Tissue Culture of Endothelial Cells.- Culture and identification of large vessel endothelial cells.- Culture of capillary endothelial cells.- Culture of endothelial cells from neural capillaries.- Culture of pulmonary endothelial cells on microcarrier beads.- Construction of an artificial blood vessel wall from cultured endothelial cells.- Determinants of Endothelial and Smooth Muscle Cell Growth.- Growth requirements for bovine aortic endothelium in vitro.- Contact inhibition in the endothelium.- Endothelial cell motility.- Factors which stimulate the growth of human umbilical vein endothelial cells in vitro.- Macrophages, neovascularization, and the growth of vascular cells.- The limited life-span of bovine endothelial cells.- Endothelium, heparin, and the regulation of vascular smooth muscle cell growth.- Morphology of Cultured Endothelial Cells.- Morphology of vascular endothelial cells in culture.- The endothelial cytoskeleton.- Synthesis of Connective Tissue Elements by Endothelial Cells.- Metabolism of thrombospondin and fibronectin by endothelial cells.- Collagen synthesis by endothelial cells in culture.- Sulfated glycosaminoglycans and vascular endothelial cells.- Elastin synthesis by endothelial cells.- Gene mapping using hybrids of human endothelial cells and rodent fibroblasts.- Interactions of Endothelial Cells with the Coagulation and Complement Systems and Formed Elements in Blood.- Properties of plasminogen activators produced by endothelial cells.- Synthesis of Factor VIII by endothelial cells.- Tissue factor activity of cultured human vascular cells.- Activation of Hageman factor by cultured rabbit endothelial cells.- Prostacyclin production by endothelial cells.- Regulation of endothelial cell function by cyclic nucleotides.- Interactions of thrombin, antithrombin III, and Protein C with endothelium.- Viral infection of endothelium and the induction of Fc and C3 receptors.- Adhesive interactions between polymorphonuclear leukocytes and endothelium.- Neutrophil endothelial interactions.- Synthesis of colony stimulating activity by endothelial cells.- Interaction with and Metabolism of Plasma Components by Endothelial Cells.- The metabolism of vasoactive peptides by human endothelial cells.- The metabolism of angiotensin I and bradykinin by endothelial cells.- Metabolism of serotonin and adenosine.- Receptors for insulin and multiplication stimulating activity (MSA) in endothelial cells.- Binding of lipoprotein lipase to cultured endothelial cells.- Role of lipoproteins in the regulation of cultured endothelial cell cholesterol metabolism.- Quantitative aspects of endocytosis in cultured endothelial cells.- Immunologic Aspects of Endothelial Cells.- The alloantigens of endothelial cells.- Accessory cell function of human endothelial cells: presentation of antigen to T cells.- Cell surface markers on endothelial cells: a developmental perspective.- Endothelial Cell and Vasular Prostheses.- Endothelial seeding of vascular prostheses.- Endothelial Cells and Cancer.- Angiogenesis.- Synthesis of collagenase and plasminogen activator by endothelial cells.- In vitro systems for studying the interaction of metastatic tumor cells with endothelial cells and subendothelial basement membranes.

Biology of endothelial cells

The purpose of this research is to evaluate the effects of a tourniquet in total knee arthroplasty (TKA). The study was done by randomized controlled trials (RCTs) on the effects of a tourniquet in TKA. All related articles which were published up to June 2013 from Medline, Embase, and Cochrane Central Register of Controlled Trails were identified. The methodological quality of the included studies was assessed by the Physiotherapy Evidence Database (PEDro) scale. The meta-analysis was performed using Cochrane RevMan software version 5.1. Thirteen RCTs that involved a total of 689 patients with 689 knees were included in the meta-analysis, which were divided into two groups. The tourniquet group included 351 knees and the non-tourniquet group included 338 knees. The meta-analysis showed that using a tourniquet in TKA could reduce intraoperative blood loss (weighted mean difference (WMD), -198.21; 95% confidence interval (CI), -279.82 to -116.60; P   0.05). Postoperative knee range of motion (ROM) in tourniquet group was 10.41° less than that in the non-tourniquet group in early stage (≤10 days after surgery) (WMD, -10.41; 95% CI, -16.41 to -4.41; P < 0.01). Moreover, the use of a tourniquet increased the risk of either thrombotic events (risk ratio (RR), 5.00; 95% CI, 1.31 to 19.10; P = 0.02) or non-thrombotic complications (RR, 2.03; 95% CI, 1.12 to 3.67; P = 0.02). TKA without a tourniquet was superior to TKA with a tourniquet in thromboembolic events and the other related complications. There were no significant differences between the two groups in the actual blood loss. TKA with a tourniquet might hinder patients' early postoperative rehabilitation exercises.

/pdf/the-effects-of-a-tourniquet-used-in-total-knee-arthroplasty-4xs1ofkh0q.pdf

The effects of a tourniquet used in total knee arthroplasty: a meta-analysis

Thrombotic cardiovascular diseases increase in incidence in the elderly, a tendency dependent on the age-related changes in vascular and hemostatic systems that include platelets, coagulation, and fibrinolytic factors as well as in the endothelium. The hypercoagulability of and advanced sclerotic changes in the vascular wall may contribute to the increased incidence of thrombosis in the elderly. One of the important key genes for aging-associated thrombosis is plasminogen activator inhibitor-1 (PAI-1), a principal inhibitor of fibrinolysis. The expression of PAI-1 is not only elevated in the elderly but also significantly induced in a variety of pathologies associated with the process of aging. These conditions include obesity, insulin resistance, emotional stress, immune responses, and vascular sclerosis/remodeling. Several cytokines and hormones, including tumor necrosis factor-alpha, transforming growth factor-beta, angiotensin II, and insulin, positively regulate the gene expression of PAI-1. The recent epidemic in obesity with aging in the industrialized society may heighten the risk for thrombotic cardiovascular disease because adipose tissue is a primary source of PAI-1 and cytokines. Emotional or psychosocial stress and inflammation also cause the elevated expression of PAI-1 in an age-specific pattern. Thus, PAI-1 could play a key role in the progression of cardiovascular aging by promoting thrombosis and vascular (athero)sclerosis. Further studies on the genetic mechanism of aging-associated PAI-1 induction will be necessary to define the basis for cardiovascular aging in relation to thrombosis.

/pdf/aging-and-plasminogen-activator-inhibitor-1-pai-1-regulation-3eby51cye9.pdf

Aging and plasminogen activator inhibitor-1 (PAI-1) regulation : Implication in the pathogenesis of thrombotic disorders in the elderly

Studies of Human Platelet α-Granule Release In Vivo

Many changes in the vasculature, hemostasis and endothelium, including alterations of platelets, coagulation and fibrinolytic factors, occur during aging. While the increasing hypercoagulability observed with aging may account for the higher incidence of thrombotic cardiovascular disorders in the elderly, the lack of genetic protective factors against thrombosis in healthy centenarians suggests that little is yet known about the age-associated changes of hemostasis. The complex inter-relationships between inherited and acquired factors influencing the hemostatic system during aging are discussed in this review.

Hemostasis and aging.

Enhanced in-vivo platelet release reaction, increased thromboxane synthesis, and decreased prostacyclin release after tourniquet ischaemia

The variability of plasma beta-thromboglobulin in healthy individuals.

Abstract Neurodegenerative diseases such as Alzheimer’s disease (AD) are multifactorial with several different pathologic mechanisms. Therefore, it is assumed that multitargeted-directed ligands (MTDLs) which interact with different biological targets relevant to the diseases, might offer an improved therapeutic alternative than using the traditional “one-target, one-molecule” approach. Herein, we describe new benzothiazole-based derivatives as a privileged scaffold for histamine H3 receptor ligands (H3R). The most affine compound, the 3-(azepan-1-yl)propyloxy-linked benzothiazole derivative 4b, displayed a Ki value of 0.012 μM. The multitargeting potential of these H3R ligands towards AChE, BuChE and MAO-B enzymes was evaluated to yield compound 3s (pyrrolidin-1-yl-(6-((5-(pyrrolidin-1-yl)pentyl)oxy)benzo[d]thiazol-2-yl)methanone) as the most promising MTDL with a Ki value of 0.036 μM at H3R and IC50 values of 6.7 µM, 2.35 µM, and 1.6 µM towards AChE, BuChE, and MAO-B, respectively. These findings suggest that compound 3s can be a lead structure for developing new multi-targeting anti-AD agents.

Novel benzothiazole derivatives as multitargeted-directed ligands for the treatment of Alzheimer’s disease

BOPPY-based novel fluorescent dopamine D2 and D3 receptor ligands.

Alzheimer’s disease (AD) is a neurodegenerative disorder, for which there is no effective cure. Current drugs only slow down the course of the disease, and, therefore, there is an urgent need to find effective therapies that not only treat, but also prevent it. Acetylcholinesterase inhibitors (AChEIs), among others, have been used for years to treat AD. Histamine H3 receptors (H3Rs) antagonists/inverse agonists are indicated for CNS diseases. Combining AChEIs with H3R antagonism in one structure could bring a beneficial therapeutic effect. The aim of this study was to find new multitargetting ligands. Thus, continuing our previous research, acetyl- and propionyl-phenoxy-pentyl(-hexyl) derivatives were designed. These compounds were tested for their affinity to human H3Rs, as well as their ability to inhibit cholinesterases (acetyl- and butyrylcholinesterases) and, additionally, human monoamine oxidase B (MAO B). Furthermore, for the selected active compounds, their toxicity towards HepG2 or SH-SY5Y cells was evaluated. The results showed that compounds 16 (1-(4-((5-(azepan-1-yl)pentyl)oxy)phenyl)propan-1-one) and 17 (1-(4-((6-(azepan-1-yl)hexyl)oxy)phenyl)propan-1-one) are the most promising, with a high affinity for human H3Rs (Ki: 30 nM and 42 nM, respectively), a good ability to inhibit cholinesterases (16: AChE IC50 = 3.60 µM, BuChE IC50 = 0.55 µM; 17: AChE IC50 = 1.06 µM, BuChE IC50 = 2.86 µM), and lack of cell toxicity up to 50 µM.

/pdf/multitargeting-histamine-h3-receptor-ligands-among-acetyl-38mb5yl5.pdf

Multitargeting Histamine H3 Receptor Ligands among Acetyl- and Propionyl-Phenoxyalkyl Derivatives

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