蜂毒素对大鼠血小板内钙浓度的影响

应用Ｆｕｒａ－２作为荧光试剂，测定大鼠血小板细胞内Ｃａ~（２＋）浓度变化。蜂毒素１．５ｍｇ／Ｌ使血小板细胞内Ｃａ~（２＋）浓度增加；悬液中加入ＣａＣｌ＿２１ｍｍｏｌ／Ｌ，血小板细胞内Ｃａ~（２＋）继续增加。维拉帕米３．１２５ｍｇ／Ｌ作用５ｍｉｎ后，蜂毒素仍可使血小板内Ｃａ~（２＋）增加．但加入ＣａＣｌ２血小板Ｃａ~（２＋）的浓度不再增加。提示蜂毒素促进大鼠血小板细胞内Ｃａ~（２＋）的释放和细胞外Ｃａ~（２＋）进入细胞内。     

风心瓣膜病变患者红细胞膜钠、钙泵活性和脂质过氧化的变化

用酶解法和Ｈ２Ｏ２分解法分别测定２８例风心瓣膜病变患者红细胞膜钠泵（Ｎａ＋、Ｋ＋－ＡＴＰ酶）、钙泵（Ｃａ２＋、Ｍｇ２＋－ＡＴＰ酶）活性和膜过氧化氢酶（ＣＡＴ）活性，并用硫代巴比妥酸比色法测定患者红细胞膜脂质过氧化物（ＬＰＯ）含量。患者红细胞膜Ｎａ＋、Ｋ＋－ＡＴＰ酶活性和Ｃａ２＋、Ｍｇ２＋－ＡＴＰ酶活性分别显著低于正常人３４．７５％（Ｐ＜０．０１）和２６．７７％（Ｐ＜０．０１）；ＣＡＴ活性显著低于正常人２０．０７％（Ｐ＜０．０１）；而患者ＬＰＯ含量却显著高于正常人９７．５０％（Ｐ＜０．０１）。结果提示风心病患者瓣膜病变与质膜钠、钙泵活性变化以及膜脂质过氧化作用有关。     

“钾异心”停搏液对缺血心肌电活动的影响

观察“钾异心”停搏液对缺血心肌的保护作用并与高钾停搏液比较。用无糖不充氧台氏液浸浴离体豚鼠右心室乳头肌３ｈ造成缺血损伤，以心肌细胞电生理参数为指标。缺血后心肌电生理参数下降，其中以“钾异心”组下降最快速彻底，复灌后只有“钾异心”组电生理各参数都恢复正常。结论“钾异心”停搏液可快速彻底抑制心肌电活动有效保护缺血心肌。     

开心散与生脉散抗阿尔茨海默症“同病异治”作用机制网络药理学分析与中枢神经免疫调控效用验证＊

目的 基于网络药理学方法研究开心散（KXS）与生脉散（SMS）“同病异治”抗阿尔茨海默症作用机制，并通过整体动物与离体细胞实验进行验证。方法 通过数据库搜集筛选开心散与生脉散复方所含药味化学成分并预测其潜在靶点，构建复方-中药-成分-靶点网络。筛选复方共有与优势靶点，构建蛋白互作网络并进行拓扑分析，进行KEGG通路和GO功能富集分析。基于网络药理学分析获得的开心散与生脉散共性与个性的生物学GO分析结果，分别建立小鼠海马Aβ注射拟阿尔茨海默症痴呆小鼠模型与小鼠小胶质BV2细胞炎性因子损伤模型，检测相应指标，采用行为学结合生化指标分析验证网络药理学分析结果。结果 筛选出开心散与生脉散复方共有成分有109个，共有靶点490个，抗AD潜在共性调控靶点375个。开心散抗AD潜在优势调控靶点92个，生脉散抗AD潜在优势调控靶点90个。淀粉样蛋白代谢与转运、cAMP与AMPK信号通路、突触功能调控等为开心散与生脉散抗AD潜在共性调控信号通路与生物学事件。NF-κB等为开心散抗AD优势调控信号通路与生物学事件；趋化因子、胆碱能突触等为生脉散抗AD优势调控信号通路与生物学事件。验证实验结果显示开心散与生脉散能够有效改善Aβ海马区注射小鼠认知功能障碍，降低小鼠海马和小胶质细胞的炎性因子表达。结论 开心散与生脉散能通过共有及各自优势靶点发挥抗AD作用。     

徐州地区1572例健康人群骨密度和骨质疏松症调查

目的通过测量徐州地区健康人群骨密度（BMD）,分析骨密度的变化规律及骨质疏松症的发病率,提高对骨质疏松症诊断的可靠性,为骨质疏松症的防治提供参考依据。方法采用GE-LUNAR公司生产的双能X线骨密度仪对徐州地区2005～2008年1572例健康人进行BMD测定,分别做股骨上端及第2～4腰椎椎体测量,并按5岁为一个年龄组分组。以峰值BMD减低2．5SD为诊断骨质疏松症标准,按性别、年龄分组进行统计学分析。结果徐州地区女性BMD峰值则在30～35岁,男性在35岁左右,女性55岁后骨量下降较男性显著,骨质疏松发病率女性高于男性。结论对于55岁女性和65岁男性,之前应加强普及骨质疏松预防知识,之后同时采取相应干预措施,以减少骨质疏松症的发生,为徐州地区骨质疏松症的诊治提供参考依据。     

Circulating dendritic cells subsets and CD4+Foxp3+ regulatory T cells in adult patients with chronic ITP before and after treatment with high-dose dexamethasome

Immune thrombocytopenic purpura (ITP) is an autoimmune disorder, and high-dose dexamethasome (HD-DXM) has been used as a first-line therapy for patients with ITP. However, little is known about the role of dendritic cells (DCs) and CD4(+)Foxp3(+) regulatory T (Treg) cells in the pathogenesis of chronic ITP and the effects of HD-DXM on DCs and Treg cells. In this study, we investigated the amounts of circulating myeloid DCs (mDCs), plasmacytoid DCs (pDCs), and CD4(+)Foxp3(+) Treg cells in 26 untreated adult patients with chronic ITP. All patients had thrombocytopenia (platelet count <50 x 10(9)/L) for more than 6 months. We also observed short-time changes of DCs and Treg cells after treatment with HD-DXM in these patients. Both mDCs and pDCs numbers in patients were comparable with that of healthy controls. In contrast, the percentage of Treg cells was significantly reduced in patients when compared with healthy controls (P < 0.0001). After 4-days treatment with HD-DXM, Treg cells and mDCs were increased (P < 0.0001 and P < 0.05), while pDCs decreased (P < 0.0001), and CD11c expression level in mDCs was downregulated (P < 0.0001). These results suggest that Treg cells are deficient in ITP and the immunosuppressive therapy of glucocorticoids could cause the short-time changes of these cells.     

The Prognostic Role of Peripheral Lymphocyte Subsets in Patients With Acute Pancreatitis

Background

The prognostic role of peripheral lymphocyte subsets in early stage of acute pancreatitis (AP) is unknown.

Sinorhizobium meliloti phospholipase C required for lipid remodeling during phosphorus limitation

Rhizobia are Gram-negative soil bacteria able to establish nitrogen-fixing root nodules with their respective legume host plants. Besides phosphatidylglycerol, cardiolipin, and phosphatidylethanolamine, rhizobial membranes contain phosphatidylcholine (PC) as a major membrane lipid. Under phosphate-limiting conditions of growth, some bacteria replace their membrane phospholipids with lipids lacking phosphorus. In Sinorhizobium meliloti, these phosphorus-free lipids are sulfoquinovosyl diacylglycerol, ornithine-containing lipid, and diacylglyceryl trimethylhomoserine (DGTS). Pulse–chase experiments suggest that the zwitterionic phospholipids phosphatidylethanolamine and PC act as biosynthetic precursors of DGTS under phosphorus-limiting conditions. A S. meliloti mutant, deficient in the predicted phosphatase {"type":"entrez-protein","attrs":{"text":"SMc00171","term_id":"1174089800","term_text":"SMC00171"}}SMc00171 was unable to degrade PC or to form DGTS in a similar way as the wild type. Cell-free extracts of Escherichia coli, in which {"type":"entrez-protein","attrs":{"text":"SMc00171","term_id":"1174089800","term_text":"SMC00171"}}SMc00171 had been expressed, convert PC to phosphocholine and diacylglycerol, showing that {"type":"entrez-protein","attrs":{"text":"SMc00171","term_id":"1174089800","term_text":"SMC00171"}}SMc00171 functions as a phospholipase C. Diacylglycerol , in turn, is the lipid anchor from which biosynthesis is initiated during the formation of the phosphorus-free membrane lipid DGTS. Inorganic phosphate can be liberated from phosphocholine. These data suggest that, in S. meliloti under phosphate-limiting conditions, membrane phospholipids provide a pool for metabolizable inorganic phosphate, which can be used for the synthesis of other essential phosphorus-containing biomolecules. This is an example of an intracellular phospholipase C in a bacterial system; however, the ability to degrade endogenous preexisting membrane phospholipids as a source of phosphorus may be a general property of Gram-negative soil bacteria.     

Epigallocatechin-3-Gallate Protects Na<Superscript>+</Superscript> Channels in Rat Ventricular Myocytes Against Sulfite

Sulfite (bisulfite/sulfite) can affect voltage-gated sodium (Na⁺) channels (VGSC) in a concentration-dependent manner in isolated rat ventricular myocytes. In this study, the effect of epigallocatechin-3-gallate (EGCG) on VGSC in isolated ventricular myocytes was studied. Ventricular myocytes were exposed to 10 μM bisulfite/sulfite for 10 min, and EGCG was then administered in different concentrations (10, 30, 50 μg ml⁻¹). Decreased activity of superoxide dismutase, catalase (CAT) and glutathione peroxidase (GPx) was observed after bisulfite/sulfite exposure, with significant increase in Na⁺ currents (I _Na) and alterations in half-activation voltage and half-inactivation voltage. Intracellular reactive oxygen species (ROS) such as hydrogen peroxide (H₂O₂), hydroxyl (OH^·), and superoxide anion (O₂^·−) were increased. After EGCG treatment, activity of the aforementioned enzymes increased while the ROS level decreased. The effects progressed with increasing amounts of EGCG, up to a level similar to blank control at the dose of 50 μg ml⁻¹ EGCG, EGCG also reduced the I _Na and reversed the alterations in half-activation voltage and half-inactivation voltage. In conclusion, EGCG could protect Na⁺ channels in rat ventricular myocytes against the oxidative damage induced by sulfite as a scavenger of the ROS.     

肝硬化及其并发症患者之凝血功能变化

目的 探讨肝硬化及其并发症患者之凝血功能变化。方法 109例肝硬化患者及其健康家属清晨空腹抽静脉血测定PT、PTA、PLT、A。结果 肝硬化组PT值明显延长,PLT、A值明显下降(P<0.001),且随肝功能分级愈差,PT值愈延长,PTA值下降愈明显(P<0.01～0.001),PLT值下降亦愈明显。脾切除者与未切除者比较,PLT值显著上升(P<0.001),PT、PTA值亦有所改善(P<0.05)。有腹水者与无腹水者比较,PT值明显延长(P<0.01),PTA、PLT值下降(P<0.05)。并发感染、肝性脑病者与无感染、无肝性脑病者比较,PT值明显延长(P<0.05～0.01),PTA值下降(P<0.05),PLT值无明显改变(P>0.05)。而并发原发性肝癌、消化道出血者与无原发性肝癌、无消化道出血者比较,PT、PTA、PLT值无明显改变(P>0.05)。结论 肝硬化患者存在不同程度的凝血功能障碍,且肝功能分级愈差,凝血功能障碍愈明显。肝硬化有腹水、并发感染、肝性脑病者,凝血功能障碍更严重。并发原发性肝癌、消化道出血者与无原发性肝癌、无消化道出血者比较,凝血功能无明显差异。而脾切除术不仅可改善脾亢,凝血功能亦有改善。