Search

Background: Cardiovascular disease accounts for at least 85 percent of deaths for those patients with type 2 diabetes mellitus (T2DM). Additionally, 75 percent of these deaths are due to ischemic heart disease. Hypothesis: Is type 2 diabetes mellitus a vascular disease (atheroscleropathy) with hyperglycemia a late manifestation? The role of NOS, NO, and redox stress. Testing of the hypothesis: The vulnerable three arms of the eNOS reaction responsible for the generation of eNO is discussed in relation to the hypothesis: (1). The L-arginine substrate. (2). The eNOS enzyme. (3). The BH4 cofactor. Implications of the hypothesis: If we view T2DM as a vascular disease initially with a later manifestation of hyperglycemia, we may be able to better understand and modify the multiple toxicities associated with insulin resistance, metabolic syndrome, prediabetes, overt T2DM, and accelerated atherosclerosis (atheroscleropathy). The importance of endothelial nitric oxide synthase, endothelial nitric oxide, tetrahydrobiopterin (BH4), L-arginine, and redox stress are discussed in relation to endothelial cell dysfunction and the development and progression of atheroscleropathy and T2DM. In addition to the standard therapies to restore endothelial cell dysfunction and stabilization of vulnerable atherosclerotic plaques, this article will discuss the importance of folic acid (5MTHF) supplementation in this complex devastating disease process. Atheroscleropathy and hyperglycemia could be early and late manifestations, respectively, in the natural progressive history of T2DM. [ABSTRACT FROM AUTHOR]

Investigates the implication of genes, diet and behavior in modifying brain aging and neurodegenerative disorders (ND). Effectivity of caloric intake restriction in reducing the risk of age-related ND; Reduction in the risk of Alzheimers' disease with the use of anti-inflammatory drugs; Efficiency of gene identification in preventing the occurrence of ND.

The article discusses the study which aims to find out whether eNOS298 gene polymorphism affects circadian blood pressure (BP) regulation in 110 healthy subjects and 155 never treated hypertensive patients recruited at Hypertension Units in Grenoble, Toulouse and Lille in France. The results support the role of the NO pathway in the circadian regulation of BP. The Asp298 variant of NOS is particularly associated with a steeper fall in nocturnal BP, independent of the BP level.

The primary goals of this study were to evaluate the gender- and age-related differences in homocysteine concentration in the general population of China and possible influencing factors. A total of 7872 subjects, divided into male and female groups, participated in this retrospective study. The average homocysteine level, prevalence of hyperhomocysteinemia, and independent factors affecting homocysteine concentration were analyzed. The homocysteine level was significantly higher in males than in females in each age range (aged 20–30, aged 30–40, aged 40–50, aged 50–60, aged 60–80, aged over 80) (P < 0.0001), and the trend did not abate with age. The homocysteine concentration first decreased and then increased, being lowest at 30–50 years of age and significantly increased after 50 years of age. Factors associated with homocysteine concentration in males were smoking status (current smokers versus ex-smokers: β: 0.112), estimated glomerular filtration rate (β = − 0.192), blood urea nitrogen (β = − 0.14), diastolic blood pressure (β = − 0.113), free triiodothyronine (β = − 0.091), serum potassium (β = − 0.107) and cystatin C (β = 0.173). In females, independent factors associated with homocysteine concentration were cystatin C (β = 0.319), albumin (β = 0.227), free thyroxine (β = 0.179), age (β = 0.148), free triiodothyronine (β = − 0.217) and serum potassium (β = − 0.153). The homocysteine level was significantly higher in males than in females and increased markedly after 50 years of age in both groups. The independent factors associated with increased homocysteine concentration differed between males and females. [ABSTRACT FROM AUTHOR]

The purpose of this study was to assess whether pharmacy database information from US Department of Veterans Affairs (VA) medical centers could be used to screen for areas of higher Parkinson's disease prevalence in patients exposed to pesticides. The authors used pharmacy data sets and compared the use of antiparkinsonian medications at 2 VA medical centers in California: one in Palo Alto, near the ocean, and one in Fresno, downwind from extensively farmed parts of the Central Valley. They found that patients at Fresno had higher odds ratios (1.5-1.8) for the use of Parkinson's disease medications than patients at Palo Alto. These data are consistent with the observations of prior epidemiologic studies and suggest that VA pharmacy databases can prioritize locations for further epidemiologic research. However, a thorough exploration of alternative explanations is needed to reach definitive conclusions regarding the findings suggested by this method. [ABSTRACT FROM AUTHOR]

Background: The aim of the present study was to examine the association of angiopoietin-like proteins-8 (ANGPTL8) rs2278426, cholesteryl ester-transfer protein (CETP) rs708272 and endothelial nitric oxide synthase (NOS3) rs1799983 variants with type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD), and to investigate the effect of the potential interaction between these variants on disease risk. Methods: Our study included 272 subjects classified into 68 patients with T2DM, 68 patients with T2DM complicated with CVD and 136 control subjects. ANGPTL8 c194C>T, CETP Taq1B and NOS3 G894T polymorphisms were genotyped using TaqMan® SNP Genotyping Assay. Results: The presence of NOS3, ANGPTL8, and homozygous CETP B1 variants were associated with increased risk of T2DM by 3.07-, 2.33- and 1.75-fold, respectively. NOS3 variant was associated with 3.08-fold increased risk of CVD (95% CI 1.70–5.60), while ANGPTL8 C allele was associated with 2.8-fold increased risk of CVD in T2DM patients (95% CI 1.13–6.97). Concomitant presence of both, CETP B1 and NOS3 T allele, associated with increased risk of T2DM, CVD and CVD in T2DM by 8.36-, 6.33- and 7.87-fold, respectively, while concomitant presence of ANGPTL8 variant with either CETP B1 or NOS3 T allele was not associated with increased risk of T2DM or CVD. However, concomitant presence of the three variants together elevated the risk of T2DM by 13.22-fold (p = 0.004), CVD risk by 8.86-fold (p = 0.03) and highly elevated the risk of CVD in T2DM patients by 13.8-fold (p = 0.008). Conclusions: Concomitant presence of CETP B1, NOS3 T and ANGPTL8 T alleles augments the risk of CVD and T2DM. Further studies to clarify the mechanism of gene–gene interaction in the pathogenesis of CVD and T2DM are needed. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article about the Sapienza University Master's degree in Headache Medicine that was published previously.

A letter to the editor is presented in response to the article concerning a clinical study of migraine evolution that was published previously.

A response by Barbara Borroni and Alessandro Padovani to a letter to the editor about their article concerning the endothelial nitric oxide synthase polymorphisms as risk factors for migraine that was published previously is presented.

A letter to the editor is presented in response to the article about his concerns for the Muggle International Headache Society and herbal-based remedies that was published previously.

Background. Elevated plasma homocysteine levels are reported to be associated with higher rates of vascular diseases. Plasma homocysteine increases in chronic kidney disease (CKD) and could contribute to the increased cardiovascular risk in CKD. Methods. Participants aged 55 years or older with CKD, defined as estimated GFRn = 307) or placebo (n = 312) daily for 5 years. The primary outcome was a composite of death from cardiovascular causes, myocardial infarction and stroke. Results. Mean baseline plasma homocysteine was 15.9 ± 7.3 μmol/l in the active treatment group and 15.7 ± 5.7 µmol/l in placebo group and decreased to 11.9 ± 3.3 µmol/l (P P = 0.25). There were no significant treatment benefits on death from cardiovascular causes (1.24; 0.84–1.83), myocardial infarction (1.10; 0.76–1.61) and stroke (1.00; 0.54–1.85). More participants in the active treatment group were hospitalized for heart failure (1.98; 1.21–3.26; P = 0.007) and for unstable angina (1.70; 1.02–2.83; P = 0.04). Incidence of primary outcome increased with decreasing GFR. Conclusions. Active treatment with B vitamins lowered homocysteine levels in participants with CKD but did not reduce cardiovascular risk. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article about the appreciation for Dr. Tfelt-Hansen's enquiry concerning the efficacy data from the comparative, double-blind, randomized clinical trial between frovatriptan and sumatriptan that was published previously.

A letter to the editor is presented in response to the article about the endothelial nitric oxide synthase polymorphisms as risk factors for migraine that was published previously.

A response by William Pryse-Phillips to a letter to the editor about his article concerning a clinical study of migraine evolution that was published previously is presented.

A response by Patricia Sulak, Sherilyn Willis, Thomas Kuehl. Andrea Coffee, and Jeffrey Clark to a letter to the editor about their article concerning the mean daily headache scores for 102 women, comparing the 28 days of the last 21/7 cycle of drospirenose/ethinyl estradiol that was published previously is presented.

Background: While it has been known that the development of chronic kidney disease (CKD) and age-related cognitive impairment involves several mediators, the evidence in clinical practice only reveals nitride oxide synthase (NOS) and klotho. However, the evidence for this topic is conflicted. The aim of this study was to assess the role of NOS and klotho single nucleotide polymorphisms (SNPs) in the pathogenesis of CKD and age-related cognitive impairment. Methods: We performed a meta-analysis during October to December 2019. Paper collection was performed in major scientific websites, and we extracted information of interest from each paper. Data were analyzed using a Z-test with either random or fixed effect model. Results: Our initial assessment identified NOS3 G894T, NOS3 T786C, NOS3 4b/4a, klotho ( KL) G395A, and KL C1818T as the gene candidate for our meta-analysis. Our pooled calculation revealed that NOS3 G894T was associated with the risk of both age-related cognitive impairment and CKD. Increased susceptibility to age-related cognitive impairment was observed in the GG genotype, and increased risk of CKD was found in patients with a single T allele and TT genotype for NOS3 nucleotide 894. For NOS3 4b/4a, increased risk of CKD was only found in 4a4a genotype. For NOS3 T786C, we failed to show the association with both CKD and age-related cognitive impairment. Subsequently, for KL G395A, A allele and GA genotype were found to correlate with increased susceptibility to CKD, while its correlation to age-related cognitive impairment was failed to clarify. For KL C1818T, our analysis failed to find the correlation with the risk of CKD. Conclusions: Our results reveal that the NOS3 G894T gene polymorphism has a crucial role in the pathogenesis of both CKD and age-related cognitive impairment.

Background: While it has been known that the development of chronic kidney disease (CKD) and age-related cognitive impairment involves several mediators, the evidence in clinical practice only reveals nitride oxide synthase (NOS) and klotho. However, the evidence for this topic is conflicted. The aim of this study was to assess the role of NOS and klotho single nucleotide polymorphisms (SNPs) in the pathogenesis of CKD and age-related cognitive impairment. Methods: We performed a meta-analysis during October to December 2019. Paper collection was performed in major scientific websites, and we extracted information of interest from each paper. Data were analyzed using a Z-test with either random or fixed effect model. Results: Our initial assessment identified NOS3 G894T, NOS3 T786C, NOS3 4b/4a, klotho ( KL) G395A, and KL C1818T as the gene candidate for our meta-analysis. Our pooled calculation revealed that NOS3 G894T was associated with the risk of both age-related cognitive impairment and CKD. Increased susceptibility to age-related cognitive impairment was observed in the GG genotype, and increased risk of CKD was found in patients with a single T allele and TT genotype for NOS3 nucleotide 894. For NOS3 4b/4a, increased risk of CKD was only found in 4a4a genotype. For NOS3 T786C, we failed to show the association with both CKD and age-related cognitive impairment. Subsequently, for KL G395A, A allele and GA genotype were found to correlate with increased susceptibility to CKD, while its correlation to age-related cognitive impairment was failed to clarify. For KL C1818T, our analysis failed to find the correlation with the risk of CKD. Conclusions: Our results reveal that the NOS3 G894T gene polymorphism has a crucial role in the pathogenesis of both CKD and age-related cognitive impairment.

Byline: Monisha. Banerjee, Pushpank. Vats Type 2 diabetes mellitus (T2DM), by definition is a heterogeneous, multifactorial, polygenic syndrome which results from insulin receptor (IR) dysfunction. It is an outcome of [...]

Byline: Shivani. Vadapalli, M. Satyanarayana, K. Chaitra, H. Rani, B.K.S.. Sastry, Pratibha. Nallari Background : Idiopathic pulmonary arterial hypertension (IPAH) is a poorly understood complex disorder, which results in progressive [...]