Biomedical subjects

K Abe

Publications and source records attributed to K Abe.

At least 901 records · Page 50Linked to original sources

PubMed1997

Developmental changes in the contractile system of the mesenteric small artery of rabbit.

This study investigated developmental changes in the contractile system of the mesenteric small arteries of the rabbit. Arteries about 1 mm in length and 100-250 microns in internal diameter were dissected out from the mesenteric bed of the fetus (29 d of gestation), newborn (3-5 d old), and adult rabbit. Vascular contraction was induced by high KCl concentration, and contractile force was measured using a tension transducer. The sensitivity of vascular contraction to high KCl was similar in the three age groups. To determine the role of Ca influx across the sarcolemma in vascular contraction, the vasorelaxant effect of diltiazem was studied in the artery precontracted with high KCl concentration. The vasorelaxant effect of diltiazem in the fetus and newborn was less than in the adult. To estimate the size of the intracellular Ca pool, caffeine-induced and noradrenaline-induced contraction were measured in the Ca- and Na-free solution. In the fetus and newborn, both the caffeine-induced contraction and noradrenaline-induced contraction were greater than in the adult. The ultrastructural study showed that the endoplasmic reticulum was abundant in the fetus and newborn, and it was scarce in the adult. These data indicate that the dependency of vascular contraction on Ca influx across the sarcolemma increases and the intracellular Ca store decreases with development in the mesenteric resistance arteries.

Aging↗

PubMed1997

Retinoid X receptors in the kidney: their protein expression and functional significance.

Retinoid X receptors (RXRs) heterodimerize with 1,25-dihydroxyvitamin D3 (VD) receptor (VDR), and play important roles in VD-regulated transactivation. VD acts on many tissues including kidney for the regulation of calcium homeostasis. In the kidney, the expression of VDR in the tubular cells has been well studied. In contrast, little is known about the localization and the functional significance of RXRs there. In order to elucidate these questions, we first performed immunohistochemical analyses of rat kidney using isoform-specific antimouse RXR antibodies we have previously reported. Interestingly, all RXR isoforms, predominantly RXR alpha, mainly localized to the proximal and the distal tubules, but not to the glomeruli. The serial section staining using anti-VDR antibody showed the colocalization of RXR alpha and VDR in those tubular cells. In order to elucidate the functional significance of endogenous receptors in the tubular cells, we next performed transient transfection studies using the tubular-cell derived Madin-Darby bovine kidney cells, which express both endogenous VDR and RXR. We transfected a reporter plasmid containing direct repeat 3 (DR3) sequence, to which only RXR/VDR heterodimer can bind, and found that VD and 9-cis retinoic acid, as well as VD and RXR selective agonist LG100153, had an additive effect for the DR3 transactivation. Taken together, we speculate that endogenous RXRs co-localize with VDR, and coregulate VD-dependent genes in the tubular cells of the kidney as RXR/VDR heterodimer.

Animals↗

PubMed1997

Acute aquaresis by the nonpeptide arginine vasopressin (AVP) antagonist OPC-31260 improves hyponatremia in patients with syndrome of inappropriate secretion of antidiuretic hormone (SIADH).

The present study was undertaken to determine whether the non-peptide V2 arginine vasopressin (AVP) antagonist 5-dimethylamino- 1[4-(2-methylbenzoylamino)benzoyl]-2,3,4,5-tetrahydro-1H-benzazepi ne hydrochloride (OPC-31260) produces water diuresis and improves hyponatremia in patients with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Eleven patients (9 males and 2 females, 64 +/- 3.5 yr) with SIADH were included in the present protocol, which was comprised of 3 successive days. Day 1 was a control day, and on days 2 and 3 OPC-31260 was administered intravenously. Five blood and urine collections were made at 1-2 h intervals during the 6 h observation period each day. A single administration of 0.25 and 0.5 mg/kg OPC-31260 increased the 4 h cumulative urine volume and decreased urinary osmolality to below 225 mOsm/kg H2O. Such a diuretic effect was independent of an increase in urinary solute excretions. This aquaresis by 0.5 mg/kg OPC-31260 caused a significant increase in serum sodium level by approximately 3 mEq/L. The antagonistic effect of OPC-31260 lasted for 4 h when it was given intravenously. These results indicate that OPC-31260 is an effective therapeutic agent for hyponatremia in patients with SIADH.

Aged↗

PubMed1997

A presenilin-1 mutation in a Japanese family with Alzheimer's disease and distinctive abnormalities on cranial MRI.

Some patients with familial Alzheimer's disease (FAD) have mutations in the presenilin-1 (PS-1) gene on chromosome 14. We report a Japanese family with AD and an Ala285Val substitution in exon 8 of the PS-1 gene. FAD in this family was characterized by relatively late onset (mean age, 50 years) and absence of myoclonus, seizures, or paratonia. Levels of tau were markedly elevated in CSF whereas CSF levels of amyloid beta protein were normal. MRI of the cranium showed marked linear signal abnormalities within white matter in the parieto-occipital lobes, consistent with cortical amyloid angiopathy of the type encountered in patients with the PS-1 gene mutation.

Alzheimer Disease↗

PubMed1997

Measurement of tissue oxygen consumption in patients with mitochondrial myopathy by noninvasive tissue oximetry.

We measured oxygen consumption in the exercising lower limb by using noninvasive tissue oximetry with the near-infrared spectra of hemoglobin in the quadriceps muscle during bicycle ergometer exercise in four normal controls and three patients with chronic progressive external ophthalmoplegia (CPEO) as well as one patient with mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS). Normal controls showed constant oxygenation during exercise and a rapid recovery after exercise. However, all four patients with mitochondrial myopathy showed abnormal oxygenation during exercise and a slow recovery afterward. The results reflected the defect in oxidative phosphorylation and the impairment in oxygen utilization in those patients. The distinctive patterns of imbalance between oxygen delivery and utilization correlated well with the severity of mitochondrial myopathy as judged by the sum of the serum lactate and pyruvate content during exercise. Noninvasive tissue oximetry may be useful to measure the severity of myopathy and exercise intolerance in patients with mitochondrial myopathy.

Adult↗

PubMed1997

Cimetidine inhibits the induction of long-term potentiation in the dentate gyrus of rats in vivo.

We investigated the effect of cimetidine, a clinically used H2-receptor antagonist, on the induction of long-term potentiation (LTP) in the dentate gyrus of anesthetized rats. Intracerebroventricular injection of cimetidine (50-100 nmol) inhibited the induction of LTP in a dose-dependent manner. The inhibitory effect of cimetidine was not mimicked by other H2-receptor antagonists (ranitidine, famotidine) or the H1-receptor antagonist diphenhydramine or the H3-receptor antagonist thioperamide. These results suggest that cimetidine inhibits hippocampal synaptic plasticity by a novel brain mechanism unrelated to H1, H2 or H3 receptors.

Animals↗

PubMed1997

Developmental changes in cyclic AMP-stimulated stellation of cultured rat cortical astrocytes.

When cultured astrocytes are treated with agents that elevate intracellular cyclic AMP, they become process-bearing stellate cells. In the present study, we investigated possible developmental changes of astrocyte stellation induced by beta-adrenoceptor stimulaton. Cultured astrocytes were prepared from the cerebral cortices of embryonic day 18 (E18) and postnatal day 2 (P2) rats. Treatment with the beta-adrenoceptor agonist isoproterenol induced stellation in P2 astrocytes more potently and rapidly than in E18 astrocytes. Isoproterenol-stimulated increase in cellular cyclic AMP levels was very similar in E18 and P2 astrocytes. The membrane-permeable cyclic AMP analog dibutyryl cyclic AMP induced stellation in P2 astrocytes more potently and rapidly than in E18 astrocytes. Stellation induced by the protein kinase C activator phorbol ester was not different between E18 and P2 astrocytes. These results suggest that beta-adrenoceptor-mediated astrocyte stellation increases during development and that this change is attributed to the development of mechanisms downstream from cyclic AMP production.

Adrenergic beta-Agonists↗

PubMed1997

Purification and properties of two isozymes of gamma-glutamyltranspeptidase from Bacillus subtilis TAM-4.

Two isozymes of gamma-glutamyltranspeptidase, GGT-A and GGT-B, were purified to electrophoretic homogeneity from a culture broth of Bacillus subtilis TAM-4, which produces poly(gamma-glutamic acid) (PGA) de novo. GGT-A was composed of three subunits with molecular weights of 23,000 (I), 39,000 (II), and 40,000 (III). GGT-B was composed of two subunits with molecular weight of 22,000 (I) and 39,000 (II). The N-terminal amino acid sequences of GGT-A subunit I and GGT-B subunit I were very similar. GGT-A subunit II and GGT-B subunit II had an identical N-terminal amino acid sequence. That of GGT-A subunit III showed no similarity to the other subunits. Both GGTs had similar enzymatic properties (optimum pH and temperature: pH 8.8 and 55 degrees C) but showed a significantly different thermal stability at 55 degrees C. Both GGT-A and -B used D-gamma-glutamyl-p-nitroanilide as well as the L-isomer as the gamma-glutamyl donor and used various amino acids and peptides as the acceptor. It was also found that the PGA produced by the strain was hydrolyzed to glutamic acid by its own GGTs.

Amino Acid Sequence↗

PubMed1997

The kidney and hypertension.

The kidney is important not only as a target organ of hypertension but also as a organ that may cause hypertension. For many years, we have studied basic and clinical aspects of the role of the kidney in hypertension, including the renin-angiotensin, kallikrein-kinin, and prostaglandin systems, glomerular hemodynamics, therapeutic modalities, and prognosis. This review summarizes some of our results together with those of other relevant studies in the literature.

Animals↗

PubMed1997

Plasma chromogranin A in pheochromocytoma, primary hyperparathyroidism and pituitary adenoma in comparison with catecholamine, parathyroid hormone and pituitary hormones.

Plasma levels of chromogranin A (CgA) were measured by ELISA in 22 patients with pheochromocytoma (18 non-metastatic, 3 metastatic, and 1 mixed neuroendocrine-neural tumor), 9 patients with primary hyperparathyroidism, and 9 patients with pituitary adenoma. The plasma levels of CgA were compared with norepinephrine, epinephrine, parathyroid hormone and pituitary hormones, i.e., growth hormone and prolactin. In pheochromocytoma, CgA in preoperative plasma of the patients without metastasis was 228 +/- 38 U/L (mean +/- SEM) and significantly higher than healthy controls (30 +/- 11 U/L, n = 40). Plasma CgA was decreased after removal of the tumors (28 +/- 6.0 U/L), except in three patients with metastatic pheochromocytoma and a mixed neuroendocrine neural tumor. The concentration of CgA in the patients with non-metastatic pheochromocytoma was significantly correlated with that of plasma norepinephrine (P < 0.005, r = 0.68) and urinary norepinephrine (P < 0.05, r = 0.65), but not with that of epinephrine. There was an exceptional case in which CgA was extremely high, but the CA level was normal. This tumor was a highly malignant pheochromocytoma with extensive metastases composed of small tumor cells which were occasionally positive for tyrosine hydroxylase immunohistochemically. These cells were considered to be poorly differentiated tumor cells and synthesized a very small amount of norepinephrine. Plasma levels of the patients with primary hyperparathyroidism and the patients with pituitary adenoma were 44 +/- 4 U/L and 48 +/- 8 U/L, respectively. Only one patient with a growth hormone-producing pituitary adenoma had a high level of CgA. Plasma CgA is a useful tumor marker for pheochromocytoma, even for malignant pheochromocytoma without elevated CA level, but not for hyperparathyroidism, or pituitary adenoma.

Adenoma, Acidophil↗

PubMed1997

Impaired vasopressin suppression and enhanced atrial natriuretic hormone release following an acute water load in primary aldosteronism.

The release of arginine vasopressin (AVP) and atrial natriuretic hormone (ANH) and their involvement in renal water and electrolyte metabolism in primary aldosteronism in humans were studied. An oral acute water load (20 ml/kg body weight) was given to each of 12 patients before and after surgical removal of their aldosterone-producing adenoma(s). Plasma AVP and ANH were measured simultaneously, and renal water and electrolyte metabolism and tubular functions were determined. The same water load was given to seven normal subjects and the same parameters were determined. In the presence of mineralocorticoid excess before the operation, plasma AVP was relatively low compared with plasma osmolality (Posm), but was not suppressed in response to decreases in Posm after the water load. Baseline plasma ANH was high and increased further after the water load; urinary dilution and diuresis both remained normal. After the operation, baseline plasma AVP was normal and decreased in response to the decrease in Posm after the water load, with normal urinary dilution and diuresis. Baseline plasma ANH was normal, and did not increase after the water load. The ratio of urinary K and Na clearances and distal tubular reabsorption of Na increased before the operation. These results suggest that there are perturbations of AVP and ANH release in primary aldosteronism, despite the normal urinary dilution after a water load.

Adenoma↗

PubMed1997

Clinical and molecular analysis of neurodegenerative diseases.

Clinical and molecular analyses of neurodegenerative diseases such as Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), and spinocerebellar ataxia type 1 (SCA1) were performed. In the present study, a Japanese family of AD with an Ala285Val substitution in exon 8 of the presenilin-1 (PS-1) gene was found. This family was characterized by relatively late onset (mean age at 50 years) in familial AD with PS-1 gene mutation and by absence of myoclonus, seizure or paratonia. Magnetic resonance image (MRI) study showed marked linear signal abnormalities in white matter of parietoocctipital lobes, suggesting a presence of cortical amyloid angiopathy of the patient with PS-1 gene mutation. Clinical characteristics of familial amyotrophic lateral sclerosis (FALS) with four different missense point mutations in exons 2, 4, and 5 of the Cu/Zn superoxide dismutase (SOD) gene were reported. Although features of progressive neurogenic muscular atrophy was common in patients of these families, patients of each family showed characteristic clinical features. Although lower motor sign was evident in all cases, hyperreflexia varied from 0 to 100% among patients with the different mutations, and Babinski sign was not observed in any cases. Bulbar palsy was frequent with a mutation, but not present with another mutation. SOD activity of red blood cells was generally reduced with minor variations. CAG trinucleotide repeat expansion was analyzed in 25 families with hereditary ataxia of Menzel type in the northeast of Japan. Twenty of 38 patients in 12 families had expanded allele for spinocerebellar ataxia type 1 (SCA1). Study of the number of CAG repeats in various tissues showed no differences in the repeat length in lymphocytes, muscle or brain; sperm, however, showed an obvious expansion. This may be a clue to a possible mechanism for the molecular basis of paternal anticipation of the disease. These results suggest that clinical features of some familial cases of neurodegenerative diseases such as AD, ALS, and SCA1 are well correlated with their genetic mutations.

Alzheimer Disease↗

PubMed1997

Detection of mineral density on the surface of mouse parietal bones: backscattered electron imaging of low accelerating voltage scanning electron microscopy.

Backscattered electron (BSE) imaging of scanning electron microscopy (SEM) was applied to a study on the mineral density of the bone surface. The neonatal and adult mouse parietal bones freed of the periosteum and covering cells were examined in a field emission scanning electron microscope equipped with a high sensitivity BSE detector at 1-30 kV accelerating voltages. The mineral density of the bone surface was observable in BSE images at 5 kV accelerating voltage while only the topographic structures of the surface were obtained under an accelerating voltage less than 5 kV. As the accelerating voltages increased from 5 kV, the bright areas were extended, probably due to the imaging of the calcified bone matrix under the uncalcified osteoid. The bone surface is usually divided into smooth and rough areas according to its irregularities. BSE images at 5 kV clearly showed that the smooth areas were further divided into dark and bright areas which apparently corresponded to the uncalcified osteoid and calcified bone matrix, respectively. Bright granules, about 1.0-3.0 microns in diameter, were sometimes observed at the border between the osteoid and calcified bone matrix; these granular calcified areas were regarded as the calcifying front forming the calcified bone matrix from the osteoid. The present study demonstrated that the distribution of the osteoid on the mouse parietal bone surface changes depending on age: the osteoid occupied a large area in the parietal bone surface in neonatal mice, but was small in adult mice. Thus, low accelerating voltage SEM using BSE provides new information on the distribution of the osteoid and the bone matrix calcification under both normal and pathological conditions.

Aging↗

PubMed1997

Involvement of IL-4 in human glomerulonephritis: an in situ hybridization study of IL-4 mRNA and IL-4 receptor mRNA.

Interleukin-4 (IL-4) has been recently implicated in the pathogenesis of glomerulonephritis. However, the expression of IL-4 and IL-4 receptor (IL-4R) in human kidney has not been fully determined. Nonradioactive in situ hybridization was used to examine the expression of IL-4 mRNA and IL-4R mRNA in tissues from normal kidneys and specimens from a variety of human kidney diseases. In normal glomeruli, a few mesangial cells and cells of the Bowman's capsule weakly expressed IL-4 and IL-4R mRNA, whereas in diseased glomeruli both mRNA types were strongly expressed in resident glomerular cells, including mesangial cells, glomerular epithelial cells, and cells of the Bowman's capsule. The relationship between the expression of these mRNA and the degree of glomerular injury was different in different types of glomerulonephritis. In IgA nephropathy and non-IgA mesangial proliferative glomerulonephritis, IL-4 expression correlated positively with the degree of mesangial hypercellularity and extracellular matrix expansion. However, IL-4R expression was relatively constant. In contrast, the expression of IL-4 and IL-4R mRNA correlated negatively with the degree of glomerular injury in lupus nephritis. Coexpression and discordant expression of these mRNA forms were observed in individual cells. In tubulointerstitium with severe lesions, IL-4 mRNA and IL-4R mRNA were observed in atrophic tubules and some of the infiltrating cells and fibroblasts. The interstitial expression of these mRNA forms was similar in IgA nephropathy, non-IGA mesangial proliferative glomerulonephritis, and lupus nephritis and correlated positively with the degree of tubulo-interstitial changes. These results suggest that an autocrine and/or paracrine pathway of IL-4 is present in human diseased kidneys and that IL-4 may be involved in tissue injury in glomerulonephritis.

Adult↗

PubMed1997

Apolipoprotein E Sendai (arginine 145-->proline): a new variant associated with lipoprotein glomerulopathy.

Lipoprotein glomerulopathy (LPG) is a novel disease characterized by proteinuria, lipoprotein thrombi in the glomeruli, and increased concentration of plasma apolipoprotein (apo) E. It is believed that a genetic disorder of apo E may be present and associated with the disease. Three patients with LPG were examined in this study. The patients' DNA sequences were analyzed, and a nucleotide G to C point mutation in exon 4 of the apo E gene was confirmed in each patient. This missense mutation denotes amino acid substitution of the proline residue for arginine residue at position 145 of apo E. This variant (apo E Sendai) may cause a marked molecular conformational change of the apo E. These findings suggest that a novel variant is etiologically related to LPG.

Aged↗

PubMed1997

Chronic inflammatory demyelinating polyneuropathy accompanied by hepatocellular carcinoma.

We report a patient with chronic inflammatory demyelinating polyneuropathy (CIDP) accompanied by hepatocellular carcinoma (HCC). Due to the remarkable weakness in the lower limbs and loss of the position sense, he could not walk. On neurophysiological examination, he had impaired nerve conduction velocities. Biopsied nerve and muscle specimens demonstrated demyelination of nerve fibers and neurogenic degeneration of muscles. After steroid therapy he showed marked improvement in muscle strength and sensory function.

Anti-Inflammatory Agents↗

PubMed1997

Three cases of Gitelman's syndrome possibly caused by different mutations in the thiazide-sensitive Na-Cl cotransporter.

Three adult Japanese cases of Gitelman's syndrome were characterized by secondary aldosteronism, hypokalemic alkalosis, hypomagnesemia, and hypocalciuria. Two were revealed to be familial cases. A mutation in the thiazide-sensitive Na-Cl cotransporter gene, which had already been confirmed in one family (Takeuchi et al. J Clin Endocrinol Metab 81: 4496,1996), was not detected in the other two cases. These observations may possibly support the previous report (Simon et al. Nature Genet 12: 24, 1996) that Gitelman's syndrome is caused by a variety of mutations in the thiazide-sensitive Na-Cl cotransporter.

Aged↗

PubMed1997

[Single photon emission computed tomography in the diagnosis of Alzheimer's disease].

Studies with single photon emission computed tomography (SPECT) have shown temporoparietal (TP) hypoperfusion in patients with Alzheimer's disease (AD). We evaluated the utility of this findings in the diagnosis of AD. SPECT images with 123I-iodoamphetamine were analyzed qualitatively by a rater without knowledge of the subject's clinical status. Sixty-seven of 302 consecutive patients were judged as having TP hypoperfusion by SPECT imaging. This perfusion pattern was observed in 44 of 51 patients with AD, in 5 with mixed dementia, 8 with cerebrovascular disease (including 5 with dementia), 4 with Parkinson's disease (including 2 with dementia), 1 with normal pressure hydrocephalus. 1 with slowly progressive aphasia. 1 with progressive autonomic failure, 2 with age associated memory impairment, and 1 with unclassified dementia. The sensitivity for AD was 86.3% (44 of 51 AD), and the specificity was 91.2% (229 of 251 non-AD). Next, we looked for differences in perfusion images between patients with AD and without AD. Some patients without AD had additional hypoperfusion beyond TP areas: deep gray matter hypoperfusion and diffuse frontal hypoperfusion, which could be used to differentiate them from the patients with AD. Other could not be distinguished from patients with AD by their perfusion pattern. Although patients with other cerebral disorders occasionally have TP hypoperfusion, this finding makes the diagnosis of AD very likely.

Adult↗