OBJECTIVE:Nowadays, the prevalence of cognitive impairment in women has gradually increased, especially in postmenopausal women. There were few studies on the mechanistic effects of iron exposure on neurotoxicity in postmenopausal women. The aim of this study is to investigate the effect of iron accumulation on cognitive ability in ovariectomized mice and its possible mechanism and to provide a scientific basis for the prevention of cognitive dysfunction in postmenopausal women. METHODS:Female C57BL/6N ovariectomized model mice were induced with ferric citrate (FAC). The mice were randomly divided into 5 groups: control, sham, ovariectomized (Ovx), Ovx + 50 mg/kg FAC (Ovx + l), and Ovx + 100 mg/kg FAC (Ovx + h). The impact of motor and cognitive function was verified by a series of behavioral tests. The levels of serum iron parameters, malondialdehyde, and superoxide dismutase were measured. The ultrastructure of mice hippocampal microglia was imaged by transmission electron microscopy. The differential expression of hippocampal proteins was analyzed by Tandem Mass Tag labeling. RESULTS:Movement and cognitive function in Ovx + l/Ovx + h mice were significantly decreased compared to control and Sham mice. Then, iron exposure caused histopathological changes in the hippocampus of mice. In addition, proteomic analysis revealed that 29/27/41 proteins were differentially expressed in the hippocampus when compared by Ovx vs. Sham, Ovx + l vs. Ovx, as well as Ovx + h vs. Ovx + l groups, respectively. Moreover, transferrin receptor protein (TFR1) and divalent metal transporter 1 (DMT1) protein expression were significantly increased in the iron accumulation mice model with ovariectomy. CONCLUSION:Iron exposure could cause histopathological damage in the hippocampus of ovariectomised mice and, by altering hippocampal proteomics, particularly the expression of hippocampal iron metabolism-related proteins, could further influence cognitive impairment in ovariectomized mice.

OBJECTIVE:The aim was to investigate the association of multidimensional sleep indicators with high blood pressure (HBP) of Chinese students. METHODS:Participants in this cross-sectional study included 11561 students aged 9-18. Sleep was characterized by sleep timing (e.g., bedtime), sleep duration and sleep consistency (e.g., bedtime/wake-up time deviations and social jet lag (SJL)). We used odds ratios (OR) and 95% confidence intervals (95% CI) to assess the relationship between sleep and HBP. RESULTS:Primary school students who slept 8.00-9.00h had a lower risk of HBP compared with sleeping >10h (OR 0.370, 95%CI 0.208, 0.658), while junior middle school students reporting ≤8.00h on weekday night had a lower risk of HBP compared with sleeping >10h (OR 0.303, 95%CI 0.111, 0.829). Moreover, compared with deviations = 0h, the OR (95%CI) for wake-up time deviations <0h and bedtime deviations >0h in primary school students with HBP were 0.314 (0.125, 0.790) and 2.155 (1.205, 3.853). Furthermore, compared with SJL = 0h, senior high school students reporting SJL = 0.01-0.50h, SJL = 0.51-1.00h and SJL = 1.01-2.00h had greater risk of HBP (OR 1.566, 95%CI 1.039, 2.361; OR 1.760, 95%CI 1.177, 2.631; OR 1.660, 95%CI 1.124, 2.452, respectively). Bedtime at night was associated with HBP for three educational periods students, however, there was no significant association between mid-day nap and HBP. CONCLUSIONS:Sleep timing, sleep duration and sleep consistency are associated with high blood pressure in children and adolescents.

To investigate the relationship between related factors and visual acuity of Chinese school students before and during the COVID-19 pandemic. Chinese students from primary and secondary schools were included from the Chinese National Surveys on Students’ Constitution and Health CNSSCH (2019). A total of 1496 participants completed follow-ups in June and December 2020, respectively. Generalized estimating equations were used to test the differences in visual environment. Logistic regression models were utilized to examine the roles of behaviors and surrounding environment changes associated with myopia before and during the pandemic. The prevalence of myopia was 47.7

Waist-to-height ratio (WHtR) with a cut-off value of 0.5 has been recognized as an anthropometric indicator of central obesity to predict the risk of the chronic disease. The aim of our study was to identify dietary related risk factors of central obesity based on WHtR. We used cross-sectional data from the China Health and Nutrition Survey (CHNS) in 2011 obtained from 2881 married women aged 19-55. The association of dietary related factors and central obesity was analyzed using binary logistic regression and back-propagation artificial neural network. Overall, central obesity prevalence was 48.4% (1394/2881). Compared to the population of women without central obesity, the population of women with central obesity had an older average age (41.84 +/- 6.89 years vs 38.45 +/- 7.91 years, P < 0.001), and meanwhile an average lower per capita annual income (13904 +/- 15916 CNY vs 16753 +/- 19163 CNY, P < 0.001). Our analysis indicated that the score of dietary knowledge (adjusted odds ratio (aOR), 0.956; 95% confidence interval (CI), 0.936-0.976) and the score of food preferences (aOR, 0.961; 95% CI, 0.926-0.997) were significantly associated with lower risk of central obesity; whereas fast food (aOR, 1.002; 95% CI, 1.000-1.003) was associated with higher risk of central obesity. The study showed the score of dietary knowledge (15.5%), fast foods (10.2%), and the score of food preferences (8.8%) were the most important modifiable factors for central obesity. In summary, aging, fast food intake, and lower per capita annual income were positively associated with higher prevalence of central obesity, while higher scores of dietary knowledge and food preferences were negatively correlated. More nutrition education programs should be implemented by the government to strengthen the pro-healthy dietary behaviors.

Cleft palate (CP) is a common birth defect with a high incidence of occurrence in humans. The 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) is a highly toxic halogenated aromatic hydrocarbon, with a strong CP effect on mice. Increasing recent evidences have shown that long-noncoding RNAs (lncRNAs) play an important role in several diseases, including CP. However, there is a paucity of studies on the role of lncRNA MEG3 in the occurrence and development of TCDD-induced CP. In this study, the relationship between MEG3 and the proliferation of palatal mesenchymal cells and the underlying molecular mechanism were studied by establishing fetal CP with TCDD (64 μg/kg) in C57BL/6N mice. The results revealed that MEG3 was highly expressed during the critical period of CP formation and that the fetal mesenchymal proliferation was significantly inhibited at certain critical periods in the mice receiving TCDD. In addition, we noted a possibility of a crosstalk between MEG3 and the TGF-β/Smad pathway, such that the inhibition of the TGF-β/Smad pathway was induced by TCDD. Cumulatively, our study suggests that TCDD-induced CP may be caused by MEG3 inhibition of the proliferation of palatal mesenchymal cells involving the TGFβ/Smad pathway, which may provide a novel perspective to understand the pathogenesis of CP.

INTRODUCTION:Results from recent trials assessing the effect of oral vitamin C supplementation on serum uric acid (SUA) have been inconsistent.OBJECTIVES:The purpose of this study was to explore the association between oral vitamin C supplementation and serum uric acid.METHODS:PUBMED, EMBASE, CNKI, Web of Science, and CENTRAL of Cochrane library databases were searched to identify relevant articles published up to February 2020. Heterogeneity was evaluated using I-square (I2) statistics. Random-effects model was used to pool weighted mean differences (WMD) and 95 % confidence interval (CI) as summary effect sizes.RESULTS:The total sixteen eligible randomized controlled trials (RCTs) containing 1,013 participants were included in this meta-analysis. The pooled findings showed that vitamin C supplementation had a significant effect of lowering SUA. The subgroup analyses showed that the effect of vitamin C supplementation on SUA has positive association with mean age of participants <65 years old, the use of placebo or blank control, duration of trials <1 month and high-quality studies. In addition, sensitivity analysis showed that the results of this study were stable. Both Egger's test and Begg's test demonstrated that no evidence of significant publication bias.CONCLUSIONS:The results of present meta-analysis have demonstrated that vitamin C supplementation could make a reduction of SUA. The use of placebo, duration of intervention, age of the subjects and study quality have an impact on the effect of oral vitamin C, but the baseline of SUA not.

2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a persistent organic pollutant that is strongly associated with a number of human diseases and birth defects, including cleft palate. Transforming growth factor (TGF) plays a significant role during mammalian palatogenesis. However, the epigenetic mechanism of transforming growth factors in the process of TCDD-induced cleft palate is unclear. The purpose of this research was to investigate the relationship and potential mechanism between TGF-β2/3 promoter DNA methylation and Smad signaling during TCDD-induced cleft palate. Pregnant C57BL/6N mice were exposed to 64 µg/kg TCDD on gestational day 10 (GD10) to establish the cleft palate model and palatal tissues of embryos were collected on GD13, GD14, and GD15 for subsequent experiments. TGF-β2/3 mRNA expression, TGF-β2/3 promoter methylation, and Smad signaling molecules expression were assessed in the palate of the two groups. The results showed that the incidence of cleft palate was 94.7% in the TCDD-treated group whereas no cleft palate was found in the control group. TCDD-treated group altered specific CpG sites of TGF-β2/3 promoter methylation. Compared to the control group, the proliferation of mouse embryonic palate mesenchymal stromal cells (MEPM), the expressions of TGF-β2/3, p-Smad2, and Smad4 were all reduced, while the expression of Smad7 was significantly increased in the atAR group. Smad signaling was downregulated by TCDD. Therefore, we suggest that TGF-β2/3 promoter methylation and Smad signaling may be involved in TCDD-induced cleft palate formation in fetal mice.

Previous studies have discovered that zinc-α2-glycoprotein (ZAG) is related to insulin resistance and lipid metabolism. The aim of the study is to explore the change of serum ZAG and its related factors in gestational diabetes mellitus (GDM). Eighty newly diagnosed GDM patients were enrolled in the case group, and 80 normal pregnant women were selected as the control group. The differences of baseline data between the two groups were compared, and the change of serum ZAG level and its relationship with related indexes was analyzed. Compared to the control group, the level of serum ZAG in GDM women decreased (P<0.001). What is more, the serum ZAG level of overweight and normal subjects in two groups was also found to have statistical differences. The Pearson correlation (or Spearman correlation) analysis showed that serum ZAG level was negatively correlated with FPG, FINS, HOMA-IR, and TG (all P<0.05) and positively correlated with HDL (P<0.05). Multiple linear regression showed that HDL and HOMA-IR were independent factors of serum ZAG (P<0.05). The level of serum ZAG in patients with gestational diabetes mellitus decreased, and HDL and HOMA-IR are the influencing factors in the case group.

As a common birth defect, Cleft palate can be caused by the disturbance during the developmental process of the palatal shelves. The 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) is a well-known environmental teratogenic agent for cleft palate and Aryl hydrocarbon receptor (AhR) pathway can be activated by dioxins. Oct4 as a pluripotent stem cell transcription factor is also involved in the process of embryonic development. The AHR and retinoid receptors have cross-talk at CYP1A1 (cytochrome P450, family 1, subfamily A, polypeptide 1) promoter. There are also bidirectional talk between AhR and Oct4. In this study, we used C57/BL6 N mice and TCDD (64 μg/Kg body weight) to establish a model of fetal cleft palate to observe the effects of dioxin on fetal mesenchymal proliferation and apoptosis, and explore the role of Oct4 in inducing cleft palate. The results showed that dioxin inhibited mesenchymal proliferation and promoted apoptosis. In addition, dioxin inhibited Oct4 expression, and preliminary data suggest that hypermethylation of the Oct4 promoter may be a putative mechanism, suggesting that TCDD might induce cleft palate by inhibiting the proliferation of palatal mesenchymal cells mediated by Oct4.

Background: Even though it is well-known that iron deficiency is the result of chronic kidney disease (CKD), whether iron will affect kidney function and disease in the general population is not clear. We thus conducted a nationwide cross-sectional study using data from the China Health and Nutrition Survey (CHNS) to assess the relationship of iron status with estimated glomerular filtration rate (eGFR) and CKD among general adults. Methods: A total of 8,339 adults from the China Health and Nutrition Survey in the wave of 2009 were included to assess the association between iron status and eGFR/CKD. Serum ferritin (SF), transferrin, soluble transferrin receptor (sTfR), and hemoglobin (Hb) were measured. The relationship of iron status and eGFR was evaluated by using multi-variable linear regression model. The effect of iron status on the odds of CKD was calculated by logistic regression model. Results: For the association between iron status and eGFR, every 100 μg/L increase in SF was correlated with 0.26 ml/min per 1.73 m2 (95% CI: 0.08–0.44) decrease in eGFR, and every 5 mg/L increase in sTfR was associated with a decrease of 6.00 ml/min per 1.73 m2 (95% CI: 3.79–8.21) in eGFR. There were no significant associations between Hb or transferrin with eGFR. For the association between iron status and CKD, every 5 g/L increase in sTfR was associated with an odds ratio of 3.72 (95% CI: 2.16–6.13) for CKD. The concentrations of Hb were associated with the odds of CKD in a U-shaped manner, with the lowest risk in the Hb range of 136–141 g/L. There was a positive correlation between SF concentration and CKD prevalence but not in a dose–response manner. The odds of CKD for participants in the highest tertile increased by 28% (98% CI: 1–63%) compared with those in the lowest tertile. Conclusion: The concentration of SF and sTfR was positively correlated with the odds of CKD, and Hb was associated with the odds of CKD in a U-shaped manner. Further large prospective researches are warranted to confirm these findings.

Lycopene, a natural carotenoid, has potential chemopreventive effects in many cancers. This study aimed to examine the effects of lycopene on regulating the inflammation and apoptosis of N-nitrosomethylbenzylamine(NMBzA) induced esophageal cancer in F344 rats. After the rats were fed normal diets containing different concentrations of lycopene for 25 weeks (10, 25, 50 mg/kg·d of lycopene, respectively), the incidence of tumors in the rats treated with lycopene was significantly lower than that in the simple exposed group (P < 0.05). The antioxidant activity of lycopene was exerted by measuring the levels of GSH-PX, SOD and MDA activity by oxidative stress kits. Furthermore, through western blotting analysis lycopene intervention was found to have significantly improved apoptosis cytokines by increasing the protein expression levels of PPARγ and caspase-3, and also significantly reduced inflammatory cytokines by decreasing the protein expression of NF-κB and COX-2 in the esophagus tissue, especially in the 25 mg/kg of lycopene intervention group (all P < 0.05). These results demonstrated that appropriate dose of lycopene intervention could inhibit the carcinogenesis of esophageal in F344 rats through the possible mechanisms of anti-inflammatory and pro-apoptosis.

Objective To investigate the correlation between type 2 diabetes mellitus (T2DM)and hepatocellular carcinoma (HCC)by case-control study. Methods From January 2006 to December 2015,the data of 1350 first diagnosis HCC patients at the First Affiliated Hospital of Zhengzhou University were collected and analyzed. The univariate and multivariate logistic regression were performed to analyze the risk factors of HCC genesis,and the risk factors were further stratified. Results The results of univariate logistic regression analysis showed that smoking and obesity were not risk factors of HCC genesis (both P > 0. 05). Alcoholism, hepatitis B virus (HBV)infection,hepatitis C virus (HCV)infection,T2DM,and family history of HCC were the risk factors of HCC genesis (odds ratio (OR)= 2. 593,4. 583,3. 732,1. 955 and 1. 622,95％ confidence interval (CI)1. 883 to 3. 549,3. 026 to 6. 940,2. 544 to 5. 367,1. 708 to 2. 477 and 1. 314 to 2. 267,all P < 0. 05). The results of multivariate logistic regression analysis indicated that alcoholism,HBV infection, HCV infection,T2DM and family history of HCC were independent risk factors of HCC genesis (OR = 2. 034, 4. 564,2. 831,1. 881 and 1. 616,95％ CI 1. 507 to 2. 745,2. 672 to 7. 765,1. 562 to 5. 047,1. 314 to 2. 671 and 1. 177 to 2. 228,all P < 0. 01),and T2DM could increase the risk of HCC genesis (P < 0. 01). In order to exclude the interference of alcoholism,HBV infection and HCV infection on above results,further stratified analysis showed that T2DM was one of the independent risk factors of HCC genesis (χ2 = 5. 190,P = 0. 023), and had synergistic effect with alcoholism,HBV infection and HCV infection (χ2 = 32. 848,P < 0. 01). There were significant differences in the propovtion,duration of disease and hemoglobin A 1c level of T2DM patients between the case group and the control group (χ2 = 46. 618,81. 644 and 43. 092,all P < 0. 01). Conclusions T2DM is one of the independent risk factors or HCC genesis. T2DM is correlated with the pathogenesis of HCC. The clinical desease course and blood glucose control in patients with T2DM are also correlated with the pathogenesis of HCC.

Purpose: Esophageal cancer is a common malignant tumor that develops rapidly and has a poor prognosis clinically. Astaxanthin (AST) is a carotenoid pigment with strong antioxidant, anti-inflammation, and antitumor activities. However, little is known about the effects of astaxanthin in esophageal cancer. The present study aimed to investigate the protective effects and related mechanisms of natural astaxanthin against N-nitrosomethylbenzylamine (NMBA)-induced esophageal cancer in rats. Methods: F344 rats were induced subcutaneously with NMBA dissolved in dimethyl sulfoxide (0.35 mg/kg body weight three times per week for 5 weeks). Rats were fed normal diets with or without 25 mg/kg/day AST at different stages. At different time points, levels of oxidative stress factors in serum and esophagus tissue were analyzed. Western blotting was performed to observe the expression of NFκB and COX2 in esophagus tissue. Results: AST clearly reduced the incidence of visible tumors in esophageal cancer during the early-stage intervention group. Furthermore, when compared with the simple exposed group, AST significantly increased levels of GPx and SOD activity, decreased the activity level of malondialdehyde (all P<0.05). Early-stage and whole-stage intervention groups effectively attenuated expression levels of NFκB and COX2 proteins compared with the simple exposed group (all P<0.05). Conclusion: Natural AST significantly suppressed the occurrence of esophageal cancer by increasing antioxidant capacity and anti-inflammation capacity by inhibiting expression levels of NFκB and COX2 proteins.

Some debates exist regarding the association of coffee consumption with hypertension risk. We performed a meta-analysis including dose–response analysis aimed to derive a more quantitatively precise estimation of this association. PubMed and Embase were searched for cohort studies published up to 18 July 2017. Fixed-effects generalized least-squares regression models were used to assess the quantitative association between coffee consumption and hypertension risk across studies. Restricted cubic spline was used to model the dose–response association. We identified eight articles (10 studies) investigating the risk of hypertension with the level of coffee consumption, including 243,869 individuals and 58,094 incident cases of hypertension. We found no evidence of a nonlinear dose–response association of coffee consumption and hypertension (P nonlinearity = 0.243). The risk of hypertension was reduced by 2% (relative risk (RR) = 0.98, 95% confidence interval (CI) 0.98–0.99) with each one cup/day increment of coffee consumption. With the linear cubic spline model, the RRs of hypertension risk were 0.97 (95% CI 0.95–0.99), 0.95 (95% CI 0.91–0.99), 0.92 (95% CI 0.87–0.98), and 0.90 (95% CI 0.83–0.97) for 2, 4, 6, and 8 cups/day, respectively, compared with individuals with no coffee intakes. This meta-analysis provides quantitative evidence that consumption of coffee was inversely associated with the risk of hypertension in a dose–response manner.

Recently, gold nanomaterials and iron oxide nanoparticles (NPs) have attracted much attention due to their unique physical, chemical and biological properties. In this study, polyethyleneimine (PEI)-modified Fe3O4 NPs (inner cores) were first prepared, and then gold shells (AuNSs) were innovatively formed on the cores using epigallocatechin gallate (EGCG) as the reducing agent to obtain Fe3O4-PEI@AuNSs-EGCG core-shell NPs. After PEG modification, the Fe3O4-PEI@AuNSs-EGCG/PEG nanoplatform was completed. This highly integrated nanoplatform has shown remarkable biostability, rapid cellular uptake, and excellent in vitro and in vivo anti-tumour activity. Moreover, this nanoplatform can also be used as a magnetic resonance (MR)/X-ray dual-mode imaging agent. In all, the results of this study showed that Fe3O4-PEI@AuNSs-EGCG/PEG is a promising, potentially effective, theranostic nanoplatform for tumour treatment.

All-trans retinoic acid (atRA), the oxidative metabolite of retinoic acid (RA), is essential for palatogenesis. Overdose RA is capable of inducing cleft palate in mice and humans. Normal embryonic palatal mesenchymal (EPM) cell growth is crucial for shelf growth. Smad signaling is involved in many biological processes. However, it is not much clear if atRA could affect Smad signaling during EPM cells growth. In this study, the timed pregnant mice with maternal administration of 100 mg/kg body weight of RA by gastric intubation were cervical dislocation executed to evaluate growth changes of palatal shelves by hematoxylin and eosin (H&E) staining. At the same time, a primary mouse EPM (MEPM) cell culture model was also established. MEPM cells were treated with atRA (0.1, 0.5, 1, 5 and 10 μM) for 24, 48 and 72 h. The results indicated that the sizes of the shelves were smaller than those in control. AtRA inhibited MEPM cell growth with both increasing concentration and increasing incubation time, especially at 72 h in vitro. Moreover, atRA significantly increased the mRNA and protein expression levels of Smad7 (P < .05), but the mRNA and protein expression levels of PCNA were reduced (P < .05). We also found atRA inhibited phosphorylation of Smad2 compared with untreated group (P < .05). However, the protein and mRNA levels of Smad2 did not change both in atRA-treated and untreated group (P > .05). We demonstrated that RA induced inhibition of MEPM cell growth that could cause cleft palate partly by down-regulation of Smad pathway.

While several epidemiological studies have investigated the association between vitamin C and risk of esophageal cancer, the results remain inconsistent. In the present study, a meta-analysis was conducted to assess the impact of dietary vitamin C intake on esophageal cancer risk. Online databases were searched up to March 29, 2015, for studies on the association between dietary vitamin C intake and esophageal cancer risk. Pooled risk ratios (RRs) or odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using a random-effects model. Dose-response analyses were performed using the method of restricted cubic splines with four knots at percentiles of 5, 35, 65 and 95% of the distribution. Publication bias was estimated using Egger's tests and funnel plots. In all, 15 articles were included in this meta-analysis, including 20 studies, containing 7063 controls and 3955 cases of esophageal cancer. By comparing the highest vs. the lowest categories of vitamin C intake, we found that vitamin C was inversely associated with the risk of esophageal cancer [overall OR=0.58, 95% CI=0.49-0.68, I-2=56%]. A linear dose-response relationship was found. With an increase in dietary vitamin C intake of 50 mg/day, the risk of esophageal cancer statistically decreased by 13% (OR=0.87, 95% CI=0.80-0.93, p(linearity)=0.0002). In conclusion, our analysis suggested that the higher intake of dietary vitamin C might have a protective effect against esophageal cancer.

The study aimed to investigate prevalence, awareness, treatment and control of type 2 diabetes mellitus (T2DM), and to explore potential risk factors in rural areas of China. A total of 16413 individuals aged 18–74 years in rural districts were recruited from the Rural Diabetes, Obesity and Lifestyle (RuralDiab) study for the epidemiological research. Meanwhile, a meta-analysis including 7 published studies was conducted to validate the result of the cross-sectional study. The rates of crude and age-standardized prevalence, awareness, treatment and control of T2DM were 12.19%, 67.00%, 62.35%, 22.20% and 6.98%, 60.11%, 54.85%, 18.77%, respectively. The prevalence, awareness, treatment and control of T2DM displayed increased trends with age ( P trend < 0.01) and were strongly associated with education, drinking, more vegetable and fruit intake, physical activity, family history of diabetes, body mass index (BMI). The results of this meta-analysis showed that the pooled prevalence, awareness, treatment and control of T2DM in China countryside were 7.3% (5.3–9.4%), 57.3% (36.9–77.6%), 48.4% (32.4–64.5%) and 21.0% (9.9–32.1%), respectively. The prevalence of T2DM was high with inadequate awareness, treatment and control of T2DM in China rural areas. Healthy lifestyles should be advocated to reduce prevalence and improve awareness, treatment, and control of T2DM in Chinese rural residents.

BACKGROUND:C1q/TNF-related protein 1 (CTRP-1), a novel adipocyte factor, may participate in the mechanisms of metabolism and inflammation. Interleukin 6 (IL-6) is a proinflammatory cytokine that is correlated with the severity of coronary heart disease (CHD). In this study, we focused on the levels of CTRP-1 and IL-6 in patients with CHD.METHODS:Circulating CTRP-1 and IL-6 levels were measured using enzyme-linked immunosorbent assay in 81 patients with acute coronary syndrome (n=41) or stable angina pectoris (n=40). CTRP-1 and IL-6 levels were also examined in 30 healthy individuals (control group). We examined the correlations between the levels of CTRP-1 and IL-6 and cardiac risk factors in CHD. Logistic regression analysis was performed to screen for factors that predict CHD.RESULTS:Both CTRP-1 and IL-6 concentrations were increased in the acute coronary syndrome or stable angina pectoris group compared with the control group (P<0.01). Both plasma levels of CTRP-1 and IL-6 in the single-, double- and triple-vessel lesion group were higher compared with the control group (P<0.01). CTRP-1 levels were positively correlated with IL-6 (r=0.667, P<0.01) and high-sensitivity C-reactive protein levels (r=0.520, P<0.01) and negatively correlated with HDL-C (r=-0.432, P<0.01). The logistic regression analysis showed that increases in CTRP-1 and IL-6 levels may be powerful predictors of CHD.CONCLUSIONS:The variation of plasma CTRP-1 and IL-6 concentrations may play an important role in reflecting the degree of inflammation in CHD and the severity of coronary arterial atherosclerosis. This potential suggests that evaluating CTRP-1 and IL-6 in combination may aid in predicting the occurrence of CHD.

OBJECTIVE:Previous studies on the association between vitamin D binding protein (DBP) polymorphisms and the risk of type 2 diabetes mellitus (T2DM) have produced conflicting results. The purpose of this meta-analysis was to examine whether DBP polymorphisms are associated with the risk of T2DM. DESIGN:Systematic review and meta-analysis. METHODS:All eligible studies were searched and acquired from the Cochrane, Pubmed, ISI, CNKI (Chinese) and Wanfang (Chinese) databases. ORs with corresponding 95% CIs were computed to estimate the association between DBP polymorphisms and T2DM. In addition, heterogeneity test, meta-regression and sensitivity analysis were also conducted. RESULTS:Six studies, which included 1191 cases and 882 controls, met the inclusion criteria and were included in the meta-analysis. The results showed that no significant associations were found between codon 416 and codon 420 polymorphisms in the DBP and the risk of T2DM in the overall analyses. In stratified analysis, significant associations between the codon 420 polymorphism and T2DM were found in Asians (allele Lys vs Thr: OR (95% CI) 1.49 (1.19 to 1.85), genotype Lys/Thr versus Thr/Thr: OR (95% CI) 1.80 (1.36 to 2.38), and Lys/Thr+Lys/Lys versus Thr/Thr: OR (95% CI) 1.81 (1.37 to 2.39), respectively) but not in Caucasians. For the codon 416, the significant association with T2DM was also detected in Asians (genotype Glu/Asp+Glu/Glu vs Asp/Asp: OR (95% CI) 1.36 (1.04 to 1.78)) but not in Caucasians. CONCLUSIONS:This meta-analysis demonstrated that the DBP polymorphism was moderately associated with increased susceptibility to T2DM in Asians, but a similar association was not found in Caucasians. It suggested that ethnicity might be the potential factor associated with heterogeneity.