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Biomedical subjects

A Tanizawa

Publications and source records attributed to A Tanizawa.

At least 55 records · Page 3Linked to original sources
PubMed1989

Cell cycle related change of Ara-C transport in HL-60 cells after differentiation induction.

Using a promyelocytic leukemia cell line, HL-60, we studied the membrane transport of Ara-C before and after differentiation induced by retinoic acid (RA). In RA-treated cells, Ara-C transport was reduced and there was a concomitant increase of the ID50 values of Ara-C in comparison with the controls. By three different procedures to synchronize untreated cells, i.e. density arrest G1 phase enrichment, aphidicolin-induced S phase accumulation and the double isoleucine block method, we found that Ara-C transport was 30-50% higher in the S phase than in the G1 phase. Therefore, the observed decrease in Ara-C transport is, in part, due to the retarded growth accompanied by an accumulation of cells in the G1 phase after differentiation induction.

Aphidicolin↗
PubMed1989

VP-16-induced nucleotide pool changes and poly(ADP-ribose) synthesis: the role of VP-16 in interphase death.

Exposure of human promyelocytic leukemia cell line (HL-60) to VP-16 resulted in accumulation of DNA strand breaks. Concomitantly, intracellular NAD levels fell at 1 h, followed by declines in ATP at 2 h and in GTP, CTP, and UTP at 3 h. Furthermore, marked morphological changes, such as loss of microvilli or bleb formation, appeared at 4 h and cell death by 8-10 h. The addition of an inhibitor of poly(ADP-ribose) polymerase, 3-aminobenzamide (5 mM), theophylline (2 mM), or thymidine (1 mM), prevented these sequential reductions of nucleotide pools and cell death. In fact, the activation of poly(ADP-ribose) synthesis was detectable within a few hours after treatment with VP-16, although it was smaller than that induced by N-methyl-N'-nitro-N-nitrosoguanidine. These results may suggest the possible role of activation of poly(ADP-ribosyl)ation in VP-16-induced nucleotide pool changes and subsequent interphase death.

Benzamides↗
PubMed1989

Synergistic effect of methotrexate and 1-beta-D-arabinofuranosylcytosine on the generation of DNA strand breaks in a human promyelocytic leukemia cell line.

We investigated the accumulation of DNA strand breaks in a human promyelocytic leukemia cell line, HL-60, treated with methotrexate (MTX) and 1-beta-D-arabinofuranosylcytosine (Ara-C). The sequential treatment with MTX then Ara-C had a synergistic effect on the formation of DNA strand breaks, which was dependent on MTX and Ara-C concentrations. On the other hand, when Ara-C preceded MTX, no such synergism was observed. The addition of both thymidine and hypoxanthine to this system, but not thymidine or hypoxanthine alone, abolished the synergism. Pretreatment with MTX augmented the generation of 1-beta-D-arabinofuranosylcytosine 5'-triphosphate. However, this augmentation did not necessarily correlate with the amount of strand breaks. Whatever the underlying mechanism of this synergism is, our present data provide one possible biochemical basis for sequential MTX and Ara-C therapy.

Aphidicolin↗
PubMed1989

[Results of a modified Stamey technique in the management of female urinary stress incontinence].

A modified Stamey technique was applied to nineteen women to control their stress incontinence. Needle puncture was reduced to one time for each side of the urethra by placing the Dacron sleeve parallel to the urethra. Postoperatively, the urethrovesical angle was reduced to be within normal limit, and functional urethral length and maximum urethral closure pressure increased significantly. All patients receiving the modified operation restored urinary continence without any significant complications.

Aged↗
PubMed1989

Biochemical characterization of U937 cells resistant to L-asparaginase: the role of asparagine synthetase.

A human histiocytic lymphoma cell line, U937, is highly sensitive to L-asparaginase with an ID50 of about 0.0001 U/ml after 72 hr of culture. When U937 cells were made resistant to either L-asparaginase (1 U/ml) or asparagine deprivation, the activity of asparagine synthetase increased to 80- or 7-fold of the wild type, respectively. The phenotype of the resistance to L-asparaginase turned out to be stable under nonselective conditions for over several months. The hybrids between L-asparaginase sensitive (Molt4) and resistant (HL-60) cell lines revealed the latter phenotype in terms of L-asparaginase sensitivity and the activity of asparagine synthetase. Furthermore, U937 cells resistant to L-asparaginase could survive in glutamine-free media with 1.5-fold elevation of glutamine synthetase activity. These results altogether clarify the role of asparagine synthetase in L-asparaginase toxicity and have a good implication for the clinical use of L-asparaginase.

Amino Acids↗
PubMed1989

[Successful induction chemotherapy for childhood RAEB-T with VP-16: a case report].

A one-year-old boy diagnosed as refractory anemia with excess of blasts in transformation is reported. Hematological examination revealed anemia, thrombocytopenia and the presence of blasts in both peripheral blood (3.5%) and bone marrow (20.1%) specimens. Chromosomal analysis showed abnormal karyotype; 48, XY, +21, +marker, r (7). Analyses with cytochemical stainings, electronmicroscopy and monoclonal antibodies to cell surface markers could not define the lineage of blasts. Induction chemotherapy was started with VP-16 (230 mg/m2 x 5 days) as a single agent and complete remission was achieved. Thereafter, he had been treated for 11 months with the intensive chemotherapy which consisted of VP-16, cytosine arabinoside, daunorubicin, vincristine, vinblastine, 6-mercaptopurine, prednisolone, mitoxantrone and CNS prophylaxis. He has been in complete remission for 18 months. The usefulness of VP-16 to MDS in pediatric patients is documented.

Anemia, Refractory, with Excess of Blasts↗
PubMed1988

Differential modulation of 1-beta-D-arabinofuranosylcytosine metabolism by hydroxyurea in human leukemic cell lines.

The ability of hydroxyurea (HU) to modulate 1-beta-D-arabinofuranosylcytosine (Ara-C) metabolism was investigated in human leukemic cell lines. Exposure of HL-60 cells to 1 mM HU enhanced the accumulation of Ara-CTP up to 2.5-fold, whereas HU did not have significant effects on Ara-C metabolism in CEM cells. In addition, two adenine nucleosides, deoxyadenosine (dAdo) and 9-beta-D-arabinofuranosyladenine (Ara-A), which are known to be activated by deoxycytidine (dCyd) kinase as Ara-C, were more effectively phosphorylated after the addition of HU only in HL-60 cells. However, the changes of intracellular dCTP and TTP pools induced by HU, i.e. decrease in dCTP and increase in TTP, were the same in both cell lines. Finally, dCyd production under normal culture conditions was at least 3- to 4-fold higher in HL-60 cells and was inhibited significantly by HU administration. These results suggest that the modulation of Ara-C metabolism by HU occurs at the level of dCyd kinase through the regulation of de novo dCyd generation.

Arabinofuranosylcytosine Triphosphate↗
PubMed1988

[A case of bilateral spermatocele].

A case of bilateral spermatocele is reported. A 46-year-old man was admitted to our hospital complaining of bilateral scrotal swelling. We obtained a colorless, opalescent fluid which contained numerous spermatozoa. The fluid volume, pH and gravity obtained from right spermatocele were 85 ml, 6.8 and 1.005, respectively, and those obtained from left side were 40 ml, 6.8 and 1.006, respectively. Spermatocelectomy was done under lumbal anesthesia. Both spematocele were found near the body of the epididymis. The wall of spermatocele had on epithelial lining of cuboidal cells. Twenty two cases of spermatocele reported in Japan since 1951 are reviewed.

Humans↗
PubMed1988

[Spontaneous rupture of the renal pelvis: a case report].

A 63-year-old man admitted to our hospital with severe pain in his right flank on June 4, 1987. After admission, his pain increased progressively and he complained of tenderness from the right flank to the right lower quadrant. Computerized tomography and intravenous pyelography demonstrated spontaneous rupture of the right renal pelvis. A retrograde ureteral catheter was indwelling into the right renal pelvis. Because extravasation had disappeared on the retrograde pyelogram, the Catheter was withdrawn after 12 days. After removal of the ureteral catheter, he did not complain of pain. The 42 patients with spontaneous rupture of the renal pelvis reported in the Japanese literature and our one case were discussed.

Catheters, Indwelling↗
PubMed1988

Changes in sensitivity to anticancer drugs during TPA-induced cellular differentiation in a human T-lymphoblastoid cell line (MOLT-4).

After four days of treatment with 10(-8) M TPA, differentiation of the human T-lymphoblastoid cell line MOLT-4 was induced along the T cell lineage, confirmed by a fall in adenosine deaminase and 5'-ectonucleotidase and a rise in purine nucleoside phosphorylase activity. TPA-treated cells became resistant to the cytotoxic effects of 1-beta-D-arabinofuranosylcytosine (Ara-C), 9-beta-D-arabinofuranosyladenine (Ara-A), and 2-chlorodeoxyadenosine. This was, in part, due to the altered cell cycle distribution (accumulation of cells in the G1 phase), since the toxicity of Ara-C and Ara-A is S phase specific. The diminished rate of Ara-C transport concomitant with Ara-CTP formation after TPA treatment is considered to be the biochemical basis for this acquired resistance.

Antineoplastic Agents↗
PubMed1987

Prevention of adriamycin-induced interphase death by 3-aminobenzamide and nicotinamide in a human promyelocytic leukemia cell line.

Adriamycin caused significant interphase death in HL-60 cells during six hours of incubation, which was abolished by the poly(ADP-ribose) polymerase inhibitors, 3-aminobenzamide or nicotinamide. Neither agent changed adriamycin uptake by HL-60 cells. Although 3-aminobenzamide did not alter the number of DNA strand breaks caused by adriamycin, it prevented adriamycin-induced depletion of intracellular NAD+ and ATP, and maintained energy charge. These findings suggest that the activation of poly(ADP-ribose) synthesis plays an important role in the adriamycin-induced interphase death of proliferating HL-60 cells.

Benzamides↗
PubMed1981

Peripheral neuropathy in children on long-term phenytoin therapy.

Nerve conduction studies of the ulnar, median, posterior tibial, peroneal and sural nerves were performed in 21 epileptic children aged 6 to 17 years on long-term phenytoin therapy. Auditory brain stem evoked responses were obtained in 16 patients to evaluate the effect of phenytoin on central nervous system synapses. Of the 21 patients examined, 15 (71.4%) showed abnormal findings. The most frequent abnormality was slowed motor conduction velocity of the ulnar nerve (33.3%) and posterior tibial nerve (23.8%), followed by slowed sensory conduction velocity of the sural nerve (20%), lowered H/M ratio (14.3%), slowed motor conduction velocity of the peroneal nerve (14.3%) and of the median nerve (14.2%). A significant correlation was noted between the total dosage and duration of therapy with PHT and the reduction of motor conduction velocity in the posterior tibial nerve. Auditory brain stem evoked responses showed no significant differences in each peak latency between the patients and the normal control group. The study indicates that long-term phenytoin therapy can cause latent impairment of peripheral nerve function in children with no clinical evidence of peripheral neuropathy.

Adolescent↗
PubMedDate not supplied

Successful treatment of essential thrombocythemia evolving into agnogenic myeloid metaplasia with interferon-alpha.

PURPOSE: Essential thrombocythemia and agnogenic myeloid metaplasia as one form of idiopathic myelofibrosis are myeloproliferative disorders and are quite rare in children. A patient with essential thrombocythemia that transformed to "adult-type" agnogenic myeloid metaplasia is described. PATIENTS AND METHODS: A routine examination of an 8-year-old girl with bronchial asthma showed thrombocytosis. Essential thrombocythemia was diagnosed 2 years later. During a 3-year follow-up without treatment, transition of the essential thrombocythemia to agnogenic myeloid metaplasia was noticed. The patient had an excellent response to interferon (IFN)-alpha therapy. CONCLUSION: This case is unique because of the availability of premorbid hematologic data and the natural progression of essential thrombocythemia to agnogenic myeloid metaplasia. Whether IFN-alpha therapy can prevent the progression of idiopathic myelofibrosis to leukemia has not yet been determined.

Child↗
PubMedDate not supplied

Serum soluble CD44 in pediatric patients with acute leukemia.

PURPOSE: CD44 is an adhesion molecule expressed on a variety of cells, and its level correlates with the metastatic potential of malignant tumors. Serum concentrations of soluble CD44 (sCD44) are elevated in various cancers. The purpose of this study was to measure the serum concentrations of CD44 in pediatric patients with acute leukemia. PATIENTS AND METHODS: Fourteen pediatric patients with acute leukemia were studied. The authors measured the serum concentration of sCD44 by enzyme-linked immunosorbent assay before and after therapy. The concentrations were compared with those of 15 control healthy children and 10 patients with bacterial infections. RESULTS: The mean serum concentration of sCD44 at presentation was significantly higher in patients than in control subjects, but decreased to a normal range in complete remission after chemotherapy. There was no difference in sCD44 concentrations between patients with acute lymphocytic leukemia and those with acute myeloid leukemia. Serum concentrations of sCD44 did not correlate with lactic dehydrogenase concentrations or bone marrow nucleated cell counts and only weakly with peripheral leukocyte count. sCD44 levels in patients with bacterial infections were similar to those of control subjects. CONCLUSION: Serum concentration of sCD44 may reflect disease status in pediatric patients with acute leukemia and might be a useful tumor marker in these patients.

Antibiotics, Antineoplastic↗