间断静脉滴注3%高渗盐水与20%甘露醇治疗小儿急性脑水肿的疗效对比

Objective To compare the clinical efficacy of 3% hypertonic saline with 20% mannitol in the treatment of acute brain edema in children.Methods Twenty children with acute brain edema were randomly divided into hypertonic saline(HS) group and mannitol group.HS group and mannitol group were given 3% HS solution or 20% mannitol respectively.Main outcome measurements included intracranial pressure(ICP),mean arterial pressure(MAP),central venous pressure(CVP),cerebral perfusion pressure (CPP),serum electrolytes,plasma osmolality,renal function and urine volume.Results Both 3% HS and 20% mannitol were effective in reducing ICP(P ＜0.05).Therapeutic effect lasted(4.5±1.2) h in HS group and(3.2±1.5) h in mannitoi group.3% HS had a longer duration of action than marmitol(P＜0.05).At the time point of 2 hours after treatment,MAP and CPP of HS group increased more than those of mannitol group(P＜0.05).Conclusion Both 3% HS and 20% mannitol could rapidly decrease ICP.3% HS has a longer duration of action in reducing ICP than 20% mannitol.3% HS is more effective in stabilizing circulation and improving CPP than 20% mannitol.     

腹水浓缩回输腹腔治疗顽固性腹水23例报告

目的：评价腹水浓缩回输腹腔治疗顽固性腹水的疗效。方法：23例顽固性腹水患者，在原治疗基础上加用腹水浓缩回输治疗，观察腹水浓缩回输前后体重、腹围、尿量、血浆总蛋白、白蛋白、血中电解质的变化。结果：治疗后所有患者体重下降，腹围减少，尿量增加（P＜0．01）；血浆总蛋白、白蛋白均升高（P＜0．05）；而血中电解质治疗前后无显著变化（P＞0．05）。结论：腹水浓缩回输腹腔对治疗顽固性腹水有良好的效果。     

利多卡因对免蛛网膜下腔出血后脑血管痉挛的防治

目的：研究枕大池注入利多卡因是否能缓解蛛网膜下腔出血后脑血管的痉挛。方法：30只新西兰大白兔随机分为假手术组、蛛网膜下腔出血组出血组、利多卡因治疗组（治疗组），每组10只。出血组和治疗组的动物于枕大池注入自体动脉血1．5ml，假手术组注入1．5ml生理盐水，30min后假手术组和出血组的动物从枕大池注入0．1ml生理盐水，治疗组注入0．1 ml 2％利多卡因。72h后观察脑基底动脉管腔面积，另测定术前和72h后血浆中的内皮素（ET）和降钙基因相关肽（CGRP）。结果：各组术前的血浆ET，CGRP无显著差别（P〉0．05）；术后72h出血组的血浆ET高于假手术组和治疗组（P〈0．05），各组术后血浆ET比术前高（P〈0．01或P〈0．001）；术后72h血浆CGRP没有统计学差别（P〉0．05），与术前比较，假手术组和出血组的术后CGRP低于术前水平（P〈0．01或P〈0．001）；出血组的血管腔面积低于假手术组和治疗组（P〈0．001）。结论：枕大池注入利多卡因能减轻兔蛛网膜下腔出血后脑血管痉挛。     

基于IP的医院信息系统存储策略

分析了医院存储系统特点，在比较现有各种存储技术的基础上，提出了基于IP的网络存储策略。     

环孢素A固体分散体的制备及体外研究

 目的利用固体分散技术改善环孢素A(CsA)的溶解性能,提高其体外溶出速率。方法以Poloxamer188为载体,溶剂熔融法制备不同比例组成的环孢素A固体分散体,考察体外溶出速率及不同转速和不同溶出介质对溶出的影响,并配合X-射线粉末衍射分析药物在载体中的存在状态。对溶出度结果用Weibull分布模型进行拟合,计算体外溶出主要参数t_d和t₅₀,并进行方差分析。结果CsA在药物-载体比例为1:4或1:6的固体分散体中呈非晶态。固体分散体的溶出速率与相应物理混合物及原料药间存在极显著差异(P<0.01),溶出介质对药物溶出无显著性影响(P>0.05)。结论制成固体分散体能显著提高CsA的溶出速率。     

云母对鼠慢性萎缩性胃炎细胞增殖作用研究

 目的探讨云母对慢性萎缩性胃炎(CAG)的细胞增殖作用和逆转机制。方法CAG模型大鼠分别用3种剂量云母和生理盐水灌胃给药4周。观察大鼠胃黏膜病理组织变化。采用放免法测定大鼠血清表皮生长因子(EGF)水平,免疫组化方法检测黏膜细胞增殖核抗原(PCNA)、表皮生长因子受体(EGFR)和C-erbB-2基因蛋白的表达。结果云母组大鼠胃窦黏膜的炎症指数明显下降(P<0.05),黏膜腺体厚度和腺体数目显著增加(P<0.01)。云母组胃黏膜氨基已糖水平较模型组显著升高(P <0.01)。云母组胃窦黏膜PCNA阳性表达高度为(117.29±11.91)μm,较模型组大鼠(57.14±6.57)μm显著增加(P<0.01);云母组大鼠的血清EGF水平较模型组大鼠显著增高(P<0.01)。模型组、云母组和正常大鼠EGFR阳性表达率分别为45.5%, 62.5%和0%(P<0.05),C-erbB-2阳性表达率分别为72.7%,12.5%和0%(P<0.05)。结论云母促进胃黏膜细胞良性增殖,可以逆转萎缩改变。     

GBE1基因突变型糖原累积病Ⅳ型1例报告

目的探讨GBE1基因突变的糖原累积病Ⅳ型(GSD Ⅳ)患儿的临床特点及其家系的基因突变情况。方法分析1例GSD Ⅳ患儿的临床表现、肝脏病理结果及其父母的全外显子基因测序情况,并进行文献复习。结果患儿,男,1岁10个月,肝脾肿大6月余伴发热7天;肝脏组织病理示慢性肝损伤,不能除外遗传代谢病。全基因外显子检测示患儿存在2种新的GBE1基因的杂合突变,分别为来自父亲的c.1694GA杂合突变(致病性变异)和来自母亲的c.218AG杂合突变(疑似致病性变异)。结合患儿临床表现、病理及基因检测结果确诊为肝型GSD Ⅳ。结论新发现GEB 1基因c. 1694 GA的致病性杂合突变,丰富了GSD Ⅳ型在中国人群的突变谱。     

6p22.3 amplification as a biomarker and potential therapeutic target of advanced stage bladder cancer

Genetic and epigenetic alterations have been identified as to contribute directly or indirectly to the generation of transitional cell carcinoma of the urinary bladder (TCC-UB). In a comparative fashion much less is known about copy number alterations in TCC-UB, but it appears that amplification of chromosome 6p22 is one of the most frequent changes. Using fluorescence in situ hybridization (FISH) analyses, we evaluated chromosomal 6p22 amplification in a large cohort of bladder cancer patients with complete surgical staging and outcome data. We have also used shRNA knockdown candidate oncogenes in the cell based study. We found that amplification of chromosome 6p22.3 is significantly associated with the muscle-invasive transitional cell carcinoma of the urinary bladder (TCC-UB) (22%) in contrast to superficial TCC-UB (9%) (p=7.2-04). The rate of 6p22.3 amplification in pN>1 patients (32%) is more than twice that in pN0 (16%) patients (p=0.05). Interestingly, we found that 6p22.3 amplification is as twice as high (p=0.0201) in African American (AA) than European American (EA) TCC-UB patients. Moreover, we showed that the expression of some candidate genes (E2F3, CDKAL1 and Sox4) in the 6p22.3 region is highly correlated with the chromosomal amplification. In particular, knockdown of E2F3 inhibits cell proliferation in a 6p22.3-dependent manner, whereas knockdown of CDKAL1 and Sox4 has no effect on cell proliferation. Using gene expression profiling, we further identified some common as well as distinctive subset targets of the E2F3 family members. In summary, our data indicate that E2F3 is a key regulator of cell proliferation in a subset of bladder cancer and the 6p22.3 amplicon is a biomarker of aggressive phenotype in this tumor type.