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Biomedical subjects

T Inukai

Publications and source records attributed to T Inukai.

At least 109 records · Page 6Linked to original sources
PubMed1992

[Clinical and cytological features of CD7 positive biphenotypic leukemias].

Clinical and cytological features of CD7 positive acute leukemias with biphenotypic characteristics in childhood were documented. From 87 patients with CD7+ acute leukemias, nine patients were selected on the basis of the biphenotypic expression of T-lymphoid and myelomonocytic antigens. The blasts of these patients expressed cell surface CD7, cytoplasmic CD3 and cytoplasmic CD13. In addition to these antigens, surface CD13 was also expressed after short term culture without any mitogens or stimulators. The double PAP method for detecting cytoplasmic antigens (CD3, CD13, beta F1, delta TCS1) was employed in this study. The average age of these patients was higher (10.2 y/o) than patients with common ALL. Mediastinal masses were observed in 4 of 9 patients. They were treated according to the diagnoses based on conventional hematological methods and surface antigen expression. In all 9 patients, complete remission was achieved, however, early relapse was noticed in 7. This study suggests that the leukemia cells of these patients may be derived at an early stage during the differentiation of multipotential hematopoietic stem cells. New therapeutic approaches are necessary to improve the outcome of such T/M biphenotypic leukemias.

Acute Disease↗
PubMed1992

Pharmacological profile of the new antidepressant levoprotiline.

The pharmacological properties of a new antidepressant, levoprotiline ((-)-R-a-[(methylamino)methyl]-9,10-ethanoanthracene-9(10H)- ethanol hydrochloride, CGP 12103 A, CAS 76496-69-0) were investigated. 1. Central nervous system: Levoprotiline did not have any marked effects on the general behaviour of mice and rats at low doses, however it slightly suppressed the righting reflex and spontaneous motor activity of mice at higher doses. In rats, chewing behaviour and salivation were observed at higher doses. Levoprotiline had no effects on the traction test (mice) and inclined screen test (rats). Levoprotiline induced a slight drowsy EEG pattern, the effect being similar to that of typical antidepressants such as maprotiline or imipramine but the degree of potency of levoprotiline was less than that of the latter two drugs. Levoprotiline and maprotiline did not inhibit the arousal response induced by physostigmine, while imipramine clearly suppressed the response. 2. Respiratory and cardiovascular system: Heart rate decrease and QT prolongation were observed in anesthetized dogs. In an in vitro study, levoprotiline caused only slight stimulation of noradrenaline transmission in the isolated guinea pig atrium. 3. Smooth muscle: The effects of levoprotiline on the contractile response to histamine, acetylcholine and serotonin in the isolated guinea pig ileum were compared with those of maprotiline or imipramine. While levoprotiline potently inhibited the contractile response to histamine, its inhibition of acetylcholine-induced contraction was the weakest of the three compounds studied. No remarkable effect was observed in serotonin induced contractions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Possible contributory role of the central histaminergic system in the forced swimming model.

Forced swimming is considered to bring about a depressive or despair state in experimental animals, usually manifested as immobility. Levoprotiline (CAS 76496-68-9), a new antidepressant, clearly reduced the duration of immobility in the forced swimming model in mice. As levoprotiline does not inhibit noradrenaline or serotonin reuptake, this effect did not seem to have been brought about through central monoaminergic systems. Histamine and tele-methylhistamine levels, the main metabolite of histamine in the cerebral cortex, were found to be significantly increased in the forced swimming model. Since the only significant known effect of levoprotiline on the neurotransmitter system is its histamine H1 receptor antagonism, a possible contribution of the central histaminergic system to the forced swimming model is proposed. The action of mepyramine, a histamine H1 receptor antagonist in reducing the duration of immobility seemed to support this proposition. It should be noted that antihistaminergic properties are shared by many antidepressant drugs.

Animals↗
PubMed1991

Purification and characterization of a novel glucooligosaccharide oxidase from Acremonium strictum T1.

A novel glucooligosaccharide oxidase was purified 495-fold from wheat bran culture of a soil-isolated Acremonium strictum strain T1 with an overall yield of 21%. This enzyme was composed of a single polypeptide chain with a molecular mass of 61 kDa as determined by sodium dodecyl sulfate polyacrylamide gel electrophoresis and size-exclusion high-performance liquid chromatography. Its isoelectric point was pH 4.3-4.5. This enzyme contained 1 mol of FAD per mol of enzyme and showed absorption maxima at 274, 379 and 444 nm. This enzyme was stable in the pH range of 5.0 to 11.0 with an optimal reaction pH of 10.0. The optimal reaction temperature was 50 degrees C. It was stable up to 50 degrees C for 1 h at pH 7.8. This enzyme oxidized those oligosaccharides with glucose residue on the reducing end and each sugar residue jointed by alpha or beta-1,4 glucosidic bond. The relative activity of this enzyme toward maltose, maltotriose, maltotetraose, maltopentaose, maltohexaose, maltoheptaose, lactose, cellobiose and glucose was 100:94:74:46:66:56:64:47:59. To our knowledge, this is the first report on the discovery of an glucooligosaccharide oxidase as judged from enzyme substrate specificity.

Acremonium↗
PubMed1991

Enhanced sensitivity to anorexia and consumption of drinking water induced by interleukin-1 beta in obese yellow mice.

Exogenously administered interleukin-1 beta (IL-1) was reported to suppress food intake and endogenous CRF in the brain was reported to be involved in mediating the IL-1-induced anorexia. The present study was undertaken to investigate the effect of IL-1 (i.p.) on food and water intake in obese yellow mice and in lean mice. Enhanced sensitivity to IL-1-induced suppression of food and water intake were observed in obese yellow mice compared to lean mice (food intake suppression: lean 29.92%, obese 88.48%; water intake suppression: lean 25.18%, obese 71.56% of respective controls). After treatment of the mice with ibuprofen (10 mg/kg i.p.), the suppression of food and water intake was prevented in lean mice but unaffected in obese mice. The results suggest that there may be differential sensitivity to activation of CRF neurons induced by the peripheral injection of IL-1 in obese yellow and in lean mice.

Animals↗
PubMed1991

Failure of anti-TSH receptor antibodies (TRAb) to predict the outcome of the course of Graves' disease following withdrawal of antithyroid drug.

Nineteen patients with Graves' disease were regarded as euthyroid at the end of therapy. Follow-up studies were performed for further 3 years. TSH binding inhibitor immunoglobins (TBII) were measured by radioreceptor assay. Thyroid stimulating antibodies (TSAb) were measured by a sensitive cAMP accumulation using FRTL-5 cells. Most of the patients showed negative TBII at the end of therapy, while TSAb-positive patients were approximately 50%. The relapse rates during post therapeutic period were 33.3% in TSAb-positive group and 40% in TSAb-negative group, which were not significantly different between the two groups. It was thought that determination of TSAb activity at the end of therapy, in addition to TBII, appears to play a permissive role in predicting the outcome of the course of Graves' disease following discontinuation of antithyroid drug therapy.

Adolescent↗
PubMed1991

Novel plasmid vectors for gene cloning in Pseudomonas.

Novel host-vector systems have been developed for gene cloning in the metabolically versatile bacterial genus Pseudomonas. We found that a new Pseudomonas strain, Pseudomonas flavida IF-4, isolated from soil, carried two small cryptic plasmids, named pNI10 and pNI20. They were multi-copy, but not self-transmissible, and the genome size was 3.7 kb for pNI10 and 2.9 kb for pNI20. Several types of cloning vectors containing a kanamycin or streptomycin resistance (Kmr or Smr) gene were constructed from pNI10 and pNI20. These plasmid vectors were efficiently transformed into several strains of Pseudomonas at a frequency up to 4 x 10(5) transformants per 1 microgram plasmid DNA by the usual competent cell method. The vectors derived from pNI10 replicated not only in Pseudomonas but also in some other Gram-negative enteric bacteria such as Escherichia coli, Enterobacter aerogenes, and Proteus mirabilis.

Blotting, Southern↗
PubMed1991

Efficacy of the glyceryl trinitrate transdermal therapeutic system in a dog model of heart failure.

The efficacy of a controlled-release topical dosage form of glyceryl trinitrate (Nitroglycerin Transdermal Therapeutic System, Nitroderm TTS, NTG-TTS; CAS 55-63-0) was studied in the experimental model of congestive heart failure in beagles. NTG-TTS suppressed the increase in left ventricular end-diastolic and central venous pressure, and total peripheral resistance resulting from propranolol, dextran and l-phenylephrine infusion. NTG-TTS antagonized the decrease in cardiac output in this model. These effects of NTG-TTS on congestive heart failure were presumably attributable to the reduction of pre-load, together with direct vasodilation of the peripheral arteries.

Administration, Cutaneous↗
PubMed1991

Effect of oxiracetam on cerebrovascular impairment in rats.

The effect of oxiracetam (CGP 21690E, CAS 62613-82-5) on cerebrovascular impairment was investigated in rats. 1. After injection of tranylcypromine (a MAO inhibitor), spontaneously hypertensive rats (SHR) which had been previously infused with norepinephrine (NE) for 14 days displayed stroke-related behaviour including kangaroo-like posture, seizures and death. Administration of oxiracetam at doses of 400 and 800 mg/kg/d p.o. for 14 days before tranylcypromine injection inhibited the stroke-related behaviour. 2. Bilateral common carotid and vertebral artery occlusion induced electroencephalogram (EEG) flattening, the EEG recovering gradually after re-perfusion of cerebral blood flow. Oxiracetam administered after the re-perfusion at a dose of 100 mg/kg, i.v. accelerated the recovery. This facilitatory effect was not seen when either piracetam (50 and 100 mg/kg i.v.) or idebenone (50 and 100 mg/kg i.v.) were administered. 3. Occlusion of middle cerebral artery produced cerebral infarction and disturbed the circadian rhythm of spontaneous motor activity with an relative increase of activity in the light period. Treatment with oxiracetam (400 mg/kg/d p.o.) for 14 days after the occlusion showed a tendency to an improvement in the disturbed circadian rhythm but did not influence the size of brain infarction. From these results, oxiracetam is thought to have a protective effect in cerebrovascular impairment.

Animals↗
PubMed1991

Effects of felodipine on vascular smooth muscle in comparison with nifedipine.

Felodipine (ethylmethyl 4-(2,3-dichlorophenyl)-1,4-dihydro-2,6-dimethyl- 3,5-pyridine dicarboxylate, CAS 72509-76-3), a vasoselective calcium antagonist, has a slow onset inhibitory effect on high K(+)-induced contractions in vascular smooth muscle and a longer duration than that of nifedipine. In addition it non-competitively inhibits Ca(++)-induced contraction in the depolarized aorta or femoral artery in the rat. Felodipine's inhibitory effect on caffeine or norepinephrine-induced contraction was observed at a micromolar range. This result suggests that felodipine may inhibity Ca++ release from intracellular Ca++ stores through a mechanism of Ca++ or inositol 1,4,5-triphosphate induced Ca++ release in addition to a blockade of Ca++ influx through the sarcolemma.

Animals↗
PubMed1991

General pharmacology of the novel angiotensin converting enzyme inhibitor benazepril hydrochloride. Effects on cardiovascular, visceral and renal functions and on hemodynamics.

The effects of benazepril hydrochloride (CGS 14824 A, CAS 86541-74-4), a novel angiotensin I converting enzyme inhibitor, on cardiovascular, visceral and renal functions and on hemodynamics, were studied in various experimental animals. Even at a high dose of 100 mg/kg p.o. benazepirl hydrochloride had no influence on the respiration, heart rate and ECG of normotensive anesthetized cats and, except at higher doses, had little effect on the contractile tension of mammalian isolated atrium, ileum, trachea, stomach fundus strips, vas deferens or uterus. Benazepril hydrochloride even at a high dose of 100 mg/kg p.o. had little effect on spontaneous uterine motility, charcoal transportation and gastrointestinal tract motility. In addition, it did not cause gastric irritation, alter the secretion of gastric and biliary juices, and did not affect the tension of the nictitating membrane or the twitch tension of the gastrocnemius muscle in various experimental animals. Benazepril hydrochloride had no effect on the blood glucose and cholesterol levels in alloxan-induced diabetic rats but decreased the triglyceride and total cholesterol levels in normotensive rats at a dose of 30 mg/kg p.o. Benazepril hydrochloride at 3 mg/kg.day s.c. for 10 weeks caused a significant decrease in aortic atherosclerosis without reducing hypercholesterolemia in cholesterol-fed rabbits. Benazepril hydrochloride at a high dose of 100 mg/kg p.o. showed no effect on the urine volume and urinary excretion of electrolytes but decreased PSP excretion in normotensive rats. At a dose of 3 or 10 mg/kg.day p.o. for 4 weeks benazepril hydrochloride inhibited the increase in the excretion of urinary protein in DOCA/salt spontaneously hypertensive rats. It caused hemolysis at concentrations as high as 0.1-1% in rabbits, however, even at a high dose of 100 mg/kg p.o. it did not affect red blood cell fragility in rats, and, except at a high dose of 10(-4) g/ml, showed little effect on the platelet aggregation response induced by collagen or arachidonic acid in rabbits. From these results, benazepril hydrochloride is considered to be a safe and well-tolerated addition to the therapeutic armamentarium of cardiovascular drugs.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1991

Effect of benazepril hydrochloride on cardiac hypertrophy in spontaneously hypertensive rats.

To study the effects of a novel angiotensin I converting enzyme inhibitor (ACEI) on hypertension-induced cardiac hypertrophy, benazepril hydrochloride (CGS 14824 A, CAS 86541-74-4) at the dose of 3 and 10 mg/kg/d p.o. was administered to spontaneously hypertensive rats from 4 to 16 weeks of age. In addition to suppression of developing blood pressure, benazepril hydrochloride reduced both the wet weights of whole heart and left ventricle dose-dependently and significantly. Benazepril hydrochloride had no effect on hydroxyproline concentration and content or protein concentration in the left ventricle, whereas is reduced the total protein content dose-dependently. Serum ACE activity was significantly reduced at 10 mg/kg/d of benazepril hydrochloride, but renin activity, aldosterone and noradrenaline concentration in serum were not changed. From the microscopic findings of the left ventricle, benazepril hydrochloride reduced the myocardial hypertrophy significantly. From these results, benazepril hydrochloride seems to suppress the increase in volume load by acting through the renin-angiotensin-aldosterone system, and dose not seem to cause a significant reflex of catecholamine which often occurs with peripheral vessels dilation. Thus, benazepril hydrochloride may be expected to suppress cardiac hypertrophy in patients with hypertension.

Aldosterone↗
PubMed1991

General pharmacology of the novel angiotensin converting enzyme inhibitor benazepril hydrochloride. Effects on central nervous and sensory systems and other functions.

The effects of benazepril hydrochloride (CGS 14824 A, CAS 86541-74-4), a novel angiotension I converting enzyme inhibitor, on the central nervous systems, were studied in experimental animals. Benazepril hydrochloride (3 or 10 mg/kg/d, p.o. for 14 days) dose-dependently inhibited the increase in the blood pressure caused by continuous norepinephrine (NE) infusion in spontaneously hypertensive rats (SHR) and suppressed in seizures induced by a monoamine oxidase inhibitor, tranylcypromine in NE infused SHR. Benazepril hydrochloride transiently increased spontaneous motor activity in mice, tended to inhibit acetic acid-induced writhing in mice and decreased fast wave sleep and slow wave deep sleep on EEG in cats at a high dose of 100 mg/kg p.o. However, benazepril hydrochloride at the same dose showed no effect on other central nervous and sensory systems in experimental animals.

Acetates↗
PubMed1991

Antihypertensive action of the novel angiotensin converting enzyme inhibitor benazepril hydrochloride in hypertensive rat models.

Single or repeated administration of benazepril hydrochloride (CGS 14824 A, CAS 86541-74-4), a novel angiotensin I converting enzyme inhibitor, (0.3-10 mg/kg p.o.) caused significant antihypertensive effects in renal and spontaneously hypertensive rats (SHR). The antihypertensive effects of benazepril hydrochloride was about 3 times as potent as that of captopril in these models. Single administration (0.3-3 mg/kg p.o.) of benazepril hydrochloride and enalapril maleate showed an equipotent antihypertensive effect in SHR. Benazepril hydrochloride (3-30 mg/kg p.o.), however, showed no clear effect on the blood pressure and heart rate in normotensive or DOCA/salt hypertensive rats.

Administration, Oral↗
PubMed1991

[Multiple sclerosis with higher cerebral dysfunction: a case report].

Higher cerebral dysfunctions such as aphasia, apraxia and agnosia have seldom been reported in multiple sclerosis (MS). 12 year-old right-handed boy felt unsteadiness of the body and headache for several days. Two months later, he had the same episode and complained of visual disturbance, and weakness and sensory disturbance on the face and the extremities. Additionally, he showed amnestic aphasia, acalculia, ideomotor apraxia, finger agnosia and right-left disorientation. Cerebrospinal fluid examinations revealed increases IgG, myelin basic protein and neuron specific enolase (11%, 25 ng/ml and 28.8 ng/ml, respectively). X-ray CT scan and MRI-CT examinations revealed sclerotic lesions on the left parietal white matter and the right mid-brain. The diagnosis was made as MS. He was treated with m-PSL (methyl-prednisolone) pulse therapy for three weeks and consecutively treated with PSL for four weeks. He recovered gradually, but visual disturbance and facial palsy remained. After seven months MRI-CT showed a high signal intensity on the left parietal white matter in spite of the disappearance of the lesion on X-ray CT scan. We suggest that these higher cerebral dysfunctions may result from the lesion of the left parietal white matter which produces a disconnection between each cortical area.

Agnosia↗
PubMed1990

Inhibitory effects of cadralazine and its metabolite, ISF-2405, on contractions and the level of cytosolic Ca2+ in vascular smooth muscle.

The inhibitory effects of a hypotensive agent, cadralazine and its metabolite, ISF-2405, on the level of cytosolic Ca2+ ([Ca2+]cyt) and on contractions were examined in isolated vascular smooth muscle. Cadralazine slightly inhibited the transient norepinephrine-induced contraction in rabbit aorta and canine femoral, renal and mesenteric arteries and saphenous vein, and prostaglandin F2 alpha-induced contractions in canine basilar and coronary arteries. In contrast, ISF-2405 inhibited the contractions induced by prostaglandin F2 alpha in canine basilar and coronary arteries and those induced by norepinephrine in canine renal and femoral arteries and rabbit aorta. In aorta, ISF-2405 inhibited the increase in [Ca2+]cyt and muscle tension caused by norepinephrine. A Ca2+ channel blocker, verapamil, inhibited the norepinephrine-stimulated increase in [Ca2+]cyt more potently than it inhibited the increase in muscle tension, and ISF-2405 inhibited the verapamil-resistant part of the contraction. In Ca2(+)-free solution, norepinephrine induced transient increases in [Ca2+]cyt and muscle tension. ISF-2405 inhibited these changes. However, ISF-2405 did not inhibit the transient contraction induced by caffeine in the aorta. These results suggest that cadralazine is metabolized to ISF-2405 and inhibits vascular smooth muscle contraction by inhibiting receptor-mediated Ca2+ influx, Ca2+ release and Ca2+ sensitization of contractile elements.

Animals↗
PubMed1990

Effects of peripheral administration of recombinant human interleukin-1 beta on feeding behavior of the rat.

This study was undertaken to investigate the changes in feeding behavior, including ambulatory activity, induced by a single injection of Interleukin-1 beta (IL-1) (2 micrograms/rat) at 18:00, just before the dark phase. For this purpose, we used the Gunma University-type automatic apparatus for continuous and direct measurement of ambulation and drinking. A significant decrease in food intake was observed for 12 hours after treatment with IL-1. Peripheral administration of IL-1 also produced a marked decrease in ambulatory activity within 3 hours which continued for 6 hours. In addition, IL-1 produced a marked decrease in drinking behavior during the first 6 hours. We reported here the changes in consummatory and ambulatory behavior of rats after acute administration of IL-1. The sickness which IL-1 produced may, at least in part, contribute to these phenomena, although precise mechanisms are still unknown.

Animals↗