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Find video protocols related to scientific articles indexed in Pubmed.
Mycobacterium ulcerans Infection Imported from Australia to Missouri, USA, 2012.
Emerging Infect. Dis.
PUBLISHED: 10-24-2014
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Buruli ulcer, the third most common mycobacterial disease worldwide, rarely affects travelers and is uncommon in the United States. We report a travel-associated case imported from Australia and review 3 previous cases diagnosed and treated in the United States. The differential diagnoses for unusual chronic cutaneous ulcers and those nonresponsive to conventional therapy should include Mycobacterium ulcerans infection.
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Prospects for a dengue vaccine: progress and pitfalls.
Mo Med
PUBLISHED: 09-13-2014
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Dengue virus is now the world's most common arboviral infection and has spread to the continental United States. The Aedes mosquito which transmits dengue is prevalent throughout Missouri, so clinicians should be familiar with dengue. While there are no licensed vaccines, five are in human trials including two tested at the Saint Louis University Center for Vaccine Development. Our deepening understanding of the correlates of protective immunity to dengue improves near-term prospects for a vaccine.
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Wnt5a-induced wnt1-inducible secreted protein-1 suppresses vascular smooth muscle cell apoptosis induced by oxidative stress.
Arterioscler. Thromb. Vasc. Biol.
PUBLISHED: 09-11-2014
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Apoptosis of vascular smooth muscle cells (VSMCs) contributes to thinning and rupture of the atherosclerotic plaque fibrous cap and is thereby associated with myocardial infarction. Wnt protein activation of ?-catenin regulates numerous genes that are associated with cell survival. We therefore investigated Wnt/?-catenin survival signaling in VSMCs and assessed the presence of this pathway in human atherosclerotic plaques at various stages of the disease process.
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Human pegivirus (GB virus C) NS3 protease activity inhibits induction of the type I interferon response and is not inhibited by HCV NS3 protease inhibitors.
Virology
PUBLISHED: 02-04-2014
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We previously found that human pegivirus (HPgV; formerly GBV-C) NS3 protease activity inhibits Human Immunodeficiency Virus (HIV) replication in a CD4+ T cell line. Given the protease?s similarity to the Hepatitis C virus (HCV) NS3 protease, we characterized HPgV protease activity and asked whether it affects the type I interferon response or is inhibited by HCV protease antagonists. We characterized the activity of proteases with mutations in the catalytic triad and demonstrated that the HCV protease inhibitors Telaprevir, Boceprevir, and Danoprevir do not affect HPgV protease activity. HPgV NS3 protease cleaved MAVS but not TRIF, and it inhibited interferon responses sufficiently to enhance growth of an interferon-sensitive virus. Therefore, HPgV?s inhibition of the interferon response could help promote HPgV persistence, which is associated with clinical benefits in HIV-infected patients. Our results also imply that HCV protease inhibitors should not interfere with the beneficial effects of HPgV in HPgV/HCV/HIV infected patients.
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miRNA-21 is dysregulated in response to vein grafting in multiple models and genetic ablation in mice attenuates neointima formation.
Eur. Heart J.
PUBLISHED: 03-25-2013
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The long-term failure of autologous saphenous vein bypass grafts due to neointimal thickening is a major clinical burden. Identifying novel strategies to prevent neointimal thickening is important. Thus, this study aimed to identify microRNAs (miRNAs) that are dysregulated during neointimal formation and determine their pathophysiological relevance following miRNA manipulation.
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Sustained reduction of vein graft neointima formation by ex vivo TIMP-3 gene therapy.
Circulation
PUBLISHED: 09-14-2011
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Coronary artery vein graft failure, resulting from thrombosis, intimal thickening, and atherosclerosis, is a significant clinical problem, with approximately 50% of vein grafts failing within 10 years. Intimal thickening is caused by migration of vascular smooth muscle cells from the media to the intima, where they proliferate. Interventions using gene transfer to inhibit vascular smooth muscle cells proliferation and migration are attractive because ex vivo access to the graft is possible. The involvement of matrix-degrading metalloproteinases in intimal thickening is well established, and we previously showed that adenoviral-delivered overexpression of an endogenous inhibitor, the tissue inhibitor of metalloproteinases-3 (TIMP-3), significantly retarded intimal thickening in short-term autologous porcine arteriovenous interposition grafts (28 days). However, it is essential to determine whether this approach will provide longer-term benefits.
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The Wnt pathways in vascular disease: lessons from vascular development.
Curr. Opin. Lipidol.
PUBLISHED: 08-16-2011
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We aim to highlight the emerging evidence for the role of the Wnt signalling pathways in vascular disease and indicate how our current understanding is supported by observations of Wnt signalling in vascular development.
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Matrix metalloproteinase (MMP)-3 activates MMP-9 mediated vascular smooth muscle cell migration and neointima formation in mice.
Arterioscler. Thromb. Vasc. Biol.
PUBLISHED: 06-30-2011
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Several matrix metalloproteinases (MMPs) have been implicated in extracellular matrix destruction and other actions that lead to plaque rupture and myocardial infarction. Conversely, other MMPs have been shown to promote vascular smooth muscle cell (VSMC)-driven neointima formation, which contributes to restenosis, fibrous cap formation, and plaque stability. MMP-3 knockout reduced VSMC accumulation in mouse atherosclerotic plaques, implicating MMP-3 in neointima formation. We therefore investigated the effect of MMP-3 knockout on neointima formation after carotid ligation in vivo and VSMC migration in vitro.
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Entorhinal cortex volume is associated with episodic memory related brain activation in normal aging and amnesic mild cognitive impairment.
Brain Imaging Behav
PUBLISHED: 02-18-2011
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The present study examined the relationship between entorhinal cortex and hippocampal volume with fMRI activation during episodic memory function in elderly controls with no cognitive impairment and individuals with amnesic mild cognitive impairment (aMCI). Both groups displayed limited evidence for a relationship between hippocampal volume and fMRI activation. Smaller right entorhinal cortex volume was correlated with reduced activation in left and right medial frontal cortex (BA 8) during incidental encoding for both aMCI and elderly controls. However, during recognition, smaller left entorhinal cortex volume correlated with reduced activation in right BA 8 for the control group, but greater activation for the aMCI group. There was no significant relationship between entorhinal cortex volume and activation during intentional encoding in either group. The recognition-related dissociation in structure/function relationships in aMCI paralleled our behavioral findings, where individuals with aMCI displayed poorer performance relative to controls during recognition, but not encoding. Taken together, these results suggest that the relationship between entorhinal cortex volume and fMRI activation during episodic memory function is altered in individuals with aMCI.
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Prevention of post-cardiopulmonary bypass acute kidney injury by endothelin A receptor blockade.
Crit. Care Med.
PUBLISHED: 01-12-2011
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The aim of this study was to determine whether administration of a specific endothelin A receptor antagonist, sitaxsentan sodium, would prevent the development of post-cardiopulmonary bypass acute kidney injury in swine.
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A selective matrix metalloproteinase-12 inhibitor retards atherosclerotic plaque development in apolipoprotein E-knockout mice.
Arterioscler. Thromb. Vasc. Biol.
PUBLISHED: 01-06-2011
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Matrix metalloproteinase (MMP)-12 has been implicated in plaque progression and instability and is also amenable to selective inhibition. In this study, we investigated the influence of a greater than 10-fold selective synthetic MMP-12 inhibitor on plaque progression in the apolipoprotein E knockout mouse model of atherosclerosis.
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Regulation of VSMC behavior by the cadherin-catenin complex.
Front Biosci (Landmark Ed)
PUBLISHED: 01-04-2011
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Vascular smooth muscle cells (VSMCs) are the predominant cell type within blood vessels. In normal vessels VSMC have low rates of proliferation, migration and apoptosis. However, increased VSMC proliferation, migration, and apoptosis rates radically alter the composition and structure of the blood vessel wall and contribute to vascular diseases such as atherosclerosis, in-stent restenosis and vein graft failure. Consequently, therapies that modulate VSMC proliferation, migration and apoptosis may be useful for treating vascular diseases. In this review article we discuss recently emerging research that has revealed that homophilic cell-cell contacts mediated by the cadherin:catenin complex and Wnt/beta-catenin signalling are important regulators of VSMC behaviour.
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Wnt4/?-catenin signaling induces VSMC proliferation and is associated with intimal thickening.
Circ. Res.
PUBLISHED: 12-30-2010
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Vascular smooth muscle cell (VSMC) proliferation causes intimal thickening in atherosclerosis and restenosis. Previously, we demonstrated that Wnt/?-catenin signaling upregulates VSMC proliferation in vitro.
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Managing cetuximab hypersensitivity-infusion reactions: incidence, risk factors, prevention, and retreatment.
J Support Oncol
PUBLISHED: 05-15-2010
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Cetuximab is an anti-epidermal growth factor receptor (EGFR) monoclonal antibody approved by the US Food and Drug Administration for the treatment of colorectal (CRC) and head and neck (H&N) cancers. Hypersensitivity-infusion reactions (HIRs) confer moderate morbidity and potential mortality. HIRs have a wide geographic incidence with few identifiable risk factors. Limited data regarding risk-reduction interventions for HIR or post-HIR retreatment are available. All patients treated with cetuximab at a single Veterans Affairs facility were monitored for development of HIRs, with baseline clinical, demographic, and supportive care data recorded. All received standard premedication based on cohort assignment. A total of 51 consecutive patients (30 CRC; 21 H&N) received at least one dose of cetuximab. Grades II-IV HIRs occurred in 14 patients (27%; 6 grade II, 6 grade Ill, 2 grade IV). There was no grade V HIR. All HIRs occurred during the first infusion. There were no differences between age, race, diagnosis, stage, concurrent chemotherapy, or radiotherapy with cetuximab, allergy history, or military service era of patients developing HIRs versus those who did not.There were no identifiable risk factors that predicted the severity of HIR. Neither premedication modifications (P = 0.34) nor bronchodilator use (P= 0.12) impacted the incidence or severity of HIR. A cetuximab test dose successfully elicited an HIR and resulted in an 87% cost savings. None of five patients receiving subsequent retreatment with anti-EGFR MoAb had recurrence of an HIR. An HIR during cetuximab infusion can be a serious and underestimated toxicity. The relatively high incidence reported here is consistent with that previously identified in the Southeastern United States. No clinical, demographic, or historic variables reliably predicted HIR in our population. Use of a test dose to elicit a HIR appears to be feasible and cost-effective. Use of panitumumab after a cetuximab HIR in select patients with CRC appears to be feasible and safe.
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Inhibition of N-cadherin retards smooth muscle cell migration and intimal thickening via induction of apoptosis.
J. Vasc. Surg.
PUBLISHED: 04-19-2010
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Inhibition of vascular smooth muscle cell (VSMC) migration is a potential strategy for reducing intimal thickening during in-stent restenosis and vein graft failure. In this study, we examined the effect of disrupting the function of the VSMC adhesion molecule, N-cadherin, using antagonists, neutralizing antibodies, and a dominant negative, on VSMC migration and intimal thickening. Migration was assessed by the scratch-wound assay of human saphenous vein VSMCs and in a human saphenous vein ex vivo organ culture model of intimal thickening.
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The first-in-human study of the hydrogen sulfate (Hyd-sulfate) capsule of the MEK1/2 inhibitor AZD6244 (ARRY-142886): a phase I open-label multicenter trial in patients with advanced cancer.
Clin. Cancer Res.
PUBLISHED: 02-23-2010
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In part A, the aim was to define the maximum tolerated dose (MTD) of the hydrogen sulfate (Hyd-Sulfate) oral capsule formulation of the mitogen-activated protein kinase kinase inhibitor AZD6244 (ARRY-142886). In part B, the aim was to compare the pharmacokinetic profile of the new Hyd-Sulfate capsule with the initial AZD6244 free-base suspension and further characterize the pharmacodynamic profile and efficacy of the new formulation.
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In situ zymography.
Methods Mol. Biol.
PUBLISHED: 02-06-2010
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In situ zymography is a unique laboratory technique that enables the localisation of matrix-degrading metalloproteinase (MMP) activity in histological sections. Frozen sections are placed on glass slides coated with fluorescently labelled matrix proteins. After incubation MMP activity can be observed as black holes in the fluorescent background due to proteolysis of the matrix protein. Alternatively frozen sections can be incubated with matrix proteins conjugated to quenched fluorescein. Proteolysis of the substrate by MMPs leads to the release of fluorescence. This technique can be combined with immunohistochemistry to enable co-location of proteins such as cell type markers or other proteins of interest. Additionally, this technique can be adapted for use with cell cultures, permitting precise location of MMP activity within cells, time-lapse analysis of MMP activity and analysis of MMP activity in migrating cells.
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MMP-7 mediates cleavage of N-cadherin and promotes smooth muscle cell apoptosis.
Cardiovasc. Res.
PUBLISHED: 02-05-2010
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Vascular smooth muscle cell (VSMC) apoptosis can lead to thinning of the fibrous cap and plaque instability. We previously showed that cell-cell contacts mediated by N-cadherin reduce VSMC apoptosis. This study aimed to determine whether matrix-degrading metalloproteinase (MMP)-dependent N-cadherin cleavage causes VSMC apoptosis.
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Dysregulation of cadherins in the intercalated disc of the spontaneously hypertensive stroke-prone rat.
J. Mol. Cell. Cardiol.
PUBLISHED: 01-26-2010
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The structural integrity of cardiac cells is maintained by the Ca(2+)-dependent homophilic cell-cell adhesion of cadherins. N-cadherin is responsible for this adhesion under normal physiological conditions. The role of cadherins in adverse cardiac pathology is less clear. We studied the hearts of the stroke-prone spontaneously hypertensive (SHRSP) rat as a genetic model of cardiac hypertrophy and compared them to Wistar-Kyoto control animals. Western blotting of protein homogenates from 12-week old SHRSP animals indicated that similar levels of beta, gamma-, and alpha-catenin and T, N and R-cadherin were expressed in the control and SHRSP animals. However, dramatically higher levels of E-cadherin were detected in SHRSP animals compared to controls at 6, 12 and 18 weeks of age. This was confirmed by quantitative Taqman PCR and immunohistochemistry. E-cadherin was located at the intercalated disc of the myocytes in co-localisation with connexin 43. Adenoviral overexpression of E-cadherin in rat H9c2 cells and primary rabbit myocytes resulted in a significant reduction in myocyte cell diameter and breadth. E-cadherin overexpression resulted in re-localisation of beta-catenin to the cell surface particularly to cell-cell junctions. Subsequent immunohistochemistry of the hearts of WKY and SHRSP animals also revealed increased levels of beta-catenin in the intercalated disc in the SHRSP compared to WKY. Therefore, remodelling of the intercalated disc in the hearts of SHRSP animals may contribute to the altered function observed in these animals.
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Vulnerable atherosclerotic plaque metalloproteinases and foam cell phenotypes.
Thromb. Haemost.
PUBLISHED: 06-04-2009
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Plaque rupture underlies most myocardial infarctions. Plaques vulnerable to rupture have thin fibrous caps, an excess of macrophages over vascular smooth muscle cells, large lipid cores, and depletion of collagen and other matrix proteins form the cap and lipid core. Production of matrix metalloproteinases from macrophages is prominent in human plaques, and studies in genetically modified mice imply a causative role for metalloproteinases in plaque vulnerability. Recent in-vitro studies on human monocyte-derived macrophages and on foam-cell macrophages generated in vivo suggest the existence of several macrophage phenotypes with distinct patterns of metalloproteinase expression. These phenotypes could play differing roles in cap, core and aneurysm formation.
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MMP-9 and -12 cause N-cadherin shedding and thereby beta-catenin signalling and vascular smooth muscle cell proliferation.
Cardiovasc. Res.
PUBLISHED: 04-11-2009
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Vascular smooth muscle cell (VSMC) proliferation contributes to intimal thickening in restenosis and atherosclerosis. Previously, we demonstrated that matrix-degrading metalloproteinase (MMP)-dependent shedding of the extracellular portion of N-cadherin increased VSMC proliferation via elevation of beta-catenin signalling and cyclin D1 expression. In this study, we aimed to determine whether MMP-2, -9, -12, or -14 regulates VSMC proliferation via N-cadherin shedding.
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Clinical, virologic, histologic, and biochemical outcomes after successful HCV therapy: a 5-year follow-up of 150 patients.
Hepatology
PUBLISHED: 04-02-2009
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One hundred fifty patients with sustained virologic response (SVR) after treatment of chronic hepatitis C were enrolled in a long-term clinical follow-up study; patients were followed for 5 years for liver-related outcomes and evidence of biochemical or virologic relapse. Patients with stage 2 or greater fibrosis on pretreatment biopsy were invited to undergo a long-term follow-up biopsy after their fourth year of follow-up. One hundred twenty-eight patients (85%) were followed through their fourth year, and long-term follow-up biopsies were obtained from 60 patients (40%). Forty-nine patients had paired pretreatment and long-term follow-up biopsies blindly rescored. Forty of these patients (82%) had a decrease in fibrosis score, and 45 (92%) had a decrease in combined inflammation score. Ten patients (20%) had normal or nearly normal livers on long-term follow-up biopsy. Two patients with pretreatment cirrhosis developed hepatocellular carcinoma (HCC), and one died. All the other patients with pretreatment cirrhosis or advanced fibrosis had improved fibrosis scores on long-term follow-up biopsy. No patient had conclusive evidence of virologic relapse. Three patients had persistently elevated alanine aminotransferase levels; two of these had new liver disease.
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Soluble N-cadherin overexpression reduces features of atherosclerotic plaque instability.
Arterioscler. Thromb. Vasc. Biol.
PUBLISHED: 02-06-2009
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Vascular smooth muscle cell (VSMC) apoptosis contributes to atherosclerotic plaque instability and myocardial infarction. Consequently, reducing VSMC apoptosis may be beneficial for reducing plaque instability and acute coronary events. We previously demonstrated that N-cadherin, a cell-cell adhesion molecule, reduces VSMC apoptosis in vitro. In this study, we examined whether a soluble form of N-cadherin (SNC) affected VSMC apoptosis and plaque stability.
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Wnt signalling in smooth muscle cells and its role in cardiovascular disorders.
Cardiovasc. Res.
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Vascular smooth muscle cells (SMCs) are the major cell type within blood vessels. SMCs exhibit low rates of proliferation, migration, and apoptosis in normal blood vessels. However, increased SMC proliferation, migration, and apoptosis rates radically alter the composition and structure of the blood vessel wall and contribute to cardiovascular diseases, such as atherosclerosis, and restenosis that occur after coronary artery vein grafting and stent implantation. Consequently, therapies that modulate SMC proliferation, migration, and apoptosis may be useful for treating cardiovascular diseases. The family of Wnt proteins, which were first identified in the wingless drosophila, has a well-established role in embryogenesis and development. It is now emerging that Wnt proteins also regulate SMC proliferation, migration, and survival. In this review article, we discuss recently emerging research that has revealed that Wnt proteins are important regulators of SMC behaviour via activation of ?-catenin-dependent and ?-catenin-independent Wnt signalling pathways.
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The GB virus C (GBV-C) NS3 serine protease inhibits HIV-1 replication in a CD4+ T lymphocyte cell line without decreasing HIV receptor expression.
PLoS ONE
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Persistent infection with GBV-C (GB Virus C), a non-pathogenic virus related to hepatitis C virus (HCV), prolongs survival in HIV infection. Two GBV-C proteins, NS5A and E2, have been shown previously to inhibit HIV replication in vitro. We investigated whether the GBV-C NS3 serine protease affects HIV replication.
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Higher antigen content improves the immune response to 2009 H1N1 influenza vaccine in HIV-infected adults: a randomized clinical trial.
J. Infect. Dis.
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The immunogenicity of a high hemagglutinin (HA) dose or a second dose of influenza vaccine in human immunodeficiency virus (HIV)-infected individuals has not been fully explored.
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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.