基于太平洋甲胁虱裂化线粒体基因组推测甲胁虱属祖先线粒体核型

[目的]动物典型的单一染色体线粒体基因组在甲胁虱属Hoplopleura已裂化成多个线粒体微环染色体.本研究旨在通过测定太平洋甲胁虱Hoplopleura pacifica的线粒体基因组来推测甲胁虱属祖先线粒体核型.[方法]利用Illumina HiSeq X Ten高通量测序技术对太平洋甲胁虱裂化线粒体基因组进行测定...     

VEGF受体功能研究进展

血管内皮生长因子受体（VEGFR）调控心血管系统的发育。VEGFR1对于造血祖细胞的招募及单核巨噬细胞的迁移是必需的;VEGFR2、VEGFR3在调控血管及淋巴管内皮细胞的功能时发挥重要作用,而现在很多研究都聚焦于阻断VEGFR信号通路以达到阻断肿瘤血管生长的目的。     

Proliferation of pulmonary endothelial cells: Time-lapse cinematography of growth to confluence and restitution of monolayer after wounding

A fundamental characteristic of vascular endothelium is that it exists as a monolayer, a condition that must be met in both vascular growth and repair. Maintenance of the monolayer is important both for the exchange of nutrients and for interactions between blood solutes and endothelial enzymes and transport systems. We have used time-lapse cinematography to compare proliferative behavior of bovine pulmonary endothelial cells in (1) establisment of a monolayer from a low-density seed (7.5 × 10⁴ cells in a 60 mm dish) and (2) restitution of a confluent monolayer (approx. 2.9 × 10⁶ cells in a 60 mm dish) following a mechanical wound (removal of cells from an area 5 × 15 mm by scraping). Culture 2 was not refed after wounding. In culture 2, approx. 30% of the cells accounted for repopulation (confluence in 40 hr). In culture I, all cells entered into division. Participating cells of culture 2 began division immediately (69 divisions/filmed area in 10 hr, vs. four divisions in culture I). Interdivision times (IDT) were longer and relatively constant in culture I until near confluence; none were < 10 h, whereas in 2, 24% of the IDT's were ≤ 10 hr. Remarkably, IDTs of culture 2 decreased steadily until confluence was re-established. Cell migration in culture 1 was multidirectional while direction of migration in culture 2 was always into the wound area. Mean migration rate (MIG) in culture 2 was related to the site of origin of the cells, those dividing farthest from the unwounded area had fastest MIGs. Neither culture formed more than a single layer of cells. Although the cell kinetics of cultures 1 and 2 differed, the same goal, confluence, was achieved in either case.     

凝血酶与血管内皮细胞

凝血酶不仅在凝血过程中起主导作用,还可以引发多种凝血酶受体介导的分子和细胞间相互作用,在动脉粥样硬化和再狭窄形成中起着重要的作用。现就凝血酶及其受体的特性,以及对血管内皮细胞的作用,包括通透性改变、内皮生长因子、基质金属蛋白酶、黏附分子表达作一综述。     

Parkinson's disease-associated DJ-1 mutations impair mitochondrial dynamics and cause mitochondrial dysfunction

Mitochondrial dysfunction represents a critical event during the pathogenesis of Parkinson's disease (PD) and expanding evidences demonstrate that an altered balance in mitochondrial fission/fusion is likely an important mechanism leading to mitochondrial and neuronal dysfunction/degeneration. In this study, we investigated whether DJ-1 is involved in the regulation of mitochondrial dynamics and function in neuronal cells. Confocal and electron microscopic analysis demonstrated that M17 human neuroblastoma cells over-expressing wild-type DJ-1 (WT DJ-1 cells) displayed elongated mitochondria while M17 cells over-expressing PD-associated DJ-1 mutants (R98Q, D149A and L166P) (mutant DJ-1 cells) showed significant increase of fragmented mitochondria. Similar mitochondrial fragmentation was also noted in primary hippocampal neurons over-expressing PD-associated mutant forms of DJ-1. Functional analysis revealed that over-expression of PD-associated DJ-1 mutants resulted in mitochondria dysfunction and increased neuronal vulnerability to oxidative stress (H(2) O(2)) or neurotoxin. Further immunoblot studies demonstrated that levels of dynamin-like protein (DLP1), also known as Drp1, a regulator of mitochondrial fission, was significantly decreased in WT DJ-1 cells but increased in mutant DJ-1 cells. Importantly, DLP1 knockdown in these mutant DJ-1 cells rescued the abnormal mitochondria morphology and all associated mitochondria/neuronal dysfunction. Taken together, these studies suggest that DJ-1 is involved in the regulation of mitochondrial dynamics through modulation of DLP1 expression and PD-associated DJ-1 mutations may cause PD by impairing mitochondrial dynamics and function.     

血管内皮生长因子受体的结构与功能

血管内皮生长因子(VEGF)受体是存在于血管内皮细胞,介导内皮细胞增殖分化的跨膜受体.研究较多的有两种VEGF特异受体:Flt和KDR.Flt和KDR的基因结构及染色体定位已基本确定,这二者均属RTK Ⅲ型受体,结构相似.细胞外区均有7个类似免疫球蛋白结构,细胞内区催化域均有酪氨酸激酶插入区.当VEGF与受体结合时,引起受体自身的磷酸化,发生细胞内反应.在血管发生与生长、创伤修复、炎症、肿瘤和某些血管疾病中起重要作用.     

定期转种法和低温冷冻法保藏致病真菌活性的能力比较

定期转种法和低温冷冻保存法是临床实验室最常用的两种真菌保存方法,为比较两种方法保藏致病真菌活性的能力,本研究使用两种保藏方法对实验室689株致病真菌保藏5年后进行检测。定期转种法是将菌落接种于马铃薯斜面培养基并将其储存在4℃冰箱,每6个月转种1次。低温冷冻法是挑取马铃薯斜面培养基上生长良好的菌落于无菌10%甘油中,放置在-80℃储存。保藏5年后,将两种方法保藏的菌株转种复苏,比较菌株的复活率。对于念珠菌属Candida、新生隐球菌Cryptococcus neoformans、毛癣菌属Trichophyton、曲霉属Aspergillus和孢子丝菌属Sporothirix真菌,两种方法的菌株复活率无统计学差异;对于小孢子菌属Microsporum真菌和马尔尼菲蓝状菌Talaromyces marneffei,使用低温冷冻法保藏的菌株复活率高于定期转种法保藏的菌株复活率;对于着色霉属Fonsecaea真菌,低温冷冻法保藏的菌株复活率低于定期转种法保藏的菌株复活率。因此,我们认为对于常见致病真菌的长期保藏,使用10%甘油作为保护剂的低温冷冻法优于定期转种法,但其不适用于着色霉属Fonsecaea真菌的长期保藏。     

缺氧条件下血管活性因子对血管内皮细胞中VEGF表达的影响

 探讨在缺氧条件下人脐静脉血管内皮细胞对血管内皮生长因子 (vascular endothelialgrowth factor,VEGF)表达及缩血管活性物质内皮素 (ET)、舒血管活性物质一氧化氮 (NO)和 NO抑制剂 LNNA对 VEGF基因表达的影响 .体外培养人脐静脉血管内皮细胞 ,经缺氧及血管活性物质处理 .Northern杂交、酶联免疫检测和计算机图象分析等观察 VEGF m RNA和蛋白表达水平 .发现缺氧 6h内皮细胞可见 VEGF表达 .ET可促进 VEGF m RNA的表达 ,NO可明显抑制 VEGFm RNA的表达 ,NO抑制剂 LNNA也影响 VEGF m RNA的表达 .ELISA检测 VEGF蛋白水平分别为 6h组 8.2± 1 .1 ng/ L,ET+6h组 9.37± 1 .0 2 ng/ L,NO+6h组 2 .86± 0 .91 ng/ L,L - NNA+6h组 1 4.75± 1 .87ng/ L.缺氧可诱导人脐静脉血管内皮细胞分泌 VEGF并受血管活性物质ET和 NO的调控 ,ET促进其表达 ,NO抑制其表达 .     

皂苷类成分对血管内皮细胞功能的调节作用研究进展

血管内皮细胞在维持血管生理稳态中发挥了重要的作用,其功能障碍是动脉粥样硬化、冠心病、脑卒中、肿瘤等多种重大疾病发生发展的病理基础,调节血管内皮细胞功能是防治上述疾病的主要途径之一。大量研究表明,皂苷类成分可通过改善血管内皮功能达到治疗疾病的目的。综述了近年来报道的皂苷类成分调节血管内皮功能的研究进展,旨在为皂苷类成分作用机制的阐明和相关重大疾病的防治提供一定参考。     

Cadmium induced Drp1-dependent mitochondrial fragmentation by disturbing calcium homeostasis in its hepatotoxicity

Mitochondria are critical targets in the hepatotoxicity of cadmium (Cd). Abnormal mitochondrial dynamics have been increasingly implicated in mitochondrial dysfunction in pathophysiological conditions. Therefore, our study aimed to investigate the effects and underlying mechanism of Cd on mitochondrial dynamics during hepatotoxicity. In the L02 liver cell lines, 12 μM cadmium chloride (CdCl₂) exposure induced excessive mitochondrial fragmentation as early as 3 h post-treatment with Cd, which preceded the mitochondrial dysfunction such as reactive oxygen species (ROS) overproduction, mitochondrial membrane potential (ΔΨm) loss and ATP reduction. Concurrent to mitochondrial fragmentation, CdCl₂ treatment increased the protein levels of dynamin-related protein (Drp1) and promoted the recruitment of Drp1 into mitochondria. Strikingly, mitochondrial fragmentation also occurred in the liver tissue of rats exposed to CdCl₂, accompanied by enhanced recruitment of Drp1 into mitochondria. Moreover, in L02 cells, Drp1 silencing could effectively reverse Cd-induced mitochondrial fragmentation and mitochondrial dysfunction. Furthermore, the increased expression and mitochondrial recruitment of Drp1 were tightly related to the disturbance of calcium homeostasis, which could be prevented by both chelating [Ca²⁺]_i and inhibiting [Ca²⁺]_m uptake. Overall, our study indicated that Cd induced Drp1-dependent mitochondrial fragmentation by disturbing calcium homeostasis to promote hepatotoxicity. Manipulation of Drp1 may be the potential avenue for developing novel strategies to protect against cadmium-induced hepatotoxicity.     

Oxidative Damage and Fragmentation of Mitochondrial DNA in Cellular Apoptosis

The molecular genetics and bioenergetics of oxidative damage, fragmentation, and fragility of mitochondrial DNA in cellular apoptosis is reviewed in connection with the redox mechanism of ageing.     

The Banking of Arterial Allografts in the United Kingdom. A Technical and Clinical Review

The standard graft materials for reconstructive vascular surgery are autologous vessels and synthetic prostheses. However, the clinical results are unsatisfactory when the diameter of the required graft is less than 6mm and attention has therefore been directed to the possibility of using vascular allografts when autologous conduits are not available. In this review, we consider the evidence that cryopreserved allogeneic vessels might meet this need. Other factors being equal, the literature suggests that arteries will give superior performance to veins when grafted into the arterial circulation. Conventional cryopreservation techniques have been developed and these can provide structurally intact and functional small elastic arteries in animal experiments. We conclude that cryopreservation per se produces only modest injury which may well be recoverable following grafting. However, both experimental and clinical studies suggest that immunological injury is a greater problem. Nevertheless, the general indication is that appropriate risk-benefit analysis in individual cases will justify the clinical use of cryopreserved allograft vessels. Immunosuppression with careful immunological monitoring may be justified in the more desperate clinical situations. Finally we conclude that the existing tissue bank network in the United Kingdom is well placed to provide surgeons with such tissue.