Prospective associations of circulating thrombospondin-2 level with heart failure hospitalization, left ventricular remodeling and diastolic function in type 2 diabetes.

BACKGROUND: Circulating thrombospondin-2 (TSP2) levels were associated with the development of heart failure (HF) in recent studies. However, these studies included only a minority of patients with type 2 diabetes, which is associated with an increased HF risk. As hyperglycemia induces TSP2 expression and its tissue expression increases in type 2 diabetes, we investigated the prospective association of circulating TSP2 with incident HF hospitalization (HHF), and its associations with longitudinal changes of echocardiographic parameters in type 2 diabetes. METHODS: Baseline serum TSP2 levels were measured in 4949 patients with type 2 diabetes to determine its association with incident HHF using multivariable Cox regression analysis. In the echocardiographic study, baseline serum TSP2 levels were measured in another 146 patients with type 2 diabetes but without cardiovascular diseases who underwent detailed transthoracic echocardiography at baseline and after 1 year. RESULTS: Over a median follow-up of 7.8 years, 330 of 4949 patients (6.7%) developed incident HHF. Baseline serum TSP2 levels were independently associated with the development of HHF (HR 1.31, 95%CI 1.06-1.62, p = 0.014) after adjustments for baseline conventional cardiovascular risk factors, atrial fibrillation, estimated glomerular filtration rate, albuminuria and high-sensitivity C-reactive protein level, use of angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, loop-diuretics, aspirin, insulin, metformin and sodium-glucose co-transporter 2 inhibitors. Moreover, baseline serum TSP2 levels were independently associated with increase in average E/e' and left atrial volume index (p = 0.04 and < 0.01, respectively). CONCLUSION: Serum TSP2 levels were independently associated with both incident HHF and deterioration in diastolic function in type 2 diabetes. TRIAL REGISTRATION: Not Applicable.

[Relationship between vitamin D receptor gene polymorphisms and gestational diabetes mellitus: a case-control study].

Objective: To investigate the relationship between vitamin D receptor (VDR) gene polymorphisms and gestational diabetes mellitus (GDM) and provide evidence for the study of the mechanism of GDM. Methods: A case-control study design was used to study pregnant women who delivered in the obstetrics department of the First Hospital of Shanxi Medical University from March 1, 2012 to July 30, 2014. Of these, 334 cases were diagnosed with GDM and were matched 1∶1 by age, gestation time and residence to corresponding healthy controls. DNA genotyping was performed for the study subjects, and those with genotyping deletions >10% were excluded. Finally 323 cases and 320 controls were included in the study. Under co-dominant, dominant, recessive, and allele genetic models, unconditional logistic regression analysis on the relationship between VDR gene locus polymorphism and GDM was conducted. And software Haploview was used to analyze the relationship between haplotype and GDM. Results: At the genetic level, VDR gene was associated with the risk of developing GDM (P<0.05). After adjusting for pre-pregnancy body mass index, family history of diabetes, it was found that rs7967152 loci was associated with an increased risk of developing GDM (AC vs. AA, OR=1.58, 95%CI: 1.13-2.21; AC+CC vs. AA, OR=1.58, 95%CI: 1.15-2.18; C vs. A, OR=1.41, 95%CI: 1.10-1.82) and rs2238140 loci was associated with an increased risk of developing GDM (AA vs. GG, OR=2.24, 95%CI: 1.19-4.20; GA+AA vs. GG, OR=1.48, 95%CI: 1.07-2.03; A vs. G, OR=1.43, 95%CI: 1.11-1.83). Carrying rs2853564 locus AG genotype and AG+GG genotype (OR=1.46, 95%CI: 1.04-2.05; OR=1.45, 95%CI: 1.05-2.00) compared with carrying AA genotype and carrying rs2853566 locus AG genotype and AG+GG genotype (OR=1.43, 95%CI: 1.03-2.00; OR=1.41, 95%CI: 1.02-1.94) compared with carrying AA genotype were risk factors for GDM. Haplotype block consisting of rs1544410, rs7967152 in the VDR gene with GC haplotype was a risk factor for GDM(OR=1.50, 95%CI: 1.15-1.97). Conclusions: VDR gene rs7967152, rs2238140, rs2853564, rs2853566 locus polymorphisms and block (rs1544410, rs7967152) GC haplotype were associated with an incrased risk of developing GDM.

[Relationship between the pre-pregnancy BMI, gestational weight gain, and risk of preeclampsia and its subtypes].

Objective: To explore the effects of maternal pre-pregnancy body mass index (BMI) and gestational weight gain and its subtypes on the risk of preeclampsia. Methods: Pregnant women delivered in the Department of Obstetrics and Gynecology of the First Affiliated Hospital of Shanxi Medical University from March 2012 to September 2016 were selected as the research subjects. According to the inclusion and exclusion criteria, 9 274 pregnant women were included. 901 preeclampsia pregnant women were selected as the case group, and 8 373 non-preeclampsia pregnant women were selected as the control group. General demographic characteristics, pre-pregnancy weight, height, lifestyle during pregnancy, reproductive history, and disease history of pregnant women were collected, and pre-pregnancy BMI and gestational weight gain were calculated. Unconditional logistic regression was used to analyze the relationship between pre-pregnancy BMI and weight gain during pregnancy and PE and its clinical subtypes. Results: Among the 901 preeclampsia after inclusion and exclusion, 401 cases were diagnosed as early-onset PE (EOPE), 500 cases were late-onset PE (LOPE), 178 cases were Mild PE (MPE), and 723 cases were severe PE (SPE). There were statistically significant differences between PE and non-PE pregnant women in terms of maternal age, residence, parity, family history of gestational diabetes and hypertension (P<0.05). After adjusting for the above factors, the logistic regression analysis results showed that pre-pregnancy BMI<18.5 kg/m2 and inadequate gestational weight gain were protective factors for PE (OR=0.74, 95%CI: 0.56-0.98; OR=0.78, 95%CI: 0.62-0.99), while pre-pregnancy BMI≥24.0 kg/m2 and excessive gestational weight gain were risk factors for PE (OR=1.82, 95%CI: 1.54-2.14; OR=1.82, 95%CI: 1.54-2.15). After subtype analysis on PE, the results showed that pre-pregnancy BMI<18.5 kg/m2 was a protective factor for EOPE and MPE (OR=0.52, 95%CI: 0.32-0.83; OR=0.47, 95%CI: 0.23-0.97), while pre-pregnancy BMI≥24.0 kg/m2 and excessive gestational weight gain were risk factors for clinical subtypes of PE. After stratification according to pre-pregnancy BMI, excessive gestational weight gain was the risk factor for PE (OR=1.86, 95%CI: 1.51-2.30; OR=1.90, 95%CI: 1.39-2.60) in pregnant women 18.5 kg/m2≤BMI<24.0 kg/m2 and ≥24.0 kg/m2. Inadequate gestational weight gain (OR=0.55, 95%CI: 0.34-0.89) was a protective factor for PE in pregnant women with pre-pregnancy BMI≥24.0 kg/m2. Excessive gestational weight gain (OR=4.05, 95%CI: 1.20-13.69) was a risk factor for EOPE in pregnant women with pre-pregnancy BMI<18.5 kg/m2. Excessive gestational weight gain was a risk factor for the clinical subtype of PE in pregnant women 18.5 kg/m2≤BMI<24.0 kg/m2 before pregnancy. Inadequate gestational weight gain was a protective factor for EOPE and MPE (OR=0.39, 95%CI: 0.19-0.80; OR=0.29, 95%CI: 0.11-0.77) in pregnant women with pre-pregnancy BMI≥24.0 kg/m2. Excessive weight gain was a risk factor for EOPE, LOPE and SPE (OR=1.60, 95%CI: 1.06-2.42;OR=2.20, 95%CI: 1.44-3.37;OR=2.28, 95%CI: 1.58-3.29). Conclusions: Pre-pregnancy BMI and gestational weight gain affect the risk of preeclampsia and its clinical subtypes. In contrast, the influence of gestational weight gain on preeclampsia varies among different pre-pregnancy BMI groups. Therefore, it is recommended to pay attention to the changes in pre-pregnancy BMI and gestational weight gain simultaneously to reduce preeclampsia.

[Studies for a new type of intellectualized multifunctional training system of rats behaviour].

AIM: To develop a type of multifunctional training examining system of rats controlled by computer-gradient voltage automatically driving rats and computer showing, recording and analysis experimental results at right moment. METHODS: Adopting the imitating Windows, using Turbo C2.0 to edit software and operating the interface of hardware directly by means of TC, so that collecting, processing of signals and managing of experimental instruments are completed. RESULTS: This system has realized that gradient voltage automatically driving rats; phonic, optical and electrical conditioned stimulation; multiple path automatically set; the results in accordance with data base are directly processed by SAS software. CONCLUSION: This system has a high-grade automation. The operation is simple and convenient. And data processing is scientific and accurate. It is also suitable for developing of acoustic, visual and another special memory model of rats.

Serum and cerebrospinal fluid immunoglobulins M, A, and G in Japanese encephalitis.

A comparison was made of virus-specific immunoglobulin M (IgM), IgA, and IgG detected by capture or indirect enzyme immunoassay in serum and cerebrospinal fluid of patients with Japanese encephalitis. The IgM capture enzyme immunoassay was more sensitive than assays for other isotypes of viral antibody; IgM was detected in 75% of specimens collected less than or equal to 4 days after the onset of illness. Specific IgA was detected in both serum and cerebrospinal fluid; however, IgA levels were significantly lower than IgM levels.