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Find video protocols related to scientific articles indexed in Pubmed.
Correlation between the expression of integrins in prostate cancer and clinical outcome in 1284 patients.
Ann Diagn Pathol
PUBLISHED: 07-10-2014
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The aim of this study was to investigate the expression of a panel of integrins in prostate cancer in order to explore their potential for tumor biology. Formalin-fixed and paraffin-embedded tissue samples of 1284 prostate cancer patients were retrieved from the archive of the Department of Pathology. Immunostaining was done with rabbit monoclonal antibodies directed against ?v?3, ?v?5, ?v?6, ?v?8, ?3, and ?v-pan. Staining results were correlated with clinicopathologic patient characteristics and patient survival. Immunostaining of tumor cells performed on whole tissue sections of 52 patients was sparse for ?v?3, ?v?6, and ?v?8, and more prevalent for ?v?5 and ?v-pan. ?v?5, ?v?8, and ?v-pan were selected for further analyses in tissue microarrays representing the entire study cohort. ?v?8 staining was generally observed in peripheral nerves. ?v?5 and ?v-pan provided strong evidence for the differential expression of these integrins in prostate cancer. The expression was variable with regard to the histoanatomical/cytoanatomical localization, cell type, intensity of immunolabeling, and Gleason pattern. ?v?5 and ?v-pan are differentially expressed in prostate cancer, and the differentiation of prostate cancer seems to influence integrin expression and subcellular distribution.
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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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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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Dynamic and volumetric variables reliably predict fluid responsiveness in a porcine model with pleural effusion.
PLoS ONE
PUBLISHED: 01-07-2013
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The ability of stroke volume variation (SVV), pulse pressure variation (PPV) and global end-diastolic volume (GEDV) for prediction of fluid responsiveness in presence of pleural effusion is unknown. The aim of the present study was to challenge the ability of SVV, PPV and GEDV to predict fluid responsiveness in a porcine model with pleural effusions.
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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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Inflammation and thrombosis in diabetes.
Thromb. Haemost.
PUBLISHED: 02-14-2011
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Patients with diabetes mellitus are at increased risk of cardiovascular morbidity and mortality. Atherothrombosis, defined as atherosclerotic lesion disruption with superimposed thrombus formation, is the most common cause of death among these patients. Following plaque rupture, adherence of platelets is followed by local activation of coagulation, the formation of a cross-linked fibrin clot and the development of an occlusive platelet rich fibrin mesh. Patients with diabetes exhibit a thrombotic risk clustering which is composed of hyper-reactive platelets, up regulation of pro-thrombotic markers and suppression of fibrinolysis. These changes are mainly mediated by the presence of insulin resistance and dysglycaemia and an increased inflammatory state which directly affects platelet function, coagulation factors and clot structure. This prothrombotic state is related to increased cardiovascular risk and may account for the reduced response to antithrombotic therapeutic approaches, underpinning the need for adequate antithrombotic therapy in patients with diabetes to reduce their cardiovascular mortality.
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PPARgamma activation attenuates T-lymphocyte-dependent inflammation of adipose tissue and development of insulin resistance in obese mice.
Cardiovasc Diabetol
PUBLISHED: 07-06-2010
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Inflammation of adipose tissue (AT) has been recently accepted as a first step towards obesity-mediated insulin resistance. We could previously show that mice fed with high fat diet (HFD) develop systemic insulin resistance (IR) and glucose intolerance (GI) associated with CD4-positive T-lymphocyte infiltration into visceral AT. These T-lymphocytes, when enriched in AT, participate in the development of fat tissue inflammation and subsequent recruitment of proinflammatory macrophages. The aim of this work was to elucidate the action of the insulin sensitizing PPARgamma on T-lymphocyte infiltration during development of IR, and comparison of the PPARgamma-mediated anti-inflammatory effects of rosiglitazone and telmisartan in diet-induced obesity model (DIO-model) in mice.
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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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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.

How does it work?

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

Video X seems to be unrelated to Abstract Y...

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.