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Biomedical subjects

K Tsuchiya

Publications and source records attributed to K Tsuchiya.

At least 235 records · Page 13Linked to original sources
PubMed1998

[A case of glioblastoma manifesting 49 years after lobotomy].

We report a case of glioblastoma manifesting 49 years after a lobotomy. He was diagnosed as having schizophrenia at age 20 and was operated on with a standard lobotomy when he was 27 years old. He had led a useful life after 40 years old without medication. Because of hallucination and delusion, he was hospitalized at the end of 1996. CT showed a well enhanced tumor adjacent to the cavity made by the lobotomy in the left frontal lobe. This is the second case report of glioblastoma just beside the cavity formed by lobotomy. The relationship between glioblastoma and old lobotomy is discussed, especially in regard to morphology and CT findings.

Aged↗
PubMed1997

Roles of heme oxygenase/carbon monoxide system in genetically hypertensive rats.

Although carbon monoxide (CO) has been suggested to be involved in the regulation of cardiovascular function through activation of soluble guanylyl cyclase, the pathophysiological significance in hypertension remains unknown. We therefore examined the effects of heme oxygenase (HO) inhibitor zinc protoporphyrin IX (ZnPP-IX) on blood pressure and determined HO mRNA expression level in various tissues in stroke-prone spontaneously hypertensive rats (SHR-SP/Izm) and Wistar Kyoto rats (WKY/Izm). Although ZnPP-IX significantly increased systolic blood pressure in both strains, the increment of blood pressure was larger in SHR-SP/Izm than in WKY/Izm. An essentially similar increase of blood pressure was demonstrated even in the ganglion blocker-pretreated rats. Constitutive type HO-2 mRNA levels in the aorta and kidney and inducible type HO-1 mRNA levels in the cardiac ventricle were significantly increased in SHR-SP/Izm compared with WKY/Izm. Clearly these results indicate the importance of the endogenous HO/CO system in the peripheral tissues in genetically hypertensive rats.

Animals↗
PubMed1997

Atrial natriuretic peptide stimulates Na+-dependent Ca2+ efflux from freshly isolated adult rat cardiomyocytes.

In the present study, we examined the effect of atrial natriuretic peptide (ANP) on Ca2+ efflux from freshly isolated adult rat cardiomyocytes. Rat ANP(1-28) stimulated the efflux of 45Ca2+ from the cells in a concentration-dependent manner (10(-8) M to 10(-6) M). The 45Ca2+ efflux was not affected by removal of extracellular Ca2+, but was dependent on the presence of extracellular Na+. In addition, rat ANP(1-28) caused 22Na+ influx into the cells. The 45Ca2+ efflux was also stimulated by C-type natriuretic peptide-22 (CNP-22), but not by rat brain natriuretic peptide-45 (BNP-45). It was also observed that both rat ANP(1-28) and CNP-22 stimulated guanosine 3',5'-cyclic monophosphate production within the cells. These results indicate that ANP stimulates Na+-dependent 45Ca2+ efflux from freshly isolated adult rat cardiomyocytes, probably through Na+/Ca2+ exchange, and that the stimulatory effect of ANP on Ca2+ efflux may be mediated via the natriuretic peptide receptor which has been shown to couple to guanylate cyclase. Since it is reported that Na+/Ca2+ exchange is important in calcium homeostasis within cells, ANP may play a role in the extrusion of intracellular Ca2+ from isolated adult rat cardiomyocytes.

Animals↗
PubMed1997

Serial brain CT in corticobasal degeneration: radiological and pathological correlation of two autopsy cases.

This report concerns serial brain computed tomography (CT) images in two patients with corticobasal degeneration (CBD). The diagnosis of CBD was confirmed by neuropathological examination. In one case, we obtained serial brain CT images for one year and five months, and in the other, for three years and four months. The CT images showed that the anterior portions of the cerebrum atrophied progressively with the length of the disease. This was also seen in the CT images with respect to the caudate nucleus. Regarding radiological and pathological correlations, we consider that the progressive atrophy of the anterior portions of the cerebrum, seen in brain CT images, is ascribed to neuronal loss and gliosis in the anterior portions of the cerebrum. We also believe that the observed caudate nucleus atrophy is due to loss of neurons and gliosis in this structure, and also to the fibrillary gliosis of the cerebral white matter. The progressive atrophy of the caudate nucleus detected in brain CT is a valuable feature for the neuroradiological diagnosis of CBD.

Aged↗
PubMed1997

Functional compartmentalization of ATP is involved in angiotensin II-mediated closure of cardiac ATP-sensitive K+ channels.

BACKGROUND: The effects of angiotensin II (Ang II) on ATP-sensitive K+ channels (K(ATP)) were investigated in ventricular myocytes enzymatically isolated from adult guinea pig heart. METHODS AND RESULTS: In the whole-cell and cell-attached configurations (including open-cell-attached mode) of the patch-clamp technique, K(ATP) currents (I(KATP)) were activated through metabolic poisoning by the use of inhibitors of both glycolytic and oxidative ATP productions at 37 degrees C. In the whole-cell mode, I(KATP) were reversibly suppressed by increasing extracellular glucose and Ang II (1 nmol/L). In the cell-attached mode, Ang II concentration-dependently inhibited single K(ATP) activities with an IC50 value of 3.2+/-0.5 pmol/L (Hill coefficient=1.3+/-0.3). CV11974 (100 nmol/L), an angiotensin 1 (AT1) receptor-selective antagonist, blocked the inhibitory action of Ang II. Preincubation of myocytes with pertussis toxin (5 microg/mL for > 120 min at 37 degrees C) virtually prevented subsequent Ang II action. The inhibitory effect of Ang II was also abolished in the open-cell-attached mode (achieved by a prior perfusion of streptolysin-O, 0.08 U/mL). In this mode, through tiny membrane holes, the intracellular ATP concentration can be controlled by bathing extracellular solutions containing a known ATP concentration. CONCLUSIONS: The inhibitory actions of Ang II on K(ATP) appear to be mediated by an increase in the subsarcolemmal ATP concentration that results from the inhibition of adenylate cyclase activities via AT1 receptors/PTX-sensitive G proteins.

Adenosine Triphosphate↗
PubMed1997

Evidence of evolutionary up-regulation of the single active X chromosome in mammals based on Clc4 expression levels in Mus spretus and Mus musculus.

Previous studies have shown that the chloride channel gene Clc4 is X-linked and subject to X inactivation in Mus spretus, but that the same gene is autosomal in laboratory strains of mice. This exception to the conservation of linkage of the X chromosome in one of two interfertile mouse species was exploited to compare expression of Clc4 from the X chromosome to that from the autosome. Clc4 was found to be highly expressed in brain tissues of both mouse species. Quantitative analyses of species-specific expression of Clc4 in brain tissues from mice resulting from M. spretus x laboratory strain crosses, demonstrate that each autosomal locus has half the level of Clc4 expression as compared with the single active X-linked locus. In contrast expression of another chloride channel gene, Clc3, which is autosomal in both mouse species is equal between alleles in F1 animals. There is no evidence of imprinting of the Clc4 autosomal locus. These results are consistent with Ohno's hypothesis of an evolutionary requirement for a higher expression of genes on the single active X chromosome to maintain balance with autosomal gene expression [Ohno, S. (1967) Sex Chromosomes and Sex-Linked Genes (Springer, Berlin)].

Animals↗
PubMed1997

Operation of an X-ray undulator in the Tristan main ring as a prototype of future super light sources.

A 5.4 m-long 239-pole undulator comprising three rigid and precise standardized-unit undulators was completed and installed in the Tristan main ring, which was operated as a light source at a beam energy from 8 to 10 GeV. This undulator was successfully tested, characterized and used as a brilliant hard X-ray source for several synchrotron radiation experiments during the last 3.5 months of 1995.

Journal Article↗
PubMed1997

Angiotensin II inhibits protein kinase A-dependent chloride conductance in heart via pertussis toxin-sensitive G proteins.

BACKGROUND: Angiotensin II receptors are reported to be abundant in the guinea pig ventricle; their coupling to adenylate cyclase in the heart, however, remains controversial. Therefore, we investigated the effect of angiotensin II on Cl- conductance activated by cAMP-dependent protein kinase. METHODS AND RESULTS: After minimizing the contribution of other ionic currents, exposure of single guinea pig ventricular cells to isoproterenol (40 to 50 nmol/L; 36 degrees C) elicited a typical protein kinase A-dependent Cl- conductance. Subsequent application of angiotensin II reduced the isoproterenol-induced conductance with an IC50 of 0.24 +/- 0.08 nmol/L. Angiotensin II also inhibited the Cl- currents, which were activated through stimulation of adenylate cyclase by forskolin and histamine receptors. CV-11974 (1 mumol/L), an antagonist selective for the angiotensin type 1 receptor, prevented the effect of angiotensin II. Angiotensin II did not inhibit the current that had been persistently activated by intracellular GTP gamma S (100 mumol/L), a nonhydrolyzable guanine nucleotide, plus isoproterenol. In addition, prior incubation of myocytes with pertussis toxin prevented the angiotensin II inhibitory action. Cl- conductance, when activated directly by intracellular dialysis with cAMP (1 mmol/L), was not affected by angiotensin II. Radioimmunologic measurement of cellular cAMP in the dissociated myocytes showed that angiotensin II inhibited the isoproterenol-induced increase of cAMP. CONCLUSIONS: Angiotensin II receptors negatively couple to adenylate cyclase via pertussis toxin-sensitive G proteins, thereby inhibiting cardiac protein kinase A-dependent Cl- conductance.

Adenylate Cyclase Toxin↗
PubMed1997

Osteoarthritis: differential expression of matrix metalloproteinase-9 mRNA in nonfibrillated and fibrillated cartilage.

Expression of matrix metalloproteinase-9 mRNA in osteoarthritic and normal cartilage was analyzed using reverse transcription-polymerase chain reaction and in situ hybridization. Fifty-four osteoarthritic cartilage samples were obtained from 24 patients undergoing total knee arthroplasty. Sixteen normal cartilage samples were obtained from non-osteoarthritic knees of four autopsy cases. With normal cartilage, reverse transcription-polymerase chain reaction analysis for matrix metalloproteinase-9 mRNA showed that chondrocytes exhibited only a trace signal. In analysis of osteoarthritic cartilage, chondrocytes of moderately and severely fibrillated cartilage exhibited a 73-fold and 110-fold increase in matrix metalloproteinase-9 mRNA signal, respectively, relative to normal cartilage. Chondrocytes of nonfibrillated osteoarthritic cartilage exhibited a 6-fold increase (p < 0.02) in matrix metalloproteinase-9 mRNA signal relative to normal cartilage. Analysis of matrix metalloproteinase-9 mRNA expression in fresh-frozen sections of normal and osteoarthritic cartilage by in situ hybridization confirmed these results. This study showed that reverse transcription-polymerase chain reaction provides a sensitive index of mRNA levels in normal and osteoarthritic cartilage samples and suggests that increased expression of matrix metalloproteinase-9 precedes fibrillation of cartilage in the development of osteoarthritis.

Aged↗
PubMed1997

Distribution of cerebral cortical lesions in corticobasal degeneration: a clinicopathological study of five autopsy cases in Japan.

We investigated five Japanese patients with autopsy-proven corticobasal degeneration (CBD) both clinically and pathologically, and examined the distribution of their cerebral cortical lesions in hemisphere specimens. The lesions were classified into three categories (slight, moderate and severe). Only two of our patients had clinical features considered to be typical of CBD. Severe lesions were present in the posterior portions of the frontal lobe, anterior to the precentral gyrus in two patients with the clinical diagnosis of CBD. By comparison, in two patients with clinically diagnosed frontal Pick's disease, and one with the clinical diagnosis of progressive supranuclear palsy (PSP), severe lesions were seen in the anterior portions of the frontal lobe. The primary motor area of all five had mostly slight to moderate lesions. We postulate that the clinical features of CBD have a much wider spectrum than previously believed. Our data also indicate that the lesion responsible for limb-kinetic apraxia in CBD is in the premotor cortex. We suggest that when the anterior portions of the frontal lobe are damaged, the clinical picture mimics those of Pick's disease and PSP. In addition, we consider that focal cerebral atrophy of CBD is multicentric.

Aged↗
PubMed1997

Analysis of sweat evaporation from clothing materials by the ventilated sweat capsule method.

The local influence of three clothing materials i.e. silk, cotton and nylon, in (1) full or (2) partial skin contact or (3) at 3 mm from the skin, on sweat evaporation from the chest skin surface of human subjects was studied. The hygrometer-ventilated capsule method was used and sweating was induced at ambient thermoneutrality by a central heat load following lower-leg immersion in water at 43 degrees C. The presence of clothing delayed the rise in capsule relative humidity (CRH) induced by heat loading. During the first 6 min of heating, CRH rose more steeply with clothing that was in full skin contact than with clothing that had partial or no contact. The rate of decrease in CRH from 1 min to 6 min after heating was not influenced by the presence of clothing or by the different degrees of skin contact. The subsequent return of CRH to the pre-heating level was delayed most by cotton, less by silk and least by nylon. For silk and nylon, partial contact with the skin prolonged the return to control conditions, as compared with full skin contact.

Adult↗
PubMed1997

Endothelin-1 inhibition of cardiac ATP-sensitive K+ channels via pertussis-toxin-sensitive G-proteins.

OBJECTIVE: Secretion of endothelin-1 (ET-1) and activation of cardiac ATP-sensitive K+ (KATP) channels are facilitated under myocardial metabolic stress. The aim of this study was to investigate the effects of ET-1 on KATP channels and to assess underlying mechanisms in ventricular myocytes. METHODS: Single channel currents were measured with the voltage-clamp technique in cell-attached patches from enzymatically-isolated single guinea pig ventricular myocytes. In some experiments, the open-cell-attached mode was employed by permeating the membrane with streptolysin-O. RESULTS: ET-1 concentration-dependently inhibited single KATP channel currents, which had been activated by metabolic poisoning, with an IC50 of 3.8 +/- 0.7 pM. BQ-123, an ETA receptor-selective antagonist, reduced the effects of ET-1. ET-1 effects were largely abolished in the myocytes pre-incubated with pertussis toxin. In the open-cell-attached mode, where the intracellular ATP concentration ([ATP]) could be virtually controlled, the effects of ET-1 were abolished. Muscarinic receptor stimulation inhibited the channels in a similar manner to ET-1, whereas beta-adrenoceptor stimulation accelerated channel activation. By analogy, ouabain also inhibited KATP channel activity under metabolic stress presumably because inhibition of the Na+/K+ pump spares subsarcolemmal ATP. ET-1 inhibited the KATP channels that had been reactivated in the continuous presence of ouabain. CONCLUSIONS: ET-1 reversibly inhibited KATP channels. This effect appears to be mediated by an increase in subsarcolemmal [ATP] which results from inhibition of adenylate cyclase activities through PTX-sensitive G-proteins coupled to ETA receptors.

Adenosine Triphosphate↗
PubMed1997

A role for Na/K adenosine triphosphatase in the pathogenesis of cyst formation in experimental polycystic kidney disease.

Multiple cyst formation with fluid retention is a characteristic structural abnormality in polycystic kidney disease (PKD). Na/K adenosine triphosphatase (ATPase) is a major transporting membrane protein that is ubiquitous in the epithelial cell, which has been thought to be involved in cystogenesis. We have investigated the molecular and histologic basis of Na/K ATPase activity in experimental PKD in vivo. Rats were treated with diphenylthiazole (100 mg/100 gm body weight), and cyst formation was examined histologically. Na/K ATPase activity was measured enzymatically by using a fluorometric method, and reverse transcription-competitive polymerase chain reaction (RT-PCR) analysis was used to quantitate mRNA levels in the isolated single nephron segment. Kidneys were immunostained with subunit-specific antibodies to determine the localization of Na/K ATPase in the epithelial cell. The enzyme activity increased in the cortical collecting duct from 25.9 +/- 3.5 mmol/Lpmol/mm/min to 72.9 +/- 6.8 pmol/mm/min and in the outer medullary collecting duct from 13.0 +/- 3.9 mmol/Lpmol/mm/min to 58.5 +/- 9.8 pmol/mm/min (n = 6, p < 0.01); however, all other segments showed no significant changes. No significant alternation in alpha 1- and beta 1-subunits of Na/K ATPase mRNA levels was observed by competitive PCR assay in either segment. The enzyme was stained at the basolateral membrane even in the cystic tubules. Na/K ATPase activity was up-regulated in the cyst-formed kidney, but this was not accompanied with transcriptional up-regulation. Increased Na/K ATPase activity at normal locations may play a role in abnormal net fluid transport in the development and progression of experimental PKD.

Animals↗
PubMed1997

Clinical assessment of the significance of platelet-derived growth factor in patients with immunoglobulin A nephropathy.

To examine the role of platelet-derived growth factor (PDGF) in the pathogenesis of IgA nephropathy (IgAN), we investigated the expression of PDGF and the PDGF receptor in glomeruli with immunohistochemistry, the plasma levels of PDGF with ELISA, and the expression of PDGF in peripheral blood monocytes (PBMCs) with reverse transcription polymerase chain reaction (RT-PCR). We also assessed the effect of corticosteroid therapy on the plasma levels of the PDGF B-chain. At the time of kidney biopsy, the expression of the PDGF B-chain and the PDGF beta receptor in the glomeruli was upregulated in patients with IgAN. In addition, the plasma concentration of the PDGF B-chain was significantly higher in patients with IgAN than in normal subjects. Moreover, mRNA expression of PDGF beta-chain in PBMCs was up-regulated in patients with IgAN when compared with other patients with glomerulonephritis. We divided the patients into two groups according to the grade of urinary protein excretion (U[p]) after corticosteroid therapy. In patients in group 1 in whom U(p) was decreased by more than 50% or 1 gm/day after corticosteroid therapy, the expression of the PDGF B-chain and the PDGF beta receptor in the glomeruli was up-regulated. Finally, corticosteroid therapy decreased the plasma levels of PDGF B-chain in patients in group 1. Up-regulation of the PDGF B-chain and beta receptor in the glomeruli, elevated plasma levels of PDGF B-chain, and increased expression of PDGF mRNA in PBMCs could be associated with the pathogenesis of IgAN. The plasma concentration of PDGF B-chain may be a useful marker for patients with IgAN who would be responsive to corticosteroid therapy.

Adolescent↗