灯盏细辛注射液治疗高粘滞血症疗效观察

目的评价灯盏细辛注射液治疗高粘滞血症的疗效。方法将76例高粘滞血症患者分成两组 ,治疗组37例患者用灯盏细辛注射液30ml静滴治疗 ,对照组39例患者用丹参注射液30ml静滴治疗 ,均连续用药14d。结果两组均有降低全血粘度、血浆粘度、红细胞聚集指数的作用 (均P<0 .05) ,而治疗组还有显著降低纤维蛋白原、延长活化部份凝血活酶时间的作用 (均P<0.01) ,两组间比较差异亦有显著性 (均P<0.01)。结论灯盏细辛注射液能改善高粘滞血症患者的血液流变性 ,尤其在降低纤维蛋白原、延长活化部份凝血活酶时间的作用方面疗效显著 ,用药安全 ,副作用少     

糖尿病肾病的血液流变学改变

本文对21例糖尿病肾病、14例糖尿病非肾病以及16例正常对照的血液流变学检查结果进行了分析.结果表明,两组糖尿病患者均呈现高粘滞血症,尤以糖尿病肾病组为著.糖尿病肾病组患者尿蛋白排泄量与血浆比粘度、红细胞刚性指数、血小板粘附率呈正相关.内生肌酐清除率(Ccr)与上述三项指标呈负相关.     

五子汤治疗阴虚阳亢型高粘血症的临床观察

目的 :观察养阴药物五子汤治疗高粘血症的疗效。方法 :筛选辨证为阴虚阳亢型的高粘血症患者 10 1例 ,按其基础病分为高血压病组 ( 48例 )、冠心病组 ( 2 8例 )、糖尿病组 ( 2 5例 ) ,均以女贞子、枸杞子、桑椹子、决明子、葶苈子为主组方治疗。各组均于治疗前后查血液流变学指标 ,观察其变化 ,作自身对照。结果 :治疗后各组红细胞压积、全血粘度较治疗前有显著差异 ( P<0 .0 5～ 0 .0 1) ;而血浆粘度、纤维蛋白原及血沉无显著差异 ( P>0 .0 5 )。高血压病组、冠心病组、糖尿病组的总有效率分别为 91.6 %、 89.2 %、 84.0 %。结论 :五子汤能够对阴虚阳亢型高粘血症患者的全血粘度、红细胞压积等指标产生良性影响。     

金纳多对2型糖尿病患者血液流变性和可溶性黏附分子的影响

目的 探讨银杏叶提取物金纳多(EGb761)对2型糖尿病患者血液流变性及可溶性黏附分子(sAM)的影响。方法 将67例2型糖尿病患者随机分为常规治疗组(33例)和金纳多治疗组(34例)，其中金纳多治疗组，在西医常规治疗基础上，加用金纳多治疗。另设健康对照组32例。观察治疗前后血液流变性及sAM的变化并与正常组比较。结果 糖尿病组的血液流变性及sAM均比正常组高，与常规治疗组相比，金纳多治疗组的血液流变性和sAM均显著下降。结论 金纳多能明显改善糖尿病患者的血液流变性，并使sAM下降。     

精制蝮蛇抗栓酶治疗糖尿病高粘血症

糖尿病血液流变学改变是糖尿病并发症的危险因素之一。而糖尿病合并症,特别是微血管病变,是糖尿病死亡的主要原因。因此降低糖尿病血液粘度的治疗具有极其重要的临床意义。我院用精制蝮蛇抗栓酶对30例糖尿病合并高粘血症患者进行治疗,并与常规组进行对比,现报道如下: 一、资料与方法 一般资料:按1981年全国糖尿病协作组会议的诊断标准,确诊为Ⅱ型糖尿病(NIDDM)且血液流变学测定指标均有显著异常的住院病人48例,随机分为治疗组30例及常规组18例。治疗组中男24例,女6例,糖尿病病程1.5—22y(12±5y)。年龄42—     

辨证施治活血化淤在血液流变性异常患者中的应用

目的研究不同的活血化淤方法对高粘滞血症的治疗效果。方法高粘滞血症患者分为对照组56例 ,单纯应用丹参、益母草、川芎、当归等活血化淤、改善血液流变学的中药 ;治疗组58例 ,在活血化淤的基础上结合中医辨证施治 ,将其分为气滞血淤型、气虚血淤型、寒凝血淤型、阴虚血淤型、痰淤互阻型 ,分别应用行气活血、补气活血、温经活血、养阴活血、祛痰活血方法治疗高粘滞血症。结果治疗组和对照组比较 ,两组临床疗效具有显著差异。结论应用中医辨证分型治疗高粘滞血症临床疗效明显优于单纯使用活血化淤药物     

2型糖尿病微血管病变患者血浆同型半胱氨酸、胱抑素C水平及血液流变学指标变化

目的:观察2型糖尿病(T2DM)微血管病变患者血浆同型半胱氨酸(Hcy)、胱抑素C(CysC)水平及血液流变学指标的变化。方法:T2DM患者120例,按有无微血管病变分为糖尿病无微血管病变组(A组,62例)和糖尿病并微血管病变组(B组,58例),检测两组病人的血浆Hcy、CysC水平和血液流变学指标并进行组间比较分析。结果:与A组比较,B组血浆Hcy、CysC、全血粘度、血浆粘度、红细胞压积、红细胞聚集指数均明显升高,差异有统计学意义(P<0.01)。结论:高Hcy、CysC及高粘血症参与了糖尿病微血管病变的发生和发展。     

血府逐瘀汤加减治疗92例高粘滞血症疗效分析

血 液粘滞异常综合征是一种常见临床综合征 ,分为血液高粘滞综合征和血液低粘滞综合征二大类 ,而临床最常见为血液高粘滞综合征 ,即高粘滞血症。按高粘滞血症的临床表现划分 ,应属于中医“血瘀”范畴。我们对 92例高粘滞血症应用古典经方血府逐瘀汤为主 ,随证加减治疗 ,取得较好效果 ,现报告如下。1　资料与方法1.1　临床资料本组 92例高粘滞血症患者 ,男 5 4例 ,女 38例 ,年龄 4 1～ 78岁 ,平均 5 7.2岁。其中冠心病 31例 ,高血压病 2 2例 ,脑梗塞 2 1例 ,糖尿病 18例。1.2　治疗方法以血府逐瘀汤为基本方随证加减 ,伴有痰湿者加陈皮、菖蒲…     

老年心脑血管疾病、糖尿病血液流变学改变

目的探讨老年冠心病、缺血性脑血管疾病、糖尿病患者血液流变学的改变是否存在差异性。方法随机选取老年冠心病95例 ,缺血性脑血管疾病93例 ,糖尿病90例 (其中合并冠心病40例 ) ,正常老年人50例。以LDYN6A型血流变测定仪测定全血粘度 (低切 ,中切 ,高切 ) ,血浆粘度 ,红细胞聚集性 ,红细胞压积 ,纤维蛋白原。运用SPSS软件行Dunnett检验。结果老年冠心病、缺血性脑血管疾病、糖尿病组全血粘度 (中切 ,高切 ) ,血浆粘度 ,红细胞压积 ,纤维蛋白原 ,红细胞电泳指数与正常对照组比较均差异显著(P<0.05)。而三组之间无显著差异。结论高血粘度和高纤维蛋白原血症为老年冠心病、缺血性脑血管疾病、糖尿病的危险因素。     

2型糖尿病并发冠心病相关因素临床分析(附40例报告)

目的 探讨2型糖尿病(T2DM)并发冠心病(CHD)的相关因素.方法 回顾性分析2008年6月～2010年6月来我院就诊的40例2型糖尿病患者的临床资料,根据是否合并冠心病分为两组,分别统计两组患者的各类因素及指标,分析2型糖尿病并发冠心病的相关因素.结果 2型糖尿病并发冠心病与患者的年龄、糖尿病病程、高血压、体重指数、空腹血清C肽、甘油三酯、血尿酸等因素有明显关系.结论 2型糖尿病患者在日常生活中应注重控制血压、体重、高胰岛素血症、高甘油三酯血症和高尿酸血症以预防并发冠心病.     

人B-CAM/Lu基因逆转录病毒载体的构建及其在L929细胞中的表达

目的 克隆人B-CAM/Lu基因,构建其逆转录病毒表达载体,获得稳定高表达B-CAM/Lu的L929细胞株.方法 RT-PCR技术克隆人B-CAM/Lu基因,并插入逆转录病毒载体pEGZ中,该重组逆转录病毒载体与pH456、pH460两个辅助病毒载体一起,共转染包装细胞293T,并感染L929细胞,经Zeocin筛选获得的细胞株通过RT-PCR、Western blot及间接免疫荧光鉴定细胞中B-CAM/Lu基因mRNA的转录和蛋白表达.结果 成功获得人B-CAM/Lu基因,测序正确,亚克隆至逆转录病毒载体pEGZ后,经转染筛选,获得的抗性L929细胞株通过RT-PCR和Western blot分析,检测到B-CAM/Lu mRNA的转录和目的 蛋白的表达,通过间接免疫荧光确定该蛋白定位表达在L929转基因细胞膜上.结论 成功克隆并构建了人B-CAM/Lu基因的重组逆转录病毒表达载体,获得稳定高表达B-CAM/Lu蛋白的L929细胞株,为将其作为免疫源,制备B-CAM/Lu单抗用于镰刀型红细胞病及一些肿瘤疾病的检测诊断打下了基础.     

Circulating adhesion molecules in sarcoidosis.

Sarcoidosis is a disease of unknown etiology characterized by non-caseating granulomata together with a number of systemic abnormalities. We have recently shown these include increased expression of the integrins CD11/CD18 on peripheral blood leucocytes. Here we have measured serum levels of the adhesion molecules intercellular adhesion molecule-1 (ICAM-1), E-selectin and vascular cell adhesion molecule-1 (VCAM-1) in 23 patients and 14 normal controls using antigen capture sandwich ELISAs. Median circulating E-selectin levels in the patients were nearly three times those of the controls (P < 0.0001, Mann-Whitney U-test), whilst ICAM-1 but not VCAM-1 levels were only slightly elevated. These results show that endothelial cell activation and shedding of E-selectin into the circulation are additional features of the pathology of sarcoidosis.     

Lymphatic development in mouse small intestine.

Lymphatic vessels in the small intestine serve as essential conduits for the absorption and transport of lipids from the intestine to the thoracic duct. Although the morphology and function of the intestinal lymphatic vasculature are well known, little is known about the embryonic development of these vessels. In this study, we examined development of lymphatic and blood vasculatures in the intestinal tube during mouse embryonic development by immunostaining with recently discovered molecular markers for lymphatic endothelial cells: LYVE-1, VEGFR3, Prox-1, and podoplanin. Immature lymphatics became detectable in mesentery, but not in intestinal tube, around E13.5-E14.5, while organized lymphatic vessel plexuses and capillaries were observed in intestinal tube and villi around E17.5. These lymphatic plexuses and capillaries in the intestinal tube appeared to be formed through an active branching process associated with activation of VEGFR3 and involvement of LYVE-1+ macrophages. Our data also reveal that the lymphatic vessels in the intestinal tube, unlike the blood vessels, have not originated from the mesoderm of intestine. All lymphatic vessels in the intestinal tube originated by extension of mesenteric lymphatic vessels through an active branching process. Although the formation of lymphatic vessels follows the formation of blood vessels in the intestine, a mature lymphatic vasculature is formed before birth. Together, our study reveals the temporal and spatial windows of intestinal lymphatic development during embryonic development in mouse.     

人受精相关抗原-1的基因克隆及原核表达

目的为了阐明免疫性不孕不育的原因,检测血清中存在的抗精子抗体的种类,构建重组人受精相关抗原-1（recombinant human Fertilization antigen-1,rhFA-1）的原核表达质粒并在大肠杆菌中诱导表达。方法采用RT-PCR法,从人睾丸组织总RNA中扩增获得人FA-1的cDNA,将其克隆入表达载体pBV220,构建人源性FA-1的重组原核表达质粒pBV220/FA-1。重组质粒经酶切和测序鉴定后,转化大肠杆菌JM109并在大肠杆菌中诱导表达目的蛋白。结果测序表明重组基因序列与人FA-1基因完全一致。SDS-PAGE电泳显示,表达产物的相对分子量为14.6KDa与预期结果相符。结论获得了人FA-1的编码基因,并在大肠杆菌中表达了人的FA-1蛋白。     

Soluble endothelium-associated adhesion molecules in patients with Graves' disease.

The targeting and recruitment of inflammatory cells to vascular endothelium in Graves' disease (GD) is mediated by intercellular adhesion molecule-1 (ICAM-1), endothelial leucocyte adhesion molecule-1 (ELAM-1), and vascular cell adhesion molecule-1 (VCAM-1). We have studied serum levels of soluble ICAM-1 (sICAM-1), soluble ELAM-1 (sELAM-1), and soluble VCAM-1 (sVCAM-1) in patients with GD (n = 21) and in patients with iodine-deficient goitre (IDG) (n = 23). The serum levels of sICAM-1 were markedly elevated in patients with GD before treatment with thiamazole (median 560 ng/ml versus 185 ng/ml in patients with IDG). In addition, elevated serum concentrations of sELAM-1 (median 85 ng/ml versus 33 ng/ml, respectively) and sVCAM-1 (median 42 ng/ml versus 15 ng/ml, respectively) were observed in patients with GD (P < 0.01 for all). The serum levels of sELAM-1 and sVCAM-1 dropped significantly after initiation of therapy and were within the normal range after 4, and 8 weeks of therapy, respectively. Serum levels of sICAM-1 were elevated even after 8 weeks of therapy. Serum levels of sVACM-1 and sICAM-1 correlated with the serum concentrations of anti-thyroid-stimulating hormone (TSH)-receptor antibodies (TSHR-R) (n = 21; r = 0.929 and r = 0.810, respectively) and anti-thyroid peroxidase antibodies (TPO-Ab) (n = 21; r = 0.673 and r = 0.750, respectively). However, no correlation between sELAM-1 and TPO-Ab, TSHR-R, and anti-thyroglobulin antibodies (Tg-Ab), respectively, could be found. In addition to thyroid hormones and autoantibodies, serum concentrations of sELAM-1 and sVCAM-1, but not sICAM-1, could be useful as clinical markers for disease activity.     

CMF1-Rb interaction promotes myogenesis in avian skeletal myoblasts.

CMF1 protein is expressed in developing striated muscle before the expression of contractile proteins, and depletion of CMF1 in myoblasts results in inability to express muscle-specific proteins. Previous studies of CMF1 identify a functional Rb-binding domain, which is conserved in the murine and human homologues. Here, we show that CMF1 binds Rb family members, while a CMF1 protein with deletion of the Rb-binding domain (Rb-del CMF1) does not. Myogenic cell lines over-expressing Rb-del CMF1 proliferate normally, but exhibit markedly impaired differentiation, including dramatically reduced contractile proteins gene expression and failure to fuse into myotubes. Furthermore, by quantitative real-time polymerase chain reaction, MyoD and Myf5 mRNA levels are comparable to wild-type, while myogenin and contractile protein mRNA levels are significantly attenuated. These data demonstrate that CMF1 regulates myocyte differentiation by interaction with Rb family members to induce expression of myogenic regulatory factors.     

Autoproliferation in HIV-1-infected patients undergoing active HIV-1-specific immunotherapy.

We have observed a treatment-associated autoproliferative response in cultured peripheral blood mononuclear cells (PBMC) of asymptomatic HIV-1-infected subjects receiving a gp120-depleted, inactivated HIV-1 antigen in incomplete Freund's adjuvant (IFA; HIV-1 Immunogen). The frequency and magnitude of the autoproliferative response appeared to be dose-related (P < 0.05), and was not observed in subjects receiving IFA alone. Immunophenotyping of the proliferating cells demonstrated the presence of both CD4+ and CD8+ lymphocytes, with the CD4+ blasts almost exclusively expressing the CD45RO+ phenotype. A comparison of this response with the HIV-1-specific antigen stimulation responses in this cohort revealed a significant correlation between increases in HIV-1-specific cell-mediated immunity and autoproliferation (r2 = 0.61, P < 0.001). These findings suggest that immunization with the HIV-1 Immunogen induces an autoproliferative response that may reflect changes in HIV-1-specific cell-mediated immunity in infected individuals.     

Decreased CD40 ligand induction in CD4 T cells and dysregulated IL-12 production during HIV infection.

During HIV infection various cytokines are overproduced in early stages, whereas in advanced disease cytokines of the T helper 1 type (e.g. interferon-gamma (IFN-gamma)) are selectively deficient. During antigenic stimulation, the production of type-1 cytokines is enhanced by IL-12, secreted by antigen-presenting cells (APC) after their interaction with activated CD4 T cells. Two factors are essential in this process: priming APC with IFN-gamma and triggering the CD40 receptor on APC by CD40 ligand (CD40L). In view of the importance of this pathway, we compared its regulation in HIV-infected and control subjects. After cross-linking of the T cell receptor (TCR)/CD3 complex, the proportional expression of CD40L was similar on CD4+ T cells from controls and from patients with high circulating CD4 T counts (> 500/microl), but CD40L up-regulation was significantly reduced in patients with more advanced disease. Simultaneous triggering of the costimulatory receptor CD28 on T cells through its natural ligand CD80 partly corrected the CD40L defect in patients with intermediate CD4 T counts (200-500), but not in AIDS patients. Early production of IFN-gamma was preserved in lymphocytes from HIV+ patients. The expression of CD40 on peripheral monocytes from HIV+ subjects was increased in a disease stage-related fashion. Stimulation of mononuclear cells through cell-bound CD40L and soluble IFN-gamma induced significantly higher IL-12 in cultures from patients with > 200 circulating CD4 T cells, whereas IL-12 production was marginally decreased in cultures from patients with < 200 CD4 T cells, compared with healthy control cultures. In conclusion, our data suggest that impaired CD40L induction on CD4 T cells contributes to deficient type-1 responses through decreased IL-12 production in AIDS infection, whereas enhanced CD40-mediated IL-12 production in less advanced stages might contribute to increased levels of various cytokines in early disease     

Transcription Factor PU.1 Represses and Activates Gene Expression in Early T Cells by Redirecting Partner Transcription Factor Binding

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