Serum Vitamin D Level is Inversely Associated With Anti-Cyclic Citrullinated Peptide Antibody Level and Disease Activity in Rheumatoid Arthritis Patients.

OBJECTIVES: This study aims to assess the relationship between serum vitamin D and anti-cyclic citrullinated peptide (anti-CCP) antibody levels, as well as disease activity in patients with newly diagnosed rheumatoid arthritis (RA). PATIENTS AND METHODS: These measurements were conducted between January 2014 and June 2014. Serum 25-hydroxy vitamin D (25-OH-D), anti- CCP antibody, and erythrocyte sedimentation rates were measured in a cohort of 154 patients (66 males, 88 females; mean age 53.5±12.4; range 29 to 79 years) with early RA. A control group of 60 healthy participants (25 males, 35 females; mean age 51.4±10.3; range 25 to 75 years) was only evaluated for serum 25-OH-D levels. Disease activity was measured by calculating the 28-Joint Disease Activity Score. Blood samples were drawn from cubital veins. After centrifugation, serum was collected and stored under minus 20 degrees. RESULTS: Vitamin D deficiency was more prevalent in RA group compared with control group (48.70% vs. 30.00%, p<0.05). Serum 25-OH-D levels were lower in RA group (19.46±8.20 ng/mL) than control group (23.18±6.71 ng/mL) (p<0.05). In the RA group, serum 25-OH-D levels were negatively correlated to anti-CCP antibody levels (rs= -0.360, p<0.001), erythrocyte sedimentation rate (rs= -0.270, p<0.001), age of patients (rs= -0.602, p<0.001), and disease activity (rs= -0.249, p<0.05), respectively. Serum 25-OH-D level did not vary according to sex in the RA group. In control group, females had lower serum 25-OH-D level (p=0.001, rs=0.404). In addition, serum 25-OH-D level was also negatively associated with age in control group (p<0.001, rs= -0.578). There were no differences between RA group and control group in terms of age and sex ratio. CONCLUSION: Serum 25-OH-D level was negatively correlated to anti-CCP antibody level and disease activity, which implied the therapeutic role of serum 25-OH-D in RA.

5,10-Methylenetetrahydrofolate reductase (MTHFR), methionine synthase (MTRR), and methionine synthase reductase (MTR) gene polymorphisms and adult meningioma risk.

The causes of meningiomas are not well understood. Folate metabolism gene polymorphisms have been shown to be associated with various human cancers. It is still controversial and ambiguous between the functional polymorphisms of folate metabolism genes 5,10-methylenetetrahydrofolate reductase (MTHFR), methionine synthase (MTRR), and methionine synthase reductase (MTR) and risk of adult meningioma. A population-based case­control study involving 600 meningioma patients (World Health Organization [WHO] Grade I, 391 cases; WHO Grade II, 167 cases; WHO Grade III, 42 cases) and 600 controls was done for the MTHFR C677T and A1298C, MTRR A66G, and MTR A2756G variants in Chinese Han population. The folate metabolism gene polymorphisms were determined by using a polymerase chain reaction­restriction fragment length polymorphism assay. Meningioma cases had a significantly lower frequency of MTHFR 677 TT genotype [odds ratio (OR) = 0.49, 95 % confidence interval (CI) 0.33­0.74; P = 0.001] and T allele (OR = 0.80, 95 % CI 0.67­0.95; P = 0.01) than controls. A significant association between risk of meningioma and MTRR 66 GG (OR = 1.41, 95 % CI 1.02­1.96; P = 0.04) was also observed. When stratifying by the WHO grade of meningioma, no association was found. Our study suggested that MTHFR C677T and MTRR A66G variants may affect the risk of adult meningioma in Chinese Han population.

Hepatitis B virus gene C1653T polymorphism mutation and hepatocellular carcinoma risk: an updated meta-analysis.

associations between the C1653T mutation and risk of HCC, the results have been inconsistent. We conducted searches of the published literature in Pubmed and Embase databases up to January 2013. Seventeen studies with a total of 1,085 HCC cases and 1,365 healthy controls were retrieved.We found a significant association between the C1653T mutation and HCC risk (OR = 2.01, 95%CI= 1.49-2.70). In the subgroup analysis by ethnicity, a significant association was also found in Asians (OR = 2.07, 95%CI= 1.71-2.51). In subgroup analysis by HBV genotype, B and C were linked with development of HCC (B:OR = 2.21, 95%CI= 1.13-4.34; C:OR = 2.26, 95%CI= 1.61-3.16). However, no significant association was found between the C1653T mutation and HCC risk in HBeAg positive cases. In conclusion, this meta-analysis suggests that the C1653T mutation may be associated with susceptibility to HCC.

Synergistic induction of miR-126 by hypoxia and HDAC inhibitors in cardiac myocytes.

HDAC inhibitors are under clinical development for the treatment of hypertrophic cardiomyopathy and heart failure although the mechanisms of protection are incompletely understood. Micro-RNA 126, an endothelium-specific miR has been assigned essential developmental roles in the heart by activating survival kinases ERK1/2 and Akt and increasing pro-angiogenic signaling. Here we provide the first evidence that hypoxia and HDAC inhibitors selectively and synergistically stimulate expression of miR-126 in cardiac myocytes. MiR-126 expression was increased 1.7-fold (p<0.05) after 1h of hypoxic exposure and this was further enhanced to 3.0-fold (p<0.01) by simultaneously blocking HDAC with the pan-HDAC inhibitor Tricostatin A (TSA). TSA alone did not increase miR-126. In parallel, hypoxia and TSA synergistically increased p-ERK and p-Akt without effecting VEGF-A level. Knockdown of miR-126 with si-RNA eliminated inductions of p-ERK and p-Akt by hypoxia, whereas miR-126 overexpression mimicked hypoxia and amplified p-ERK and p-Akt in parallel with miR-126. The results suggest that miR-126 is a hypoxia-inducible target of HAT/HDAC and its activation in cardiac myocytes may contribute to cardioprotection by activating cell survival and pro-angiogenic pathways selectively during ischemia.

[Transcription factors networks and their roles in plant responses to environmental stress].

The regulation networks of gene expression mediated by transcription factors play important roles in plant responses to a range of environmental stresses. Transcription factors and their families identified to be involved in plant stress responses include APETALA2/EREBP, bZIP, WRKY, MYB, etc., which can constitute regulation networks to regulate the temporal-spatial expression of each kind of related genes in plant stress responses. The genetic modifications of transcription factors and their regulation networks are increasingly becoming the effective approaches for understanding stress biology at system level, and a new way for enhancing the stress tolerance and resistance of plants.