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In this study, a wave generation boundary capable of absorbing secondary reflections is embedded in an OpenFOAM-based numerical toolbox to model the wave-structure interactions of a Jarlan-type caisson breakwater (JTCB). Numerical simulations of wave structure interactions of a JTCB have been compared to experimental data where the reflection coefficient, the velocity field and the wave load of the JTCB, are analyzed in detail. It has been found that conventional two-dimensional (2D) simulation will underestimate the reflection coefficient, especially when the value of the nondimensional wave dissipation chamber length is in the range [0.12, 0.21]. This underestimation of the reflection coefficient could be related to an overestimation of the porosity of the perforated wall considered in conventional 2D structure simplifications. A porosity-equivalent 2D structure, whose porosity is the same as that of the three-dimensional (3D) structure, is presented and shown to effectively avoid this problem. In addition, in terms of wave loads, the agreement between the 2D simulation and the experiment has also been improved significantly using the porosity-equivalent 2D structure. Additionally, the interaction process, including the run-up on the back wall and the eddy formation process, is described via the changes of the velocity field and the free surface. Relatively good overall agreement between the calculated values and the experimental values is observed, indicating that this toolbox is useful and efficient for simulating wave-structure interactions of this kind. This study is expected to be useful to engineers concerned with the numerical modeling, preliminary feasibility assessment and conceptual design of JTCBs. • A wave generation boundary with the capacity of absorbing secondary reflection is presented. • Conventional two-dimensional structure simplification results in underestimations on the reflection coefficient. • The process of the interaction between waves and perforated structures is analyzed in detail. • Good overall agreement between the numerical and experimental results is obtained. • The porosity should keep unchanged during the 2D simplification process for such perforated structures. [ABSTRACT FROM AUTHOR]

Depression and cancer are both prevalent diseases worldwide. Numerous cancer patients experience psychological illnesses, especially depression, following a malignancy's dismal prognosis. Although some research has suggested that caffeine may be protective against depressive symptoms, it is still unclear how caffeine and cancer patients are related. Thus, we hypothesized that moderate daily caffeine intake may reduce the risk of depression in both the cancer and noncancer populations. Data were extracted and combined from the National Health and Nutrition Examination Survey from 2007 to 2016. After controlling for potential confounding factors, interaction effects analysis was used to clarify the interaction between caffeine and cancer on depressive symptoms. Linear regression analysis and restricted cubic splines were used to further analyze the relationship between caffeine and depression in cancer and noncancer populations. A total of 24,145 participants were included in the analysis. In the noncancer population, the quartile 3 group of caffeine intake showed a negative association between caffeine intake and Patient Health Questionnaire-9 (PHQ-9) scores (β = –0.23, 95% confidence interval, –0.45 to –0.01; P =.041). No association between caffeine intake and PHQ-9 scores was observed in the cancer population. In both cancer and noncancer populations, restricted cubic splines indicated a nonlinear trend between caffeine and PHQ-9 scores, with the lowest PHQ-9 scores when caffeine intake was 119.52 mg. In the noncancer population, moderate daily caffeine intake (quartile 3 group; range, 119.5-236.5 mg) was associated with reduced depressive symptoms, whereas in the cancer population, no association was found between caffeine intake and depression. Our study included 24,145 participants in NHANES. In the noncancer population, moderate caffeine intake (119.5-236.5 mg) is associated with less severe depressive symptoms. In the cancer population, however, caffeine intake bears no relationship to depression severity. NHANES, National Health and Nutrition Examination Survey. [Display omitted] [ABSTRACT FROM AUTHOR]

Adiposity is associated with an increased risk of primary liver cancer (PLC). As the most commonly used indicator of adiposity, the body mass index (BMI) has been questioned for its limitations in reflecting visceral fat. This study aimed to investigate the role of different anthropometric indicators in identifying the risk of PLC by accounting for potential non-linear associations. Systematic searches were conducted in the PubMed, Embase, Cochrane Library, Sinomed, Web of Science, and CNKI databases. Hazard ratios (HRs) and the corresponding 95% confidence intervals (CIs) were used to assess the pooled risk. The dose-response relationship was assessed using a restricted cubic spline model. Sixty-nine studies involving more than 30 million participants were included in the final analysis. Regardless of the indicator used, adiposity was strongly associated with an increased risk of PLC. When comparing the HRs per 1-standard deviation increment across indicators of adiposity, the association was strongest for waist-to-height ratio (WHtR) (HR = 1.39), followed by waist-to-hip ratio (WHR) (HR = 1.22), BMI (HR = 1.13), waist circumference (WC) (HR = 1.12), and hip circumference (HC) (HR = 1.12). A strong non-linear association was observed between each anthropometric parameter and the risk of PLC, regardless of whether the original or decentralised value was used. The positive association between WC and PLC risk remained substantial after adjusting for BMI. The incidence of PLC was higher with central adiposity (52.89 per 100,000 person-years, 95% CI = 50.33–55.44) than general adiposity (39.01 per 100,000 person-years, 95% CI = 37.26–40.75). Central adiposity seems to contribute more to the development of PLC than general adiposity. A larger WC, independent of BMI, was strongly associated with the risk of PLC and might be a more promising predictive indicator than BMI. [Display omitted] • BMI, WC, WHR, WHtR, and HC were, respectively, positively associated with the risk of PLC. • Elevated WC, independent of BMI, was associated with an increased risk of PLC. • The incidence of PLC was higher in central adiposity than that in general adiposity. • WC might be a more promising predictive indicator for PLC beyond BMI. [ABSTRACT FROM AUTHOR]

Mouse embryonic fibroblasts (MEFs) are multi-potent progenitor cells (MPCs), can differentiate into different lineages, such as osteogenic, and adipogenic. PTEN, a tumor suppressor, may be involved in regulating bone development through interacting with COX-2. BMP9, the most potent osteogenic BMPs, can up-regulate COX-2 in MPCs. Whether PTEN is involved in BMP9 induced osteogenic differentiation in MPCs remains unknown. The goal of this investigation is to identify the effect of PTEN on BMP9-induced osteogenic differentiation in MPCs and dissect the possible mechanism underlay this. We found that BMP9 down-regulates PTEN, and PTEN inhibitor (VO) effectively increases different osteogenic markers induced by BMP9 in MEFs. Exogenous expression of PTEN inhibits BMP9 induced ectopic bone formation apparently. Mechanistically, we found that VO can enhance BMP9 induced BMPs/Smads signaling prominently without no substantial effects on cell cycle. Further analysis indicates that VO can promote BMP9-induced expression of COX-2 in MEFs, which can be eliminated by PI3K inhibitor. Additionally, COX-2 knockdown abolishes the effect of VO on BMP9-induced ALP activities in MEFs. Our findings suggest that PTEN plays an important role in regulating BMP9 induced osteogenic differentiation in MPCs, which may be mediated by PTEN/PI3K/Akt signaling to modulate the expression of COX-2. [ABSTRACT FROM AUTHOR]

Cerebral ischemia-reperfusion (CIR) injury is one of the main diseases leading to death and disability. Acanthopanax senticosus (Rupr. & Maxim.) Harms (AS), also known as Panax ginseng, has neuroprotective effects on anti-CIR injury. However, the underlying molecular mechanism of its therapeutic effects is not clear. To systematically study and explore the mechanism of Acanthopanax senticosus (Rupr. & Maxim.) Harms extract (ASE) in the treatment of CIR injury based on metabolomics and transcriptomics. The pharmacological basis of ASE in the treatment of CIR was evaluated, and samples were used in plasma metabolomics and brain tissue transcriptomics to reveal potential biomarkers. Finally, according to online database, we analyzed biomarkers identified by the two technologies, explained reasons for the therapeutic effect of ASE, and identify therapeutic targets. A total of 53 differential metabolites (DMs) were identified in plasma and 3138 differentially expressed genes (DEGs) were identified in brain tissue from three groups of rats, including sham, ischemia-reperfusion (I/R), and ASE groups. Enrichment analysis showed that Nme6, Tk1, and Pold1 that are involved in the production of deoxycytidine and thymine were significantly up-regulated and Dck was significantly down-regulated by the intervention with ASE. These findings indicated that ASE participates in the pyrimidine metabolism by significantly regulating the balance between dCTP and dTTP. In addition, ASE repaired and promoted the lipid metabolism in rats, which might be due to the significant expression of Dgkz, Chat, and Gpcpd1. The findings of this study suggest that ASE regulates the significant changes in gene expression in metabolites pyrimidine, and lipid metabolism in CIR rats and plays an active role in the treatment of CIR injury through multiple targets and pathways. Image 1 [ABSTRACT FROM AUTHOR]