8%, with similar incidence in patients treated with and without NIV. Among NIV users (26.4%), NIV failure occurred in 39.3%. Higher MPI scores at admission significantly predicted in-hospital mortality (β=4.46, p<0.0001) among patients with ARF and NIV failure (β=7.82, p=0.001) among NIV users. MPI showed good discriminatory power for NIV failure (area under the curve 0.72, 95% CI 0.58-0.85, p<0.001) with optimal cut-off at MPI value of 0.84. MPI at admission might be a useful tool to early detect patients more at risk of in-hospital death and NIV failure among older adults with ARF. MPI at admission might be a useful tool to early detect patients more at risk of in-hospital death and NIV failure among older adults with ARF.Pollution in soil by petroleum hydrocarbon has become a global environmental problem. The bioremediation of petroleum hydrocarbon-contaminated soil was enhanced with the combination of an isolated indigenous bacterial consortium and biosurfactant. The biodegradation efficiency of total petroleum hydrocarbon (TPH) was increased from 12.2% in the contaminated soil to 44.5% and 57.7% in isolated consortium and isolated consortium & 1.5 g sophorolipid (SL)/kg dry soil, respectively. https://www.selleckchem.com/products/buloxibutid.html The half-life of TPH degradation process was decreased from 32.5 d in the isolated consortium reactor to 20.4 d in the isolated consortium & 1.5 g SL/kg dry soil. The addition of biosurfactant into contaminated soils improved the TPH desorption from solid matrix to the aqueous solution and the subsequent solubilization, which ultimately improved the bioavailability of TPH in contaminated soils. Biosurfactant also served as carbon sources which contributed to the stimulation of cell growth and microbial activity and accelerated the biodegradation process via co-metabolism. The enzyme activities and quantities of functional genes were demonstrated to be incremented in SL reactors. The biosurfactant improved the TPH bioavailability, stimulated the microbial activities and participated in the co-metabolism. The combination of bioaugmentation and SL benefitted the bioremediation of petroleum hydrocarbon-contaminated soil.Particulate matter (PM) is the most important air pollution problem that leads to substantial health effects. However, very few studies focused on the effects of ultrafine particles (UFPs, particles less then 0.1 μm) on children respiratory health. We performed a panel study with 3 rounds of follow-up among 65 pupils at the Elementary School Affiliated to Shanghai Normal University in China from November 2018 to June 2019. Real-time concentrations of UFPs were measured in the campus. In each visit, we detected biomarkers in saliva and microflora in buccal mucosa, fractional exhaled nitric oxide (FeNO) and lung function. We applied a linear mixed-effect (LME) model to examine the associations of UFPs and each health outcome. We found increased levels of FeNO and tumor necrosis factor-α (TNF-α) and reduced lung function in association with higher UFP exposure. For each interquartile range increase of UFPs, the largest changes were found in lag 0-72 h for forced vital capacity [-69.02 ml (95% CI -114.20, -23.84)], TNF-α [13.41 pg/ml (95% CI 7.08, 19.73)], and FeNO [26.85% (95% CI 11.84%, 43.88%)]. UFP exposure was associated with reduced diversity in buccal microflora with largest reduction in lag 0-72 h [12.24 (95% CI 7.76, 16.71) for Ace index; 8.78 (95% CI 2.96, 14.60) for Chao1 index]. UFP exposure was also associated with increased Streptococcus, Gemella, and decreased Actinomyces. Short-term UFP exposures may impair the respiratory system by inducing inflammation, decreasing lung function and attenuating buccal microbe diversity in children.Both legacy and emerging per- and polyfluoroalkyl substances (PFAS) have been found to be threats to human health. In particular, fetuses are sensitive to xenobiotics and the placenta functions as a significant barrier for environmental pollutants. The placental transfer of PFAS is closely related to their interactions with proteins. In this study, 54 human placental samples were collected to investigate the occurrence of legacy and emerging PFAS in human placenta, including perfluorinated carboxylates (PFCAs), perfluorinated sulfonates (PFSAs), chlorinated polyfluoroalkyl ether sulfonic acids (Cl-PFESAs), and fluorotelomer sulfonates (FTSAs). Among the legacy PFAS, perfluorooctanesulfonate (PFOS), perfluorooctanoic acid (PFOA), and perfluorononanoic acid (PFNA) were detected in all samples, with PFOS and PFOA being the two predominant (mean 0.457 and 0.242 ng/g wet weight, respectively). Among the emerging PFAS, 62 Cl-PFESA was detected in all samples with the mean value of 0.104 ng/g wet weight, while the detect frequency (DF) of 82 Cl-PFESAs was only 24%. The concentration and DF of the four FTSA congeners were low in the placentas. Molecular docking calculation results showed that the binding affinities of PFAS to the human serum albumin (HSA) were increased with chain length in each category except for the PFCAs, of which the perfluoroundecanoic acid (PFUnDA) was the turning point of binding affinity to HSA. For PFSAs, their binding affinities to organic anion transporter 4 (OAT4) were increased with the chain length except for the sodium perfluoro-1-heptanesulfonate (PFHpS) and sodium perfluoro-1-nonanesulfonate (PFNS). The calculation results demonstrated that the placental transfer of PFAS is closely related to chain length. The findings in the study can help better understand the occurrence of the PFAS in the human placenta and the placental transfer mechanisms of PFAS in human beings.Phthalate ester pollution in the environment and food chain is frequently reported. Microbial treatment is a green and efficient method for solving this problem. The isolation and systematic investigation of microorganisms generally recognized as safe (GRAS) will provide useful resources. A GRAS Bacillus subtilis strain, BJQ0005, was isolated from Baijiu fermentation starter and efficiently degraded phthalate esters (PAEs). The half-lives for di-isobutyl phthalate, di-butyl phthalate and di-(2-ethylhexyl) phthalate were 3.93, 4.28, and 25.49 h, respectively, from the initial amount of 10 mg per 10 mL reaction mixture, which are records using wild-type strains. Genome sequencing and metabolic intermediate analysis generated the whole metabolic pathway. Eighteen enzymes from the α/β hydrolase family were expressed. Enzymes GTW28_09400 and GTW28_13725 were capable of single ester bond hydrolysis of PAEs, while GTW28_17760 hydrolyzed di-ester bonds of PAEs. Using molecular docking, a possible mechanism affecting enzymatic ester bond hydrolysis of mono-butyl phthalate was proposed of GTW28_17760.