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1.
Chemosphere ; 280: 130669, 2021 Oct.
Article in English | MEDLINE | ID: mdl-33940451

ABSTRACT

The presence of hydrogen peroxide (H2O2) in ozonation process can resist the formation of carcinogenic bromate (BrO3¯) efficiently, and the bromate depression is closely related with background water qualities, especially in high bromide-containing seawater. In this study, the freshwater and seawater were selected to investigate the effects of H2O2 on ozone (O3) decomposition kinetics, bromide transformation and bromate depression, and the evolutions of BrO3¯ under different scavengers were explored to speculate the primary bromate formation pathways. The results showed that the initial O3 half-live period (t1/2-O3) in seawater was only one-sixth of that in freshwater, and its attenuation rate increased analogously with the increase of H2O2 concentration in both freshwater and seawater. The H2O2 could promote the formation of BrO3¯ via hydroxyl radical (•OH) based bromate pathways, nevertheless higher concentration of H2O2 facilitated the reduction of HOBr/OBr¯ back to Br¯, resulting in 87.0% and 73.2% of BrO3¯ retardment in freshwater and seawater, respectively. The suppression ratios of BrO3¯ were up to 48.4% and 35.3% in freshwater with the addition of •OH and •O2¯ scavengers, and the corresponding depressions in seawater decreased to 35.3% and 12.7%, indicating that •OH was dominant on bromate formation when the concentration of residual ozone was adequate to generate some bromine intermediates, meanwhile H2O2 and •O2¯ functioned as the key reductants for bromate depression. Based on these results, the Br¯ transformation mechanisms via O3, •OH, H2O2, and •O2¯ reactions were speculated, and the feasibility of H2O2-ozonation was verified for the treatment of high Br¯-containing seawater.


Subject(s)
Ozone , Water Pollutants, Chemical , Water Purification , Bromates , Depression , Hydrogen Peroxide , Oxidation-Reduction , Seawater , Water Pollutants, Chemical/analysis
2.
Crit Care Med ; 45(12): e1218-e1225, 2017 Dec.
Article in English | MEDLINE | ID: mdl-28902121

ABSTRACT

OBJECTIVES: Data about the critical care resources in China remain scarce. The purpose of this study was to investigate the variation and distribution of critical care resources in Guangdong province from 2005 to 2015. DESIGN: Data in regard to critical care resources were collected through questionnaires and visits every 5 years from 2005. SETTING: All hospitals in Guangdong province were screened and hospitals that provide critical care services were enrolled. INTERVENTION: None. MEASUREMENTS AND MAIN RESULTS: One hundred eleven, 158, and 284 hospitals that provide critical care services were enrolled in the three consecutive surveys respectively. The number of ICUs, ICU beds, intensivists, and nurses increased to 324, 3,956, 2,470, and 7,695, respectively, by 2015. Adjusted by population, the number of ICU beds per 100,000 (100,000) population increased by 147.7% from 2005 to 2015, and the number of intensivists and nurses per 100,000 population increased by 35.3% and 55.1% from 2011 to 2015. However, the numbers in the Pearl River Delta, a richer area, were higher than those in the non-Pearl River Delta area (ICU beds: 4.64 vs 2.58; intensivists: 2.90 vs 1.61; nurses: 9.30 vs 4.71 in 2015). In terms of staff training, only 17.85% of intensivists and 14.29% of nurses have completed a formal accredited critical care training program by 2015. CONCLUSIONS: Our study was the first one to investigate the trend and distribution of critical care resources in China. The quantity of ICU beds and staff has been increasing rapidly, but professional training for staff was inadequate. The distribution of critical care resources was unbalanced. Our study can be beneficial for healthcare policymaking and the allocation of critical care resources in Guangdong province and other provinces in China.


Subject(s)
Critical Care/statistics & numerical data , Intensive Care Units/supply & distribution , China , Equipment and Supplies/supply & distribution , Gross Domestic Product , Hospital Bed Capacity/statistics & numerical data , Humans , Personnel, Hospital/supply & distribution
3.
Chem Commun (Camb) ; 50(16): 1989-91, 2014 Feb 25.
Article in English | MEDLINE | ID: mdl-24413586

ABSTRACT

A new perovskite-like compound [N(CH3)4][Cd(N3)3] is reported here, which undergoes a series of reversible phase transitions including an above-room-temperature ferroelastic phase transition. An order-disorder mechanism is found in these structural transitions owing to the sway of the rod-like N3(-) bridges as well as the rotation of the tetrahedron-like [N(CH3)4](+) guests.

4.
Apoptosis ; 15(1): 41-54, 2010 Jan.
Article in English | MEDLINE | ID: mdl-19904610

ABSTRACT

This study was undertaken to determine the in vitro effect of lentivirus-mediated siPin1 on cell cycle and apoptosis of vascular smooth muscle cells (VSMCs). Further we sought to provide insight into the mechanisms behind these processes. Human umbilical artery smooth muscle cells (HUASMCs) were transfected with lentiviral siPin1. Real-time RT-PCR and Western blotting were used to examine Pin1 mRNA and protein expression. MTT and [(3)H]thymidine incorporation assays were employed to observe cell proliferation status. The apoptotic rate and cell cycle were analyzed by Hoechst33258 staining and flow cytometry. Finally we measured the expression of cyclin D1, beta-catenin, CDK4, cytochrome c, procaspase-3, cleaved caspase-3, procaspase-9, cleaved caspase-9, Bcl-2, Bax, STAT3, phosphorylated STAT3 and VEGF in lentiviral siPin1 infected VSMCs. Lentivirus-mediated siPin1 effectively diminished endogenous Pin1 expression in VSMCs resulting in cell cycle arrest and enhancement of apoptosis. This was accompanied by downregulation of cyclin D1, beta-catenin, CDK4, increase of Bax/Bcl-2 ratio, release of cytochrome c, and activation of caspase-3 and -9. We concluded that this effect was mediated, at least in part, via the beta-catenin/cyclin D1/CDK4 cascade, and that the mitochondrial pathway was responsible for VSMC apoptosis in the absence of Pin1. Our observations raised the possibility that Pin1 might be a potential therapeutic target to prevent stenosis.


Subject(s)
Apoptosis , Cell Cycle , Down-Regulation , Muscle, Smooth, Vascular/cytology , Muscle, Smooth, Vascular/enzymology , Peptidylprolyl Isomerase/metabolism , Cell Cycle Proteins/genetics , Cell Cycle Proteins/metabolism , Cells, Cultured , Gene Expression , Humans , Isomerism , Muscle, Smooth, Vascular/chemistry , NIMA-Interacting Peptidylprolyl Isomerase , Peptidylprolyl Isomerase/chemistry , Peptidylprolyl Isomerase/genetics
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