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T Taoka

Publications and source records attributed to T Taoka.

At least 55 records · Page 3Linked to original sources

The role of Ca2+ and protein kinase C in the differentiation of HL-60 cells induced by 1 alpha,25(OH)2D3 and diltiazem.

The roles of calcium (Ca2+) and protein kinase C in the differentiation of HL-60 cells induced by 1 alpha,25(OH)2D3 (D3) and/or a Ca2+ antagonist, diltiazem(D-cis, L-cis), were elucidated. D3 and diltiazem (100 microM) inhibited cell proliferation, and diltiazem enhanced the D3-induced differentiation. There was no difference in potency between the two isomers of diltiazem in the enhancing activity, in spite of their different pharmacological activity. The concentration of free Ca2+ in the HL-60 cells following D3 and/or diltiazem treatment significantly increased. A protein kinase C inhibitor, H-7, inhibited the phenotypic differentiation induced by D3. These results suggest that Ca2+ and protein kinase C play an important role in the differentiation of HL-60 cells induced by D3 and diltiazem.

Calcitriol↗

[Treatment of myelodysplastic syndrome and acute myelogenous leukemia with vitamin D3 [1 alpha(OH)D3]].

It is known that 1 alpha, 25(OH)2D3 is an inducer of nonlymphoid leukemic cell differentiation to monocyte-macrophage-like in vitro. The effects of oral administration of 4.5-15 micrograms/d 1 alpha (OH)D3, which is converted to 1 alpha, 25(OH)2D3 in vivo by liver cells, on leukemic cells were studied in two patients with AML and one with RAEB. In these three cases, 1 alpha (OH)D3 reduced the number of leukemic cells in the bone marrow and aggregated the dispersed chromatin of leukemic cells as heterochromatin. Furthermore, this drug induced atypical lymphocyte-like cells, which were considered to be differentiated from leukemic cells in case 1, and improvement of pancytopenia in case 3. While hypercalcemia developed during 1 alpha (OH)D3 therapy in case 1, it disappeared within three days after discontinuation. We also studied the in vitro effects of 1 alpha, 25 (OH)2D3 on leukemic cells freshly isolated from the bone marrow in these three cases. After incubation with 10(-8) M 1 alpha, 25(OH)2D3 at 37 degrees C for 72 h, the number of adherent cells on the bottom of Petri dishes had increased. These cells were quite similar to monocyte-macrophages. These leukemic cells, after differentiation induced by 1 alpha, 25(OH)2D3, reacted strongly with monoclonal antibodies My-4 and My-7. Both 100 microM D-cis and L-cis diltiazem (calcium channel blocker) enhanced the differentiation of HL-60 cells induced by 1 alpha, 25 (OH)2D3. There was no significant difference between D-cis and L-cis diltiazem with regard to this enhancing effect. The cytoplasmic free Ca2+ concentration in HL-60 cells induced by 1 alpha, 25(OH)2 D3 and/or diltiazem, was increased significantly as compared with that in HL-60 cells incubated without inducers.

Administration, Oral↗

[Therapeutic effect of ranimustine (MCNU) on essential thrombocythemia and polycythemia vera].

Seven patients with essential thrombocythemia and two patients with polycythemia vera were treated with ranimustine (MCNU). MCNU was given intravenously by drip infusion at a dose of 40-80 mg/m2 with intervals arranged in terns of the counts of both white blood cell and platelets. All cases with essential thrombocythemia obtained complete response, but the cases with polycythemia vera needed the combination of phlebotomy. The therapeutic effects were maintained for 2-5 months. No serious side effect was recognized except in two cases (22%) of mild nausea. Our study indicates that MCNU is useful for chemotherapy of chronic myeloproliferative disorders, especially, essential thrombocythemia.

Adult↗

[VAMA salvage regimen (VP-16, ARA-C, MTX and L-asparaginase) in relapsed or resistant non-Hodgkin's lymphoma].

A new salvage treatment protocol consisting of VP-16, cytosine arabinoside (Ara-C), methotrexate (MTX) and L-asparaginase, known as VAMA, was administered to twelve patients with relapsed or resistant non-Hodgkin's lymphoma. All twelve patients were in advanced stage with aggressive histologic type. Four of eight patients whose tumor cells had been immunologically determined, had T-cell phenotype. Three complete and five partial responses were obtained, for an overall response rate of 67%. It is of particular interest that all four patients with T-cell phenotype responded(CR; 3 cases, PR; 1 case), and a CR duration over 31 months has been achieved in a case of T-lymphoblastic lymphoma. Severe myelosuppression was the major toxic effect, but it was generally well-tolerated with supportive therapy. These results indicate that VAMA salvage regimen can play an important role in the treatment of relapsed or resistant non-Hodgkin's lymphoma.

Adult↗

[Treatment with K-18 (IgG-melphalan) in recurrent cases of hematopoietic malignancies].

K 18, an IgG-Melphalan conjugate was administered to 30 patients, who had recurrent hematopoietic malignancy. Ten out of the 30 patients received single doses of 1 to 20 enteric tablets containing 10 mg of K 18, as a phase I study. No side effects were observed. K 18 was administered every day to the remaining 20 patients in order to evaluate the side effects and therapeutic effects, as a phase II study. One patient attained partial remission. Although no remission effect was obtained in 14 of the 20 patients, antitumor effects such as a decrease in leukemia cells, were observed in 4 of 20 patients. As to side effects, neither recurrence of tumor nor cumulative toxicity were shown in one patient with NHL who received only K 18 for 14 months as maintenance therapy. Evaluation of antitumor effect was difficult in the case of the remaining 4 patients. In the 20 cases who entered the phase II study, a decrease in neutrophils was observed in 2 patients, a slight decrease in platelets in 3 patients and increased transaminase activity in one patient as side effects of K 18. In brief, compared with Melphalan, K 18 has between 1.3 and 2 times a more potent therapeutic effect, with extremely low side effects.

Administration, Oral↗

Long-term palliative treatment of hepatocellular carcinoma extending into the portal vein and bile duct by chemoembolization and metallic stenting.

We present a patient with hepatocellular carcinoma accompanied by portal vein and bile duct tumor thrombi. The patient was treated with a spiral Z-stent covered by a polyethylene sheet placed in the bile duct, a Wallstent placed in the portal vein, chemoembolization, and external radiation therapy. The patient is alive with patency of both endoprostheses 18 months later.

Antibiotics, Antineoplastic↗

Age correlation of the time lag in signal change on EPI-fMRI.

PURPOSE: We measured the time lags between the start or end of tasks and signal changes in functional MRI (fMRI) for various age groups and evaluated the age correlation of the time lags. METHODS: Forty subjects, 20-76 years old, were evaluated. fMRI was performed with and echo planar imaging sequence at 0.5 s intervals. We measured the time for the signal of the precentral gyrus to make a half-maximal increase after starting the task (T-inc) and the time to reach the initial level after ceasing the task (T-dec). RESULTS: Average T-inc was 3.09 s and T-dec was 6.63 s. The values of T-inc could be correlated to age. T-dec had no age correlation. CONCLUSION: The time lag in fMRI was revealed to be prolonged with increasing age. Our results suggest that the time lag in fMRI is influenced by some factors associated with aging.

Adult↗

Hippocampal damage in the human brain after cardiac arrest.

BACKGROUND AND PURPOSE: Very few reports are available on changes in the human hippocampus after cardiac arrest. The objective of this study was to investigate if specific hippocampal volume losses can be demonstrated in the human brain following reperfusion after cardiac arrest. METHODS: We assessed the volumes of the hippocampal formation (HF) and temporal lobe excluding HF (TL) as the contrast using magnetic resonance (MR)-imaging-based volumetry in 11 vegetative patients after cardiac arrest and in 22 healthy controls of similar age, sex and body size distribution. The measured volumes were normalized for differences in the head size among subjects by dividing by the total intracranial volume (TICV). The MR images of the 11 patients were obtained between days 8 and 21 after cardiac arrest. RESULTS: The observed volumes of HFs and TLs of both patient and control groups were as follows: right HF volume (HFV): 2.67 +/- 0.19 (mean +/- SD, cm(3)) in patients versus 3.89 +/- 0.44 in controls; left HFV: 2.72 +/- 0.17 versus 3.74 +/- 0.35; right TL volume (TLV): 73.37 +/- 6.54 versus 80.08 +/- 7.62, and left TLV: 72. 45 +/- 6.77 versus 78.59 +/- 6.68. The normalized indices (HFV/TICV and TLV/TICV) were as follows: right HF: 0.0021 +/- 0.0002 (mean +/- SD) in patients versus 0.0031 +/- 0.0001 in controls, p < 0.0001, left HF: 0.0022 +/- 0.0002 versus 0.0030 +/- 0.0001, p < 0.0001, right TL: 0.058 +/- 0.002 versus 0.064 +/- 0.004, p = 0.0007, and left TL: 0.058 +/- 0.002 versus 0.062 +/- 0.004, p = 0.0014. The HFV-TLV ratios (HFV/TICV divided by TLV/TICV) of both groups were: right HFV-TLV ratio: 0.037 +/- 0.004 in patients versus 0.049 +/- 0. 004 in controls, p < 0.0001, left HFV-TLV ratio: 0.038 +/- 0.004 versus 0.048 +/- 0.004, p < 0.0001. CONCLUSIONS: The patient group had HFs that were 26.8-30.6% smaller than those of the control group, but in the patient group, the TLs slightly decreased in size by only 7.8-8.2% of the volume of those in the control group within 21 days after cardiac arrest. The volume reductions in the bilateral HFs of patients after cardiac arrest were significantly larger than those in the bilateral TLs. We speculate that this specific rapid hippocampal shrinkage reflects its greater vulnerability to global brain ischemia.

Aged↗