Aerobic degradation of parent triisobutyl phosphate and its metabolite diisobutyl phosphate in activated sludge: Degradation pathways and degrading bacteria.

Although organophosphate esters (OPEs) degradation has been widely studied, the degradation of their metabolites is always ignored. Triisobutyl phosphate (TiBP), a typical alkyl-OPEs, is of emerging concern because of its potential ecotoxicity in the environment. This study provides comprehensive understanding about the degradation of TiBP and one of its metabolites, diisobutyl phosphate (DiBP) using activated sludge (AS).

Triisobutyl phosphate biodegradation by enriched activated sludge consortia: Degradation mechanism and bioaugmentation potential.

This study investigated the ability of activated sludge (AS) to biodegrade triisobutyl phosphate (TiBP) after acclimation in an AS bioreactor by adding 50 mg/L TiBP. The bioreactor significantly increased the biotransformation rate of TiBP (2.15-12.

Exosomal miR-552-5p promotes tumorigenesis and disease progression via the PTEN/TOB1 axis in gastric cancer.

Gastric cancer (GC) is associated with rapid disease progression and poor patient prognosis, highlighting the pressing need for new biomarkers to facilitate disease management. Exosomes are released by all cells and are ubiquitous in body fluids, thus giving them great potential as diagnostic biomarkers and therapeutic targets. MicroRNAs (miRNAs) can be transported by exosomes, and are a common target for regulation in cancer.

Ear ischemia induced by endovascular therapy for arteriovenous fistula of the sigmoid sinus: A case report.

Background: Arteriovenous fistula of the sigmoid sinus is an abnormal connection of arteries with the sigmoid sinus. Endovascular treatments of such lesions are considered safe and with low rates of complications.

Case Summary: A 62-year-old female patient underwent endovascular treatment of an arteriovenous fistula of the right sigmoid sinus on February 7, 2017, but her tinnitus was not cured.

Silencing ROCK1 ameliorates ventilator-induced lung injury in mice by inhibiting macrophages' NLRP3 signaling.

Rho kinase, including two subtypes, ROCK1 and ROCK2, controls a variety of biological processes helping coordinate the tissues response to stress and injury. Some authors believe that alveolar macrophages (AMs) play a key role in the early phase of ventilator-induced lung injury (VILI), which is closely related to the activation of NLRP3 inflammasome and NF-κB signaling. However, there is currently little known about the relationship between ROCK signaling and NLRP3 inflammasome.

Morphine may act via DDX49 to inhibit hepatocellular carcinoma cell growth.

Pain in hepatocellular carcinoma (HCC) is a frequent cause of low quality of life, and morphine is routinely used as a first-line opiate analgesic in HCC. Morphine may exert not only analgesic effects but also anti-cancer effects via unknown mechanisms. Here we show that morphine can inhibit HCC cell proliferation.

Mitophagy-Mediated mtDNA Release Aggravates Stretching-Induced Inflammation and Lung Epithelial Cell Injury via the TLR9/MyD88/NF-κB Pathway.

Background: In animal models of ventilation-induced lung injury, mitophagy triggers mitochondria damage and the release of mitochondrial (mt) DNA, which activates inflammation. However, the mechanism of this process is unclear.

Methods: A model of cyclic stretching (CS)-induced lung epithelial cell injury was established.

Ly-6C inflammatory-monocyte recruitment is regulated by p38 MAPK/MCP-1 activation and promotes ventilator-induced lung injury.

Lymphocyte antigen 6Chigh (Ly-6C) inflammatory monocytes, as novel mononuclear cells in the innate immune system, participate in infectious diseases. In this study, we investigated the potential role of these monocytes in ventilator-induced lung injury (VILI) and the possible mechanism involved in their migration to lung tissue. Our results showed that mechanical ventilation with high tidal volume (HTV) increased the accumulation of Ly-6C inflammatory monocytes in lung tissues and that blocking C‑C chemokine receptor 2 (CCR2) could significantly reduce Ly-6C inflammatory-monocyte migration and attenuate the degree of inflammation of lung tissues.

Non-intubated anesthesia in patients undergoing video-assisted thoracoscopic surgery: A systematic review and meta-analysis.

Introduction: Non-intubated anesthesia (NIA) has been proposed for video-assisted thoracoscopic surgery (VATS), although how the benefit-to-risk of NIA compares to that of intubated general anesthesia (IGA) for certain types of patients remains unclear. Therefore, the aim of the present meta-analysis was to understand whether NIA or IGA may be more beneficial for patients undergoing VATS.

Methods: A systematic search of Cochrane Library, Pubmed and Embase databases from 1968 to April 2019 was performed using predefined criteria.

Celecoxib Inhibits Hepatocellular Carcinoma Cell Growth and Migration by Targeting PNO1.

BACKGROUND Celecoxib has shown anti-tumor activities against several types of cancer. Although the majority of research focuses on its mechanism via cyclooxygenase-2 (COX-2) enzyme inhibition, we identified a distinct mechanism behind celecoxib anti-cancer abilities. MATERIAL AND METHODS We treated hepatocellular carcinoma (HCC) Huh-7 cells and tumor xenograft mice models with celecoxib to test its effects on the tumor.

RhoA inhibitor suppresses the production of microvesicles and rescues high ventilation induced lung injury.

Microvesicles (MVs) have been extensively identified in various biological fluids including bronchoalveolar lavage fluid (BALF), peripheral blood and ascitic fluids. Our previous study showed that MVs are responsible for acute lung injury, but the exact mechanism underlying MVs formation remains poorly understood. In the present study, we investigate the potential role of RhoA/Rock signaling in MVs generation and the biological activity of MVs in ventilator-induced lung injury (VILI).

[Effect of high tidal volume mechanical ventilation on pulmonary autophagy and mitochondrial damage in rats].

Objective: To investigate the relationship between different tidal volume (VT) mechanical ventilation (MV) and autophagy and mitochondrial damage in rats.

Methods: A total of 120 clean-grade male Sprague-Dawley (SD) rats were divided into five groups (n = 24) by random number table method, and then given 0 (spontaneous breathing), 10, 20, 30, 40 mL/kg VT for MV. The rats in each group were subdivided into four subgroups of 1, 2, 3, and 4 hours according to ventilation time, with 6 rats in each subgroup.

Microvesicles packaging IL-1β and TNF-α enhance lung inflammatory response to mechanical ventilation in part by induction of cofilin signaling.

Microvesicles shed from pulmonary cells are capable of transferring inflammatory cargo to recipient cells nearby or in distant to enhance inflammation. Some authors believe that cofilin controls actin dynamics and regulates vesicle mobilization. We therefore investigated the potential role and mechanism of microvesicles in ventilator-induced lung injury (VILI).

Down-regulation of TRAF4 targeting RSK4 inhibits proliferation, invasion and metastasis in breast cancer xenografts.

Ribosomal S6 protein kinase 4 (RSK4) was known as a novel tumor suppressor gene, and the tumor necrosis factor receptor-associated factor 4 (TRAF4) was linked to carcinogenesis. The purpose of this study is to further investigate the effect of the TRAF4 gene on cell proliferation, invasion and metastasis in vivo and explore whether there is an interaction between TRAF4 and RSK4 in breast cancer. MDA-MB-231 cells were transfected with lentivirus TRAF4-shRNA to specifically block the expression of TRAF4, or transfected with lentivirus negative-shRNA as a negative control.