Two Categories of Approximately mu-tau Symmetric Neutrino Mass Textures

Our approximately \mu-\tau symmetric neutrino mass textures fall into two different categories, whose behaviors in the \mu-\tau symmetric limit are characterized by either \sin(theta_{13})->0 (referred to as C1)), or \sin(theta_{12})->0 (referred to as C2)). We present ten phenomenologically viable neutrino mass textures: two for the normal mass hierarchy, three for the inverted mass hierarchy, and five for the quasi degenerate mass pattern. Tiny \mu-\tau symmetry breaking ensures that \sin^2(theta_{13}) << 1 for C1), and \Delta m^2_\odot/\Delta m^2_{atm} (\equiv R) << 1 for C2). A correlation among small quantities is provided by \cos 2(theta_{23}) \sim \sin(theta_{13}) for C1), and by either \cos(2theta_{23}) \sim R, or \cos(2theta_{23})\sin(theta_{13}) \sim R for C2). It is further shown that \tan(2theta_{12}) \sim \cos(2theta_{23})/\sin(theta_{13}) is satisfied for C2). We find specific properties for each mass ordering, which are discussed in this article.Comment: 31 pages, 15 figures (High-resolution figures can be downloaded from http://www.sp.u-tokai.ac.jp/~yasue/two_categories_of.pdf.tar.gz

Role of Differential Signaling Pathways and Oxidative Stress in Diabetic Cardiomyopathy

Diabetes mellitus increases the risk of heart failure independently of underlying coronary artery disease, and many believe that diabetes leads to cardiomyopathy. The underlying pathogenesis is partially understood. Several factors may contribute to the development of cardiac dysfunction in the absence of coronary artery disease in diabetes mellitus. There is growing evidence that excess generation of highly reactive free radicals, largely due to hyperglycemia, causes oxidative stress, which further exacerbates the development and progression of diabetes and its complications. Hyperglycemia-induced oxidative stress is a major risk factor for the development of micro-vascular pathogenesis in the diabetic myocardium, which results in myocardial cell death, hypertrophy, fibrosis, abnormalities of calcium homeostasis and endothelial dysfunction. Diabetes-mediated biochemical changes show cross-interaction and complex interplay culminating in the activation of several intracellular signaling molecules. Diabetic cardiomyopathy is characterized by morphologic and structural changes in the myocardium and coronary vasculature mediated by the activation of various signaling pathways. This review focuses on the oxidative stress and signaling pathways in the pathogenesis of the cardiovascular complications of diabetes, which underlie the development and progression of diabetic cardiomyopathy

A Simple, Fast, Sensitive LC-MS/MS Method to Quantify NAD(H) in Biological Samples: Plasma NAD(H) Measurement to Monitor Brain Pathophysiology

Nicotinamide adenine dinucleotide (NAD) is a cofactor in redox reactions and an essential mediator of energy metabolism. The redox balance between NAD+ and NADH affects various diseases, cell differentiation, and aging, and in recent years there has been a growing need for measurement techniques with improved accuracy. However, NAD(H) measurements, representing both NAD+ and NADH, have been limited by the compound’s properties. We achieved highly sensitive simultaneous measurement of NAD+ and NADH under non-ion pairing, mobile phase conditions of water, or methanol containing 5 mM ammonium acetate. These were achieved using a simple pre-treatment and 7-min analysis time. Use of the stable isotope 13C5-NAD+ as an internal standard enabled validation close to BMV criteria and demonstrated the robustness of NAD(H) determination. Measurements using this method showed that brain NAD(H) levels correlate strongly with plasma NAD(H) levels in the same mouse, indicating that NAD(H) concentrations in brain tissue are reflected in plasma. As NAD(H) is involved in various neurodegenerative diseases and cerebral ischemia, as well as brain diseases such as mitochondrial myopathies, monitoring changes in NADH levels in plasma after drug administration will be useful for development of future diagnostics and therapeutics

Circulating interleukin-6 (IL-6) levels are associated with aortic dimensions in genetic aortic conditions.

BACKGROUND:Biomarkers that reflect progression of dilatation of the aorta in patients with aortic conditions are needed as surrogate tools to assist in monitoring the condition in a non-invasive manner in combination with imaging procedures. This study aimed to investigate whether biomarkers are associated with aortic dimensions in patients enrolled in the Genetically-Triggered Thoracic Aortic Conditions (GenTAC) registry. METHODS:Plasma samples of 159 patients enrolled in the GenTAC registry were assessed for circulating biomarkers [interleukin-6 (IL-6), matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase-1 (TIMP-1), tissue inhibitor of metalloproteinase-2 (TIMP-2) and transforming growth factor-β1 (TGFβ1)]. Association of circulating biomarker levels with aortic dimensions was investigated. RESULTS:IL-6 showed significant positive correlations with aortic dimensions at each segment of the aorta, with the correlation increasing in more distal aortic regions (ascending aorta, R = 0.26, p = 0.004; proximal arch, R = 0.35, p<0.0001; transverse arch, R = 0.30, p = 0.0005; mid-descending thoracic aorta, R = 0.40, p<0.0001; thoracoabdominal aorta, R = 0.38, p<0.0001; suprarenal abdominal aorta, R = 0.42, p<0.0001; and infrarenal aorta, R = 0.43, p<0.0001). TIMP-1 showed a significant correlation albeit weaker than IL-6, and also showed increasing correlation towards the distal areas of the aorta. CONCLUSIONS:Circulating IL-6 and TIMP-1 were associated with aortic dimensions in patients with aortopathies enrolled in the GenTAC cohort