BACKGROUND & AIMS: :Over the past decade, the old idea that the bone marrow contains endothelial cell precursors has become an area of renewed interest. While some still believe that there are no endothelial precursors in the blood, even among those who do, there is no consensus as to what they are or what they do. In this review, we describe the problems in identifying endothelial cells and conclude that expression of endothelial nitric oxide synthase may be the most reliable antigenic indicator of the phenotype. The evidence for two different classes of endothelial precursors is also presented. We suggest that, though there is no single endothelial cell precursor, we may be able to use these phenotypic variations to our advantage in better understanding their biology. We also discuss how a variety of genetic, epigenetic, and methodological differences can account for the seemingly contradictory findings on the physiological relevance of bone marrow-derived precursors in normal vascular maintenance and in response to injury. Data on the impact of tumor type and location on the contribution of bone marrow-derived cells to the tumor vasculature are also presented. These data provide hope that we may ultimately be able to predict those tumors in which bone marrow-derived cells will have a significant contribution and design therapies accordingly. Finally, factors that regulate bone marrow cell recruitment to and function in the endothelium are beginning to be identified, and several of these, including stromal derived factor 1, monocyte chemoattractant factor-1, and vascular endothelial growth factor are discussed.

背景与目标： ：在过去的十年中，关于骨髓中含有内皮细胞前体的古老观念已经引起人们的广泛关注。尽管有些人仍然认为血液中没有内皮前体，即使在有血液的人中也没有，但是关于它们是什么或它们的行为尚无共识。在这篇综述中，我们描述了鉴定内皮细胞的问题，并得出结论，内皮一氧化氮合酶的表达可能是最可靠的表型抗原指示剂。还提供了两种不同类别的内皮前体的证据。我们建议，尽管没有单个内皮细胞前体，但我们也许能够利用这些表型变异来更好地了解它们的生物学特性。我们还将讨论各种遗传，表观遗传学和方法学上的差异如何解释在正常血管维持和对损伤的反应中，骨髓来源的前体的生理相关性看似矛盾的发现。还提供了有关肿瘤类型和位置对骨髓衍生细胞对肿瘤脉管系统的影响的数据。这些数据提供了希望，使我们最终能够预测那些骨髓来源的细胞将发挥重要作用的肿瘤，并据此设计治疗方法。最后，已开始确定调节骨髓细胞向内皮募集并在内皮中起作用的因子，并讨论了其中的几种，包括基质衍生因子1，单核细胞趋化因子-1和血管内皮生长因子。

BACKGROUND & AIMS: OBJECTIVE:To compare prostate carcinoma, with and with no lymph node metastasis, to benign prostatic hyperplasia (BPH) tissue for lymphatic vessel density (LVD) and the expression of the lymph-endothelial specific growth factor, vascular endothelial growth factor C (VEGF-C), to determine their role in lymphogenic metastasis. PATIENTS, MATERIALS AND METHODS:Lymphatic vessels were stained using lymphatic vessel endothelial hyaluronan receptor 1 and assessed in standard areas. The expression of VEGF-C was assessed by the number of positive epithelial cells. The data were compared with the clinical staging. RESULTS:The lowest LVD was found in tumorous areas as opposed to periphery and nontumorous tissue (P = 0.007; P < 0.001). The highest LVD was in BPH tissue (P < 0.001). There was no correlation with clinical staging. There was more VEGF-C staining in pN1 than in pN0 and in BPH specimens (P = 0.002). CONCLUSION:LVD is not a prognostic variable for the process of lymphogenic metastasis in prostate cancer. VEGF-C is up-regulated in prostate cancer and its correlation with lymph node status suggests a role for the development of lymph node metastasis, e.g. via an increased permeability of lymphatic vessels.

背景与目标： 目的：比较有无淋巴结转移的前列腺癌与良性前列腺增生（BPH）组织的淋巴管密度（LVD）以及淋巴内皮特异性生长因子，血管内皮生长因子C（VEGF- C），确定其在淋巴转移中的作用。
患者，材料和方法：使用淋巴管内皮透明质酸受体1对淋巴管进行染色，并在标准区域进行评估。通过阳性上皮细胞的数量评估VEGF-C的表达。将数据与临床分期进行比较。
结果：与周围和非肿瘤组织相比，在肿瘤区域发现的LVD最低（P = 0.007； P <0.001）。 LVD最高的是BPH组织（P <0.001）。与临床分期无关。 pN1和BPH标本中的VEGF-C染色要多于pN0和PPH（P = 0.002）。
结论：LVD不是前列腺癌淋巴转移的预后变量。 VEGF-C在前列腺癌中被上调，并且其与淋巴结状态的相关性暗示了淋巴结转移的发展，例如肝癌的发生。通过增加淋巴管的通透性

BACKGROUND & AIMS: :The band alignment at an Al2O3/SrTiO3 heterointerface forming a two-dimensional electron gas (2DEG) was investigated using scanning photocurrent microscopy (SPCM) in an electrolyte-gated environment. We used a focused UV laser source for above-the-bandgap illumination on the SrTiO3 layer, creating electron-hole pairs that contributed to the photocurrent through migration towards the metal electrodes. The polarity of the SPCM signals of a bare SrTiO3 device shows typical p-type behavior at zero gate bias, in which the photogenerated electrons are collected by the electrodes. In contrast, the SPCM polarity of 2DEG device indicates that the hole carriers were collected by the metal electrodes. Careful transport measurements revealed that the gate-dependent conductance of the 2DEG devices exhibits n-type switching behavior. More importantly, the SPCM signals in 2DEG devices demonstrated very unique gate-responses that cannot be found in conventional semiconducting devices, based on which we were able to perform detailed investigation into the electronic band alignment of the 2DEG devices and obtain the valence band offset at the heterointerface.

背景与目标： ：使用扫描光电流显微镜（SPCM）在电解质门控环境中研究了形成二维电子气（2DEG）的Al2O3 / SrTiO3异质界面处的能带排列。我们使用聚焦的UV激光源在SrTiO3层上进行带隙以上照明，从而创建电子-空穴对，这些电子-空穴对通过向金属电极的迁移而有助于光电流。裸露的SrTiO3器件的SPCM信号的极性在零栅极偏置下显示出典型的p型行为，其中光生电子被电极收集。相反，2DEG器件的SPCM极性表明空穴载流子被金属电极收集。仔细的传输测量表明，2DEG器件的依赖于栅极的电导表现出n型开关行为。更重要的是，2DEG器件中的SPCM信号表现出非常独特的门响应，这是常规半导体器件中找不到的，基于此，我们能够对2DEG器件的电子能带对准进行详细研究，并获得价带偏移。异类接口。

BACKGROUND & AIMS: :With recent advances in synthetic biology, CO2 could be utilized as a carbon feedstock by native or engineered organisms, assuming the availability of electrons. Two key enzymes used in autotrophic CO2 fixation are the CO dehydrogenase (CODH) and acetyl coenzyme A (acetyl-CoA) synthase (ACS), which form a bifunctional heterotetrameric complex. The CODH/ACS complex can reversibly catalyze CO2 to CO, effectively enabling a biological water-gas shift reaction at ambient temperatures and pressures. The CODH/ACS complex is part of the Wood-Ljungdahl pathway (WLP) used by acetogens to fix CO2, and it has been well characterized in native hosts. So far, only a few recombinant CODH/ACS complexes have been expressed in heterologous hosts, none of which demonstrated in vivo CO2 reduction. Here, functional expression of the Clostridium carboxidivorans CODH/ACS complex is demonstrated in the solventogen Clostridium acetobutylicum, which was engineered to express CODH alone or together with the ACS. Both strains exhibited CO2 reduction and CO oxidation activities. The CODH reactions were interrogated using isotopic labeling, thus verifying that CO was a direct product of CO2 reduction, and vice versa. CODH apparently uses a native C. acetobutylicum ferredoxin as an electron carrier for CO2 reduction. Heterologous CODH activity depended on actively growing cells and required the addition of nickel, which is inserted into CODH without the need to express the native Ni insertase protein. Increasing CO concentrations in the gas phase inhibited CODH activity and altered the metabolite profile of the CODH-expressing cells. This work provides the foundation for engineering a complete and functional WLP in nonnative host organisms.IMPORTANCE Functional expression of CO dehydrogenase (CODH) from Clostridium carboxidivorans was demonstrated in C. acetobutylicum, which is natively incapable of CO2 fixation. The expression of CODH, alone or together with the C. carboxidivorans acetyl-CoA synthase (ACS), enabled C. acetobutylicum to catalyze both CO2 reduction and CO oxidation. Importantly, CODH exhibited activity in both the presence and absence of ACS. 13C-tracer studies confirmed that the engineered C. acetobutylicum strains can reduce CO2 to CO and oxidize CO during growth on glucose.

背景与目标： ：随着合成生物学的最新进展，假设电子的可用性，CO2可以被天然或工程有机体用作碳原料。自养性CO2固定中使用的两个关键酶是CO脱氢酶（CODH）和乙酰辅酶A（乙酰-CoA）合酶（ACS），它们形成了双功能异四聚体复合物。 CODH / ACS复合物可以可逆地将CO2催化转化为CO，从而有效地实现了在环境温度和压力下进行生物水煤气变换反应。 CODH / ACS复合物是乙酸原用于固定CO2的Wood-Ljungdahl途径（WLP）的一部分，并且在天然宿主中已得到很好的表征。迄今为止，在异源宿主中仅表达了少数重组CODH / ACS复合物，但均未显示体内CO2减少。在此，在溶剂原丙酮丁醇梭菌（Clostridium acetobutylicum）中证明了碳氧化梭菌CODH / ACS复合物的功能表达，该溶剂被改造成单独或与ACS一起表达CODH。两种菌株均表现出CO 2还原和CO氧化活性。使用同位素标记对CODH反应进行了询问，从而验证了CO是CO2还原的直接产物，反之亦然。 CODH显然使用天然的丙酮丁醇梭菌铁氧还蛋白作为电子载体来减少CO2。异源CODH活性取决于活跃生长的细胞，并需要添加镍，而无需表达天然Ni插入酶蛋白即可将其插入CODH。气相中CO浓度的增加会抑制CODH活性并改变表达CODH的细胞的代谢产物谱。这项工作为在非天然宿主生物中工程化完整且功能性的WLP提供了基础。重要提示在丙酮丁醇梭菌中证明了碳氧化梭菌中CO脱氢酶（CODH）的功能性表达，这本来就无法进行CO2固定。 CODH的表达，单独或与碳氧化单胞菌乙酰辅酶A合酶（ACS）一起表达，可使丙酮丁醇梭菌既催化CO2还原又催化CO氧化。重要的是，在有或没有ACS的情况下，CODH均具有活性。 13C示踪剂研究证实，工程改造的丙酮丁醇梭菌菌株可以在葡萄糖生长期间将CO2还原为CO，并氧化CO。

BACKGROUND & AIMS: :The objective of the study was to evaluate the association between peripheral venous disease (PVD) and arterial endothelial dysfunction (ED). Arterial and venous diseases have been always considered as two completely different entities, but the recent discovery of a relationship between arterial and venous thrombosis have challenged this assumption. ED, considered to be an early process in the pathophysiology of atherosclerotic disease, could represent a common pathogenetic background. We studied 39 healthy volunteers (median age: 34 years; men: 25.6%). PVD was diagnosed using ultrasound examination, arterial ED using flow-mediated dilation (FMD) and FMD normalized for the peak shear rate (nFMD). Compared with controls, participants with PVD had a lower FMD (15.2 versus 23.4%, P < 0.001) and nFMD (12.7 × 10(-3) versus 19 × 10(-3)/second, P < 0.001). People with the most clinically evident disease had the worst endothelial function. In conclusion, our findings, if confirmed in larger population, might corroborate the idea that venous and arterial disease could have common causes.

背景与目标： ：该研究的目的是评估周围静脉疾病（PVD）与动脉内皮功能障碍（ED）之间的关联。动脉和静脉疾病一直被认为是两个完全不同的实体，但是最近发现动脉和静脉血栓形成之间的关系挑战了这一假设。 ED被认为是动脉粥样硬化疾病病理生理的早期过程，可能代表了常见的致病背景。我们研究了39名健康志愿者（中位年龄：34岁；男性：25.6％）。使用超声检查诊断PVD，使用流介导的扩张（FMD）诊断动脉ED，并针对峰剪切速率（nFMD）归一化FMD。与对照组相比，PVD参与者的FMD较低（15.2比23.4％，P <0.001）和nFMD（12.7×10（-3）/ 19×10（-3）/秒，P <0.001）。临床上最明显的疾病的人的内皮功能最差。总之，我们的发现，如果在更大的人群中得到证实，可能证实静脉和动脉疾病可能是常见原因的观点。

BACKGROUND & AIMS: PURPOSE:The issue of unidentified volume expansion is well recognized as a cause for resistance to antihypertensive therapy. The aim of study is to identify contribution of negative fluid balance to hypertension control and impact on endothelial and cardiac functions among primary hypertensive patients who do not have kidney failure. MATERIALS AND METHODS:This is a prospective interventional study with one-year follow-up. Preceded by volume status measurements were performed by a body composition monitor (BCM), the patients were put on ambulatory blood pressure monitoring for 24 hours. Then, echocardiographic assessments and flow-mediated dilation (FMD) and carotid intima-media thickness (CIMT) measurements were completed. Patients in one of the two groups were kept negative hydrated during trial with diuretic treatment. RESULTS:At the end of one-year follow-up, patients in negative hydrated group were found to have significantly lower CIMT, left ventricle mass index, left ventricular end-diastolic diameter, mean systolic and diastolic BP, non-dipper patient ratio, and higher FMD. In negatively hydrated group, target organ damage significantly reduced during trial. CONCLUSIONS:The significance of negative hydration status with respect to blood pressure control, endothelial and cardiac functions within primary hypertensive patients who do not suffer from kidney failure has been demonstrated.

背景与目标： 目的：不明原因的体积膨胀问题已被公认为是抗高血压治疗耐药的原因。研究的目的是在没有肾衰竭的原发性高血压患者中确定负流体平衡对高血压控制的贡献以及对内皮和心脏功能的影响。
材料与方法：这是一项为期一年的随访的前瞻性干预研究。在通过身体成分监测仪（BCM）进行体积状态测量之前，将患者进行动态血压监测24小时。然后，完成了超声心动图评估以及血流介导的扩张（FMD）和颈动脉内膜中层厚度（CIMT）的测量。两组中的一组患者在利尿剂治疗试验期间保持负水分状态。
结果：在一年的随访结束时，负水合组患者的CIMT，左心室质量指数，左心室舒张末期直径，平均收缩压和舒张压，非北斗七星患者比率显着降低，和更高的FMD。在负水合组中，试验期间靶器官损伤显着减少。
结论：在没有肾脏衰竭的原发性高血压患者中，负水合状态对血压控制，内皮和心脏功能的重要性已得到证实。

BACKGROUND & AIMS: :Human coronary artery endothelial cells (HCAECs) have the potential to undergo fibrogenic endothelial-mesenchymal transition (EndMT), which results in matrix-producing fibroblasts and thereby contributes to the pathogenesis of cardiac fibrosis. Recently, the profibrotic cytokine transforming growth factor-β (TGF-β) is shown to be the crucial pathogenic driver which has been verified to induce EndMT. C-Ski is an important regulator of TGF-β signaling. However, the detailed role of c-Ski and the molecular mechanisms by which c-Ski affects TGF-β-induced EndMT in HCAECs are not largely elucidated. In the present study, we treated HCAECs with TGF-β of different concentrations to induce EndMT. We found that overexpression of c-Ski in HCAECs either blocked EndMT via hindering Vimentin, Snail, Slug, and Twist expression while enhancing CD31 expression, with or without TGF-β treatment. In contrast, suppression of c-Ski further enhanced EndMT. Currently, miRNA expression disorder has been frequently reported associating with cardiac fibrosis. By using online tools, we regarded miR-155 as a candidate miRNA that could target c-Ski, which was verified using luciferase assays. C-Ski expression was negatively regulated by miR-155. TGF-β-induced EndMT was inhibited by miR-155 silence; the effect of TGF-β on Vimentin, CD31, Snail, Slug, and Twist could be partially restored by miR-155. Altogether, these findings will shed light on the role and mechanism by which miR-155 regulates TGF-β-induced HCAECs EndMT via c-Ski to affect cardiac fibrosis, and miR-155/c-Ski may represent novel biomarkers and therapeutic targets in the treatment of cardiac fibrosis.

背景与目标： ：人冠状动脉内皮细胞（HCAEC）有可能经历纤维化内皮-间充质转变（EndMT），这会导致产生基质的成纤维细胞，从而促进心脏纤维化的发病机理。最近，已证明原纤维化细胞因子转化生长因子-β（TGF-β）是关键的致病性驱动因子，已被证实可诱导EndMT。 C-Ski是TGF-β信号传导的重要调节剂。然而，在很大程度上没有阐明c-Ski的详细作用以及c-Ski影响HCAECs中TGF-β诱导的EndMT的分子机制。在本研究中，我们用不同浓度的TGF-β处理HCAEC，以诱导EndMT。我们发现，无论是否使用TGF-β处理，HCAEC中c-Ski的过表达要么通过阻碍波形蛋白，蜗牛，Slug和Twist的表达而阻断EndMT，同时增强CD31的表达。相反，抑制c-Ski进一步增强了EndMT。当前，miRNA表达障碍经常被报道与心脏纤维化有关。通过使用在线工具，我们将miR-155视为可以靶向c-Ski的候选miRNA，这已通过荧光素酶测定法进行了验证。 C-Ski表达受到miR-155的负调控。 TGF-β诱导的EndMT被miR-155沉默抑制； TGF-β对波形蛋白，CD31，蜗牛，Slug和Twist的作用可以被miR-155部分恢复。总而言之，这些发现将阐明miR-155通过c-Ski调节TGF-β诱导的HCAECs EndMT通过影响心脏纤维化的作用和机制，而miR-155 / c-Ski可能代表了新型的生物标志物和治疗靶点。心脏纤维化的治疗。

BACKGROUND & AIMS: :Maintenance of the lipid composition is important for proper function and homeostasis of the mitochondrion. In Trypanosoma brucei, the enzymes involved in the biosynthesis of the mitochondrial phospholipid, phosphatidylglycerol (PG), have not been studied experimentally. We now report the characterization of T. brucei phosphatidylglycerophosphate synthase (TbPgps), the rate-limiting enzyme in PG formation, which was identified based on its homology to other eukaryotic Pgps. Lipid quantification and metabolic labelling experiments show that TbPgps gene knock-down results in loss of PG and a reduction of another mitochondria-specific phospholipid, cardiolipin. Using immunohistochemistry and immunoblotting of digitonin-isolated mitochondria, we show that TbPgps localizes to the mitochondrion. Moreover, reduced TbPgps expression in T. brucei procyclic forms leads to alterations in mitochondrial morphology, reduction in the amounts of respiratory complexes III and IV and, ultimately, parasite death. Using native polyacrylamide gel electrophoresis we demonstrate for the first time in a eukaryotic organism that TbPgps is a component of a 720 kDa protein complex, co-migrating with T. brucei cardiolipin synthase and cytochrome c1, a protein of respiratory complex III.

背景与目标： ：脂质成分的维护对于线粒体的正常功能和体内平衡非常重要。在布鲁氏锥虫中，尚未对线粒体磷脂，磷脂酰甘油（PG）的生物合成中涉及的酶进行研究。现在，我们报告T.brucei磷脂酰甘油磷酸合酶（TbPgps）的表征，PG形成中的限速酶，是根据它与其他真核Pgps的同源性鉴定的。脂质定量和代谢标记实验表明，TbPgps基因敲低会导致PG丢失并降低另一种线粒体特异性磷脂心磷脂。使用免疫组化和指印蛋白分离的线粒体的免疫印迹，我们显示TbPgps定位于线粒体。此外，布鲁氏杆菌前环形式的TbPgps表达降低导致线粒体形态改变，呼吸道复合物III和IV数量减少，最终导致寄生虫死亡。使用天然聚丙烯酰胺凝胶电泳，我们首次在真核生物中证明了TbPgps是720 kDa蛋白复合物的一个成分，与T. brucei心磷脂合酶和细胞色素c1（呼吸复合物III的蛋白）共同迁移。

BACKGROUND & AIMS: :The soya-derived phytoestrogen genistein has been suggested to be protective in cardiovascular diseases. In the present study, we have analysed whether chronic oral genistein might influence endothelial function in male SHRs (spontaneously hypertensive rats) via ERs (oestrogen receptors), changes in eNOS (endothelial NO synthase) activity and vascular O(2)(-) (superoxide) production. Rats (23-weeks old) were divided into the following groups: WKY (Wistar-Kyoto)-vehicle, SHR-vehicle, WKY-genistein (10 mg.kg(-1) of body weight.day(-1)); SHR-genistein; SHR-genistein-faslodex (ICI 182780; 2.5 mg.kg(-1) of body weight.day(-1)). Vascular expression of eNOS, caveolin-1 and calmodulin-1 were analysed by Western blotting, eNOS activity by conversion of [(3)H]arginine into L-[(3)H]citrulline and O(2)(-) production by chemoluminescence of lucigenin. In SHRs, after 5 weeks of treatment, genistein reduced systolic blood pressure and enhanced endothelium-dependent aortic relaxation to acetylcholine, but had no effect on the vasodilator responses to sodium nitroprusside. Compared with WKY rats, SHRs had up-regulated eNOS and down-regulated caveolin-1 and calmodulin-1 expression, increased NADPH-induced O(2)(-) production, but reduced eNOS activity. Genistein increased aortic calmodulin-1 protein abundance and eNOS activity, and reduced NADPH-induced O(2)(-) production in SHRs. The pure ERalpha and ERbeta antagonist faslodex did not modify any of the changes induced by genistein in SHRs, suggesting that these effects are unrelated to ER stimulation. In conclusion, genistein reduced the elevated blood pressure and endothelial dysfunction in SHRs. This latter effect appears to be related to increased eNOS activity associated with increased calmodulin-1 expression and decreased O(2)(-) generation.

背景与目标： 大豆来源的植物雌激素染料木黄酮已被建议在心血管疾病中具有保护作用。在本研究中，我们分析了慢性口服染料木黄酮是否可能通过ER（雌激素受体），eNOS（内皮型NO合酶）活性和血管O（2）（-）（超氧化物）生产。将大鼠（23周龄）分为以下几组：WKY（Wistar-Kyoto）车辆，SHR车辆，WKY-染料木黄酮（10 mg.kg（-1）体重.day（-1））； SHR-染料木黄酮; SHR-genistein-faslodex（ICI 182780; 2.5 mg.kg（-1）体重.day（-1））。通过蛋白质印迹分析eNOS，caveolin-1和钙调蛋白-1的血管表达，通过将[（3）H]精氨酸转化为L-[（3H）]瓜氨酸和通过生成O（2）（-）来分析eNOS活性。发光素的化学发光。在SHR中，经过5周的治疗，金雀异黄素降低了收缩压，增强了内皮依赖性的主动脉对乙酰胆碱的舒张作用，但对血管扩张剂对硝普钠的反应没有影响。与WKY大鼠相比，SHRs上调了eNOS，下调了Caveolin-1和calmodulin-1的表达，增加了NADPH诱导的O（2）（-）的产生，但降低了eNOS的活性。金雀异黄素增加主动脉钙调蛋白1蛋白的丰度和eNOS的活性，并减少NADPH诱导SHRs中的O（2）（-）生产。单纯的ERalpha和ERbeta拮抗剂faslodex并未改变染料木黄酮在SHRs中诱导的任何变化，表明这些作用与ER刺激无关。总之，金雀异黄素减轻了SHRs的血压升高和内皮功能障碍。后者的作用似乎与增加的钙调蛋白-1表达和减少的O（2）（-）生成有关的eNOS活性有关。

BACKGROUND & AIMS: :Extracellular magnesium ions [Mg2+]o are known to regulate functions of endothelial cells, but whether [Mg2+]o can alter intracellular free ionized magnesium [Mg2+]i in these cells remains unknown. The present studies, using digital imaging microscopy and the Mg2+ fluorescent probe, mag-fura-2, determined effects of elevation of [Mg2+]o on [Mg2+]i in cultured human aortic endothelial cells. With normal Mg2+(1.2 mM)-containing incubation media, [Mg2+]i was 0.51+/-0.04 mM with a heterogeneous distribution. The ratio of [Mg2+]i/[Mg2+]o was 0.52+/-0.07. Elevation of [Mg2+]o up to 4.8 mM increased [Mg2+]i to 0.80+/-0.07 mM in 2-10 min and lowered the ratio of [Mg2+]i/[Mg2+]o to 0.16+/-0.02. Irrespective of the observed increments of [Mg2+]i, a subcellular heterogeneous distribution of [Mg2+]i was always evident in all cells tested. Our results suggest that [Mg2+]o can regulate [Mg2+]i more rapidly than heretofore believed, supporting the hypothesis that extracellular Mg2+ can exert regulatory effects on endothelial cell functions and probably act as extracellular regulatory cations

背景与目标： ：已知细胞外镁离子[Mg2] o调节内皮细胞的功能，但是[Mg2] o是否可以改变这些细胞中的细胞内游离离子化镁[Mg2] i，仍然未知。本研究使用数字成像显微镜和Mg2荧光探针mag-fura-2，确定了培养的人主动脉内皮细胞中[Mg2] o升高对[Mg2] i的影响。在含有正常Mg2（1.2 mM）的培养培养基中，[Mg2] i为0.51 / 0.04 mM，分布不均。 [Mg 2] i / [Mg 2] o的比例为0.52 / -0.07。 [Mg2] o升高至4.8 mM会使[Mg2] i在2-10分钟内增加到0.80 /-0.07 mM，并使[Mg2] i / [Mg2] o的比率降低到0.16 /-0.02。不管观察到的[Mg2] i增量如何，在所有测试的细胞中[Mg2] i的亚细胞异质分布总是很明显的。我们的结果表明，[Mg2] o可以比以前认为的更快地调节[Mg2] i，支持以下假设：细胞外Mg2可以对内皮细胞功能发挥调节作用，并且可能充当细胞外调节阳离子

BACKGROUND & AIMS: CONTEXT:Oestrogens play an important protective role on the vascular system. The endothelial cell layer is a direct target for these hormones, and expresses at least two oestrogen receptors, ER-alpha and ER-beta. Recent studies have shown that vascular healing is significantly modulated by circulating bone marrow-derived cells. A subset of these stem cells, endothelial progenitor cells (EPCs), have recently been described as a population of pluripotent cells within the peripheral blood capable of differentiating into endothelial cells. OBJECTIVE:In the present study we investigated the expression of ER-alpha and ER-beta on human EPCs and the effect that oestrogens have on the function of EPCs in vitro. METHODS:EPCs were isolated and cultured from healthy donors. RT-PCR, western blotting and immunohistochemistry were used to assess expression of ER-alpha and ER-beta. Proliferation and CFU assays were used to assess the response of EPCs to different doses of 17,beta-oestradiol. MAIN OUTCOME MEASURES:Expression of ER-alpha and ER-beta in EPCs, and the effect of 17,beta-oestradiol on proliferation of EPCs. RESULTS:Human EPCs express ER-alpha mRNA and protein. 17,beta-oestradiol increases proliferation of EPCs and CFU in a dose-dependent manner. CONCLUSIONS:Human EPCs express ER-alpha but not ER-beta, and oestrogens can stimulate the proliferation of these cells in vitro. Oestrogens exert these effects at concentrations that are usually reached during stimulation for in vitro fertilization in women, and therefore further studies are needed to clarify the clinical significance of these effects.

背景与目标： 背景：雌激素对血管系统起重要的保护作用。内皮细胞层是这些激素的直接靶标，并表达至少两种雌激素受体，即ER-α和ER-β。最近的研究表明，循环的骨髓来源的细胞显着地调节了血管的愈合。这些干细胞的一个子集，内皮祖细胞（EPC），最近被描述为能够分化为内皮细胞的外周血中的多能细胞群。
目的：在本研究中，我们研究了ER-α和ER-β在人EPC上的表达以及雌激素在体外对EPC功能的影响。
方法：从健康供体中分离并培养EPC。 RT-PCR，蛋白质印迹和免疫组化被用于评估ER-alpha和ER-beta的表达。增殖和CFU分析用于评估EPC对不同剂量的17-β-雌二醇的反应。
主要观察指标：EPCs中ER-α和ER-β的表达，以及17-β-雌二醇对EPCs增殖的影响。
结果：人EPCs表达ER-αmRNA和蛋白。 17，β-雌二醇以剂量依赖性方式增加EPC和CFU的增殖。
结论：人类EPCs表达ER-α而不表达ER-β，并且雌激素可以刺激这些细胞的体外增殖。雌激素以刺激女性体外受精时通常达到的浓度发挥这些作用，因此需要进一步的研究以阐明这些作用的临床意义。

BACKGROUND & AIMS: Histochemical, immunohistochemical, and biochemical evidence is reported showing that the ink gland of the cuttlefish Sepia officinalis contains a calcium-dependent isoform of nitric oxide synthase as well as an NMDA R1 receptor subunit localized for the most part in the immature inner cells of the epithelial layer of the gland. These results may be taken to implicate a hitherto unrecognized regulatory role of the glutamate-nitric oxide pathway in the maturation and metabolic activity of melanin-producing cells in the cephalopod defense system.

背景与目标： 据组织化学，免疫组化和生物化学证据表明，乌贼墨Sep的墨腺含有一氧化钙合酶的一氧化氮合酶同工型，以及NMDA R1受体亚基，其大部分位于上皮的未成熟内细胞中。腺体层。这些结果可能暗示了迄今为止尚未认识到的谷氨酸一氧化氮途径在头足防御系统中黑色素生成细胞的成熟和代谢活性中的作用。

BACKGROUND & AIMS: :Soybean [Glycine max (L.) Merr.] embryogenic cultures were transformed by particle bombardment with the feedback-insensitive tobacco anthranilate synthase (AS) gene ASA2 driven by the CaMV 35S promoter and selected using hph as the selectable marker gene. Only one of eight regenerated lines that set seed and contained ASA2 expressed the gene highly and contained increased free tryptophan (Trp) levels in leaves, seeds and embryogenic cultures. Leaf extracts of the ASA2 expressing line contained about twice as much AS enzyme activity as the untransformed control and this activity was only slightly more feedback-insensitive. Amino acid analysis showed that both leaves and embryogenic tissue cultures of the ASA2 expressing line had four to five-times the normal levels of free Trp and slightly higher free tyrosine and phenylalanine. The seed total Trp content was only slightly increased. Metabolic profiling-analysis by GC-MS detected no other consistent differences. These studies show that the ASA2 gene can be expressed in soybean and that modest changes in Trp synthesis occurs.

背景与目标： ：大豆[Glycine max（L.）Merr。]胚性培养物通过由CaMV 35S启动子驱动的反馈不敏感的烟草邻氨基苯甲酸合酶（AS）基因ASA2进行粒子轰击进行转化，并使用hph作为选择标记基因进行选择。八个定植种子并含有ASA2的再生系中只有一个表达该基因，并且在叶片，种子和胚发生培养物中的游离色氨酸（Trp）水平升高。表达ASA2的品系的叶提取物所含的AS酶活性约为未转化对照的两倍，该活性对反馈的敏感性稍高。氨基酸分析表明，ASA2表达株系的叶片和胚发生组织培养物的游离Trp含量是正常水平的4至5倍，游离酪氨酸和苯丙氨酸含量稍高。种子总色氨酸含量仅略有增加。 GC-MS进行的代谢谱分析没有发现其他一致的差异。这些研究表明，ASA2基因可以在大豆中表达，并且Trp合成发生适度的变化。

BACKGROUND & AIMS: :The ATP synthase, isolated from Wolinella (formerly Vibrio) succinogenes could be fully incorporated into liposomes without significant cleavage of the enzyme or loss of activity. These proteoliposomes, but not the isolated enzyme, catalyzed phosphate-ATP exchange and the phosphorylation of ADP which was driven by an artificially imposed delta mu H across the liposomal membrane. Phosphorylation driven by light was catalyzed by proteoliposomes containing also bacteriorhodopsin. The three activities were similarly sensitive to protonophores or dicyclohexylcarbodiimide. This sensitivity was similar to that of the electron-transport-driven phosphorylation catalyzed by bacterial membrane vesicles. With a delta mu H value 280 mV to drive phosphorylation the turnover number of the enzyme was in the same order of magnitude as that measured in the electron-transport-driven phosphorylation catalyzed by the bacterial membrane. When the delta mu H was below 150 mV, the phosphorylation activity of the incorporated enzyme was two orders of magnitude slower, and was about as fast as light-driven phosphorylation or as the exchange reaction.

背景与目标： 从沃林氏菌（以前为弧菌）琥珀酸基因中分离出的ATP合酶可以完全掺入脂质体中，而无需酶的显着裂解或活性降低。这些蛋白脂质体（而非分离的酶）催化磷酸-ATP交换和由人为施加的δH跨脂质体膜驱动的ADP磷酸化。含有细菌视紫红质的蛋白脂质体可催化光驱动的磷酸化。这三种活性对质子体或二环己基碳二亚胺同样敏感。这种敏感性类似于细菌膜囊泡催化的电子传输驱动的磷酸化。在280 mV的ΔmuH值驱动磷酸化的情况下，酶的周转数与细菌膜催化的电子传输驱动的磷酸化反应的量级处于相同的数量级。当ΔμH低于150mV时，掺入的酶的磷酸化活性慢两个数量级，并且大约与光驱动的磷酸化或交换反应一样快。

BACKGROUND & AIMS: :Acute kidney injury (AKI) represents a significant clinical concern that is associated with high mortality rates and also represents a significant risk factor for the development of chronic kidney disease (CKD). This article will consider alterations in renal endothelial function in the setting of AKI that may underlie impairment in renal perfusion and how inefficient vascular repair may manifest post-AKI and contribute to the potential transition to CKD. We provide updated terminology for cells previously classified as 'endothelial progenitor' that may mediate vascular repair such as pro-angiogenic cells and endothelial colony-forming cells. We consider how endothelial repair may be mediated by these different cell types following vascular injury, particularly in models of AKI. We further summarize the potential ability of these different cells to mitigate the severity of AKI, improve perfusion and maintain vascular structure in pre-clinical studies.

背景与目标： ：急性肾损伤（AKI）代表了与高死亡率相关的重要临床问题，并且还代表了慢性肾脏疾病（CKD）发生的重要危险因素。本文将考虑在AKI的背景下肾内皮功能的改变，这可能是肾脏灌注受损的基础，以及AKI后的低效血管修复可能如何表现出来，并可能导致向CKD的转变。我们为以前被归类为“内皮祖细胞”的细胞提供了更新的术语，这些细胞可能介导血管修复，例如促血管生成细胞和内皮集落形成细胞。我们考虑血管损伤后这些不同细胞类型可能如何介导内皮修复，尤其是在AKI模型中。在临床前研究中，我们进一步总结了这些不同细胞减轻AKI严重性，改善灌注和维持血管结构的潜在能力。