手足口病的预防控制及护理对策

从手足口病概述,流行概况,预防措施、护理对策及健康教育等方面综述了近年来手足口病的流行及护理进展,并阐述了手足口病的预防及健康教育措施.     

五白散胶囊治疗慢性消化道溃疡出血15例观察

目的:观察五白散胶囊治疗慢性消化道出血的疗效.方法:治疗组15例用五白散胶囊治疗,对照组15例用维霉素、果胶铋、止血敏治疗.结果:治疗组总有效率100%,对照组总有效率86.6%,两组比较有显著性差异(P<0.05).结论:五白散胶囊治疗消化道溃疡出血止血功效良好.     

全腹膜外补片植入术中补片不固定的实验研究

目的评价全腹膜外补片植入术中补片不固定的安全性和有效性。方法将50只SD大鼠建立疝缺损(3cm2)模型,按随机数字表分为2组,使用聚丙烯补片(12 cm2)采用腹膜外补片植入术进行修复。甲组为补片固定组,乙组为补片不固定组。大鼠于术后不同时间分批处死,记录补片的挛缩度、腹壁抗张强度以及组织细胞学变化。结果所有大鼠术后腹腔均无粘连。2组大鼠在术后7 d、14 d、30 d、60 d和90 d补片的挛缩度分别为6.7%±1.3%vs 7.3%±1.5%、12.3%±1.3%vs 12.4%±1.6%、14.0%±2.0%vs 14.5%±1.3%、17.4%±2.1%vs 18.4%±1.5%和18.9%±2.2%vs19.5%±2.6%(P>0.05);2组大鼠的腹壁抗张强度分别为(288.4±8.4)mm Hg vs(286.6±10.2)mm Hg、(300.4±11.2)mm Hg vs(298.8±11.4)mm Hg、(305.0±11.7)mm Hg vs(303.3±16.1)mm Hg、(309.0±10.8)mm Hg vs(307.6±8.9)mm Hg和(311.8±9.8)mm Hg vs(310.0±8.6)mm Hg(P>0.05);2组大鼠的组织细胞学变化一致。结论当补片面积是大鼠疝缺损的4倍以上时,不固定的腹膜外补片植入术是安全有效的。     

宫腔镜在辅助生殖技术中的应用

目的：探讨宫腔镜检查术在辅助生殖技术中应用的重要性。方法：对150例拟行辅助生殖技术的不育妇女行常规宫腔镜检查。结果：宫腔镜150例中47例（31％）有镜下异常，其中：子宫内膜息肉或息肉样增生18例（12％），子宫内膜单纯性增生17例（11％），子宫畸形7例（5％），宫腔粘连狭窄3例（2％），子宫内膜结核1例（0．7％），子宫黏膜下肌瘤或腺肌瘤1例（0．7％）。以宫腔镜诊断为标准，阴道超声诊断敏感性、特异性、阳性预测值、阴性预测值、准确率分别为66％（31／47）、98％（101／103）、94％（31／33）、86％（101／117）、88％（132／150），子宫造影分别为26％（12／47）、100％（95／95）、100％（12／12）、73％（95／130）、75％（107／142）。结论：宫腔镜检查术具有良好的可接受性和准确性，应作为辅助生殖技术前的常规检查。     

泌尿系肿瘤基础研究的热点及中国在研究中存在的问题

随着高新技术的发展和人们对生物医学认识的不断提高和更新，近年来医学基础研究呈现出飞跃式发展。人们利用不断发展开发的新技术，对人类各种疾病的发生发展进行了深入的研究和探讨。以下就泌尿系肿瘤基础研究的热点及我国存在的问题做一简要介绍。     

PRO 1000 V3型心电监护仪LCD逆变器的升级及注意事项

介绍了该型心电监护仪黑屏故障的常见原因，对升级前后的LCD逆变器电路作了对比分析，并详细介绍了升级更换的方法和注意事项。     

大脑中动脉支架内血栓形成1例报告

支架内血栓形成是支架置入术后的一种常见并发症。术后血管内皮损伤、胶原组织暴露和作为异物的支架均为引发血栓形成的可能机制。不能及时识别处理则成为再狭窄的重要原因。我们报告1例发生在大脑中动脉（middle cerebral artery，MCA）支架内的血栓形成，探讨其识别处理过程和可能的机制。     

Elevated hepatic SULT1E1 activity in mouse models of cystic fibrosis alters the regulation of estrogen responsive proteins.

BACKGROUND: Previous studies with cystic fibrosis transmembrane conductance regulator (CFTR) DeltaF508 mice indicate that estrogen levels may play a role in the occurrence or severity of CF-associated liver disease. However, the underlying mechanisms of liver disease in CF are poorly understood. METHODS: The levels of SULT1E1 (estrogen sulfotransferase) were measured in livers of control and CFTR-knockout (KO) mice. The impact of increased SULT1E1 activity on hepatic protein expression was assessed by immunoblot and MALDI mass spectrometric analysis. RESULTS: SULT1E1 expression was significantly elevated in livers of several CFTR-KO mice. SULT1E1 and CFTR were specifically detected in hepatocytes and cholangiocytes, respectively. Elevated SULT1E1 activity may result in lower levels of free beta-estradiol thereby altering estrogen-responsive hepatic protein expression. Estrogen receptors (ER)-alpha and beta were differentially regulated in CFTR-KO and CFTR-DeltaF508 mice. ERalpha expression was reduced in mice with high SULT1E1 activity. Glutathione S-transferase-P1 and carbonic anhydrase III were significantly decreased in CFTR (-/-) mice with high SULT1E1 activity. Furthermore, cytochrome P450 2B9, also estrogen regulated, was significantly induced in the livers of CFTR (-/-) mice with high SULT1E1 activity. CONCLUSIONS: Elevated SULT1E1 levels and associated alterations in estrogen-regulated hepatic protein expression may play an important role in CF liver disease.     

Histamine and tryptase modulate asthmatic airway smooth muscle GM-CSF and RANTES release.

Degranulating mast cells are increased in the airway smooth muscle (ASM) of asthmatics, where they may influence ASM function. The aim of the present study was to determine whether histamine and tryptase modulate ASM cell granulocyte-macrophage colony-stimulating factor (GM-CSF) and RANTES (regulated on activation, normal T-cell expressed and secreted) release and also to examine which receptors are involved in this release. Confluent, quiescent ASM cells from asthmatic and nonasthmatic donors were treated with histamine (1 microM-100 microM) with and without histamine receptor antagonist pre-treatment, or the protease-activated receptor (PAR)-2 agonists tryptase (0.5-5 nM) and SLIGKV (100 and 400 microM). The cells were then stimulated with interleukin (IL)-1beta and/or tumour necrosis factor (TNF)-alpha (10 ng.mL(-1)) or left unstimulated for 24 h. Release of GM-CSF and RANTES was determined by ELISA and prostaglandin (PG)E(2) measured by enzyme immunoassay. Neither histamine nor tryptase induced ASM GM-CSF or RANTES secretion. However, histamine increased IL-1beta-induced GM-CSF release and markedly reduced TNF-alpha-induced RANTES release by both asthmatic and nonasthmatic cells to a similar extent, but did not modulate PGE(2) release. All changes involved activation of the histamine H1 receptor as they were partially or fully blocked by chlorpheniramine, but not ranitidine. Tryptase, via its proteolytic activity, also potentiated GM-CSF, but not RANTES, release from asthmatic and nonasthmatic ASM cells induced by both cytokines. PAR-2 involvement in the tryptase potentiation was unlikely because SLIGKV had no effect. In conclusion, mast cells, through histamine and tryptase, may locally modulate airway smooth muscle-induced inflammation in asthma.