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Attrition is a major obstacle for lifestyle interventions sustained for the medium-to-long term and can have significant consequences on the internal validity of a trial. When the degree of attrition differs between active and control arms this is termed differential attrition and is an important consideration during initial stages of trial planning.
The primary research question of this study was what is the differential attrition between treatment arms in lifestyle interventions for prevalent chronic diseases?
We performed a systematic review and meta-analysis of 23 studies involving a lifestyle intervention component in cohorts with chronic diseases. The search accessed three databases Scopus, Medline Ovid and Web of Science. Attrition between treatment arms was analysed using a random-effects model and examined the relationship between the relative attrition and potential moderators, such as time to final follow-up, time to first follow-up, type of disease, type of control, type of intervention and length of treatment.
The pooled risk ratio was 1.00 (95% CI 0.97 - 1.03) and only one study fell outside this range. A univariable association was described between the pooled risk ration and length (years) to final follow-up, which did not remain in the multivariable model.
Ultimately, we found no evidence of differential attrition in medium-to-long term lifestyle intervention studies for chronic disease, increasing confidence in conducting such studies with minimal potential of attrition bias.
PROSPERO registration number CRD42018084495 .
PROSPERO registration number CRD42018084495 .
Migraine is a multifactorial disorder that is more frequent (two to four times) in women than in men. In recent years, our research group has focused on the role of neurotransmitter release and its regulation. Neurexin (NRXN2) is one of the components of the synaptic vesicle machinery, responsible for connecting intracellular fusion proteins and synaptic vesicles. Our aim was to continue exploring the role and interaction of proteins involved in the control and promotion of neurotransmission in migraine susceptibility.
A case-control study was performed comprising 183 migraineurs (148 females and 35 males) and 265 migraine-free controls (202 females and 63 males). Tagging single nucleotide polymorphisms of NRXN2 were genotyped to assess the association between NRXN2 and migraine susceptibility. The χ
test was used to compare allele frequencies in cases and controls and odds ratios were estimated with 95% confidence intervals. Haplotype frequencies were compared between groups. Gene-gene interactions werthe synergetic effect between those genes and its relation with migraine susceptibility. These gene interactions, which may be a part of a larger network, can potentially help us in better understanding migraine aetiology and in development of new therapeutic approaches.
This study unravels, for the first time, the gene-gene interactions between NRXN2, GABRE - a GABAA-receptor - and CASK, importantly it shows the synergetic effect between those genes and its relation with migraine susceptibility. These gene interactions, which may be a part of a larger network, can potentially help us in better understanding migraine aetiology and in development of new therapeutic approaches.
Histone modification constitutes a basic mechanism for the genetic regulation of gene expression. In early 2000s, a powerful technique has emerged that couples chromatin immunoprecipitation with high-throughput sequencing (ChIP-seq). This technique provides a direct survey of the DNA regions associated to these modifications. In order to realize the full potential of this technique, increasingly sophisticated statistical algorithms have been developed or adapted to analyze the massive amount of data it generates. Many of these algorithms were built around natural assumptions such as the Poisson distribution to model the noise in the count data. In this work we start from these natural assumptions and show that it is possible to improve upon them.
Our comparisons on seven reference datasets of histone modifications (H3K36me3 & H3K4me3) suggest that natural assumptions are not always realistic under application conditions. We show that the unconstrained multiple changepoint detection model with alternative noise assumptions and supervised learning of the penalty parameter reduces the over-dispersion exhibited by count data. G007-LK concentration These models, implemented in the R package CROCS ( https//github.com/aLiehrmann/CROCS ), detect the peaks more accurately than algorithms which rely on natural assumptions.
The segmentation models we propose can benefit researchers in the field of epigenetics by providing new high-quality peak prediction tracks for H3K36me3 and H3K4me3 histone modifications.
The segmentation models we propose can benefit researchers in the field of epigenetics by providing new high-quality peak prediction tracks for H3K36me3 and H3K4me3 histone modifications.
Although many studies showed that the risk of congenital heart disease (CHD) was closely related to genetic factors, the exact pathogenesis is still unknown. Our study aimed to comprehensively assess the association of single nucleotide polymorphisms (SNPs) of maternal MTHFR gene with risk of CHD and its three subtypes in offspring.
A case-control study involving 569 mothers of CHD cases and 652 health controls was conducted. Thirteen SNPs were detected and analyzed.
Our study showed that genetic polymorphisms of maternal MTHFR gene at rs4846052 and rs1801131 were significantly associated with risk of CHD in the homozygote comparisons (TT vs. CC at rs4846052 OR = 7.62 [95%CI 2.95-19.65]; GG vs. TT at rs1801131 OR = 5.18 [95%CI 2.77-9.71]). And six haplotypes of G-C (involving rs4846048 and rs2274976), A-C (involving rs1801133 and rs4846052), G-T (involving rs1801133 and rs4846052), G-T-G (involving rs2066470, rs3737964 and rs535107), A-C-G (involving rs2066470, rs3737964 and rs535107) and G-C-G (involvital CHD in the Chinese population. Additionally, there were significantly interactions among different SNPs on risk of CHD. However, how these SNPs affect the development of fetal heart remains unknown, and more studies in different ethnic populations and with a larger sample are required to confirm these findings.
Here's my website: https://www.selleckchem.com/products/g007-lk.html
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