Vildagliptin,a dipeptidyl peptidase-4 (DPP-4) inhibitor,is always used in combination with metformin.Data from multiple clinical trials showed that vildagliptin and metformin combination therapy can improve HbA1c,fasting blood glucose,and postprandial blood glucose without weight gain,good gastrointestinal (GI)tolerance,and no increase in the incidence of hypoglycemia.Vildagliptin increases plasma levels of glucagon-like peptide-1 ( GLP-1 ).When glucose levels are above normal fasting levels,enhanced GLP-1 levels stimulate insulin secretion.Mefformin has been shown to increase insulin sensitivity and inhibit hepatic glucose production.The effect of vildagliptin to increase plasma levels of intact GLP-1 was enhanced in patients receiving concomitant metformin.

Objective To explore the effects of various location methods on the successful rate of placement nails by the entrance spot of lumbar vertebra pedicle. Methods The clinical data of 105 patients with 462 times of internal nail fixation of lumbar vertebra pedicle were analyzed, and the successful rates of placement nails one time were compared among 5 location methods. Results 462 times of internal nail fixation of lumbar vertebral pedicle were performed safely. Postoperative X-ray imagining showed that 322 nails were located in the middle of pedicle of lumbar vertebra, 58 nails in its inferior part, and 82 nails in its superior part. The successful rate of placement nails one time by the location method of four quadrants technique was 86.9%, which was significantly different compared with the other 4 location methods(P

Gastrointestinal tumor patients are characterized by malnutrition resulting from various elements. So it is necessary to analyze,assess, and treat malnutrition of patients with gastrointestinal tumor. Nutrition support is an indispensable step in tumor therapy.

Objective To evaluate an improved modification of TTC staining method for measuring myocardial in-farct size after ischemia-reperfusion in rats.Methods Twenty healthy SPF male 8-week-old SD rats were randomly divided into two groups:Group A with conventional TTC staining, and group B with the modified TTC staining method for measuring myocardial ischemia-reperfusion injury.The infarct size was caculated and the serum cTnI levels were determined.Results The infarcted myocardium was well detected in both groups A and B.There were no significant differences in the myocardial infarct sizes measured in the groups A and B (48.69 ±5.37 %vs.47.41 ±3.28%, P>0.05).There were no significant differences in the serum cTnI levels assayed in the groups A and B (4.51 ±0.88 ng/mL vs.4.70 ±0.71 ng/mL, P>0.05). But compared with the group A, the color contrast of stained myocardial slice and the distinguishing infarction area and non-infarction area were much clearer in the group B.Conclusions Our modified TTC staining technique using in vivo staining is an economic, convenient, fast and efficient method, being easy to control, time-saving and inexpensive, and enhances the staining effect in evaluating the size of myocardial ischemia/reperfusion injury more accurately.

Objective To investigate the correlation between serum uric acid (SUA) level and early-phase insulin secretion in subjects with normal glucose regulation (NGR).Methods Totally 367 community NGR residents confirmed by a 75g oral glucose tolerance test were enrolled.The insulin resistance index (HOMA-IR) and the early-phase insulin secretion index after a glucose load (ΔI30/ΔG30) were used to estimate the insulin sensitivity and the early-phase insulin secretion, respectively.The subjects were divided into 4 groups according to the SUA level quartiles.Differences in early-phase insulin levels, ΔI30/ΔG30, and HOMA-IR were compared among the 4 groups.Results Age, BMI, waist circumference, systolic blood pressure, diastolic blood pressure, fasting insulin (FINS), 30 minutes postprandial insulin (30 minINS), 2 hours postprandial insulin(2hlNS), HOMA-IR and TG levels increased across the rising categories of SUA levels, while the HDL-C was decreased across the SUA groups (P ＜ 0.01).The SUA level was positively correlated with age (r =0.157, P ＜ 0.01), BMI (r =0.262, P ＜ 0.01), waist circumference(r =0.372, P ＜ 0.01), systolic blood pressure (r =0.200, P ＜ 0.01), diastolic blood pressure(r =0.254,P ＜ 0.01) , 30 minutes postprandial plasma glucose(r =0.118 ,P =0.023), FINS(r =0.249, P ＜ 0.01), 30minlNS (r =0.189, P ＜ 0.01) ,2hlNS (r =0.206, P ＜ 0.01), glycosylated hemoglobin (HbAlc, r=0.106,P =0.042), HOMA-IR(r =0.244,P ＜0.01), TG(r =0.350,P ＜0.01), ΔI30/ΔG30 (r =0.144, P ＜ 0.01), and negatively correlated with HDL-C level (r =-0.321, P ＜ 0.01).Multiple stepwise regression analysis showed that SUA (β =0.292, P ＜ 0.01) and HOMA-IR (β3 =29.821, P ＜ 0.01)were positively associated with ΔI30/ΔG30.Conclusion SUA level is closely related with the early-phase insulin secretion in NGR subjects.

Objective To investigate the clinical festures and CLCN1 gene mutation screen on a myotonia congenital kindred.Methods The clinical data of 22 patients in the myotonia congenital kindred were analysed. Results There were total 68 people in 5 generations, including 24 patients in 4 generations .Both male and female were suffered. All patientes of this kindred showed myotonia with onset the illness from the infant, and 16 cases accompanied with hypermyotrophy.The levels of creatases and dielectric in serum were normal in all the cases. Spontaneous myotonic electric potential were observed on electromyography( EMG ) in 2 cases.The proband was found in light microscope by biopsy that muscle fibers arranged loosenly , size of them mismatched , transverse striation was unclear and some of them was hyperplasia and hypertrophy. Muscle cells degenerated gently with a few inflammatory cells infiltration. No mutation was found in the whole 23 extrons of CLCN1 gene in the 3 patients.Conclusions This kindred accords with the autosomal dominant heredity form Thomsen's disease. The affected numbers have the typical clinical characteristics. No mutation is found when 23 extrons of CLCN1 gene screened in the patients which indicate the genetic heterogeneity may be exist in this kindred.

Objective To investigate the effect of Icariin ( ICA) experimental IgA nephropathy in rats and to explore related mechanisms .Methods Experimental IgA nephropathy rat model was established and then model rat were treated with or without different doses of ICA .Then, urine RBC, Urine protein and urine NAG were analyzed; IgA precipitation was detected with immunofluorescence staining;the protein level of NF-κBp65 and MCP-1 were examined by immunohistochemical staining;the mRNA level of IL-4, IL-10 and IL-13 were determined by quantitative PCR .Results The concentrations of urine RBC, Urine protein and urine NAG were reduced after ICA treatment , as companied by a decrease of IgA precipitation .Moreover, ICA treatment also decreased the protein level of NF-κBp65 and MCP-1, and the mRNA level of IL-4, IL-10 and IL-13.Conclusions ICA exerts a certain degree of efficacy on the treatment of experimental IgA nephropathy through regulating NF-κBp65 and MCP-1 expression and the immunoregulation mechanism .

time of infusion. Data analysis indicated that A1B3C2 was the best combination of the 3 factors according to the degree of lung injury. Conclusion Adequate amount of HES 200/0.5 infused during compensated stage of hypovolemic shock produces best result.

Objective To investigate the retinal toxicity and verify the safe dose of intravitreal injection of nonsteroid anti inflamatory drug, diclofenac sodium. Methods Twenty eight healthy adult white rabbits were divided at random into 7 groups and received in every right eye the intravitreal injection of a single dose of diclofenac sodium solution ranging from 0.4～1.0 mg/0.1ml respectively,the left eyes were regarded as control ones. Before injection and on the 1st, 3rd, 7th, 14th, 21st, and 28th day after injection the electroretinography on both eyes was examined. On the 28th day after injection the retinas of two rabbits of every group were examined by using light microscopy. On the 10th and 30th day after injection the retinal tissues around the optic nerve disk of two eyes from every group at random were tested by using transmission electron microscopy. Results The ratio of amplitude of b wave of electroretinography in 0.4 mg and 0 5 mg groups had no significant difference from groups before injection,the retinal tissues showed no structural changes in light and electron microscopy examination. The ratio of amplitude of b wave of photoptic electroretinography in 0.6 mg groups in the early stage after injection was markedly reduced ( P

Objective To access the changes in blood gases and electrolytes during anaphylactic shock induced by Echinococcus granulosus (EG) in sheep.Methods Fifteen healthy sheep of either sex weighing 31.2 ? 3.5 kg were repeatedly infected with EG for six months. The infected sheep were anesthetized with intramuscular thiopental 20mg?kg-1 and ketamine 15 mg?kg-1. The animals were breathing spontaneously and placed on the left side. ECG (lead Ⅱ) was monitored. Swan-Ganz catheter was placed via right internal jugular vein for hemodynamic monitoring. Anaphylactic shock was induced with antigen prepared from fluid in EG capsules. Blood samples were taken from right internal carotid artery before shock (T0) and 3.5 min (T1 ), 8 min (T2), 15 min (T3), 30 min (T4) and 60 min (T5 ) after shock was induced for determination of blood Na+ , K+ , Hct, Hb, pH, PaO2 , PaGO2 and HCO3-. Shock was confirmed by hypotension (MAP decreased by 30%), tachypnea, dyspnea, agitation and pupil dilation. Results Three sheep did not develop shock and two sheep died of severe shock within 10 min after iv antigen challenge. Blood K+ significantly increased at T1 and T2 after antigen challenge and then gradually returned to baseline value at T5 . PaO2 decreased, PaGO2 increased and pH deceased after challenge. Hct and Hb also increased significantly after challenge. Conclusion There are significant changes in blood gas and electrolytes indicated by hyperkalemia, acidosis and hypoxemia during anaphylactic shock induced by EG.