Effects of inhaled corticosteroids on growth in asthmatic children

This article presents a brief review of the effects of inhaled corticosteroids on growth in children with asthma. All currently available inhaled corticosteroids, where there is adequate data, have been shown to cause significant growth suppression in children in a dose-dependent manner. It is now apparent that there are differences in the growthsuppressive effects of different corticosteroids. Recent evidence confirms that the growth-suppressive effects are short lived and that, at conventional doses, inhaled corticosteroids do not affect final attained adult height.     

Galectin-3 modulates ureteric bud branching in organ culture of the developing mouse kidney

Galectin-3 is a mammalian beta-galactoside-specific lectin with functions in cell growth, adhesion, and neoplastic transformation. On the basis of expression patterns in humans, it is proposed that galectin-3 modulates fetal collecting duct growth. This article provides evidence that galectin-3 can modulate branching morphogenesis of the mouse ureteric bud/collecting duct lineage. With the use of immunohistochemistry, galectin-3 was not detected in early metanephrogenesis but was upregulated later in fetal kidney maturation when the protein was prominent in basal domains of medullary collecting ducts. Addition of galectin-3 to embryonic days 11 and 12 whole metanephric cultures inhibited ureteric bud branching, whereas galectin-1 did not perturb morphogenesis, nor did a galectin-3 mutant lacking wild-type high-affinity binding to extended oligosaccharides. Exogenous galectin-3 retarded conversion of renal mesenchyme to nephrons in whole metanephric explants but did not affect nephron induction by spinal cord in isolated renal mesenchymes. Finally, addition of a blocking antiserum to galectin-3 caused dilation and distortion of developing epithelia in embryonic day 12 metanephroi cultured for 1 wk. The upregulation of galectin-3 protein during kidney maturation, predominantly at sites where it could mediate cell/matrix interactions, seems to modulate growth of the ureteric tree.     

Expression of a soluble complement inhibitor protects transgenic mice from antibody-induced acute renal failure

Crry is a potent complement regulator in rodents that inhibits C3 convertases. In rats, intrarenal arterial injection of anti-glomerular endothelial cell (GEN) antibodies leads to complement-dependent microvascular injury and acute renal failure. In this study, a mouse variant of this model and the effects of complement inhibition were examined. Transgenic mice that overexpressed soluble Crry systemically and in their kidneys were studied. Anti-GEN IgG was injected intravenously into eight Crry transgenic mice and seven transgene-negative littermates (which were used as control animals). Thirty h after injection, blood urea nitrogen (BUN) levels were 30.3 +/- 4.4 and 114.8 +/- 23.5 mg/dl for transgene-positive and -negative animals, respectively (P = 0.012). Four of five transgene-negative animals with BUN levels of > 100 mg/dl were anuric; the remaining animal exhibited minimal albuminuria and no detectable urinary C3. In animals with renal failure, glomerular capillary collapse and tubular necrosis were observed. There was significant tubular staining for C3 in transgene-negative animals, with cellular and basal distributions, both of which were statistically greater than those in transgene-positive animals. Tubular cell C3 staining was strongly correlated with BUN values (r = 0.83, P < 0.001), as was C9 staining (r = 0.56, P = 0.037), suggesting that complement activation to the C5b-9 membrane attack complex had a casual role in renal failure. Thus, systemic injection of anti-GEN antibodies into mice leads to acute renal failure, with glomerular and tubular injury. Animals that overexpress soluble Crry in renal tubules and elsewhere are protected from the acute renal failure that occurs in this model, which ultimately seems to develop because of complement activation focused on tubules.     

上海市南汇区广州管圆线虫病自然疫源地调查

目的了解上海市南汇区广州管圆线虫疫源地的分布及感染情况，为预防控制广州管圆线虫病提供科学依据。方法随机抽取南汇区新场镇作为调查点。在调查点野外、自由市场、餐饮场所对广州管圆线虫的中间宿主、转续宿主和保虫宿主感染情况进行调查。结果在调查点内发现广州管圆线虫中间宿主螺类1种（铜锈环棱螺）、蛞蝓1种（双线嗜黏液蛞蝓）和蜗牛1种（中华灰尖巴蜗牛），同时查到保虫宿主（鼠）和转续宿主（淡水鱼、河虾、青蛙、河蟹，蟾蜍）。经检测均无广州管圆线虫感染。结论南汇区目前尚无广州管圆线虫疫源地存在，但具备了该病流行的基本条件，是个潜在的疫源地，一旦有广州管圆线虫传入则可引起传播，故应加强健康教育、加强监测。     

健康教育对慢性病控制的效果观察

目的探索健康教育和行为干预降低高血压等慢性生活方式病患病率的效果途径。方法采用随机抽样方法,抽取参与健康体检的社区居民和单位干部职工,有针对性地开展健康教育。3年以后,再对这些人群体检时进行健康知识、健康行为测试,并对其慢性病患病情况进行对比分析。结果社区居民和单位干部职工6项健康知识知晓率分别提高了17.22%和7.34%;6项有益健康行为正确率分别提高了4.55%和3.38%;高血压等慢性病患病率分别下降了7.42%和12.49%。结论慢性病与人们的健康知识水平和行为习惯有密切关系,通过健康知识教育、干预不良生活习惯,可有效降低慢性病的患病率。     

医院建设中的网络综合布线系统

医院计算机网络建设中的综合布线系统是整个医院系统的物理层，是应用系统运行的高速路。合理、科学的规划网络布线可以使医院整个系统运行在稳定可靠、安全高效的健康网络环境中。     

盐酸多西环素调释胶囊生物等效性研究

目的：考察自制（受试）与进口（参比）盐酸多西环素调释胶囊两种制剂的药动学与人体生物等效性。方法：20名男性健康志愿者按交叉单剂量双周期试验设计，随机单剂量口服含100mg多西环素的两种制剂。以HPLC内标法测定各时间点的多西环素血药浓度，计算两种制剂的药动学参数和相对生物利用度，并评价其生物等效性。结果：受试和参比制剂的Cmax分别为（859．2±253．1）和（917．2±220．6）μg/L，tmax分别为（3．8±0．8）和（4．4±1．8）h，t1／2分别为（18．9±2．8）和（18．0±3．5）h，AUC0-72分别为（18．2±5．9）和（18．7±3．9）mg·h／L，AUC0-inf村分别为（18．7±5．9）和（19．2±3．9）mg·h／L，受试制剂的相对生物利用度为94．56％。结论：自制与进口盐酸多西环素调释胶囊生物等效。     

看病难和看病贵问题:基于医生角度的实证分析

从医生角度对上海市看病难和看病贵问题进行了实证分析.研究共调查了上海市包括三级、二级医院和社区卫生服务中心在内的14家医疗机构的1305名医生.调查结果显示了医生在对看病难看病贵问题及其成因上与患者和居民的认识上存在的一致及差异之处,并探讨了可能的原因.     

用两种不同方法检测血糖的对比分析

糖尿病是常见的代谢性疾病,血糖测定是评估糖尿病的重要指标之一。目前最常采用的有两种测定方法,即血清葡萄糖氧化酶法和血糖仪快速检测干化学法[1],在工作中发现两种方法检测结果存在一定的差异,给临床诊断和糖尿病患者带来一些困惑,为了解不同方法间的差异,随机选择宝鸡市中     

舒芬太尼复合异丙酚抑制气管插管应激反应的效果

【目的】比较靶控输注不同剂量舒芬太尼复合异丙酚抑制气管插管应激反应的效果。【方法】60例择期上腹部手术患者，ASAⅠ～Ⅱ级，随机分为3组m=20），全麻诱导时，A组、B组、C组分别靶控输注效应室浓度为0．3、0．5、0．7ng／mL的舒芬太尼2min后．均输注效应室靶浓度为4μg／mL的异丙酚，病人意识消失后给予维库溴铵行气管插管。记录全麻诱导前1min（T1）、气管插管后1min（T2）、3min（T3、10min（T4）各时点平均动脉压（MAP）、心率（HR）；并于T1、T2、T4时点采集桡动脉血，测定血浆肾上腺素（AD）和去甲肾上腺素（NA）浓度。【结果】（1）A组T2时点MAP、HR比T。时点明显升高（P〈0．0S），C组T2、T3、T4时点MAP明显低于A组（P〈0．05），C组T2、T3时点HR明显低于A组（P〈0．05），C组L、T4时点MAP低于B组（P〈0．05）；（2）A组T2时点血浆AD和NA浓度较T1时点明显升高（P〈0．05）、较B组高（P〈0．05）、较C组高（P〈0．05）。【结论】靶控输注舒芬太尼复合异丙酚可以有效抑制气管插管应激反应，其中舒芬太尼效应室浓度0．5ng／mL复合异丙酚效应室浓度4μg／mL靶控输注的效果较好。