Objective: To investigate the effects of the link between overweight/obesity and type 2 diabetes mellitus (T2DM) on leptin and visfatin levels. Methods: Males without T2DM and male patients with T2DM hospitalized in Lishui Municipal Central Hospital from January to June, 2017 were enrolled. Subjects' age and medical history of diseases were collected. The height and body weight were measured, and the body mass index (BMI) was estimated. The leptin and visfatin levels were determined, and compared between patients with and without T2DM, and between patients with and without overweight/obesity. The effect of the link between overweight/obesity and T2DM on leptin and visfatin levels was examined using a generalized linear regression model. Results: There were 66 patients with T2DM, with a mean age of (49.70±9.45) years and a mean diabetes duration of (4.99±4.46) years, and there were 64 patients without T2DM, with a mean age of (43.89±0.20) years. The leptin [ (3.17±0.36) vs. (3.03±0.30) ng/mL; t=2.387, P=0.018] and visfatin levels [ (29.14±3.16) vs. (21.81±3.32) ng/mL; t=12.900, P<0.001] were significantly greater in T2DM patients than in patients without T2DM. The leptin level was significantly greater in patients with overweight/obesity than in those without overweight/obesity [ (3.27±0.32) vs. (2.92±0.26) ng/mL; t=6.634, P<0.001], and the visfatin level was significantly lower in patients with overweight/obesity than in those without overweight/obesity [(24.38±5.14) vs. (26.71±4.36) ng/mL; t=2.780, P=0.006]. Generalized linear regression analysis showed interacting effects of overweight/obesity and T2DM on leptin (β=0.286, P=0.003) and visfatin levels (β=2.709, P=0.008). Conclusion The interaction between overweight/obesity and T2DM affects leptin and visfatin levels.

OBJECTIVETo develop a HPLC method for the determination of plasma concentration of oridonin (ORI) and study the pharmacokinetics of ORI in mice.

METHODBlood was sampled from mice which were injected ORI by 10 mg x kg(-1) at different time intervals, and the concentration of ORI was determined by HPLC. The pharmacokinetic parameters were accessed by 3P97.

RESULTThe calibration curve was linear (r = 0.998 7) within the range of 0.202-20.0 mg x L(-1) for ORI in plasma. The average recoveries were more than 93%. The within-day and between-day precisions were no more than 9%. After i.v. oridonin in mice, the plasma concentration-time course fitted well to two-compartment model. The pharmacokinetic equation was C = 16.192 5e(-0.554 6t) + 5.475 7e(-0.016 3t). The pharmacokinetic parameters were below: t1/2alpha 1.249 9 min, t1/2beta 42.638 4 min, K21 0.152 3 min(-1), K12 0.359 3 min(-1), K10 0.0592 min(-1), AUC 366.035 0 microg x min x mL(-1), CL 0.0273 L x min(-1) x kg(-1), V(c)0.461 5 L x kg(-1).

CONCLUSIONThe method can be used to determine the concentration and to investigate the pharmacokinetics of ORI in mice. ORI was absorbed and distributed very fast in mice. The effect of ORI was rapid. The elimination was the main process.

Animals ; Chromatography, High Pressure Liquid ; methods ; Diterpenes, Kaurane ; pharmacokinetics ; Female ; Male ; Mice

Objective: To investigate the influence of abaR gene knockout on growth metabolism and biofilm formation of Acinetobacter baumannii. Methods: The abaR gene was knocked out from Acinetobacter baumannii standard strain ATCC 17978 (wild strain) by homologous recombination method, and then the ATCC 17978 abaR knockout strain (ATCC 17978/ΔabaR: : Kn) was obtained and verified by polymerase chain reaction (PCR) electrophoresis and sequencing. The growth curves of Acinetobacter baumannii wild strain and Acinetobacter baumannii knockout strain were determined by microplate reader within cultivation hour (CH) 18, and the biofilm formation ability was measured by crystal violet staining at CH 8, 24, and 48, respectively. The sample number at each time point was 3.The results were denoted as absorbance value. Data were processed with analysis of variance of factorial design, one-way analysis of variance, t test, and least-significant difference test. Results: (1) The length of PCR product of target fragment ΔabaR: : Kn was 3 029 bp. The abaR gene was knocked out to obtain the knockout strain ATCC 17978/ΔabaR: : Kn. The length of PCR product of the knockout strain was 3 300 bp. The abaR gene was successfully knocked out. (2) At CH 2, 3, and 4, the absorbance values of Acinetobacter baumannii wild strain were slightly higher than those of the knockout strain. The absorbance values of Acinetobacter baumannii wild strain and knockout strain were similar from CH 5 to 18. (3) At CH 8 and 24, the biofilm formation ability of Acinetobacter baumannii wild strains (0.644±0.066, 0.574±0.184) was similar to that of knockout strains (0.559±0.008, 0.394±0.030, t=2.209, 1.167, P>0.05). At CH 48, the biofilm formation ability of Acinetobacter baumannii wild strains (1.157±0.259) was significantly stronger than that of Acinetobacter baumannii knockout strains (0.576±0.026, t=3.865, P<0.05). The biofilm formation ability of Acinetobacter baumannii wild strains at CH 48 was significantly stronger than that at CH 8 and 24 (P<0.05). The biofilm formation ability of Acinetobacter baumannii knockout strains at CH 24 was significantly weaker than that at CH 8 and 48 (P<0.05). Conclusions The abaR gene of Acinetobacter baumannii ATCC 17978 can be successfully knocked out by homologous recombination to obtain its knockout strain ATCC 17978/ΔabaR: : Kn. The abaR gene does not affect the growth and metabolism of Acinetobacter baumanniibut can weaken its biofilm formation ability.