Exposure and potential risks of thirteen endocrine- disrupting chemicals in pharmaceuticals and personal care products for breastfed infants in China.

Ingestion of breast milk represents the primary exposure pathway for endocrine-disrupting chemicals (EDCs) in newborns. To elucidate the associated risks, it is essential to quantify EDC levels in both breast milk and infant urine. This study measured the concentrations of 13 EDCs, including parabens (methyl paraben (MP), ethyl paraben (EP), propyl paraben (PP), iso-propyl paraben, butyl paraben, and iso-butyl paraben), bisphenols (bisphenol A (BPA), bisphenol F, bisphenol S, bisphenol AF, and bisphenol Z), triclosan (TCS), and triclocarban, in breast milk and infant urine to assess their potential health effects and endocrine disruption risks.

Impact of internet plus health education on urinary stoma caregivers in coping with care burden and stress in the era of COVID-19.

Objective: To explore the impact of "Internet Plus Health Education" on coping with care burden and pressure in urinary stoma caregivers in the era of COVID-19.

Materials And Methods: Eighty caregivers of patients with urinary ostomy were equally randomized to experimental and control groups. Caregivers in the experimental group received digital nursing education intervention, which involved nursing intervention of Internet Plus Health Education (IPHE), and those in the control group received conventional care instructions.

Interference with lncRNA NEAT1 promotes the proliferation, migration, and invasion of trophoblasts by upregulating miR-411-5p and inhibiting PTEN expression.

Preeclampsia (PE) is an idiopathic hypertensive disorder of pregnancy, which is related to abnormal placental villi development. Our previous study has found that lncRNA NEAT1 promotes apoptosis of trophoblasts, but the role of NEAT1 in proliferation, migration, and invasion is still unclear. This study explores the role of NEAT1 in proliferation, migration, and invasion of trophoblasts.

Up-regulation of LncRNA NEAT1 induces apoptosis of human placental trophoblasts.

The trophoblast apoptosis induced by placental oxidative stress is a contributor to the pathological development of preeclampsia (PE), whereas the molecular mechanism remains unclear. In this study, we explored the role and mechanism of Long non-coding RNA (LncRNA) NEAT1 in trophoblasts apoptosis. In the placenta tissues of PE patients and HO-treated human trophoblast cell line HTR-8/SVneo, the expressions of LncRNA NEAT1, p53, and estrogen receptor α (ESRα) were increased whereas miR-18a-5p expression was decreased.

Epigenetically-Regulated MicroRNA-9-5p Suppresses the Activation of Hepatic Stellate Cells via TGFBR1 and TGFBR2.

Background/aims: Recently, microRNAs (miRNAs) have been demonstrated to act as regulators of activation of hepatic stellate cells (HSCs). It is well known that the main profibrogenic inducer transforming growth factor-β1 (TGF-β1) contributes to HSC activation, which is a key event in liver fibrosis. Increasing studies show that miR-9-5p is down-regulated in liver fibrosis and restoration of miR-9-5p limits HSC activation.

Serum lincRNA-p21 as a potential biomarker of liver fibrosis in chronic hepatitis B patients.

Serum long non-coding RNAs (lncRNAs) are emerging as promising biomarkers for various human diseases. The aim of this study was to investigate the feasibility of using serum long intergenic non-coding RNA-p21 (lincRNA-p21) as a biomarker for chronic hepatitis B patients. Serum lincRNA-p21 levels were quantified using real-time PCR in 417 CHB patients and 363 healthy controls.

Activation of Hepatic Stellate Cells is Inhibited by microRNA-378a-3p via Wnt10a.

Background/aims: Wnt/β-catenin pathway is involved in liver fibrosis and microRNAs (miRNAs) are considered as key regulators of the activation of hepatic stellate cells (HSCs). A recent study showed the protective role of miR-378a-3p against cardiac fibrosis. However, whether miR-378a-3p suppresses Wnt/β-catenin pathway in liver fibrosis is largely unknown.

Inhibition of ATIR by shRNA prevents collagen synthesis in hepatic stellate cells.

Currently, strategies aimed at disrupting renin-angiotensin-aldosterone system (RAAS) are extensively investigated for treating liver fibrosis. However, the experiment results remain unsatisfactory, mainly due to excessive level of angiotensin II (AngII) in gene expression. In this article, we aim to investigate whether suppression of AngII-type I receptor (ATIR) expression by short hairpin RNA (shRNA) expression vectors decreases the level of collagen synthesis in hepatic stellate cells (HSCs).