for compression and burst fractures utilizing the short contoured rod derotation technique and the instrumented stabilization of the fractured spine are found to be effective procedures which contribute to the fractured vertebral body consolidation without recollapse and maintain the motion segment function.     

Principles and Practice of Hemofiltration and Hemodiafiltration

There is growing interest in the convective dialysis therapies, hemofiltration (HF) and hemodiafiltration (HDF). Both require dialysis membranes which are highly permeable to solutes as well as fluid, and in both cases large volumes of ultrafiltration are the condition for convective transport. In HDF the convection is combined with diffusion, and as a consequence, maximum clearance over the entire molecular weight spectrum is achieved. Optimal forms of HDF provide urea clearance 10–15% higher than the corresponding diffusive mode. The larger the solute, the greater is the impact of convection, and β₂-microglobulin (β₂m) levels may be up to 70% reduced. Traditional postdilution HF provides high clearance of medium sized and large molecules. Satisfactory clearance of small solutes requires blood flows in excess of 500 ml/min. With access to practically unlimited volumes of substitution solution through on-line ultrafiltration, predilution HF can now be used. This increases the clearance of small solutes to an acceptable range. For HDF as well as HF, large patient populations consistently treated for longer periods of time are needed to make valid outcome comparisons with other therapies.     

骨折不愈合与延迟愈合的成因与治疗

目的探讨骨折不愈合与延迟愈合的成因、报肯治疗的方法与设果。方法对1990年7月～2004年12月间收治的107例骨折不愈台、54例骨折延迟愈合2例先天性胫骨骨不连进行回顾性研究，分析原因，随访治疗结果。18例延迟愈合行保守治疗，本组其他145例行手术治疗，结果除2例先天性胫骨骨不连外，其余161例的成因中均有医源性因素。10例失去随访，153例平均随访17（6-28）个月，骨折均获骨性连接，愈合时间平均10（6-14）个月，肢体功能恢复良好，结论医源性技术缺陷是骨折不愈合与延迟愈合的主要原因，针对各种不同因素进行合理治疗可获得满意效果。     

Recognition and management of phaeochromocytoma and paraganglioma

Phaeochromocytomas and paragangliomas (PPGL) are catecholamine-secreting neuroendocrine tumours arising from the chromaffin cells in the adrenal medulla. These tumours may be identified incidentally, as part of a work-up for multiple endocrine neoplasia or following haemodynamic surges during unrelated procedures. Advances in perioperative management and improved management of intraoperative haemodynamic instability have significantly reduced surgical mortality from around 40% to less than 3%. Surgery is the definitive treatment in most cases and laparoscopic resection where possible is associated with improved outcomes. Anaesthetic management of PPGL cases represents a unique haemodynamic challenge both before and after tumour resection. In this article we describe the physiology of these tumours, their diagnosis, preoperative optimization methods, intraoperative anaesthetic management and management of postoperative complications.     

Physiology and pharmacology of nausea and vomiting

Nausea and vomiting are both very unpleasant experiences. The physiology is poorly understood; however, understanding what we do know is key to tailoring a preventative or therapeutic antiemetic regime. There are two key sites in the central nervous system implicated in the organization of the vomiting reflex: the vomiting centre and the chemoreceptor trigger zone. There are five key neurotransmitters involved in afferent feedback to these areas. These are histamine (H₁ receptors), dopamine (D₂), serotonin (5-HT₃), acetyl choline (muscarinic) and neurokinin (substance P). Postoperative nausea and vomiting will occur in around one-third of elective patients who have no prophylaxis. This can result in many detrimental effects including patient dissatisfaction, unplanned admission and prolonged recovery. It is therefore essential that clinicians understand how they can prevent and treat nausea and vomiting using either a single agent or a combination of antiemetics to target relevant receptors. Commonly used drugs include antihistamines, dopamine antagonists, serotonin antagonists and steroids. More novel agents are being developed such as aprepitant, a neurokinin receptor antagonist, palonosetron, a 5HT₃ receptor antagonist and nabilone, a synthetic cannabinoid.     

Physiology and pharmacology of nausea and vomiting

Nausea and vomiting are both very unpleasant experiences. The physiology is poorly understood; however, understanding what we do know is key to tailoring a preventative or therapeutic antiemetic regime. There are two key sites in the central nervous system implicated in the organization of the vomiting reflex: the vomiting centre and the chemoreceptor trigger zone. There are five key neurotransmitters involved in afferent feedback to these areas. These are histamine (H₁ receptors), dopamine (D₂), serotonin (5-HT₃), acetyl choline (muscarinic) and neurokinin (substance P). Postoperative nausea and vomiting will occur in around one-third of elective patients who have no prophylaxis. This can result in many detrimental effects including patient dissatisfaction, unplanned admission and prolonged recovery. It is therefore essential that clinicians understand how they can prevent and treat nausea and vomiting using either a single agent or a combination of antiemetics to target relevant receptors. Commonly used drugs include antihistamines, dopamine antagonists, serotonin antagonists and steroids. More novel agents are being developed such as aprepitant, a neurokinin receptor antagonist, palonosetron, a 5HT₃ receptor antagonist, and nabilone, a synthetic cannabinoid.