三七皂甙单体2A-1-1对人血小板聚集和钙内流的作用

目的观察三七皂甙单体2A-1-1对人血小板聚集和钙内流的影响,并探讨其对受体操纵性钙通道的作用.方法比浊法测定血小板聚集;Fura-2/Am荧光探针双波长测定细胞胞浆游离钙浓度,观察2A-1-1、硝苯地平、SK＆F96365对二磷酸腺苷(ADP)、环匹阿尼酸(CPA)介导的人血小板钙内流的变化.结果硝苯地平(20μmol/L)不能抑制ADP诱导的血小板聚集,不能抑制ADP或CPA介导的血小板钙内流;SK＆F96365(20μmol/L)可以抑制ADP诱导的血小板聚集,抑制率为59.83%;SK＆F96365(15μmol/L)可以抑制CPA和ADP介导的钙内流;2A-1-1(5,10,20,μmol/L)可抑制ADP诱导的血小板聚集,抑制率分别为47.06%,53.47%,71.52%;2A-1-1(10,20 μmol/L)可抑制CPA和ADP介导的钙内流.结论三七皂甙单体2A-1-1能抑制人血小板聚集,抑制血小板受体操纵性钙通道,从而抑制钙内流,有抗血小板作用.     

A possible mechanism for island formation by rat ascites hepatoma cells with special reference to the function of aggregation factor at the cell surface

Summary Two tumor cell-aggregation factors of glycoprotein nature, separated from rat ascites hepatoma AH136B cells (forming cell islands in vivo), had different antigenicity; one was not absorbed by immunoadsorbent chromatography with anti-rat serum antibody and the other was. The unabsorbed factor induced aggregation (as shown in the form of simple apposition) of rat ascites hepatoma AH109A cells (present as a free form in vivo) and cell adhesiveness characterized by well-defined tripartite junctional complexes, including intermediate junctions, desmosomes, and tight junctions. In contrast, the absorbed factor from AH136B cells, AH109A cells or normal rat serum aggregated AH109A cells but failed to develop the junctional complexes; only simple apposition was observed. AH109A cells themselves contained the absorbed factor but not the unabsorbed factor. AH136B cells proliferating in the skin developed the junctional complexes, while AH109A cells proliferating in the skin did not from any junctional complexes.This is No. 7 of the studies on tumor cell aggregation-promoting factor     

Polyphenolic grape extract inhibits platelet activation through PECAM-1: an explanation for the French paradox

BACKGROUND: Moderate and prolonged consumption of red wine is associated with decreased cardiovascular morbidity and mortality. Inhibition of platelet functions by ingredients in red wine is thought to be one of the causes. However, the molecular mechanism of this inhibition has remained unexplained. MATERIALS AND METHODS: We measured aggregation, changes in cytosolic Ca(2+) and tyrosine phosphorylation of the inhibitory receptor platelet endothelial cell adhesion molecule-1 (PECAM-1) in platelets stimulated with thrombin receptor (PAR-1) activating peptide (TRAP) and ADP and investigated the effects of alcohol-free polyphenolic grape extract (PGE), alcohol, and the polyphenols catechin, epi-catechin, resveratrol, trans-resveratrol, and gallic acid. RESULTS: Polyphenolic grape extract induced dose-dependent inhibition of TRAP-induced and ADP-induced platelet aggregation and Ca(2+) mobilization. Inhibition was accompanied by activation of PECAM-1. Apart from a slight inhibition by catechin, ethanol or other individual polyphenols failed to inhibit aggregation or activate PECAM-1. CONCLUSIONS: Red wine inhibits platelet functions through its PGE content, which stimulates the inhibitory receptor PECAM-1, thereby attenuating platelet activation.     

Genetic Etiology for Alcohol-Induced Cardiac Toxicity

Background

Alcoholic cardiomyopathy (ACM) is defined by a dilated and impaired left ventricle due to chronic excess alcohol consumption. It is largely unknown which factors determine cardiac toxicity on exposure to alcohol.

某部队结核病聚集流行的现场调查与控制研究

目的探讨部队某部新兵连一起结核病聚集的流行因素,控制结核的进一步蔓延。方法对该部所有新兵及密切接触者进行流行病学调查、X线检查、结核菌素试验、X线检查异常者进行痰结核菌检查,查找结核菌,确诊结核病人,追踪传染源。结果 2008年2月-2009年2月1年内,640名新兵中共确诊活动性结核34例,罹患率5.31%。时间分布呈现两个小高峰,在春秋季。PPD检测人数扩大到新兵密切接触者,共833例,阳性共598例,结核感染率71.79%;强阳性48例,强阳性率5.76%。大大高于对照的未发病部队(P<0.01)。结论首发病例的误诊和未隔离是本次暴发的源头。应加强上下级卫生防疫部门的沟通,采取综合性的结核病防治措施,预防结核病的聚集流行。     

2010-2013年天津市河东区水痘流行特征分析

目的 了解天津市河东区水痘流行病学特征,为制定水痘预防控制策略提供参考依据.方法 对2010-2013年天津市河东区水痘病例应用描述流行病学及统计学分析方法,利用excel 97-2003和SPSS 13.0软件进行数据处理和分析.结果 2010-2013年天津市河东区共报告水痘病例2 684例,年平均发病率74.22/10万.每年3-5月、11月至次年1月发病较多.4年间发生聚集疫情20起,暴发疫情8起;涉及605例患者,其中身体上出皮疹数＜50个的占71.89％,无发热或仅有低热的占68.99％.4年间突破病例占68.28％,且呈逐年上升趋势.结论 天津市河东区水痘发病率较高,突破病例逐年上升,应在保证按时接种首剂水痘疫苗的前提下,适时接种第2剂水痘疫苗,以降低水痘发病率.     

Radiopharmaceutical evaluation of 131I-protohypericin as a necrosis avid compound

Hypericin is a necrosis avid agent useful for nuclear imaging and tumor therapy. Protohypericin, with a similar structure to hypericin except poorer planarity, is the precursor of hypericin. In this study, we aimed to investigate the impact of this structural difference on self-assembly, and evaluate the necrosis affinity and metabolism in the rat model of reperfused hepatic infarction. Protohypericin appeared less aggregative in solution compared with hypericin by fluorescence analysis. Biodistribution data of ¹³¹I-protohypericin showed the percentage of injected dose per gram of tissues (%ID/g) increased with time and reached to the maximum of 7.03 at 24?h in necrotic liver by gamma counting. The maximum ratio of target/non-target tissues was 11.7-fold in necrotic liver at 72?h. Pharmacokinetic parameters revealed that the half-life of ¹³¹I-protohypericin was 14.9?h, enabling a long blood circulation and constant retention in necrotic regions. SPECT-CT, autoradiography, and histological staining showed high uptake of ¹³¹I-protohypericin in necrotic tissues. These results suggest that ¹³¹I-protohypericin is a promising necrosis avid compound with a weaker aggregation tendency compared with hypericin and it may have a broad application in imaging and oncotherapy.     

原发性高血压患者血小板聚集性与L-精氨酸转运功能的改变

为探讨高血压病患者血小板功能的改变及其可能的机制．本文观察了23名原发性高血压患者和14名健康成年人血小板体积、数量、聚集性和一氧化氮产生量及L-精氨酸转运特征。结果发现，原发性高血压患者血小板数目、体积无明显改变．而最大聚集率较对照组高1．3倍（P＜0．05），在二磷酸腺苷刺激下一氧化氮产生量较对照组低71％（P＜0．01），且血小板最大聚集率与一氧化氮产生量之间成明显负相关（r＝0．63）。原发性高血压患者血小板L-精氨酸转运能力明显降低，其最大转运速率仅为对照组的79％（P＜0．01），但两组间米氏常数无明显差异。结果提示，原发性高血压患者血小板聚集功能增强可能与一氧化氮生成减少及L-精氨酸转运功能降低有关。     

Baicalin prevents the production of hydrogen peroxide and oxidative stress induced by Aβ aggregation in SH-SY5Y cells

Alzheimer's disease (AD) is a common form of neurodegenerative disease. Mounting evidence suggests that metal ions play a key role in the aggregation of amyloid β peptide (Aβ), which acts as a factor or cofactor in the etiopathogenesis of AD. Therefore, inhibition of Aβ aggregation emerges as a potential approach for the treatment of AD. We have found that baicalin can interact with copper directly and inhibits Aβ1–42 aggregation. In addition, baicalin protects SH-SY5Y cells from oxidative injuries induced by Aβ1–42 aggregation through decreasing H₂O₂ production that is normally formed as a deleterious by-product of beta amyloid aggregation and the formation of plaques. Taken together, these data indicate that baicalin may be a potential agent to inhibit Aβ aggregation and thereby delay, mitigate or modify the progression of neurodegenerative diseases such as AD.