ObjectiveTo investigate the effect of urinary kallidinogenase for injection on neurological function and serum matrix metalloproteinase 9(MMP-9) in patients with cerebral infarction.Methods Ninety patients of acute cerebral infarction were divided into observation group and control group by random digits table with 45 cases each.The control group was treated with conventional therapy.The observation group was treated with conventional therapy and additional urinary kallidinogenase for injection treatment,0.15 PNA U/day,for 10 days.National institutes of health stroke scale(NIHSS) score and Barthel index (BI) score were used to evaluate the neurological impairment and the abilities of activities of daily living.The serum MMP-9 levels was tested by enzyme linked immunosorbent assay.The treatment outcome,NIHSS score,BI score and serum MMP-9 level were compared.ResultsThe total effective rate in observation group [ 88.9％ (40/45) ] was higher than that in control group [ 71.1％ (32/45) ],and there was significant difference (P ＜ 0.05).NIHSS score after 3 months treatment was decreased and BI score was increased compared with before treatment in two groups,and there were significant differences(P＜ 0.05).NIHSS score after 3 months treatment in observation group[ (6.56 ± 0.74) scores] was lower than that in control group [ (9.06 ± 0.87 ) scores ],and there was significant difference (P ＜ 0.05 ).BI score after 3 months treatment in observation group [ (79.98 ± 7.32) scores ] was higher than that in control group [ (72.57 ± 6.95 ) scores ],and there was significant difference(P ＜ 0.05).Compared with before treatment,the serum MMP-9 level after 10 days treatment was significantly decreased in two groups (P＜ 0.05 ).The serum MMP-9 level after 10 days treatment in observation group[ ( 187.58 ± 14.52) ng/L] was lower than that in control group[ (238.89 ± 17.48 ) ng/L ] with significant difference (P ＜ 0.05 ).ConclusionsUrinary kallidinogenase for injection can significantly improve neurological function in patients with cerebral infarction,significantly decrease serum MMP-9 levels.It has good effect and high clinical value.

Objective To explore the influence of thyroid dysfunction in the first half pregnancy (≤20 gestational weeks) on gestational diabetes. Methords By adopting the method of prospective intervention study, general data of pregnant-women in the care clinics of our hospital were collected. Thyroid function was detected and evaluated by ATA criteria. All cases were divided into two groups: normal thyroid function group and thyroid dysfunction group. The thyroid dysfunction group was intervened. 75 g OGTT were conducted in all cases in 24-28 gestational-weeks. GDM was diagnosed by IADPSG diagnostic criteria. GDM prevalence was compared between normal thyroid function group and abnormal thyroid function groups. Results 1 062 cases of pregnant women were collected. 857 cases of pregnant women were normal, while 14 cases were subclinical hyperthyroidism (1.32%), 164 cases were subclinical hypothyroidism (15.4%), 22 cases were hypothyroxinemia (2.07%). Compared with normal thyroid function, prevalence rate of GDM was the highest in hypothyroxinemia group (54.5% vs 27.8%). There was no significant difference between subclinical hypothyroidism group and normal thyroid function group. Conclusion Thyroid dysfunction in the first half pregnancy is associated with GDM , Screening and treatment of pregnant thyroid dysfunction should be attached.

In recent years, the incidence of diabetic kidney disease(DKD) has been increasing gradually, and it has become the leading cause of end-stage renal disease. However, current therapies show limited efficacy in preventing the progression of DKD. Against the backdrop of chip and high-throughput sequencing, long non-coding RNAs are revealed to an important role in the pathogenesis of DKD. This article summarizes the research progress of long non-coding RNA in DKD, and look forward to the more extensive application of long non-coding RNA in the future.

Objective To investigate the association between single nucleotide polymorphisms ( SNPs) of FOXO1 gene and type 2 diabetic nephropathy(T2DN). Methods A total of 654 Chinese Han patients with type 2 diabetes mellitus (T2DM;394 without and 260 with T2DN) were enrolled. Six FOXO1 gene tags SNPs were selected using the Hapmap database. The genotypes of six SNPs in FOXO1 were determined by PCR-RFLP, and the clinical characteristics of the subjects were also evaluated. The interaction of SNPs with these clinical factors was analyzed by multiple factor reduction(MDR) method. Results After adjusting for age, gender, DM course, body mass index ( BMI ) , HbA1C , total cholesterol ( TC ) , triglycerides ( TG ) , high-density lipoprotein-cholesterol ( HDL-C ) , low-density lipoprotein-cholesterol ( LDL-C ) , hypertension history, DM family history, smoking, and drinking, FOXO1 rs17446614 variant genotype was significantly associated with an increased risk of T2DN, while rs17446593 variant genotype was associated with a decreased T2DN risk. In the stratified analysis of risk factors, the correlation between rs17446614 and T2DN was unrelated with patient' s gender, hypertension history, and blood TC level. Simultaneously, rs17446614 variant genotype significantly increased the risk of T2DN in people older than 60 years,BMI less than 24 kg/m2 , LDL-C less than or equal to 3. 5 mmol/L , or DM family history. rs2721068 variant genotype significantly decreased the risk of T2DN in people less than 60 years old or without DM family history. rs2951787 variant genotype significantly increased the risk of T2DN in people with DM duration longer than 10 years or with DM family history. A variant genotype rs17592236 significantly increased the risk of T2DN in male or TC higher than 5 mmol/L. A variant genotype rs17446593 significantly decreased the risk of T2DN in male or those DM duration longer than 10 years, or BMI≥24 kg/m2 . The interactions among rs17446614, DM duration, TC, and hypertension history were also observed. Conclusion The genetic variants rs17446614, rs2721068, rs2951787, rs17592236, and rs17446593 in FoxO1 may contribute to the risk of T2DN in T2DM patients.