OBJECTIVE:To observe clinical efficacy and safety of sitagliptin combined with metformin in the treatment of type 2 diabetes complicating with metabolic syndrome. METHODS:Totally 80 patients with type 2 diabetes complicating with meta-bolic syndrome were divided into the observation group and control group with 40 cases in each group according to simple random sampling method. Both groups were given same diet and exercise plan;control group was additionally given metformin orally,0.5 g each time,tid;observation group was additionally given sitagliptin,100 mg each time,qd,on the basis of control group. Treat-ment course of 2 groups lasted for 12 weeks. The waist circumference(WC),body mass index(BMI),blood glucose,blood lip-id,fasting insulin (FINS) and serum adiponectin were detected in 2 groups,and steady-state model insulin resistance index (HOMA-IR)and whole body insulin sensitivity index(WBISI)were calculated. The occurrence of ADR was observed. RESULTS:Before treatment,there were no statistically significant differences between 2 groups in WC,BMI,systolic blood pressure,diastol-ic blood pressure,triglycerides,cholesterol,high-density lipoprotein cholester,low-density lipoprotein cholesterol,fasting plasma glucose,2 h postprandial blood glucose,FINS,HOMA-IR,WBISI and serum adiponectin(P>0.05). After treatment,the above indexes of 2 groups were obviously improved,and the improvement of observation group was significantly better than that of con-trol group,with statistical significance(P<0.05). 2 cases and 3 cases were withdraw from the study in control group and observa-tion group because of ADR,respectively.There was no statistically significant difference in the incidence of ADR between 2 groups (P>0.05). CONCLUSIONS:Sitagliptin combined with metformin shows significant clinical efficacy in the treatment of type 2 di-abetes complicating with metabolic syndrome. Its mechanism may be related to reducing insulin resistance,enhancing insulin sensi-tivity,decreasing patients’body weight and up-regulating serum adiponectin level.

Objective:To explore the influence of childhood psychological abuse, neglect and alexithymia on the boredom proneness of college students.Methods:The boredom proneness scale for college students(BPS), child psychological abuse and neglect scale (CPANS) and the Toronto alexithymia scale (TAS-20) were used to investigate 1 557 college students, and SPSS 22.0 was used for descriptive statistics, correlation analysis and regression analysis.Results:Childhood psychological abuse (26.540±8.985), neglect (32.665±10.651), recognition emotion in alexithymia dimension (19.359±4.835), description emotion dimension (14.173±3.001), extroverted thinking dimension in alexithymia (20.383±3.429) had positive correlation with the total score of boredom tendency (101.109±19.735) and the dimension of external stimulus (66.022±21.079)( r=0.160-0.559, all P<0.01). And there were negative correlations with the internal stimulus dimension (35.132±8.207)( r=-0.302--0.104, all P<0.01). The hierarchical regression analysis showed that after controlling the effects of gender and age, psychological abuse and neglect were the influencing factors of boredom proneness, internal stimulus and external stimulus, which explained 14.3%, 5.1% and 18.2% of the total variation (△ F=130.561, 41.968, 172.711, all P<0.01). Recognition of emotions, description of emotions and extroverted thinking in alexithymia were the influencing factors of boredom proneness, internal stimulus and external stimulus, which explained 17.5%, 9.9% and 25.5% of the total variation (△ F=134.274, 60.696, 234.383, all P<0.01). Conclusion:Childhood psychological abuse, neglect and alexithymia have significant effect on boredom proneness of college students, and mainly on external stimuli of boredom proneness. Among them, alexithymia has the greatest influence and the highest explanatory power.

Objective To investigate the correlation between XRCC1 R280H,XRCCl TSS+29C/T genetic polymorphisma and susceptibility to non-Hodgkin lymphoma (NHL). Methods The MassARRAY method was applied to detect the DNA repair gene XRCC1 genetic polymorphisms in 73 cases of NHL and 540 cases of normal healthy controls. Chi-square test was performed to calculate the adjusted odds ratios (OR) and 95% confidence intervals (CI). Results For XRCCl R280H genotypes, there was a significant difference between frequencies of the G and A among patients and controls (P=0.001). However, XRCCl TSS+29C/T genotypes had no statistical difference as for the T and C frequencies between patients and controls (P = 0.383). The frequency of XRCCI R280H with at least one A genotype was lower in the NHL cases than in controls, indicating a decreased risk for NHL development (OR=0.309, 95 % CI =0.168-0.567), comparing with GG genotype. In XRCC1 TSS+29C/T genotypes, the frequeney of TC and CC genotype was higher in NHL cases than in controls and associated with an increased risk of NHL development (P=0.472, OR =1.262, 95 % CI =0.669-2.379). Conclusion DNA repair XRCCl gene possesses significant correlation with NHL.

Objective To investigate the relationship between HbA1c in blood and IL-6 in tear fluid of the elderly patients with diabetic retinopathy ( DR ) in Shijiazhuang urban communities , and the relationship between IL-6 in tear fluid and the severity of DR. Methods The elderly people who lived more than 5 years , older than ≥45 year old. in nine urban communities of Shijiazhuang were stratified randomly sampled and received cross-sectional epidemiology questionnaire survey and OGTT. A total of 1 447 subjects (509 males and 938 females) were included. Each participant underwent epidemiological surveys and oral glucose tolerance test (OGTT), according to the 1999 WHO diabetes mellitus (DM) diagnostic criteria established. For patients who were newly or previously diagnosed as DM. HbA1c level, tear fluid IL-6 and serum IL-6 tested.The severity of DR was evaluated by fundus examination, the people were divided into normal group(NGT), non-diabetic retinopathy ( NDR ) , non-proliferative diabetic retinopathy ( NPDR ) , and proliferative diabetic retinopathy ( PDR ) . The correlation of serum IL-6 and tear fluid IL-6,blood HbA1c and tear fluid IL-6 were assessed by SPSS 19.0 statistical software. Results Concentrations of tear fluid IL-6 were (3.10 ± 1.25)pg/mL in the NGT group, (10.25 ± 3.22)pg/mL in the NDR group,(16.80 ± 5.76)pg/mL in the NPDR group,(25.11 ± 5.20)pg/mL in the PDR group(P < 0.01). SNK-q test revealed significant differences between every two groups (P < 0.01,P <0.05,P < 0.05) Concentrations of serum IL-6 were (88.04 ± 17.06)pg/mL in the NGT group,(126.38 ± 20.73) pg/mL in the NDR group, (239.83 ± 40.33)pg/mL in the NPDR group, (268.36 ± 27.72)pg/mL in the PDR group(P < 0.01). SNK-q test revealed significant differences between every two groups (P < 0.01). Tear fluid IL-6 level was positively correlated with serum IL-6 level(R = 0.756,P < 0.01). Tear fluid IL-6 level was positively correlated with blood IL-6 level (R = 0.338, P < 0.01). Conclusion The tear fluid IL-6 levels of the elderly patients with DM in Shijiazhuang urban communities , increased; with the increased severity of DR , the levels of tear fluid IL-6 gradually increase. The level of tear fluid IL-6, serum IL-6, HbA1c closely correlates with the severity of DR.

Plasticity in the glutamatergic synapses on striatal medium spiny neurons (MSNs) is not only essential for behavioral adaptation but also extremely vulnerable to drugs of abuse. Modulation on these synapses by even a single exposure to an addictive drug may interfere with the plasticity required by behavioral learning and thus produce impairment. In the present work, we found that the negative reinforcement learning, escaping mild foot-shocks by correct nose-poking, was impaired by a single in vivo exposure to 20 mg/kg cocaine 24 h before the learning in mice. Either a single exposure to cocaine or reinforcement learning potentiates the glutamatergic synapses on MSNs expressing the striatal dopamine 1 (D1) receptor (D1-MSNs). However, 24 h after the cocaine exposure, the potentiation required for reinforcement learning was disrupted. Specific manipulation of the activity of striatal D1-MSNs in D1-cre mice demonstrated that activation of these MSNs impaired reinforcement learning in normal D1-cre mice, but inhibition of these neurons reversed the reinforcement learning impairment induced by cocaine. The results suggest that cocaine potentiates the activity of direct pathway neurons in the dorsomedial striatum and this potentiation might disrupt the potentiation produced during and required for reinforcement learning.