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Biomedical subjects

T Tahara

Publications and source records attributed to T Tahara.

At least 127 records · Page 7Linked to original sources
PubMed1989

Evaluation of the significance of "redistribution" in I-123 IMP SPECT in cerebrovascular disorders--a comparative study with PET.

We evaluated the significance of redistribution in 123I-IMP SPECT study using PET. Twelve lesions in ten patients were selected. These lesions were classified into the following three groups; ischemia, infarction of subacute phase and infarction of chronic phase. All lesions with ischemia or subacute infarction showed good or moderate redistribution. Three of four lesions with chronic infarction showed no redistribution. The mean values of rCBF and rCMRO2 were highest in the lesions with good redistribution, but there was no differences in rOEF with the degree of redistribution. In conclusion, the tissue with good redistribution is not always viable and it was impossible to predict a region with increased rOEF by redistribution alone.

Adult↗
PubMed1989

Cerebral blood flow, oxygen and glucose metabolism with PET in progressive supranuclear palsy.

Cerebral blood flow, cerebral oxygen metabolic rate and cerebral glucose metabolic rate were measured with positron emission tomography (PET) in four patients with progressive supranuclear palsy (PSP). Decreased blood flow and hypometabolism of oxygen and glucose were found in both subcortical and cortical regions, particularly in the striatum including the head of the caudate nucleus and the frontal cortex. The coupling between blood flow and metabolism was preserved even in the regions which showed decreased blood flow and hypometabolism. These findings indicated the hypofunction, as revealed by decreased blood flow and hypometabolism on PET, both in the striatum and the frontal cortex, and which may underlie the pathophysiological mechanism of motor and mental disturbance in PSP.

Adult↗
PubMed1989

[Thromboxane synthetase inhibitors. I. Synthesis of some imidazolylarylmethanols and their inhibitory activity on platelet aggregation].

Several imidazolylpyridinemethanols and imidazolylbenzenemethanols were prepared and evaluated for an inhibitory activity against arachidonic acid-induced platelet aggregation. The result shows that the arylmethanol moiety is essential for the activity and may correspond to the 15-OH group of prostagrandin H2 (PGH2). Among the compounds tested, 4-[alpha-hydroxy-5-(1-imidazolyl)-2-methylbenzyl]-3,5-dimethylbenzoic acid (XV) was found to have a potent inhibitory activity and a long duration of action. Structure-activity relationships are also discussed briefly.

Animals↗
PubMed1989

[Neuroleptic properties of Y-20024, a new benzofurancarboxamide derivative].

N-[(1-butyl-2-pyrrolidinyl)methyl]-2-methyl-5-sulfamoyl-2,3- dihydrobenzofuran-7-carboxamide hydrochloride (Y-20024) was synthesized in our laboratories in anticipation of developing a new psychotropic drug. In the present study, the pharmacological properties of Y-20024 were compared with those of sulpiride (SPR) and haloperidol (HPD). Administered orally, Y-20024 was 10 times stronger than SPR in inhibiting apomorphine (0.5 mg/kg, s.c.)-induced hyperactivity in mice; administered intravenously or intracerebroventricularly, it was 2 times or one third as strong, respectively. Y-20024 was almost equipotent to SPR in antagonizing apomorphine (0.1 mg/kg, s.c.)-induced vomiting in dogs. Combined with methamphetamine (5 mg/kg, i.p.), Y-20024 and SPR induced mortality dose-dependently in rats, but HPD did not. The mammotropic activity of Y-20024 administered orally once a day for 5 days was almost equipotent to that of SPR. From these results, Y-20024, pharmacologically similar to SPR, but superior in bioavailability and penetration through the blood brain barrier, may have potential usefulness as an antipsychotic drug.

Animals↗
PubMed1988

Morphological changes of the villous microvascular architecture and intestinal growth in rats with streptozotocin-induced diabetes.

Using intact tissues and vascular corrosion casts, morphological changes in the small intestine of streptozotocin-induced diabetic rats present 1 month after onset were investigated using scanning and transmission electron microscopy. Although there were increases in the height of the villi in the jejunum and not in the ileum, characteristic changes in surface morphology in the diabetic rats were observed only in the ileum. Use of a vascular corrosion cast technique clearly demonstrated the prominent thick marginal vessels of the intestinal villi of the control rats. In the diabetic rats, the central arterioles in the villi were dilated both in the jejunum and the ileum. Marginal vessels were small in the ileum but prominent in the jejunum. Using transmission electron microscopy, decreases in diameter and the number of endothelial fenestra were also evident in the marginal vessels of the ileal villi in the diabetic rats. Thus in rats made diabetic, fine structural alterations of the marginal vessels are induced in the villi of the distal ileum, in addition to quantitative changes in the jejunal villi, presumably related to hyperphagia. The marginal vessels seem to be involved in the regulation of microcirculation of the intestinal villi in the rat.

Animals↗
PubMed1988

Generation and characterization of lymphokine-activated killer cells against fresh human leukemia cells.

Lymphokine-activated killer (LAK) cells generated from 15 acute leukemia patients in remission showed significant levels of cytotoxicity against Daudi 1A4, a natural killer-resistant cell line. This indicates that lymphocytes of leukemia patients in remission could respond to interleukin-2 to generate conventional LAK cells. However, LAK cells caused lysis of autologous leukemia cells at considerably lower levels in seven out of the 15 patients, with the exception of one case (48.6% cytolysis). None of the remaining eight patients exhibited LAK activity against autologous leukemia cells. On the other hand, patients' LAK could lyse allogeneic leukemia cells including those resistant to autologous LAK. Thus, patients' LAK seem not to be defective in lysis of leukemia cells. In the cold target competition analysis, the binding of patients' LAK to leukemia cells could be inhibited by autologous and allogeneic leukemia cell competitors, implying that almost all leukemia cells could be recognized by patients' LAK. Most LAK cells from normal donors showed significant lysis of allogeneic leukemia cells, but some leukemia cells were found to be resistant to lysis. LAK cells against both leukemia cells and Daudi 1A4 were phenotypically heterogenous, and were predominantly observed in the T3- fraction in the precursor phase. In the effector phase, whereas LAK activity against leukemia cells was also predominantly shown in the T cell-depleted fraction, similar levels of LAK activity against Daudi 1A4 were found in both the T cell-depleted and -enriched fractions.

Acute Disease↗
PubMed1987

Antagonistic activity of etizolam on platelet-activating factor in vivo experiments.

The ability of etizolam, 6-(o-chlorophenyl)-8-ethyl-1-methyl-4H-s-triazolo[3,4-c]thieno[2,3-e] [1,4]diazepine (Y-7131), an anti-anxiety drug, to inhibit platelet-activating factor (PAF)-induced reactions was investigated in experimental animals in vivo. Etizolam (0.01-0.3 mg/kg, i.v.) dose dependently inhibited PAF (0.3 microgram/kg, i.v.)-induced bronchoconstriction (Konzett and Rössler's method) in guinea pigs, but even at doses as large as 3 mg/kg, i.v., it had no effect on bronchoconstriction induced by histamine, serotonin, acetylcholine, arachidonic acid, bradykinin, angiotensin l or leukotriene D4. Etizolam (0.1-1 mg/kg, i.v.) also dose-dependently reversed PAF (1 microgram/kg, i.v.)-induced hypotension in anesthetized rats. Injection of PAF into the tail veins of mice produced lethal shock within 10-30 min. Etizolam (0.1-3 mg/kg, i.v. and 1-10 mg/kg, p.o.) protected against the lethal effect of PAF (75 micrograms/kg, i.v.) in a dose-dependent manner. These results indicate that etizolam specifically inhibits the action of PAF in vivo.

Animals↗
PubMed1987

An antagonistic activity of etizolam on platelet-activating factor (PAF). In vitro effects on platelet aggregation and PAF receptor binding.

The antagonistic effect of etizolam, an anti-anxiety drug, on platelet-activating factor (PAF) was investigated in rabbit platelets in vitro. Etizolam inhibited PAF-induced aggregation in a dose-dependent manner, with an IC50 of 3.8 microM, about one tenth that of triazolam (IC50 = 30 microM). At 300 microM, it inhibited both ADP and arachidonic acid-induced aggregation only slightly, while the other anti-anxiety drugs tested had no effect on PAF-induced aggregation even at this concentration. Etizolam and triazolam inhibited the specific binding of 3H-PAF to PAF receptor sites on washed rabbit platelets with IC50 values of 22 nM and 320 nM, respectively. Diazepam and estazolam were inactive even at 1 microM. These results indicate that etizolam is a specific antagonist of PAF.

Animals↗
PubMed1987

Treatment of adult T cell leukemia with mega-dose cyclophosphamide and total body irradiation followed by allogeneic bone marrow transplantation.

A 43-year-old patient with adult T cell leukemia (ATL) was treated with mega-dose cyclophosphamide and total body irradiation (TBI) followed by bone marrow transplantation (BMT) from his HLA-identical sibling who was not a carrier of ATL virus. After BMT, ATL cells rapidly decreased and disappeared, and the engraftment of marrow was confirmed on day 20. The patient showed normal hematologic recovery. However, he died on day 205 with interstitial pneumonitis caused by cytomegalovirus infection. Neither autopsy findings nor serologic and cytologic examinations showed any evidence of ATL relapse after BMT. This pilot study suggests that mega-dose chemotherapy and TBI followed by allogeneic BMT should be considered for such treatment of ATL.

Adult↗