血浆纤维连接蛋白含量对肺性脑病预后判断的临床价值

采用火箭电泳法对６４例（８０例次）肺性病患者进行血浆纤维连接蛋白（Ｆｎ）测定。合并肺性脑病１９例，并与１０６例健康人及１０４例其他呼吸疾患进行对比．结果表明：正常组、肺性病缓解组、急性发作组、肺性脑病组血浆Ｆｎ水平分别为３４．２７±６．３６ｍｇ／ｄｌ，２９．６１±４．２５ｍｓ／ｄｌ，１５．２１±５．２０ｍｇ／ｄｌ，１１．８２±５．６７ｍｇ／ｄｌ．肺性脑病患者血浆Ｆｎ显著降低，并随病情恶化而进一步下降。同时，其含量变化与ｐＨ值和ＰａＯ２呈正相关，与ＰａＣＯ２，呈负相关。因此动态观察肺性脑病患者血浆Ｆｎ含量可作为判断顶后一项较为可靠的指标。     

Carbonic anhydrase gene expression in CA II-deficient (Car2−/−) and CA IX-deficient (Car9−/−) mice

Using real-time PCR and immunohistochemistry, we have examined the expression of carbonic anhydrase isozymes (CA) I, II, III, IV, IX, XII, XIII and XIV in the brain, kidney, stomach and colon of the wild-type, CA II-deficient ( Car2^−/− ), and CA IX deficient ( Car9^−/− ) mice. The expression of Car4, Car12, Car13 and Car14 mRNAs did not show any significant deviations between the three groups of mice, whereas both groups of CA deficient mice showed decreased expression levels of Car1 in the colon and Car3 in the kidney. The Car2 mRNA level was greatly reduced but not completely abolished in all four tissues from the Car2^−/− mice in which no CA II protein was expressed. Sequencing the Car2 cDNA isolated from C57BL6 Car2^−/− mice revealed two nucleotide differences from the wild-type C57BL6 mice. One is a silent polymorphism found in Car2 mRNA from wild-type DBA mice, which is the strain that provided the original mutagenized chromosome. The second change is a mutation that causes prematurely terminated translation at codon 155 (Gln155X). Car9 mRNA and CA IX protein expression levels were up-regulated about 2.5- and 3.6-fold, respectively, in the stomach of the Car2^−/− mice. These results suggest that the loss of function of cytosolic CA II in the stomach of Car2^−/− mice leads to up-regulation of an extracellular CA, namely CA IX, which is expressed on the cell surface of the gastric epithelium.     

磁共振血管成像在布—加综合征诊断中的价值

目的：就磁共振血管成像（ＭＲＡ）对布—加综合征（Ｂｕｄｄ－Ｃｈｉａｒｉｓｙｎｄｒｏｍｅ）的诊断价值进行初步观察。方法：１０例患者,先行中上腹常规ＭＲＩ扫描再行肝静脉、下腔静脉ＭＲＡ检查。结果：常规ＭＲＩ发现１例存在两支肝静脉同时狭窄,３例肝段下腔静脉处狭窄,其中１例下腔静脉肝段及以下广泛血栓形成。ＭＲＡ显示６例肝段下腔静脉狭窄,１例肝静脉狭窄、变细,３例肝段下腔静脉合并肝静脉狭窄、变细。其中３例发现下腔静脉内血栓形成。全部病例均显示门静脉、脾静脉增宽等门脉高压表现。结论：ＭＲＡ检查对诊断布—加综合征有重要价值。     

几种为Authorware制作的CAI课件节省磁盘空间的方法

文章结合实践介绍了在应用Authorware制作CAI课件时,通过采用对媒体素材的压缩、程序方面的压缩和文件发布及安装时的压缩等操作,使课件“减肥”,以达到节省磁盘空间的几种措施和方法。     

尿激酶静脉溶栓治疗急性心肌梗死的临床观察

目的观察评价尿激酶静脉溶栓治疗急性心肌梗死临床疗效,分析用药时机、剂量对患者预后的影响。方法我院2009年4月至2013年8月应用尿激酶静脉溶栓治疗急性心肌梗死35例,行回顾性分析,统计对比不同溶栓时间患者再通率、死亡率、并发率、不良反应发生率。结果 <3 h溶栓者12例、3~6 h溶栓者15例、>6 h溶栓者8例;<3 h溶栓者与≥3 h溶栓者年龄、性别、合并症、梗死部位、吸烟、饮酒、高同型半胱胺酸血症、HCY水平差异无统计学意义(P>0.05);不同时间应用尿激酶溶栓再通率差异无统计学意义(P>0.05);溶栓再通20例,平均溶栓时间(1.9±1.5)h,低于溶栓失败15例(4.3±1.0)h,差异具有统计学意义(P<0.05);血管再通再灌注心率失常发生率与发生类型差异无统计学意义(P>0.05);死亡2例,死亡率5.71%,<3 h溶栓者、病发≥6 h溶栓者死亡率、肺水肿发生率、牙龈出血率差异无统计学意义(P>0.05);<3 h溶栓者、≥6 h溶栓者心源性休克发生率差异具有统计学意义(P<0.05)。结论<3h,应积极行尿激酶溶栓,有助于降低并发、死亡风险,发病3~6 h可以溶栓,大于6 h不应溶栓,可增加并发风险,收益小,风险高。     

Store–Operated Ca2+ Channels in Mesangial Cells Inhibit Matrix Protein Expression

Accumulation of extracellular matrix derived from glomerular mesangial cells is an early feature of diabetic nephropathy. Ca²⁺ signals mediated by store–operated Ca²⁺ channels regulate protein production in a variety of cell types. The aim of this study was to determine the effect of store–operated Ca²⁺ channels in mesangial cells on extracellular matrix protein expression. In cultured human mesangial cells, activation of store–operated Ca²⁺ channels by thapsigargin significantly decreased fibronectin protein expression and collagen IV mRNA expression in a dose-dependent manner. Conversely, inhibition of the channels by 2-aminoethyl diphenylborinate significantly increased the expression of fibronectin and collagen IV. Similarly, overexpression of stromal interacting molecule 1 reduced, but knockdown of calcium release–activated calcium channel protein 1 (Orai1) increased fibronectin protein expression. Furthermore, 2-aminoethyl diphenylborinate significantly augmented angiotensin II–induced fibronectin protein expression, whereas thapsigargin abrogated high glucose– and TGF-β1–stimulated matrix protein expression. In vivo knockdown of Orai1 in mesangial cells of mice using a targeted nanoparticle siRNA delivery system resulted in increased expression of glomerular fibronectin and collagen IV, and mice showed significant mesangial expansion compared with controls. Similarly, in vivo knockdown of stromal interacting molecule 1 in mesangial cells by recombinant adeno–associated virus–encoded shRNA markedly increased collagen IV protein expression in renal cortex and caused mesangial expansion in rats. These results suggest that store–operated Ca²⁺ channels in mesangial cells negatively regulate extracellular matrix protein expression in the kidney, which may serve as an endogenous renoprotective mechanism in diabetes.     

地塞米松对护骨素基因敲除小鼠骨微结构的影响

目的探讨小剂量地塞米松对生长期小鼠骨密度及骨微结构的影响及其与OPG途径的关系。方法 20只4周龄OPG~(-/-)雌性小鼠及20只野生型小鼠随机分四组(n=10):野生型安慰剂组(WT+saline),野生型地塞米松干预组(WT+DEX,地塞米松1mg/kg体重,肌肉注射,每周3次),OPG~(-/-)敲除小鼠安慰剂组(OPG~(-/-)+saline),OPG~(-/-)敲除小鼠DEX干预组(OPG~(-/-)+DEX,地塞米松1 mg/kg体重,肌肉注射,每周3次)。6周后处死小鼠,一侧胫骨行显微CT扫描分析。结果OPG~(-/-)组的组织骨密度、骨小梁体积分数、骨小梁数量、骨小梁厚度均较其他三组降低(P0.05)。OPG~(-/-)+DEX组的组织骨密度、骨小梁体积分数、骨小梁数量、骨小梁厚度均较WT及WT+DEX组降低(P0.05)。OPG~(-/-)组的骨小梁模型因子及骨小梁分离度均较其他三组增加(P0.05);OPG~(-/-)+DEX组的骨小梁模型因子及骨小梁分离度均较WT及WT+DEX组增加(P0.05)。WT及WT+DEX组之间骨小梁微结构参数均无统计学差异。结论在生长期小鼠OPG基因功能缺失时,地塞米松有部分拮抗骨量丢失的作用,表明除了OPG/RANKL途径,地塞米松对骨代谢的影响是多途径的。     

闽南地区部分脆性髋部骨折的发病特点及治疗现状

目的通过回顾分析闽南地区到我院骨科住院治疗的脆性髋部骨折患者的发病特点以及治疗的现状,为本地区老年人脆性髋部骨折的预防和治疗提供依据。方法采用回顾性研究方法,收集我院2010~2012年骨科收治的年龄大于50岁的脆性髋部骨折患者的病历资料及部分获得随访的患者的随访资料,采集患者个人特征(性别与年龄)、受伤的年份与季节、骨折类型、治疗方式、抗骨质疏松方案、随访1年的死亡率,并进行统计分析整理。结果 3年间我院收治年龄大于50岁的脆性髋部骨折患者560例,发病有地区性特点,各年份病例数基本持平(2010年190例,2011年184例,2012年186例),各年份构成比差异无统计学意义(P0.05);女性患者(373例)明显多于男性(187例),男女比例为1∶2,男女构成比差异有显著的统计学意义(P0.05);股骨颈骨折(316例)多于股骨转子间骨折(244例);平均年龄高达77.19±10.38岁,各年龄段构成比差异有显著的统计学意义(P0.05);发病例数以春季(149例)、冬季(145例)为多,冬春季与夏秋季间的构成比差异有统计学意义(P0.05);采用手术治疗比例89.11%(499/560);住院期间有进行骨密度检查的患者80例,住院期间有抗骨质疏松治疗的患者比例63.93%(358/560),获得随访的患者出院后继续抗骨质疏松治疗的比例仅20.63%(59/286);随访超过1年的231例患者中,手术组1年死亡率(6.57%)明显低于非手术组(72.73%),差异有显著性统计学意义(P0.05)。结论闽南地区脆性髋部骨折发病有其地区特点,尤其在年龄、性别、发病部位、发病季节、治疗方法有一定分布规律,目前抗骨质疏松治疗重视程度仍然不够,应加强宣传,深入开展防治策略研究来预防骨折的发生。     

双膦酸盐治疗骨质疏松症时每日补充维生素D 800~1200 IU是否足够？

目的观察双膦酸盐治疗时每日补充800~1200 IU维生素D是否可以获得理想的25羟维生素D(25OHD)水平。方法将112例骨质疏松症女性患者根据补充维生素D的剂量分为800 IU组和1200 IU组,在双膦酸盐治疗前和16周时检测血清25OHD,比较治疗前后25OHD的变化和获得理想25OHD水平的患者例数。结果 112例患者治疗前25OHD 24.26±7.98 ng/ml,治疗16周时25OHD 32.04±8.12 ng/ml。补充维生素D 800 IU组治疗后25OHD提高5.08±8.35 ng/ml,25OHD≥30 ng/ml患者为55.56%,25OHD≥33 ng/ml为38.89%;补充维生素D 1200 IU组治疗后25OHD提高10.29±8.20 ng/ml,25OHD≥30 ng/ml患者为60.34%,25OHD≥33 ng/ml为46.55%。结论双膦酸盐治疗时每日补充维生素D800~1200 IU可以显著提高25OHD水平,但仍然约有50%的患者不能达到理想的血清25OHD水平。