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H Matsui

Publications and source records attributed to H Matsui.

At least 451 records · Page 25Linked to original sources
PubMed1995

[Effect of branched-chain amino acids on glutamate neurotoxicity in primary cultured rat cerebral neurons].

The neurotoxicity of glutamate has recently been postulated to participate in the pathogenesis of amyotrophic lateral sclerosis (ALS), and branched-chain amino acids have been proposed as possible therapeutic compounds for this disease. This study was undertaken to investigate whether branched-chain amino acids have any protective effect on cultured neurons exposed to glutamate. Primary cultures of cerebral neurons were prepared from fetal rats, using an established technique. For the assessment of glutamate toxicity, photomicrographs were taken before and after glutamate exposure both with phase-contrast and with bright field following incubation in trypan blue, a dye normally excluded by healthy cells. The activity of lactate dehydrogenase released from damaged cells was also measured. Exposure to glutamate in various concentrations was carried out, and leucine, isoleucine and varine, each separately, were added in advance to culture dishes. Glutamate neurotoxicity was confirmed, but no protective effect of branched-chain amino acids was observed. Although possible clinical benefit of branched-chain amino acids in ALS may not be denied, they do not prevent glutamate neurotoxicity in cultured cerebral neurons.

Amino Acids, Branched-Chain↗
PubMed1995

Angiotensin II stimulates sodium-hydrogen exchange in adult rabbit ventricular myocytes.

OBJECTIVE: The aim was to characterise the effects of angiotensin II on Na+/H+ exchange in adult ventricular myocytes. METHODS: Intracellular pH (pHi) was continuously measured with the fluorescent pH indicator, SNARF-1, in single resting myocytes obtained from adult rabbits by enzymatic dissociation. In some experiments cells were electrically paced to elicit contractions. All experiments were performed at 36 degrees C in HEPES buffered solution containing no added CO2 or HCO3- (pHo 7.4). RESULTS: Rapid application of angiotensin II caused pHi to rise. The initial rate of rise and initial net H+ efflux responded to angiotensin II in a concentration dependent manner, EC50 = 7.8. Buffering of cytosolic calcium with the calcium chelator BAPTA did not affect the initial net H+ efflux elicited by 1 microM angiotensin II. The increase in steady state pHi was blocked by inhibitors of Na+/H+ exchange, amiloride (1 mM) and EIPA (10 microM). Angiotensin II also increased the rate of pHi recovery from intracellular acidosis at pHi values above approximately 6.9. During inhibition of Na+/H+ exchange the application of angiotensin II decreased steady state pHi. This acidosis was blocked by preincubation in dextrose-free solution containing 20.0 mM 2-deoxy-D-glucose and 10 microM EIPA. The positive inotropic effect of angiotensin II was markedly suppressed by amiloride. CONCLUSIONS: Angiotensin II exerts a concentration dependent stimulatory effect on Na+/H+ exchange in adult rabbit ventricular myocytes. This effect does not appear to involve changes in cytosolic calcium. During inhibition of Na+/H+ exchange, angiotensin II causes pHi to fall, perhaps by stimulating metabolic acid production. The positive inotropic action of angiotensin II depends, in part, on stimulation of Na+/H+ exchange.

Amiloride↗
PubMed1995

[DNA content analysis and expression of human leucocyte antigen on esophageal cancer].

To examine the usefulness of DNA analysis of cancer cells in estimating the prognosis of the patients with cancer, we measured the DNA content of cancer cells using flow cytometry in 82 patients bearing esophageal cancer. Although neither DNA content nor DNA ploidy alone was a prognostic factor, the aneuploid pattern with a DNA index greater than 1.3 was an indicator of poor prognosis. In addition, we studied the HLA class I expression in the same patient group using immunochemical staining (anti-HLA class I monoclonal antibody; w6/32). Forty-four cases (53.7%) were HLA class I positive and 38 (46.3%) were negative. Pathological lymph node metastasis was found more frequently in HLA class I negative patients than positive patients with statistical significance (p < 0.05). The tumors with positive HLA expression induced significantly more TILs around them (p < 0.05). The patients with the aneuploid pattern and negative HLA class I appeared to have the poorest prognosis from the survival curve study, although the difference was not statistically significant. These findings suggest that the expression of HLA class I on tumors is an important prognostic factor in patients with esophageal cancer.

DNA, Neoplasm↗
PubMed1995

The effects of PSK, a biological response modifier, on congenital ocular abnormalities induced by X-ray irradiation.

The antiteratogenic effects of PSK, a biological response modifier, were examined using histological and developmental analysis. The whole bodies of pregnant mice were irradiated with X-rays and injected with PSK within ten minutes after irradiation on day 7 of gestation (E7). The foetuses on E18 were examined and a high incidence of malformations were observed in X-ray irradiated embryos. Microphthalmia was the most frequent malformation. PSK administration suppressed the X-ray irradiation-induced ocular anomalies in not only the frequency, as deduced by external observation, but also in histopathological changes in the retina, lens, and cornea. In particular, the incidence of lens aplasia was significantly decreased by PSK administration. Developmental analysis using E10 and E13 embryos revealed that the decrease in the incidence of histopathological changes was first observed within 72 hours after PSK administration. In addition, X-ray irradiation-induced early foetal death (E10-13) was also suppressed by PSK administration. The possible mechanisms of the antiteratogenic effects of PSK are discussed.

Abnormalities, Radiation-Induced↗
PubMed1995

Oophorectomy predisposes to degenerative spondylolisthesis.

We performed a case-control study on the influence of oophorectomy on the development of degenerative spondylolisthesis, including a clinical review and determination of serum oestradiol levels. We also compared the radiological appearance of the lumbar spine at L4/5 in patients with and without spondylolisthesis and with and without oophorectomy. Oophorectomy was a risk factor for degenerative spondylolisthesis with an odds ratio of 7.5 (95% confidence interval, 1.6 to 46). The incidence of degenerative spondylolisthesis in 69 oophorectomised patients was about three times higher than in 69 non-oophorectomised matched control subjects. There was also a difference in spinal variation between oophorectomised and non-oophorectomised patients with spondylolisthesis. A high incidence of sagittal-plane orientation of the L4/5 facet and an increase in pedicle-facet angle were seen in both groups and are typical radiological features of this disease. An increase in lumbosacral angle and in disc-space narrowing was seen only in the non-oophorectomised patients with this condition. Our results suggest that the abrupt decrease in oestradiol level caused by oophorectomy may be a predisposing factor in degenerative spondylolisthesis at L4/5.

Adult↗
PubMed1995

Probing of the location of the allosteric site on m1 muscarinic receptors by site-directed mutagenesis.

In an attempt to locate the allosteric site on muscarinic receptors to which gallamine binds, 21 residues in the putative external loops and loop/transmembrane helix interfaces have been mutated to alanine. These residues are conserved in mammalian m1-m5 receptors. All mutant receptors can be expressed in COS-7 cells at high levels and appear to be functional, in that acetylcholine binding is sensitive to GTP. The gallamine binding site does not appear to involve the first, second, and most of the third extracellular loops. Tryptophan-400 and -101 inhibit gallamine binding when mutated to alanine or to phenylalanine and may form part of the allosteric site. Several mutations also affect antagonist binding. Surprisingly, tryptophan-91, a residue conserved in monoamine and peptide receptors, is important for antagonist binding. This residue, present in the middle of the first extracellular loop, may have a structural role in many G protein-coupled receptors. Antagonist binding is also affected by mutations of tryptophan-101 and tyrosine-404 to alanine or phenylalanine. In a helical wheel model, trytophan-101 and tyrosine-404, in conjunction with serine-78, aspartate-105, and tyrosine-408, form a cluster of residues that have been reported to affect antagonist binding when mutated, and they may therefore be part of the antagonist binding site. It is suggested that the allosteric site may be located close to and just extracellular to the antagonist binding site. The binding of methoctramine, an antagonist with allosteric properties, is not substantially affected by mutations at tryptophan-91, -101, and -400 and tyrosine-404, and thus these amino acids are not important for its binding. The binding of himbacine, another antagonist with allosteric properties, is affected by these mutations but in a manner different from that of gallamine or competitive antagonists. It has not been possible to determine whether methoctramine and himbacine bind exclusively to the allosteric site or to both the competitive site and the allosteric site.

Acetylcholine↗
PubMed1995

Hypothalamus regulates calcium metabolism in rats.

Hypothalamic mechanisms of blood calcium homeostasis and their functional heterogeneity were investigated in rats. Electrical and chemical stimulation of the lateral hypothalamic area (LHA), the paraventricular nucleus (PVN) and the ventromedial nucleus of the hypothalamus (VMH) induced hypocalcemia. The hypocalcemic effect of PVN stimulation was suppressed by vagotomy of the thyroid/parathyroid branches, while that of LHA and VMH stimulation was eliminated by gastric vagotomy. Immobilization (IMB) stress elicited hypocalcemia through VMH-gastric vagal activation. Both IMB- and LHA stimulation-induced hypocalcemia was antagonized by muscarinic antagonist and histamine H2 blocker. The former was also blocked by alpha-blocker and gastrin release inhibitor, while the latter was antagonized by an beta-blocker. The results suggest that hypothalamic nuclei are involved in regulation of blood calcium homeostasis via the gastric or thyroid/parathyroid vagus. Muscarinic, histamine H2, adrenergic and gastrin receptors mediate the hypocalcemic effect of the hypothalamo-vagal activation depending on behavioral conditions and receptor subtypes.

Animals↗
PubMed1994

Back muscle injury after posterior lumbar spine surgery. Part 1: Histologic and histochemical analyses in rats.

STUDY DESIGN: Back muscle injury caused by retractor application during posterior spine surgery in rats was examined histologically and histochemically according to the postoperative time with reference to the retraction time-pressure relationship. OBJECTIVES: The results were correlated to provide the risk factors for back muscle injury during posterior spine surgery. SUMMARY OF BACKGROUND DATA: Back muscles were examined histologically and histochemically after application of quantitative pressure and retraction time. No previous study has assessed this relationship. METHODS: Five groups were studied: Group 1, 1-hour low-pressure load group; Group 2, 1-hour high-pressure load group; Group 3, 3-hour low-pressure load group; Group 4, 3-hour high-pressure load group; and sham group. In each group, the multifidus muscle was evaluated 3 hours, 48 hours, 1 week, 3 weeks, and 6 weeks after surgery. RESULTS: In all groups except the sham group, degeneration of the muscle and neuromuscular junction was found at a very early postoperative time, but regeneration began at 1 week, and recovery was attained by 6 weeks. The extent of muscle fiber necrosis and the severity of degeneration of the neuromuscular junctions showed a parallelism with the magnitude of the pressure load and retraction time. As the duration and pressure load increased, the time required for regeneration also increased. The fiber type grouping in group 3 and 4 was consistent with the severity of degeneration of neuromuscular junctions. CONCLUSIONS: The muscular degeneration and the regeneration was largely dependent on the retraction pressure-time product. These results suggest that denervation muscle injuries are likely secondary responses to muscle retraction injury in any case of posterior spine surgery.

Animals↗
PubMed1994

Back muscle injury after posterior lumbar spine surgery. Part 2: Histologic and histochemical analyses in humans.

STUDY DESIGN: The histologic and histochemical changes in back muscle were studied in virgin surgery patients with lumbar spine disorders and in patients who underwent repeat posterior lumbar surgery. OBJECTIVES: The results were correlated to provide the evidences of histologic changes of back muscle after posterior lumbar surgery. SUMMARY OF BACKGROUND DATA: Back muscles were examined histologically and histochemically after posterior lumbar surgery. No previous study has assessed these changes. METHODS: Back muscles were obtained before and after retraction from 18 virgin surgery cases with lumbar spine disorders. In four patients, the retraction pressure was monitored and the retraction pressure-time products ([P][T]) were calculated. In 21 repeat lumbar surgery cases, muscle samples were obtained before muscle retraction. Samples were evaluated by histologic and histochemical methods. RESULTS: Abnormal findings were slight in virgin surgery cases. Early back muscle injury tended to depend on operation time and [P][T] products. Late back muscle injury in reoperated patients was marked. Various types of neurogenic changes were observed more than 10 months after the first operation. CONCLUSIONS: Histologic damages of back muscle due to previous surgical intervention were long-lasting. To avoid permanent muscle injury, the retraction time and pressure should be shortened or the pressure on the back muscle should be monitored during posterior surgery.

Adult↗
PubMed1994

Functional anatomy of taste perception in the human brain studied with positron emission tomography.

Regional cerebral blood flow (rCBF) was measured with positron emission tomography (PET) in 10 normal volunteers with the purpose of measuring rCBF changes related to taste physiology. Discrimination of 0.18% saline from pure water was associated with significantly increased rCBF values in the thalamus, the insular cortex, the anterior cingulate gyrus, the parahippocampal gyrus, the lingual gyrus, the caudate nucleus, and the temporal gyri. The results indicate that rCBF changes in these structures may reflect oral exposure to salt.

Adolescent↗
PubMed1994

In situ localization of rat testis-specific calcineurin B subunit isoform beta 1 in the developing rat testis.

In situ localization and developmental changes in expression of testis-specific calcineurin B subunit isoform beta 1 was examined in rat testis. Two different sizes of mRNA signal, 4.0 kb and 0.9 kb, were detected by Northern blot hybridization. Both signals were expressed synchronously with the start of meiosis at 3 weeks after birth, and increased depending on the maturation of spermatogenesis. In situ hybridization using non-radioactive riboprobes showed that the beta 1 mRNA was specifically localized to spermatocytes where meiosis occurs but none or very little was observed in spermatogonia, spermatids, Sertoli or Leydig cells.

Animals↗
PubMed1994

Activation of the alternative pathway of complement by apoptotic Jurkat cells.

Jurkat T cells die of apoptosis upon exposure to anti-Fas mAb. Here we show that although the alternative complement pathway generally does not attack homologous cells, anti-Fas-induced apoptotic Jurkat T cells were attacked antibody-independently by the alternative pathway of human complement and opsonized with iC3b, which is a ligand of the complement receptor type 3 (CR3) of phagocytes. These results suggest that apoptotic cells become the targets of the homologous alternative complement pathway, which facilitates the clearance of apoptotic cells by phagocytes.

Antibodies, Monoclonal↗
PubMed1994

Immunosuppressants and calcineurin inhibitors, cyclosporin A and FK506, reversibly inhibit epileptogenesis in amygdaloid kindled rat.

Calcineurin (CaN) immunoreactivity and content increased markedly in kindled rat brain, and this increment was due to CaN in the membrane fraction. Investigation of the effects of cyclosporin A and FK506 (immunosuppressants which inhibit CaN activity in T lymphocytes) in the kindling phenomena showed that the kindling stage progression was reversibly blocked by these drugs. These findings suggest that calcineurin may play an essential role in acquiring epileptogenesis in kindling.

Amygdala↗
PubMed1994

Mutual interaction between host and graft tissues in embryonic neural transplantation.

The differentiation of AChE-positive cells in embryonic neural grafts from various brain regions into the hippocampus after fimbria-fornix transection was investigated. Rat fetal cell suspensions of basal forebrain, hippocampus, mesencephalon or cortex were prepared from fetuses of either embryonic day 14 (E14) or day 19 (E19) gestational age, and these were transplanted into the rat brain after unilateral fimbria-fornix transection. Dense acetylcholinesterase (AChE) positive fibres were observed in both E14 and E19 basal forebrain grafts. These fibres were also found in E14 hippocampal grafts. However E19 hippocampal grafts did not have any AChE-positive fibres. These results suggest that E14 hippocampal grafts might be affected by the host brain tissues and differentiate into cholinergic neurones.

Acetylcholinesterase↗
PubMed1994

Purified vacuolar inorganic pyrophosphatase consisting of a 75-kDa polypeptide can pump H+ into reconstituted proteoliposomes.

Inorganic pyrophosphatase was purified to homogeneity from the vacuolar membranes of pumpkin hypocotyl tissue. The purified Inorganic pyrophosphatase consists of a single kind of 75-kDa polypeptide, and the stacked molecules with a repeating unit of 5.8 x 3.8 nm are seen under electron micrography. It exhibits H(+)-translocating activity across membranes coupled with PPi hydrolysis when it is reconstituted into proteoliposomes. A monovalent cation is required for the H+ translocation with the K+ ion being the most effective, but evidence for active transport of 42K+ into proteoliposomes was not obtained under the conditions tested. The hydrolysis of PPi by the reconstituted proteoliposomes is stimulated by the addition of a H+ ionophore, carbonyl cyanide p-trifluoromethyoxyphenylhydrazone, but not by a K+ ionophore, valinomycin. Both hydrolysis of PPi and PPi-dependent H+ translocation of the proteoliposomes are inhibited by N,N'-dicyclohexylcarbodiimide.

Amino Acid Sequence↗
PubMed1994

Calcitonin receptors on neoplastic mononuclear cells cultured from a human giant-cell tumor of the sacrum.

Saturable, specific, high-affinity calcitonin receptors were demonstrated in cultured neoplastic mononuclear spindle cells from a giant-cell tumor of the sacrum of a 38-year-old woman. The receptor was analyzed by autoradiography and 125I-calcitonin binding assay. Binding reversibility of 125I-calcitonin to the cells was not complete and the structural specificity was indicated by the inability of unrelated hormones to compete with calcitonin. The 24,000 receptors/cell and dissociation constant (Kd) of 8.0 x 10(-10) M, calculated from linear Scatchard plots, suggested the existence of a single class of calcitonin binding sites in the neoplastic mononuclear cells. Flow-cytometric analysis in the primary culture showed that mononuclear cells consisted of mononuclear round cells of monocyte/macrophage lineage, which express more calcitonin receptors than neoplastic mononuclear spindle cells. Administration of calcitonin caused morphological and physiological alterations, resulting in involutional or irregular cytoplasmic shapes and inhibition of DNA synthesis in neoplastic mononuclear cells accompanied by the escape phenomenon. Cells preincubated with calcitonin showed a decrease in 125I-calcitonin binding activity, which could account for the escape phenomenon. The decrease in 125I-calcitonin binding was rapid, but the recovery was not observed for 24 h after elimination of calcitonin. This decrease may be caused by the disappearance of residual receptors or by a decrease in calcitonin affinity. The calcitonin-induced morphological changes and the inhibition of DNA synthesis of cells were revealed to be mediated by calcitonin receptors.

Adult↗
PubMed1994

Autofluorescence in onset of gastric mucosal injury induced by hemorrhagic shock in rats.

In an attempt to clarify whether gastric mucosal autofluorescence can help us to recognize gastric lesions at the onset of their formation, we investigated the fluorescence generated from the gastric mucosa of rats under ischemia-reperfusion stress. Red-colored fluorescence appeared and began to increase within 5 min after reperfusion. Such an increase in fluorescence did not occur in the gastric mucosa under prolonged ischemia without reperfusion. The epifluorescence microscopy of mucosal cryosections revealed that fluorescence was present even when only superficial mucosal damage occurred. Spectrofluorometric and high-performance liquid chromatographic analysis of the fluorescent mucosa extract identified the fluorescent substances as porphyrins. These findings suggested that fluorescent porphyrins are generated in the mucosal layer during the introductory phase of mucosal lesion formation induced by ischemia-reperfusion stress.

Animals↗