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Find video protocols related to scientific articles indexed in Pubmed.
The role of lectin-like oxidised low-density lipoprotein receptor-1 in vascular pathology.
Diab Vasc Dis Res
PUBLISHED: 09-12-2014
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The lectin-like oxidised low-density lipoprotein receptor-1 (LOX-1) is a vascular scavenger receptor that plays a central role in the pathogenesis of atherothrombotic disease, which remains the main cause of mortality in the Western population. Recent evidence indicates that targeting LOX-1 represents a credible strategy for the management vascular disease and the current review explores the role of this molecule in the diagnosis and treatment of atherosclerosis. LOX-1-mediated pro-atherogenic effects can be inhibited by anti-LOX-1 monoclonal antibodies and procyanidins, whereas downregulation of LOX-1 expression has been achieved by antisense oligonucleotides and a specific pyrrole-imidazole polyamide. Furthermore, LOX-1 can be utilised for plaque imaging using monoclonal antibodies and even the selective delivery of anti-atherosclerotic agents employing immunoliposome techniques. Also, plasma levels of the circulating soluble form of LOX-1 levels are elevated in atherosclerosis and therefore may constitute an additional diagnostic biomarker of vascular pathology.
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Hypofibrinolysis in type 2 diabetes: the role of the inflammatory pathway and complement C3.
Diabetologia
PUBLISHED: 04-29-2014
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Plasminogen activator inhibitor-1 (PAI-1) has been regarded as the main antifibrinolytic protein in diabetes, but recent work indicates that complement C3 (C3), an inflammatory protein, directly compromises fibrinolysis in type 1 diabetes. The aim of the current project was to investigate associations between C3 and fibrinolysis in a large cohort of individuals with type 2 diabetes.
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Genetic and environmental determinants of dimethylarginines and association with cardiovascular disease in patients with type 2 diabetes.
Diabetes Care
PUBLISHED: 11-01-2013
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ObjectiveTo investigate determinants of asymmetric dimethylarginine (ADMA) and symmetric dimethylarginine (SDMA), including single nucleotide polymorphisms (SNPs) in the DDAH1, DDAH2 and AGXT2 genes and their associations with prevalent and incident cardiovascular disease (CVD) in older adults with type 2 diabetes mellitus.Research Design and MethodsPrevalent CVD was assessed in men and women aged 60-75 years with type 2 diabetes as part of the Edinburgh Type 2 Diabetes Study (ET2DS), and the participants were prospectively followed up for 4 years for incident CVD. Dimethylarginines were measured in 783 of these subjects and genotyping for tagSNPs in the DDAH1, DDAH2 and AGXT2 genes was performed in 935 subjects.ResultsPlasma ADMA levels were significantly associated with SNPs in DDAH1 (top SNP rs1554597; p= 9.0E-09), whilst SDMA levels were associated with SNPs in AGXT2 (top SNP rs28305; p= 1.3E-04). Significant, independent determinants of plasma ADMA were sex, L-arginine, creatinine, fasting glucose and rs1554597 (all p<0.05, combined R(2)=0.213). Determinants of SDMA were age, sex, creatinine, L-arginine, diabetes duration, prevalent CVD and rs28305 (all p<0.05, combined R(2)=0.425). Neither dimethylarginine was associated with incident CVD. None of the investigated SNPs was associated with overall CVD, although subgroup analysis revealed a significant association of AGXT2 rs28305 with intermittent claudication.ConclusionOur study in a well characterized population with type 2 diabetes does not support reported associations or causal relationship between ADMA and features of diabetes or CVD.
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Diabetes is associated with posttranslational modifications in plasminogen resulting in reduced plasmin generation and enzyme-specific activity.
Blood
PUBLISHED: 05-22-2013
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Diabetes is associated with hypofibrinolysis by mechanisms that are only partially understood. We investigated the effects of in vivo plasminogen glycation on fibrinolysis, plasmin generation, protein proteolytic activity, and plasminogen-fibrin interactions. Plasma was collected from healthy controls and individuals with type 1 diabetes before and after improving glycemia. Plasma-purified plasmin(ogen) functional activity was evaluated by chromogenic, turbidimetric, and plasmin conversion assays, with surface plasmon resonance employed for fibrin-plasminogen interactions. Plasminogen posttranslational modifications were quantified by mass spectrometry and glycation sites located by peptide mapping. Diabetes was associated with impaired plasma fibrin network lysis, which partly normalized upon improving glycaemia. Purified plasmin(ogen) from diabetic subjects had impaired fibrinolytic activity compared with controls (723 ± 16 and 317 ± 4 s, respectively; P < .01), mainly related to decreased fibrin-dependent plasmin generation and reduced protease activity (Kcat/KM 2.57 ± 1.02 × 10?³ and 5.67 ± 0.98 × 10?³ M?¹s?¹, respectively; P < .05). N?-fructosyl-lysine residue on plasminogen was increased in diabetes compared with controls (6.26 ± 3.43 and 1.82 ± 0.95%mol, respectively; P < .01) with preferential glycation of lysines 107 and 557, sites involved in fibrin binding and plasmin(ogen) cleavage, respectively. Glycation of plasminogen in diabetes directly affects fibrinolysis by decreasing plasmin generation and reducing protein-specific activity, changes that are reversible with modest improvement in glycemic control.
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A comparison of cardiovascular risk indices in patients with polycystic ovary syndrome with and without coexisting nonalcoholic fatty liver disease.
Clin. Endocrinol. (Oxf)
PUBLISHED: 04-29-2013
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Women with polycystic ovary syndrome (PCOS) have an adverse cardiovascular risk profile and an increased prevalence of nonalcoholic fatty liver disease (NAFLD), which is also associated with an adverse cardiovascular risk profile.
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Diabetes mellitus is associated with adverse prognosis in chronic heart failure of ischaemic and non-ischaemic aetiology.
Diab Vasc Dis Res
PUBLISHED: 01-24-2013
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It is unclear whether diabetes mellitus (DM) is an adverse prognostic factor in chronic heart failure (CHF) of ischaemic and non-ischaemic aetiology managed with contemporary evidence-based care.
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Fibrin clot structure and platelet aggregation in patients with aspirin treatment failure.
PLoS ONE
PUBLISHED: 01-01-2013
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Aspirin is a cornerstone in prevention of cardiovascular events and modulates both platelet aggregation and fibrin clot formation. Some patients experience cardiovascular events whilst on aspirin, often termed aspirin treatment failure (ATF). This study evaluated both platelet aggregation and fibrin clot structure in patients with ATF.
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Clot architecture is altered in abdominal aortic aneurysms and correlates with aneurysm size.
Arterioscler. Thromb. Vasc. Biol.
PUBLISHED: 09-15-2011
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Abdominal aortic aneurysm (AAA) is characterized by widening of the aorta. Once the aneurysm exceeds 5.5 cm, there is a 10% risk of death due to rupture. AAA is also associated with mortality due to other cardiovascular disease. Our aim was to investigate clot structure in AAA and its relationship to aneurysm size.
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Vascular insulin-like growth factor-I resistance and diet-induced obesity.
Endocrinology
PUBLISHED: 07-16-2009
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Obesity and type 2 diabetes mellitus are characterized by insulin resistance, reduced bioavailability of the antiatherosclerotic signaling molecule nitric oxide (NO), and accelerated atherosclerosis. IGF-I, the principal growth-stimulating peptide, which shares many of the effects of insulin, may, like insulin, also be involved in metabolic and vascular homeostasis. We examined the effects of IGF-I on NO bioavailability and the effect of obesity/type 2 diabetes mellitus on IGF-I actions at a whole-body level and in the vasculature. In aortic rings IGF-I blunted phenylephrine-mediated vasoconstriction and relaxed rings preconstricted with phenylephrine, an effect blocked by N(G)-monomethyl L-arginine. IGF-I increased NO synthase activity to an extent similar to that seen with insulin and in-vivo IGF-I led to serine phosphorylation of endothelial NO synthase (eNOS). Mice rendered obese using a high-fat diet were less sensitive to the glucose-lowering effects of insulin and IGF-I. IGF-I increased aortic phospho-eNOS levels in lean mice, an effect that was blunted in obese mice. eNOS activity in aortae of lean mice increased 1.6-fold in response to IGF-I compared with obese mice. IGF-I-mediated vasorelaxation was blunted in obese mice. These data demonstrate that IGF-I increases eNOS phosphorylation in-vivo, increases eNOS activity, and leads to NO-dependent relaxation of conduit vessels. Obesity is associated with resistance to IGF-I at a whole-body level and in the endothelium. Vascular IGF-I resistance may represent a novel therapeutic target to prevent or slow the accelerated vasculopathy seen in humans with obesity or type 2 diabetes mellitus.
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Symmetric dimethylarginine predicts all-cause mortality following ischemic stroke.
Atherosclerosis
PUBLISHED: 04-09-2009
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Methylarginines have been shown to interfere with nitric oxide (NO) formation by inhibiting NO synthase (asymmetric dimethylarginine, ADMA, and monomethylarginine, NMMA) and the cellular l-arginine uptake system (ADMA, NMMA and symmetric dimethylarginine, SDMA), thereby causing endothelial dysfunction. ADMA is a predictor of cardiovascular events and mortality in diverse populations.
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Nanoscale probing reveals that reduced stiffness of clots from fibrinogen lacking 42 N-terminal Bbeta-chain residues is due to the formation of abnormal oligomers.
Biophys. J.
PUBLISHED: 03-18-2009
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Removal of Bbetal-42 from fibrinogen by Crotalus atrox venom results in a molecule lacking fibrinopeptide B and part of a thrombin binding site. We investigated the mechanism of polymerization of desBbeta1-42 fibrin. Fibrinogen trinodular structure was clearly observed using high resolution noncontact atomic force microscopy. E-regions were smaller in desBbeta1-42 than normal fibrinogen (1.2 nm +/- 0.3 vs. 1.5 nm +/- 0.2), whereas there were no differences between the D-regions (1.7 nm +/- 0.4 vs. 1.7 nm +/- 0.3). Polymerization rate for desBbeta1-42 was slower than normal, resulting in clots with thinner fibers. Differences in oligomers were found, with predominantly lateral associations for desBbeta1-42 and longitudinal associations for normal fibrin. Clot elasticity as measured by magnetic tweezers showed a G of approximately 1 Pa for desBbeta1-42 compared with approximately 8 Pa for normal fibrin. Spring constants of early stage desBbeta1-42 single fibers determined by atomic force microscopy were approximately 3 times less than normal fibers of comparable dimensions and development. We conclude that Bbeta1-42 plays an important role in fibrin oligomer formation. Absence of Bbeta1-42 influences oligomer structure, affects the structure and properties of the final clot, and markedly reduces stiffness of the whole clot as well as individual fibrin fibers.
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Gender-specific alterations in fibrin structure function in type 2 diabetes: associations with cardiometabolic and vascular markers.
J. Clin. Endocrinol. Metab.
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Diabetes is associated with increased incidence of atherothrombotic disease. The fibrin network forms the backbone of the arterial thrombus, and fibrin clot structure determines predisposition to cardiovascular events.
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Effects of MASP-1 of the complement system on activation of coagulation factors and plasma clot formation.
PLoS ONE
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Numerous interactions between the coagulation and complement systems have been shown. Recently, links between coagulation and mannan-binding lectin-associated serine protease-1 (MASP-1) of the complement lectin pathway have been proposed. Our aim was to investigate MASP-1 activation of factor XIII (FXIII), fibrinogen, prothrombin, and thrombin-activatable fibrinolysis inhibitor (TAFI) in plasma-based systems, and to analyse effects of MASP-1 on plasma clot formation, structure and lysis.
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Complement C3 is a novel plasma clot component with anti-fibrinolytic properties.
Diab Vasc Dis Res
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Increased plasma clot density and prolonged lysis times are associated with cardiovascular disease. In this study, we employed a functional proteomics approach to identify novel clot components which may influence clot phenotypes.
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Insulin Resistance and Cardiovascular Risk Marker Evaluation in Morbid Obesity 12 Months After Bariatric Surgery Compared to Weight-Matched Controls.
Obes Surg
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Insulin resistance (IR) after bariatric surgery is significantly lower than controls matched for body mass index (BMI) and is indistinguishable from lean subjects however it is not known if this is the same for associated cardiovascular risk (CVR) markers (endothelial function (EF) and clot structure and function (maximum absorbance (MA) lysis potential (LT) and clot formation time (FT).
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What is Visualize?

JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

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We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

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In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.