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 observe the clinical effect , blood glucose time , clearance time of ketone body , correction time of acidosis and influence on average daily dosage of insulin of supplementing Qi and nourishing Yin combined with insulin treatment of patients with diabetic ketoacidosis (DKA).Methods 67 cases of DKA were divided into 2 groups.Control group (n=32) was giv-en micro injection of pump continuous infusion of insulin and aggressive fluid resuscitation for potassium supplement , water and elec-trolyte maintaining and acid -base balance;the observation group ( n=35 ) was given oral Chinese medicine for supplementing Qi and nourishing Yin on the basis of control group .The clinical effect after treatment , blood glucose time , clearance time of ketone body, correction time of acidosis , average daily dosage of insulin and the average number of hypoglycemia per capita were compared and analyzed .Results Blood sugar could be controlled faster in observation group .Clearance time of urine ketone and correction time of acidosis were significantly shortened .The dosage of insulin and number of hypoglycemia per capita were greatly reduced .There were significant differences compared with the control group (p<0.01);in terms of clinical effect, 19 cases of observation group were markedly effective , 14 cases effective , and 2 cases ineffective with the efficiency rate of 94.29%; 13 cases of control group were markedly effective , 10 cases effective , and 9 cases ineffective with the efficiency rate of 71.88%.There were differences between the two groups (p<0.05).Conclusion Supplementing Qi and nourishing Yin can significantly improve the curative effect in the treat -ment of DKA .

Objective To evaluate the copy number variation of FCGR3B gene in Henan Han systemic lupus erythematosus (SLE) patients and healthy controls,and explore the association between FCGR3B gene copy number variants (CNVs) and lupus nephritis (LN) susceptibility in Henan Han population.Methods FCGR3B CNVs was investigated in 142 SLE patients with nephritis,187 SLE patients without nephritis and 328 healthy controls.A modified methodology based on competitive PCR named Multiplex AccuCopyTM Kit was used to detect FCGR3B copy number.Clinical and laboratory data were collected retrospectively from the medical record.Logistic regression analysis was used to determine the association of FCGR3B copy number variants with LN susceptibility.Rank correlation was used to determine the correlations between FCGE3B copy number variants and clinical phenotypes of LN.Results No significant difference was detected in the copy number variations of FCGR3B in different groups.Low copy number of FCGR3B was more commonly seen in patients with nephritis (P=0.042),and was a risk factor for LN (OR=2.059; 95％ CI:1.081-3.921; P=0.028).However,high copy number (＞ 2) had no effect on SLE patients without nephritis(OR=1.152; 95％CI:0.711-1.866; P=0.565) and LN patients (OR=0.838; 95％ CI:0.529-1.329; P=0.454).There were no associations between FCGR3B copy number variants and clinical phenotypes and immunologic characteristics of LN.Conclusion The low copy number of FCGR3B is a risk factor for LN in Henan Han population.

OBJECTIVETo study the role of poly (ADP-ribose) polymerase-l (PARP-1) in formaldehyde-induced DNA damage response in human bronchial epithelial (HBE) cells and to investigate the mechanism of formaldehyde carcinogenicity.

METHODSThe protein levels were measured by Western blot. The interaction between different proteins was determined by co-immunoprecipitation assay. The chemical inhibitor was used to confirm the relationship between PARP-1 and DNA damage repair.

RESULTSAfter being exposed to different concentrations of formaldehyde for 4 h, HBE cells showed no significant changes in cell viability. Cell viability was significantly reduced after 24-h exposure to 80 and 160 µmol/L formaldehyde (P < 0.05). The 10 µmol/L formaldehyde resulted in significant increases in the protein levels of PARP-1 and XRCC-1. However, 80 µmol/L formaldehyde led to a significant decrease in the protein level of PARP-1 of 124 KD molecular weight but a significant increase in the protein level of PARP-1 of 89 KD molecular weight; there was no significant change in the protein level of XRCC-1. The co-immunoprecipitation assay showed that 10 µmol/L formaldehyde induced increased binding between PARP-1 and XRCC-1, but 80 µmol/L formaldehyde led to no significant change in binding between PARP-1 and XRCC-1. Here, we confirmed the role of 10 µmol/L formaldehyde in strand breaks by comet assay which showed an increase in the tail DNA content of HBE cells after 4-h formaldehyde exposure. No significant difference was observed in tail DNA content between treated HBE cells and control cells at 2 h after formaldehyde was removed. Moreover, compared with control, inhibition of PARP-1 induced a significant increase in tail DNA content, and a significant difference was observed in tail DNA content between inhibited HBE cells and control cells at 2 h after formaldehyde was removed. Inhibition of PARP-1 significantly reduced DNA repair capacity.

CONCLUSIONPARP-1 mediated the repair of DNA damage induced by low-concentration formaldehyde through recruiting XRCC-1 protein, and may be involved in the regulation of cell apoptosis induced by high-concentration formaldehyde.

Apoptosis ; drug effects ; Cells, Cultured ; DNA Damage ; drug effects ; DNA Repair ; drug effects ; DNA-Binding Proteins ; metabolism ; Epithelial Cells ; drug effects ; metabolism ; pathology ; Formaldehyde ; toxicity ; Humans ; Poly (ADP-Ribose) Polymerase-1 ; Poly(ADP-ribose) Polymerases ; metabolism ; X-ray Repair Cross Complementing Protein 1