Severe vitamin D deficiency is associated with endothelial inflammation in healthy individuals even in the absence of subclinical atherosclerosis.

OBJECTIVE: Vitamin D has beneficial effects, some of which involve the cardiovascular system. No study to date has investigated the association between serum endocan levels, as a biomarker of endothelial inflammation, and vitamin D levels in the absence of subclinical atherosclerosis detected by carotid intima-media thickness (CIMT) in healthy individuals. PATIENTS AND METHODS: Subjects were categorized into three groups based on vitamin D levels according to Endocrine Society guidelines. Mean CIMT was calculated from six measurements on two scans. Statistical significance was set at p < 0.05, and all testing was two-sided. RESULTS: The concentration of serum endocan was 802.8 ± 411.4 ng/L in the group with the lowest serum vitamin D level, 454.8 ± 334.3 ng/L in the mild/moderately low serum vitamin D level group, and 269.4 ± 180.2 ng/L in the group with normal serum vitamin D levels (p < 0.01). Receiver operating characteristics curve analysis revealed that a serum vitamin D concentration of 7.5 ng/mL had a 97% sensitivity and 81% specificity for the prediction of serum endocan level greater than 270 ng/L, which could be an indicator for endothelial inflammation. CONCLUSIONS: Demonstrating that vitamin D deficiency can cause endothelial damage in the early period of atherosclerosis without the development of clinical cardiovascular disease will have a pivotal role in the prevention of cardiovascular mortality and morbidity.

Identification of gene variants related to the nitric oxide pathway in patients with acute coronary syndrome.

Dysfunction of vascular endothelium is known to have an essential role in the atherosclerotic process by releasing mediators including nitric oxide (NO). Nitric oxide maintains endothelial balance by controlling cellular processes of vascular smooth muscle cells. Evidence suggests that variations in the NO pathway could include atherosclerotic events. The objective of this study was to determine the possible effects of genes on the nitric oxide pathway in the development of acute coronary syndrome (ACS). The blood samples of 100 patients with ACS and 100 controls were collected at Istanbul University, Department of Cardiology. DNA samples were genotyped by using Illumina Cyto-SNP-12 BeadChip. The additive model and Correlation/Trend Test were selected for association analysis. Afterwards, a Q-Q graphic was drawn to compare expected and obtained values. A Manhattan plot was produced to display p-values that were generated by -log10(P) function for each SNP. The p-values under 1×10(-4) were selected as statistically significant SNPs while p-values under 5×10(-2) were considered as suspicious biomarker candidates. Nitric oxide pathway analysis was then used to find the single nucleotide polymorphisms (SNPs) related to ACS. As a result, death-associated protein kinase 3 (DAPK) (rs10426955) was found to be most statistically significant SNP. The most suspicious biomarker candidates associated with the nitric oxide pathway analysis were vascular endothelial growth factor A (VEGFA), methionine sulfoxide reductase A (MSRA), nitric oxide synthase 1 (NOS1), and GTP cyclohydrolase I (GCH-1). Further studies with large sample groups are necessary to clarify the exact role of nitric oxide in the development of disease.

Association of genetic polymorphisms with endothelial dysfunction in chronic heart failure.

OBJECTIVES: Endothelial dysfunction can be shown very early in the cardiovascular disease. In the present study the association between congestive heart failure (CHF), endothelial function and 3 gene polymorphisms was investigated. PATIENTS AND METHODS: In 104 healthy controls and 104 CHF patients, endothelial constitutive nitric oxide synthase (ecNOS), angiotensin converting enzyme (ACE) and angiotensin II type 1 receptor (AT1R) gene polymorphisms were assessed. The cause of CHF was ischemic in 68 patients and dilated cardiomyopathy (DCMP) in 36 patients. High resolution brachial artery ultrasound was used in 37 CHF patients and 37 healthy controls to assess the endothelial function. Endothelium-dependent vasodilation (EDD) and endothelium-independent vasodilation (EID) were determined. RESULTS: There no was difference between controls and CHF patients for the ACE, ecNOS, and AT1R genotype frequencies. Compared to controls CHF patients had significantly impaired EDD (9.0+5% vs 16±7%, p < 0.001) and EID (13±6% vs 19+8%, p = 0.001). EDD (7±4% vs 12+6%, p = 0.005), but not EID, was significantly impaired in ischemic CHF as compared to DCMP patients. In the CHF group ecNOS a allele and AT1R C allele influence the EDD. CONCLUSIONS: Endothelial dysfunction was present in CHF group and the presence of ecNOS a allele and AT1R C allele further impaired EDD.

Continuous vs. discontinuous force application and root resorption.

The aim of this study was to compare the effects on root resorption of continuous and discontinuous force application. The experimental material consisted of 22 first premolars that were to be extracted as part of orthodontic treatment. Prior to extraction, a 100 g tipping force was applied to the experimental teeth by means of elastics. One side was randomly selected to be the continuous force side, and the contralateral side became the discontinuous force side. Elastics were worn 24 hours per day on the continuous force side and 12 hours per day on the discontinuous side. The experimental procedure lasted 9 weeks. Composite electron micrographs of the buccal surface of each specimen were digitized and areas affected by resorption were determined. The degree of root blunting was assessed by visual scoring. Mean percentage of resorption-affected areas was smaller and apical blunting was less severe on the discontinuous force side. The results of this study show that the application of discontinuous force results in less root resorption than does the application of continuous force.