Detection of mild Alzheimer's disease and mild cognitive impairment from elderly speech: Binary discrimination using logistic regression.

In this research, we have developed a novel data-mining approach for detection of cognitive impairment, SPCIR (Speech Prosody-Based Cognitive Impairment Rating), which can discriminate between mild cognitive impairment and mild Alzheimer's disease from elderly using prosodic sign extracted from elderly speech during questionnaire test. This paper proposes a binary discrimination model of SPCIR using multivariate logistic regression and model selection using receiver operating characteristic (ROC) curve analysis, and reports the sensitivity and specificity of SPCIR for diagnosis (control; mild cognitive impairment/mild Alzheimer's disease).

LVQ-SMOTE - Learning Vector Quantization based Synthetic Minority Over-sampling Technique for biomedical data.

Background: Over-sampling methods based on Synthetic Minority Over-sampling Technique (SMOTE) have been proposed for classification problems of imbalanced biomedical data. However, the existing over-sampling methods achieve slightly better or sometimes worse result than the simplest SMOTE. In order to improve the effectiveness of SMOTE, this paper presents a novel over-sampling method using codebooks obtained by the learning vector quantization.

Mutual regulation of conventional protein kinase C and a ubiquitin ligase complex.

Several isoforms of protein kinase C (PKC) are degraded by the ubiquitin-proteasome pathway after phorbol ester-mediated activation. However, little is known about the ubiquitin ligase (E3) that targets activated PKCs. We recently showed that an E3 complex composed of HOIL-1L and HOIP (LUBAC) generates linear polyubiquitin chains and induces the proteasomal degradation of a model substrate.

Anxiety-induced plasma norepinephrine augmentation increases reactive oxygen species formation by monocytes in essential hypertension.

Background: An association between anxiety and depression and increased blood pressure (BP) and cardiovascular disease risk has not been firmly established. We examined the hypothesis that anxiety and depression lead to increased plasma catecholamines and to production of reactive oxygen species (ROS) by mononuclear cells (MNC) in hypertensive individuals. We also studied the role of BP in this effect.

Reactive oxygen species formation by polymorphonuclear cells and mononuclear cells as a risk factor of cardiovascular diseases.

To better identify patients at high risk for cardiovascular events, several markers of risk have been proposed for use in screening. Recently, oxidative stress and inflammation have been evaluated as potential tools for prediction of the risk of cardiovascular events. Among them, we have measured reactive oxygen species (ROS) formation by polymorphonuclear cells (PMNs) and mononuclear cells (MNCs), since they may be a possible link between inflammation and oxidative stress.

Oxidative stress by peripheral blood mononuclear cells is increased in hypertensives with an extreme-dipper pattern and/or morning surge in blood pressure.

Because oxidative stress and inflammation are known to play important roles in the pathogenesis of cardiovascular events that occur most frequently in the morning, we studied the association between reactive oxygen species (ROS) formation by polymorphonuclear leukocytes (PMNs) or mononuclear cells (MNCs) and morning blood pressure (BP) rhythm. A total of 31 hypertensives in whom ambulatory BP monitoring was performed participated in this study. They were first divided into three groups according to their nocturnal BP rhythm (non-dippers, dippers and extreme dippers), and then into two groups according to their morning BP change (surge-type and sustained-type).

Benidipine, a long-acting calcium channel blocker, inhibits oxidative stress in polymorphonuclear cells in patients with essential hypertension.

To study the relationship between blood pressure and oxidative stress in leukocytes, the effect of benidipine on these variables was compared with that of a placebo. Hypertensive patients were randomly assigned benidipine 4 mg (n=40) or placebo (n=40), and treated for 6 months. Oxidative stress in polymorphonuclear cells (PMNs) was measured by gated flow cytometry.

Pharmacological and clinical studies with temocapril, an angiotensin converting enzyme inhibitor that is excreted in the bile.

Temocapril is an angiotensin converting enzyme inhibitor (ACEI), a prodrug with a thiazepine ring. Its active form, temocaprilat, is slightly more potent than enalaprilat in inhibiting ACE isolated from rabbit lung. The inhibitory potency of temocaprilat on isolated rat aorta is 3 times that of enalaprilat.

Comparative effects of valsartan versus amlodipine on left ventricular mass and reactive oxygen species formation by monocytes in hypertensive patients with left ventricular hypertrophy.

Objectives: To compare the effects of the angiotensin receptor blocker (ARB) valsartan versus the calcium channel blocker amlodipine, reactive oxygen species (ROS) formation by monocytes, C-reactive protein (CRP), and left ventricular (LV) mass were studied in 104 hypertensive patients with left ventricular hypertrophy (LVH).

Background: There is evidence that ARBs have blood pressure (BP)-independent effects on LV mass. Whether regression of LV mass by ARBs is correlated to ROS formation by monocytes and CRP is not fully understood yet.

Effects of carvedilol on oxidative stress in polymorphonuclear and mononuclear cells in patients with essential hypertension.

Purpose: To compare the effects of carvedilol and propranolol on oxidative stress in leukocytes and C-reactive protein levels in patients with hypertension.

Methods: Sixty hypertensive patients were randomly assigned to carvedilol (20 mg; n = 30) or propranolol (60 mg; n = 30) for 6 months. Thirty normotensive subjects who were given placebo served as controls.

Converting enzyme inhibitor temocaprilat prevents high glucose-mediated suppression of human aortic endothelial cell proliferation.

We examined the involvement of the oxidative stress in high glucose-induced suppression of human aortic endothelial cell proliferation. Chronic glucose treatment for 72 h concentration-dependently (5.6-22.

Dopamine as a novel anti-migration factor of vascular smooth muscle cells through D1A and D1B receptors.

To elucidate the roles of rat vascular dopamine D1A and D1B receptors in vascular smooth muscle cell migration, the effect of antisense oligonucleotides to D1A receptors (+1 to +21 of rat D1A receptors) and to D1B receptors (-12 to +6 of rat D1B receptors) on dopamine-mediated suppression of platelet-derived growth factor BB-mediated vascular smooth muscle cell migration, evaluated by the Boyden's chamber method, was studied. Increased vascular smooth muscle cell migration by platelet-derived growth factor BB (5 ng/ml) was suppressed significantly by co-incubation with dopamine (0.025-10 micromol/l) (by 15-59%).

Carvedilol inhibits pressure-induced increase in oxidative stress in coronary smooth muscle cells.

The cellular mechanisms by which hypertension enhances atherosclerosis are still not known in detail. Recently, evidence has been obtained that oxidative stress plays a role in the pathogenesis of pressure-induced atherosclerosis. We examined the effects of pressure on oxidative stress in cultured human coronary smooth muscle cells (SMCs).

Oxidative stress in leukocytes is a possible link between blood pressure, blood glucose, and C-reacting protein.

Because oxidative stress and inflammation are believed to play roles in the pathogenesis of cardiovascular diseases, oxidative stress in polymorphonuclear leukocytes (PMNs) and mononuclear cells (MNCs) has been measured. A total of 529 subjects participated this study. Intracellular oxidative stress in PMNs and MNCs was measured by gated flow cytometry using carboxyfluorescin diacetate bis-acetoxymethyl ester.

Pressure promotes angiotensin II--mediated migration of human coronary smooth muscle cells through increase in oxidative stress.

Angiotensin II--mediated oxidative stress may play a role in the pathogenesis of coronary atherosclerosis. We examined the effects of pressure on the angiotensin II--mediated increase in oxidative stress and migration of cultured human coronary smooth muscle cells (SMCs). Increased pressure (100 mm Hg) by helium gas for 48 hours increased angiotensin II--mediated oxidative stress as evaluated by flow cytometry and SMC migration (from 15.