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Find video protocols related to scientific articles indexed in Pubmed.
Chronic effects of shift work on cognition: findings from the VISAT longitudinal study.
Occup Environ Med
PUBLISHED: 11-05-2014
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Shift work, like chronic jet lag, is known to disrupt workers' normal circadian rhythms and social life, and to be associated with increased health problems (eg, ulcers, cardiovascular disease, metabolic syndrome, breast cancer, reproductive difficulties) and with acute effects on safety and productivity. However, very little is known about the long-term consequences of shift work on cognitive abilities. The aim of this study was to assess the chronicity and reversibility of the effects of shift work on cognition.
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Breslow Thickness, Clark Index and Ulceration Are Associated with Sentinel Lymph Node Metastasis in Melanoma Patients: A Cohort Analysis of 612 Patients.
Dermatology (Basel)
PUBLISHED: 08-26-2014
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Background: Sentinel lymph node biopsy (SLNB) is the most sensitive procedure for assessing nodal status in patients with primary melanoma. Objective: To evaluate the predictive ability of usual primary melanoma prognosis factors of detecting sentinel lymph node (SLN) metastasis in patients with melanoma. Patients and Methods: A cohort of 612 consecutive patients presenting with primary skin melanoma who underwent a SLNB was evaluated. Assessment of the determinants of SLN metastasis was based on general linear model analysis. The model performance was studied using the concordance statistic and the net reclassification index. The calibration was estimated using the Hosmer-Lemeshow test. Results: The discrimination ability did not differ significantly between Breslow thickness (0.57), Clark index (0.61), ulceration (0.57) and histological subtype (0.55). Clark index, ulceration and Breslow thickness were all significant and independent determinants of SLN metastasis. The predictive ability of the final model was 0.657. Conclusion: Breslow thickness, Clark index and ulceration are independent predictors of a SLN metastasis. © 2014 S. Karger AG, Basel.
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Front-line transplantation program with lenalidomide, bortezomib, and dexamethasone combination as induction and consolidation followed by lenalidomide maintenance in patients with multiple myeloma: a phase II study by the Intergroupe Francophone du Myélome.
J. Clin. Oncol.
PUBLISHED: 07-14-2014
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The three-drug combination of lenalidomide, bortezomib, and dexamethasone (RVD) has shown significant efficacy in multiple myeloma (MM). The Intergroupe Francophone du Myélome (IFM) decided to evaluate RVD induction and consolidation therapies in a sequential intensive strategy for previously untreated transplantation-eligible patients with MM.
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Reduced sphingosine kinase-1 and enhanced sphingosine 1-phosphate lyase expression demonstrate deregulated sphingosine 1-phosphate signaling in Alzheimer's disease.
Acta Neuropathol Commun
PUBLISHED: 01-09-2014
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The accumulation of beta amyloid (A?) peptides, a hallmark of Alzheimer's disease (AD) is related to mechanisms leading to neurodegeneration. Among its pleiotropic cellular effects, A? accumulation has been associated with a deregulation of sphingolipid metabolism. Sphingosine 1-phosphate (S1P) derived from sphingosine is emerging as a critical lipid mediator regulating various biological activities including cell proliferation, survival, migration, inflammation, or angiogenesis. S1P tissue level is low and kept under control through equilibrium between its synthesis mostly governed by sphingosine kinase-1 (SphK1) and its degradation by sphingosine 1-phosphate lyase (SPL). We have previously reported that A? peptides were able to decrease the activity of SphK1 in cell culture models, an effect that could be blocked by the prosurvival IGF-1/IGF-1R signaling.
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DNA polymerase theta up-regulation is associated with poor survival in breast cancer, perturbs DNA replication, and promotes genetic instability.
Proc. Natl. Acad. Sci. U.S.A.
PUBLISHED: 07-12-2010
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"Replicative stress" is one of the main factors underlying neoplasia from its early stages. Genes involved in DNA synthesis may therefore represent an underexplored source of potential prognostic markers for cancer. To this aim, we generated gene expression profiles from two independent cohorts (France, n=206; United Kingdom, n=117) of patients with previously untreated primary breast cancers. We report here that among the 13 human nuclear DNA polymerase genes, DNA Polymerase (POLQ) is the only one significantly up-regulated in breast cancer compared with normal breast tissues. Importantly, POLQ up-regulation significantly correlates with poor clinical outcome (4.3-fold increased risk of death in patients with high POLQ expression), and this correlation is independent of Cyclin E expression or the number of positive nodes, which are currently considered as markers for poor outcome. POLQ expression provides thus an additional indicator for the survival outcome of patients with high Cyclin E tumor expression or high number of positive lymph nodes. Furthermore, to decipher the molecular consequences of POLQ up-regulation in breast cancer, we generated human MRC5-SV cell lines that stably overexpress POLQ. Strong POLQ expression was directly associated with defective DNA replication fork progression and chromosomal damage. Therefore, POLQ overexpression may be a promising genetic instability and prognostic marker for breast cancer.
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Genome-wide analysis of cutaneous T-cell lymphomas identifies three clinically relevant classes.
J. Invest. Dermatol.
PUBLISHED: 02-04-2010
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This study was undertaken to identify recurrent genetic alterations of the three main types of cutaneous T-cell lymphomas (CTCLs): mycosis fungoides (MF), Sézary syndrome (SS), and cutaneous anaplastic large-cell lymphoma (CALCL). Using array-based comparative genomic hybridization, the molecular cytogenetic profiles of 72 samples obtained from 58 patients with CTCL corresponding to 24 transformed MF (T-MF), 16 SS, and 18 CALCLs were determined. T-MF was characterized by gains of 1q25-31, 7p22-11.2, 7q21, 7q31, and 17q12, and losses of 9p21, 10p11.2, and 10q26. SS exhibited gains of 8q23-24.3 and 17q23-24, as well as losses of 9p21, 10p12-11.2, 10q22-24, 10q25-26, and 17p13-q11.1. Finally, CALCL exhibited 6q27 and 13q34 losses. Such imbalances were statistically associated with one CTCL subtype. Unsupervised hierarchical clustering defined three categories of clinical relevance: (1) CALCL apart from epidermotropic-CTCL, (2) an SS-only category, and (3) a mixed category with T-MF and SS cases, with both primary and secondary SS cases. In rare cases, the genetic classification did not correspond to the inclusion diagnosis, possibly reflecting the association of two diseases in the same patient or initial misdiagnosis according to follow-up. Finally, different samples in the same patient clustered together, showing reproducibility of such a classifier.
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CDKN2A-CDKN2B deletion defines an aggressive subset of cutaneous T-cell lymphoma.
Mod. Pathol.
PUBLISHED: 01-29-2010
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Inactivation of the CDKN2A-CDKN2B locus has been reported in the most frequent subtypes of cutaneous T-cell lymphomas (CTCLs), mycosis fungoides, Sézary syndrome (SS) and CD30+ cutaneous anaplastic large cell lymphoma. To investigate whether genetic or epigenetic inactivation of CDKN2A-CDKN2B is more specifically observed in certain CTCL subtypes with clinical impact, we used array-comparative genomic hybridization, quantitative PCR, interphase fluorescent in situ hybridization and methylation analyses of p14(ARF) p16(INK4A) and p15(INK4B) promoters. We studied 67 samples from 58 patients with either transformed mycosis fungoides (n=24), SS (n=16) or CD30+ cutaneous anaplastic large cell lymphoma (n=18). We observed combined CDKN2A-CDKN2B deletion in both transformed mycosis fungoides (n=17, 71%) and SS patients (n=7, 44%), but, surprisingly, in only one CD30+ cutaneous anaplastic large cell lymphoma case. Interphase fluorescent in situ hybridization showed 9p21 loss in 17 out of 19 cases, with 9p21 deletion indicating either hemizygous (n=4) or homozygous (n=2) deletion, with mixed patterns in most patients (n=11). The limited size of 9p21 deletion was found to account for false-negative detection by either BAC arrays (n=9) or fluorescent in situ hybridization (n=2), especially in patients with Sézary syndrome (n=6). Methylation was found to be restricted to the p15(INK4B) gene promoter in patients with or without 9p21 deletion and did not correlate with prognosis. In contrast, CDKN2A-CDKN2B genetic loss was strongly associated with a shorter survival in CTCL patients (P=0.002) and more specifically at 24 months in transformed mycosis fungoides and SS patients (P=0.02). As immunohistochemistry for p16(INK4A) protein was not found to be informative, the genetic status of the CDKN2A-CDKN2B locus would be relevant in assessing patients with epidermotropic CTCLs in order to identify those cases where the disease was more aggressive.
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Autocrine control of glioma cells adhesion and migration through IRE1?-mediated cleavage of SPARC mRNA.
J. Cell. Sci.
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The endoplasmic reticulum (ER) is an organelle specialized for the folding and assembly of secretory and transmembrane proteins. ER homeostasis is often perturbed in tumor cells because of dramatic changes in the microenvironment of solid tumors, thereby leading to the activation of an adaptive mechanism named the unfolded protein response (UPR). The activation of the UPR sensor IRE1? has been described to play an important role in tumor progression. However, the molecular events associated with this phenotype remain poorly characterized. In the present study, we examined the effects of IRE1? signaling on the adaptation of glioma cells to their microenvironment. We show that the characteristics of U87 cell migration are modified under conditions where IRE1? activity is impaired (DN_IRE1). This is linked to increased stress fiber formation and enhanced RhoA activity. Gene expression profiling also revealed that loss of functional IRE1? signaling mostly resulted in the upregulation of genes encoding extracellular matrix proteins. Among these genes, Sparc, whose mRNA is a direct target of IRE1? endoribonuclease activity, was in part responsible for the phenotypic changes associated with IRE1? inactivation. Hence, our data demonstrate that IRE1? is a key regulator of SPARC expression in vitro in a glioma model. Our results also further support the crucial contribution of IRE1? to tumor growth, infiltration and invasion and extend the paradigm of secretome control in tumor microenvironment conditioning.
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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.