Background The impacts of air pollution on circulatory and respiratory systems have been extensively studied. However, the associations between air pollution exposure and the risk of noncommunicable diseases of other organ systems, including diseases of the digestive, musculoskeletal, and genitourinary systems, remain unclear or inconclusive. We aimed to systematically assess the associations between short-term exposure to main air pollutants (fine particulate matter [PM 2.5 ] and ozone) and cause-specific risk of hospital admission in China over a wide spectrum of human diseases. Methods and findings Daily data on hospital admissions for primary diagnosis of 14 major and 188 minor disease categories in 252 Chinese cities (107 cities in North China and 145 cities in South China) from January 1, 2013, to December 31, 2017, were obtained from the Hospital Quality Monitoring System of China (covering 387 hospitals in North China and 614 hospitals in South China). We applied a 2-stage analytic approach to assess the associations between air pollution and daily hospital admissions. City-specific associations were estimated with quasi-Poisson regression models and then pooled by random-effects meta-analyses. Each disease category was analyzed separately, and the P values were adjusted for multiple comparisons. A total of 117,338,867 hospital admissions were recorded in the study period. Overall, 51.7% of the hospitalized cases were male, and 71.3% were aged <65 years. Robust positive associations were found between short-term PM 2.5 exposure and hospital
BackgroundGallbladder cancer is the most frequent malignancy of the bile duct with high aggressive and extremely poor prognosis. The main objective of the paper was to investigate the inhibitory effects of oridonin, a diterpenoid isolated from Rabdosia rubescens, on gallbladder cancer both in vitro and in vivo and to explore the mechanisms underlying oridonin-induced apoptosis and cell cycle arrest.MethodsThe anti-tumor activity of oridonin on SGC996 and NOZ cells was assessed by the MTT and colony forming assays. Cell cycle changes were detected by flow cytometric analysis. Apoptosis was detected by annexin V/PI double-staining and Hoechst 33342 staining assays. Loss of mitochondrial membrane potential was observed by Rhodamine 123 staining. The in vivo efficacy of oridonin was evaluated using a NOZ xenograft model in athymic nude mice. The expression of cell cycle- and apoptosis-related proteins in vitro and in vivo was analyzed by western blot analysis. Activation of caspases (caspase-3, -8 and -9) was measured by caspases activity assay.ResultsOridonin induced potent growth inhibition, S-phase arrest, apoptosis, and colony-forming inhibition in SGC996 and NOZ cells in a dose-dependent manner. Intraperitoneal injection of oridonin (5, 10, or 15 mg/kg) for 3 weeks significantly inhibited the growth of NOZ xenografts in athymic nude mice. We demonstrated that oridonin regulated cell cycle-related proteins in response to S-phase arrest by western blot analysis. In contrast, we observed inhibition of NF-κB nuclear translocation and an increase Bax/Bcl-2 ratio accompanied by activated caspase-3, caspase-9 and PARP-1 cleavage after treatment with oridonin, which indicate that the mitochondrial pathway is involved in oridonin-mediated apoptosis.ConclusionsOridonin possesses potent anti-gallbladder cancer activities that correlate with regulation of the mitochondrial pathway, which is critical for apoptosis and S-phase arrest. Therefore, oridonin has potential as a novel anti-tumor therapy for the treatment of gallbladder cancer.
BackgroundGallbladder carcinoma is a malignant tumor with a very low 5-year survival rate because of the difficulty with its early diagnosis and the very poor prognosis of the advanced cancer state. The aims of this study were to determine whether curcumin could induce the apoptosis of a gallbladder carcinoma cell line, GBC-SD, and to clarify its related mechanism.MethodsFirst, the anti-proliferative activities of curcumin-treated and untreated GBC-SD cells were determined using the MTT and colony formation assays. Then, the early apoptosis of cells was detected by the annexin V/propidium iodide double-staining assay and Hoechst 33342 staining assay. Detection of mitochondrial membrane potential was used to validate the ability of curcumin on inducing apoptosis in GBC-SD cells. Cell cycle changes were detected by flow cytometric analysis. Finally, the expressions of the apoptosis-related proteins or genes caspase-3, PARP, Bcl-2, and Bax were analyzed by western blot and quantitative real time PCR assay. Statistical analyses were performed using the Student’s t-test for comparison of the results obtained from cells with or without curcumin treatment.ResultsThe MTT assay revealed that curcumin had induced a dose- and a time-dependent decrease in cell viability. Colony counting indicated that curcumin had induced a dose-dependent decrease in the colony formation ability in GBC-SD cells. Cells treated with curcumin were arrested at the S phase, according to the flow cytometric analysis. A significant induction of both the early and late phases of apoptosis was shown by the annexin V-FITC and PI staining. Morphological changes in apoptotic cells were also found by the Hoechst 33342 staining. After treatment with curcumin fluorescence shifted from red to green as ΔΨm decreased. Furthermore, western blot and quantitative real time PCR assays demonstrated that the curcumin induced apoptosis in GBC-SD cells by regulating the ratio of Bcl-2/Bax and activating the expression of cleaved caspase-3.ConclusionsTaken together, the results indicate that curcumin may be a potential agent for the treatment of gallbladder cancer.
It is very imperative to improve delayed fracture properties of high strength steel, which may enlarge its usage. The published literature shows that the susceptibility to hydrogen embrittlement of a novel 1 500 MPa bainite/martensite dual-phase high strength steel is inferior to that of conventional quench-tempered high strength steel. The stress corrosion cracking (SCC) in a 3.5 % NaCl solution for novel 1 500 MPa bainite/martensite dual-phase high strength steel was investigated in this paper by using modified wedgeopening-loading (WOL) specimens. The experimental results show that K ISCC for novel 1 500 MPa bainite/martensite dual-phase high strength steel is larger than 50 MPa · m 1/2 , exceeding conventional high strength steel. Its crack growth rate (da/dt) II is about 1ϫ10 Ϫ5 mm/s, which is less than that of conventional high strength steel. Hydrogen trapping phenomena in the steel were investigated by electrochemical permeation technique. The lath boundaries and stable retained austenite are beneficial hydrogen trap, slowing down the segregation of hydrogen on the crack tip, hence K ISCC increases and crack growth rate decreases.KEY WORDS: delayed fracture; hydrogen embrittlement; bainite/martensite dual-phase high strength steel; stress corrosion cracking; electrochemical permeation technique.
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