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Plant and fruit extracts exhibit fewer side effects than pharmaceuticals and can display therapeutic qualities. Consequently, they have attracted increased attention among health-conscious individuals, and many studies related to their health-promoting effects are being actively conducted. Vitis coignetiae is well-known for its antioxidant, anti-inflammatory, and anticancer properties. However, the immune-enhancing effects of Vitis coignetiae have not yet been studied. In this study, Vitis coignetiae extract (VCE) increased immune-related activity in Wistar rat splenocytes and cyclophosphamide (Cy)-induced immunosuppressed rats. In splenocytes, VCE was nontoxic up to 300 μg/mL and increased cell viability in the presence of Cy. VCE also recovered Cy-induced decreases in cytokine (tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), interleukin-2 (IL-2), and IL-12) levels and natural killer (NK) cell activity in splenocytes. In Cy-induced immunosuppressed rats, VCE protected against Cy-induced spleen tissue damage and decreases in body and spleen weight, cytokine (TNF-α, IFN-γ, IL-2, and IL-12) levels, and NK cell activity. We also observed recovery of immunoglobulin G (IgG) and IgM levels following VCE treatment. In conclusion, the ability of VCE to restore immune activity from an immunosuppressive state to normal levels suggests its immune-enhancing efficacy. Therefore, VCE may have the potential for application in the development of immune-enhancing functional foods and medicines. [ABSTRACT FROM AUTHOR]

Aim: The link between periodontitis and intestinal dysbiosis, two factors that contribute to atherosclerosis, has not been clearly defined. We investigated the integrative effects of oral infection with Porphyromonas gingivalis (PG), the major pathogen for periodontitis, on intestinal microbiota and atherosclerosis. Materials and Methods: ApoE−/− mice were fed a normal chow diet (NC), a Western diet (WD) or a WD with oral PG infection (PG). The PG infection was investigated by placing a total of 109 CFUs of live PG into the oral cavity of each mouse using a feeding needle five times a week for 3 weeks. Atherosclerotic lesions of the aortae were measured, and blood lipoproteins and the expression of molecules related to lipid metabolism in the liver were analysed. We also performed 16S RNA sequencing and a microbiome analysis using faeces. Results: En face bloc preparation of the aortae showed that the PG group had a 1.7‐fold increase in atherosclerotic lesions compared with the WD group (p <.01). Serum analyses showed that oral PG infection induced a significant decrease in high‐density lipoprotein (HDL) and triglyceride. Western blots of hepatic tissue lysates revealed that PG infection reduced the expression of scavenger receptor class B type 1 (SR‐B1) in the liver by 50%. Faecal microbiota analysis revealed that species richness estimates (Chao1, ACE) decreased immediately after PG infection. PG infection also induced a significant decrease in Shannon diversity and an increase in Simpson's indices in the WD‐fed mice. PG infection significantly increased the phyla Actinobacteria and Deferribacteres, along with the species Mucispirillum schaedleri and Lactobacillus gasseri, in the mice. The functional study showed that PG infection increased the expression of proteins that function in carbohydrate and glucose metabolism, including phosphotransferase system (PTS) proteins and the GntR family transcriptional regulator. Conclusions: Oral PG infection promotes atherosclerosis and induces significant metabolic changes, including reduced serum HDL and reduced hepatic SR‐B1 and ABCA1 expression, as well as changes in intestinal microbiota. Our study suggests that intestinal dysbiosis accompanies periodontitis and could play a role in atherosclerosis. [ABSTRACT FROM AUTHOR]

Flat plate systems are commonly designed as a gravity-force-resisting system (GFRS) along with stiffer lateral-force- resisting systems (LFRS) such as shear walls, and moment resisting frames; however, deformation compatibility between the GFRS and LFRS results in positive moments (producing tension at the slab bottom) at the slab-column connections in flat plate systems. Continuous slab-bottom reinforcement (integrity reinforcement) passing through the column is required to prevent progressive collapse; however, for posttensioned flat plate (PT-flat plate) systems, there have been arguments among engineers on applying continuous slab-bottom reinforcement since ACI 318 and 352 provisions do not clearly specify the requirement on the slab-bottom reinforcement for PT flat plates. The purpose of this study is to investigate the effects of continuous slab-bottom reinforcement passing through the column core on the hysteretic behavior of the PT slab-column connections. Test results for six, 3/5 scaled specimens for interior PT flat plate connections subjected to constant gravity loads and quasistatic reversed cyclic lateral loads are presented and indicate that the slab-bottom reinforcement conforming to ACI-ASCE 352R.1 is not required to prevent collapse, but does significantly improves the hysteretic energy absorption capacity. DOI: 10.1061/(ASCE)0733-9445 (2009) 135:9(1019) CE Database subject headings: Post tensioning; Slabs; Connections; Lateral forces; Plates; Reinforcement.

Effective beam width model (EBWM) has been widely used for predicting lateral drifts and slab moments in fiat slab structures under lateral loads. As the slab moment due to lateral loads increases, slab stiffness decreases due to crack formation. The accuracy of the EBWM strongly depends on how the reduced slab stiffness is estimated. For this purpose, this study developed equations for calculating slab stiffness reduction factor ([beta]) by conducting nonlinear regression analysis using stiffness reduction factors estimated from collected test results. The slab stiffness reduction factor ([beta]) is defined as a ratio of reduced slab stiffness due to crack formation to the stiffness of the uncracked slab section. For verifying the proposed equation, the lateral stiffness of two slab-column connection specimens tested by the writers was compared with the lateral stiffness calculated using the EBWM with the proposed stiffness reduction factor. Further, two fiat plate specimens having two continuous spans were also considered for verifying the proposed equations for [beta]. DOI: 10.1061/(ASCE)ST.1943-541X.0000001 CE Database subject headings: Slabs; Beams; Stiffness; Experimentation; Drift; Lateral loads.

The trapping of lipid-laden macrophages in the arterial intima is a critical but reversible step in atherogenesis. However, the mechanism by which this occurs is not clearly defined. Here, we tested in mice the hypothesis that CD36, a class B scavenger receptor expressed on macrophages, has a role in this process. Using both in vivo and in vitro migration assays, we found that oxidized LDL (oxLDL), but not native LDL, inhibited migration of WT mouse macrophages but not CD36-deficient cells. We further observed a crucial role for CD36 in modulating the in vitro migratory response of human peripheral blood monocyte--derived macrophages to oxLDL. oxLDL also induced rapid spreading and actin polymerization in CD36-sufficient but not CD36-deficient mouse macrophages in vitro. The underlying mechanism was dependent on oxLDL-mediated CD36 signaling, which resulted in sustained activation of focal adhesion kinase (FAK) and inactivation of Src homology 2-containing phosphotyrosine phosphatase (SHP-2). The latter was due to NADPH oxidase--mediated ROS generation, resulting in oxidative inactivation of critical cysteine residues in the SHP-2-active site. Macrophage migration in the presence of oxLDL was restored by both antioxidants and NADPH oxidase inhibitors, which restored the dynamic activation of FAK. We conclude therefore that CD36 signaling in response to oxLDL alters cytoskeletal dynamics to enhance macrophage spreading, inhibiting migration. This may induce trapping of macrophages in the arterial intima and promote atherosclerosis., Introduction Cardiovascular disease is currently the leading cause of death in many developed countries, and atherosclerosis is the most important underlying pathology (1). Atherosclerosis is a disease characterized by accumulation [...]

Simple Summary: Enzymatic porcine placental hydrolyzing (EPPH) was extracted using enzymatic hydrolysis to extract placental-derived peptides recently reported as excellent bioactive substances, and EPPH was administered to HepG2 cells and alcohol-derived animal models. As a result, it was confirmed that inflammation and antioxidant activity could be regulated through CYP2E1 inhibition. Through these results, we confirmed that the antioxidant and anti-inflammatory effects mediated by CYP2E1 regulation of EPPH have potential for improvement and protection of liver disease in alcoholic liver disease animal models. Alcoholic liver disease is associated with the production of highly reactive free radicals by ethanol and its metabolites. Free radicals not only induce liver oxidation and damage tissues, but also stimulate an inflammatory response in hepatocytes, leading to severe liver disease. In order to improve alcoholic liver disease, enzymatic porcine placenta hydrolysate was studied by exploring various materials. Enzymatic porcine placenta hydrolysate (EPPH) contains various amino acids, peptides, and proteins, and is used as a useful substance in the body. In this study, changes were confirmed in indicators related to the antioxidant efficacy of EPPH in vitro and in vivo. EPPH inhibits an EtOH-induced decrease in superoxide dismutase and catalase activity through inhibition of free radicals without endogenous cytotoxicity. EPPH has been observed to have a partial effect on common liver function factors such as liver weight, ALT, AST, ALP, and GGT. In addition, EPPH affected changes in fat regulators and inflammatory cytokines in blood biochemical assays. It was confirmed that EPPH was involved in fat metabolism in hepatocytes by regulating PPARα in an alcoholic liver disease animal model. Therefore, EPPH strongly modulates Bcl-2 and BAX involved in apoptosis, thereby exhibiting cytochrome P450 (CYP)-inhibitory effects in alcoholic liver disease cells. As a result, this study confirmed that EPPH is a substance that can help liver health by improving liver disease in an alcoholic liver disease animal model. [ABSTRACT FROM AUTHOR]