MiR-467g suppresses the osteogenic differentiation and mineralization of mouse preosteoblasts via down-regulation of Runx-2 expression / 中国组织工程研究

BACKGROUND: Preliminary studies have found miR-467g inhibits bone regeneration, however, there is little information about the underlying mechanism. OBJECTIVE: To explore the effect of miR-467g on osteogenic differentiation and mineralization of mouse preosteoblasts and the underlying mechanism. METHODS: C57 mouse preosteoblasts were isolated and cultured in vitro. The expression levels of Runx-2, Osterix, and Osteocalcin, as well as alkaline phosphatase and mineralization activities were determined by western blot, real-time PCR, alkaline phosphatase and Alizarin red staining, respectively. miR-467g-overexpressed preosteoblasts were constructed to investigate the effect of miR-467g on osteogenic differentiation and mineralization of preosteoblasts by lipofection transfection. Dual luciferase reporter assay was used to identify whether the 3’UTR of Runx-2 mRNA was a binding target of miR-467g. RESULTS AND CONCLUSION: The primary mouse preosteoblasts had a good osteogenic proliferation and differentiation ability in vitro. Expression level of miR-467g was decreased with the increase in osteogenic induction time. MiR-467g suppressed the osteogenic differentiation and mineralization of mouse preosteoblasts. Luciferase assay confirmed that miR-467g targeted Runx-2 directly. In summary, miR-467g can suppress the osteogenic differentiation and mineralization of mouse preosteoblasts via down-regulation of Runx-2 expression.

Study on acute and subchronic toxicity of ammonium dinitramide / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the acute, subacute and subchronic toxicity induced by ammonium dinitramide (ADN), and to ascertain the gradation and target organs of acute toxicity induced by AND.</p><p><b>METHODS</b>According to technical specifications for toxicity determination of chemicals, the oral tests for acute, subacute and subchronic toxicity induced by AND were performed for 90 days.</p><p><b>RESULTS</b>The oral LDx for mouse and rat was 568.9 mg/kg and 616.6 mg/kg ADN respectively. The gradation of acute toxicity induced by AND was low level. The results of oral subacute and subchronic toxicity tests (for 28 and 90 days) showed that a gain in weight in group exposed to 123 mg/kg AND was significantly lower than that in control group (P<0.05), the TBIL and ALT in group exposed to 61.6 and 123 mg/kg AND significantly increased and the ratio of liver weight to body weight obviously decreased, as compared with control group, the number of animals with hepatic pathological changes in group exposed to 61.6 and 123 mg/kg AND was significantly higher than that in control group (P<0.05).</p><p><b>CONCLUSION</b>The gradation of acute toxicity induced by ADN was low level. When the exposure dose of AND was 30.8 mg/kg, the adverse effect was not observed, and the target organ was liver.</p>

Study on mutagenicity and teratogenicity of ammonium dinitramide / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the mutagenicity and teratogenicity induced by ammonium dinitramide(ADN).</p><p><b>METHODS</b>According to technical specifications for toxicity determination of chemicals, Salmonella typhimurium reverse mutation assay (Ames assay), in vivo mammalian erythrocyte micronucleus test, sperm malformation test and teratogenesis test were used to detect the mutagenicity and teratogenicity induced by AND.</p><p><b>RESULTS</b>When the exposure doses of AND were 8-5000 pg/plate, the result of Ames assay was negative. As compared with control group, the micronucleus rate of mice exposed to 113.8 mg/kg AND significantly increased(P<0.05), the sperm malformation rates of mice exposed to 54.4-272.0 mg/kg AND did not increased significantly. The survival rate of fetuses decreased, the rate of assimilated fetuses increased, the rate of fetus sternum agenesis enhanced in mice exposed to 319 mg/kg AND, as compared with controls. The rates of in the 4th-6th fetus sternum agenesis in groups exposed to 21.3, 79.7 and 319 mg/kg AND were higher than that in control group. The malformation rate of fetus bowels in groups exposed to 319 mg/kg AND was higher than that in control group. The teratogenic index of ADN was 30.</p><p><b>CONCLUSION</b>AND may be a mutagen and induce the teratogenic effect.</p>

A novel beta-glucan produced by Paenibacillus polymyxa JB115 induces nitric oxide production in RAW264.7 macrophages

The effect of extracellular beta-(1-->3), (1-->6)-glucan, produced by Paenibacillus polymyxa JB115, on nitric oxide (NO) production in RAW264.7 macrophages was investigated. beta-glucan induced the production of NO by RAW264.7 macrophages in a concentration- and time-dependent manner. Moreover, beta-glucan stimulation increased the mRNA expression of iNOS, COX-2 and IL-6 in RAW264.7 macrophages in a concentration-dependent manner.

Clinical pharmacokinetics of norfloxacin-glycine acetate after intravenous and oral administration in pigs

The pharmacokinetics and dosage regimen of norfloxacin-glycine acetate (NFLXGA) was investigated in pigs after a single intravenous (i.v.) or oral (p.o.) administration at a dosage of 7.2 mg/kg body weight. After both i.v. and p.o. administration, plasma drug concentrations were best fitted to an open two-compartment model with a rapid distribution phase. After i.v. administration of NFLXGA, the distribution (t1/2alpha) and elimination half-life (t1/2beta) were 0.36 +/- 0.07 h and 7.42 +/- 3.55 h, respectively. The volume of distribution of NFLXGA at steady state (Vdss) was 4.66 +/- 1.39 l/kg. After p.o. administration of NFLXGA, the maximal absorption concentration (Cmax) was 0.43 +/- 0.06 microgram/ ml at 1.36 +/- 0.39 h (Tmax). The mean absorption (t1/2ka) and elimination half-life (t1/2beta) of NFLXGA were 0.78 +/- 0.27 h and 7.13 +/- 1.41 h, respectively. The mean systemic bioavailability (F) after p.o. administration was 31.10 +/- 15.16%. We suggest that the optimal dosage calculated from the pharmacokinetic parameters is 5.01 mg/kg per day i.v. or 16.12 mg/kg per day p.o.