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Biomedical subjects

T Ogihara

Publications and source records attributed to T Ogihara.

At least 613 records · Page 34Linked to original sources

Regression of hypertension-induced vascular hypertrophy by an ACE inhibitor and calcium antagonist in the spontaneously hypertensive rat.

This study was designed to investigate the effects of antihypertensive drugs on vascular hypertrophy and vascular angiotensin II in vivo in spontaneously hypertensive rats (SHR). Hydralazine (10 mg/kg/day), delapril (angiotensin converting enzyme inhibitor; 20 mg/kg/day), manidipine (calcium channel blocker; 10 mg/kg/day), and vehicle were given by gavage to four groups of SHR between 4 and 5 months of age. The aortic angiotensin II level was measured by highly sensitive radioimmunoassay coupled with high pressure liquid chromatography; aortic morphologic studies were performed. Each drug treatment effectively lowered blood pressure to the same level. However, the aortic wall thickness, medial-intimal areas, and wall to lumen ratio of abdominal aorta decreased significantly (p < 0.05, p < 0.01, p < 0.01, respectively) with delapril and manidipine but not hydralazine. Delapril significantly decreased aortic angiotensin II levels (p < 0.05), whereas manidipine treatment significantly increased them (p < 0.05). The aortic angiotensin II level was not changed by hydralazine. These results show that delapril and manidipine caused regression of hypertension-induced vascular hypertrophy in SHR. The probable mechanism of regression of aortic hypertrophy by delapril was inhibition of vascular angiotensin II formation, but the mechanism for manidipine was unclear.

Angiotensin II↗

[Renin gene analysis of familial Bartter's syndrome].

Familial Bartter's syndrome is considered to be an autosomal recessive disease. Because an activation of the renin-angiotensin system is a characteristic feature of this disease, we evaluated a possible changes in renin gene. However, we could not detected any molecular abnormalities of renin gene, i.e. gene duplication, insertion/deletion polymorphism, nor peculiar frequencies of renin RFLPs. For further study, we must collect large numbers of affected families of this disease, and examine more various candidate genes including Cl(-)-transport proteins.

Bartter Syndrome↗

[Abnormalities in acid-base balance in the elderly].

Physiological decline in the ability to adjust acid-base balance and increase the incidence of diseases with aging, modifies pathophysiological and clinical features of acid-base disturbance in the elderly. Regulation of pH ultimately depends on the kidney and lung, however, the ability of the two organs is decreased with physiological aging. Moreover, the elderly are more prone to suffer from renal insufficiency and/or chronic obstructive pulmonary disease. Furthermore, medication with various drugs, such as diuretics, often affect the acid-base balance in the elderly. This paper describes the characteristics of the abnormalities in acid-base balance in the elderly, including metabolic acidosis and alkalosis, and respiratory acidosis and alkalosis.

Acid-Base Imbalance↗

Analysis of the apolipoprotein B3' hypervariable region in patients with essential hypertension.

1. The typing of the apolipoprotein B 3' hypervariable region was investigated in hypertensive and normotensive subjects using rapid typing of a variable number of tandemly repeated short DNA sequences (VNTR) by the polymerase chain reaction. 2. In the DNA samples of 89 normotensive and 99 hypertensive patients, 13 different-sized alleles were detected. The most frequent allele has 35 repeat units in both groups with frequencies of 0.624 and 0.596 in normotensive and hypertensive patients, respectively. Frequency distribution of 13 alleles was similar in both groups. 3. These results demonstrate no association between the apolipoprotein B gene polymorphism and essential hypertension.

Aged↗

EDTA induces differentiation and suppresses proliferation of promyelocytic leukemia cell line HL-60--possible participation of zinc.

Effects of ethylenediaminetetraacetic acid (EDTA), a chelator of divalent cations, on the proliferation and differentiation of human promyelocytic leukemia cell line HL-60 were examined. Incubation of HL-60 cells with 200 microM of EDTA suppressed cell proliferation, and induced differentiation assessed by reductivity of nitro blue tetrazolium and activity of alpha-naphthyl butyrate esterase. These effects were inhibited by zinc (Zn) dose-dependently at concentrations of up to 20 microM, but not by other divalent cations including Ca, Mg, Fe, Cu, Ni, or Cd. Although addition of 200 microM EDTA for 24 hr decreased the c-myc mRNA level of HL-60 cells, coaddition of 20 microM of Zn also reversed this effect on c-myc mRNA level. Treatment with EDTA did not change the half-life time of degradation of c-myc mRNA after addition of actinomycin D (5 micrograms/ml). These findings suggest that Zn deficiency suppresses c-myc gene transcription which is followed by suppression of proliferation and induction of differentiation of HL-60 cells.

Blotting, Northern↗

[Endoscopic treatment of early colorectal cancer].

Early cancer of the colon and rectum is currently treated by endoscopic or surgical resection. We studied the indications for endoscopic treatment of early colorectal cancers (80 lesions) in relation to the size and macroscopic findings. The endoscopic treatment consists of polypectomy for a pedunculated or a sessile polyp and strip biopsy for a plaque-like or a depressive lesion. Microscopic or most small cancers were completely treated endoscopically. From macroscopic findings of the early cancers, type Ip (less than 2cm and 2cm in diameter) was completely treated by polypectomy, type I s and type II a (less than 1cm and 1cm in diameter) by polypectomy or strip biopsy, and type II c (less than 0.5cm and 0.5cm in diameter) by strip biopsy.

Colonic Neoplasms↗

The 717Val----Ile substitution in amyloid precursor protein is associated with familial Alzheimer's disease regardless of ethnic groups.

Alzheimer's disease (AD) is a devastating neurological disorder and the leading cause of dementia among aged individuals. The human amyloid beta protein, which is a cleavage product of amyloid precursor protein (APP), is a major component of the amyloid deposited in the brain of patients with AD. By using PCR direct sequencing of exon 17 (encoding part of the beta protein) of the APP gene, we have found that a Japanese AD patient harbours a C to T substitution, responsible for a valine to isoleucine change at position 717, heterogeneously. The mutation is exactly the same as that found in a Caucasian AD family by Goate et al. (1). Furthermore, the mutation was shown to co-segregate with AD in his family. These results suggest that the Val----Ile change in the APP causes AD, regardless of ethnic background.

Alzheimer Disease↗

Studies on the role of platelet-activating factor in blood pressure regulation.

Circulating levels of 1-O-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine (C16PAF) in human subjects were measured by gas chromatography/mass spectrometry using negative ion chemical ionization. The mean (+/- S.D.) circulating C16PAF levels in patients with essential hypertension (18.1 +/- 5.3 pg/mL, n = 16) were not significantly different from those in normotensive subjects (17.2 +/- 7.2 pg/mL, n = 14). During a salt balance study, high salt intake (20 g/day) significantly increased the circulating level of C16PAF, and changes in circulating C16PAF significantly and positively correlated with changes in mean arterial blood pressure (r = 0.47, p less than 0.05). Changes in C16PAF also correlated with changes in creatinine clearance (r = 0.55, p less than 0.05), but did not correlate with changes in plasma sodium concentration, plasma chloride concentration and plasma volume. An intravenous injection of 50 micrograms of human atrial natriuretic peptide (hANP) decreased circulating C16PAF levels from 20.0 +/- 2.7 to 13.9 +/- 2.4 pg/mL of blood (n = 10, p less than 0.01) in healthy subjects. The data appear to indicate that C16PAF levels are changed by salt intake-induced mild increase in blood pressure, and that hANP may be an endogenous factor which lowers circulating C16PAF.

Atrial Natriuretic Factor↗

Urinary C-peptide as an index of unstable glycemic control in insulin-dependent diabetes mellitus (IDDM)

In order to investigate whether urinary C-peptide (UCP) excretion can be a useful index of insulin-dependent diabetes mellitus (IDDM) with unstable glycemic control, UCP was measured in nine IDDM patients with unstable glycemic control, nine IDDM patients with stable glycemic control, and 12 non-insulin-dependent diabetic (NIDDM) patients treated with insulin. The UCPs in overnight urine (U1) and fasting single void urine (U2) in IDDM patients with unstable glycemic control were significantly lower than those in IDDM patients with stable glycemic control (U1: 0.03 +/- 0.03 vs 0.24 +/- 0.20 nmol/mmol-Creatinine, U2: 0.02 +/- 0.01 vs 0.20 +/- 0.20 nmol/mmol-Cr, mean +/- SD, both P less than 0.01). The UCPs in U1 and U2 in both groups of IDDM were significantly lower than those in NIDDM (U1: 0.97 +/- 0.52, U2: 0.73 +/- 0.41 nmol/mmol-Cr, both P less than 0.01). The UCPs in U1 and U2 significantly correlated with incremental C-peptide response to intravenous glucagon injection and with glycemic stability assessed by the standard deviation of 10 previous fasting plasma glucose levels. These results suggest that UCP reflects their residual insulin secretory capacity and that UCP can be a useful index which distinguishes patients with unstable IDDM from those with stable diabetes mellitus.

Adult↗

Renal handling of glycated albumin in non-insulin-dependent diabetes mellitus with nephropathy.

Renal handling of glycated albumin in diabetic nephropathy was examined by studies on renal selectivity for glycated albumin in 23 normal controls and 52 patients with non-insulin-dependent diabetes mellitus (NIDDM) with various degrees of nephropathy. The serum and urinary levels of glycated albumin were measured by enzyme-immunoassay with monoclonal antibody to glucitol-lysine residues in human glycated albumin. The diabetic patients were divided into 3 groups according to the albumin index (AI): patients with normoalbuminuria [AI less than or equal to 30 mg/g creatinine(Cr)], with microalbuminuria (30 less than AI less than or equal to 270 mg/g Cr), and with macroalbuminuria (AI greater than 270 mg/g Cr). The renal selectivity for glycated albumin was calculated from the ratio of the urinary to serum level of glycated albumin. In the controls, the renal selectivity was as high as 4.40 +/- 0.48, and significantly higher than those in patients with normo- (2.87 +/- 0.29), micro- (1.72 +/- 0.20) and macroalbuminuria (1.26 +/- 0.23). The renal selectivity was inversely correlated with the AI in diabetic patients (r = -0.58, P less than 0.01). These data indicate that glycated albumin was selectively excreted in the urine and that the renal selectivity in diabetic patients gradually decreased to a value of 1 with increase in albuminuria. When the patients with normoalbuminuria were divided into two subgroups with high and low albumin excretion, the renal selectivities for glycated albumin in both subgroups were still significantly lower than that in controls. These results suggested that early diabetic nephropathy which cannot be detected clinically by albuminuria can be diagnosed by measurement of renal selectivity for glycated albumin.

Aged↗

Two-dimensional computer color graphics of gastric mucosal blood distribution in normal subjects and ulcer patients.

The mucosal blood volume in 20 to 24 different regions of stomach was estimated by reflectance spectrophotometry during endoscopy, and an image showing mucosal blood distribution was made by two-dimensional computer color graphics with the aid of a personal computer. In 55 normal controls, the estimated mucosal blood volume (EMBV) was greater in the corpus mucosa than in the antral mucosa, and less in the lesser curvature than in the greater curvature. The volume in the anterior and posterior walls was almost the same. In 15 patients with active gastric ulcers in the angular region, the EMBV was decreased in all regions in the stomach. In 37 patients with healing ulcers, the EMBV increased, resuming the same levels as in normal controls. However, the EMBV around the ulcer increased remarkably at this stage. In 35 patients with ulcers in the scarring stage, the distribution of the EMBV was similar to that in the normal controls. These hemodynamic changes were shown clearly in a color display with the aid of a personal computer. This method could offer new possibilities in endoscopic research.

Adult↗