Architectural remodelling in lungs of rabbits induced by type V collagen immunization: a preliminary morphologic model to study diffuse connective tissue diseases

The pathogenesis of diffuse connective tissue diseases (DCTD) is still unknown and has been extensively studied regarding its autoimmunity aspects related to extracellular matrix (ECM) remodelling, with an emphasis on the collagens at the inflammatory site. The present paper describes the pulmonary architectural and repair/remodelling responses to injury after immunization of rabbits with human type V collagen. The animal model consisted of rabbits immunized with collagen mixed with Freund's adjuvant and sacrificed 7, 15, 30, 75, and 120 days after the first of four doses of antigen. Pulmonary architecture remodelling response was evaluated by histology, morphometry, and the immunofluorescence method, according to compartments of reference (parenchyma and interstitium) and injury: 1 inflammation (polymorphonuclear and mononuclear cells); 2-repair (fibrosis) and 3-ECM remodelling (collagen system). The results showed an intense inflammatory involvement of the pulmonary vascular and bronchiolar parenchyma, characterized by increased wall thickness in small arteries, infiltrations by pseudoeosinophils, and mononuclear cells. Progressive remodelling of the pulmonary ECM was characterized by collagen deposition in the septal and bronchovascular interstitium, especially in rabbits sacrifices at 75 and 120 days. The ECM remodelling process was not reproduced when rabbits were inoculated with collagen types I and III. We conclude that the model reproduces morphologic changes similar to those observed in many DCTD, encouraging realization of other experiments to gain a better understanding of the pathogenesis of these diseases.     

企业员工应激源的因素结构研究

目的 :该研究旨在确立企业员工应激源的因素结构。方法 :经过对 394 6名被试的探索性因素分析 ,提出企业员工应激源的 9因素结构。结果 :因素分别命名为职业发展、住房问题、工作特征、社会环境、人际关系、经济收入、子女问题、组织气氛和夫妻关系。结论 :企业员工应激源的 9因素结构获得了验证性因素分析的支持。     

Immunohistochemical differentiation between lymphangiographically verified lymphatic vessels and blood vessels

Summary In order to investigate the antigen profile in human lymphatic vessels when compared with blood vessels, postmortem retrograde lymphangiography was done via the thoracic duct on six patients. Formalin fixed, paraffin embedded tissue was stained immunohistochemically for Factor VIII-Related antigen (F VIII R:Ag), with Ulex Europaeus 1 lectin (UEA-1) and for laminin. The results show that the endothelium of blood vessels and lymphatics at all levels of the lymphatic system react positively following staining for Factor VIII-R:Ag and with UEA-1 lectin. The staining for F VIII R:Ag was generally weaker in the endothelial cells lining lymphatic vessels. Staining for the basement membrane component laminin can be used to distinguish lymphatic capillaries and smaller lymphatic collecting vessels from blood vessels.     

Activated protein C resistance shows an association with pregnancy-induced hypertension

A common mutation in the factor V gene, the Leiden mutation, is the most frequent genetic cause of resistance to activated protein C (APC). Recent studies have shown that the prevalence of APC resistance is associated with severe pregnancy-induced hypertension (PIH). Our objective was to determine whether the factor V Leiden mutation is more prevalent in patients who developed severe PIH than in normotensive pregnant women. In 70 women with a history of severe PIH, of whom 15 had pre-eclampsia, we investigated common coagulation factors as well as APC resistance (factor V related). We found that seven of these 70 women showed low values for APC. Out of these, five were heterozygous and none was homozygous for factor V Leiden mutation. In a control group of normotensive pregnant women we found a 3.0% rate of APC resistance and a 3.0% rate of carriers of the Leiden mutation. These results indicate a significantly higher prevalence of both APC resistance and factor V Leiden mutation in women with severe PIH. Placental infarctions and micro-embolisms are considered to be one of the principle pathophysiological changes in severe PIH. Our results suggest that APC resistance is a risk factor for severe PIH, in addition to its well-known role in macrothrombo-embolism.     

2型糖尿病患者血清von Willebrand因子变化与微血管并发症的关系

目的 :探讨 2型糖尿病患者的微血管内皮细胞功能损伤与微血管并发症之间的关系。方法 :从 3 3 4名 2型糖尿病患者中选择合并微血管并发症但未合并大血管并发症者 3 2人作为微血管并发症组 ,并选择年龄与之匹配的无大血管及微血管并发症 55人作为无并发症组 ,观察二组患者血清vonWillebrand因子 (vWF)水平 ,并与年龄相接近的正常对照组 ( 4 0例 )比较。结果 :血清vWF水平正常对照组 0 .92U± 0 .44U/ml;无并发症组 1.15U± 0 .42U /ml ;微血管并发症组 1.3 7U± 0 .44U/ml;三组之间均有显著性差异 (P <0 .0 5～ 0 .0 1)。多因素Logistic回归分析表明vWF、空腹血糖分别与糖尿病人是否合并微血管病变显著相关 (ExpB分别为 3 .0 2 3 ,1.3 3 7,P <0 .0 5～ 0 .0 1) ,以vWF为应变量的多元逐步回归分析表明年龄、糖尿病病程、甘油三酯分别与vWF呈显著独立正相关 (B =0 .53 ,0 .3 5,0 .2 9,P <0 .0 5～ 0 .0 1)。结论 :在糖尿病患者中存在不同程度的微血管内皮细胞的损伤 ,此变化随着微血管并发症的进展呈进行性加重。以vWF升高所反映的微血管内皮细胞损伤是一项值得临床推广的研究方法     

The effect of AVP‐V1 receptor stimulation on local GFR in the rat kidney

Aim: Arginine vasopressin (AVP) might influence urinary concentration ability by altering the intrarenal distribution of glomerular filtration rate (GFR). Methods: To study this possibility we have measured the intracortical distribution of GFR following acute AVP‐V₁ receptor stimulation in anaesthetized female Sprague–Dawley (SPD) rats during euvolemia and water diuresis by the aprotinin method, allowing two consecutive measurements of zonal GFR in the same kidney. Results: Acute i.v. bolus injection of 50 ng V₁ receptor agonist ([Phe², Ile³, Orn⁸]‐vasopressin) followed by a continuous infusion of 5 ng min^?1 in euvolemic rats reduced GFR by 25% in outer cortex (OC), 20% in middle cortex (MC) and 19% in inner cortex (IC) relative to vehicle infusion (all P < 0.05). In water diuretic rats V₁ receptor agonist reduced GFR by 22% in OC, 10% in MC and 11% in IC relative to vehicle infusion (P < 0.05). GFR decreased slightly more in OC than in MC and IC in both euvolemic and water diuretic rats (P < 0.05) indicating a distribution of GFR towards MC and IC. Acute infusion of the selective non‐peptide V₁ receptor antagonist OPC‐21268 in euvolemic rats reduced GFR by 14% in OC, 13% in MC and 11% in IC relative to vehicle infusion (P < 0.05), with no significant difference between the layers. Conclusions: The change in distribution of GFR not only between OC and IC, but also between OC and MC suggests that the afferent/efferent arterioles and not the medullary vasa recta is the main site of resistance change. We conclude that acute i.v. infusion of V₁ receptor agonist in high doses reduces GFR more in superficial than in deep cortex in both euvolemic and water diuretic rats and that this may be of some importance for water conservation, adding to the V₂‐ receptor effect on water permeability of the collecting ducts.     

Identification of histiocytic reticulum cells by the immunohistochemical demonstration of factor XIII (F-XIIIa) in human lymph nodes

Morphologically and enzyme histochemically distinguishable tissue macrophages and stromal cells of human reactive lymph nodes were characterized by the cytoplasmic presence of the subunit A of factor XIII and by the expression of surface antigenic determinants reacting with monoclonal antibodies directed against monocyte/macrophage populations (Mo 1, Leu M3) and HLA-DR antigens. The distribution of F-XIIIa positive cells was studied on formaldehyde-fixed paraffin-embedded sections with immunoperoxidase techniques. established on cryostat section with double immunofluorescence. Alpha-Naphthyl acetate esterase (ANAE) reaction was The immunophenotype was established on cryostat sections with double immunofluorescence. Alpha-Naphthyl acetate esterase (ANAE) reaction was carried out on these cryostat sections to identify tissue macrophages. The antibody against F-XIIIa detected histiocytes in both intra- and extra-sinusoidal locations which were ANAE+, Mo 1+, Leu M3+ and HLA-DR-. F-XIIIa was also present in fibroblast-like mesenchymal cells with the following phenotypic characteristics: ANAE-, Mo 1+, Leu M3+ and HLA-DR+. The anti F-XIIIa antibody did not stain lymphoid cells, granulocytes, epithelial cells, endothelial cells and mast cells. The immunohistochemical detection of F-XIIIa works on formaldehyde-fixed paraffin-embedded sections. The most promising application seems to be the identification of histiocytes in lymphoid and histiocytic proliferations.     

Coreceptor Switch of [MLV(SIVagm)] pseudotype vectors by V3-loop exchange

Retroviral vectors derived from murine leukemia virus (MLV) have been pseudotyped with a variant of the envelope glycoprotein (Env) of nonpathogenic simian immunodeficiency virus from African green monkeys (SIVagm) to result in [MLV(SIVagm-wt)] vector particles. The variant env gene encodes a full-length surface envelope glycoprotein (SU) and a C-terminally truncated transmembrane protein (TM). To change the coreceptor usage of this vector from CCR5 to CXCR4, which is predominant on human CD4-positive lymphocytes, the putative V3-loop of SIVagm SU was replaced by that of the T cell tropic HIV-1 variant BH10. The resulting [MLV(SIVagm-X4)] vectors were shown to specifically transduce CD4/CXCR4-positive cell lines, demonstrating the equivalent function in cell entry and choice of coreceptor usage of the V3-loops of SIVagm and HIV-1. These modified vectors were able to transduce primary human lymphocytes and were resistant to neutralization by sera from HIV-1-infected individuals. The [MLV(SIVagm-X4)] pseudotype vector generated is thus a promising candidate vector, e.g., for in vivo gene therapy of HIV-1 infection.     

企业员工应对方式与心理健康之间的关系

目的：验证不同应对方式对心理健康的单独与共同影响。方法：对4745名被试用分层回归的方法分析不同应对方式对心理健康的单独影响和交互作用。结论：单独使用“消极应对”的应对方式,对心理健康水平存在不利影响;而单独使用“积极应对”的应对方式能在一定程度上改善心理健康水平。“消极应对”与“积极应对”两种应对方式结合使用能显著改善心理健康水平,比单独使用这两种应对方式对心理健康更有利。     

人类免疫缺陷病毒包膜糖蛋白V3区对细胞结合能力的研究

目的：研究人类免疫缺陷病毒（ＨＩＶ）不同亲嗜株包膜糖蛋白Ｖ３区结合于靶细胞的能力。方法：合成来源于不同嗜性ＨＩＶ－１Ｖ３区的生物素标记和非标记的多肽。采用流式细胞计数分析生物素化的 Ｖ３多肽对细胞的结合能力以及细胞表面的结合配体。结果：ＨＩＶ－１Ｘ４　亲嗜株ＩＩＩＢＶ３区能结合于多种细胞的表面，包括辅助受体ＣＸＣＲ４；竞争实验结果显示蛋白酶抑制剂能抑制该结合。Ｒ５亲嗜株 ＡＤＡ Ｖ３区只极微弱地结合于外周血单核细胞和表达ＣＣＲ５ 的人星形胶质细胞表面。结论：不同嗜性ＨＩＶ－１Ｖ３区结合于细胞表面的能力不同从亲嗜株Ｖ３区直接结合于细胞表面并被其自身所增强，其靶分子至少包括辅助受体 ＣＸＣＲ４和蛋白酶分子；而Ｒ５亲嗜株 ＡＤＡ Ｖ３区则不结合于 ＣＣＲ５和蛋白酶。