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Biomedical subjects

Y Sakurai

Publications and source records attributed to Y Sakurai.

At least 523 records · Page 29Linked to original sources
PubMed1985

[A case of moyamoya disease accompanied by arterio-venous malformation].

It is well known that moyamoya disease is sometimes accompanied by cerebral aneurysm. However, a case of moyamoya disease with arterio-venous malformation is not found out on the literature. In this paper, a rare case of moyamoya disease accompanied by arterio-venous malformation is reported. The patient is a 33-year-old male who developed transient left motor weakness and visual disturbance on September 5, 1983. He was admitted to our hospital on October 3, 1983. On admission, there were no abnormal neurological findings. Plain CT scan showed low density area in the left parietooccipital cortex. Enhanced CT scan revealed a ribbon-shaped enhanced area in the right temporooccipital cortex and spotty enhanced area in the right frontal subcortex. Cerebral angiogram was a typical angiogram of moyamoya disease, namely, stenosis of the terminal portions of both internal carotid arteries and basal, ethmoidal and vault moyamoya vessels were seen. On the basis of Suzuki's angiographical classification the patient was diagnosed as being in stage III. Interesting was that a right carotid angiogram revealed an arterio-venous malformation fed by basal moyamoya vessels and drained to Trolard and Sylvian veins in the right frontal lobe. This arterio-venous malformation consisted with feeders, nidus and drainers. The size of arterio-venous malformation was about 8 X 11 X 12 mm on the angiogram. Another interesting fact was that Trolard vein which was one of the draining veins of the arterio-venous malformation flows into the right parietal vault moyamoya vessels as if it was feeding the moyamoya vessels.

Adult↗
PubMed1984

Identification of canine lymphocyte subpopulations by immunofluorescence assay.

Experiments were performed to identify subpopulations of lymphocytes in lymphoid tissues of dogs. Anti-canine thymocyte serum (ATS) and anti-canine brain-associated T-cell antigen (ABAT) were obtained by immunization of rabbits with canine thymocytes and canine brain tissue homogenate, respectively. The ATS and ABAT antisera were absorbed using canine RBC, liver powder, and bone marrow cells. Part of the ABAT antiserum was further absorbed using canine thymocytes (ABAT-T antiserum). The ATS, ABAT, ABAT-T, and antiasialo GM1 antisera were used for identification of lymphocyte subpopulations by means of indirect immunofluorescent antibody (FA) techniques. For bone marrow-derived lymphocytes, surface immunoglobulin (SIg) was measured by direct FA using fluorescein isothiocyanate-conjugated rabbit anti-dog immunoglobulin G antiserum. The specificities of the various antisera were proven by treatment of the lymphocytes by means of nylon wool columns or rosette-forming techniques followed by treatment with antisera and rabbit complement. Results indicated that ATS reacted with T-lymphocytes, and ABAT antiserum reacted with T-lymphocytes, with ABAT-T-positive cells, and with antiasialo GM1-positive cells The ABAT-T and asialo GM1 antisera reacted with the same cell populations, but did not react with ATS-positive cells and ABAT-positive cells. Lymphocytes from 21 clinically normal mixed-breed dogs and from 2 Beagle dogs were identified by various antisera. For mixed-breed dogs, the positive percentages of peripheral blood lymphocytes with respect to SIg, ATS, ABAT, and ABAT-T were 36.3 +/- 3.2%, 52.7 +/- 3.5%, 56.1 +/- 3.6%, and 2.4 +/- 0.3%, respectively; in the spleens, the positive percentages were 44.8 +/- 3.8%, 39.6 +/- 2.8%, 42.6 +/- 2.6%, and 1.9 +/- 0.5%, respectively; and in the lymph nodes, 39.0 +/- 2.7%, 49.4 +/- 3.6%, 52.1 +/- 3.9%, and 1.6 +/- 0.5%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Effects of quinidine and related compounds on cytotoxicity and cellular accumulation of vincristine and adriamycin in drug-resistant tumor cells.

Quinidine, which has antiarrhythmic activity, greatly enhanced the cytotoxicity of vincristine (VCR) in tumor cells and especially in VCR-resistant sublines of P388 leukemia (P388/VCR) and human myelogenous leukemia. A nontoxic concentration of quinidine increased VCR cytotoxicity in these resistant tumor cells about 50 to 80 times, and the drug in combination with VCR could completely reverse VCR resistance of these cell lines. Quinidine also enhanced the cytotoxicity of Adriamycin, especially in the Adriamycin-resistant subline of P388 leukemia; this enhancement (8-fold) was less than that of VCR toxicity in the VCR-resistant tumor line. When administered daily for 10 days with VCR, quinidine at doses of 50 to 125 mg/kg significantly enhanced the chemotherapeutic effect of VCR in P388/VCR-bearing mice. Some other antiarrhythmic agents also showed similar effects in vitro, but these effects were considerably lower than that of quinidine. Quinidine increased the cellular levels of VCR and daunomycin in VCR-resistant sublines of mouse and human tumors and the ADM-resistant mouse tumor line in vitro, respectively. Quinidine also enhanced the cellular accumulation of VCR in P388/VCR cells in vivo. Thus, the therapeutic effect observed in P388/VCR-bearing mice might be due to the enhanced accumulation of VCR in P388/VCR cells by quinidine. The increase of cellular accumulation of VCR was partly explained by inhibition of efflux of VCR and daunomycin from the resistant tumor cells. The mechanism of this phenomenon is discussed in relation to previous findings on calcium channel blockers.

Animals↗
PubMed1984

Spontaneous metastasis of highly metastatic variants of mouse tumors and the effect of drugs on the metastasis.

Spontaneous metastasis of highly metastatic variants, B16 melanoma BL-6 and colon adenocarcinoma 26 NL-22, was examined. Tumor cells were inoculated into the right front footpad and the original tumors were removed by amputation of the forelimb at an appropriate time after tumor inoculation. Spontaneous lymph node and lung metastases occurred with B16 BL-6 and spontaneous lung metastasis occurred with NL-22. Analysis of the time-dependent formation of lymph node and lung metastases of BL-6 indicated that lung metastasis could be formed after the lymph node metastasis. Metastasis is influenced by the mouse strain, and both inbred and F1 hybrid mice of syngeneic origin could be used as host animals. By using these metastatic variants, two spontaneous metastasis systems were established. In order to evaluate the systems, the effects of 5-fluorouracil (5-FU) and adriamycin (ADM) were examined. 5-FU was effective against the metastases of both tumors, and ADM was moderately effective against B16 BL-6 metastasis.

Adenocarcinoma↗
PubMed1984

Cross-resistance of vincristine-resistant sublines of P388 leukemia to mitoxantrone with special emphasis on the relationship between in vitro and in vivo cross-resistance.

In vitro and in vivo cross-resistance to mitoxantrone of two vincristine-resistant sublines of P388 leukemia with different degrees of resistance in vitro was compared with that to adriamycin. A subline with a lower degree of resistance to vincristine exhibited approximately the same responses in vivo to mitoxantrone and adriamycin as the original P388 leukemic cell line, although it was evidently cross-resistant in vitro to these agents. Another subline having a higher degree of resistance to vincristine showed a 25-fold cross-resistance in vitro and gave no response in vivo to adriamycin. With mitoxantrone, on the other hand, this subline was solidly resistant as compared with the sensitive line but still retained significant responsiveness in vivo irrespective of a 150-fold cross-resistance in vitro. These results suggest that cross-resistance on a cellular basis does not necessarily correspond to in vivo cross-resistance. The relationship between in vitro and in vivo cross-resistance is discussed.

Animals↗
PubMed1984

[Intrapulmonary reactions of workers exposed to dust and ozone].

Forty-one dust-and-ozone-exposed and 37 nonexposed workers, belonging to the Research and Development Division of a photo-copier manufacturing industry, were examined to assess the effect of the exposure to carbon, iron and resin dust and ozone in the air of the work environment by means of questionnaires on their physical condition, smoking habits and exposure history by interview, chest X-rays, testing of ventilatory functions, transcutaneous PO2 (tcPO2) test and H2O2-induced hemolysis test. The following results were obtained. Respirable dust concentrations in the air of the work place were 0.1-1.0 mg/m3, total dust concentrations 0.2-2.0 mg/m3, and ozone concentrations 0.004-0.06 ppm (0.008-0.12 mg/m3). According to the Japanese Classification of Radiographs of Pneumoconioses, the exposed workers showed a higher rate of profusion 0/1 and over, and category 1 and over (1/0 and over) than the nonexposed workers. Ventilatory function testing revealed no difference between exposed workers and nonexposed workers, but small airway narrowing was suspected in smoking workers in comparison with nonsmoking workers. Transcutaneous PO2 showed no difference between exposed and nonexposed workers, between smoking and nonsmoking workers, and between any of the paired six combinations out of the four groups of workers, i.e., nonsmoking and nonexposed, nonsmoking and exposed, smoking and nonexposed, and smoking and exposed. It was estimated by H2O2-induced hemolysis test that smoking and/or dust exposure, especially long-term exposure, gave rise to aggravation of fragility of the erythrocyte membrane by lipid peroxidation with ozone or active oxygen produced by the reaction of dust and alveolar macrophages. The questionnaire was considered indispensable to ascertain the workers' exposure history. No worker in this work environment showed clinical signs indicating a need for medical care or home response. There results may indicate that in resolving the pathogenesis of pneumoconiosis further studies will be required on the prevalence rate of profusion 0/1 and over (or category 1 and over) under low concentrations of dust exposure and on the intrapulmonary reactions induced by low doses of dust exposure.

Adult↗
PubMed1984

Establishment of human KB cells resistant to 1-beta-D-arabinofuranosylcytosine, and mechanisms of cellular resistance in isolated clones.

A subline of human KB cells that was resistant to 1-beta-D-arabinofuranosylcytosine (ara-C) was established by continuous exposure of the cells to increasing concentrations of ara-C. Thirteen resistant clones were isolated from the resistant subline (KB/ara-C). KB/ara-C showed 1,300-fold higher resistance than the parent KB cells to ara-C; the most resistant clones, clones 7 and 10, showed 1,330-fold higher resistance. In the absence of ara-C, the resistance of the parent KB/ara-C cells was stable for at least 14 weeks, whereas that of clone 7 was stable for 10 weeks, but was slightly less after 14 weeks. The ara-C kinase and ara-C deaminase activities of the 13 clones and the cellular uptake of ara-C by several clones were measured. In general the clones showed decreased deoxycytidine kinase activity and decreased cellular uptake of ara-C. Most clones had higher cytidine deaminase activity than KB cells, but some had activity similar to that of the KB cells. A clear inverse relationship was found between the ara-C sensitivity of the clones and their kinase activity, but not their deaminase activity or their ara-C uptake. These results clearly demonstrate that a major mechanism of ara-C resistance of these human KB cells was a decrease in the activity of the ara-C activating enzyme deoxycytidine kinase. The parent KB/ara-C cells showed no clear cross-resistance to various antitumor agents other than an ara-C derivative, including metabolic inhibitors, alkylating agents, DNA binders and mitotic spindle poisons.

Antineoplastic Agents↗
PubMed1984

Relative contribution of antiproliferative and host immunity-associated activity of mouse interferon in murine tumor therapy.

Administration of mouse interferon (IFN; 0.5 to 1 X 10(7) reference units/mg protein) inhibited the growth of Meth A and Meth 1 fibrosarcomas, but to a lesser extent, if at all, the growth of Colon 26 adenocarcinoma in BALB/c mice. The in vitro IFN sensitivity of these three tumors was not consistent with the in vivo therapeutic response in mice bearing these tumors under the present experimental conditions; Colon 26, the most sensitive of the three tumors in the in vitro antiproliferation test, did not respond or responded most poorly to IFN therapy; furthermore, Meth A and Meth 1 tumors responded similarly well to IFN therapy, although there was about a 100-fold difference in their in vitro IFN sensitivity. These results as well as the kinetic analysis of IFN concentrations of the serum of Meth A- or Colon 26-bearing mice did not indicate that the antiproliferative activity of IFN was solely responsible for its in vivo therapeutic effect. In contrast, abrogation of T-cell immunity by alpha mouse thymocyte globulin completely nullified the IFN-dependent therapeutic effect in Meth A-bearing mice. Furthermore, the IFN-dependent therapeutic response in Meth A tumors was much weaker in T-cell-defective BALB/c (nu/nu) mice than that in immunologically competent BALB/c (+/+) mice and was marginal, if present at all, confirming that T-cell immunity was involved in the IFN-dependent therapeutic effect and suggesting that the antiproliferative activity of IFN may only be responsible to a small extent for the therapeutic effect.

Animals↗
PubMed1984

6-Mercaptopurine-induced potentiation of active immunotherapy in L1210-bearing mice treated with concanavalin A-bound leukemia cell vaccine.

While the combination of L1210 murine leukemia cell vaccine (L1210 vaccine) with 6-mercaptopurine (6-MP) or 6-thioguanine produces a therapeutic response greater than that induced by either of these agents alone, its combination with cyclophosphamide, N4-behenoyl-1-beta-D-arabinofuranosylcytosine, or 5-fluorouracil does not produce such a response. The administration of cyclophosphamide, N4-behenoyl-1-beta-D-arabinofuranosylcytosine, or 5-fluorouracil alone resulted in a response as great as, or greater than, that induced by 6-MP alone. This and the finding that the 6-MP-induced response was more pronounced upon its delayed rather than its early administration indicate that 6-MP-induced reduction of the tumor burden does not explain this augmentation. The combination of 6-MP and L1210 vaccine was not effective in mice bearing 6-MP-resistant L1210 leukemia; however, an augmented response occurred when the tumor burden was reduced by N4-behenoyl-1-beta-D-arabinofuranosylcytosine, indicating that reduction of the tumor burden by 6-MP was only partially associated with augmentation of the therapeutic response. Augmentation was associated with vaccine-induced antitumor immunity because it was induced by the combination of 6-MP and concanavalin A-bound, but not concanavalin A-free L1210 vaccine. This augmentation was dependent on the timing of the L1210 vaccine administration. The combination was not effective in mice bearing P388 leukemia, indicating the tumor specificity of the augmentation. These results show that 6-MP not only reduced the tumor burden but also potentiated the vaccine-dependent antitumor immunity, resulting in the induction of an augmented therapeutic response.

Animals↗
PubMed1984

Enhancement of antiproliferation activity of vincristine and adriamycin by interferon.

Vincristine (VCR) combined with interferon (IFN)-beta suppressed H.Ep #2 cell proliferation more than additively, whereas 6-mercaptopurine combined with IFN-beta suppressed it less than additively. Factors associated with the more-than-additive effect were examined. The enhanced antiproliferation was achieved in HeLa cells as well as H.Ep #2 cells but not in Daudi or M-14 cells, indicating cell dependency of the enhancement. This enhancement was not dependent on the IFN species, including IFN-beta, IFN-alpha (leukocyte), and IFN-alpha (lymphoblastoid), although the cells were variably sensitive to these IFN species. In contrast, the enhance antiproliferation was critically dependent on the species of antineoplastic agents, and was selective to VCR and adriamycin among those tested under the present experimental conditions. The sequential exposure of H.Ep #2 cells to IFN and VCR induced the enhancement but exposure to VCR followed by IFN did not, suggesting that IFN-induced cell modification made the cells more sensitive to VCR. Either IFN or VCR was successfully replaced by colchicine, an antimicrotubule agent, but not by cytochalasin D, an antimicrofilament agent, suggesting the involvement of microtubule modification in the enhanced antiproliferation observed with IFN and VCR.

Cell Division↗
PubMed1984

High calcium content of pleiotropic drug-resistant P388 and K562 leukemia and Chinese hamster ovary cells.

The calcium content of pleiotropic drug-resistant tumor cells was estimated and compared with that of the parent tumor lines. P388 leukemia cells resistant to vincristine and Adriamycin contained more calcium (1.5- to 1.8-fold) in the cells and on the cell surface than the parent P388 cells. Similar results were obtained with human K562 myelogenous leukemia cells resistant to vincristine and also with Chinese hamster ovary cells resistant to colchicine. However, the calcium content of P388 cells resistant to 5-fluorouracil was almost the same as that of the parent P388 cells. The calmodulin content of pleiotropic resistant tumor lines and a 5-fluorouracil-resistant tumor line was almost the same as that of the corresponding parent lines. The isolated plasma membrane of K562 cells resistant to vincristine contained approximately 1.5-fold higher calcium than the parent cells. These results indicate that the higher cellular calcium content might be a characteristic phenotype of pleiotropic resistant tumor lines.

Animals↗
PubMed1984

Reversal of multidrug resistance by non-antitumor anthracycline analogs.

It was found that three synthetic anthracycline analogs lacking not only antitumor activity but also calcium-antagonizing action possessed an activity to potentiate vincristine cytotoxicity against vincristine-resistant P388 leukemia. ID-8279, one of these analogs, significantly reversed resistance to vincristine and daunorubicin by increasing their intracellular accumulation.

Animals↗
PubMed1984

Antitumor effects and pharmacology of orally administered N4-palmitoyl-1-beta-D-arabinofuranosylcytosine in mice.

The antitumor activity and the pharmacological fate of N4-palmitoyl-1-beta-D-arabinofuranosylcytosine (N4-palmitoyl-ara-C) administered p.o. were examined in mice and were compared with those of the parent compound 1-beta-D-arabinofuranosylcytosine (ara-C). N4-Palmitoyl-ara-C administered p.o. showed chemotherapeutic effects superior to those of ara-C when used against P388 leukemia, L1210 leukemia, mammary adenocarcinoma 755, and colon 38 adenocarcinoma. The derivative also inhibited the spontaneous pulmonary metastasis of s.c.-inoculated Lewis lung carcinoma more efficiently than did ara-C. After a single p.o. injection of a suspension of N4-palmitoyl-[2-14C]ara-C at a therapeutic dose of 350 mu/kg, a high concentration of the drug was found in the liver, lung, and plasma of portal venous blood. The level of the drug in other tissues and peripheral plasma was rather low. The two main metabolites, identified as ara-C and 1-beta-D-arabinofuranosyluracil, were found in plasma and various tissues. Plasma ara-C concentration was maintained for at least 6 hr in the range of 2.3 to 5.1 nmol/ml after p.o. administration of N4-palmitoyl-ara-C (350 mu/kg). On the other hand, when an equimolar amount of ara-C was given, the plasma levels of the drug decreased rapidly; from 2 to 6 hr after administration, the level (1.0 to 4.1 nmol/ml) was less than that obtained with N4-palmitoyl-ara-C. These results suggested that N4-palmitoyl-ara-C administered p.o. is absorbed as an intact form from the gastrointestinal tract and that the absorbed compound is the depot form of ara-C, releasing ara-C over a prolonged period of time.

Adenocarcinoma↗