Poly-4-hydroxybutyrate, P(4HB), is a biosynthetic thermoplastic polymer that has been studied as a bio-absorbable medical material. In order to explore the in vivo biodegradation behaviour of porous P(4HB) membranes with specified apertures (89-150 µm), membranes with different porosities were implanted subcutaneously into the backs of 27 eight-week-old Sprague Dawley® rats. The implanted specimens were examined with Masson and hematoxylin and eosin staining. Masson staining indicated that the P(4HB) membranes were encased in fibrous cysts and that more collagen fibers were present within the sections of the hyper-porosity group. Hematoxylin and eosin staining showed that the residual area of the P(4HB) membranes in the hyper-porosity group decreased sharply compared to the hypo-porosity group, which implied that the P(4HB) membranes with higher porosity degraded faster than those with lower porosity. A slow degradation phase persisted for approximately 14 weeks during the degradation process. After the 16th week, the P(4HB) scaffolds fell into a fast degradation phase. The residual areas of the hyper-porosity P(4HB) membranes at the 32nd week were reduced by 39.76% compared with the second week after implantation. We concluded that P(4HB) membranes manifest a special biodegradation behavior in vivo and that the increased porosity of these membranes is an important factor favoring their biodegradation rates.

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Background: Microcystin-LR (MC-LR) and hepatitis B virus (HBV) are associated with hepatocellular carcinoma (HCC). However, the concentrations of MC-LR in drinking water and the synergistic effect of MC-LR and HBV on hepatocellular carcinogenesis through their disturbance of redox balance have not been fully elucidated. Methods: We measured the MC-LR concentrations in 168 drinking water samples of areas with a high incidence of HCC. The relationships between MC-LR and both redox status and liver diseases in 177 local residents were analyzed. The hepatoma cell line HepG2 transfected with C-terminal truncated hepatitis B virus X gene (Ct-HBX) were treated with MC-LR. Reactive oxygen species (ROS), superoxide dismutase (SOD), glutathione (GSH) and malondialdehyde (MDA) were measured. Cell proliferation, migration, invasion, and apoptosis were assessed with cell activity assays, scratch and transwell assays, and flow cytometry, respectively. The mRNA and protein expression-related redox status genes were analyzed with qPCR and Western blotting. Results:The average concentration of MC-LR in well water, river water and reservoir water were 57.55 ng/L, 76.74 ng/L and 132.86 ng/L respectively, and the differences were statistically significant (P < 0.05). The MC-LR levels in drinking water were correlated with liver health status, including hepatitis, clonorchiasis, glutamic pyruvic transaminase abnormalities and hepatitis B surface antigen carriage (all P values < 0.05). The serum MDA increased in subjects who drank reservoir water and were infected with HBV (P < 0.05). In the cell experiment, ROS increased when Ct-HBX-transfected HepG2 cells were treated with MC-LR, followed by a decrease in SOD and GSH and an increase in MDA. MC-LR combined with Ct-HBX promoted the proliferation, migration and invasion of HepG2 cells, upregulated the mRNA and protein expression of MAOA gene, and downregulated UCP2 and GPX1 genes. Conclusion: MC-LR and HBV may synergistically affect redox status and play an important role in hepatocarcinoma genesis.

In the present study, subcutaneous fat was obtained from adult women that had undergone conventional liposuction surgery. A comparative study was performed to investigate the effect of transparent and white poly-β-hydroxyethyl methacrylate (PHEMA) stents, which have different surface and cross-sectional morphological characteristics, on the differentiation of adipose-derived stem cells (ASCs) into myocardial cells. The cell counting kit-8 assay revealed that cell growth increased at varying rates among the different treatment groups. The absorbance of the experimental transparent PHEMA treated group increased in a time-dependent manner with the duration of incubation. The highest levels of proliferation were observed in the transparent PHEMA group. In addition, the transparent PHEMA treated group exhibited the strongest cell adhesion ability, which was significantly different to that of the white PHEMA group (P<0.01 and P<0.05 for Matrigel and fibronectin assay, respectively). Comparisons between the two stent materials with the inducer control group revealed statistically significant differences in the rate of ASC differentiation (P<0.05). The level of differentiation was the greatest in the transparent PHEMA group, and was significantly different to the white PHEMA group (P<0.05) and the blank control group (P<0.01). The results suggest that the inducers 5-aza-2-deoxycytidin and laminin, and material microstructure stents effectively promote the proliferation, growth and adhesion of ASCs. However, the transparent material microstructure may be a more suitable candidate for ASC-associated injections. The present study provides further evidence that a PHEMA stent structure, comprised of a high number of matrixes and a low water content, induces a high level of ASC differentiation to myocardial cells.

Objective: To investigate whether sequential regimen such as traditional anti-reabsorption medications followed by zoledronic acid could reduce the side effects after initiation of zoledronic acid in postmenopausal osteoporosis patients. Methods: A total of 156 postmenopausal osteoporosis patients who presented at our osteoporosis outpatient clinic were enrolled in this study. They were randomly divided into four groups: the control group, alendronate group, calcitonin group, and raloxifene group. All participants were treated with Caltrate 600 mg per day and calcitriol 0.25 ug per day as a baseline treatment, followed by administrating 5 mg/100 mL of zoledronic acid intravenously for one single time three months afterwards. During the abovementioned course of three months, the alendronate group received 70 mg of alendronate sodium orally once a week, the calcitonin group received nasal spray form of salmon calcitonin 10iu daily, the raloxifene group received 60mg of raloxifene orally daily, and the control group received nothing but only the baseline treatment. We tested parameters such as β-cross, blood calcium level, renal function both pre and post zoledronic acid treatment. We also documented those side effects that typically occurred within one week of treatment initiation, which included the proportion, severity, onset time, and duration of the fever, demand for pain medication, severity of bone and joint pain, flu-like symptoms, arrhythmia, blood calcium level, and kidney function impairment. We also evaluated how willing the patients were to receive a second dose of zoledronic acid. Then we did comparative analysis between control group and sequential group. Results: The side effects such as fever, bone and joint pain, flu-like symptoms after zoledronic acid treatment in alendronate group and calcitonin group were all significantly lower than that in control group, while raloxifene group showed no significant difference compared to that in the control group. The proportions of patients who needed NSAIDs in the alendronate group and the calcitonin group were significantly lower than that in control group. However, the raloxifene group showed no significant difference in the NSAIDs demand from that of the control group. The percentages of patients who consented to a second dose of zoledronate therapy in the alendronate, calcitonin and raloxifene groups were significantly higher than that in the control group. Conclusions: Sequential treatment with alendronate sodium or calcitonin can significantly reduce the side effects such as fever, bone/joint pain, flu-like symptoms caused by first-time zoledronic acid therapy. Raloxifene sequential treatment does not seem to have decreased or increased the side effects of zoledronic acid treatment. Also, sequential treatment can improve the patient compliance with a second dose of zoledronic acid.