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Objective This study aims to evaluate the association between lower grip strength and mortality hazard. Methods We selected 10,280 adults aged 45 to 96 years old from the China Health and Retirement Longitudinal Study and used multivariate Cox proportional hazard models to assess the association of grip strength with mortality hazard. In addition, we explored the possibility of a nonlinear relationship using a 4-knot restricted spline regression. Results We found that elevated grip strength was associated with lower mortality up to a certain threshold. The baseline quartile values of grip strength were 30, 37, and 44 kg for males and 25, 30, and 35 kg for females. After adjusting for confounders, with category 1 as the reference group, the adjusted HRs were 0.58 (0.42–0.79) in males and 0.70 (0.48–0.99) in females (category 4). We also found a linear association between grip strength values and all-cause death risk (males, P = 0.274; females, P = 0.883) using restricted spline regression. For males with a grip strength < 37 kg and females with a grip strength < 30 kg, grip strength and death were negatively associated. Conclusion Grip strength below a sex-specific threshold is inversely associated with mortality hazard among middle-aged and older Chinese adults with chronic diseases.
Objective This study aimed to estimate spatiotemporal variations of global heat-related cardiovascular disease (CVD) burden from 1990 to 2019. Methods Data on the burden of heat-related CVD were derived from the Global Burden of Disease Study 2019. Deaths and disability-adjusted life years (DALYs) were used to quantify heat-induced CVD burden. We calculated the age-standardized mortality rate (ASMR) and DALY rate (ASDR) per 100,000 population to compare this burden across regions. Generalized linear models were applied to evaluate estimated annual percentage changes (EAPC) for temporal trends from 1990 to 2019. The correlation between the socio-demographic index (SDI) and age-standardized rate was measured using the Spearman rank test. Results Heat-induced CVD caused approximately 90 thousand deaths worldwide in 2019. Global ASMR and ASDR of heat-related CVD in 2019 were 1.17 [95% confidence interval (CI): 0.13–1.98] and 25.59 (95% CI: 2.07–44.17) per 100,000 population, respectively. The burden was significantly increased in middle and low-SDI regions and slightly decreased in high-SDI regions from 1990 to 2019. ASMR showed an upward trend, with the most considerable increase in low-latitude countries. We observed a negative correlation between SDI and EAPC in ASMR (rs = −0.57, P < 0.01) and ASDR (rs = −0.59, P < 0.01) among 204 countries. Conclusion Heat-attributable CVD burden substantially increased in most developing countries and tropical regions.
Objective To evaluate the association between serum uric acid (SUA) and kidney function decline. Methods Data was obtained from the China Health and Retirement Longitudinal Study on the Chinese middle-aged and older population for analysis. The kidney function decline was defined as an annual estimated glomerular filtration rate (eGFR) decrease by > 3 mL/min per 1.73 m2. Multivariable logistic regression was applied to determine the association between SUA and kidney function decline. The shape of the association was investigated by restricted cubic splines. Results A total of 7,346 participants were included, of which 1,004 individuals (13.67%) developed kidney function decline during the follow-up of 4 years. A significant dose-response relation was recorded between SUA and the kidney function decline (OR 1.14, 95% CI 1.03–1.27), as the risk of kidney function decline increased by 14% per 1 mg/dL increase in SUA. In the subgroup analyses, such a relation was only recorded among women (OR 1.22, 95% CI 1.03–1.45), those aged < 60 years (OR 1.22, 95% CI 1.05–1.42), and those without hypertension and without diabetes (OR 1.22, 95% CI 1.06–1.41). Although the dose-response relation was not observed in men, the high level of SUA was related to kidney function decline (OR 1.83, 95% CI 1.05–3.17). The restricted cubic spline analysis indicated that SUA > 5 mg/dL was associated with a significantly higher risk of kidney function decline. Conclusion The SUA level was associated with kidney function decline. An elevation of SUA should therefore be addressed to prevent possible kidney impairment and dysfunction.
Objective Programmed cell death 6 (PDCD6), a Ca2+-binding protein, has been reported to be aberrantly expressed in all kinds of tumors. The aim of this study was to explore the role and mechanism of PDCD6 in hepatocellular carcinomas (HCCs). Methods The expression levels of PDCD6 in liver cancer patients and HCC cell lines were analyzed using bioinformatics and Western blotting. Cell viability and metastasis were determined by methylthiazol tetrazolium (MTT) and transwell assays, respectively. And Western blotting was used to test related biomarkers and molecular pathway factors in HCC cell lines. LY294002, a PI3K inhibitor inhibiting AKT, was used to suppress the AKT/GSK3β/β-catenin pathway to help evaluate the role of this pathway in the HCC carcinogenesis associated with PDCD6. Results The analysis of The Cancer Genome Atlas Database suggested that high PDCD6 expression levels were relevant to liver cancer progression. This was consistent with our finding of higher levels of PDCD6 expression in HCC cell lines than in normal hepatocyte cell lines. The results of MTT, transwell migration, and Western blotting assays revealed that overexpression of PDCD6 positively regulated HCC cell proliferation, migration, and invasion. Conversely, the upregulation of PDCD6 expression in the presence of an AKT inhibitor inhibited HCC cell proliferation, migration, and invasion. In addition, PDCD6 promoted HCC cell migration and invasion by epithelial-mesenchymal transition. The mechanistic investigation proved that PDCD6 acted as a tumor promoter in HCC through the AKT/GSK3β/β-catenin pathway, increasing the expression of transcription factors and cellular proliferation and metastasis. Conclusion PDCD6 has a tumor stimulative role in HCC mediated by AKT/GSK3β/β-catenin signaling and might be a potential target for HCC progression.
Objective Arsenic (As) and fluoride (F) are two of the most common elements contaminating groundwater resources. A growing number of studies have found that As and F can cause neurotoxicity in infants and children, leading to cognitive, learning, and memory impairments. However, early biomarkers of learning and memory impairment induced by As and/or F remain unclear. In the present study, the mechanisms by which As and/or F cause learning memory impairment are explored at the multi-omics level (microbiome and metabolome). Methods We stablished an SD rats model exposed to arsenic and/or fluoride from intrauterine to adult period. Results Arsenic and/fluoride exposed groups showed reduced neurobehavioral performance and lesions in the hippocampal CA1 region. 16S rRNA gene sequencing revealed that As and/or F exposure significantly altered the composition and diversity of the gut microbiome, featuring the Lachnospiraceae_NK4A136_group, Ruminococcus_1, Prevotellaceae_NK3B31_group, [Eubacterium]_xylanophilum_group. Metabolome analysis showed that As and/or F-induced learning and memory impairment may be related to tryptophan, lipoic acid, glutamate, gamma-aminobutyric acidergic (GABAergic) synapse, and arachidonic acid (AA) metabolism. The gut microbiota, metabolites, and learning memory indicators were significantly correlated. Conclusion Learning memory impairment triggered by As and/or F exposure may be mediated by different gut microbes and their associated metabolites.
Objective Late 2019 witnessed the outbreak and widespread transmission of coronavirus disease 2019 (COVID-19), a new, highly contagious disease caused by novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Consequently, considerable attention has been paid to the development of new diagnostic tools for the early detection of SARS-CoV-2. Methods In this study, a new poly-N-isopropylacrylamide microgel-based electrochemical sensor was explored to detect the SARS-CoV-2 spike protein (S protein) in human saliva. The microgel was composed of a copolymer of N-isopropylacrylamide and acrylic acid, and gold nanoparticles were encapsulated within the microgel through facile and economical fabrication. The electrochemical performance of the sensor was evaluated through differential pulse voltammetry. Results Under optimal experimental conditions, the linear range of the sensor was 10−13–10−9 mg/mL, whereas the detection limit was 9.55 fg/mL. Furthermore, the S protein was instilled in artificial saliva as the infected human saliva model, and the sensing platform showed satisfactory detection capability. Conclusion The sensing platform exhibited excellent specificity and sensitivity in detecting spike protein, indicating its potential application for the time-saving and inexpensive detection of SARS-CoV-2.
2023, 36(3): 284-288.
doi: 10.3967/bes2023.031
2015, 28(1): 57-71.
doi: 10.3967/bes2015.006
2018, 31(2): 87-96.
doi: 10.3967/bes2018.011
2022, 35(7): 573-603.
doi: 10.3967/bes2022.079
2012, 25(3): 317-324.
doi: 10.3967/0895-3988.2012.03.010
2003, 16(3): 246-255.
2019, 32(9): 659-672.
doi: 10.3967/bes2019.085
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doi: 10.3967/bes2018.088
2019, 32(8): 578-591.
doi: 10.3967/bes2019.076
2019, 32(6): 419-426.
doi: 10.3967/bes2019.057
2014, 27(8): 606-613.
doi: 10.3967/bes2014.093
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doi: 10.3967/bes2016.026
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doi: 10.3967/bes2019.096
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2019, 32(8): 559-570.
doi: 10.3967/bes2019.074
2019, 32(10): 739-754.
doi: 10.3967/bes2019.094
2017, 30(5): 384-389.
doi: 10.3967/bes2017.051
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