双氯灭痛药膜体外透皮速率的实验研究

作者选择乙基纤维素、聚乙烯醇等高分子材料制成涂膜剂，用大鼠皮进行双氯灭痛药膜的体外透皮速率测定。结果表明，氮酮与丙二醇可以促进药物渗透。不同的高分子材料可影响药物的扩散与释放，从而影响其透皮速率。与无膜无促透剂处方相比，药物在乙基纤维素中的透皮速率没有增加，在聚乙烯醇膜中的透皮速率有显著增加。     

Inhaled natural human interferon alpha induces bronchospastic reactions in asthmatics.

There is a relationship between viral infection and aggravation of bronchial asthma symptoms. Viruses belong to the strongest and fast acting inducers of interferon (IFN), which, in turn, may enhance histamine release from effector cells. We have administered IFN intrabronchially to 49 patients suffering from bronchial asthma. The impairment of lung ventilation with significant decrease of forced expiratory volume in one second (FEV1) have been observed in majority of the patients who inhaled crude or purified IFN preparations.     

战士体内VitB_1、VitB_2储备水平检测

选择南方热区某特种部队战士５２人，分两组分别口服５ｍｇＶｉｔＢ１和ＶｉｔＢ２，收集４ｈ尿液，用荧光法进行负荷试验。结果：ＶｉｔＢ１组，所测２９人中，１５人缺乏，９人不足，２人正常，３人充裕；ＶｉｔＢ２组，所测２３人中，１１人缺乏，１２人不足，反映该部队全年约５％的发病是由于ＶｉｔＢ１、ＶｉｔＢ２缺乏不足所致。其原因为膳食摄入不够     

反相HPLC法同时测定饮料中的两种人造甜味剂

应用反相HPLC法，探讨了同一色谱条件下，食品中安赛蜜，糖精钠、咖啡因及苯甲酸的分离条件，并在此基础上建立了饮料中人造甜味剂安赛蜜、糖精钠的测定方法，取得了满意的结果。在反相C_(18)柱上，使用甲醇-冰乙酸-水（20+3.5+76.5）为流动相，可使安赛蜜、糖精钠、咖啡因，苯甲酸快速而良好地分离，254nm波长下检测，安赛蜜的线性范围为0.002～1.00g／L，最小检测量为0.04μg；糖精钠的线性范围为0.005～1.00g／L，最小检测量为0.08μg，在饮料分析中，外标单点校正法测得数据再用标准添加法处理进而求出的回收率分别为安赛蜜97.6％（n=5,CV=0.74%)、103.5%（n=5，CV=1.l%）、95.l%（n=5，CV=0.73%）；糖精钠97.9%（n=5，CV=0.66％）、99.9%（n=5，CV=0.73%)、102.1％（n=5，CV=0.18%）。本方法分析步骤简便，且检测波长适用于国产单波长检测器。     

Phenotypic heterogeneity associated with defective apolipoprotein B-100 and occurrence of the familial hypercholesterolemia phenotype in the absence of an LDL-receptor defect within a Canadian kindred

Of 163 individuals with a diagnosis of heterozygous familial hypercholesterolemia (FH), only one subject was found to be positive for familial defective apo B-100 (FDB). The eight-member kindred ascertained through this subject who presented with both a clinical phenotype of FH and the FDB apo B-100 (Arg₃₅₀₀→-Gln) mutation was studied. Plasma lipid and lipoprotein profiles, apo E phenotypes, apo B gene markers at the 3′ hypervariable region and LDL-receptor haplotypes (ApaLI, PvuII, NcoI), were determined, together with LDL-receptor activity on freshly isolated blood lymphocytes. The FDB mutation, present in four relatives, was associated with three different phenotypes: FH and severe hypercholesterolemia, moderate hypercholesterolemia and normolipidemia. The FH phenotype occurred in the absence of any functional LDL-receptor defect. In homozygotes for the absence of the PvuII cutting site who had the apo B mutation, LDL-cholesterol levels were low in the presence of the apo E3/2 phenotype and high in the presence of the apo E4/4 phenotype. None of the major known environmental influences accounted for the wide range of variation in LDL-cholesterol among the affected members. Further observations in the spouse and offspring of the normolipidemic FDB subject confirmed the association of apo E4, the FDB mutation and the PvuH(-/-) genotype with high cholesterol levels. It is concluded that the phenotypic expression of the FDB mutation may vary widely as a function of the genetic environment within a family. The presence of phenotypic heterogeneity among individuals with the same apo B mutation may result from epistatic interaction of the apo B locus with genetic factors regulating cholesterol homeostasis, including possible involvement of the apo E and the LDL-receptor gene loci. This study also confirms that the clinical diagnosis of FH is not necessarily associated with an LDL-receptor defect.     

用化学计量法研究CO2—n—C7H16系的高压相平衡

测定了在温度３１０．６５Ｋ、３２３．１５Ｋ和压力３．１３～７．５４ＭＰａ条件下的气液平衡数据，实验结果与文献值具有较好的一致性。用ＴＲＫ状态方程对实验所得数据进行关联，取得了较满意的结果。     

贲门失弛缓症术式探讨

目的 探讨治疗贲门失弛缓症的理想术式。方法 回顾分析66例贲门失弛缓症患者的治疗效果，评估手术方式与其疗效的关系。结果 单纯Heller肌层切开术15例，Heller手术附加Belsey MarkⅣ底折叠术17例，自行设计的改良Heller手术附加胃底折叠术34例。全组随访3年以上，失访3例按无效计算，疗效优，良者占91．2％（60／66）／单纯Heller手术病例术后复发3例（3／15，20．0％），发生反流性食管炎4例（4／15，26．7％）;Heller手术附加Belsey MarkⅣ底折叠发生反流性食管炎2例（2／17，11．8％），膈裂孔疝1例（1／17，5．9％），而改良Heller手术附加胃底折叠术无复发及反流。全组无手术死亡及其他并发症。结论 改良式Heller手术加胃底折叠术式治疗贲门失弛缓症疗效较好。     

微粒皮肤移植治疗特大面积烧伤：附7例报告

报告应用微粒皮肤移植技术抢救成功７例特大面积烧伤病人。文中介绍了手术方法、注意事项，指出了本术式的优缺点，并对该领域国内外的发展状况，作了简单叙述。     

缺指(趾)综合征

本文报告—缺指(趾)综合征之家族。在4代62人中手足畸形者20人,对3代7人拍照了双手足正位X线片,发现足部2-4跖趾均缺如,1、5跖趾呈现跖外翻,趾内曲。外形酷似龙虾爪样。手部1-3指大多数病人缺如。也有2、3指并指畸形或指骨分叉畸形。全身其他骨关节正常,智力发育良好。本文讨论了该病的命名、分类和有关鉴别诊断。     

Activated neutrophils aggravate endothelial dysfunction after reperfusion of the ischemic feline myocardium.

Endothelial dysfunction, as evidenced by decreased stimulated release of endothelium-derived relaxing factor (EDRF), occurs after reperfusion of the ischemic myocardium. To better understand this endothelial dysfunction, isolated cat hearts were perfused under constant flow by the Langendorff procedure with Krebs-Henseleit solution devoid of blood cells. Following global ischemia (90 minutes) and reperfusion (20 minutes), coronary vasorelaxation to the endothelium-dependent vasodilator acetylcholine (ACh) was 70 +/- 3% of initial values (p less than 0.01) compared with 90 +/- 4% in nonischemic control perfused hearts. No decrement occurred in response to the endothelium-independent vasodilator nitroglycerin (NTG). Coronary artery rings isolated from the ischemic left circumflex coronary artery showed a similar degree of endothelial dysfunction to ACh, with normal relaxation in response to NaNO2. Autologous cat neutrophils (100 million cells), activated with 100 nmol/L f-met-leu-phe infused into the heart directly before and throughout reperfusion, resulted in a further decrement in ACh-induced vasodilation, to 55 +/- 5% of initial response, with no effect on NTG-induced vasodilation. Similar results were obtained with coronary artery rings isolated from perfused cat hearts and exposed to neutrophils. This neutrophil-enhanced endothelial dysfunction was inhibited by human superoxide dismutase as well as by an antibody to the adherence glycoprotein complex CD-18 (i.e., MAbR 15.7). Therefore endothelial dysfunction occurs initially upon reperfusion of the previously ischemic heart and is aggravated by superoxide radicals produced by activated neutrophils.