Free fatty acids(FFAs) provide an important energy source and also act as signaling molecules.Medium to long-chain free fatty acids can activate the intracellular signal pathways in the pancreatic ?-cells and play a role in regulating insulin secretion as an extracellular signal molecular via binding to the FFA receptor G protein-coupled receptor 40(GPR40). Furthermore,GPR40 is associated with several biological effects including cell proliferation and antiapoptosis of nerve cells.GPR40 act an important role in the connection of obesity and diabetes or cancers.GPR40 will probably become a novel kind of antidiabetic and anticancer drugs.

Objective To investigate whether the effect of pioglitazone on TNF-α-induced insulin resistance is associated with altering IRS-1-induced signaling. Methods 3T3-L1 adipocytes were treated with TNF-α for 24 hours with or without being pretreated with 10μM piglitazone for 6 hours or with pioglitazone alone.Insulin-stimulated glucose uptake of 3T3 adipocytes was measured by using 2-deoxy 3H glucose.The Western blot was used to measure IRS-1, PKB, PKC-λ protein and tyrosine phosphorylation on IRS-1, PKB and PKC-λ phosphorylation. Results Both TNF-α and pioglitazone increased glucose uptake of 3T3 adipocytes under basal status.On TNF-α treated cells, insulin-stimulated glucose uptake was decreased by about 50%, accompanied with the reductions of IRS-1 protein level, tyrosine-phosphorylation of IRS-1 and PKB phosphorylation.TNF-α treatment had no effect on PKC-λ phosphorylation. Pioglitazone pretreatment was able to antagonize TNF-α-induced insulin resistance in 3T3 adipocytes partly reverse IRS-1 protein, increase insulin-stimulated tyrosine phosphorylation of IRS-1,and increase phosphorylations of PKB and PKCλ. Conclusion TNF-α-induced insulin resistance in 3T3-L1 adipocytes is related to impaired tyrosine phosphorylation of IRS-1. Pioglitazone antagonizes the above TNF-α induced insulin resistance.

Objective To explore the secondary inventory appropriate to improve the stomatological hospital in cost control for medical consumables,standardizing patient charging,dynamic materials management,zero inventory and enhancing hospital economic benefit.Methods An enterprise resource planning (ERP) secondary inventory information system was developed to solve the problems in medical materials management of the stomatological hospital,and then went through practical trials in three departments to determine its efficacy and deficiencies.Results The information system facilitated cost control,standardized patient charging,and the trials in three departments showed the rate for material consumption was decreased greatly.The deficiencies still existed in the traceability,mobile App,manual input and etc.Conclusion The ERP secondary inventory information system reduces the running cost of the department,increases the hospital abilities in cost control and management,and thus is worthy promoting practically.

Objective:To investigate glucose uptake and IRS-1-associated signaling pathway by stimulated insulin under TNF-? treatment.Methods:3T3-L1 adipocytes were treated with TNF-? within 6 hours and 24 hours respectively. 2-deoxy ~3H glucose was used to measure glucose uptake and western blot was used to measure IRS-1, PKB protein, tyrosine and serine307 phosphorylation on IRS-1, and PKB phosphorylation.Results:On basal status, glucose uptake of 3T3-L1 cells and phospho-tyrosine of IRS-1, PKB phosphorylation, and serine307 phosphorylation on IRS-1 were all low. Insulin stimulation induced glucose uptake and IRS-1 tyrosine phosphorylation, serine307 phosphorylation, PKB phosphorylation rapidly. TNF-? inhibited insulin-induced glucose uptake, tyrosine phosphorylation of IRS-1 and PKB phosphorylation. Rapamycin reversed the effects of TNF-?. Treated with TNF-? within 6 hours increased serine307 phosphorylation but had no effect on IRS-1 protein level. TNF-?-induced serine307 phosphorylation of IRS-1 was not affected by rapamycin. IRS-1 level was decreased under 24 hours TNF-? treatment and rapamycin can reverse the effect.Conclusion:TNF-? induced insulin resistance in 3T3-L1 adipocytes mightbe related to impaired IRS-1 tyrosine phosphorylation, rapamycin could reverse the effects of TNF-?. Treated with TNF-? within 6 hours stimulate phosphrylation of serine307 of IRS-1 and 24 hours treatment decreased IRS-1 protein level. Rapamycin antagonist TNF-?-induced loses of IRS-1.

Objective:To establish the drug release determination conditions and method for phencynonate hydrochloride extended release tablets. Methods:The drug release of the tablets was determined by HPLC using a Diamonsil C18 (250 mm × 4. 6 mm, 5 μm) column with the mobile phase of acetonitrile-water-phosphoric acid-triethylamine (270∶400∶1. 3∶2), the detection wavelength was 220 nm, the flow rate was 1. 0 ml·min-1 , the column temperature was 30 ℃ and the injection volume was 20 μl. The effects of different release apparatus, release media and rotation speeds on the release of phencynonate hydrochloride extended-release tablets were studied as well. Results:The established drug release determination method had a good linear relationship within the range of 0. 3-5. 0 μg· ml-1(r=0. 999 8), and the average recovery was 100. 6%(RSD=1. 16%, n=15). Under the conditions of 900ml pH 3. 0 phos-phate buffer solution as the release medium, rotation speed of 50 r·min-1 and the settlement basket as the apparatus, the release be-havior of the product was complied with a zero-level model in vitro, and the release equation was as follows:Q=6. 141 2t-9. 328 7(r=0. 996). Conclusion:The method is simple, accurate and reliable, and suitable for the quality control of phencynonate hydrochlo-ride extended-release tablets.

ObjectiveTo evaluate the relationship between microalbuminuria(MAU) and cardiac autonomic neuropathy in diabetes.MethodsThe urinary albumin excretion (UAE) was measured,and the cardiac autonomic function was detected using 24 hour ambulatory ECG spectral analysis of heart rate variability (HRV) in 46 patients with diabetes and 31 normal control subjects.ResultsParameters of time and frequencydomain of HRV were reduced in patients with diabetes.The high frequency at night reflecting the cardiac vagus nerve function was significantly lower in diabetic patients than control group.In diabetic patients with MAU,the detected values of HRV were significantly decreased,combined vagosympathetic impairment occurred,and 24 hour rhythm from day to night in autonomic nervous activity disappeared.ConclusionMAU in diabetes is related with HRV.

Objective:To enhance the ability of organizing, commanding, decision-making and contingency-meeting of campaign medical support commanding officers so as to qualify them for their positions by simulation training. Methods: Based on the decision support theory, modern medical support theory, health service optimized decision support system and medical support command simulation training system, we designed and constructed a simulation training platform for medical support decision optimization. Results: A network-based simulation training platform was successfully constructed, which gives a strong support to the simulation training in medical support decision optimization under the network circumstance. Conclusion: The application of the simulation training platform has enriched the content and renewed the pattern of training in decision optimization for campaign medical support commanding officers.

NIT-1 cells were exposed to various concentrations of glucose for 24,48,and 72 hours.The content of triglyceride in NIT-1 cells increased in dose-and time-dependent manners (P ＜ 0.05).Long-term exposure of NIT-1 cells to high glucose concentrations caused an inverse "v"-like induction of HSL mRNA and protein expressions,which increased from beginning,and then decreased,along with similar changes of lipolysis.These results suggest that the adaptation of HSL may play an important role in regulating the intracellular triglyceride pool and the development of glucolipotoxicity in pancreatic β cells.

Objective To establish the biological reference intervals of serum immunoglobulin ( Ig) for children ( neonates to young adults) in our laboratory.Methods This was a retrospective study.Serum IgG, IgA and IgM of the neonatal ( 1-28 days ) to 18 years old who visited the First Hospital of Jilin University during January 2011 to July 2014 were measured.The inclusion criteria were normal C-reactive protein content, normal liver and kidney function and without history of chronic diseases, allergic reactions, connective tissue diseases, rheumatic diseases and human immunodeficiency diseases.Children whose Ig tests were below upper limit of adult reference range were divided into 19 age groups.By eliminating outliers within each group, 9 466 cases of reference individuals conformed to the establishment of reference intervals were selected.Rank sum test was applied in comparing Ig levels of each two adjacent age groups, if there was not statistical significance ( P>0.05 ) , the two age groups were merged; otherwise not merged.The upper and lower limit of Ig reference range for each age group were calculated using nonparametric method, and biological reference intervals of children′s serum Ig were established.Results The neonatal serum IgG decreased grually after birth and reached the lowest point at 29 days-3 months, then the concentration increased gradually along with age growth and reached adult level by 11 years old.Neonatal serum IgA and IgM levels were at the lowest point and the concentration increased along with age growth then reached adult levels by 11 and 2 years old respectively.The children′s serum Ig reference intervals were as below:IgG:3.59-7.90, 2.26-5.40, 2.72-6.62, 2.87-7.74, 3.38-8.07, 3.80-9.08, 4.86-11.40, 4.97-11.70, 5.51-12.40, 6.17-13.10, 6.41-13.60, 6.53-14.20 and 6.84-14.30 g/L for neonatal, 29 days-3 months, 4-6 months, 7 months, 8-9 months, 10 months-1 year old, 2, 3, 4, 5-6, 7, 8 and 9-10 years old, respectively;IgA:0.23-0.45, 0.24-1.02, 0.23-0.79, 0.23-0.92, 0.24-1.03, 0.24-1.56, 0.26-1.93, 0.31-2.16, 0.44-2.56, 0.56-2.85, 0.52-3.35 and 0.63-3.23 g/L for neonatal-3 months, 4 months, 5-7 months, 8-9 months, 10 months-1 years old, 2, 3, 4, 5-6, 7, 8, and 9-10 years old, respectively;IgM:0.16-0.70, 0.21-1.20, 0.30-1.62, 0.38-2.16 and 0.44-2.17 g/L for neonatal, 29 days-3 months, 4-7 months, 8-9 months and 10 months-1 years old, respectively.Conclusions There were great differences of the serum Ig concentrations between children and adults, thus children′s immunologic function should not be assessed based on adult Ig reference intervals.According to the research, reference intervals of Ig were obtained for children at different age groups in the laboratory and reference in evaluating children′s immunologic function was provided for clinicians.

Objective To investigate the effect of curcumin on tumor necrosis factor-alpha (TNF-α)-in-duced expression and release of monocyte chemoattractant protein-1 (MCP-1) in rat astrocytes.Methods The primary astrocytes were prepared from the cerebral cortex of 5 neonatal Sprague-Dawley rats and cultured.The cultured cells were identified by immunofluorescence staining with glial fibrillary acid protein.The cells were then divided into 6 groups (n =15 each):control group (group C),TNF-α group (group T),TNF-α+ different concentrations of curcumin groups (Cur5,Cur10 and Cur20 groups),and TNF-α+ solvent control group (D group).TNF-α with the final concentration of 20 ng/ml was added and the cells were incubated for 2h in T group.In Cur5,Cur10 and Cur20 groups,curcumin with the final concentrations of 5,10 and 20μmol/L was added,respectively,the cells were incubated for 24h and then the culture medium was abandoned,TNF-α with the final concentration of 20 ng/ml was added and the cells were then incubated for another 2h.In group D,dimethyl sulfoxide with the final concentration of 1 μl/ml was added,the cells were then incubated for 24h,then TNF-α with the final concentration of 20 ng/ml was added and the cells were incubated for another 2h.After treatment in each group,the expression of MCP-1 was determined by immunohistochemistry and the release of MCP-1 was determined by ELISA.Results Compared with group C,the expression and release of MCP-1 was significantly increased in the other five groups (P ＜ 0.05).Compared with group T,the expression and release of MCP-1 was significantly decreased in group Cur20 (P ＜ 0.05),and no significant changes in the expression and release of MCP-1 were found in Cur5,Cur10 and D groups (P ＞ 0.05).Compared with group Cur5,the expression and release of MCP1 was significantly decreased in group Cur20 (P ＜ 0.05),and no significant change in the expression and release of MCP-1 was found in group Cur10 (P ＞ 0.05).Conclusion Curcumin can inhibit TNF-α-induced expression and release of MCP-1 in rat astrocytes and the effect is dose-related and may be one of the mechanisms of curcumin-induced reduction of neurophathic pain.