Mucosal glucosamine synthetase activity in inflammatory bowel disease

Abnormalities in colonic glycoprotein synthesis have been implicated in the pathogenesis of ulcerative colitis and Crohn's disease. Glucosamine synthetase is the rate-limiting step in the biosynthesis of gastrointestinal glycoprotein and has been measured in control subjects (N=23) and patients with ulcerative colitis (N=26) or Crohn's disease of the colon (N=20) classified according to the macroscopic status of the rectum. Glucosamine synthetase activity was relatively constant around the normal colon but lower levels were found in the terminal ileum. In ulcerative colitis, glucosamine synthetase activity was similar to controls (24.0±1.9) mmol/g wet (wt/hr) irrespective of disease activity (quiescent:N=13, =27.3±1.9; activeN=16, =26.2±2.3). Rectal glucosamine synthetase activity was normal in the presence of active Crohn's proctocolitis (29.4±3.1) but raised in patients with Crohn's colitis and rectal sparing (37.2±4.9P<0.02). Glucosamine synthetase activity was strongly influence by the degree of epithelial preservation.     

甘薯的抗家兔主动脉粥样硬化形成作用

为观察甘薯糖蛋白对家兔实验性动脉粥样硬化形成的影响并探讨其可能的发病机制。将 4 0只新西兰白兔随机分为正常组 (饲以普通饲料 )、高脂组 (饲以胆固醇饲料 )、低剂量甘薯糖蛋白 (简称低剂量 )组 [饲以胆固醇饲料 +糖蛋白 0 .0 6g/ (kg·d) ]和高剂量甘薯糖蛋白 (简称高剂量 )组 [饲以胆固醇饲料 +糖蛋白 0 .1g/ (kg·d) ]。在实验开始时和 12周时分别检测血清总胆固醇、甘油三酯、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇、超氧化物歧化酶和丙二醛含量。第 12周末处死动物 ,行主动脉病理形态学观察。结果发现 ,实验前各组血清检测指标无明显差异。实验 12周 ,高脂组、低剂量组和高剂量组血清总胆固醇、甘油三酯、低密度和高密度脂蛋白胆固醇以及丙二醛含量均高于或明显高于正常组 (正常组、高脂组、低剂量组和高剂量组的总胆固醇分别为 1.2 7± 0 .73、2 0 .2 6± 0 .13、15 .2 7± 0 .83和 11.2 8± 1.6 2mmol/L ;甘油三酯分别为 0 .85± 0 .18、1.85± 0 .35、1.71± 0 .2 8和 1.5 1± 0 .11mmol/L ;低密度脂蛋白胆固醇分别为 0 .5 0± 0 .0 7、18.99± 2 .6 5、14 .2 7± 3.0 4和 12 .13± 3.5 6mmol/L ;高密度脂蛋白胆固醇分别为 0 .5 4± 0 .11、0 .75± 0 .10、0 .81± 0 .0 6和 0 .94± 0 .0     

The effects of anagrelide on human megakaryocytopoiesis

Anagrelide, an inhibitor of platelet aggregation, decreases the number of platelets in normal subjects and in patients with myeloproliferative disorders. We describe studies aimed at discovering the general mechanism(s) by which anagrelide acts. We examined three hypotheses: (1) anagrelide shortens platelet survival, (2) anagrelide inhibits the proliferation of megakaryocytic-committed progenitor cells (CFU-M), and (3) anagrelide inhibits maturation of megakaryocytes. We observed that anagrelide did not shorten platelet survival. Proliferation of CFU-M in vivo was not affected by anagrelide, although high concentrations of anagrelide inhibited CFU-M in vitro . In-vivo and in-vitro anagrelide altered the maturation of megakaryocytes, causing a decrease in their size and changing other morphometric features. We conclude that anagrelide decreases the number of platelets primarily by interfering with the maturation of megakaryocytes.     

不同磷脂肽段诱导的实验性自身免疫性脑脊髓炎模型病理特征多样性的研究

目的:探索是否不同磷脂肽段可以诱导Lewis大鼠产生不同的病理学表现。方法:采用髓鞘碱性蛋白82-99(MBP82-99)、MBP68-86、髓鞘少突胶质细胞糖蛋白35-55(MOG35-55)免疫Lewis大鼠,每天进行神经功能评分。免疫后取各组大鼠大脑、小脑、脑干和脊髓组织,观察炎性细胞浸润部位和浸润程度、有无脱髓鞘和轴索损害。结果:MBP68-86和MBP82-99两组大鼠的大脑、脑干、小脑和脊髓组织均有炎性细胞浸润,脊髓炎症程度重于其他部位;MBP68-86和MBP82-99诱导的脊髓炎症程度无统计学差异;MOG35-55组大鼠仅脊髓组织受累,且炎症程度明显低于MBP组,其余各组未见炎性细胞浸润。各组大鼠神经组织均未见脱髓鞘和轴索受累。结论:不同磷脂肽段诱导Lewis大鼠神经组织炎性细胞浸润的分布和程度不同。     

Platelet Glycoprotein IIb/IIIa Integrin Blockade in Coronary Artery Disease: Current State of the Art

Platelets have been shown to play an important role in the pathogenesis of atherosclerosis, acute coronary syndromes, and ischemic complications after percutaneous coronary intervention. Fibrinogen binding via platelet surface glycoprotein (GP) IIb/IIIa receptors constitutes the "final pathway" in platelet aggregation leading to thrombus formation. The GP IIb/IIIa receptor inhibitors, a new class of antiplatelet agents that have emerged in recent years, show great promise in reducing complications of coronary angioplasty and acute coronary syndromes. This review will examine the biology of platelet GP IIb/IIIa receptors, the various classes of GP IIb/IIIa receptor antagonists, the results of the latest clinical trials, and their implications in current clinical practice.     

Vascular access site complications with the use of closure devices in patients treated with platelet glycoprotein IIb/IIIa inhibitors during rescue angioplasty.

The objective of this study was to evaluate the effectiveness of two different closure devices in patients undergoing rescue percutaneous coronary intervention (PCI) using IIb/IIIa inhibitors and to compare it with patients undergoing elective PCI. One hundred sixty-two patients undergoing rescue PCI treated with IIb/IIIa inhibitors underwent vascular access site closure (6 Fr Perclose, n = 92, or 6 Fr Angioseal, n = 70). Vascular complications were compared with a sex- and age-matched group (n = 100) of patients undergoing manual compression after sheath removal and a similar group of patients undergoing elective PCI (n = 196). The incidence of access site complications was not significantly different between the three groups undergoing rescue PCI and was not higher than in patient receiving GP IIb/IIIa inhibitors without fibrinolysis (RR = 0.95; 95% CI = 0.88-1.01). In patients undergoing rescue PCI and receiving IIb/IIIa inhibitors, closure devices allow early sheath removal and are associated with similar outcomes compared with manual compression and elective PCI regardless of the type of closure device used.     

A recombinant varicella vaccine harboring a respiratory syncytial virus gene induces humoral immunity

The varicella-zoster virus (VZV) Oka vaccine strain (vOka) is highly efficient and causes few adverse events; therefore, it is used worldwide. We previously constructed recombinant vOka (rvOka) harboring the mumps virus gene. Immunizing guinea pigs with rvOka induced the production of neutralizing antibodies against the mumps virus and VZV.Here, we constructed recombinant vOka viruses containing either the respiratory syncytial virus (RSV) subgroup A fusion glycoprotein (RSV A–F) gene or RSV subgroup B fusion glycoprotein (RSV B–F) gene (rvOka-RSV A–F or rvOka-RSV B–F). Indirect immunofluorescence and Western blot analyses confirmed the expression of each recombinant RSV protein in virus-infected cells. Immunizing guinea pigs with rvOka-RSV A–F or rvOka-RSV B–F led to the induction of antibodies against RSV proteins. These results suggest that the current varicella vaccine genome can be used to generate custom-made vaccine vectors to develop the next generation of live vaccines.     

代谢综合征危险因素与锌α2糖蛋白相关性研究进展

代谢综合征的危险性因素包括胰岛素抵抗、高血压、肥胖、高脂血症和高尿酸血症.并且全球发病率有逐年升高的趋势.代谢综合征损害了人类的健康,降低了患者的生活质量.锌α2糖蛋白(ZAG)是一种脂溶性糖蛋白,广泛存在于人体体液及多种分泌上皮细胞中,ZAG的结构类似于主要组织相溶性抗原家族工(MHCⅠ)类抗原呈递分子.其作为脂肪动员因子参与代谢综合征和某些恶性病质的发生.     

社区获得性肺炎患者的外周血TNF-α、sTREM-1、α1-APG水平

目的观察肿瘤坏死因子-α(TNF-α)、可溶性髓系细胞触发受体-1(sTREM-1)、α1-酸性糖蛋白(α1-APG)水平在社区获得性肺炎(CAP)患者外周血中变化,了解TNF-α、sTREM-1、α1-APG在CAP患者中的临床价值。方法 ELISA双抗夹心法检测110例CAP患者(CAP组)与52例对照组外周血TNF-α、sTREM-1水平,免疫散射速率比浊法检测α1-APG水平;观察CAP组住院第1天、第4天、第7天及不同病情时的TNF-α、sTREM-1、α1-APG水平变化趋势。结果 CAP组住院第1天、第4天及第7天的TNF-α、sTREM-1及α1-APG水平均显著高于对照组(P<0.001)。经治疗后,第4天TNF-α、sTREM-1、α1-APG水平较第1天显著降低(P<0.001);第7天TNF-α、sTREM-1水平较第4天显著降低(P<0.001),第7天α1-APG水平较第4天升高(P<0.05)。CAP组住院第1天,PSI高危患者TNF-α、sTREM-1、α1-APG水平显著高于中、低危患者(P<0.001)。CAP组住院第1天,呼吸衰竭与非呼吸衰竭患者TNF-α、sTREM-1及α1-APG水平差异有统计学意义(P<0.001)。CAP组住院第7天,与非糖皮质激素治疗患者相比,糖皮质激素治疗患者sTREM-1、α1-APG水平显著下降(P<0.01),但TNF-α水平差异无统计学意义(P>0.05)。结论在CAP患者中存在着炎性细胞因子TNF-α、sTREM-1、α1-APG的过度释放,TNF-α、sTREM-1、α1-APG水平可反映CAP患者的病情严重程度及治疗效果;糖皮质激素的应用可降低sTREM-1及α1-APG水平。TNF-α、sTREM-1、α1-APG可作为CAP患者诊断治疗及预后的指导指标。     

Utilization of anticoagulants and outcomes in STEMI patients undergoing PPCI in the US hospitals: Bivalirudin,heparin plus GPI or heparin alone?

Objective. Despite major trials showing the opposite, one of three small randomized trials conducted outside the US has raised questions about whether heparin alone is a viable antithrombotic strategy for primary percutaneous coronary interventions (PPCI). We determined the frequency and in-hospital outcomes of anticoagulation strategies in patients undergoing PPCI. Methods. We analyzed records from 2008 through 2013 in the Premier Research Database of patients hospitalized with ST-segment elevation myocardial infarction (STEMI) undergoing PPCI. Patients were categorized into one of four anticoagulation strategies: bivalirudin alone, bivalirudin plus glycoprotein IIb/IIIa inhibitors (GPI), unfractionated or low-molecular-weight heparin alone or heparin plus GPI. In-hospital clinical outcomes were compared between treatment groups after propensity score matching. Results. Among 114,134 eligible STEMI patients, heparin alone was the least frequent anticoagulation strategy, used in 14.4% to 18.1% of cases per year. Bivalirudin alone nearly tripled during the study period, from 12.7% to 37.8% and surpassed that of heparin plus GPI by 2013. Bivalirudin alone performed better than heparin alone for mortality (4.7% vs 5.3%, p = 0.010), clinically apparent bleeding (5.7% vs 6.7%, p < 0.001), transfusion rates (4.1% vs 4.8%, p = 0.003) and mean length of stay (4.1 vs 4.2 days, p < 0.001). The in-hospital death rate was lower with heparin plus GPI than with heparin alone (4.9% vs 5.9%, p < 0.001), but clinically apparent bleeding was higher in heparin plus GPI than in heparin alone (9.4% vs 7.1%, p < 0.001). Conclusion: In patients hospitalized for STEMI undergoing PPCI, heparin alone is not commonly used and is inferior to bivalirudin for mortality, bleeding and length of stay outcomes. Heparin is also inferior to heparin plus GPI for ischemic protection but associated with less bleeding.