Raunmclamb6428

There has been an exponential growth in research on loneliness among older adults. However, differing measurements and definitions of loneliness mean the incidence and prevalence, associated risk factors and health consequences are often conflicting or confusing especially for those developing policy and services.

Visceral adipose tissue (VAT) is closely related to obesity complications. We aimed to determine the optimal sex-specific and age-specific VAT thresholds for predicting metabolic complications among individuals living in the United Arab Emirates (UAE).

Retrospective cross-sectional study.

We reviewed medical records of adults who visited a hospital in the UAE.

A total of 369 subjects were included in the final analysis after application of inclusion and exclusion criteria.

The prevalence of metabolic syndrome (MES).

MES measures excluding waist circumference were present in 73.4% of women and 78.5% of men. VAT areas adjusted for age were significantly greater in the MES group compared with the non-MES group regardless of sex (p<0.05 for all relations); however, subcutaneous adipose tissue areas adjusted for age were not significantly different. Areas under the curve used to predict MES were statistically significant for VAT and visceral to subcutaneous fat ratios among both men and women. Identified cut-off values of VAT to predict MES were 132.0 cm

in both sexes for individuals under the age of 50 years. For those over 50 years of age, VAT thresholds were greater in women compared with men (173 cm

vs 124.3 cm

, respectively).

Optimal VAT cut-offs to predict MES were 132 cm

for individuals under 50 years old living in the UAE. These measures are potential target visceral fat values that could be used to reduce obesity-related morbidity in populations with pre-existing metabolic complications.

Optimal VAT cut-offs to predict MES were 132 cm2 for individuals under 50 years old living in the UAE. click here These measures are potential target visceral fat values that could be used to reduce obesity-related morbidity in populations with pre-existing metabolic complications.Prenatal depression is common, underrecognized, and undertreated. It has negative consequences on child behavior and brain development, yet the relationships among prenatal depression, child behavior, and children's brain structure remain unclear. The aim of this study was to determine whether altered brain connectivity mediates relationships between prenatal maternal depressive symptoms and child behavior. This study included 54 human mother-child pairs. Mothers completed the Edinburgh Postnatal Depression Scale during the second and third trimesters of pregnancy and 3 months postpartum. Their children had diffusion MRI at age 4.1 ± 0.8 years, and children's behavior was assessed using the Child Behavior Checklist within 6 months of their MRI scan. Structural brain connectivity of the amygdala, fornix, uncinate fasciculus, and cingulum was assessed using fractional anisotropy and mean diffusivity and analyzed with maternal prenatal depressive symptoms as well as child behavior. Third trimester maternal Edinbressive symptoms. Children of mothers with worse depressive symptoms had weaker white matter connectivity between areas related to emotional processing. Furthermore, connectivity between the amygdala and prefrontal cortex mediated the relationship between maternal depressive symptoms and externalizing behavior in boys, showing that altered brain structure is a possible mechanism via which maternal prenatal depression impacts children's behavior. This provides important information for understanding why children of depressed mothers may be more vulnerable to depression themselves and may help shape future guidelines on maternal prenatal care.High-risk human papillomaviruses (HPVs) constitutively activate the ataxia telangiectasia and Rad3-related (ATR) DNA damage response pathway, and this is required for viral replication. In fibroblasts, activated ATR regulates transcription of inflammatory genes through its negative effects on the autophagosome cargo protein p62. In addition, suppression of p62 results in increased levels of the transcription factor GATA4, leading to cellular senescence. In contrast, in HPV-positive keratinocytes, we observed that activation of ATR resulted in increased levels of phosphorylated p62, which in turn lead to reduced levels of GATA4. Knockdown of ATR in HPV-positive cells resulted in decreased p62 phosphorylation and increased GATA4 levels. Transcriptome sequencing (RNA-seq) analysis of HPV-positive cells identified inflammatory genes and interferon factors as negative transcriptional targets of ATR. Furthermore, knockdown of p62 or overexpression of GATA4 in HPV-positive cells leads to inhibition of viral replicat DNA repair and facilitating HPV replication.

Obesity is growing global health concern and highly associated with increased risk of metabolic diseases including type 2 diabetes. We aimed to discover new differential DNA methylation patterns predisposing obesity and prioritize surrogate epigenetic markers in Koreans.

We performed multistage epigenome-wide analyses to identify differentially expressed CpGs in obesity using the Illumina HumanMethylationEPIC array (EPIC). Forty-eight CpGs showed significant differences across three phases 902 whole blood DNAs from two cohorts (phase 1 n=450, phase 2 n=377) and a hospital-based sample (phase 3 n=75). Samples from phase III participants were used to examine whether the 48 CpGs are significant in the fat tissue and influenced gene expression. Furthermore, we investigated the epigenetic effect of CpG loci in childhood obesity (n=94).

Seven of the 48 CpGs exhibited similar changes in the fat tissue along with gene expression changes. In particular, hypomethylated CpG (cg13424229) on the GATA1 transcription factor cluster of CPA3 promoter was related to its increased gene expression and showed consistent effect in childhood obesity. Interestingly, subsequent analysis using RNA sequencing data from 21 preadipocytes and 26 adipocytes suggested CPA3 as a potential obesity-related gene. Moreover, expression patterns from RNA sequencing and public Gene Expression Omnibus showed the correlation between CPA3 and type 2 diabetes (T2D) and asthma.

Our finding prioritizes influential genes in obesity and provides new evidence for the role of CPA3 linking obesity, T2D, and asthma.

Our finding prioritizes influential genes in obesity and provides new evidence for the role of CPA3 linking obesity, T2D, and asthma.