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Biomedical subjects

T Matsuda

Publications and source records attributed to T Matsuda.

At least 1,279 records · Page 71Linked to original sources
PubMed1988

Bacillus cereus bacteremia in an adult with acute leukemia.

Bacillus cereus, which used to be considered non-pathogenic, was isolated from the blood of a patient with acute leukemia who was receiving intensive chemotherapy. Fatal bacteremia developed with a clinical syndrome of acute gastroenteritis, followed by both meningoencephalitis with subarachnoid hemorrhage and multiple liver abscesses probably caused by infective vasculitis. Surveillance stool cultures revealed colonization with the organism prior to the onset of diarrhea, and repetitive blood cultures were found to be positive. Thus, this case suggested some new important clinicopathologic features of true B. cereus bacteremia complicating acute leukemia.

Acute Disease↗
PubMed1988

Beta 1- and beta 2-adrenoceptor-mediated relaxation responses in peripheral arteries from spontaneously hypertensive rats at pre-hypertensive and early hypertensive stages.

Beta-adrenoceptor-mediated relaxation of isolated arteries from spontaneously hypertensive rats (SHR) was studied. The relaxation responses of the femoral arteries of pre-hypertensive SHR (PHSHR) to isoprenaline (ISO) and dibutyryl cyclic AMP were less than those of the age-matched tissues of rats of the Wistar-Kyoto strain (WKY). The responses of the mesenteric arteries of PHSHR to ISO and noradrenaline (NA) but not fenoterol (FEN) and forskolin were diminished when compared to those from the WKY tissues. The diminished relaxation response to ISO was observed in the SHR arteries with and without endothelial cells as compared to similar arteries from WKY. Relative potency ratios of ISO:FEN:NA and the Schild plot data for atenolol and butoxamine suggested that there were only beta 1-adrenoceptors and predominantly beta 2-adrenoceptors mediating relaxation in the femoral and mesenteric arteries, respectively. There was no difference in beta-adrenoceptor subtypes between the SHR and WKY arteries. The evidence in this study suggests that beta 1-adrenoceptor-mediated relaxation was diminished in the femoral and mesenteric arteries of PHSHR.

Adrenergic beta-Agonists↗
PubMed1988

Antagonism of alpha 1-adrenoceptor-mediated vascular contraction by urapidil in isolated arterial strips of spontaneously hypertensive rats.

Antagonism of alpha 1-adrenoceptor-mediated vascular contraction by urapidil was examined in helical strips of femoral and mesenteric arteries isolated from 13-week-old Aoki spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar-Kyoto (WKY) rats, since this agent has antihypertensive effect through antagonizing peripheral alpha-adrenoceptors. Schild plot analyses clearly demonstrated the existence of only alpha 1-adrenoceptors in these arteries from both strains. Therefore, it is possible to demonstrate alpha 1-adrenoceptor blocking effects of nonselective alpha-adrenoceptor antagonists as well as selective alpha 1-adrenoceptor antagonists. Urapidil antagonized the alpha 1-adrenoceptor-mediated vascular contraction in a competitive fashion. The pA2 value for urapidil against alpha 1-adrenoceptors was not significantly different between SHR and WKY rats. The addition of 10(-5) M norepinephrine (NE) produced a sustained contraction in a SHR femoral artery, whereas in a WKY rat femoral artery this agonist produced a transient contraction followed by a sustained relaxation. Urapidil elicited a dose-dependent relaxation with a IC50 value of 6.50 in the SHR femoral artery precontracted with NE. In the presence of 3 x 10(-7) M timolol, a beta-adrenoceptor antagonist, femoral arteries from both strains exhibited similar magnitude of contraction in response to the stimulation with 10(-5) M NE. Under these conditions, urapidil elicited a similar extent of relaxation between SHR and WKY rats. On the other hand, the addition of 10(-5) M NE produced a sustained contraction in mesenteric arteries from both SHR and WKY rats. The contraction expressed as a ratio to the maximum developed by KCl depolarization was significantly greater in SHR than in WKY rats. In these arteries, the relaxing effect of urapidil was more evident in SHR than in WKY rats. Contractile responses to NE and relaxing effects of urapidil were not affected by timolol. These results suggest that urapidil effectively antagonized enhanced alpha 1-adrenoceptor responses seen in SHR arteries.

Age Factors↗
PubMed1988

Primary pulmonary artery sarcoma. Report of two autopsy cases studied by immunohistochemistry and electron microscopy, and review of 110 cases reported in the literature.

Two cases of primary pulmonary artery sarcoma are reported. The patient in the first case was a 61-year-old male with a two-year history of cough and exertional dyspnea, who died of intractable cardiac failure two months after admission without establishment of a diagnosis related to the etiology of cardiac failure. Autopsy revealed a sessile tumor within the pulmonary trunk and a solitary metastatic lesion in the lung. Histologic, immunohistochemical and electron microscopic studies were performed and a diagnosis of malignant mesenchymoma was made. The patient in the second case was a 32-year-old male complaining of exertional dyspnea and back pain. Radiologic studies indicated a mediastinal tumor involving the pulmonary artery. Exploratory thoracotomy revealed that the mediastinal mass arose from the left pulmonary artery. He died of respiratory failure 26 months after onset of his initial symptoms. Histologic, immunocytochemical and electron microscopic studies of both surgical and autopsy materials revealed a malignant fibrous histiocytoma. One hundred ten previously reported cases of this tumor are reviewed, and its clinicopathologic and morphologic features and probable histogenesis are discussed.

Adult↗
PubMed1988

Evidence for reduced beta-adrenoceptor coupling to adenylate cyclase in femoral arteries from spontaneously hypertensive rats.

1. Arterial relaxant responses via beta-adrenoceptors have been demonstrated to be decreased in spontaneously hypertensive rats (SHR) when compared with normotensive Wistar-Kyoto rats (WKY). To determine which process of the beta-adrenoceptor.adenylate cyclase (AC) system is involved in the decreased responsiveness to beta-adrenoceptor stimulation, relaxant responses to forskolin and dibutyryl cyclic AMP (db cyclic AMP) were compared strips of femoral and mesenteric arteries isolated from 13 week-old SHR and age-matched WKY. 2. The relaxant response to either forskolin, an activator of AC, or db cyclic AMP was not significantly different between the SHR and WKY, when the strips of both arteries from both strains were contracted with K+ to an equivalent magnitude (85% of the maximum). 3. Under the same conditions, however, the relaxant response to noradrenaline (NA) via beta-adrenoceptors was significantly decreased in the SHR arteries. 4. When the strips of femoral arteries were contracted with the same concentration of K+, there was a precontraction of greater magnitude in response to the K+ and a decreased relaxation in response to forskolin, db cyclic AMP or NA in the SHR. On the other hand, when the strips of mesenteric arteries were contracted with the same concentration of K+, the precontraction was smaller in magnitude and there was an increased relaxation in the SHR. 5. The relationship between the relaxant responses and the K+-induced precontractions clearly showed that the ability of forskolin and NA to relax the K+-contracted strips depends on the magnitude of precontraction. Therefore, a difference in magnitude of precontraction between the two groups may produce a meaningless difference. 6. The relaxant responses to forskolin and NA were significantly potentiated by the addition of isobutyl methylxanthine (IBMX), an inhibitor of cyclic AMP phosphodiesterase. Even in the presence of IBMX, relaxant responses to forskolin were the same for the two strains. The difference in the pD2 value for NA-induced relaxation between the two strains was the same in the presence and absence of IBMX. 7. The relaxant effect of either nitroprusside or nifedipine, agents which are independent of this system, was not significantly different between the strips from SHR and WKY. These relaxations were not potentiated by IBMX. 8. From these results, it is concluded that the reduced beta-adrenoceptor coupling to AC is mainly involved in the decreased responsiveness to beta-adrenoceptor stimulation. Furthermore, for an accurate comparison to be made, it is necessary to minimize the influence of variations in the magnitude of precontraction on the relaxant responses.

1-Methyl-3-isobutylxanthine↗
PubMed1988

Role of stimulatory GTP-binding protein (Gs) in reduced beta-adrenoceptor coupling in the femoral artery of spontaneously hypertensive rats.

1. Arterial relaxant responses to beta-adrenoceptor agonists are decreased in spontaneously hypertensive rats (SHR) when compared with normotensive Wistar-Kyoto rats (WKY). To establish which component of the beta-adrenoceptor.adenylate cyclase (AC) system is impaired in the SHR arteries, effects of two activators of AC--cholera toxin (CTX) and forskolin--and of dibutyryl cyclic AMP (db cyclic AMP) were compared between strips of femoral arteries isolated from 13 week-old SHR and age-matched WKY. 2. In the absence of timolol, a beta-adrenoceptor antagonist, contractile responses of the strips to noradrenaline (NA) were significantly greater in the SHR than in the WKY. Timolol augmented the contractile responses to NA to a smaller extent in the SHR than in the WKY. 3. After blockade by timolol of beta-adrenoceptors, contractile responses of the strips to NA through the activation of alpha-adrenoceptors were not significantly different between the two strains. 4. Pre-treatment of the strips with CTX, an activator of the stimulatory GTP-binding protein (Gs), produced a slow-onset and long-lived antagonism of the alpha-adrenoceptor-mediated contractions. The antagonism was much smaller in the SHR than in the WKY. 5. The dose-response curves of the strips from both strains for alpha-adrenoceptor stimulation with NA determined after pretreatment with CTX were comparable to those determined in the absence of timolol. 6. Forskolin, an activator of the catalytic subunit of AC, and DB cyclic AMP also antagonized the alpha-adrenoceptor-mediated contractions. However, these antagonisms were not significantly different between the two strains. 7. Isobutyl methylxanthine (IBMX), an inhibitor of cyclic AMP phosphodiesterase, produced a similar antagonism of the alpha-adrenoceptor-mediated contractions between the two strains. 8. These results suggest that a reduced function of Gs is the main factor responsible for the decreased responsiveness to beta-adrenoceptor stimulation in the SHR femoral artery.

1-Methyl-3-isobutylxanthine↗
PubMed1988

Induction of neuronal differentiation in PC12 cells by B-cell stimulatory factor 2/interleukin 6.

B-cell stimulatory factor 2 (BSF-2) is a lymphokine which induces the final maturation of B cells. BSF-2 acts on a variety of cells other than B cells, and moreover, expression of BSF-2 mRNA is detected in interleukin-1 beta-stimulated glioblastoma and astrocytoma cell lines. Here, we studied the function of BSF-2 on pheochromocytoma PC12 cells, a model system for induction of neuronal differentiation. PC12 cells possess specific receptors for BSF-2. The BSF-2-stimulated PC12 cells expressed the c-fos proto-oncogene transiently, and they began to change morphologically to neurite-extending cells after several days. The number of voltage-dependent Na+ channels was also increased.

Adrenal Gland Neoplasms↗
PubMed1988

Transient neonatal hyperthyroidism and maternal thyroid stimulating immunoglobulins.

Serum thyroid stimulating hormone binding inhibitor immunoglobulins (TBII) and thyroid stimulating antibody (TSAb) concentrations were measured in three pregnant women with hyperthyroidism and then in their infants. The results suggested that TBII concentrations in infants in the neonatal period or from mothers during the third trimester of pregnancy showed a good correlation with the development of neonatal hyperthyroidism.

Adult↗
PubMed1988

Difference between two isozymes of (Na+ + K+)-ATPase in the interaction with omeprazole.

The difference in functional SH groups between two isozymes (alpha(+) and alpha forms) of (Na+ + K+)-ATPase was examined using omeprazole, a hydrophobic drug which was reported to modify SH groups of gastric (H+ + K+)-ATPase. Omeprazole inhibited rat brain and kidney (Na+ + K+)-ATPase activities in a time- and dose-dependent manner, and it inhibited incorporation of [3H]NEM into the catalytic subunit of the enzymes. The inhibition was greater in the brain enzyme than in the kidney enzyme. The inhibition of the brain enzyme showed a lag time, whereas the kidney enzyme was inhibited according to pseudo-first order kinetics. The inhibition by omeprazole of Na+-dependent phosphorylation and K+-stimulated phosphatase activity in the brain enzyme preparation was parallel with that of the overall (Na+ + K+)-ATPase reaction, while the partial reactions of the kidney enzyme showed different sensitivities to inhibition by omeprazole. Furthermore, the inhibition by omeprazole of [3H]NEM reactivity in the brain alpha(+) form was greater in the presence of SDS than in the absence, whereas the inhibition in the brain and kidney alpha forms was less in the presence of SDS than in the absence. These findings suggest that the isozymes of (Na+ + K+)-ATPase differ in hydrophobicity of SH groups of their catalytic subunits.

Animals↗
PubMed1988

Comparison of inhibitory effects of calcium channel blockers and that of a calmodulin antagonist in strips of mesenteric arteries from spontaneously hypertensive and normotensive rats.

Effects of calcium channel blockers and of calmodulin antagonist on the contractile responses to norepinephrine (NE) were compared between strips of mesenteric arteries from 6- and 14-week-old spontaneously hypertensive rats (SHR) and age-matched, normotensive Wistar-Kyoto rats (WKY). The ratio of the maximum contraction developed by NE to that by 60 mM KCl was significantly increased in strips from 14-week-old SHR. Niludipine, verapamil and diltiazem antagonized the maximum NE contraction to a greater extent in strips from 14-week-old SHR than in those from the WKY. However, the antagonism by niludipine of the KCl- or caffeine-induced contraction was not significantly different between the strips from 14-week-old SHR and those from WKY. In strips from 6-week-old rats, there was no difference in the antagonism by niludipine of the maximum NE contraction. On the other hand, the effect of W-7 on the maximum NE contraction was not significantly different between the strips from 14-week-old SHR and those from WKY. Schild plot analyses demonstrated that alpha 1-adrenoceptors were the same for the strips from SHR and WKY. These results suggest that the enhanced maximum NE contraction in the mesenteric artery from 14-week-old SHR reflects the increased transmembrane influx of calcium, and the activity of calmodulin seems to be the same for the two strains.

Adrenergic alpha-Antagonists↗
PubMed1988

Effect of intraoperative radiotherapy on pancreatic carcinoma: histopathological findings from autopsy cases.

Histopathological examinations of 18 necropsy patients with pancreatic carcinoma who died after receiving intraoperative radiotherapy (IOR) revealed the following: 1) Cancer cells were suspected of remaining in the periphery of the irradiated areas. 2) Thickening of intima of small arteries, some of which were obstructed, was found in the tumor tissues. 3) Highly degenerated nerve fibers were observed within the necrotic or viable tumor tissues. These findings provide evidence of the effects of IOR, while they also demonstrate the problems encountered in improving this treatment and the necessity of a complementary therapy for complete local control of pancreatic cancer by IOR.

Adult↗
PubMed1988

Edwardsiella tarda septicemia complicating acute leukemia.

We describe here an unusual case of Edwardsiella tarda septicemia preceded by acute gastroenteritis in a patient with acute leukemia in complete remission receiving maintenance chemotherapy. She also had ulcerated rectal cancer with bleeding, which was thought to serve as the portal of entry into the blood stream. She was successfully treated with cefmetazole and gentamicin in combination. However, the concomitant resolution of chemotherapy-induced granulocytopenia may have had a favorable effect as well.

Acute Disease↗
PubMed1988

Reduced function of the stimulatory GTP-binding protein in beta adrenoceptor-adenylate cyclase system of femoral arteries isolated from spontaneously hypertensive rats.

Arterial relaxant responses to beta adrenoceptor agonists are decreased in spontaneously hypertensive rats (SHR) when compared with normotensive Wistar-Kyoto rats (WKY). To determine which component of the beta adrenoceptor-adenylate cyclase (AC) system is involved in the decreased beta adrenoceptor responses, effects of two activators of AC-forskolin and cholera toxin and of dibutyryl cyclic AMP (DBcAMP) were compared between the strips of femoral arteries isolated from 13-week-old SHR and age-matched WKY. Arterial relaxant responses to either forskolin, an activator of AC or DBcAMP were not significantly different between the SHR and WKY, whereas the relaxant responses to norepinephrine (NE) via beta adrenoceptors were significantly weaker in the SHR than in the WKY. In the absence of timolol, a beta adrenoceptor antagonist, contractile responses to NE were significantly greater in the SHR than in the WKY. Timolol augmented the contractile responses to NE to a greater extent in the WKY than in the SHR. After the blockade by timolol of beta adrenoceptors, contractile responses to alpha adrenoceptor stimulation with NE were not significantly different between the two strains. The pretreatment of the strips with cholera toxin, an activator of stimulatory GTP-binding protein (Gs), antagonized the alpha adrenoceptor-mediated contractions much greater in the WKY than in the SHR. The alpha adrenoceptor-mediated contractions after the pretreatment with cholera toxin were comparable to the contractile responses to NE determined in the absence of timolol in either the SHR or the WKY. Forskolin and DBcAMP also antagonized the alpha adrenoceptor-mediated contractions. However, these antagonisms were not significantly different between the two strains. The cellular cAMP content in arterial strips after the stimulation with NE was significantly less in the SHR than in the WKY, whereas the cAMP contents were similar in arterial strips from both strains which were stimulated with forskolin. These results suggest that the reduced function of Gs is involved in the abnormality of beta adrenoceptor-AC system in the SHR femoral artery.

1-Methyl-3-isobutylxanthine↗
PubMed1988

Altered vascular beta adrenoceptor-mediated relaxation in deoxycorticosterone-salt hypertensive rats.

Beta adrenoceptor-mediated relaxation was studied on femoral and mesenteric arteries and thoracic aorta from deoxycorticosterone-salt hypertensive and age-matched normotensive rats. Maximum relaxations to isoproterenol (ISO), fenoterol and norepinephrine were less in hypertensive than in normotensive tissues. Mean negative log EC50 values of ISO and norepinephrine, but not fenoterol, were smaller in femoral and mesenteric strips from hypertensive rats than those from oil-water-treated rats. In thoracic aortas from hypertensive rats, the mean negative log EC50 values of ISO and fenoterol decreased, whereas those of norepinephrine increased as compared with those in oil-water-treated rats. In oil-salt- and deoxycorticosterone-water-treated rats, hypertension did not develop nor were the responses to ISO reduced. Relative potencies of the beta adrenoceptor agonists and Schild plot data for atenolol and butoxamine indicate that femoral arteries of normotensive and hypertensive rats possess beta-1 adrenoceptors mediating relaxation. It also is suggested that the mesenteric artery and thoracic aorta of both normotensive and hypertensive rats predominantly possess beta-2 adrenoceptors mediating relaxation. The present results suggest that an elevation in blood pressure is associated with the reduction of beta-1 adrenoceptor-mediated relaxation in femoral arteries and of beta-2 adrenoceptor-mediated relaxation in mesenteric arteries.

Animals↗
PubMed1988

[Clinical trial of high-dose etoposide].

In eleven patients with recurrent or refractory malignant lymphomas or lung cancers, a phase I study of high-dose etoposide without autologous bone marrow transplantation was performed. As a starting dose of etoposide 200 mg/m2 was administered for five consecutive days and the daily dose was increased step by step to a dose of 50 mg/m2. The dose of etoposide was escalated in order to define dose-limiting extramedullary toxicity, which was oropharyngeal mucositis and arrhythmias (PVC) at a dose level of 350 mg/m2/day. Bone marrow toxicity was completely reversible, supported by thrombocyte transfusion and antibiotics. Of nine evaluable patients with malignant lymphomas, two complete remissions and one partial remission were obtained. However, some patients unresponsive to standard-dose etoposide did not exhibit any response to the augmented dose of etoposide. Etoposide is thus a suitable drug for high-dose chemotherapy.

Adult↗