乌司他丁在预防不同胃肠术后吻合口瘘中的效果观察

目的探讨乌司他丁在预防不同胃肠术后吻合口瘘中的效果。方法选取2005年6月～2011年8月于本院进行胃肠术进行治疗的220例患者为研究对象,将其随机分为对照组和观察组各110例,观察组在对照组的基础上加用乌司他丁,后将两组患者中不同术式的吻合口瘘发生率及术前、术后1 d及3 d的血清超敏C反应蛋白（hs-CRP）、白介素2（IL-2）、白介素6（IL-6）、肿瘤坏死因子α（TNF-α）、血液流变学指标进行统计及比较。结果观察组不同术式的吻合口瘘发生率及总发生率均低于对照组,血清hs-CRP、IL-6、TNF-α水平低于对照组,IL-2高于对照组,血液流变学指标改变幅度小于对照组,差异均有统计学意义（均P〈0.05）。结论乌司他丁可以改善胃肠手术患者的炎性状态及血液循环情况,对于降低吻合口瘘的发生率有着积极的作用。     

Diagnostic Splenectomy for Visceral Leishmaniasis

A 57-year-old-man with a history of malaise, fever,night sweats and shortness of breath presented a diagnostic challenge to his medical team. He was pancytopaenic and had splenomegaly on admission but other investigations, including bone marrow aspiration, proved inconclusive. After the patient deteriorated clinically, the general surgical team was requested to perform a diagnostic splenectomy. The histology of this showed infection with visceral leishmaniasis. He recovered completely with Amphotericin treatment. Although this is a rare condition, particularly for the general surgeon, this case highlights the difficult position surgeons are often put in when performing major surgery diagnostically.     

多聚（ADP-核糖）聚合酶抑制剂对大鼠缺血再灌注肾脏损伤的保护作用

目的探讨多聚（ADP-核糖）聚合酶（PARP）抑制剂3-氨基苯甲酰胺（3-AB）在大鼠-肾脏缺血再灌注损伤中的保护作用及对肾组织血管内皮生长因子A（VEGF-A）和中性粒细胞明胶酶相关脂质运载蛋白（NGAL）mRNA表达的影响。方法将54只大鼠随机分为假手术组（S组）、再灌注后模型组（M组）和PARP抑制剂组（P组）,每组8只。比较各组大鼠右侧肾动脉缺血再灌注后2、6、12h后的血肌酐和尿素氮水平、肾脏组织病理学变化、肾组织PARP蛋白表达及肾组织VEGF-A和NGAI．mRNA表达。结果（1）M组各时间点的血肌酐、尿素氮水平均高于S组,P组各时间点血肌酐、尿素氮明显低于M组,差异均有统计学意义（P〈0．01）;（2）P组肾组织病理学表现较M组改善;（3）P组各时间点肾组织PARP表达明显低于M组,差异有统计学意义（P〈0．05）;（4）与M组相比,P组肾组织的VEGF-AmRNA的表达升高,NGALmRNA表达降低,有统计学差异（P〈0．05）。结论PARP抑制剂3AB对大鼠肾脏缺血再灌注损伤具有保护作用,可下调NGAL及上调VEGF-AmRNA表达。     

A novel class of amino-alkylcyclohexanes as uncompetitive,fast, voltage-dependent,N-methyl-D-aspartate (NMDA) receptor antagonists – <Emphasis Type="Italic">in vitro</Emphasis> characterization

The fact that potent NMDA receptor channel blockers produce phencyclidine-like psychotropic symptoms in man and rodents implies that uncompetitive antagonism of NMDA receptors may not be a promising therapeutic approach. However, recent data indicate that agents with moderate affinity such as memantine and neramexane (MRZ 2/579) are useful therapeutics due to their strong voltage-dependency and rapid unblocking kinetics. Merz has developed a series of novel uncompetitive NMDA receptor antagonists based on an amino-alkylcyclohexane structure. These compounds displaced [(3)H]-MK-801 binding to rat cortical membranes with K(i) values between 1 and 100 microM and inward current responses of cultured hippocampal neurons to NMDA were antagonized in a strongly voltage-dependent manner with rapid blocking/unblocking kinetics. Three of these compounds, with similar biophysical properties to memantine, were chosen for development. MRZ 2/759 (1-ethenyl-3,3,5,5-tetramethyl-cyclohexylamine), 2/1010 (1,3,3,5-tetramethyl-6-azabicyclo[3.2.1]octane) and 2/1013 (8,8,10,10-tetramethyl-1-azaspiro[5.5] undecane) displaced [(3)H]-MK-801 binding with K(i) values of 1.18, 2.59 and 3.64 microM, respectively. They were similarly potent against NMDA-induced currents in hippocampal neurons - IC(50) values of 1.51, 3.06 and 2.20 microM, respectively. In line with their moderate affinity, all were voltage-dependent (delta = 0.86, 0.96 and 0.89, respectively) and fast, open-channel blockers (k(on) 7.90, 1.70 and 2.60 x 10(4) M(-1) sec(-1), k(off) 0.13, 0.12 and 0.24 sec(-1), respectively). These compounds are also NMDA receptor antagonists in the CNS following systemic administration and have good therapeutic indices in a variety of in vivo behavioural models where glutamate is known to play a pivotal role. In view of their relatively low affinity and associated rapid kinetics, they should prove to be useful therapeutics in a wide range of CNS disorders.     

预防和治疗抗生素相关性腹泻的药学体会

目的:促进抗生素相关性腹泻的有效预防和治疗。方法:选用临床实例对以益生菌酸奶、活菌制剂及益生元等多种微生态制剂预防和治疗抗生素相关性腹泻的结果进行分析和总结。结果:实例表明,有抗生素相关性腹泻危险因素的患者给予益生菌酸奶和益生元后,能有效预防抗生素相关性腹泻的发生;已发生抗生素相关性腹泻的患者,应用微生态制剂后取得显著疗效。结论:合理应用微生态制剂能预防和治疗抗生素相关性腹泻。     

大连市乙肝疫苗查漏补种情况调查

[目的]了解大连市乙肝疫苗漏种的情况及其影响因素。[方法]2006年10月至2007年5月开展了大连市2002年7月1日至2006年9月3013出生儿童的乙肝疫苗查漏补种工作,对于在补种过程中新发现的漏种儿童,按照“随时发现,随时补种”的原则进行补种。[结果]本次“查漏补种”工作共摸底调查263727名儿童,查出漏种儿童2017人,漏种率为0．76％,应补种针次4198针次;实补种1933人,补种率为95．84％。大连市乙肝疫苗近5年平均接种率为99．9％,漏种率较低;流动儿童较本地常住儿童漏种率高（P〈0.05）,补种率低（P〈0．05）。[结论]流动儿童中仍存在免疫空白现象。     

Phosphoinositide 3-kinase is involved in the induction of the human sperm acrosome reaction downstream of tyrosine phosphorylation

In somatic cells phosphoinositide 3-kinase (PI 3-kinase) is activated upon interaction with both receptor tyrosine kinases (RTK) and G- proteins resulting in the production of moieties involved in the inositol phospholipid signalling pathway. As G proteins, RTK and the inositol phospholipids have all been implicated in the human sperm acrosome reaction, experiments were carried out to determine whether PI 3-kinase was also involved in this phenomenon. Wortmannin is a selective inhibitor of PI 3-kinase and was shown to significantly inhibit the acrosome reaction induced by both mannose-bovine serum albumin (mannose-BSA) (10, 50 and 100 nM) and a polyclonal antibody raised against an extracellular region of the sperm zona receptor kinase (ZRK, at 100 nM only). Wortmannin did not inhibit the A23187- or progesterone-induced acrosome reaction. These results suggest that PI 3- kinase is involved in the human sperm acrosome reaction. The levels of tyrosine phosphorylation of sperm proteins as detected by Western blotting using antiphosphotyrosine antibodies was not affected by wortmannin in agonist (A23187 and mannose-BSA)-stimulated spermatozoa. This indicated that PI 3-kinase operates downstream of tyrosine phosphorylation in the signal transduction cascade which leads to the human sperm acrosome reaction.      

The binding of ouabain to normal and chronic lymphocytic leukemic lymphocytes

The binding of the cardiac glycoside, ouabain, to cells had been used to quantify the number of active cation pumps. In this study, lymphocytes were incubated with 3H-ouabain and the equilibrium binding analyzed for the maximal number of specific binding sites. Lymphocytes from normal peripheral blood bound 44,200 +/- 9920 molecules/cell, compared with 29,200 +/- 8370 molecules/cell for the lymphocytes of chronic lymphocytic leukemia (CLL) subjects. This difference was significant (p less than 0.01) and did not reflect a lower number of sites on B cells than T cells, since B-cell-enriched lymphocytes from normal peripheral blood showed the same ouabain binding characteristics as the standard T-cell-rich preparation. Although monocytes bind threefold more ouabain than lymphocytes, the small monocyte contamination (3.0%) in normal lymphocyte preparations could not account for the difference between normal and CLL. The fewer ouabain binding sites on CLL lymphocytes may reflect both their smaller size (by 10%) and lower mitotic activity compared with lymphocytes from normal peripheral blood.     

Inhibition of thromboxane formation in vivo and ex vivo: implications for therapy with platelet inhibitory drugs

The capacity of platelets to generate thromboxane A2, reflected by measurement of serum thromboxane B2 (TxB2), greatly exceeds the systemic production of thromboxane in vivo. Thus, it is possible that substantial but incomplete inhibition of thromboxane formation ex vivo would still allow marked augmentation of thromboxane production in vivo. To address this hypothesis, we administered aspirin 120 mg, a selective inhibitor of thromboxane synthase (TxSl), 3-(1H-imidazol-1-yl- methyl)-2-methyl-1H-indole-1-propanoic acid (UK-38, 485) 200 mg, and a combination of both drugs to 12 healthy volunteers and measured the effects on serum TxB2 and urinary 2,3-dinor-thromboxane B2 (Tx-M), an index of endogenous thromboxane biosynthesis. Although serum TxB2 was maximally inhibited by 94 +/- 1% after aspirin and 96 +/- 2% after the TxSl, maximal depression of Tx-M was only 28 +/- 8% and 37 +/- 9%, respectively. Combination of aspirin with the TxSl resulted in a small but significant increase in inhibition of thromboxane generation ex vivo (98 +/- 1% v 94 +/- 1%; P less than 0.05), but a disproportionately greater fall in thromboxane synthesis in vivo (58 +/- 7%; P less than 0.01). Consistent with further inhibition of platelet thromboxane synthesis, addition of the TxSl abolished the transient decline in prostacyclin formation after aspirin alone. Administration of a lower dose of aspirin (20 mg) to 6 healthy subjects caused a small reduction in Tx-M (12 +/- 4%; P less than 0.05) and inhibited serum TxB2 by 48 +/- 2%. The relationship between inhibition of platelet capacity to form thromboxane ex vivo (serum TxB2) and synthesis in vivo (Tx-M) departed markedly from the line of identity. When total blockade of the capacity of platelets to generate thromboxane is approached, minor decrements in capacity result in a disproportionate depression of actual thromboxane biosynthesis. These results imply that pharmacologic inhibition of serum TxB2 must be virtually complete before thromboxane- dependent platelet activation is influenced in vivo.