Finding flaws in the spatial distribution of health workforce and its influential factors: An empirical analysis based on Chinese provincial panel data, 2010-2019.

Background: The maldistributions of the health workforce showed great inconsistency when singly measured by population quantity or geographic area in China. Meanwhile, earlier studies mainly employed traditional econometric approaches to investigate determinants for the health workforce, which ignored spillover effects of influential factors on neighboring regions. Therefore, we aimed to analyze health workforce allocation in China from demographic and geographic perspectives simultaneously and then explore the spatial pattern and determinants for health workforce allocation taking account of the spillover effect.

The Influence of Parents on Medication Adherence of Their Children in China: A Cross-Sectional Online Investigation Based on Health Belief Model.

Objective: To explore the influence of parents on the medication adherence of their children.

Study Design: A cross-sectional online investigation.

Methods: A questionnaire with 41 questions was designed based on the health belief model (HBM) distributed and collected online in 28 cities around China through multi-stage stratified sampling.

Multilayered control of splicing regulatory networks by DAP3 leads to widespread alternative splicing changes in cancer.

The dynamic regulation of alternative splicing requires coordinated participation of multiple RNA binding proteins (RBPs). Aberrant splicing caused by dysregulation of splicing regulatory RBPs is implicated in numerous cancers. Here, we reveal a frequently overexpressed cancer-associated protein, DAP3, as a splicing regulatory RBP in cancer.

ADARs act as potent regulators of circular transcriptome in cancer.

Circular RNAs (circRNAs) are produced by head-to-tail back-splicing which is mainly facilitated by base-pairing of reverse complementary matches (RCMs) in circRNA flanking introns. Adenosine deaminases acting on RNA (ADARs) are known to bind double-stranded RNAs for adenosine to inosine (A-to-I) RNA editing. Here we characterize ADARs as potent regulators of circular transcriptome by identifying over a thousand of circRNAs regulated by ADARs in a bidirectional manner through and beyond their editing function.

SIRT3 deficiency exacerbates early-stage fibrosis after ischaemia-reperfusion-induced AKI.

Background: Sirtuin 3 (SIRT3) is a crucial regulator of mitochondrial function and is associated with injury and repair in acute kidney injury (AKI). To investigate whether mitochondrial damage and early renal fibrosis are associated with decreased renal SIRT3 levels, we established an in vivo model.

Methods: In vivo, we established ischaemia-reperfusion-induced AKI (IR-AKI) models in wild-type (WT) and SIRT3-knockout (SIRT3-KO) mice.

Topography of transcriptionally active chromatin in glioblastoma.

Molecular profiling of the most aggressive brain tumor glioblastoma (GBM) on the basis of gene expression, DNA methylation, and genomic variations advances both cancer research and clinical diagnosis. The enhancer architectures and regulatory circuitries governing tumor-intrinsic transcriptional diversity and subtype identity are still elusive. Here, by mapping H3K27ac deposition, we analyze the active regulatory landscapes across 95 GBM biopsies, 12 normal brain tissues, and 38 cell line counterparts.

The influence of TCM constitutions and neurocognitive function in elderly Macau individuals.

Background: Traditional Chinese medicine (TCM) constitution contributes to predicating disease occurrence and pathological progress. In this study, we investigate the correlation between TCM constitution and neurocognitive function in elderly Macau individuals.

Methods: A total of 313 older adults from elderly healthcare centers were recruited at random.

Homocysteine induced a calcium-mediated disruption of mitochondrial function and dynamics in endothelial cells.

Homocysteine (Hcy) is a sulfur-containing amino acid that originated in methionine metabolism and the elevated level of Hcy in plasma is considered to be an independent risk factor for cardiovascular diseases (CVD). Endothelial dysfunction plays a major role in the development of CVD, while the potential mechanism of Hcy-induced endothelial dysfunction is still unclear. Here, in Hcy-treated endothelial cells, we observed the destruction of mitochondrial morphology and the decline of mitochondrial membrane potential.

MNK1 and MNK2 enforce expression of E2F1, FOXM1, and WEE1 to drive soft tissue sarcoma.

Soft tissue sarcoma (STS) is a heterogeneous disease that arises from connective tissues. Clinical outcome of patients with advanced tumors especially de-differentiated liposarcoma and uterine leiomyosarcoma remains unsatisfactory, despite intensive treatment regimens including maximal surgical resection, radiation, and chemotherapy. MAP kinase-interacting serine/threonine-protein kinase 1 and 2 (MNK1/2) have been shown to contribute to oncogenic translation via phosphorylation of eukaryotic translation initiation factor 4E (eIF4E).

"3G" Trial: An RNA Editing Signature to Guide Gastric Cancer Chemotherapy.

Gastric cancer cases are often diagnosed at an advanced stage with poor prognosis. Platinum-based chemotherapy has been internationally accepted as first-line therapy for inoperable or metastatic gastric cancer. To achieve greater benefits, selection of patients eligible for this treatment is critical.

The Potential Use of RNA-based Therapeutics for Breast Cancer Treatment.

Breast cancer is one of the most lethal cancers in women worldwide, and the development of efficient treatments faces several challenges. Breast cancer is characterized by histological and functional heterogeneity in aspects such as tumorigenesis, metastasis, and drug resistance. RNA therapy has emerged as a highly attractive class of drugs for the treatment and prevention of breast cancer.

Targetable BET proteins- and E2F1-dependent transcriptional program maintains the malignancy of glioblastoma.

Competitive BET bromodomain inhibitors (BBIs) targeting BET proteins (BRD2, BRD3, BRD4, and BRDT) show promising preclinical activities against brain cancers. However, the BET protein-dependent glioblastoma (GBM)-promoting transcriptional network remains elusive. Here, with mechanistic exploration of a next-generation chemical degrader of BET proteins (dBET6), we reveal a profound and consistent impact of BET proteins on E2F1- dependent transcriptional program in both differentiated GBM cells and brain tumor-initiating cells.