Amorphous-selenium (a-Se) based photodetectors are promising candidates for imaging devices, due to their high spatial resolution and response speed, as well as extremely high sensitivity enhanced by an internal carrier multiplication. In addition, a-Se is reported to show sensitivity against wide variety of wavelengths, including visible, UV and X-ray, where a-Se based flat-panel X-ray detector was proposed. In order to develop an ultra high-sensitivity photodetector with a wide detectable wavelength range, a photodetector was fabricated using a-Se photoconductor and a nitrogen-doped diamond cold cathode. In the study, a prototype photodetector has been developed, and its response to visible and ultraviolet light are characterized.

Maternal malnutrition, which causes prenatal exposure to excessive glucocorticoid, induces adverse metabolic programming, leading to hypertension in offspring. In offspring of pregnant rats receiving a low-protein diet or dexamethasone, a synthetic glucocorticoid, mRNA expression of angiotensin receptor type 1a ( Agtr1a ) in the paraventricular nucleus (PVN) of the hypothalamus was upregulated, concurrent with reduced expression of DNA methyltransferase 3a ( Dnmt3a ), reduced binding of DNMT3a to the Agtr1a gene, and DNA demethylation. Salt loading increased BP in both types of offspring, suggesting that elevated hypothalamic Agtr1a expression is epigenetically modulated by excessive glucocorticoid and leads to adult-onset salt-sensitive hypertension. Consistent with this, dexamethasone treatment of PVN cells upregulated Agtr1a , while downregulating Dnmt3a , and decreased DNMT3a binding and DNA demethylation at the Agtr1a locus. In addition, Dnmt3a knockdown upregulated Agtr1a independently of dexamethasone. Hypothalamic neuron–specific Dnmt3a -deficient mice exhibited upregulation of Agtr1a in the PVN and salt-induced BP elevation without dexamethasone treatment. By contrast, dexamethasone-treated Agtr1a -deficient mice failed to show salt-induced BP elevation, despite reduced expression of Dnmt3a . Thus, epigenetic modulation of hypothalamic angiotensin signaling contributes to salt-sensitive hypertension induced by prenatal glucocorticoid excess in offspring of mothers that are malnourished during pregnancy.

It is widely known that salt is an accelerating factor for the progression of metabolic syndrome and causes cardiovascular diseases, most likely due to its pro-oxidant properties. We hypothesized that excessive salt intake also facilitates the development of nonalcoholic steatohepatitis (NASH), which is frequently associated with metabolic syndrome. We examined the exacerbating effect of high-salt diet on high-fat diet-induced liver injury in a susceptible model to oxidative stress, apoE knockout and lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) transgenic mice. High-salt diet led to NASH in high-fat diet-fed LOX-1 transgenic/apoE knockout mice without affecting high-fat diet-induced dyslipidemia or hepatic triglyceride accumulation. Additionally, a high-salt and high-fat diet stimulated oxidative stress production and inflammatory reaction to a greater extent than did a high-fat diet in the liver of LOX-1 transgenic/apoE knockout mice. We demonstrated that high-salt diet exacerbated NASH in high-fat diet-fed LOX-1 transgenic /apoE knockout mice and that this effect was associated with the stimulation of oxidative and inflammatory processes; this is the first study to suggest the important role of excessive salt intake in the development of NASH.

High salt intake is a risk for developing resistant hypertension, and even under triple therapy with diuretics, an angiotensin-converting enzyme inhibitor/angiotensin receptor blocker and a calcium channel blocker, the volume is occasionally not controlled. In such cases, a mineralocorticoid receptor (MR) antagonist additively lowers the circulating blood volume and blood pressure despite the lower circulating aldosterone level. This mechanism may be explained by the increase in the number of MR under some conditions or the activation of these receptors independent of aldosterone. Future diagnostic tools to evaluate receptor activity may be valuable for the proper diagnosis and choice of therapy. Additionally, basic research has suggested that oxidative stress and the renin–angiotensin–aldosterone system in the brain represent new targets for the treatment of resistant hypertension.