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Biomedical subjects

H Iida

Publications and source records attributed to H Iida.

At least 559 records · Page 31Linked to original sources
PubMed1983

Establishment and properties of vincristine-resistant human myelogenous leukemia K562.

A vincristine (VCR)-resistant subline of human K562 myelogenous leukemia was established in vitro, and several clones with different susceptibilities to VCR were isolated by the limiting dilution technique. The most resistant clone (H-1) had a 17-fold greater resistance to VCR when compared to the parent K562 cells. The clone gradually lost the resistance during prolonged culture in vitro. These clones generally accumulated smaller amounts of VCR in their cells as compared to the parent cells. The size of H-1 clone cells was almost the same as that of the parent cells. The numbers of potential binding sites of VCR in the K562 cells and the resistant H-1 clone were almost the same. Similar results were obtained for P388 and its VCR-resistant subline. The cells derived from the VCR-resistant H-1 clone were highly cross-resistant to vindesine and moderately resistant to vinblastine. Cells derived from clone H-1 exhibited marginal degrees of cross-resistance to adriamycin, maytansine and VP-16-213, whereas VCR-resistant P388 leukemia cells exhibited significant resistance to these agents, especially to maytansine.

Cell Line↗
PubMed1983

Vincristine-resistant P388 leukemia cells contain a large amount of calcium.

P388 leukemia cells resistant to vincristine contained more calcium in the cells than the parent sensitive line, especially in the form of EGTA-removable (surface-bound) calcium. Although the relationship, if any, between the high cellular calcium of resistant cells and drug-resistant phenotype is not clear, the possible implications of this result for the elucidation of the mechanisms of drug resistance are interesting.

Animals↗
PubMed1983

[Postoperative chemotherapy of perforating appendicitis in children; with special reference to latamoxef therapy].

We employed latamoxef (LMOX) as antibiotic therapy subsequent to the performance of appendectomies in children. Fifteen patients, consisting of 8 cases of catarrhal appendicitis and 7 cases of gangrenous appendicitis, were administered LMOX at 50 mg/kg/day, while 13 patients with peritonitis due to a perforated appendix were treated with a dosage of 90 mg/kg/day. Both of these dosages were administered in 3 equally-divided doses, as one shot intravenous injections. All of the cases of catarrhal and gangrenous appendicitis showed good, steady recovery after the surgery, and there were no instances of complications. With regard to the 13 cases of perforating appendicitis, a clinical efficacy of at least "good" was obtained in 12 patients, for an efficacy rate of 92.3%. In addition, bacteriologically, 35 out of 36 strains that were isolated initially could no longer be detected after the LMOX therapy, indicating an eradication rate of 97.2%. Complications consisted of 1 case of dehiscence of the wound, and 1 case of adhesive ileus. Comparison of the values of the laboratory tests before and after the LMOX therapy revealed no development of abnormalities. Moreover, with regard to side effects, with the exception of 1 case of transient diarrhea, there were no side effects which presented clinical problems. It was found that the causative microbes involved in these cases of appendicitis--especially in the perforative appendicitis cases--were Gram-negative bacilli such as E. coli, and an anaerobic bacterium, B. fragilis.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Bacterial Agents↗
PubMed1983

Potentiation of vincristine and Adriamycin effects in human hemopoietic tumor cell lines by calcium antagonists and calmodulin inhibitors.

verapamil, a calcium-influx blocker, enhanced the cytotoxicity of vincristine (VCR) in vitro 6- to 12-fold in eight human hemopoietic tumor cell lines established from acute lymphatic leukemia, acute myelogenous leukemia, and Burkitt's lymphoma. Great enhancement of VCR cytotoxicity was obtained in a VCR-resistant subline of K562 myelogenous leukemia. A maximum of approximate 100-fold increase in VCR cytotoxicity occurred. Heterogeneity in VCR sensitivity (80-fold difference in sensitivity) was observed in vitro among these human tumor cells. BALL and Daudi cells of B-cell type were more susceptible to VCR. At 6.6 or 20 microM of verapamil, the values for the concentration of drug required for 50% inhibition of cell growth for each cell line fell into a rather narrow range, and heterogeneity in VCR sensitivity among cell lines was circumvented in vitro. Verapamil also enhanced the cytotoxicity of Adriamycin, although the extent of enhancement was considerably small. Enhancement of VCR cytotoxicity also occurred with other calcium antagonists and calmodulin inhibitors. At maximum effective concentration of these reagents, a 3- to 5-fold increase in VCR cytotoxicity occurred in K562 cells. In VCR-resistant K562 cells, a more prominent enhancement (20- to 45-fold) was observed with these reagents. VCR resistance was circumvented in vitro. The mechanism of enhancement of VCR cytotoxicity was explained by the enhanced accumulation of VCR in K562, especially in resistant cells.

Calcium↗
PubMed1983

Promotion by verapamil of vincristine responsiveness in tumor cell lines inherently resistant to the drug.

Cultured cell lines LL, B16, C26, and C38 established from mouse solid tumors of Lewis lung carcinoma, B16 melanoma, and colon adenocarcinomas 26 and 38, respectively, showed inherently different resistance to vincristine (VCR) in vitro. The inherent resistance to VCR of these cell lines was related to the ability of the cells to accumulate VCR. Verapamil, a calcium antagonist with coronary vasodilator activity, enhanced the cytotoxicity of VCR against these cell lines depending upon their susceptibility to VCR. C26 cells, the most resistant, became the most susceptible to VCR with a nontoxic dose of verapamil. A 12-fold increase in VCR cytotoxicity occurred. Only a 2.5-fold increase in VCR cytotoxicity was observed for B16 cells, the most sensitive cells. VCR cytotoxicity against each cell line reached almost the same level by verapamil (2.2 to 6.6 microM). Thus, the inherent resistance to VCR among the tumor lines was circumvented. Verapamil enhanced the cellular accumulation of VCR. A 3- to 4-fold increase in cellular VCR occurred in C26 cells, while approximately a 2-fold increase was observed for B16 and LL cells. A similar rate of enhancement was observed for both bound and free VCR, indicating that verapamil does not enhance the affinity of VCR to tubulin. Verapamil inhibited the outward transport of VCR from the cells. The most prominent inhibition was observed for C26 cells. Circumvention of inherent resistance of tumor cells to VCR by verapamil could be attained through an enhanced cellular accumulation of VCR in each of the tumor cells. The enhancement of VCR cytotoxicity and circumvention of inherent VCR resistance by verapamil could be explained by the cellular concentration of VCR, and also it might be related to the extent of VCR binding to tubulin in the cell. The chemotherapeutic effect of VCR is significantly enhanced by verapamil in colon adenocarcinoma 26-bearing mice.

Adenocarcinoma↗
PubMed1983

Circumvention of vincristine and Adriamycin resistance in vitro and in vivo by calcium influx blockers.

Calcium influx blockers, diltiazem, nicardipine, nifedipine, niludipine, and nimodipine, which possess coronary vasodilator activity, greatly enhanced the cytotoxicity of vincristine (VCR) in tumor cells and especially in VCR-resistant sublines of P388 leukemia (P388/VCR) and human K562 myelogenous leukemia. The extent of enhancement was different among the drugs, and up to a 50- to 70-fold increase in VCR cytotoxicity occurred in P388/VCR cells with nontoxic or marginally toxic concentrations of diltiazem and nicardipine. A 50- to 100-fold enhancement occurred in VCR-resistant human K562 myelogenous leukemia cells with diltiazem, nicardipine, niludipine, and nimodipine. VCR resistance of these cell lines was circumvented completely by these blockers. Calcium influx blockers also enhanced the cytotoxicity of Adriamycin in P388 leukemia cells and especially in its Adriamycin-resistant subline. The extent of enhancement, however, was lower than that which occurred in VCR-resistant tumor lines with VCR. An approximately 10- to 30-fold increase in Adriamycin cytotoxicity occurred in P388 Adriamycin-resistant subline cells with diltiazem, nicardipine, niludipine, and nimodipine. Although VCR alone at 10 to 200 micrograms/kg did not confer a significant therapeutic effect in P388/VCR-bearing mice, calcium influx blockers in doses of 30 to 125 mg/kg administered daily for 10 days with VCR enhanced the chemotherapeutic effect of VCR in P388/VCR-bearing mice. A maximum of approximately a 40 to 50% increase in life span occurred with diltiazem, nicardipine, niludipine, and nimodipine. The calcium influx blockers also enhanced the therapeutic effect of Adriamycin in P388 Adriamycin-resistant subline-bearing mice, although the extent of enhancement was smaller than that observed with VCR in P388/VCR-bearing mice.

Animals↗
PubMed1982

Enhancement of vincristine- and adriamycin-induced cytotoxicity by verapamil in P388 leukemia and its sublines resistant to vincristine and adriamycin.

A calcium antagonist, verapamil, enhanced the cellular uptake and cytotoxicity of vincristine (VCR) in adriamycin-resistant P388 leukemia (P388/ADM) cells and also enhanced the cellular uptake and cytotoxicity of adriamycin (ADM) in vincristine-resistant P388 leukemia (P388/VCR) and P388/ADM cells. The enhancement of cytotoxicity and cellular uptake of VCR in P388 and P388/VCR cells has been reported previously. [1]. VCR and ADM resistance was circumvented by verapamil. A common transport mechanism for VCR and ADM, which is responsive to verapamil, seems to exist in VCR- and ADM-resistant cells. However, the enhancement of ADM cytotoxicity and cellular uptake by verapamil was not evident in P388 cells.

Animals↗
PubMed1982

Ontogeny of the leucine-enkephalin neuron system of the rat: immunohistochemical analysis. I. Lower brainstem.

Ontogeny of the leucine-enkephalin (L-Enk) neuron system in the lower brainstem of the rat was investigated by means of indirect immunofluorescence. L-Enk-containing cells first appear in the primordium of the medullary reticular formation just medial to the n. tractus spinalis nerve trigemini at the level of the the rostral half of the inferior olivary nucleus, in the n. cuneiformis, and in the mesencephalic reticular formation of the fetus at gestational day 16 (14-15-mm embryos). From that time onward, L-Enk-containing cells appear in various areas of the lower brainstem one after another until birth. After birth, although L-Enk-containing cells decrease slightly in number as the rats grow, L-Enk-containing fibers continue to increase in number.

Animals↗
PubMed1982

[A case with Bartter's syndrome associated with type II hyperlipidemia, increased fluidity of plasma VLDL and abnormal configuration of peripheral erythrocytes (author's transl)].

A 34-year-old female complaining of numbness and weakness of the extremities was examined. Consanguineous marriage was contracted between mother and father. She was of short stature (149 cm), and her blood pressure was normal (118/60 mmHg). Her serum potassium concentration had decreased to a level between 2.5 and 3.2 mEq/L, and hypokalemic alkalosis was present. Potassium clearance had increased and urinary concentrating capacity was impaired. Plasma renin activity was high at 25 ng/ml/hr but plasma aldosterone concentration was normal. Hypertensive response to angiotensin II (50 ng/kg/min) was weak but improved to nearly the normal value after the administration of indomethacin for 17 days at a dose of 50 mg/day. A slight elevation in blood pressure was observed during the infusion of norepinephrine (250 ng/kg/min). A decrease in blood pressure was observed during the infusion of 1-sarcosine, 8-isoleucine angiotensin II (600 ng/kg/min) with concomitant increase of plasma renin activity. Twenty-four hour urinary excretion of prostaglandin E decreased somewhat (225 approximately 252 ng/day), and hyperplasia of the juxtaglomerular cells and increased JG index were demonstrated in the biopsy specimens of the right kidney. From the findings, the present case were diagnosed as Bartter's syndrome. Although mild enlargement of the sella turcica was found in skull x-ray films, no abnormalities in pituitary function were demonstrated. Other unusual complications, i.e. hyperlipidemia (type II, beta-dominant) and abnormal configuration of peripheral erythrocytes, were demonstrated. Phospholipid composition of the erythrocyte membrane was normal. The fluidity of plasma VLDL examined by electron spin resonance was increased. Hypokalemia and hyperreninemia were improved through the administration of indomethacin. However, because of headache as an adverse effect, further administration could not be accepted. The patient's complaints were resolved by the rectal application of indomethacin with oral administrations of spironolactone and triamterene. Changes in serum lipid levels did not occur with the above mentioned treatment. alpha-tocopheryl nicotinate lowered the levels of serum lipids and normalized the configuration of peripheral erythrocytes. But increased fluidity of plasma VLDL remained, and phospholipid composition of erythrocyte membrane was also unchanged. The relationship between the rare complications mentioned above and the pathophysiology of Bartter's syndrome is still obscure.

Adult↗
PubMed1982

Ontogeny of somatostatin-containing neuron system of the rat: immunohistochemical analysis. II. Forebrain and diencephalon.

The ontogeny of the somatostatin (SRIF) neuron system in the forebrain and diencephalon the rat was investigated by means of the indirect immunofluorescence method. SRIF-positive cells first appear in the primordium of the hypothalamus surrounding the fasciculus mammillothalamicus of the fetus at gestational day 14 (10-12-mm embryo). At gestational days 16-17 (14-17-mm embryo, SRIF-positive cells appear in the developing piriform cortex and entopeduncular nucleus. The fetus at gestational days 18-19 (17-26-mm embryos) showed a remarkable increase in the number of SRIF-positive cells and numerous groups of such cells are detectable in various forebrain and diencephalic areas such as the hypothalamic periventricular zone, zona incerta, area lateral to the commissura posterior (ACP), area between the optic tract and capsula interna, pars retrolenticularis (AOR), n. caudatus putamen, hippocampus, somatic sensory cortex, and n. accumbens, etc. At gestational day 20, SRIF-positive cells newly appear in the septum, olfactory bulb, diagonal band of Broca, claustrum, lateral preoptic area, and lateral habenular nucleus. The majority of SRIF-positive structures found in the forebrain and diencephalon increase in number during the perinatal stage (between gestational day 21 and postnatal day 2) and more or less maintain their immunoreactivity even in adult rats. However, SRIF-positive cells located in the AOR, ACP, and lateral septal area, etc., begin to decrease in number during the perinatal stage and no or only a few SRIF-containing cells are identified in these areas of infant and adult rats.

Animals↗
PubMed1982

Ontogeny of somatostatin-containing neuron system of the rat cerebellum including its fiber connections: an experimental and immunohistochemical analysis.

Ontogeny of somatostatin (SRIF) neuron system of the rat cerebellum was investigated by means of the indirect immunofluorescent method. In addition, several operations were performed to provide the evidence of understanding the cerebellar SRIF innervation. SRIF-positive structures appeared in the primordium of the cerebellum of the fetus at gestational day 16 (14-15 mm embryos). From that time on, SRIF-positive structures identified in the cerebellum increased in number and the greatest number of SRIF-positive structures were detected in the cerebellum of the rat between newborn and 7-day-olds. Afterwards, these structures decreased remarkably in number and only a few if any SRIF-positive structures were observed in the cerebellum of the adult rats. These facts might suggest that SRIF might perform some important roles in the development of the cerebellum. The present study further elucidated that cerebellar SRIF was supplied by at least two types of sources; one was situated within the cerebellum and the other in the extracerebellar regions. The former one innervates mainly the vermis and partly the hemisphere, while the latter one projects mainly to the hemisphere and partly to the vermis.

Aging↗