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INTRODUCTION This study aimed to investigate the association between T-wave morphology and impaired left ventricular ejection fraction (LVEF) in patients with complete left bundle branch block (cLBBB), and the predictive value of T-wave morphology for response to cardiac resynchronization therapy (CRT). METHODS AND RESULTS We enrolled 189 patients with cLBBB on electrocardiogram performed between January 2007 and December 2011 who underwent standard echocardiography. Repolarization parameters, including the QRS-to-T angle (TCRT), T-wave morphology dispersion (TMD), T-wave loop area (PL), and T-wave residuum (TWR), were reconstructed from digital standard 12-lead electrocardiograms by T-wave morphology analysis. CRT response was defined as ≥15% reduction in left ventricular end-systolic volume at 12 months after CRT implantation. The clinical outcome endpoint was a composite of heart failure hospitalization, heart transplantation, or death during follow up (mean, 5.8 years). On logistic regression, a higher heart rate, longer QRS duration, increased TMD, and larger TWR were all independently associated with LVEF less then 40%. Among 40 patients who underwent CRT, those with a larger TMD (p=0.007), larger PL (p=0.025), and more negative TCRT (p=0.015) had better response to CRT. A large TMD (p=0.018) and large PL (p=0.003) were also independent predictors of the clinical outcome endpoint. CONCLUSION Increases in repolarization heterogeneity in patients with cLBBB are associated with impaired LVEF. A large TMD and large PL may be useful as additional predictors of response to CRT, improving patient selection for CRT. this website This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.A genetic evaluation may lead to a clinical or molecular diagnosis, which helps clarify prognosis, tailor surveillance protocols based on risks associated with the genetic condition, and aid in assessment of risk to family members. However, individuals of low socioeconomic and/or minority status often have limited access to genetics services, which contributes to healthcare disparities (Journal of Community Genetics, 2018, 9, 233). Our county hospital system, dedicated to providing health care to the underserved, offers a unique opportunity to reduce healthcare inequalities in genetics. This retrospective chart review included 2,304 patients evaluated at an outpatient county hospital genetics clinic between January 1, 2013, and December 31, 2018, during which time genetic testing was recommended for most patients (58.5%) for a total of 1,429 recommended genetic tests. Most tests were obtained through non-hospital financial resources (56.5%), and loss to follow-up during the phlebotomy stage was the most common reason for tests not to be ordered (41.9%) and not to be completed (36.4%). The experience in our clinic suggests that identifying financial avenues, such as commercial laboratory financial assistance programs in addition to county hospital funds, can support obtaining genetic testing and allow healthcare providers to overcome financial barriers to genetic testing. © 2020 National Society of Genetic Counselors.Lung adenocarcinoma (LUAD) is one of the most common diagnosed pathological categories of lung cancer. Long noncoding RNAs (lncRNAs) have been manifested to be key regulators in modulating multiple cancers. Nevertheless, the pathologic role of lncRNA WDFY3-AS2 in LUAD remains elusive. The relative messenger RNA and protein levels were assessed by quantitative reverse transcription-polymerase chain reaction and Western blot analyses, respectively. Colony formation, carboxyfluorescein succinimidyl ester, terminal deoxynucleotidyl transferase dUTP nick-end labeling, wound-healing, and transwell invasion assays were performed to study the underlying role of WDFY3-AS2 in LUAD. Luciferase reporter assay, chromatin immunoprecipitation, RNA pull down, and RNA immunoprecipitation assays were conducted to probe into the interactions between relevant genes. WDFY3-AS2 expression was elevated in LUAD and WDFY3-AS2 transcription was activated by transcription factor USF1. Silencing WDFY3-AS2 could suppress cell proliferation, migration, and invasion, whereas accelerate cell apoptosis in LUAD. Molecular mechanism assays revealed that WDFY3-AS2 could bind to miR-491-5p and miR-491-5p inhibition could reverse the inhibitory effect of WDFY3-AS2 silence on LUAD progression. Besides, zinc finger protein 703 (ZNF703) was identified as a downstream target of miR-491-5p and its expression could be upregulated by WDFY3-AS2. Further, rescue assays uncovered that ZNF703 overexpression could restore the suppressive influence of silenced WDFY3-AS2 on LUAD development. USF1-acitvated WDFY3-AS2 promotes LUAD progression via targeting miR-491-5p/ZNF703 axis, suggesting the potential value of WDFY3-AS2 as a novel target for LUAD treatment. © 2020 Wiley Periodicals, Inc.During aging humans lose midbrain dopamine neurons, but not all dopamine regions exhibit vulnerability to neurodegeneration. Microglia maintain tissue homeostasis and neuronal support, but microglia become senescent and likely lose some of their functional abilities. Since aging is the greatest risk factor for Parkinson's disease, we hypothesized that aging-related changes in microglia and neurons occur in the vulnerable substantia nigra pars compacta (SNc) but not the ventral tegmental area (VTA). We conducted stereological analyses to enumerate microglia and dopaminergic neurons in the SNc and VTA of 1-, 6-, 9-, 18-, and 24-month-old C57BL/J6 mice using sections double-stained with tyrosine hydroxylase (TH) and Iba1. Both brain regions show an increase in microglia with aging, whereas numbers of TH+ cells show no significant change after 9 months of age in SNc and 6 months in VTA. Morphometric analyses reveal reduced microglial complexity and projection area while cell body size increases with aging. Contact sites between microglia and dopaminergic neurons in both regions increase with aging, suggesting increased microglial support/surveillance of dopamine neurons. To assess neurotrophin expression in dopaminergic neurons, BDNF and TH mRNA were quantified. Results show that the ratio of BDNF to TH decreases in the SNc, but not the VTA. Gait analysis indicates subtle, aging-dependent changes in gait indices. In conclusion, increases in microglial cell number, ratio of microglia to dopamine neurons, and contact sites suggest that innate biological mechanisms compensate for the aging-dependent decline in microglia morphological complexity (senescence) to ensure continued neuronal support in the SNc and VTA. © 2020 Wiley Periodicals, Inc.
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