Objective To evaluate the efficacy of metformin on liver fat content in schizophrenia patients with olanzapine-induced weight gain, and the relationship between the change of LFC and the other metabolic indices. Methods In a double-blind study, the clinically stable inpatients with first-episode schizophrenia under olanzapine monotherapy who gained more than 7% of their baseline weight were randomly assigned to two groups, one with olanzapine plus metformin (1 000 mg/d) (metformin group), the other with olanzapine plus placebo(placebo group) for 16 weeks. All patients continued to maintain the original olanzapine dosage. Liver fat content was measured by MRI at baseline and at the end of 16 weeks, respectively. At the same time, glucose and lipid metabolism (including fasting blood glucose, hemoglobin A1c, total cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein-cholesterol), homeostasis model assessment of insulin resistance index were measured respectively, analysing the correlation between the change value of LFC and other indicators. Results (1)Over the 16-week study period, LFC value in metformin group decreased compared with baseline ((16.55 ± 7.51)% vs.(19.47 ± 8.99)%, t=2.909,P<0.05).LFC change across the 16-week treatment period was-2.91%for the metformin group and 0.59%for the placebo group, with a between-group difference of-3.5%(95%CI=-6.08 to-0.93, P=0.009). (2) Compared to baseline, in the metformin group, triglyceride and HOMA-IR reduced significantly, while high density lipoprotein cholesterol increased significantly at weeks 16(t=2.242, 2.116, 3.226, all P<0.05).(3)There was positive correlation between LFC changes and TG,HOMA-IR changes significantly(r=0.505,0.578,both P<0.05).Conclusion Metformin can significantly attenuate liver fat content in schizophrenia patients with olanzapine-induced weight gain. It may be related to the improvement of the part of the glucolipid metabolic indices.

Objective To evaluate the efficacy of metformin on liver fat content in schizophrenia patients with olanzapine-induced weight gain, and the relationship between the change of LFC and the other metabolic indices. Methods In a double-blind study, the clinically stable inpatients with first-episode schizophrenia under olanzapine monotherapy who gained more than 7% of their baseline weight were randomly assigned to two groups, one with olanzapine plus metformin (1 000 mg/d) (metformin group), the other with olanzapine plus placebo(placebo group) for 16 weeks. All patients continued to maintain the original olanzapine dosage. Liver fat content was measured by MRI at baseline and at the end of 16 weeks, respectively. At the same time, glucose and lipid metabolism (including fasting blood glucose, hemoglobin A1c, total cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein-cholesterol), homeostasis model assessment of insulin resistance index were measured respectively, analysing the correlation between the change value of LFC and other indicators. Results (1)Over the 16-week study period, LFC value in metformin group decreased compared with baseline ((16.55 ± 7.51)% vs.(19.47 ± 8.99)%, t=2.909,P<0.05).LFC change across the 16-week treatment period was-2.91%for the metformin group and 0.59%for the placebo group, with a between-group difference of-3.5%(95%CI=-6.08 to-0.93, P=0.009). (2) Compared to baseline, in the metformin group, triglyceride and HOMA-IR reduced significantly, while high density lipoprotein cholesterol increased significantly at weeks 16(t=2.242, 2.116, 3.226, all P<0.05).(3)There was positive correlation between LFC changes and TG,HOMA-IR changes significantly(r=0.505,0.578,both P<0.05).Conclusion Metformin can significantly attenuate liver fat content in schizophrenia patients with olanzapine-induced weight gain. It may be related to the improvement of the part of the glucolipid metabolic indices.

Objective To investigate the correlation between enlarged perivascular space (EPVS) and post-stroke depression (PSD) in patients with ischemic stroke. Methods Consecutive patients with acute cerebral infarction admitted to hospital from March 2010 to March 2014 were enroled prospectively. The patients completed head MRI examination after admission and performed EPVS grading. At 3 months after symptom onset, they performed PSD assessment according to Hamilton Depression Scale (HAMD) and Classification and Diagnostic Criteria of Mental Disorders in China, 3rd edition (CCMD-3). The relationship between EPVS and PSD was analyzed. Results A total of 249 patients were enroled; including 62 patients (4. 9% ) experienced PSD at 3 months. There were significant differences in the proportions of the EPVS classification patients of the baseline National Institutes of Health Stroke Scale score ( the median [interquartile range]; 4 [3 - 6] vs. 3 [2 - 5]; Z = - 2. 950, P = 0. 003), centrum semiovale (χ2 = 14. 370, P = 0. 001), and periventricular (χ2 = 11. 590, P = 0. 003)between the PSD group and the non-PSD group. Multivariable logistic regression analysis showed that centrum semiovale EPVS grade 2 (odds ratio [OR] 3. 89, 95% confidence interval [ CI] 1. 59 - 9. 56) and grade 3 (OR 3. 28, 95% CI 1. 04 - 10. 33) were significantly correlated with PSD; periventricular EPVS grade 2 (OR 0. 72, 95% CI 0. 27 - 1. 91) and grade 3 (OR 2. 24, 95% CI 0. 68 - 7. 37) were not correlated with PSD. Conclusions Centrum semiovale EPVS is independently associated with PSD, and periventricular EPVS is not.

Objective To investigate the clinical value of serum cystatin C in the early renal function impairment in elderly patients wtih chronic congestive heart failure (CHF). Methods Serum cystafin Cwas measured in 60 cases with chronic CHF (CHF group), 40 cases with cardiovascular diseases and compensated heart function (compensated heart function group), and other 20 elderly normal volunteers(controlgroup). The correlation between cystafin C, B-type natriuretic peptide (BNP) and LVEF was evaluated. Results The levels of eystatin C in CHF group [(1.86±0.37)mg/L]was higher than that in compensated heart function group [(1.32±0.56) mg/L]and control group [(1.05±0.43) mg/L], P < 0.01. Cystatin C was positively correlated with BNP (r = 0.528,P< 0.01)and negatively correlated with LVEF (r=-0.463, P<0.01). In CHF group, the level of cystatin C and the incidence rate of renal failure was higher in the patients with BNP≥500 ng/L than those with BNP < 500 ng/L. Conclusions Cystatin C is a marker dearly impairment of renal function in elderly patients with chronic CHF. The more severe the heart failure, the more obvious the glomorular filtration function impairment shows.