Different divergence processes of isoglosses of folk nomenclature between wild trees and rice landraces imply the need for different conservation planning based on the type of plant resources.

Background: The intensification of production and socio-economic changes have accelerated the loss of local traditional knowledge and plant resources. Understanding the distribution and determinants of such biocultural diversity is essential in planning efficient surveys and conservation efforts. Because the concept of biocultural diversity in socio-ecological adaptive systems comprises biological, cultural, and linguistic diversity, linguistic information should serve as a surrogate for the distribution of local biological and cultural diversity.

High-salt in addition to high-fat diet may enhance inflammation and fibrosis in liver steatosis induced by oxidative stress and dyslipidemia in mice.

Background: 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.

Methods: 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.

Mineralocorticoid receptor activation: a major contributor to salt-induced renal injury and hypertension in young rats.

Excessive salt intake is known to preferentially increase blood pressure (BP) and promote kidney damage in young, salt-sensitive hypertensive human and animal models. We have suggested that mineralocorticoid receptor (MR) activation plays a major role in kidney injury in young rats. BP and urinary protein were compared in young (3-wk-old) and adult (10-wk-old) uninephrectomized (UNx) Sprague-Dawley rats fed a high (8.

Mineralocorticoid receptor activation contributes to salt-induced hypertension and renal injury in prepubertal Dahl salt-sensitive rats.

Background: Excessive prepubertal salt intake permanently increases blood pressure (BP). We examined the role that the mineralocorticoid receptor (MR) plays in the salt-induced hypertension and renal damage of prepubertal Dahl salt-sensitive (SS) rats.

Methods: Prepubertal (6 weeks old) and adult (10 weeks old) Dahl SS rats fed a high (8.

Antioxidant, EUK-8, prevents murine dilated cardiomyopathy.

Background: Mice lacking manganese-superoxide dismutase (Mn-SOD) activity exhibit the typical pathology of dilated cardiomyopathy (DCM). In the present study, presymptomatic and symptomatic mutant mice were treated with the SOD/catalase mimetic, EUK-8.

Methods And Results: Presymptomatic heart/muscle-specific Mn-SOD-deficient mice (H/M-Sod2(-/-)) were treated with EUK-8 (30 mg x kg(-1) .

Protective effect of dietary potassium against cardiovascular damage in salt-sensitive hypertension: possible role of its antioxidant action.

It is well known that high salt intake induces hypertension and cardiovascular damage, while dietary potassium supplementation counteracts these harmful effects. Actually, the protective effect of potassium is strengthened with excess salt as compared with salt depletion. Although the precise mechanisms have not been fully elucidated, in our previous reports, the antihypertensive effect of dietary potassium was accompanied by sympathetic nerve inhibition in salt-sensitive hypertension.

Additive Pummerer reaction of 3,5-O-(di-tert-butyl)silylene-4-thiofuranoid glycal: a high-yield and beta-selective entry to 4'-thioribonucleosides.

Upon reacting 3,5-O-(di-tert-butyl)silylene-4-thiofuranoid glycal S-oxide (6) with Ac(2)O/TMSOAc/BF(3) x OEt(2) in CH(2)Cl(2), the additive Pummerer reaction proceeded to furnish the corresponding 1,2-di-O-acetyl-4-thioribofuranose 7. Compound 7 serves as a highly beta-selective glycosyl donor in the Vorbruggen condensation carried out in the presence of TMSOTf. Thus, the 4-thio-beta-D-ribofuranosyl derivatives of uracil, thymine, N (4) -acetylcytosine, 6-chloropurine, and 2-amino-6-chloropurine were synthesized.

Sympathoexcitation by oxidative stress in the brain mediates arterial pressure elevation in obesity-induced hypertension.

Background: Obesity is one of the major risk factors for cardiovascular disease and is often associated with increased oxidative stress and sympathoexcitation. We have already suggested that increased oxidative stress in the brain modulates the sympathetic regulation of arterial pressure in salt-sensitive hypertension, which is often associated with obesity. The present study was performed to determine whether oxidative stress could mediate central sympathoexcitation in the initial stage of obesity-induced hypertension.

Salt excess causes left ventricular diastolic dysfunction in rats with metabolic disorder.

Metabolic syndrome is a highly predisposing condition for cardiovascular disease and could be a cause of excess salt-induced organ damage. Recently, several investigators have demonstrated that salt loading causes left ventricular diastolic dysfunction associated with increased oxidative stress and mineralocorticoid receptor activation. We, therefore, investigated whether excess salt induces cardiac diastolic dysfunction in metabolic syndrome via increased oxidative stress and upregulation of mineralocorticoid receptor signals.

Paradoxical mineralocorticoid receptor activation and left ventricular diastolic dysfunction under high oxidative stress conditions.

Background: Salt status plays a pivotal role in angiotensin-II-induced organ damage by regulating reactive oxygen species status, and it is reported that reactive oxygen species activate mineralocorticoid receptors.

Method: To clarify the role of reactive oxygen species-related mineralocorticoid receptor activation in angiotensin-II-induced cardiac dysfunction, we examined the effect of the following: salt status; an MR antagonist, eplerenone; and an antioxidant, tempol in angiotensin-II-loaded Sprague-Dawley rats.

Results: Angiotensin-II/salt-loading elevated blood pressure, and neither eplerenone nor tempol antagonized the rise in blood pressure significantly.

Additive Pummerer reaction of 3,5-O-(di-t-butylsilylene)-4-thiofuranoid glycal and stereoselective synthesis of beta-anomer of 4'-thioribonucleosides.

Upon reacting 3,5-O-(di-t-butylsilylene) (DTBS)-4-thiofuranoid glycal S-oxide (7) with Ac2O in the presence of TMSOAc and BF3.OEt2, additive Pummerer reaction proceeded to furnish 1,2-di-O-acetyl-3,5-O-DTBS-4-thioribofuranose (8) in 61% yield. When 8 was reacted with bis-O-TMS-uracil and TMSOTf, 2'-O-acetyl-3',5'-O-DTBS-4'-thiouridine (13a) was obtained along with it's beta-anomer (13b) in 93% yield (13a/13b = 22/1).

Salt-induced nephropathy in obese spontaneously hypertensive rats via paradoxical activation of the mineralocorticoid receptor: role of oxidative stress.

Aldosterone is implicated in the pathogenesis of proteinuria and chronic kidney disease. We previously demonstrated the contribution of elevated serum aldosterone in the early nephropathy of SHR/NDmcr-cp (SHR/cp), a rat model of metabolic syndrome. In the present study, we investigated the effect of salt loading on renal damage in SHR/cps and explored the underlying mechanisms.

Suppression of catechol-O-methyltransferase activity through blunting of alpha2-adrenoceptor can explain hypertension in Dahl salt-sensitive rats.

Catecholamines have been reported to be involved in the development of salt-sensitive hypertension. We investigated the relation between catechol-O-methyltransferase (COMT) and salt-sensitivity. In the first experiment, Dahl salt-sensitive (DS) rats were given a normal-salt (NS), high-salt (HS), or HS+hydralazine (80 mg/l water) diet for 4 or 13 weeks, and Dahl salt-resistant (DR) rats were given a NS or HS diet.

New synthesis of (+/-)-isonucleosides.

[Structure: see text] A novel method for synthesizing isonucleosides, a new class of anti-HIV nucleosides, is described. 2,2-Dimethyl-1,3-dioxan-5-one was converted into a dioxabicyclohexane derivative in six steps. After cleaving the epoxide group with thiophenol, the resulting product was subjected to the Mitsunobu reaction in the presence of a nucleobase to give the desired isonucleoside derivative via migration of the thiophenyl group.

Adrenomedullin inhibits angiotensin II-induced oxidative stress via Csk-mediated inhibition of Src activity.

We have demonstrated that adrenomedullin (AM) protects against angiotensin II (ANG II)-induced cardiovascular damage through the attenuation of increased oxidative stress observed in AM-deficient mice. However, the mechanism(s) that underlie this activity remain unclear. To address this question, we investigated the effect of AM on ANG II-stimulated reactive oxygen species (ROS) production in cultured rat aortic vascular smooth muscle cells (VSMCs).

Protective effect of potassium against the hypertensive cardiac dysfunction: association with reactive oxygen species reduction.

Potassium supplementation has a potent protective effect against cardiovascular disease, but the precise mechanism of it against left ventricular abnormal relaxation, relatively early functional cardiac alteration in hypertensive subjects, has not been fully elucidated. In the present study, we investigated the effect of potassium against salt-induced cardiac dysfunction and the involved mechanism. Seven- to 8-week-old Dahl salt sensitive rats were fed normal diet (0.

Two cases of renovascular hypertension and ischemic renal dysfunction: reliable choice of examinations and treatments.

We experienced two aged patients with atherosclerotic renovascular stenosis associated with hypertension and ischemic nephropathy. Both patients exhibited sudden rise in blood pressure (BP) and progressive aggravation of renal dysfunction. In these patients, the use of contrast medium to screen for renal artery stenosis (RAS) ran the risk of further deterioration of renal function.

Angiotensin II-induced insulin resistance is enhanced in adrenomedullin-deficient mice.

Insulin resistance and hypertension are common disorders that are closely related. Among several factors, oxidative stress has been reported to be intimately related to these diseases. To elucidate the involvement of oxidative stress in the development of insulin resistance in a hypertensive model, we administered angiotensin II (Ang II), which raises blood pressure and induces reactive oxygen radicals, to adrenomedullin (AM)-knockout heterozygous mice and examined the resulting changes in blood pressure and insulin resistance.

Adrenomedullin can protect against pulmonary vascular remodeling induced by hypoxia.

Background: Chronic hypoxia is one of the major causes of pulmonary vascular remodeling associated with stimulating reactive oxygen species (ROS) production. Recent studies have indicated that hypoxia upregulates expression of adrenomedullin (AM), which is not only a potent vasodilator but also an antioxidant. Thus, using heterozygous AM-knockout (AM+/-) mice, we examined whether AM could attenuate pulmonary vascular damage induced by hypoxia.

Deficiency of adrenomedullin induces insulin resistance by increasing oxidative stress.

Hypertension, insulin resistance, and obesity are common age-related metabolic disorders that are often associated with increased oxidative stress and the resultant vascular damage. Underlying mechanisms have been suggested, and age-related overproduction of oxidative stress is one possible candidate. Since we recently found a vasoactive peptide, adrenomedullin, to be an endogenous antioxidant that potently inhibits oxidative stress-induced vascular damage, in the current study we evaluated oxidative stress-induced changes in aged mice.

Organ-protective effects of adrenomedullin.

Adrenomedullin (AM), a vasodilatory peptide, has recently been shown to have multipotent properties. Among its other pharmacological actions, AM has been hypothesized to protect organs from hypertension, hypoxia, or infection. In vitro studies have shown that AM has an inhibitory effect on vascular smooth muscle cell proliferation and oxidative stress, but that it enhances nitric oxide (NO) production, which in turn is thought to protect against organ damage.