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Find video protocols related to scientific articles indexed in Pubmed.
Independent replication of an association of CNVR7113.6 with Crohns disease in Caucasians.
Inflamm. Bowel Dis.
PUBLISHED: 03-06-2011
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A recent genome-wide association study (GWAS) of copy number variants (CNVs) in Crohns disease (CD) confirmed association of three CNVs. The GWAS also provided evidence that a fourth CNV, CNVR7113.6, on chromosome 17 may alter susceptibility to CD (P = 0.0018). The aim of our study was to confirm the CNVR7113.6 association by genotyping two independent inflammatory bowel disease (IBD) cohorts and by conducting a subsequent meta-analysis.
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Differential association of two PTPN22 coding variants with Crohns disease and ulcerative colitis.
Inflamm. Bowel Dis.
PUBLISHED: 02-01-2011
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The PTPN22 gene is an important risk factor for human autoimmunity. The aim of this study was to evaluate for the first time the role of the R263Q PTPN22 polymorphism in ulcerative colitis (UC) and Crohns disease (CD), and to reevaluate the association of the R620W PTPN22 polymorphism with both diseases.
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Analysis of the influence of two CD24 genetic variants in Crohns disease and ulcerative colitis.
Hum. Immunol.
PUBLISHED: 01-19-2011
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The aim of this study was to evaluate the possible implication of CD24 gene in the genetic predisposition to inflammatory bowel disease (IBD). Our study population consisted of 1321 female Spanish individuals (369 Crohns disease [CD] patients, 323 ulcerative colitis [UC] patients, and 629 healthy matched controls). Two putative functional polymorphisms, a C to T coding polymorphism (rs8734) and a TG deletion in the 3 untranslated region (rs3838646), were used as CD24 genetic markers and genotyped using a Taqman 5 allelic discrimination assay. The "del" allele of the dinucleotide deletion was associated with an increased risk of CD (odds ratio = 1.61, 95% confidence interval = 1.17-2.21, p(FDR) = 6.4E-03) but not with UC. Moreover, this allele was significant associated with the age of CD diagnosis between 17 and 40 years, the ileocolonic location, and the inflammatory behavior of CD. We observed no significant differences between the allelic or genotypic frequencies of the A57V polymorphism in our studied IBD cohort. Our results suggest that the rs3838646 CD24 polymorphism is part of the genetic background of CD.
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[Evaluation of bone mineral density, bone turnover markers, the OPG/RANKL system and sTNF-RI in Crohns disease].
Gastroenterol Hepatol
PUBLISHED: 01-08-2011
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Patients with Crohns disease are at risk of developing osteoporosis, a disease in which the inflammatory process seems to be gaining importance. We performed a cross-sectional study to evaluate bone metabolism, osteoclastogenic factors [receptor activator of NF-kB ligand (RANK-L) and osteoprotegerin (OPG)] and soluble tumor necrosis factor-? receptor I (sTNF-RI) in patients with Crohns disease and to correlate the findings with the degree of disease activity.
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CD40: novel association with Crohns disease and replication in multiple sclerosis susceptibility.
PLoS ONE
PUBLISHED: 04-26-2010
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A functional polymorphism located at -1 from the start codon of the CD40 gene, rs1883832, was previously reported to disrupt a Kozak sequence essential for translation. It has been consistently associated with Graves disease risk in populations of different ethnicity and genetic proxies of this variant evaluated in genome-wide association studies have shown evidence of an effect in rheumatoid arthritis and multiple sclerosis (MS) susceptibility. However, the protective allele associated with Graves disease or rheumatoid arthritis has shown a risk role in MS, an effect that we aimed to replicate in the present work. We hypothesized that this functional polymorphism might also show an association with other complex autoimmune condition such as inflammatory bowel disease, given the CD40 overexpression previously observed in Crohns disease (CD) lesions.
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[Vitamin D deficiency and bone mineral density in Crohns disease].
Med Clin (Barc)
PUBLISHED: 02-20-2010
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Inadequate serum levels of 25-hydroxyvitamin D (25OHD(3)) are deemed as a possible risk factor for osteoporosis in Crohns disease (CD). Our aim is to determine the prevalence of inadequate serum levels of 25OHD(3) and its possible relationship with low bone mineral disease (BMD) in CD.
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STAT4 gene influences genetic predisposition to ulcerative colitis but not Crohns disease in the Spanish population: a replication study.
Hum. Immunol.
PUBLISHED: 01-21-2010
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Recently, the signal transducer and activator of transcription 4 (STAT4) gene has been associated with multiple autoimmune diseases. Interestingly, a recent work showed that the T allele of the rs7574865 STAT4 SNP was associated with inflammatory bowel disease (IBD) in a Spanish population. The aim of the present study was to reevaluate the role of the STAT4 rs7574865 polymorphism on IBD. The present case-control study included 498 Crohns disease (CD) patients, 402 ulcerative colitis (UC) patients, and 1296 healthy matched controls. Genotyping was performed using a PCR system with a pre-developed TaqMan allelic discrimination assay for the rs7574865 STAT4 SNP. Moreover, a meta-analysis was performed with the previous work in a Spanish population and the current study, including a final sample size of 1574 IBD patients (820 with CD and 754 with UC) and 2012 healthy controls. No evidence of association was found for the current case-control study (CD: p = 0.23, OR = 0.9, 95% CI = 0.75-1.1; UC: p = 0.17, OR = 1.14, 95% CI = 0.95-1.38). However, the meta-analysis showed that the STAT4 rs7574865 T allele was significantly associated with susceptibility to UC (p = 0.012 pooled; OR = 1.20, 95% CI = 1.04-1.39) but not CD (p = 0.71 pooled; OR = 0.93, 95% CI = 0.65-1.34). Our data suggest that the rs7574865 STAT4 SNP is a genetic susceptibility variant for UC but not CD in the Spanish population.
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Glibenclamide-pregnenolone derivative has greater hypoglycemic effects and biodistribution than glibenclamide-OH in alloxan-rats.
Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub
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The present study was designed to investigate the activity of two glibenclamide derivatives on glucose concentration. An additional aim was to identify the biodistribution of glibenclamide derivatives in different organs in a diabetic animal model.
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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.