湖北省35~75岁人群高血压流行状况及影响因素分析

目的 了解湖北省35~75岁人群高血压患病、知晓、治疗、控制情况及其影响因素。方法 在6个湖北省心血管病高危人群早期筛查与综合干预项目（简称“高危筛查项目”）点,整群抽样法抽取了35~75岁常住人口共计95371人,采用多水平混合模型分析高血压患病、知晓、治疗和控制情况及其影响因素。结果 50.30%的筛查对象患有高血压,标化后患病率为39.13%,男性患病率（53.60%）高于女性（48.38%）,差异有统计学意义（t=-8.966,P <0.001）。知晓率、治疗率、控制率分别为48.51%、41.83%和10.68%。高血压患者中,年龄较大、受教育程度高、饮酒、罹患糖尿病、肥胖、既往发生过心血管事件的患者具有较高的高血压知晓率、治疗率和控制率(P<0.05)。在接受治疗的高血压人群里,90.49%服用1种降压药物（男:88.94%,女:91.49%）。最常用的降压药物为钙通道阻滞剂（61.09%）。结论 湖北省35~75岁成人患病率高,但知晓率、治疗率和控制率都偏低,且单药使用比例高,应采取有效的干预策略和措施,加强高血压防控。     

促性腺激素释放多肽(GRP)对体外培养小鼠垂体分泌LH的影响

合成的促性腺激素释放多肽(GRP)及其类似物GRp～NH₂,[Glu^7.9.14Lys^6.10]GRP(6～14),[phe¹⁴]GRP(5～14)和[phe¹⁴]GRP浓度在0.05mmol·L^-1时,具有刺激体外培养的小鼠垂体分泌LH的作用。其活性依此相当对照垂体的115.4,114.2,140,160和179%。小鼠于妊振第7～9天或第1～5天,每只sc[phe¹⁴]GRP1mg·d^-1,或于妊娠第2～4天每只sc[phe¹⁴]GRP(5～14)1mg·d^-1,有40～60%的妊娠动物出现死胎。     

江苏省镇江市2009-2018年15岁以下少年儿童法定报告传染病流行特征

目的 了解2009-2018年镇江市15岁以下少年儿童法定传染病的流行趋势,为开展防控工作提供依据。方法 从中国疾病预防控制信息系统中收集2009-2018年镇江市15岁以下少年儿童法定传染病疫情资料进行分析。结果 2009-2018年镇江市累计报告15岁以下少年儿童法定传染病病例22种65135例,年报告发病率134.51/万～263.23/万之间,发病率呈现上升波动趋势（〖XC小五号.EPS;P〗趋势=1932.389,P<0.001）;死亡病例12例,年均死亡率0.03/万;累计病例中男童发病数为38156例（58.58%）,年均发病率204.86/万;女童发病数为26979例（41.42%）,年均发病率159.81/万,不同性别间发病率差异有统计学意义（〖XC小五号.EPS;P〗=997.605,P<0.001）。无甲类传染病报告;乙类传染病累计报告病例16种2587例,年均发病率为7.29/万,发病呈下降趋势（〖XC小五号.EPS;P〗趋势=78.566,P<0.001）;丙类传染病累计报告病例6种62548例,年均发病率176.16/万,发病呈上升趋势（〖XC小五号.EPS;P〗趋势=2177.178,P<0.001）。肠道传染病、呼吸道传染病、血源及性传播传染病、自然疫源及虫媒传染病、其它传播途径传染病分别占累计发病总数的86.95%（56636例）、12.65%（8240例）、0.25%（166例）、0.03%（17例）、0.12%（76例）。发病率前2位的传染病为手足口病和流行性腮腺炎,分别占发病总数的78.43%（51088例）和8.42%（5485例）。结论 少年儿童是传染病发病的重点高危人群,应重点加强手足口病、流行性腮腺炎传染病的监测,采取针对性措施控制少年儿童传染病的发生。     

Development and Validation of a Stability-Indicating HPLC-DAD Method for the Determination of Canagliflozin and Metformin Simultaneously in Combination Dosage Form

Pharmaceutical Chemistry Journal - The purpose of this study was to develop and validate a rapid, simple, easy, and precise high-performance liquid chromatography (HPLC) method with diode array...     

心理一致感在脑卒中患者主要照顾者照顾负担与抑郁间的中介效应研究

目的 探讨心理一致感在主要照顾者照顾负担与抑郁间的中介作用,为提高主要照顾者身心健康提供理论参考。方法 用便利抽样方法抽取某三甲医院神经内科的脑卒中患者主要照顾者,使用一般情况调查表、照顾负担量表、心理一致感量表和流调中心抑郁量表进行调查。采用SPSS 21.0与AMOS 22.0对数据进行统计分析。结果 回收有效问卷436份,有效回收率为96.88%。主要照顾者照顾负担得分为36.50±7.49分、心理一致感得分为63.15±8.46分、抑郁得分为14.03±6.77分。心理一致感与照顾负担、抑郁得分均呈负相关(r=-0.642、-0.592,P<0.01);照顾负担与抑郁得分呈正相关(r=0.625,P<0.01)。Bootstrap 法进一步验证了心理一致感的中介效应,中介效应占总效应的16.6%。结论 心理一致感是脑卒中患者主要照顾者照顾负担与抑郁间的中介变量。     

贵州省2014-2018年人感染H7N9禽流感病例流行病学调查分析

目的 了解贵州省Ｈ７Ｎ９禽流感病例的特征,为进一步防控提供参考。方法 收集贵州省2014-2018年人感染Ｈ７Ｎ９禽流感临床及流行病学疫情资料,用描述性流行病学方法分析其流行特征。结果 2014-2018年贵州省共确诊21例人感染H7N9人禽流感病例,死亡11例,病死率52.3%。以男性、中老年、农民为主,61.9%的病例发生在黔东南和黔南地区,2017年病例数占总病例数的80.9%,未发现聚集性疫情和二代病例。病例发现以不明原因肺炎监测发现为主,从暴露到发病、发病到首诊、发病到确诊、发病到抗病毒药物使用及发病到死亡的时间中位数分别为5天、3天、7天、7天和14天;有无基础性疾病的病死率差异无统计学意义（〖XC小五号.EPS;P〗=0.38,P=0.54）,后期病例病死率低于前期（〖XC小五号.EPS;P〗=4.24,P=0.04）。19例本地病例均有明确的活禽或活禽市场相关环境接触史,其中94.7%的活禽市场或活禽相关场所均检出H7核酸阳性,平均阳性率为32.3%(1.34%～82%),全面长期关闭活禽市场后疫情得到有效控制。 结论 接触活禽或活禽市场环境是感染的主要因素;加强活禽市场外环境监测,规范化管理及长期关闭活禽市场,可有效预警和控制疫情;加强基层医疗机构救治水平可有效降低病死率。     

Modified proteinase-activated receptor-1 and -2 derived peptides inhibit proteinase-activated receptor-2 activation by trypsin.

Trypsin activates proteinase-activated receptor-2 (PAR(2)) by a mechanism that involves the release of a tethered receptor-activating sequence. We have identified two peptides, FSLLRY-NH(2) (FSY-NH(2)) and LSIGRL-NH(2) (LS-NH(2)) that block the ability of trypsin to activate PAR(2) either in PAR(2)-expressing Kirsten virus-transformed kidney (KNRK) cell lines or in a rat aorta ring preparation. The reverse PAR(2) peptide, LRGILS-NH(2) (LRG-NH(2)) did not do so and FSY-NH(2) failed to block thrombin activation of PAR(1) in the aorta ring or in PAR(1)-expressing human embryonic kidney cells. Half-maximal inhibition (IC(50)) by FSY-NH(2) and LS-NH(2) of the activation of PAR(2) by trypsin in a PAR(2) KNRK calcium-signaling assay was observed at about 50 and 200 microM, respectively. In contrast, the activation of PAR(2) by the PAR(2)-activating peptide, SLIGRL-NH(2) (SL-NH(2)) was not inhibited by FSY-NH(2), LS-NH(2), or LRG-NH(2). In a casein proteolysis assay, neither FSY-NH(2) nor LS-NH(2) inhibited the proteolytic action of trypsin on its substrate. In addition, FSY-NH(2) and LS-NH(2) were unable to prevent trypsin from hydrolyzing a 20-amino acid peptide, GPNSKGR/SLIGRLDTPYGGC representing the trypsin cleavage/activation site of rat PAR(2). Similarly, FSY-NH(2) and LS-NH(2) failed to block the ability of trypsin to release the PAR(2) N-terminal epitope that is cleaved from the receptor upon proteolytic activation of receptor-expressing KNRK cells. We conclude that the peptides FSY-NH(2) and LS-NH(2) block the ability of trypsin to activate PAR(2) by a mechanism that does not involve a simple inhibition of trypsin proteolytic activity, but possibly by interacting with a tethered ligand receptor-docking site.     

Direct evidence for endothelial vascular endothelial growth factor receptor-1 function in nitric oxide-mediated angiogenesis

Vascular endothelial growth factor-A (VEGF) is critical for angiogenesis but fails to induce neovascularization in ischemic tissue lesions in mice lacking endothelial nitric oxide synthase (eNOS). VEGF receptor-2 (VEGFR-2) is critical for angiogenesis, although little is known about the precise role of endothelial VEGFR-1 and its downstream effectors in this process. Here we have used a chimeric receptor approach in which the extracellular domain of the epidermal growth factor receptor was substituted for that of VEGFR-1 (EGLT) or VEGFR-2 (EGDR) and transduced into primary cultures of human umbilical vein endothelial cells (HUVECs) using a retroviral system. Activation of HUVECs expressing EGLT or EGDR induced rapid phosphorylation of eNOS at Ser1177, release of NO, and formation of capillary networks, similar to VEGF. Activation of eNOS by VEGFR-1 was dependent on Tyr794 and was mediated via phosphatidylinositol 3-kinase, whereas VEGFR-2 Tyr951 was involved in eNOS activation via phospholipase Cgamma1. Consistent with these findings, the VEGFR-1-specific ligand placenta growth factor-1 activated phosphatidylinositol 3-kinase and VEGF-E, which is selective for VEGFR-2-activated phospholipase Cgamma1. Both VEGFR-1 and VEGFR-2 signal pathways converged on Akt, as dominant-negative Akt inhibited the NO release and in vitro tube formation induced following activation of EGLT and EGDR. The identification Tyr794 of VEGFR-1 as a key residue in this process provides direct evidence of endothelial VEGFR-1 in NO-driven in vitro angiogenesis. These studies provide new sites of modulation in VEGF-mediated vascular morphogenesis and highlight new therapeutic targets for management of vascular diseases.