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H Matsui

Publications and source records attributed to H Matsui.

At least 433 records · Page 24Linked to original sources

Sarcoplasmic reticulum gene expression in pressure overload-induced cardiac hypertrophy in rabbit.

Pressure overload (PO)-induced cardiac hypertrophy in rabbits has been utilized extensively to study alterations in systolic and diastolic functions of the heart. In earlier studies we showed that the levels of mRNA encoding two important sarcoplasmic reticulum (SR) proteins, the cardiac/slow-twitch muscle Ca(2+)-ATPase (SERCA2a) and phospholamban, were decreased in PO rabbit hearts. In this study, we analyzed the expression of the Ca(2+)-release channel (ryanodine receptor), calsequestrin, SERCA2a, and phospholamban in PO-induced cardiac hypertrophy after 2, 4, 8, and 16 days of pulmonary artery banding. Northern blot and slot blot analyses showed that the steady-state level of mRNA encoding the cardiac ryanodine receptor, SERCA2a, and phospholamban was decreased significantly as early as 2 days after PO. In 16-day PO hearts, SERCA2a mRNA was reduced to 7.9 +/- 3.4% (P < 0.05), phospholamban mRNA was reduced to 15.9 +/- 6.5% (P < 0.05), and ryanodine receptor mRNA was reduced to 49.2 +/- 23.6% (P < 0.05). In this study, calsequestrin mRNA levels were also reduced to 29.9 +/- 15.2% by day 16 (P < 0.05). ATP-dependent Ca2+ uptake was reduced to 78% (P < 0.05); in contrast, the steady-state formation of ATPase phosphoenzyme was reduced to 81% of control (P < 0.05) and Ca(2+)-ATPase protein was reduced to 78% of control (P < 0.05) in crude SR vesicles or total muscle homogenate obtained from 16-day PO hearts. On the basis of these data, we propose that decreases in the expression of SR proteins may contribute to dysfunctions seen in systolic and diastolic properties of the hypertrophied myocardium.

Actins↗

In vivo effects of endothelin A- and B-receptor antagonists in guinea pigs.

Endothelin (ET)-1, a novel 21-amino acid constrictor peptide, has been recently reported to have a potential pathophysiological role in asthma. We hypothesized that ET-1 might affect guinea pig lung via different ET receptor subtypes, i.e., ETA and ETB, in vivo. To test this hypothesis, we investigated the effects of ET-1 on airways in anesthetized, open-chest, mechanically ventilated [frequency (f) = 1 Hz; tidal volume (VT) = 9 ml/kg; positive end-expiratory pressure (PEEP) = 4 cmH2O] guinea pigs in the absence or the presence of ETA and ETB selective antagonists, i.e., BQ-123 and BQ-788, respectively. We affixed alveolar capsules to the lungs to measure alveolar pressure and calculated the elastance of lung (EL) and the resistance of lung (RL), tissue (Rti), and airway (R(aw)) under control conditions and after intravenous administration of ET-1 (10(-8) mol/kg). ET-1 induced a concentration-dependent increase in RL, Rti, R(aw), and EL.BQ-123 (2 mg/kg) partially blocks delta RL and delta R(aw) during ET-1 induced constriction, while delta Rti and delta EL were not significantly affected. BQ-788 (2 mg/kg) significantly inhibited delta RL, delta Rti, delta R(aw), and delta EL during ET-1-induced constriction. The combination of BQ-123 and BQ-788 completely ablated the response to ET-1. These data suggest that both ET receptor subtypes, i.e., ETA and ETB, may have physiological roles in guinea pig airways in response to ET-1, a potential mediator of asthma.

Airway Resistance↗

Central actions of parathyroid hormone on blood calcium and hypothalamic neuronal activity in the rat.

The central actions of parathyroid hormone (PTH) on the blood ionized calcium level in anesthetized rats and the neuronal activity of the ventromedial nucleus of the hypothalamus (VMH) in vitro were investigated. An intracerebroventricular injection of PTH (0.01, 0.1, and 1 microgram) prevented urethan-induced hypocalcemia in a dose-dependent manner, whereas either an intravenous or an intracisternal injection of PTH (1 microgram) was ineffective. Eighty-three of 177 VMH neurons responded to a bath application of PTH (10(-7) or 3 x 10(-7) M): a majority (72, 83%) of the responsive cells decreased, whereas 11 increased their activity. This inhibitory effect of PTH on neuronal activity still persisted after synaptic blocking in a Ca(2+)-free/high-Mg2+ medium. A PTH receptor antagonist, [Tyr34]bPTH-(7-34)-NH2, suppressed the effect of PTH on the neuronal activity. These findings thus suggest that brain PTH has a calciotropic function and that one of the possible target sites is the VMH, where PTH inhibits its neuronal activity through a postsynaptic mechanism mediated by PTH receptors.

Analysis of Variance↗

Cytokeratin fragment 21-1 in gynecologic malignancy: comparison with cancer antigen 125 and squamous cell carcinoma-related antigen.

We measured serum cytokeratin fragment 21-1 (CYFRA 21-1) levels by a solid-phase immunoradiometric assay in 102 healthy Japanese women, and set the reference value at 1.9 ng/ml (mean +2 SD of the serum levels based on a linear distribution). Pretreatment serum CYFRA 21-1 levels were also analyzed in 235 women with benign (n = 94) or malignant (n = 141) gynecologic disease, and were compared with the serum levels of CA 125 and SCC. The respective positivity rates for CYFRA 21-1 and CA 125 were 64.0 and 77.2% in ovarian malignancy, while they were 4.2 and 30.8% in benign ovarian masses. CYFRA 21-1 had an accuracy of 61.3% in diagnosing ovarian malignancy, which was higher than that of CA 125 (53.4%). The positive predictive value of CYFRA 21-1 for ovarian malignancy reached 94.1%, which was significantly (p < 0.005) higher than that of CA 125 (68.8%). These findings indicate the potential usefulness of CYFRA 21-1 as a tumor marker for ovarian malignancy. In addition, the positivity rates fo CYFRA 21-1 in cervical cancer (51.2%) and endometrial cancer (52.2%) were also similar to the respective rates for SCC and CA 125, which suggests that CYFRA 21-1 seems to be a general tumor marker for gynecologic malignancy.

Adolescent↗

Antagonism of ICAM-1 attenuates airway and tissue responses to antigen in sensitized rats.

Airway inflammation is involved in the pathogenesis of bronchial asthma. Intercellular adhesion molecule-1 (ICAM-1) is a ligand for lymphocyte function-associated antigen-1 alpha (LFA-1 alpha) and has been shown to be required for leukocyte migration into inflamed area. The purpose of this report was to investigate the role of ICAM-1/LFA-1 alpha pathway in a rat model of extrinsic asthma using monoclonal antibodies (mAbs). We chose to study ovalbumin (OA)-sensitized Brown-Norway rats, an animal model in which there is a high prevalence of both early (ER) and late responses (LR) after antigen challenge. We measured tracheal and alveolar pressure using alveolar capsules in open-chested, mechanically ventilated animals to calculate resistance of lung (RL), tissue (Rti), and airway (Raw). In the OA group, both ER (RL, Rti, Raw = 263 +/- 16, 235 +/- 10, 309 +/- 38% baseline) and LR (RL, Rti, Raw = 265 +/- 26, 238 +/- 13, 316 +/- 55% baseline) were observed. The administration of mAbs to ICAM-1 and LFA-1 alpha significantly attenuated the ER (RL, Rti, Raw = 146 +/- 9, 141 +/- 11, 156 +/- 8% baseline) and LR (RL, Rti, Raw = 128 +/- 8, 124 +/- 5, 137 +/- 1% baseline), indicating that both airway and lung tissues were involved in this mechanism. The current observations suggest that ICAM-1/LFA-1 alpha pathway is involved in both the early and late responses in a rat model of allergic asthma. The antagonism of ICAM-1 and LFA-1 alpha may provide a potential therapeutic approach to the early and late responses of bronchial asthma.

Airway Resistance↗

Expression of immunoreactive and bioactive activin A protein in adult murine lung after bleomycin treatment.

Activin A is a homodimeric protein structurally and functionally related to transforming growth factor beta (TGF-beta), and the expression of activin A is modulated by TGF-beta. Here, we demonstrate the expression of activin A in normal and bleomycin (BLM)-treated murine lungs. ICR mice were treated with BLM intraperitoneally for 10 days, whereas saline vehicle was injected into control mice. Intra-alveolar fibrotic changes were observed in the lung tissue obtained from the mice at day 14 after the final BLM administration. Immunohistochemical studies using a polyclonal antibody to activin A revealed the presence of activin A in the bronchiolar epithelium and smooth muscle cells of veins in both control and BLM-treated mice. In the BLM-treated mice at days 7 and 14, the marked infiltration of immunoreactive alveolar macrophages was observed in the area of fibrotic changes. Bioactivity of activin A measured by erythroid differentiation factor assay in the conditioned medium of alveolar macrophages obtained from BLM-treated mice at day 14 was significantly increased. These findings indicate that alveolar macrophages are a potent source of activin A after BLM treatment. The present study demonstrates for the first time the abundant expression of activin A in murine lung tissues after BLM administration, suggesting that activin A may play a role in the pathogenesis of BLM-induced pulmonary fibrosis.

Activins↗

Involvement of annexin-I in glucose-induced insulin secretion in rat pancreatic islets.

Annexin-I was demonstrated to specifically present in islets and not in exocrine tissues of the rat pancreas and to have a diffuse and homogeneous distribution in all islet cells in our previous study. In the present report, to clarify the functions of annexin-I in rat pancreatic islets, especially in beta-cells, we investigated the role of annexin-I in insulin secretion. Immunoelectron microscopic analysis of pancreatic beta-cells demonstrated that immunogold particles reactive to annexin-I were almost exclusively observed on most of the insulin-containing granules (approximately 90%) and less frequently located in cytosol and other organelles, such as the endoplasmic reticulum and mitochondria. The number of annexin-I gold particles located on insulin granules after oral glucose administration was significantly increased compared with that observed in fasted rats. Moreover, when the isolated islets were stimulated by a high concentration of glucose (20 mM), the phosphorylation of annexin-I was markedly enhanced, and it was synchronized to insulin secretion. This phosphorylation mainly occurred on serine residues. H-7 (100 microM), a potent inhibitor of protein kinase-C, inhibited the phosphorylation to about 90%. These findings suggest that annexin-I might be involved in the regulatory mechanism of glucose-induced insulin secretion in rat pancreatic islets via phosphorylation-dephosphorylation processes.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

Solitary T-cell lymphoma of the sciatic nerve: case report.

In lymphoproliferative disorders, primary involvement of the peripheral nerve is rare. This report describes a very rare case of a solitary extranodal T-cell lymphoma of the sciatic nerve. Magnetic resonance imaging and gallium scintigraphy were useful for the identification of the lesion of the sciatic nerve. The histological analysis of an open-biopsy specimen disclosed a T-cell lymphoma (non-Hodgkin's lymphoma, lymphoblastic type). Radiotherapy and chemotherapy resulted in a partial regression of the disease.

Adult↗

Thromboxane A2 synthetase inhibitors with histamine H1-blocking activity: synthesis and evaluation of a new series of indole derivatives.

A novel series of N-substituted 3-(1H-imidazol-1-ylmethyl)indole carboxylic acid derivatives were prepared and evaluated for thromboxane A2 (TXA2) synthetase-inhibitory and histaminergic H1-blocking activity. Among the compounds synthesized, indole-6-carboxylic acid derivatives showed higher activities than the other positional isomers of carboxylic acid. 1-[3-(4-Benzhydryl-1-piperazinyl)propyl]-3-(1H-imidazol-1-ylmethyl )-1H-indole-6-carboxylic acid (12) had the strongest thromboxane synthetase inhibitory activity (IC50 = 5 x 10(-8) M) and H1-blocking activity (IC50 = 8 x 10(-9) M).

Animals↗

Chemical modification and amino acid sequence of active site in sugar beet alpha-glucosidase.

The modification of amino acid residues in sugar beet alpha-glucosidase with conduritol B epoxide (CBE), an affinity labeling reagent, inactivated the enzyme. The inactivation followed pseudo-first-order kinetics. The enzyme was protected from inactivation by a competitive inhibitor, Tris, and the partially inactivated enzymes showed only the decrease of V values and no change in Km value. An 3H-CBE labeled peptide isolated from the digest of the inactivated enzyme with Lys-C protease was sequenced. The -COO- group of Asp was found to be specifically labeled, implicating that it is a catalytic group of the enzyme. The sequence around the essential Asp was determined to be -DGIWIDMNE-, which showed a high homology with those of other alpha-glucosidases.

Amino Acid Sequence↗

Effect of cigarette smoking on pulmonary function in each phenotype M of alpha-1-protease inhibitor.

Human alpha-1-protease inhibitor (alpha-1-Pi) has been known to be a highly polymorphic protein. We hypothesized that antiprotease activity of each phenotype M of alpha 1-protease inhibitor (PiM) might be different among smokers and that a variation of decrease in pulmonary function for a given amount of cigarette smoking might be associated with PiM phenotypes. To test this, we investigated the effect of cigarette smoking on pulmonary function in each PiM phenotype. The serum level of alpha 1-Pi was measured by the turbidimetric immunoassay and the distribution of PiM phenotypes was determined using isoelectric focusing technique in 247 healthy subjects and 20 COPD patients. Serum levels of alpha-1-antitrypsin of healthy and COPD subjects were 205.1 +/- 31.1 and 179.2 +/- 44.4 (+/- SD) mg/dL, respectively (p > 0.01). The frequency of each PiM phenotype in healthy subjects was shown as follows: M1, 0.555; M1M2, 0.328; M2, 0.041; M1M3, 0.057; M2M3, 0.016; M3, 0.004. The difference in the distribution of PiM phenotypes between healthy and COPD subjects was not significant. Single- and multiple-regression analyses showed that the ratio of FEV1 to forced vital capacity (FVC), in which FEV1 is expressed as percentage of FVC, the maximum flow rate at 50% of FVC divided by measured body height (V50/Ht), and the maximum flow rate at 25% of FVC divided by body height (V25/Ht) were closely related to age and that V25/Ht also was related to smoking index. However, PiM phenotype was unrelated to those pulmonary function variables. We conclude that PiM phenotype is not a major determinant of difference in magnitude of pulmonary impairments caused by cigarette smoking in each individual.

Adult↗

Effects of exercise and amenorrhea on bone mineral density in teenage runners.

In order to elucidate whether exercise and calcium intake can offset bone loss due to hypoestrogenemia in teenage girls, the lumbar and femoral bone mineral density (BMD) in elite amenorrheic runners (group 1 (n = 8)) was compared with those in eumenorrheic athletes (group 2 (n = 15)) and two groups of eumenorrheic non-athletic subjects, group 3 (n = 14), and group 4 (n = 15). BMD was measured by dual energy x-ray absorptiometry. The subjects in group 1 lived in the dormitory, and their calcium intake was controlled to > 1400 mg/day. The subjects in groups 1, 2 and 3 were age matched (16-17 years old), but the body weight of those in group 2 was significantly greater than that of others. The subjects in groups 1, 3 and 4 were weight matched, but group 4 subjects were older by 5 years (21.0 +/- 0.2 years old). The lumbar BMD of group 1 was 1.0460 +/- 0.0259, which was not statistically different from those in the other groups, while the femoral BMD of group 1 was significantly higher than those of groups 3 and 4 at trochanter. The lumbar and femoral BMD of group 2 was significantly higher than in groups 3 and 4, but was not statistically different from group 1. There were no significant differences in serum parathyroid hormone levels, but osteocalcin and calcitonin levels of group 1 were significantly lower than those of groups 2 and 3, and groups 2, 3 and 4, respectively, suggesting that the rate of bone formation is suppressed in amenorrheic runners.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Morphological evaluation of cyclophosphamide testicular toxicity in rats using quantitative morphometry of spermatogenic cycle stages.

The testicular toxicity of cyclophosphamide (Cp) in rats was evaluated by quantitative morphometry of spermatogenic cycle stages. Nine-week-old male Sprague-Dawley rats in Group 1 were given a single oral administration of 100 mg/kg of Cp, and were sacrificed at 1, 7, 14 and 21 days thereafter. Rats in Group 2 were orally given 100 mg/kg/day of Cp for 2 days, followed by 50 mg/kg/day for the next 3 days, and were sacrificed at 1 and 4 days after the last administration. The numbers of seminiferous epithelia were counted in the seminiferous tubules of stages II, V, VII and XII of the spermatogenic cycle. The data were expressed as numbers of spermatogenic cells per Sertoli cells per seminiferous tubule cross section. Animals in Group 1 showed decreased preleptotene spermatocytes at Day 7, decreased zygotene spermatocytes at Day 14, and decreased pachytene spermatocytes at Day 21. In group 2, testicular toxicity could also be clearly detected by this morphometric approach. The present morphometric study thus indicates that testicular toxicity can be detected from Day 7 even after a single administration of Cp.

Animals↗

The influence of scattering on temporo-regional proliferation in the cultured Madin-Darby canine kidney (MDCK) cells.

An epithelial Madin-Darby canine kidney (MDCK) cell line was grown in two kinds of standard media and a medium conditioned by MRC-5 embryonic lung cells, and temporo-regional differences in cell proliferation were examined by immunohistochemical detection of incorporated bromodeoxyuridine (BrdU). MRC-5-conditioned medium is known to contain scatter factor, which induces scattering of MDCK cells. In a proliferation assay, the BrdU labeling index (percentage ratio of BrdU-positive to total nuclei) was highest in day 2 cultures in the standard media, but on day 3 in the conditioned medium. MDCK cells in the standard media formed multiple epithelial sheets by day 2. In the conditioned medium, however, epithelial sheet formation was retarded and observed only after day 3. Once epithelial sheets had formed, cells close to the edge of the sheet were more proliferative than those distant from the edge in both standard and conditioned media. These findings suggest that proliferation of MDCK cells is suppressed during the scattering induced by the conditioned medium, and that their DNA synthesis becomes most active when cell scattering has ceased and epithelial sheets have begun to form.

Animals↗

Posterior canal-activated excitatory vestibuloocular relay neurons participate in the vestibulocortical pathways in cats.

We have previously reported that axon collaterals of posterior canal-activated excitatory vestibular (PC) neurons project to the contralateral oculomotor nucleus, and rostrally to the thalamus. To elucidate the vestibulothalamocortical pathways we investigated the synaptic connections of the PC neurons with the thalamic neurons by post-spike averaging of compound potentials triggered by spikes of the PC neuron in anesthetized cats. The averaged field potential evoked in the ventrobasal complex (VBC) revealed a spike followed by a negative wave. Latencies of the wave ranged from 0.8 to 1.5 ms. Next, we examined the location and axonal projection of 36 thalamic neurons which were activated by nose-up head rotation and by contralateral labyrinth stimulation. Most of them were located in the VBC and some in the medial geniculate body. Thirteen of the 36 neurons were antidromically activated from the anterior suprasylvian sulcus or postcruciate dimple of the cortex. These results suggest that the PC neurons participate, at least in part, in the vestibulocortical pathways contributing to spatial orientation.

Animals↗

[Treatment of refractory hypoxemia due to right-to-left interatrial shunt complicating right ventricular infarction: successful short-term percutaneous catheter closure of the patent foramen ovale].

Refractory hypoxemia as a complication of right ventricular infarction is rare. A 74-year-old man developed persistent hypoxemia due to right-to-left interatrial shunting through a patent foramen ovale during the acute phase of right ventricular infarction. Short-term percutaneous transvenous closure of the patent foramen ovale with a large balloon occlusion catheter was life-saving.

Aged↗

Opaque eyes developed in transgenic mice with T-cell receptor delta gene.

PURPOSE: During the generation of transgenic mice (TGs) introduced with mouse T-cell receptor delta (TCR delta) gene, the authors found a TG line with corneal opacity that coincided with the presence of the transgene. The authors investigated the pathogenesis and molecular mechanisms of this corneal opacity in this line. METHODS: The pathologic features and pathogenesis of the corneal opacity in TGs were examined histologically using transmission and scanning electron microscopy, as well as light microscopy. DNA and RNA blot analyses were performed to examine the copy number and the expression of the transgenes, respectively. RESULTS: Histologically, edema of the corneal epithelium and adhesion of the iris to the cornea were observed in adult TGs. In the developmental analysis, the authors first observed relative hypoplasia of the ciliary body on day 18 of gestation and dysgenesis of the anterior chamber angle from postnatal day 2. Corneal opacity was observed from postnatal day 8, coinciding with the histologic vesicular change of the epithelium. No inflammation was observed through its life. In the sublines that have different copy numbers of the transgene, the occurrence of the opacity depended on the copy number of the transgene. Expression of the transgene in the thymus was consistent with the number of the introduced transgene. CONCLUSION: In a TCR delta TG line, the overexpression of transgenes coincided with abnormal development of the ocular anterior segment and the corneal opacity. Pathogenesis is described, and possible molecular mechanisms are discussed.

Animals↗

Effects of the novel water-soluble calcium antagonist (+/-)-3-(4-allyl-1-piperazinyl)-2,2-dimethylpropyl methyl 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylate dihydrochloride on the responses of isolated canine arteries.

The effects of NKY-722 ((+/-)-3-(4-allyl-1-piperazinyl)-2,2-dimethylpropyl methyl 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylate dihydrochloride, CAS 117241-46-0), a new water soluble dihydropyridine derivative on the responses of isolated canine arteries were examined. NKY-722 (IC50: 5-16 x 10(-10) mol/l), nicardipine (IC50: 5-10 x 10(-10) mol/l) and nifedipine (IC50: 44-195 x 10(-10) mol/l) relaxed four arteries in the potency order of basilar > coronary > mesenteric > intrarenal arteries. NKY-722 was nearly equipotent to nicardipine and about 10 times more potent than nifedipine. [3H]NKY-722 was accumulated in the four arteries in the same order of amount as the vasoinhibitory effect. All three drugs inhibited the contraction induced by Ca2+ and methyl 1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylophenyl)-p yri dine-5- carboxylate (Bay K 8644) in the mesenteric arteries, indicating their Ca2+ antagonistic actions. NKY-722 and nicardipine were nearly equipotent and about 100 times more potent than nifedipine on the Ca(2+)-induced contraction and was about 4 times more potent than nicardipine and 400 times more potent than nifedipine on the Bay K 8644-induced contraction. NKY-722, nicardipine and nifedipine relaxed the mesenteric arteries precontracted with KCl by more than 90%, while they relaxed the arteries contracted with PGF2 alpha, 9,11-dideoxy-9 alpha, 11 alpha-methanoepoxy-PGF2 alpha (U-46619) and endothelin-1 only by 40-70%. The IC50 values of NKY-722 and nicardipine were similar and much smaller than that of nifedipine for all four contracting agents.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗