肝脏外科患者术后输注脂肪乳剂对蛋白质代谢的影响

将32例肝脏外科疾病患者随机分为Ⅰ组（单能源TPN组10例）；Ⅱ组（双能源TPN组11例，其中脂肪乳剂用量为1g·kg－1·d－1）；Ⅲ组（双能，TPN组11例，其中脂肪乳剂用量为2g·kg－1·d－1）。术后按组别给予TPN支持共6天，术前1天、术后第1和第6天测定肝功，糖代谢及蛋白质合成代谢指标。结果：①Ⅱ、Ⅲ组术后第6天肝脏酶学指标明显下降（P＜0．05），而Ⅰ组仍高于术前水平（P＜O．05）；②Ⅱ、Ⅲ组术后糖代谢基本恢复正常，而Ⅰ组出现高血糖症及高胰岛素血症（P＜0．05）；③Ⅱ组肝脏蛋白质合成水平恢复术前水平或略有提高（P＜0．05），而Ⅰ和Ⅲ组术后蛋白质合成功能仍低（P＜0．05）。结果提示：含脂肪乳剂的TPN支持对肝脏外科患者术后的肝功恢复有益，能促进蛋白质合成及肝细胞再生，并且在进行TPN支持时按1g·kg－1·d－1给予脂肪乳剂较为安全合理。     

Role of tyrosine kinase activity in cardiac slow delayed rectifier channel modulation by cell swelling

 We studied the effects of cell swelling on membrane currents of canine ventricular myocytes using the whole-cell patch-clamp method. Cell swelling was induced by lowering the osmolarity of the bath solution to 60% of control. Cell width and currents were measured simultaneously. Cell swelling induced little or no change in the L-type Ca, the inward rectifier, and the transient outward currents, but a marked increase in the slow delayed rectifier current (I _Ks) was seen. We further examined the role of protein kinase activities in I _Ks modulation by cell swelling. This modulation was not affected by inhibiting serine/threonine kinases using H-8. On the other hand, the modulation was inhibited by genistein (a protein tyrosine kinase inhibitor) although not by daidzein (an inactive analogue of genistein). Our data suggest that in canine ventricle cell swelling can increase protein tyrosine kinase activity, which can augment I _Ks and contribute to changes in membrane electrical activity observed under these conditions. Received: 20 September 1996 / Received after revision and accepted: 5 December 1996     

Accentuated antagonism by angiotensin II on guinea-pig cardiac L-type Ca-currents enhanced by β-adrenergic stimulation

 To examine mechanism(s) underlying the accentuated antagonism by angiotensin II (A-II) on twitch tension, we recorded L-type Ca²⁺ currents (I _Ca,L) using conventional patch-clamp techniques in single, guinea-pig, ventricular myocytes. I _Ca,L was recorded by a step-pulse protocol after eliminating K⁺ conductances (internal Cs⁺ plus tetraethylammonium chloride and K⁺-free extracellular solution). A-II (100 nM) did not affect basal I _Ca,L, but inhibited I _Ca,L that had been enhanced (approximately 200% of control) by (ISO, isoproterenol 100 nM). The inhibitory action of A-II was concentration dependent (concentration eliciting 50% inhibition 88±9 pM, n=41) and the ISO-enhanced component of I _Ca,L was completely blocked by A-II at concentrations above 10 nM. CV-11974 (500 nM), an A-II type-1 receptor (AT₁) antagonist, prevented the inhibitory action of A-II. Pre-incubation with pertussis toxin (PTX) abolished the inhibitory effect of A-II. A-II also inhibited the I _Ca,L enhanced by histamine (500 nM) and forskolin (1 μM), but failed to affect I _Ca,L enhanced by intracellular cyclic adenosine monophosphate (1 mM). The inhibitory action of A-II may therefore involve AT₁ receptors/PTX-sensitive, guanine nucleotide-binding (G) proteins (Gi)/adenylate cyclase and partially explains the A-II-dependent accentuated antagonism of inotropy.     

锌及复合微量营养素的营养干预对学龄前儿童蛋白质营养状况的影响

选择重庆市近郊农村学龄前儿童１４０名，男、女各半，随机分为单纯补锌组、补锌及复合微量营养素组和单纯补充微量营养素组，另一组为对照。实验组每组４０人，对照组为２０人，进行１０周营养干预实验。结果显示，在补锌的同时服用硒、锰、维生素Ａ等多种微量营养素或单纯补充多种微量营养素均能有效改善受试儿童体内锌营养状况，使血浆中前白蛋白、转铁蛋白、铜蓝蛋白含量增加，血清中多种必需及非必需氨基酸，３甲基组氨酸浓度下降。提示，儿童营养状况改善后其体内蛋白质合成代谢加强，而分解减少，这种变化除缘于血清锌含量增加外，可能还与其它微量营养素的作用有关。而单纯补锌儿童血清锌变化并不显著，血清中几种转运蛋白与对照均无明显差异。     

振动对急性缺氧小鼠肺损伤的影响

本文观察了频率为20Hz、振幅为0．67mm和作用时间为40min的振动预处理对急性缺氧小鼠肺损伤的影响。结果发现实验组的肺组织匀浆脂质过氧化物LghdPeroxde（LPO）、支气管肺泡灌洗液（BALF）中蛋白含量和白细胞数明显低于对照组（P＜0．05）。这表明在特定率数的振动作用下能明显减轻急性缺氧小鼠肺的损伤。     

非创伤性股骨头坏死患者的血液学改变

目的测定非创伤性股骨头坏死(nontraumaticosteonecrosisoffemoralhead,NONFH)患者的血液学指标变化,筛选敏感分子标记物用于早期诊断和筛选高危人群。方法研究对象共分三组:(1)NONFH早期组(塌陷前期)30例,(2)NONFH晚期组(塌陷后期)30例,(3)正常对照组30例。各组对象均抽取空腹肘静脉血。应用酶联免疫吸附法(ELISA)测定血小板α-颗粒膜蛋白(GMP-140)、血浆蛋白C(PC)、D-二聚体(D-Dimer)含量;发色底物法测定血浆纤溶酶原激活剂抑制剂(PAI)活性。结果(1)NONFH早、晚期组血小板GMP-140含量均高于正常对照组,血浆PC含量均低于正常对照组,D-Dimer含量均高于正常对照组,PAI活性均高于正常对照组(P均<0.05)。骨坏死情况越严重,各项指标上升或降低的趋势越明显,而且各项指标早、晚期组间比较差异均有显著性(P均<0.05)。(2)经判别分析,筛选出PAI、D-Dimer、PC三个指标,建立NONFH早期、晚期和正常对照三类判别函数式。NONFH早期:Y1=?26.3966 41.4916X10 0.0512X4 4.1390X1;NONFH晚期:Y2=?66.7566 82.1315X10 0.1082X4 2.7233X1;正常对照组:Y3=?26.7049 20.5695X10 0.0327X4 6.1900X1。回代判对率97.78%。结论(1)NONFH患者各期均存在高凝和低纤溶状态。(2)PAI、D-Dimer、PC为NONFH患者的血液学敏感指标。     

Chronic lithium treatment increases the phosphorylation of a 64-kDa protein in rat brains

Despite the wide clinical use of lithium in the treatment of manic depressive illness there is no adequate explanation for its mechanism of action. In the light of lithium's suggestive effects on the second messenger system in the brain, we studied the effects of chronic dietary lithium treatment (achieving blood levels in the therapeutic range) on protein phosphorylation in different areas of rat brain. An increase in the phosphorylation of a 64-kDa membrane-associated protein was evident in the lithium-treated rats compared to controls. This increase was observed only under basal phosphorylating conditions and was abolished when the phosphorylation was performed in the presence of Ca²⁺ or Ca²⁺ and calmodulin. The possibility that this 64-kDa protein affected by lithium is the beta-subunit of the calmodulin-dependent protein kinase or a different protein which co-migrates with it is discussed.     

Ethanol-Induced Enhancement of Cocaine Bioactivation and Irreversible Protein Binding: Evidence Against a Role of Cytochrome P-450IIE1

Chronic ethanol consumption potentiates cocaine-induced liver injury in rodents. Since cocaine has to be bioactivated by a cytochrome P-450-dependent N-oxidative pathway to exert its hepatotoxic effects, we studied the role of the ethanol-inducible P-450IIE1 for cocaine metabolism. Male Sprague-Dawley rats were pretreated with either a liquid diet containing ethanol (30% of calories) for 4 weeks or injected with pyrazole (200 mg/kg/day, ip, for 3 days). Both agents induced microsomal p-nitrophenol hydroxylation which is a probe for the catalytic activity of P-450IIE1. However, only ethanol, but not pyrazole, increased both microsomal cocaine N-demethylase activity (by 47%) and the extent of irreversible binding of [3H]-cocaine to microsomal proteins (by 100%), which was taken as a quantitative endpoint for the formation of a reactive metabolite. Cocaine N-demethylation and irreversible protein binding of cocaine were not inhibited by P-450IIE1 isozyme-selective substrates, nor was the rate of cocaine metabolism and binding decreased by functionally active polyclonal anti-rat P-450IIE1 antibodies. Furthermore, pyrazole pretreatment sensitized cultured hepatocytes to the glutathione-dependent cytotoxic effects of nontoxic concentrations of cocaine. These results indicate that (a) cocaine is not a major substrate for the ethanol-inducible P-450IIE1, (b) the enhancing effects of ethanol on cocaine bioactivation may be due to induction of other P-450 isoforms, and (c) induction of P-450IIE1 may potentiate cocaine-induced hepatocellular toxicity in vitro independently of cocaine metabolism, e.g., by P-450IIE1-dependent oxidative stress.     

蛋白芯片检测系统(多肿瘤标志物C12系统)的应用评价

目的：应用并评价蛋白芯片检测系统(多肿瘤标志物C12)的临床价值。方法：应用雅培电化学发光系统(ECL)和C12系统双盲法检测41份血清标本。结果：在对照检测达10份标本的AFP、CEA、β-HCG三个项目，C12系统和ECL系统符合性达81．8％以上；C12系统多个指标间可相互支持其准确性，并有助于判断肿瘤来源。结论：C12系统具有较高准确性，其指标间可相互支持，并有助于判断肿瘤源性。