No abstract

Polygonatum alte-lobatum Hayata, a rhizomatous perennial herb, belongs to the Liliaceae family and is endemic to Taiwan. We investigated the antioxidant and anti-fatigue activities of P. alte-lobatum in exercised rats. Levels of polyphenols, flavonoids and polysaccharides and 2,2-diphenyl-1-picrylhydrazyl (DPPH) free-radical scavenging activity were measured in extracts of P. alte-lobatum (EPA). Sprague-Dawley rats were randomly divided into four groups for 8-week treatment with vehicle (control) and low-, medium-, and high-dose EPA (LEPA, MEPA, HEPA; 0, 75, 150, and 375 mg/kg/day, respectively). Exercise performance was evaluated by exhaustive treadmill exercise time and by changes in body composition and biochemical variables at the end of the experiment. EPA contained polyphenols, flavonoids and polysaccharides, with polysaccharide content at least 26 times greater than that of polyphenols and flavonoids. Trend analysis revealed that EPA dose-dependently scavenged DPPH free radicals. EPA treatment dose-dependently increased endurance running time to exhaustion and superoxide dismutase activity and total antioxidant ability of blood. EPA dose-dependently decreased serum urea nitrogen and malondialdehyde levels after exercise. Hepatic glycogen content, an important energy source for exercise, was significantly increased with EPA treatment. EPA could be a potential agent with an anti-fatigue pharmacological function.

Human placental multipotent mesenchymal stromal cells (hPMSCs) can be isolated from term placenta, but their angiogenic ability and the regulatory pathways involved are not known. hPMSCs were shown to express integrins αv, α4, α5, β1, β3, and β5 and could be induced to differentiate into cells expressing endothelial markers. Increases in cell surface integrins α5 and β1, but not α4, αvβ3, or αvβ5, accompanied endothelial differentiation. Vascular endothelial growth factor-A augmented the effect of fibronectin in enhancing adhesion and migration of differentiated hPMSC through integrin α5β1, but not αvβ3 or αvβ5. Formation of capillary-like structures in vitro from differentiated cells was inhibited by pre-treatment with function-blocking antibodies to integrins α5 and β1. When hPMSCs were seeded onto chick chorioallantoic membranes (CAM), human von Willebrand factor-positive cells were observed to engraft in the chick endothelium. CAMs transplanted with differentiated hPMSCs had a greater number of vessels containing human cells and more incorporated cells per vessel compared to CAMs transplanted with undifferentiated hPMSCs, and overall angiogenesis was enhanced more by the differentiated cells. Function-blocking antibodies to integrins α5 and β1 inhibited angiogenesis in the CAM assay. These results suggest that differentiated hPMSCs may contribute to blood vessel formation, and this activity depends on integrin α5β1.

We verify a high visualization rate (93%) of normal appendices on MDCT by using multiplanar reformation display.

Objective: Excess postpartum weight retention (PPWR) is related to long-term weight gain. Therefore, this study was conducted to identify the risk factors for PPWR to provide guidance for preventive strategies. Methods: This cohort study surveyed 461 women who gave birth at a medical center between March 2014 and March 2016. The participants completed a questionnaire within 1 month of delivery, and their 6-month postpartum weight was tracked. Results: The results showed that the mean pre-pregnancy BMI was 21.4 ± 3.3 kg/m², and the mean gestational weight gain (GWG) was 12.8 ± 4.1 kg. The mean PPWR was 4.6 ± 3.5 kg at 1 month and 2.1 ± 3.3 kg at 6 months. Multivariate analysis revealed that GWG (adjusted OR: 1.92 (1.70-2.17)), pre-pregnancy BMI (adjusted OR: 0.85 (0.77-0.94)), and exclusive breastfeeding (adjusted OR: 0.55 (0.32-0.94)) were significantly correlated with a 1-month PPWR higher than the median value. In addition, GWG (adjusted OR: 1.30 (1.22-1.39)) and exclusive breastfeeding (adjusted OR: 0.37 (0.24-0.58)) were significantly correlated with a 6-month PPWR higher than the median value. Conclusion: Our findings indicate that the key to reducing PPWR is to control GWG and engage in exclusive breastfeeding.

No abstract

Soy extract is highly efficacious at relieving menopausal symptoms and demonstrates a positive effect on the cardiovascular system and skeleton.

Reactive oxygen species may cause oxidative damage in the placenta, yet some mechanisms must exist to reduce or prevent such damage. We investigated whether oxidative injury to placental endothelial cells is inhibited by activation of antioxidant enzymes by paracrine factors secreted by human placental multipotent mesenchymal stromal cells (hPMSC). hPMSC-conditioned medium and umbilical endothelial cells were assayed for cytokines and cytokine receptor expression by immunoassay and real-time PCR. Endothelial cell survival was evaluated by MTS [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt] assay and caspase 3 activity assay. tert-Butyl hydroperoxide was used to induce oxidative injury in endothelial cells, with fluorescent microscopy and flow cytometry used to detect intracellular peroxides and cell apoptosis. Western blot, real-time PCR, STAT3 DNA-binding activity assay, and STAT3 siRNA were used to assess endothelial cell antioxidant enzymes. hPMSC-conditioned medium supported endothelial cell survival and reduced endothelial cell intracellular peroxides and apoptosis. hPMSCs expressed the transcripts of the interleukin (IL) 6 cytokine family, including IL6 and leukemia-inhibitory factor. hPMSC-conditioned medium activated STAT3 expression in endothelial cells, which was inhibited by neutralizing antibody to interleukin 6 signal transducer (IL6ST) but not to IL6 or leukemia-inhibitory factor. STAT3 siRNA or manganese superoxide dismutase (SOD2) siRNA transfected into endothelial cells inhibited the antiapoptotic effect of conditioned medium. SOD2 was significantly upregulated in endothelial cells by conditioned medium via STAT3 activation that, in turn, was inhibited by IL6ST-neutralizing antibody or STAT3 siRNA. Paracrine factors secreted by hPMSCs support endothelial cell survival. STAT3 activation and SOD2 production protect against oxidative stress-induced endothelial cell damage.