2015—2018年西安市百日咳流行特征分析

目的 分析西安市2015—2018年百日咳流行病学特征,为预防和控制百日咳传播提供参考。方法 采用描述流行病学方法,对中国疾病预防控制信息系统中2015—2018年期间西安市百日咳报告病例和此期间西安市百日咳哨点监测病例的数据进行统计学分析。结果 西安市2015—2018年共报告百日咳确诊病例1 635例,发病率分别为3.97/10万、4.11/10万、4.85/10万和5.28/10万,发病有逐年上升趋势（χ2趋势 = 21.719,P＜0.001）;高发季为3—8月（2015—2018年分别占该年度总发病数的75.73%、66.76%、78.97%和80.27%）;以3～6月龄发病比例最高（2015—2018年分别占该年度总发病数的50.58%、48.60%、48.36%和41.22%）;未全程接种疫苗患儿所占比例最大（2015—2018年分别为36.26%、23.74%、42.76%和33.73%）,未到接种年龄就发病所占比例有逐年升高趋势（χ2趋势 = 10.302,P = 0.001）,无免疫史患儿比例呈逐年降低趋势（χ2趋势 = 36.088,P＜0.001）;3种实验室检测方法中荧光PCR的检出率最高（40.12%）;传播模式除了散发病例,出现了家庭聚集现象,且所有流行病学相关病例均被漏诊或误诊。结论 西安市近年来百日咳发病率有明显上升趋势,＜6月龄婴儿为主要发病人群,百日咳的日常监测仍有待加强,且其家庭聚集式传播现象值得关注。     

白芨多糖对大鼠血小板聚集、疑血功能及TXB2、6-keto-PGF1α表达的影响

目的：观察白芨多糖对大鼠血小板聚集、凝血功能及血浆血栓素B2（TXB2）、6-酮-前列腺素F1α（6-keto-PGF1α）水平的影响,探讨白芨多糖的止血机制.方法：健康SD大鼠60只,随机分为正常对照组（生理盐水）、白芨多糖高剂量组（12 g/kg）、白芨多糖中剂量组（6 g/kg）、白芨多糖低剂量组（3 g/kg）、云南白药组（0.4g/kg）,连续给药14 d;股动脉采血,测定各组大鼠血小板聚集率、凝血酶原时间（PT）、凝血酶时间（TT）、部分凝血活酶时间（APTT）、纤维蛋白原（FIB）、TXB2和6-keto-PGF1α水平.结果：与空白对照组比较,白芨多糖中、高剂量能增加大鼠血小板聚集率,缩短PT、APTT和TT,显著增加FIB、TXB2含量和降低6-keto-PGF1α含量（P＜0.05或P＜0.01）.结论：白芨多糖可能通过激活内源性,外源性凝血系统,促进血小板聚集和调节TXB2、6-ke-to-PGF1α的水平,发挥止血功能.     

血液流变学特性改变在＋Gz致大鼠脑损害中的意义

目的：探讨＋Ｇｚ重复作用后大鼠血液流变学特性的变化规律及其在＋Ｇｚ致脑损害中的作用．方法：利用动物离心机将大鼠重复暴露于＋１０Ｇｚ３ｍｉｎ三次，观察暴露后不同时间血液流变学特性及脑组织形态学的变化．结果：＋Ｇｚ重复暴露３次后即刻及１ｈ，大鼠全血粘度、全血还原粘度、血浆纤维蛋白原含量、红细胞聚集指数及屈服应力较对照组均显著升高（Ｐ＜０．０５）；暴露后６ｈ，全血粘度、全血还原粘度及血浆纤维蛋白原含量已基本恢复至对照组水平，红细胞聚集指数及屈服应力也呈现出恢复趋势，但仍明显高于对照组（Ｐ＜０．０５）．＋Ｇｚ暴露后各时间组的血浆粘度、红细胞体积分数、红细胞刚性指数及Ｃａｓｓｏｎ粘度则均无明显变化．＋Ｇｚ重复暴露后大鼠脑皮层少数神经元出现缺血性改变．结论：＋１０Ｇｚ３ｍｉｎ重复暴露３次可引起大鼠血液流变学特性的改变．全血粘度的增高可能主要与红细胞聚集程度增加有关．血液流变学特性的改变可能对加重＋Ｇｚ重复暴露引起的脑损害有一定影响．     

不同银杏内酯化合物抗血小板活聚集(PAF)活性的研究

目的:探讨不同银杏内酯化合物对家兔血小板聚集作用的影响。方法:进行体外实验观察不同银杏内酯化合物对由血小板活化因子(PAF)诱导的家兔血小板聚集作用的影响。结果:不同银杏内酯化合物体对PAF诱导的血小板聚集均有抑制作用,IC50在0.24～27.44μg/mL之间。结论:不同银杏内酯化合物体外对血小板聚集均有抑制作用差异明显。     

流行性出血热出血机理的探讨

为阐明流行性出血热(简称出血热)的出血机理,我们将31例出血热患者各病期血小板和红细胞涂片,用羊抗人IgG和C3荧光素作荧光染色后,再用出血热单克隆荧光抗体作特异性染色。血小板、红细胞表面的免疫复合物在发热期即出现,检出率分别为33.3％和25.8％,至休克少尿期仍存在,到多尿和恢复期则基本消失。发热期患者的血小板计数及其聚集率均显著下降。各病期血标本纤维蛋白原半定量测定的结果均属正常。但纤维蛋白(原)裂解产物(FDP)在发热期已有增高,休克少尿期增高显著,多尿期仍高于正常。直至恢复期渐趋正常。本文资料提示免疫复合物在组织细胞表面沉积是引起出血的重要原因。     

Effects of Ginsenosides and Ketoprofen on Smoke Inhalation Injury in Rabbits and Rats

Six hours after smoke inhalation injury in rabbits, the permeability of pulmonary vesselsand the aggregation of circulating platelets increased markedly accompanied with apparent patholog-ical changes in the trachea and lungs. Fifteen minutes after smoke inhalation injury in rabbits, an intravenous dose of ginsenosides or ketoprofenwas given to the animals respectively. 6 hours after medication, it was found that both the drugscould significantly alleviate the platelet aggregation, but only ginsenosides could alleviate theaugmentation of pulmonary vascular permeability and the pathological lesions in the trachea andlungs. In those rats injured by smoke inhalation, l hour after an intravenous dose of ginsenosides, theplasma PGI_2 level was elevated and TXA_2/PGI_2 ratio decreased significantly.     

脾切除后血小板聚集及ATP释放增高机制的探讨

测定了32例脾切除患者血小板聚集(PAg),其中包括16例同步测定PAg及ATP释放(ATP-R)的结果。脾切除组由ADP、Coll及ADR所致5分钟内最大聚集率(M~1)及ATP-R的均值较脾切除前组及正常对照组均有一定程度升高,其中以肝硬化代偿期脾切除组升高最明显(P<0.05～0.001)。其发生机制与血小板数增多、凝血因子增加、抗凝活性减低、继发性纤溶活性增加及血小板代谢活性指标TXB_2增高等因素有关,提示脾切除患者PAg及ATP-R升高与临床存在的高凝状态有关。     

APN FO 1341抗血小板聚集的研究

APNFO1341为穿心莲第三代提取物之一。本文采用血小板聚集(PAG)试验比浊法观察发现APN FO 1341在一定剂量范围内呈剂量依赖性抑制二磷酸腺苷(ADP)和血小板活化因子(PAF)诱导的人富血小板血浆(PRP)的PGA。其对虫ADP诱导第1分钟和第5分钟PAG的IC_(50)分别为2.6mg/L和1.4 mg/L;对由PAF诱导PAG的IC_(50)分别为0.58mg/L和0.38mg/L。通过血小板鲁米诺化学发光技术证明APN FO 1341 2mg/L即显著抑制静息及刺激后人洗涤血小板的化学发光,提示其尚具有清除活性氧的作用。APN FO 1341 2mg/L与PRP孵育后上清液中乳酸脱氢酶活性没有明显变化。表明APN FO 1341没有破坏血小板的作用。     

Book of the Month—A Report

There are four grades of the three main types of ophthalmoscopic hypertensive signs which occur in the retinal arterioles. Acute and chronic hypertension can be differentiated on the basis of these signs and, therefore, a better evaluation of the treatment can be achieved. The changes occurring in the retinal arterioles are illustrated by both diagrams and photographs.     

Relationship between urinary biopyrrins and pneumoconiosis

Abstract

Background: Test 1 is a recently introduced technique claiming to determine Erythrocyte Sedimentation Rate (ESR) in 20 s. In contrast to the original Westergren procedure this new technique uses undiluted blood and operates at 37°C. It is hypothesized that Test 1 is in fact an erythrocyte aggregometer and does not measure any sedimentation. Methods: Test 1 results were compared to those obtained with StaRRsed, an automated ESR analyser based on the Westergren technique, and the results of both were correlated to various indices of red blood cell (RBC) aggregation, obtained with an aggrego - meter (LORCA). Measurements were made on blood from 75 patients with various rheumatic disorders. Furthermore, blood that was experimentally manipulated in order to affect RBC aggregation, i.e. by changing the hematocrit, by diminishing plasma protein concentration, by inducing hyperaggregation or by RBC rigidification, was tested on all three instruments. Results: Generally in patient blood, Test 1 results demonstrated a higher correlation with the various aggregation parameters than StaRRsed. Highest correlation (R = ?0.8)) with both Test 1 and StaRRsed outcome were seen with I₂₀, a RBC aggregation parameter directly related to the backscatter intensity. All experimentally induced changes in RBC aggregation paralleled closely those obtained with Test 1 while StaRRsed results followed a different course. Conclusions: The results obtained in this study strongly support the hypothesis that Test 1 measures only the RBC aggregation process and does not cover any of the indices directly linked to the sedimentation process as determined by the Westergren method.