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Find video protocols related to scientific articles indexed in Pubmed.
Does tranexamic acid stop haemoptysis?
Interact Cardiovasc Thorac Surg
PUBLISHED: 08-21-2013
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A best evidence topic in thoracic surgery was written according to a structured protocol. The question addressed was Does tranexamic acid stop haemoptysis? Altogether 49 papers were found using the reported search strategy, of which 13 represented the best evidence to answer the clinical question. The authors, journal, date and country of publication, patient group studied, study type, relevant outcomes and results of these papers are tabulated. This consisted of one systematic review including a meta-analysis of two double-blind randomized controlled trials (RCTs), the two RCTs, one cohort study, two case-series and seven case reports. Main outcomes included bleeding time, bleeding volume and occurrence of thromboembolic complications after start of treatment. Based on results from the meta-analysis, no difference in remission of bleeding within 1 week was found between tranexamic acid (TA) and placebo groups (odds ratio 1.56, 95% CI: 0.44-5.46). However, overall bleeding time was significantly shorter for the TA group (weighted mean difference -19.47, 95% CI: -26.90, -12.03 h). In one RCT, TA reduced both the duration and the volume of bleeding compared with patients receiving placebo (both P < 0.0005). However, the other RCT failed to find a difference in bleeding time (P = 0.2). In these studies, no patient suffered from thromboembolic complications. Two case reports, however, describe development of pulmonary embolism during TA treatment. Several case reports on the use of TA for treatment of haemoptysis secondary to cystic fibrosis were found. In general, they suggest that TA may be a useful and well-tolerated medication for the treatment of intractable haemoptysis in this patient group. We conclude that limited research on the use of TA for treatment of haemoptysis exists. As aetiology of haemoptysis as well as length of treatment, dosage and form of TA administration varied between the studies, strong recommendations are difficult to give. Current best evidence, however, indicates that TA may reduce both the duration and volume of bleeding, with low risk of short-term thromboembolic complications, in patients with haemoptysis.
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Galacturonosyltransferase (GAUT)1 and GAUT7 are the core of a plant cell wall pectin biosynthetic homogalacturonan:galacturonosyltransferase complex.
Proc. Natl. Acad. Sci. U.S.A.
PUBLISHED: 11-30-2011
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Plant cell wall pectic polysaccharides are arguably the most complex carbohydrates in nature. Progress in understanding pectin synthesis has been slow due to its complex structure and difficulties in purifying and expressing the low-abundance, Golgi membrane-bound pectin biosynthetic enzymes. Arabidopsis galacturonosyltransferase (GAUT) 1 is an ?-1,4-galacturonosyltransferase (GalAT) that synthesizes homogalacturonan (HG), the most abundant pectic polysaccharide. We now show that GAUT1 functions in a protein complex with the homologous GAUT7. Surprisingly, although both GAUT1 and GAUT7 are type II membrane proteins with single N-terminal transmembrane-spanning domains, the N-terminal region of GAUT1, including the transmembrane domain, is cleaved in vivo. This raises the question of how the processed GAUT1 is retained in the Golgi, the site of HG biosynthesis. We show that the anchoring of GAUT1 in the Golgi requires association with GAUT7 to form the GAUT1:GAUT7 complex. Proteomics analyses also identified 12 additional proteins that immunoprecipitate with the GAUT1:GAUT7 complex. This study provides conclusive evidence that the GAUT1:GAUT7 complex is the catalytic core of an HG:GalAT complex and that cell wall matrix polysaccharide biosynthesis occurs via protein complexes. The processing of GAUT1 to remove its N-terminal transmembrane domain and its anchoring in the Golgi by association with GAUT7 provides an example of how specific catalytic domains of plant cell wall biosynthetic glycosyltransferases could be assembled into protein complexes to enable the synthesis of the complex and developmentally and environmentally plastic plant cell wall.
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Epigenetic mechanisms in multiple sclerosis and the major histocompatibility complex (MHC).
Discov Med
PUBLISHED: 03-31-2011
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Multiple sclerosis (MS) is a complex disorder of the central nervous system characterized by demyelination, axonal loss, and inflammation. The cause of MS is currently unknown although genetic and environmental factors contribute to etiology. The relative importance of each has been disputed; however, now it is clear that much of the disease results from the interaction of the environment and the genetics. Epigenetic modifications within the major histocompatibility complex (MHC) likely mediate interactions at this locus with current known environmental risk factors--vitamin D, Epstein-Barr virus, and smoking. Maternal parent-of-origin effects, month of birth effects and transgenerational differences in allele frequency are also evident in MS and may be mediated by sex-specific epigenetic mechanisms. Differences in epigenetic marks characterize monozygotic twin pairs and may explain discordance. There is promise of potential therapeutic strategies to be found in the epigenetic mechanisms at work in MS.
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Heterogeneity in multiple sclerosis: scratching the surface of a complex disease.
Autoimmune Dis
PUBLISHED: 09-08-2010
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Multiple Sclerosis (MS) is the most common demyelinating disease of the central nervous system. Although the etiology and the pathogenesis of MS has been extensively investigated, no single pathway, reliable biomarker, diagnostic test, or specific treatment have yet been identified for all MS patients. One of the reasons behind this failure is likely to be the wide heterogeneity observed within the MS population. The clinical course of MS is highly variable and includes several subcategories and variants. Moreover, apart from the well-established association with the HLA-class II DRB1*15:01 allele, other genetic variants have been shown to vary significantly across different populations and individuals. Finally both pathological and immunological studies suggest that different pathways may be active in different MS patients. We conclude that these "MS subtypes" should still be considered as part of the same disease but hypothesize that spatiotemporal effects of genetic and environmental agents differentially influence MS course. These considerations are extremely relevant, as outcome prediction and personalised medicine represent the central aim of modern research.
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A ChIP-seq defined genome-wide map of vitamin D receptor binding: associations with disease and evolution.
Genome Res.
PUBLISHED: 08-24-2010
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Initially thought to play a restricted role in calcium homeostasis, the pleiotropic actions of vitamin D in biology and their clinical significance are only now becoming apparent. However, the mode of action of vitamin D, through its cognate nuclear vitamin D receptor (VDR), and its contribution to diverse disorders, remain poorly understood. We determined VDR binding throughout the human genome using chromatin immunoprecipitation followed by massively parallel DNA sequencing (ChIP-seq). After calcitriol stimulation, we identified 2776 genomic positions occupied by the VDR and 229 genes with significant changes in expression in response to vitamin D. VDR binding sites were significantly enriched near autoimmune and cancer associated genes identified from genome-wide association (GWA) studies. Notable genes with VDR binding included IRF8, associated with MS, and PTPN2 associated with Crohns disease and T1D. Furthermore, a number of single nucleotide polymorphism associations from GWA were located directly within VDR binding intervals, for example, rs13385731 associated with SLE and rs947474 associated with T1D. We also observed significant enrichment of VDR intervals within regions of positive selection among individuals of Asian and European descent. ChIP-seq determination of transcription factor binding, in combination with GWA data, provides a powerful approach to further understanding the molecular bases of complex diseases.
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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.