-
Carney Penn posted an update 6 hours, 18 minutes ago
amount of time and show the cost of including additional items. The Type I Error rate study demonstrates that hypothesis tests for genetic associations with latent variable models follow the hypothesized uniform distribution. Taken together, we suggest that GW-SEM may provide substantially deeper insights into the underlying genomic architecture for multivariate behavioral and psychological systems than is currently possible with standard GWAS methods. The current release of GW-SEM 2.0 is available on CRAN (stable release) and GitHub (beta release), and tutorials are available on our github wiki ( https//jpritikin.github.io/gwsem/ ).Anxiety not only concerns mental wellbeing but also negatively impacts other areas of health. click here Yet, there is limited research on (a) the genetic and environmental aetiology of such relationships; (b) sex differences in aetiology and (c) non-European samples. In this study, we investigated the genetic and environmental variation and covariation of anxiety symptoms and eight components of health-related quality of life (QoL), as measured by the short form health survey (SF-36), using genetic twin model fitting analysis. Data was drawn from the Colombo Twin and Singleton Study (COTASS), a population-based sample in Sri Lanka with data on twins (N = 2921) and singletons (N = 1027). Individual differences in anxiety and QoL traits showed more shared environmental (family) effects in women. Men did not show familial effects. Anxiety negatively correlated with all eight components of QoL, mostly driven by overlapping unique (individual-specific) environmental effects in both sexes and overlapping shared environmental effects in women. This is the first study in a South Asian population supporting the association between poor mental health and reduced QoL, highlighting the value of integrated healthcare services. Associations were largely environmental, on both individual and family levels, which could be informative for therapy and intervention.Candida species are opportunistic fungi that can cause mucosal or invasive infections. Especially in biofilm-related infections, resistance is very high to anifungals; therefore more effective treatment strategies are needed. Farnesol(3,7,11-trimethyl-2,6,10-dodecatriene-1-ol) is the quorum sensing (QS) signal molecule and can interact with Candida species both as a QS molecule and as an exogenous agent. The aim of this study was to investigate the effects of farnesol on both the planktonic and biofilm forms of Candida species by colorimetric, microbiological, and electron microscopic methods. Obtained results demonstrated the inhibitory effect of farnesol on the planktonic and biofilm forms of Candida. Farnesol showed a biofilm-enhancing effect at lower concentrations. TEM findings showed the membrane and wall damage, vacuolization, or granulation in cells. SEM images confirmed biofilm reduction in pre-/post-biofilm applications as a result of farnesol treatment. In conclusion, farnesol can be used as an alternative agent to reduce the Candida biofilms, with future studies.
In the present study, we characterized the microbiomes of acute leukemia (AL) patients who achieved complete remission following remission induction chemotherapy (RIC) as outpatients, but who did not receive antimicrobials to treat or prevent febrile neutropenia.
Saliva and stool samples from 9 patients with acute myeloid leukemia, 11 patients with acute lymphoblastic leukemia, and 5 healthy controls were subjected to 16S ribosomal RNA sequencing at baseline and at 3 months following RIC. Only patients who achieved remission at 3 months post-treatment were included. We excluded anyone who used antimicrobials within 2 months of enrollment or at any time during the study period.
At baseline, the relative abundances of species of Prevotella maculosa (P=0.001), Megasphaera micronuciformis (P=0.014), Roseburia inulinivorans (P=0.021), and Bacteroides uniformis (P=0.004) in saliva and Prevotella copri (P=0.002) in the stools of controls were significantly higher than in AL patients. Following RIC, the relativa might have an effect on clinical outcomes of AL patients.
To compare the impact of different statins therapies on the reduction of carotid intima-media thickness (CIMT) may reflect their cardiovascular benefits which is useful in clinical decision.
PubMed, EMBASE, Cochrane Library, and Web of Science were searched, and 3539 articles published from 1992 to 2020 were retrieved. CIMT in randomized controlled trials for statins therapies were included for traditional and network meta-analyses analyzed by Stata 16. The quality of included studies was assessed by the Cochrane Collaboration’s tool.
Thirty-three randomized controlled trials (n=8762) were eligible for network meta-analysis, of which 18 randomized controlled trials (n=5252) were included for comparison between statins and no statins and 11 randomized controlled trials (n=1338) were included for comparison between high-intensity statins or combination with niacin/ezetimibe and moderate/low-intensity statins in 2 traditional meta-analyses. In the traditional meta-analyses, the statins groups significantly reduce CIMT compared to no statins (standard mean difference=-0.207, 95% confidence interval -0.291 to -0.123, p<0.001), while high-intensity statins or combination with niacin/ezetimibe performed significant CIMT reduction compared to moderate/low-intensity statins (standard mean difference=-0.287, 95% confidence interval -0.460 to -0.114, p=0.001). In the network meta-analysis, a relative rank for the ability to reduce CIMT was given as follows combination therapy with niacin (mean rank 1.7), high-intensity statins, combination therapy with ezetimibe, and moderate/low-intensity statins.
Statins combined with niacin performed a greater CIMT reduction compared to high-intensity statins alone and combination therapies with ezetimibe. The advantage of niacin-combined statins therapies to improve cardiovascular endpoint needs further validation through randomized controlled trials.
PROSPERO, CRD42020175972.
PROSPERO, CRD42020175972.