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Biomedical subjects

K Kitajima

Publications and source records attributed to K Kitajima.

At least 271 records · Page 15Linked to original sources

Chromosome 8-14 translocation in a non-African Burkitt's lymphoma with leukemic conversion.

A specific chromosome translocation, t(8q-; 14q+), was observed in a 43-year-old female with non-African Burkitt's lymphoma in which leukemic conversion had occurred. The chromosome studies used cells from ascites. The ascites was apparently the result of a primary tumor involving the ovaries and contained 68% of lymphoma cells. The frequent occurrence of abnormalities related to chromosomes 1, 8 and 14 in African and non-African Burkitt's lymphomas was emphasized.

Adult↗

Treatment of relapsed acute myelocytic leukemia with a combination of aclarubicin and cytosine arabinoside.

Relapses in nine patients with acute myelocytic leukemia were treated with a combination of aclarubicin (ACR) and cytosine arabinoside (ara-C). ACR, 40 mg/m2/day, was administered daily by intravenous injection from day 1 to day 3 and ara-C, 60-80 mg/m2/day, divided into 2 doses, was given every 12 h by intravenous infusion from day 1 to day 7. Depending on the state of the bone marrow, ACR-ara-C regimen was modified in administration period and repeated after the resting periods of at least 7 days. Complete remission was obtained in 7 of 9 patients (77.8%). The time required for achieving the complete remission varied from 20 to 55 days with a median of 39 days. The duration of complete remission was from 8 to 52 weeks with a median of 22 weeks. Side effects on digestive system such as nausea, vomiting and anorexia, were seen in all patients, although they were managed by symptomatic treatment. The results indicate the effectiveness of this ACR-ara-C regimen in the clinical management of acute nonlymphocytic leukemia.

Aclarubicin↗

Non-A, non-B (type 1) hepatitis agent capable of inducing tubular ultrastructures in the hepatocyte cytoplasm of chimpanzees: inactivation by formalin and heat.

We have reported two kinds of viruslike particles derived from human sera that induced morphologically and serologically different types of non-A, non-B hepatitis in chimpanzees. A chimp serum containing one such agent capable of inducing a type of hepatitis with cytoplasmic tubular ultrastructures (non-A, non-B, type 1) was titrated for its infectivity in chimps. Two chimps who received 1 ml of a 10(-2) dilution of the original serum developed the characteristic morphological changes in the liver together with elevated serum transaminase levels, while the other two who received 1 ml of a 10(-4) dilution failed to show such changes. The two who escaped the infection were proven to be susceptible to the agent, because they developed non-A, non-B, type 1 hepatitis when they were challenged by 1 ml of a 10(-1) dilution of the same serum on the 23rd week after the first inoculation. One milliliter of a 10(-1) dilution containing more than 10 chimp infecting units were inactivated in the presence of 1/2000 formalin or by heating at 100 degrees C for 5 min and then given to four other chimps. None of them developed clinical or histologic evidence of non-A, non-B, type 1 hepatitis, thereby indicating that both formalin and heat could destroy the ability of the agent to induce this type of hepatitis.

Animals↗

[Chemotherapy for chronic leukemia].

Chemotherapy for chronic myelogenous leukemia is divided into two parts; chronic phase and blastic phase. The most distinguished new attempt for chronic phase in recent years in the former was the L-15 protocol, intensive multicombination chemotherapy by Clarkson and his group, which destroyed a large fraction of the leukemic population and permitted repopulation of the marrow with predominantly Ph1-negative cells in about half of the patients. However, most of the complete remissions were of short duration. On the other hand, much progress has been made in the chemotherapy for blastic phase cases. Using a combination chemotherapy of vincristine and prednisolone, over one-third of the patients with CML in blastic crisis have achieved a complete remission. Survivors over one year from the blastic crisis are rapidly increasing in recent years. Chemotherapy for chronic lymphocytic leukemia at the stage III of Rai's staging is recommended to start with chlorambucil, cyclophosphamide or corticosteroids.

Antineoplastic Agents↗

[Clinical management of acute lymphocytic leukemia in adults. 1. Treatment of acute lymphocytic leukemia with VP (vincristine, prednisolone)--DVMP (daunorubicin, vincristine 6-mercaptopurine, prednisolone) regimen].

Eighteen patients with acute lymphocytic leukemia (ALL) were treated with VP (vincristine, prednisolone) followed by DVMP (daunorubicin + vincristine + 6-mercaptopurine + prednisolone) regimen (VP-DVMP regimen). Patients were all previously untreated. Complete remission (CR) was obtained in 11 of 18 patients (61.1%,) by VP alone and 4 patients, by VP-DVMP. The time required for CR varied from 14 to 60 days with a median of 28 days. The duration of CR and survivals in responders were from 1.2 to 42.3 + months with a median of 24.0 months. The hematological toxicities in VP-DVMP regimen were lower than those in NVP (neocarzinostatin + vincristine + prednisolone) and NVMP (neocarzinostatin + vincristine + 6-mercaptopurine + prednisolone) regimens.

Adolescent↗

[Comparative evaluation of a combination of daunorubicin and cytosine arabinoside and that of aclarubicin and cytosine arabinoside in remission induction in acute non-lymphocytic leukemia].

A comparative trial of a combination of daunorubicin and cytosine arabinoside (Regimen A) and a combination of aclarubicin and cytosine arabinoside (Regimen B) was performed. Sixteen patients with acute non-lymphocytic leukemia, previously untreated, were entered into this study. Five of 8 patients (62.5%) obtained a complete remission (CR) in Regimen A and B, respectively. The days required for achieving a CR varied from 37 to 46 days in Regimen A and from 22 to 56 days in Regimen B. The total doses of daunorubicin and cytosine arabinoside were from 100 to 240 mg and from 640 to 1,120 mg in Regimen A, respectively. Those of aclarubicin were from 180 to 300 mg and from 660 to 1,000 mg in cytosine arabinoside in Regimen B. In a comparative study on hematological changes, toxic effects on peripheral white blood cell, platelet and nucleated cell counts in bone marrow tended to appear later in Regimen B compared to those in Regimen A. Side effects on digestive system such as nausea and vomiting and vascular pain were more frequently recognized in patients treated with Regimen B, although they were managed by symptomatic treatment. The results indicated the usefullness of aclarubicin in combination chemotherapy for the treatment of acute non-lymphocytic leukemia.

Aclarubicin↗

Karyotypic findings and prognosis of adult T-cell leukemia patients.

Twelve patients with abnormal karyotypes out of 18 patients with adult T-cell leukemia died within 5 months on average after initial diagnosis; in contrast, three patients with normal karyotypes are still alive without having received any cancer chemotherapy at 12 to 21 months after diagnosis. The significance of the chromosome abnormality is discussed.

Adult↗

[Recovery from cyclophosphamide-induced myelosuppression accelerated by bestatin].

In this experiment, the effect of bestatin on cyclophosphamide (CYC)-induced myelosuppression was studied to evaluate the hemopoietic activity. Bestatin administrated i.p. from -day 5 to -day 1, showed no influence on the peripheral blood pictures and bone marrow nucleated cell counts (NCC) in normal mice. On the other hand, in mice treated with CYC, 300 mg/kg, i.p. on day 0, bestatin accelerated the recovery from CYC-induced leukopenia and myelosuppression. The accelerated recovery of the total WBC count and bone marrow NCC were solely due to the enhanced granulocyte recovery. These findings indicated a promising effect of bestatin in the clinical management of myelosuppression induced by cancer chemotherapy.

Aminopeptidases↗

Effect of streptococcal lipids on Ehrlich ascite tumor cells.

The lipids extracted from group A hemolytic streptococci (strain Su, Blackmore and C203U) were examined for their antitumor effect against Ehrlich ascites carcinoma in mice. Total lipids were extracted from streptococcal cells according to the method of Folch et al, and separated into 9 lipid fractions by thin-layer chromatography, using various solvent systems. Three fractions were compound lipids (diphosphatidyl glycerols, monoglucosyl diglycerides and diglucosyl diglycerides), and the remaining 6 fractions were neutral lipids such as free fatty acids, glycerides, sterols and sterol esters. For biological testing, the lipid fractions suspended in physiological saline containing Tween 20 (0.02%) were incubated with Ehrlich tumor cells at 37 degrees C for 90 min, and the cell mixture was given intraperitoneally into mice thereafter. Among 9 lipid fractions, free fatty acids and monoglycerides from the streptococci examined were highly active in suppressing the depressing the development of ascites carcinoma in mice. Diphosphatidyl glycerols from two strains of streptococci (BLackmore and C203U) were also effective in suppressing the tumor growth in mice. However, the other lipid fractions had little effect on the tumor growth.

Animals↗

Abnormalities in the contact activation through factor XII in Fujiwara trait: a deficiency in both high and low molecular weight kininogens with low level of prekallikrein.

Fujiwara trait, the first case of kininogen deficiency in Japan previously reported which did not show any clinical symptom except the prolonged activated partial thromboplastin time was further examined. The activated partial thromboplastin time of the patient was corrected by addition of normal, Factor XII deficient or Fletcher plasma, but not corrected by Fitzgerald or Williams plasma. It was also corrected by addition of highly purified bovine or human high molecular weight (HMW) kininogen, but not by low molecular weight (LMW) kininogen. When total kininogen was measured as the amount of bradykinin released by trypsin, only a trace amount was detected in Fujiwara as well as Williams plasma. No immunoreactive protein against anti-human-HMW-kininogen nor anti-human-LMW-kininogen was found in Fujiwara plasma. Acetone-kaolin-activated plasma kallikrein was not generated by Fujiwara plasma. Substitution with normal plasma in various ratios showed the generation of various plasma kallikrein activities. Calculations with these activities of mixed plasma gave the prekallikrein content of Fujiwara trait plasma about 30% of the normal level. These results suggest that Fujiwara trait is very similar to Williams trait in that both plasmas were deficient in HMW and LMW kininogens with reduced content of prekallikrein.

Factor XII↗

Abnormalities of chromosome no. 1 related to blood dyscrasias: study of 10 cases.

Partial excess of chromosome 1 (q25-q32) was noted in malignant cells from all of 10 patients who had disorders such as non-African Burkitt's lymphoma, adult T-cell leukemia, myelofibrosis, malignant lymphoma, chronic lymphocytic leukemia or chronic myelocytic leukemia in blast crisis. The break points on chromosome 1 were at centromere, q12, q21, q23, q25 and q32. Variations in the specific region of the long arm of chromosome 1, q25-q32, were thought to be important in the evolution of malignant cell proliferation.

Adult↗