Search PubMed⌕ Search

Biomedical subjects

M Morikawa

Publications and source records attributed to M Morikawa.

At least 163 records · Page 9Linked to original sources
PubMed1993

Exercise-induced upward shift of diastolic left ventricular pressure-volume relation in patients with dilated cardiomyopathy. Effects of beta-adrenoceptor blockade.

BACKGROUND: The effectiveness of beta-blocker therapy for dilated cardiomyopathy (DCM) may be attributed to the inhibition of detrimental effects on the failing heart of sympathetic stimulation during exertion. However, the harmful effects of activity as well as the protective effects of beta-blockers have not been demonstrated. Diastolic ventricular function is known to be sensitive to transient myocardial metabolic insult. In this study, we investigated the effect of modest exercise with or without beta-blockade on the diastolic left ventricular pressure-volume (P-V) relation in patients with DCM. METHODS AND RESULTS: The diastolic left ventricular P-V relation was obtained by high-fidelity pressure measurements and digital subtraction left ventriculography at rest and immediately after modest supine bicycle exercise in 12 patients with DCM. The effects of intravenous administration of 0.1 mg/kg propranolol on resting and exercise P-V relations were studied. The end-diastolic and lowest left ventricular pressures were significantly elevated by exercise (20 +/- 9 to 32 +/- 13 mm Hg, P < .01, and 12 +/- 6 to 21 +/- 11 mm Hg, P < .01, respectively) despite insignificant changes in left ventricular volumes. The administration of propranolol did not alter the resting diastolic P-V relation. However, propranolol significantly attenuated the exercise-induced upward shift of the diastolic P-V relation despite a significant increase in end-diastolic volume. The significant upward shift and attenuation by propranolol were also observed even when the left ventricular pressure was corrected by the subtraction of right atrial pressure. CONCLUSIONS: These results indicate that even modest exercise exerts detrimental effects on diastolic left ventricular function of the failing heart through beta-adrenergic stimulation. The clinical effectiveness of beta-blocker therapy in patients with DCM can be attributed in part to the inhibition of detrimental myocardial effects of sympathetic stimulation during daily activity.

Adrenergic beta-Antagonists↗
PubMed1993

Morphological changes and reorganization of actinfilaments in human myeloid leukemia cells induced by a novel protein phosphatase inhibitor, tautomycin.

A protein phosphatase inhibitor, tautomycin induces blebs on the surface of human myeloid leukemia K562 cells within 10 min. In this paper we examined the cytoskeleton of tautomycin-treated cells. In the presence of tautomycin, cells with blebs turned into segmented forms with smooth surfaces after 15 min and into smooth round shapes without microprotuberance after 60 min. Observation with fluorescence microscopy showed that F-actin detached from the plasma membrane at the site of the blebs. Further treatment with tautomycin induced the accumulation of F-actin at the segmentation centers. Under electron microscopy, an electron dense ring-structure was detected at the segmentation center. Tautomycin did not induce major changes of the microtubule network although F-actin accumulated near the microtubule organizing center. The amount of F-actin increased in tautomycin-treated cells. These results indicate that the morphological changes are induced by reorganization of actinfilaments.

Actin Cytoskeleton↗
PubMed1993

Availability of dihydrofolate reductase affinity handle in expressing human prolactin as a soluble fusion protein.

Human prolactin (PRL) cDNA was successfully expressed in Escherichia coli cells with the aid of a dihydrofolate reductase (DHFR) affinity handle. The formed DHFR-PRL fusion protein was accumulated in E. coli cells as a soluble protein with DHFR activity at 30 degrees C. The fusion protein was highly purified with monitored the DHFR activity by methotrexate-bound affinity chromatography, suggesting the usefulness of the handle even in expressing a large polypeptide as a fusion protein.

Amino Acid Sequence↗
PubMed1993

Study on high-strength plastic teeth. Tooth discoloration.

Conventional plastic teeth (CV teeth) are inferior to porcelain teeth in maintaining an adequate esthetic appearance with wear and discoloration, and thus have a shorter period of durability. Recently, high-strength plastic teeth (HS teeth) have been developed and applied to overcome the wear problems of CV teeth. Since HS teeth made of hard resin are still susceptible to staining with pigments, it has been observed that the esthetics of removable partial dentures made from such plastic teeth are gradually impaired in many patients. To investigate the susceptibility of HS teeth to pigments, we conducted an in vitro study by immersing three types of artificial teeth in three coloring liquids. It was found that the HS teeth tended to be less susceptible to the test pigments than the CV teeth to various degrees. In contrast, they showed markedly stronger susceptibility to the pigments than porcelain teeth. For all three artificial tooth types, daily tooth cleaning with an ultrasonic vibrator had a tendency to reduce the coloration in comparison with their counterparts without ultrasonic cleaning.

Acrylic Resins↗
PubMed1993

Contribution of plasmin to sex differences in platelet aggregation in the rat.

Platelet aggregation was induced more strongly in male than in female 5, 12, and 45 week-old rats by both collagen and arachidonic acid. This is in agreement with our previous reports which suggested that the sex differences in platelet aggregation may be a primary characteristic of rat platelets. In plasma, plasmin-like activity was higher in male than in female rats. Plasmin alone induced aggregation, and low concentrations of plasmin synergistically enhanced collagen-induced aggregation in both male and female rats. Platelets potentiated plasmin generation by plasminogen activator at various Ca2+ concentrations in both male and female rats. Platelets from males displayed more efficient plasmin generation in 2 mM extracellular Ca2+ than those from females. If platelets were activated by abnormal causes in plasma, generated plasmin could make a greater contribution to the potentiated effect of platelet aggregation in male than in female rats. This study suggests that plasmin may be a partial cofactor in sex differences in platelet aggregation in the rat.

Animals↗
PubMed1993

[Surgical treatment of double-outlet right ventricle with left ventricular outflow tract obstruction].

Three patients with double-outlet right ventricle (DORV) and left ventricular outflow tract obstruction (LVOTO) were described. In each patient, LVOTO was produced by restrictive VSD which resulted from malalignment of the conal musculature and a discrete subaortic membrane. All patients underwent surgical repair with enlargement of the ventricular septal defect and rerouting of the outflow tract from the left ventricle to the aorta. One patient died of congestive heart failure three months postoperatively. Causes of LVOTO and surgical management of DORV with LVOTO were discussed.

Cardiac Surgical Procedures↗
PubMed1993

[A case of malignant paraganglioma].

Herein we report a case of paraganglioma. The metastatic lesion was incidentally found in a 64-year-old man by chest roentgenography. The primary tumor was extra-adrenal and was revealed to be malignant. The patient was normotensive without clinical symptoms despite extreme high serum and urinary dopamine levels. A venous injection of 5 mg metoclopramide elicited a significant increase of the blood pressure. This phenomenon disappeared after surgical excisions of the primary and metastatic lesions. The metoclopramide test is considered to be useful to diagnose asymptomatic paraganglioma.

Humans↗
PubMed1993

[Two cases of male infertility with pathological dilatation of ejaculatory duct].

Two cases of male infertility with pathological dilatation of ejaculatory duct are reported. In both cases, the dilatated wall of the ejaculatory duct was incised at the vermontanum with a cold knife endoscopically. After the incision, the findings of semen analysis of one case improved markedly and his wife became pregnant. In another case, semen analysis was not improved. Transurethral incision seemed to be a useful modality for the treatment of pathological dilatation of ejaculatory duct.

Adult↗
PubMed1992

Inhibitory actions of prostaglandin E1 on neurogenic plasma extravasation in rat airways.

To determine whether neurogenic inflammation can be inhibited by prostaglandin E1 (PGE1), that is suggested to have an inhibitory effect on neuropeptide release from airway sensory nerves, we examined plasma extravasation in the airways of anesthetized rats in vivo with Evans blue due as a marker. Neurogenic inflammation was produced by an i.v. injection of capsaicin (100 micrograms/kg) or by antidromic electrical stimulation of the right vagus nerve (4 Hz, 1 ms, 4 V for 1 min). Capsaicin injection significantly increased leakage of dye in the trachea and main bronchi. Similar increases in leakage were seen in the trachea and right bronchus on electrical stimulation of the right vagus nerve. PGE1 (1-1000 micrograms/kg) inhibited the leakage induced by capsaicin in the trachea and bronchi concentration dependently with complete inhibition at a concentration of 1000 micrograms/kg. Likewise, PGE1 (1000 micrograms/kg) significantly inhibited electrical stimulation-induced leakage in the trachea and right bronchus (P less than 0.01). I.v. substance P (SP; 1 microgram/kg) increased Evans blue dye extravasation in the same way as the leakage induced by capsaicin and electrical stimulation but PGE1 (1000 micrograms/kg) failed to inhibit SP-induced leakage in the trachea and main bronchi (P greater than 0.20). These results suggest that PGE1 inhibits neurogenic plasma leakage by presynaptic inhibition of the release of neuropeptides from sensory nerves.

Alprostadil↗
PubMed1992

Activation of calpain I in thrombin-stimulated platelets is regulated by the initial elevation of the cytosolic Ca2+ concentration.

The source and concentration of Ca2+ required to activate calpain I were investigated in thrombin-stimulated platelets. The concentration of cytosolic free Ca2+ ([Ca2+]i) was measured in platelets containing fura-2-AM, and exhibited a biphasic response after stimulation with 0.05, 0.1 or 0.5 NIH units of thrombin/ml. An initial transient elevation, which was predominantly dependent upon Ca2+ released from the internal stores into the cytosol, peaked at 15 s after stimulation, and a secondary sustained elevation, which was due to Ca2+ influx, was observed following the initial elevation. Calpain I was present at about 540 ng/10(8) unstimulated platelets, as measured by immunoblotting using rabbit anti-(human calpain I) IgG. Calpain I was activated 10 s after thrombin stimulation, as determined by the appearance of the 78 kDa and 76 kDa forms on immunoblots. The activation ratio of calpain I was calculated as the amount of the 78 + 76 kDa forms as a percentage of the total (80 + 78 + 76 kDa), and was influenced by the extent of the initial transient [Ca2+]i elevation after stimulation. An initial increase in [Ca2+]i of 300 nM was required to achieve the maximal activation (60%) of calpain I, and half-maximal activation occurred at 160 nM- Ca2+]i. These results suggest that the activation of calpain I in platelets is regulated by the initial elevation in Ca2+]i after thrombin stimulation, and does not necessarily require a Ca2+ influx.

Adult↗
PubMed1992

Growth retardation due to idiopathic growth hormone deficiencies: MR findings in 24 patients.

In this study we evaluated the pituitary-hypothalamic abnormalities of "idiopathic growth hormone (GH) deficiency" as demonstrated by MR imaging. Twenty-four patients were examined with a 1.5-T unit using spin echo T-1 weighted images. The patients were divided into two groups according to MR findings: those with ectopic posterior pituitary glands (12 patients), and those with normal posterior pituitary glands (12 patients). Ten patients in the former group and four in the latter group had small anterior pituitary glands. All patients in the former group but only four in the latter group had severe GH deficiencies. Multiple hormone deficiencies were found in eight patients in the former group, but in only two in the latter group. Among the 12 patients with posterior pituitary ectopia, 11 were males, 10 had been born by breech delivery, and four had a history of asphyxia. It is speculated that perinatal abnormalities can cause posterior pituitary ectopia and that there is a close correlation between breech delivery and the male disadvantage of posterior pituitary ectopia. Half of our patients with "idiopathic GH deficiency" had ectopic posterior pituitaries. GH deficiency with posterior pituitary ectopia should no longer be considered idiopathic because organic lesions can now be identified during life.

Adolescent↗
PubMed1992

Induction of phosphatidylinositol-glycan-linked Fc gamma RIII in human monocytic THP-1 cells by transforming growth factor-beta 1 and retinoic acid.

Human monocytic leukemic cell line THP-1 was incubated with transforming growth factor-beta 1 (TGF-beta 1) and retinoic acid (RA) and the expression of Fc gamma RIII was investigated. Fc gamma RIII was induced after incubation of the cells with both TGF-beta 1 and RA but not with either TGF-beta 1 or RA alone. Such effects of TGF-beta 1 and RA were not detected on human promyelocytic HL-60 cells. Northern blot analysis revealed the induction of Fc gamma RIII transcripts in THP-1 cells. Furthermore, the Fc gamma RIIIs newly expressed on the cell surface were cleaved by phosphatidylinositol-specific phospholipase C (PI-PLC) and reacted with monoclonal antibody MG38 which specifically binds to granulocyte-type Fc gamma receptors. These results indicated that TGF-beta 1 could induce phosphatidylinositol-glycan-linked Fc gamma RIII (Fc gamma RIII-I) in THP-1 cells in the presence of RA.

Antigens, Differentiation↗
PubMed1992

Regulation of myeloid-specific calcium binding protein synthesis by cytosolic protein kinase C.

Two calcium binding proteins, MRP-8 and MRP-14, are specifically synthesized in human myeloid cells. This paper shows that Me2SO, all-trans-retinoic acid (RA) and 1 alpha,25-dihydroxyvitamin D3 (1 alpha,25(OH)2D3), but not 12-O-tetradecanoyl phorbol-13-acetate (PMA) are potent inducers of MRP-8/14 protein complex in human leukemic cells. Transforming growth factor-beta 1 (TGF-beta 1) is shown to enhance the inductive effect of RA and 1 alpha,25(OH)2D3. We have examined the possibility that MRP expression is regulated through the protein kinase pathway. Both cytosolic and membrane-bound protein kinase C (PKC) activities increased during differentiation by RA and 1 alpha,25(OH)2D3. PMA-treatment led to a decrease of cytosolic PKC activity and an increase of membrane-bound PKC activity in the presence of these differentiation inducers, while PMA alone resulted in low cytosolic and high membrane-bound PKC activities. PKC inhibitor H7 inhibited MRP synthesis in HL-60 cells treated with RA and 1 alpha,25(OH)2D3. These results suggest that cytosolic PKC activity may be involved in a stimulatory pathway of MRP synthesis and that protein phosphorylation reactions may play important roles in MRP expression during myelocytic differentiation.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1992

The role of cyclic AMP in non-adrenergic non-cholinergic contraction in guinea-pig bronchi.

1. We investigated the role of adenosine 3':5'-cyclic monophosphate (cyclic AMP) in non-adrenergic non-cholinergic (NANC) contraction in guinea-pig bronchial strips. 2. Forskolin (3 nM to 1 microM) reduced NANC contraction induced by electrical field stimulation (EFS) in a concentration-dependent fashion (-log EC50 was 7.22 +/- 0.12 M and maximum inhibition was 100 +/- 0.01%). However, forskolin (less than 1 microM) did not alter the contraction induced by substance P (SP, 1 microM). 3. Dibutyryl cyclic AMP (1 mM) also reduced NANC contractions induced by EFS (100 +/- 0.01%) without significant effect on SP (1 microM)-induced contractions. In contrast, dibutyryl cyclic GMP (1 mM) was without effect against either NANC or SP-induced contractions. 4. Both the beta 2-adrenoceptor agonist, procaterol (0.1 nM to 3 nM) and theophylline (100 nM to 1 mM) concentration-dependently reduced EFS-induced NANC contractions without significant effect on SP (1 microM)-induced contractions. 5. In contrast to forskolin, procaterol and theophylline, both sodium nitroprusside and cromakalim inhibited the EFS-induced contractions only at those concentrations that similarly reduced the contractions induced by SP (1 microM). 6. These results suggest that cyclic AMP may mediate pre-junctional inhibition of NANC contractions in guinea-pig bronchi.

Animals↗
PubMed1992

Possible mechanisms of inhibition with atropine against noradrenaline-induced contraction in the rabbit aorta.

1. In the rabbit isolated aorta, atropine (3 x 10(-6) M-10(-4) M) inhibited contractile response to noradrenaline without affecting contraction to KCl. 2. In the presence of contraction to noradrenaline, atropine (3 x 10(-7) M-10(-4) M) caused concentration-dependent relaxation. Pretreatment with theophylline (10(-3) M) potentiated the relaxant action of atropine. Relaxation to atropine was not affected by the specific guanosine 3':5'-cyclic monophosphate phosphodiesterase inhibitor, M & B 22,948 (10(-4) M), tetraethylammonium (10 mM), indomethacin (10(-5) M), propranolol (10(-7) M), nifedipine (10(-6) M) or removal of the endothelium. 3. Relaxation to either atropine or prazosin was not affected by preincubation with prazosin and atropine, respectively. 4. In Ca(2+)-free medium containing EGTA and nifedipine, atropine (10(-7) M-10(-4) M) inhibited the residual noradrenaline response more than the subsequent Ca(2+)-induced contraction. Pretreatment with either theophylline (10(-3) M), forskolin (3 x 10(-7) M) or a low concentration of prazosin (3 x 10(-9) M) also inhibited the residual contraction to noradrenaline and Ca2+. The effect of combined treatment of atropine and any of these agents was much greater than with each individual agent. 5. Atropine (10(-6) M-10(-4) M) also inhibited increases in the level of inositol monophosphates (IP) in response to noradrenaline. Theophylline (10(-3) M) and a low concentration of prazosin (3 x 10(-9) M) also inhibited IP formation. Combined with atropine, the effect was much greater than with each of these agents individually. 6. Atropine did not affect adenosine 3':5'-cyclic monophosphate (cyclic AMP) levels in the aorta and also failed to displace specific [3H]-prazosin binding.7. These results suggest the possibility that smooth muscle relaxation to atropine may be due to the inhibition of phosphoinositide metabolism. The relaxation is not apparently due to an action of atropine on ax-adrenoceptors, or a change in the level of cyclic AMP.

Animals↗
PubMed1992

Effect of mammalian lignans on fMLP-induced oxidative bursts in human polymorphonuclear leucocytes.

We examined the effects of mammalian lignans, enterolactone, prestegane B and 2,3-dibenzylbutane-1,4-diol (DBB) on superoxide production and luminol-dependent chemiluminescence (LCL) response in human polymorphonuclear leucocytes (PMNs). The three lignans had no direct effect on the responses of human PMNs. DBB and prestegane B enhanced the superoxide production and LCL response induced by formylmethionyl-leucyl-phenylalanine (fMLP), but enterolactone inhibited fMLP-induced effects. The effects of DBB were stronger than those of prestegane B and the effects of DBB were inhibited by bromophenacyl bromide, mepacrine, N-(6-aminophenyl)-5-chloro-1-naphthalene, sulphonamide and trifluoroperazine, but not by gossypol, nordihydroguaretic acid, indomethacin, staurosporine, 1-(5-isoquinolinesulphonyl)-2-methylpiperazine dihydrochloride or (R,S)-2-methoxy-3-(octadecyl-carbamoyloxy)-propyl-2-(2-thiazoli o)-ethylphosphate. These results suggest that DBB primes the responses of human PMNs, and the priming effect is caused by the activation of phospholipase A2--and Ca(2+)-calmodulin-pathways, but not by the activation of lipoxygenase, cyclo-oxygenase and protein kinase C or by the release of platelet activating factor.

Humans↗
PubMed1992

Effective site of bronchodilation by beta-adrenergic and anticholinergic agents in patients with chronic obstructive pulmonary disease: direct measurement of intrabronchial pressure with a new catheter.

To study the effective site of bronchodilators in patients with chronic obstructive pulmonary disease (COPD), a catheter tip micromanometer sensing lateral pressure of the airway was wedged into the right lower lobe of a bronchus, 3 mm inner diameter, in 14 patients with COPD. We simultaneously measured mouth flow, transpulmonary pressure (PL) and intra-airway lateral pressure during quiet tidal breathing. Total pulmonary resistance (RL) was calculated from PL and mouth flow, and central airway resistance (RC) was calculated from intra-airway lateral pressure and mouth flow. Peripheral airway resistance (RP) was obtained by the subtraction of RC from RL. This technique permitted identification of the site of changes in airway resistance. Atropine sulfate (5 mg/ml) was continuously inhaled during tidal breathing for 1 min by seven patients (Group A), and the other seven patients (Group B) inhaled fenoterol (1 mg/ml) for 1 min. The doses that were actually delivered were 0.75 mg for atropine sulfate and 0.15 mg for fenoterol. The baseline resistances of RC and RP were 3.9 +/- 0.8 and 3.7 +/- 0.6 cm H2O/L/s in Group A, and 4.3 +/- 0.5 and 3.5 +/- 0.4 cm H2O/L/s in Group B, respectively. Both atropine sulfate and fenoterol significantly decreased RL by an average of 2.4 and 2.6 cm H2O/L/s, and there was no significant difference between them (p greater than 0.20). The percentage decrease in resistance from the baseline values by fenoterol did not differ significantly between RC and RP (p greater than 0.20). However, atropine sulfate significantly decreased RC more than RP.(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Resistance↗