干细胞诱导分化为胰腺β细胞的研究现状

学术背景：干细胞体外诱导分化成的胰岛细胞可以发挥对血糖的生理性调节作用。大量研究证明可以从胚胎干细胞、胰腺干细胞、骨髓间充质干细胞、神经干细胞、肝脏干细胞或脐血干细胞等诱导分化出胰腺β细胞。目的：深入认识干细胞诱导分化为胰腺β细胞的研究现状。检索策略：由该论文的研究人员应用计算机检索Pubmed数据库1990—01，2006—07的相关文献，检索词“stem cell，differenliation，culture，pancreas”，并限定文章语言种类为English。同时计算机检索维普数据库2000-01，2006—07的相关文献，检索词“干细胞，胰岛，诱导分化”，并限定文章语言种类为中文。共检索到142篇文献，对资料进行初审，纳入标准：①与干细胞和干细胞向胰腺β细胞诱导分化相关的文章。②若内容相似，选取首次实验报告及近5年较权威杂志发表的文章。排除标准：重复或类似的研究。文献评价：文献的来源主要是通过对干细胞向胰腺β细胞诱导分化方面内容进行汇总分析。所选用的30篇文献中，1篇为综述，其余均为临床或基础实验研究。资料综合：胰岛移植是目前治疗Ⅰ型糖尿病和部分Ⅱ型糖尿病效果最理想的方法。由干细胞诱导分化得到的胰腺β细胞可以发挥调节血糖的作用，在许多小鼠糖尿病模型研究中起到了降低血糖的作用。目前用于诱导分化为胰腺β细胞的干细胞来源包括胚胎干细胞、胰腺干细胞、骨髓间充质干细胞、神经干细胞、肝脏干细胞或脐血干细胞等。在不同的干细胞诱导分化为胰腺β细胞的研究中，分为体内和体外两种诱导分化方法，而体外诱导法多数采用分步诱导的方式，也有部分实验利用基因技术的方法进行诱导。结论：不同来源的干细胞可以在体外通过多种方法诱导分化得到胰腺β细胞，但得到的胰腺β细胞数量及其诱导分化方法还有待进一步研究。     

终末期肝病模型在肝病中的应用进展

终末期肝病模型(modelforend-stageliverdisease,MELD)是近年来新创立的判断晚期肝病病情的方法,最初他是用于评估行经颈静脉肝内门体分流术(transjugularintrahepaticportosystemicshunt,TIPS)后患者的生存率,目前已被广泛应用于肝移植、终末期肝病患者预后、评估肝癌患者术后(手术切除癌灶或局部治疗等)生存率等方面,现认为MELD模型可以有效的预测终末期肝病患者的预后,能准确的反映病情的危急程度.     

老年肾病综合征28例

1 临床资料 2002/2004年行肾活检的老年(≥60岁)住院肾病综合征患者28(男19,女9)例,按WHO标准进行病理学分类(表1).全部病例给予强的松每日1 mg/kg,晨顿服,8～12 wk后渐减量至最小量维持治疗.9例患者因激素反应欠佳而加用环磷酰胺治疗.完全缓解: 水肿消退,24 h尿蛋白＜300 mg;部分缓解: 水肿消退,24 h尿蛋白300～1500 mg;无效: 临床征状改善或无改善,肾功能恶化(表1,2).     

Immunological studies in placentas with villitis of unknown etiology: complement components and immunoglobulins in chorionic villi.

Villitis of unknown etiology (VUE) is a common placental lesion and complement-fixing immune complexes is one of the mechanisms proposed for its development. We examined 16 placentas with VUE and 16 without VUE by immunofluorescence in order to compare the distribution and amount of C1q, C3d, IgG and IgM in the chorionic villi between the two groups. We found both in cases with and without VUE a distribution of the complement components and immunoglobulins similar to that described in normal placentas. The amount of deposit was also not significantly different in the two groups. Only the inflamed villi showed an abnormal distribution of C1q which was present diffusely in the stroma of these villi.     

Relationship between disease severity and inflammatory markers in cystic fibrosis

To evaluate the clinical use of measuring neutrophil, lymphocyte, and eosinophil activities, serum myeloperoxidase (MPO), soluble interleukin-2 receptors (sIL-2R), and eosinophil cationic protein (ECP) were measured in 98 patients with cystic fibrosis and in 85 healthy children. Serum concentrations of MPO, sIL-2R, and ECP were increased in patients with cystic fibrosis (median 807 micrograms/l, 4452 pg/ml, 48.8 micrograms/l, respectively) compared with the controls (median 319 micrograms/l, 2743 pg/ml, 9.4 micrograms/l). ECP concentrations, but not serum MPO or sIL-2R, were significantly related to disease severity assessed by the Shwachman-Kulczycki score and by pulmonary function (forced expiratory volume in one second % predicted). Neither ECP nor sIL-2R was influenced by Pseudomonas aeruginosa infection, acute pulmonary exacerbation, or atopy. Serum MPO, however, was strongly correlated with acute pulmonary exacerbation. In the light of these findings the measurement of serum ECP might thus be used for clinical monitoring and for assessing disease severity in cystic fibrosis. The measurement of serum MPO and sIL-2R did not correlate with the disease severity.     

脉压水平与经皮冠状动脉介入术患者的危险分层及预后评价

目的:通过对接受经皮冠状动脉介入治疗患者的临床特征,围手术期并发症和远期的疗效分析,了解脉压水平与经皮冠状动脉介入术患者的危险分层和预后关系。方法:选择2003-10/2005-10就诊于解放军第三○五医院心脏介入中心符合冠心病诊断标准并接受经皮冠状动脉介入治疗的631例患者。外周肱动脉压力测定收缩压、舒张压,脉压水平通过收缩压与舒张压差表示,冠状动脉病变的严重程度用冠脉病变积分表示。采用横断面前瞻性多变量观察研究,根据脉压>65mm Hg(1mm Hg=0.133kPa)和≤65mm Hg进行分组,其中脉压>65mm Hg组154例,男110例,女44例;脉压≤65mm Hg组477例,男288例,女189例。观察患者临床特征,随访[随访时间(18.6±4.3)个月]主要心血管事件发生率。结果:631例患者均进入结果分析。①与脉压≤65mm Hg组比较,脉压>65mmHg组年龄偏大,男性多见,高血压病史和糖尿病史多,C型病变和三支病变常见,冠脉病变积分高。②脉压>65mmHg组围手术期并发症发生率、住院期非致死性心肌梗死发生率和远期心源性死亡发生率显著高于脉压≤65mmHg组(16.8%,8.8%;5.2%,2.3%;1.3%,0.8%,P均<0.05)。③多因素logistic分析冠脉病变严重程度与脉压、年龄、糖尿病有正相关,OR分别为1.181(95%CI1.120～1.321),1.012(95%CI1.009～1.213),1.273(95%CI1.042～1.359)。结论:脉压与冠状动脉病变的严重程度密切相关,与经皮冠状动脉介入术围手术期及远期不良心血管事件发生率增加密切相关,可作为全身心血管疾病的一个危险信号,指导早期干预。     

Regulation of human monocyte surface antigen expression. I. Up- modulation of Mo3e antigen expression on U-937 and HL-60 cells stimulated by pharmacologic activators of protein kinase C

Mo3e is a protein (p 50,80) that is expressed on the surface of human monocytic cells after exposure in vitro to soluble activating factors that include bacterial lipopolysaccharide, muramyl dipeptide, and phorbol myristate acetate (PMA). The surface expression of Mo3e may represent a cellular event that occurs in response to the formation of "secondary messengers" that include diacylglycerol, inositol trisphosphate, and calcium ions. This postulate is based on the stimulatory effect of agents that can mimic the activity of endogenous diacylglycerol (PMA and other biologically active phorbol compounds, mezerein, and L-alpha-1,2 dioctanoylglycerol) and inositol trisphosphate (ionomycin) on Mo3e expression by U-937 and HL-60 cells. The inhibitory effect of phospholipid-active calmodulin inhibitors (trifluoperazine, chlorpromazine, and dibucaine), calcium antagonists (nicardipine and TMB-8), and EGTA further support the involvement of phospholipid- and calcium-dependent protein kinase (protein kinase C) and calcium ions in the up-modulation of Mo3e surface expression.     

The expression of the Hodgkin's disease associated antigen Ki-1 in reactive and neoplastic lymphoid tissue: evidence that Reed-Sternberg cells and histiocytic malignancies are derived from activated lymphoid cells

Ki-1 is a monoclonal antibody (raised against a Hodgkin's disease- derived cell line) that, in biopsy tissue affected by Hodgkin's disease, reacts selectively with Reed-Sternberg cells. The expression of Ki-1 antigen has been analyzed by immunocytochemical techniques in a wide range of human tissue and cell samples, including fetal tissue, malignant lymphomas (290 cases), and mitogen- and virus-transformed peripheral blood lymphocytes. The antigen was detectable on a variable proportion of cells in all cases of lymphomatoid papulosis and angio- immunoblastic lymphadenopathy and in 28% of the cases of peripheral T cell lymphomas (including lympho-epithelioid lymphomas). It was also expressed (more strongly) on tumor cells in 45 cases of diffuse large- cell lymphoma, most of which had originally been diagnosed as malignant histiocytosis or anaplastic carcinoma, because of their bizarre morphology. However, all of these cases lacked macrophage and epithelial antigens. Thirty-five cases expressed T cell-related antigens (associated in nine cases with the coexpression of B cell- related antigens), seven bore B cell-related antigens alone, and three were devoid of T and B cell markers. DNA hybridization with a JH specific probe showed a germline configuration in 11 cases of T cell phenotype, in two cases lacking T and B cell antigens, and in one case of mixed T/B phenotype, while rearrangement was found in two cases of clear B cell type and in one mixed T/B case. Expression of the Ki-1 antigen could be induced, together with interleukin 2 (IL 2) receptor, on normal lymphoid cells of both T and B cell type by exposure to phytohemagglutinin, human T leukemia viruses, Epstein-Barr virus, or Staphylococcus aureus. The results obtained indicate that Ki-1 antigen is an inducible lymphoid-associated molecule that identifies a group of hitherto poorly characterized normal and neoplastic large lymphoid cells. Tumors comprised solely of these cells show both morphological and immunological similarities to the neoplastic cells in Hodgkin's disease. This suggests that both disorders represent the neoplastic proliferation of activated lymphoid cells of either T cell or, less commonly, B cell origin. Disorders in which only a minority of cells express Ki-1 antigen (lymphomatoid papulosis, angio-immunoblastic lymphadenopathy, and certain T cell lymphomas) probably represent lesions in which only some of the abnormal cells have transformed into an "activation state." In direct support of this view is the finding that the Ki-1 expression in these lesions is accompanied by the expression of HLA-DR and IL 2 receptors.