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The stilling basin has been one of the most powerful hydraulic structures for the dissipation of the flow energy. Meshfree and particle methods have special advantages in modeling incompressible flows with free surfaces. In this paper, an integrated smoothed particle hydrodynamics (SPH) method is developed to model energy dissipation process of stilling basins. The integrated SPH includes the kernel gradient correction (KGC) technique, the dynamic solid boundary treatment, δ -SPH model and density reinitialization. We first conducted the simulations of dam-breaking and hydraulic jump to validate the accuracy of the present method. The present simulation results agree well with the experimental observations and numerical results from other sources. Then the discharge process of stilling basin with baffle-blocks is simulated with the integrated SPH. It is demonstrated that the detailed discharge process can be well captured by this method. The energy dissipation effect of stilling basin could be significantly improved by the baffle-blocks. The structure and position of the baffle-block directly affect the energy dissipation effect, while the height of the baffle-block has big influence on the drainage capacity. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Diabetes mellitus is involved in inflammation, immunity, and metabolism during osteoarthritis (OA). It destroys the normal synthesis and degradation balance of chondrocytes (CHs) and extracellular matrix (ECM). The purpose of this study was to explore the possible way of SIRT2 influencing the progress of diabetic OA. PATIENTS AND METHODS: Proteins of diabetic OA and normal OA cartilage samples were extracted from patients undergoing knee joint operation. CHs were also isolated from the cartilage exempted from diabetes for cell culture. Glucose was used to treat CHs for imitating the microenvironment of diabetes. The expressions of SIRT2, acetylated H3K9, H3K14, and H3K56 protein were determined by Western blotting. SIRT2, 8-hydroxy-2' deoxyguanosine (8-OH), and MMP-13 expressions were analyzed using immunofluorescence. RT-PCR was performed to measure the mRNA levels of SOD1, SOD2, CAT, MMP-13, ADAMTS-4, and ADAMTS-5. Total ROS level was performed by flow cytometry assay. RESULTS: SIRT2 expression was reduced, whereas acetylated H3K9, H3K14, and H3K56 were upregulated in diabetic cartilage compared to normal. High glucose suppressed the expression of SIRT2 but accelerated the acetylation of H3K9, H3K14, and H3K56. Besides, high glucose promoted the expression of 8-OH, and inhibited SOD1, SOD2, and CAT mRNA expressions, resulting in the up-regulated ROS level of CHs. In addition, high glucose activated the inflammatory response by upregulation of MMP-13, ADAMTS-4, and ADAMTS-5 expressions. SirReal2 suppressed SIRT2 and resulted in several acetylations of H3, more ROS, less antioxidant enzymes, and stronger inflammatory response caused by high glucose. However, supplied rh-SIRT2 reversed these negative effects of high glucose in CHs. CONCLUSIONS: SIRT2 expression is reduced along with the diabetic OA process with increased acetylation of H3, oxidative stress, and inflammatory response. Suppression of SIRT2 accelerates the progress of diabetic OA and upregulation of SIRT2 alleviates diabetic OA development by suppressing oxidative stress and inflammatory response that are likely to be related to the deacetylation of H3. [ABSTRACT FROM AUTHOR]

Based on the fundamental theory of smoothed-particle hydrodynamics (SPH), a feasible algorithm for fluid–solid coupling on interface is applied to describe the dynamic behavior of fluid and solid by utilizing continuum mechanics governing equations. Numerical simulation is conducted based on the proposed SPH model and the fluid–solid interface coupling algorithm, and good agreement is observed with the experiment results. It is shown in the results that the present SPH model is able to effectively and accurately simulate the free-surface flow of fluid, deformation of the elastic solid and the fluid–solid impacting. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of this study was to explore the influence of roflumilast on sepsis mice through the Janus kinase/signal transducer and activator of transcription (JAK/ STAT) signaling pathway. MATERIALS AND METHODS: A total of 36 Sprague-Dawley mice were randomly divided into normal group (n=12), model group (n=12) and roflumilast group (n=12). Mice in the normal group were fed normally. However, mice in the model group and roflumilast group were intraperitoneally injected with endotoxin to establish the sepsis mouse model. Furthermore, mice in the model group and roflumilast group were intraperitoneally injected with 0.9% sodium chloride and roflumilast once a day, respectively. After 7 d of intervention, mice were sampled. Lung tissue morphology was observed via hematoxylin-eosin (HE) staining, and the pathological score was given. The protein expression levels of JAK and STAT-3 were detected via Western blotting. The expression levels of interleukin-6 (IL-6) and tumor necrosis factor- α (TNF-α) were detected via enzyme-linked immunosorbent assay (ELISA). Meanwhile, the mRNA expression levels of JAK, STAT-3, IL-6 and TNF-α were detected via quantitative Polymerase Chain Reaction (qPCR). The number of inflammatory cells in the lavage fluid was counted by a biochemical detector. RESULTS: The survival rate of mice in the roflumilast group was significantly higher than that of the model group (p<0.05). The results of HE staining revealed that lung tissue morphology in roflumilast group was significantly improved when compared with the model group. Meanwhile, the pathological score in the roflumilast group was significantly lower than that of the model group (p<0.05). Western blotting showed that the protein expression levels of JAK and STAT-3 in the roflumilast group were markedly lower than those of the model group (p<0.05). According to the results of ELISA, the expression levels of IL-6 and TNF-α in the roflumilast group were remarkably lower than the model group (p<0.05). Further qPCR results manifested that the mRNA expression levels of JAK, STAT-3, IL-6 and TNF-α in the roflumilast group were significantly lower than those of the model group (p<0.05). Moreover, the number of neutrophils, monocytes and lymphocytes in the roflumilast group was significantly smaller than the model group. CONCLUSIONS: Roflumilast can improve lung tissue morphology of sepsis mice by inhibiting the JAK/STAT signaling pathway. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of this study was to investigate the expression of UPK1B in bladder cancer (BCa), and to further explore the correlation between UPK1B expression and pathological parameters as well as the prognosis of BCa. PATIENTS AND METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of UPK1B in 92 pairs of BCa tissues and adjacent normal tissues. The relationship between UPK1B expression and pathological features as well as the prognosis of BCa patients was further analyzed. For in vitro experiments, the mRNA expression level of UPK1B in BCa cell lines (EJ and T-24) was detected by qRT-PCR. In addition, knockdown of UPK1B in BCa cells was constructed using small interfering RNA. Effects of UPK1B knockdown on biological functions of BCa cells were analyzed by Cell Counting Kit-8 (CCK-8), colony formation assay and transwell assay, respectively. Furthermore, the underlying mechanism of UPK1B in regulating BCa was evaluated by Western blot and qRT-PCR, respectively. RESULTS: The expression of UPK1B in BCa tissues was remarkably higher than that of adjacent normal tissues (p<0.05). Compared with BCa patients with lower UPK1B expression, those with higher UPK1B expression exhibited higher tumor stage, lymph node metastasis and distant metastasis. In vitro experiments indicated that cell proliferation, invasion and metastasis were remarkably decreased in cells transfected with si-UPK1B when compared with those transfected with negative controls. Western blot showed that the expression of key proteins in the Wnt/β-catenin signaling pathway in cells transfected with si-UPK1B was significantly down-regulated compared with those transfected with negative controls, including β-catenin, c-myc and cyclinD1. In addition, rescue experiments found that UPK1B was regulated by β-catenin. CONCLUSIONS: UPK1B is upregulated in BCa, and is significantly correlated with tumor stage, lymph node metastasis, distant metastasis and poor prognosis of BCa. Moreover, UPK1B promotes the proliferation, invasion and migration of BCa via regulating the Wnt/β-catenin signaling pathway. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To study the alteration of CD8+ memory T cell subsets under different immune statuses during the spontaneous clearance of hepatitis B virus (HBV) in Chinese patients with chronic HBV infection. PATIENTS AND METHODS: We analyzed Chinese patients with chronic HBV infection including 10 patients with Hepatitis B surface Antigen (HBsAg) spontaneous seroconversion, 25 patients with Hepatitis B virus e Antigen (HBeAg) spontaneous seroconversion, 25 patients with chronic hepatitis B (CHB), and 25 chronic HBV carriers. The CD8+ T cells in peripheral blood were isolated, and flow cytometry was used to determine the percent change of CD8+ T memory cell subsets. ELISA was used to measure the levels of Interferon-γ (IFN-γ) secretion from CD8+ T cells. RESULTS: (1) The percentage of CD8+ TN cells in peripheral blood was lower in the HBsAg seroconversion group than in the HBeAg seroconversion group (p<0.01), and higher in the CHB group and chronic HBV carrier group (p<0.01, 0.01); (2) The percentage of CD8+ TEM-2 memory T cells in peripheral blood was higher in the HBsAg seroconversion group than the HBeAg seroconversion group (p<0.05), CHB group, and chronic HBV carrier group (p<0.01, 0.01); (3) The percentage of CD8+ TEM-1 and CD8+ TCM cells in peripheral blood was higher in the CHB group and HBV carrier group than the HBsAg seroconversion group and HBeAg group, but there were no significant differences between groups (p>0.05); (4) IFN-γ production from CD8+ T cells in peripheral blood was higher in the HBsAg seroconversion group than the HBeAg seroconversion group (p<0.05), CHB group, and chronic HBV carrier group (p<0.05, 0.01). CONCLUSIONS: The consistent increase of CD8+ TEM-2 cell subsets may be an important cause of spontaneous clearance of HBV. The disorder of CD8+ memory T cell differentiation may be an important mechanism of chronic HBV infection. [ABSTRACT FROM AUTHOR]