不同剂量L-精氨酸对严重烧伤患者辅助性T淋巴细胞型细胞因子的影响

目的 了解不同剂量L-精氨酸对严重烧伤患者血清辅助性T淋巴细胞1(Th1)/Th2型细胞因子水平的影响.方法 选择笔者单位收治的伤后20 h内入院、烧伤总面积为50%～80%TBSA的患者29例,按随机数字表法分为对照组[10例,经鼻肠管给予葡萄糖盐水500 mL(含50 g/L葡萄糖及9 g/L氯化钠,下同)]、L-精氨酸200 mg组(10例,经鼻肠管给予L-精氨酸200 mg/kg+葡萄糖盐水500 mL)、L-精氨酸400 mg组(9例,经鼻肠管给予L-精氨酸400 mg/kg+葡萄糖盐水500mL).于伤后1 d(行肠内营养前)及3、5、7 d,取各组患者空腹静脉血,用放射免疫法及酶联免疫吸附测定法检测血清Th1型细胞因子TNF-α、IL-1β和Th2型细胞因子TGF-β_1、IL-4含量.结果 各组患者血清TNF-α及IL-1β含量伤后均呈快速上升趋势,L-精氨酸200 mg组血清TNF-α及IL-1β含量伤后5 d达高峰[(318±57)ng/mL、(218±47)pg/mL],但仍显著低于同时相点对照组[(389±34)ng/mL、(272±40)pg/mL,P<0.05],伤后7 d此2种细胞因子含量下降;L-精氨酸400 mg组各时相点血清TNF-α及IL-1β含量与对照组相近(P>0.05).各组患者血清TGF-β_1及IL-4含量伤后呈较缓慢上升趋势;伤后5 d,L-精氨酸200 mg组血清TGF-β_1含量为(110±16)pg/mL,显著高于对照组[(83±20)pg/mL,P<0.05],L-精氨酸400mg组各时相点血清TGF-β_1含量与对照组相近(P>0.05).结论 在严重烧伤患者感染期,相对于400 mg/kg的用量,200 mg/kg的L-精氨酸通过调节血清Th1/Th2型细胞因子释放,能更有效地保持两者之间的比例,从而产生更好的免疫调理作用.     

胃肠道左旋精氨酸营养干预对严重烧伤患者休克期复苏的影响

目的观察严重烧伤患者休克期经胃肠道给予左旋(L)精氨酸对休克复苏的影响,探讨其机制。方法选取烧伤面积≥30%TBSA的患者20例,并随机分为:L-精氨酸组,伤后24h内开始从鼻肠管给予L-精氨酸;对照组,伤后24h内开始从鼻肠管给予50g/L葡萄糖盐水500ml/d,连续4d,每组10例。在伤后1、2、3、4d分别抽取两组患者静脉血,检测其血清超氧化物歧化酶(SOD)活性及丙二醛(MDA)和一氧化氮(NO)含量,并抽取患者动脉血检测其乳酸含量。结果L-精氨酸组患者SOD活性在伤后呈上升趋势,于伤后4d达峰值(68±23)U/ml,与对照组(31±9)U/ml比较,差异有统计学意义(P<0·01)。两组患者伤后MDA、NO含量均呈下降趋势,伤后2dL-精氨酸组NO[(50±14)μmol/L]下降最明显,与对照组(78±22)μmol/L比较,差异有统计学意义(P<0.01)。伤后4d两组患者MDA下降最明显[(3.4±0.8)、(3.5±1.3)μmol/L],L-精氨酸组血乳酸含量在伤后2、3d显著低于对照组(P<0.05或0.01)。结论严重烧伤患者休克期经胃肠道给予L-精氨酸可抑制其体内NO含量过度升高,使血乳酸含量降低,血清SOD活性增加,改善组织脏器血流灌注及氧合状态,减轻缺血再灌注损伤,有利于预防隐性休克的发生或减轻其损害。     

L-精氨酸诱导大鼠暴发型胰腺炎模型建立

目的 建立L-精氨酸诱导大鼠暴发性胰腺炎动物模型.方法 用20%L-精氨酸(450 mg,120 ms/100 g大鼠体重)序贯腹腔和皮下给药建立大鼠暴发性胰腺炎模型.结果 实验大鼠胰腺有广泛变性、坏死,48 h达高峰,胰腺病理评分13.21±3.02;大鼠6～48 h死亡率为56.67%;血清淀粉酶和脂肪酶显著升高,皆12 h达到高峰,分别是(4120±759)、(1490±354)U/L;肺功、肝脏酶学和肾功能皆有显著性改变,48 h PaO2(78.24±3.56)InnlHg(1mmHg=0.133 kPa),48 h谷丙转氨酶(224.67±4.73)U/L,12 h肌酐(94.53±13.49)tunol/L;肺、肝、肾分别有轻到重度病理改变.结论 L-精氨酸能诱导出大鼠暴发性胰腺炎动物模型     

L-精氨酸对内毒素诱导急性肺损伤大鼠肺表面活性物质的影响

目的 评价L-精氨酸对内毒素(LPS)诱导急性肺损伤大鼠肺表面活性物质的影响.方法 健康雄性SD大鼠48只,随机分为4组:正常对照组(C组,n=16)、LPS组(n=16)、LPS 3 h+L-精氨酸治疗组(L1组,n=8)和LPS 6 h+L-精氨酸治疗组(L2组,n=8).LPS组、L1组和L2组静脉注射LPS 5mg/kg,C组给予等容量生理盐水.L1组和L2组分别于给予LPS后3 h或6 h腹腔注射L-精氮酸500 mg/kg.L1组和L2组于给予L-精氨酸后3 h(C组和LPS组分别于给予生理盐水或LPS后6、9 h)取8只大鼠,取肺组织,测定表面活性物质结合蛋白A(SP-A)mRNA的表达水平、肺泡灌洗液(BALF)中总磷脂(TPL)和总蛋白(TP)浓度,光镜下观察肺组织病理学结果.结果 与C组比较,LPS组SP-A mRNA表达下调,BALF中TPL浓度降低,TP浓度升高(P＜0.01).与LPS组比较,L1组SP-A mRNA表达上调,BALF中TPL浓度升高,TP浓度降低(P＜0.05或0.01);L2组上述指标差异无统计学意义(P＞0.05).L1组肺损伤程度轻于LPS组和L2组.结论 L-精氨酸可促进肺表面活性物质合成,从而对大鼠内毒素诱导急性肺损伤具有治疗作用.     

L-精氨酸经一氧化氮途径对人结肠癌细胞株LS174的增殖及iNOS表达和细胞周期的影响

目的探讨L-精氨酸经一氧化氮（NO）途径对人结肠癌细胞株LS174的增殖及诱导型一氧化氮合酶（iNOS）的表达和细胞周期的影响。方法LS174细胞经不同浓度L-精氨酸干预后,采用MTT法检测细胞增殖活性,硝酸还原酶法检测细胞培养液中NO的含量,流式细胞仪检测细胞周期,Western blot和免疫细胞化学染色SP法检测iNOS蛋白的表达。结果低浓度（0.125mmol/L）的L-精氨酸对LS174细胞的增殖有促进作用,高浓度（0.5、2、8及32mmol/L）的L-精氨酸对LS174细胞的增殖有抑制作用;培养液中的NO浓度伴随L-精氨酸浓度的增加而升高;与对照组相比,高浓度（0.5、2、8及32mmol/L）L-精氨酸处理48h后S期细胞比例增加（P〈0.05,P〈0.01）,低浓度（0.125mmol/L）者差异则无统计学意义（P〉0.05）;随着L-精氨酸浓度的增加,iNOS蛋白的表达较对照组有增高趋势,浓度越高,效果越明显。结论L-精氨酸通过诱导iNOS的表达,可提高NO的生成;低浓度的L-精氨酸对LS174细胞的增殖有促进作用,高浓度的L-精氨酸对LS174细胞的增殖有抑制作用;高浓度的L-精氨酸诱导细胞周期停滞于S期。     

填充床反应器中固定化假单胞菌细胞连续制备L-瓜氨酸

对实验室筛选的产精氨酸脱亚胺酶的假单胞菌( Pseudomonas sp.)进行了固定化,以及对固定化细胞转化L-精氨酸生产L-瓜氨酸进行了研究.比较4种不同固定化方法,确定卡拉胶包埋结合戊二醛后处理为假单胞菌的细胞固定化方法.固定化反应的最适pH值为6.5,细胞固定化后细胞精氨酸脱亚胺酶的热稳定性增加.在50 mm×240 mm固定填充床反应器中,底物浓度为0.5 mol/L L-精氨酸盐酸盐,pH值6.5,温度37 ℃,稀释速率为0.147/h的条件下,连续运转54 d,固定化细胞对底物的摩尔转化率在95%以上,平均生产强度 0.010 8 g/(h*g)(每单位质量的固定化细胞每小时生产的瓜氨酸质量).转化液经732阳离子树脂吸附,氨水洗脱,及浓缩、结晶,得到纯度为99%的L-瓜氨酸晶体,提取总收率约为87%.     

早期应用L-精氨酸治疗急性出血坏死性胰腺炎的实验研究

目的: 探讨早期应用L-精氨酸对急性出血坏死性胰腺炎(AHNP)的治疗作用. 方法: 经大鼠胰胆管注射牛磺酸钠制备AHNP模型,分别静注L-精氨酸、生理盐水、山莨菪碱;观察血清淀粉酶、白介素6(IL-6)、丙二醛(MDA)、一氧化氮(NO)改变及胰腺的病理改变. 结果: 应用L-精氨酸后,能升高血NO浓度,清除氧自由基,降低血清IL-6水平,降低血清淀粉酶,改善胰腺病变,其作用优于山莨菪碱. 结论: 早期应用一定剂量的L-精氨酸对AHNP具有一定的治疗效果.     

L-精氨酸——一氧化氮代谢通路对在体心肌缺血/再灌注大鼠心功能的影响

目的 用在体方法于大鼠心肌缺血/再灌注过程的不同时相给予L-精氨酸,以观察一氧化氮(NO)的"双刃性"作用对心功能的影响.方法 雄性Wistar大鼠48只,随机均分为4组:伪手术组(Sham组),心肌缺血I再灌注(MI/R)+生理盐水组(Vehicle组),MI/R+L-精氨酸早期处理组(Early组)和MI/R+L-精氨酸晚期处理组(Late组).结扎大鼠心脏左冠状动脉前降支,缺血30min、再灌注5 h;分别在缺血/再灌注早期和晚期给予L-精氨酸,动态监测大鼠左心室功能.用比色法测定心肌组织Caspase3活性;用化学发光法检测总NO(NOx)含量;用免疫印迹法测定iNOS含量.结果 与Vehicle组相比,早期给予L-精氨酸使大鼠心功能明显改善,Caspase3活性大幅度下降;而晚期给予L-精氨酸使大鼠心功能明显恶化,Caspase3活性进一步增加,心肌NOx含量升高,iNOS表达显著上调(P<0.05).结论 在再灌注早期给予L-精氨酸可通过抑制心肌细胞凋亡,降低再灌注损伤,起到改善心功能的作用;而晚期给予L-精氨酸,可促进细胞凋亡,进而使心功能恶化.     

L-丝氨酸产生菌的分离筛选及发酵条件

在含50mL／L的甲醇、5g／L的甘氨酸的基本培养基平板上，从土壤中分离出130多株细菌，测定了它们利用甘氨酸生产L-丝氨酸的能力，获得了一株产L-丝氨酸较好的菌株A3，L-丝氨酸产量最高为1．4g／L，分类学鉴定为微球菌科(Micrococcaceae)，对菌株A3利用甘氨酸发酵生产L-丝氨酸的发酵条件进行了初步研究，包括甘氨酸和甲醇添加量，不同碳源、氮源，初始pH值以及发酵时间对产酸的影响．结果表明，菌株A3在不添加甲醇、只以甘氨酸为惟一碳源的发酵培养基中也能产L-丝氨酸，培养基中较高质量浓度的甘氨酸存在对L-丝氨酸生产是必需的．添加葡萄糖、甘油等外源碳源对菌体生长有利但不利于L-丝氨酸的生产。     

一种新型大鼠高脂血症急性胰腺炎模型的构建和评价

背景与目的:目前高脂血症急性胰腺炎(HTG-AP)研究中,动物模型的构建方法尚不统一,且模型制备有一定困难。故本研究探讨一种采用高脂血症诱导物poloxamer-407(P-407)联合L-精氨酸构建大鼠HTG-AP模型的新方法。方法:将72只雄性SD大鼠随机均分为正常对照组和低(0.12 g/kg)、中(0.25 g/kg)、高(0.50 g/kg)3个剂量P-407组。正常对照组大鼠不予干预,其余3组大鼠分别腹腔注射各自剂量的P-407,1次/d诱导高脂血症,每组分别于1、2、4周后随机各取6只大鼠,腹腔注射20% L-精氨酸(2.5 g/kg)2次(间隔1 h)诱导胰腺炎,并于24 h后剖杀,取血检测各组大鼠血清肝肾功能指标以及血清甘油三酯(TG)、总胆固醇(TC)、淀粉酶(AMY)、脂肪酶(LIPA)水平,取胰腺组织观察组织病理学变化并评分。结果:各剂量P-407组与正常对照组比较,血清肝肾功能指标在各时间点均无明显变化(均P0.05);而血清TG、TC水平在每个时间点均明显升高,且呈时间与剂量依赖性(均P0.05),其中低剂量P-407组各时间点TG水平未达到HTG-AP血脂标准(TG11.3 mmol/L),而高、中剂量P-407组分别在实验1、2周后TG水平达HTG-AP血脂标准。各剂量P-407组与正常对照组比较,血清AMY、LIPA明显升高,胰腺病理损伤评分明显增加,且均呈明显的时间与剂量依赖性(均P0.05)。结论:采用适当剂量的P-407(0.25～5.0 g/kg)联合L-精氨酸的方法可在短时间内(1～2周)构建稳定的大鼠HTG-AP模型。该模型操作简便,可靠性好,可为相关领域的研究提供便利的工具。     

Comparaison des dispositifs Orth-Evac™ et Solcotrans Plus™ pour l'autotransfusion du sang drainé après arthroplastie totale du genou

Surgical wound blood which is ched through drains after total knee replacement surgery with a tourniquet may be returned to the patient using special collecting devices. This study aimed to compare two systems, Orth-Evac™ and Solcotrans Plus™ an to assess the safety of the reinfusion of non washed blood cells. It included 30 patients scheduled for total knee replacement surgery, free from tumoral or coagulation disease and allocated randomly in three groups of 10 each : the Orth-Evac™ group (OGr), the Solcotrans Plus™ group (SGr) and the Control group (CGr). The devices, not containing an anticoagulant, were connected to the deep suction drains in the operating room, after skin closure and before the tourniquet removal. The salvaged blood was reinfused in the subsequent six hours via a 40 μm filter. The volume of collected blood was measured and homologous blood was added as required, to maintain a hematocrit of 30 %. A blood sample was obtained the day before surgery (D − 1), before reinfusion (D0), two hours later (D + 2 h), one day later (D + 1), and from the collecting device before reinfusion. The statistical analysis used the Kruskal-Wallis test and Steel-Dwass procedure to confirm the difference between two groups. The three groups did not differ in age, weight, height and gender. The volume of salvaged and autotransfused blood was 925 ± 156 mL in OGr and 605 ± 178 mL in SGr respectivelly. transfusion of homologous blood was required in two patients of OGr, four of SGr and six of CGr. At D + 1, the hematocrit was comparable in all groups (OGr = 28 %, SGr = 28.2 % and CGr = 28.5 %). At D + 1 the moderate decrease of PT, aPTT, fibrinogen and platelets count was also similar between the groups and correlated with haemodilution (protein concentration). At D + 1, blood lipids and blood gases were comparable in all groups and no symptoms of fat embolism were seen. At D + 2 h, the plasma concentration of D-dimers, assessed by Elisa technique, was significantly higher in SGr (89 ± 99 μg · mL⁻¹ vs 39 ± 34 μg · mL⁻¹ in the OGr), and in one patient of this group it reached 306 μg · mL⁻¹. In the CGr the concentration was 22 ± 15 μg · mL⁻¹. At D + 1 no significant difference was observed. This effect may be related to the reinfused blood which contained over 1 000 μg · mL⁻¹ of D-dimers. The collected blood did not coagulate. The PT was over 120 s, the aPTT over 180 s and the presence of fibrinogen and factors V and II could not be detected. The high concentration of D-dimers in the salvaged blood can be explained by the activation of coagulation in the surgical site. As this blood is not clotable, the addition of an anticoagulant is not required. The collected blood has similar characteristics in the two devices. The amount was always more than 500 mL. Therefore the Orth-Evac™ system is more appropriate as its content is 1 000 mL vs 550 mL for the Solcotrans system. Moreover, the cost of the former is lower. The economy of homologous blood was more significant with the Orth-Evac™ system, as only two patients out of 10 required the transfusion of homologous blood. D-dimers at high concentration may decrease the platelets' aggregation. In this study, neither bleeding nor other adverse effects occurred with retransfusion of salvaged blood at amounts never exceeding 1 000 mL, which is probably the upper limit of this technique.     

两个时期肾结核的临床比较

目的：探讨近年来肾结核的流行病学和临床变化趋势.方法：对收治的842例肾结核患者,以1980年底为界,分为先期组和近期组进行临床比较.结果：两组患者分别：占同期泌尿外科住院人数的8.74%和1.95%（P＜0.05）;就诊年龄中位数为28岁、38岁;病程平均为33.6个月、45.9个月.尿频91.1%,66.0%;血尿82.6%、64.7%;伴发肺结核18.4%、12.3%;伴发膀胱结核37.2%、19.6%;伴发附睾结核47.0%、36.6%（以上各项均P＜0.05）;IVU检查阳性率分别为90.0%、85.9%.结论：肾结核发病率近年来明显下降,其典型临床表现比例降低,不典型肾结核病例呈明显增加趋势.     

免疫抑制剂对嗜铬细胞瘤12细胞和L929细胞增殖的影响

目的 初步探讨多种免疫抑制剂对嗜铬细胞瘤12（pheochromocytoma 12，PC12）细胞和L929细胞增殖的影响。方法 对数生长期PC12细胞和L929细胞传代，取细胞株复苏后第3代细胞均以1×10^6／ml密度接种于培养板中，分别加入10、10、10^-7和10^8mol／L环孢菌素A（cyclosporin A，CsA），10^-6、10^-7、10^-8和10^-9mol／LFK506以及10^-3、10^-4、10^-6和10^-8mol／L甲基强地松龙，并设立空白对照组。于培养24、48和72h后，取各浓度药物作用的细胞，采用MTT法检测细胞增殖。结果 高浓度（10mol／L）甲基强地松龙和较低浓度（10^-8～10^-7mol／L）CsA，在给药后48h内对PCI2细胞增殖有明显促进作用，此后促增殖作用不明显；而各个浓度的FK506均无促进PCI2细胞增殖的作用。高浓度甲基强地松龙（10^-3mol／L）和CsA（10^-6～10mol／L）作用24h后，对L929细胞增殖有显著抑制作用，FK506仅在较高浓度（10^-6mol／L）有一过性（仅出现于给药后48h）促进L929细胞增殖的作用。结论 10^-3mol／L甲基强地松龙和10^-8～10^-7mol／LCsA能够在短时间内促进PC12细胞增殖，而10^-3mol／L甲基强地松龙和10^-6～10^-5mol／L CsA对L929细胞增殖有显著抑制作用。     

Effect of ammonium chloride and dietary phosphorus in the azotaemic rat. I. Renal function and biochemical changes.

BACKGROUND: Both dietary phosphorus restriction and the ingestion of ammonium chloride (NH(4)Cl) given to rats on a high-phosphorus diet have been shown to preserve renal function in the azotaemic rat. Parathyroidectomy also has been reported to preserve renal function and, in addition, to prevent kidney hypertrophy in the remnant kidney model. Our goals were (i) to evaluate in azotaemic rats the effect of dietary phosphorus on renal function in a shorter time frame than previously studied and (ii) to determine whether NH(4)Cl administration (a) enhances the renoprotective effect of dietary phosphorus restriction and (b) improves renal function in the absence of parathyroid hormone (PTH). METHODS: High (H; 1.2%), normal (N; 0.6%) and low (L; <0.05%) phosphorus diets (PD) were given for 30 days to 5/6 nephrectomized rats. In each dietary group, one-half of the rats were given NH(4)Cl in the drinking water. The six groups were HPD + NH(4)Cl, HPD, NPD + NH(4)Cl, NPD, LPD + NH(4)Cl and LPD. The effect of NH(4)Cl administration was also evaluated in 5/6 nephrectomized, parathyroidectomized (PTX) rats on NPD. RESULTS: In each of the three dietary phosphorus groups, creatinine and urea clearances were greater (P<0.01) in rats receiving NH(4)Cl. Neither creatinine nor urea clearance was reduced by high dietary phosphorus. Urine calcium excretion was greatest in the LPD group and was increased (P < or = 0.001) in all three groups by NH(4)Cl ingestion. An inverse correlation was present between plasma calcium and phosphorus in the parathyroid intact (r = -0.79, P<0.001) and PTX groups (r = -0.46, P = 0.02). In PTX rats, NH(4)Cl ingestion increased (P < or = 0.01) creatinine and urea clearances and both an increasing plasma calcium concentration (r = 0.67, P<0.001) and urine calcium excretion (r = 0.73, P<0.001) increased urine phosphorus excretion. CONCLUSIONS: At 30 days of renal failure (i) NH(4)Cl ingestion increased creatinine and urea clearances, irrespective of dietary phosphorus; (ii) high urine calcium excretion, induced by dietary phosphorus restriction and NH(4)Cl ingestion, did not adversely affect renal function; (iii) high dietary phosphorus did not decrease renal function; (iv) the absence of PTH did not preserve renal function or prevent NH(4)Cl from improving renal function; and (v) both an increasing plasma calcium concentration and urine calcium excretion resulted in an increase in urine phosphorus excretion in PTX rats.     

Sepsis alters vessel contraction by adrenoceptor-induced nitric oxide and prostanoid

BACKGROUND: Alpha-adrenergic agents contract vascular smooth muscle (VSM) and stimulate endothelial release of secondary factors which modulate VSM contraction. Our study examined constrictor prostanoid (cPN) and nitric oxide (NO) as secondary factors which could alter alpha-1 adrenoceptor-mediated contraction during sepsis. METHODS: Sepsis was induced in rats by inoculation of an implanted sponge with Escherichia coli and Bacteroides fragilis. Aortic rings at 24 h from septic (n = 21) and control (n = 21) rats were suspended in physiological salt solution (PSS) with or without blockers to NO (N(G)-monomethylarginine), cPN (mefenamic acid, MFA), or thromboxane A2 (SQ29548). Contraction dose-response curves were generated to determine maximal contraction force (F(max)) and pD2 (sensitivity) to phenylephrine in each experimental group. RESULTS: Sepsis increased F(max) to phenylephrine (PHE) (1.18 vs 0.90 g, SEM 0.0703). COX inhibition reduced the F(max) in control (0.63 vs 0.90 g, SEM 0.0675) but not in septic animals (1.19 vs 1.18 g, SEM 0.0433). TXA2 receptor inhibition did not alter F(max) in control (1.017 vs 0.973 g, SEM 0.0959) or septic animals (1.28 vs 1.12 g, SEM 0.0823). NOS inhibition enhanced the F(max) in both nonseptic (2.03 vs 0.83 g, SEM 0.0523) and septic rats (1.96 vs 1.15 g, SEM 0.0526), but did less so in the septic animals. CONCLUSIONS: PHE-induced F(max) is determined by a balance between PHE-stimulated VSM alpha-adrenoceptor activity, and PHE-stimulated endothelial release of cPN and NO. Sepsis enhances total PHE-induced F(max) by increasing VSM alpha-adrenoceptor activity and reducing PHE-stimulated endothelial release of dilator NO. Sepsis abolishes the PHE-stimulated endothelial release of cPN. PHE-stimulated cPN is not thromboxane A2, but could be a nonprostanoid dilator in the lipoxygenase (HETE) or cytochrome P450 (EET) pathways.     

A Prospective Randomized Study Comparing Two Different Techniques for Laparoscopic Sleeve Gastrectomy

BACKGROUND: Laparoscopic sleeve gastrectomy (LSG) represents a relatively new restrictive operation for obesity. We report a prospective randomized study comparing two different techniques of performing this procedure. METHODS: Between January and August 2006, 20 patients (group A) and 20 patients (group B) were prospectively and randomly submitted to LSG. The characteristics of the patients in the two groups were similar for age and sex. The median preoperative weight was of 120 kg (95-180) (A) and 133 kg (83-175) (B) (NS). The median preoperative BMI was of 42.5 kg/m2 (35-58) (A) and 47 kg/m2 (37-58) (B) (NS). The two techniques differ in that in A, stapling is performed after full devascularization and mobilization of the gastric curve, whereas in B stapling is performed as soon as the lesser sac is entered and the greater curve is devascularized after full completion of the sleeve. The staple-line is reinforced at the end of stapling in both techniques. RESULTS: Median operative time was 34 min (12-54) (A) and 25 min (9-51) (B) (P = 0.06). Median peroperative bleeding was 5 mL (0-450) (A) and 5 mL (0-100) (B) (P = 0.37). Median number of staple cartridges used was 6 (5-7) (A) and 6 (4-7) (B) (P = 0.63). Peroperative complications were a small hiatal hernia requiring repair and a bleeding in two patients of A. Postoperative leak occurred in 1 patient of A, and minor early complications affected 2 patients of A and 1 patient of B. Peroperative and postoperative mortality was 0. Median hospital stay was 3 days (1-10) (A) and 3 days (2-7) (B) (P = 0.59). One stenosis as a late complication appeared in a patient of B. %EWL at 6 months and 1 year was respectively 43.4% (A), 42.2% (B) and 48.3% (A) 49.5% (B) (P = 0.82). CONCLUSION: LSG can be performed by two different techniques. The technique B (section of the stomach followed by its mobilization) appears familiar to surgeons usually performing laparoscopic RYGBP. No observed differences are significant, but the technique B when looking at observed distributions, seems to be better than the technique A (mobilization of the stomach followed by its section) in terms of operative time, peroperative bleeding and hospital stay.     

Ets-1和VEGF在膀胱移行细胞癌中的表达及意义

目的:探讨血管内皮生长因子(VEGF)和E26转录因子(Ets-1)的表达与膀胱移行细胞癌生物学行为的关系。方法:应用免疫组织化学的方法对48例膀胱移行细胞癌以及正常膀胱组织中的VEGF和Ets-1进行检测。结果:Ets-1的阳性率在Ta~1和T2~4分别为32.1%和65.5%(P<0.05);Ⅰ级和Ⅲ级的表达率分别为31.3%和66.7%(P<0.05);在初发肿瘤和复发肿瘤中的表达分别为33.3%和66.7%(P<0.05)。VEGF的阳性表达率在Ta~1和T2~4分别为28.6%和85.0%(P<0.01);Ⅰ级和Ⅲ级的表达率分别为25.0%和77.8%(P<0.01);在初发肿瘤和复发肿瘤中的表达分别为36.7%和77.7%(P<0.01)。结论:Ets-1和VEGF可以作为了解膀胱移性细胞癌生物学行为的参考指标。     

膀胱移行细胞癌组织中黑色素瘤抗原基因及蛋白的表达

目的探讨膀胱移行细胞癌(TCC)中黑色素瘤抗原(MAGE)基因mRNA的表达及其临床意义。方法采用逆转录聚合酶链反应(RT PCR)技术检测3个膀胱TCC细胞株和20例膀胱TCC患者癌组织(新鲜标本,T1期7例,T2期5例,T3期6例,T4期2例;G11例,G211例,G38例)MAGE A1,A2,A3,A4mRNA表达,免疫组化法检测105例膀胱TCC患者癌组织(石蜡标本,T1期35例,T2期12例,T3期26例,T4期13例,另19例无法确定分期;G113例,G244例,G348例)MAGE A4蛋白的表达。结果3个膀胱TCC细胞株均有MAGE基因mRNA的表达;20例膀胱TCC新鲜标本组织MAGEmRNA阳性:A112例(60%),A216例(80%),A311例(55%),A418例(90%),A1～A4均阳性8例(40%)。105例膀胱TCC石蜡标本组织中MAGE A4蛋白阳性53例(50%),高分级膀胱TCC组织中强表达(++或+++)率为27%(13/48),显著高于低分级的4%(2/57)(F=12.00,P<0.01),高分期膀胱TCC组织中强表达率为27%(14/51),显著高于低分期的0%(0/35)(F=11.48,P<0.01)。结论MAGE基因在膀胱TCC中有较高表达,分级或分期高的膀胱TCC中MACE A4蛋白明显强表达。     

NK2 tachykinin receptors mediate contraction of the pig intravesical ureter: tachykinin-induced enhancement of non-adrenergic non-cholinergic excitatory neurotransmission

The current study was designed to characterize the functionally active tachykinin receptors involved in tachykinin-elicited contractions in the pig intravesical ureter, and to investigate the possible modulation exerted by the natural tachykinins substance P (SP) and neurokinin A (NKA) on the non-adrenergic non-cholinergic (NANC) excitatory ureteral neurotransmission. In pig intravesical ureteral strips pretreated with phosphoramidon (10(-5) mol/L) to block the endopeptidase activities, isometric force recordings showed that SP, NKA, and the NK2 receptor selective agonist [beta-Ala(8)]-NKA (4-10), all three induced contractions, with the following potency order: NKA > [beta-Ala(8) ]-NKA (4-10) > SP. [Sar(9), Met(O(2))(11)]-SP and senktide, selective agonists of the NK1 and NK3 receptors, respectively, failed to modify the ureteral tone. Urothelium removal and incubation with tetrodotoxin (10(-6) mol/L), phentolamine (10(-7) mol/L), propranolol (3 x 10(-6) mol/L), atropine (10(-7) mol/L) and indomethacin (3 x 10(-6) mol/L), did not alter the contraction induced by a submaximal (10(-7) mol/L) dose of [beta-Ala(8)]-NKA (4-10). MEN 10,376 (10(-8)-10(-7) mol/L), a NK2 receptor antagonist, reduced the contraction to 3 x 10(-8) mol/L NKA. GR 82334 (10(-6) -10(-5) mol/L) and SR 142801 (10(-8)-10(-7) mol/L), selective antagonists of the NK1 and NK3 receptors, respectively, did not modify that contraction. In pig intravesical ureteral strips in NANC conditions, SP and NKA induced a potentiation of the contractions to electrical field stimulation (EFS) and to exogenous ATP. The results suggest that the tachykinins evoke a direct contraction of pig intravesical ureteral strips through NK2 receptors located in the smooth muscle. SP and NKA exert an enhancement of the NANC excitatory neurotransmission of the pig intravesical ureter.