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Biomedical subjects

Y Kitamura

Publications and source records attributed to Y Kitamura.

At least 559 records · Page 31Linked to original sources
PubMed1989

Androgen dependency of a tumor produced by a cell line derived from androgen-responsive Shionogi carcinoma 115.

An androgen-dependent tumor (SCC8 tumor) was obtained by inoculating an androgen-responsive cell line derived from the androgen-responsive Shionogi carcinoma 115 (SC115) into mice and then treating the mice with testosterone propionate (TP) at a pharmacological dose (400 micrograms/day). The SCC8 tumor differed in histological appearance from the SC115 tumor and its growth was less stimulated by androgen than that of the SC115 tumor. However, its growth was completely androgen dependent; SCC8 tumors did not develop in castrated mice and regressed when TP treatment was discontinued. The decreased sensitivity of the SCC8 tumor seemed to be attributable in part to its rapid metabolism of testosterone to metabolites with lower androgenic actions. The effects of TP at doses of 0, 100, 200, and 400 micrograms/day on cell division and cell death in SCC8 tumors of medium size were examined by measurements of the mitotic index and the retention of 5-[125I]iodo-2'-deoxyuridine incorporated into the whole tumor. TP increased the mitotic index dose dependently and at all doses reduced the decrease in the retention of 5-[125I]iodo-2'-deoxyuridine. These results suggest that steroids may not only stimulate cell division but also reduce cell death in steroid-dependent tumors.

Androgens↗
PubMed1989

Regulation of mast cell differentiation.

Mast cells are a unique class of blood cell. Unlike most blood cells, undifferentiated precursors of mast cells migrate in the bloodstream, invade tissues, proliferate there and then differentiate. Even after differentiation, some mast cells may proliferate extensively. Differentiation of mast cells is regulated by both diffusible growth factors and direct contact with fibroblasts.

Animals↗
PubMed1989

Differentiation of germ cells in seminiferous tubules transplanted to testes of germ cell-deficient mice of W/Wv and Sl/Sld genotypes.

(WB X C57BL/6)F1-W/Wv (hereafter, WBB6F1-W/Wv) mice and (WC X C57BL/6)F1-Sl/Sld (hereafter, WCB6F1-Sl/Sld) mice are sterile due to the deficient spermatogenesis in the testes. The cause of deficient spermatogenesis in WBB6F1-W/Wv mice is considered to be a defect in germ cells themselves, whereas that in WCB6F1-Sl/Sld mice is considered to be a defect in tissue environment necessary for differentiation of germ cells. Seminiferous tubules isolated from cryptorchid testes of C57BL/6- +/+ mice were transplanted into the testes of WBB6F1-W/Wv and WCB6F1-Sl/Sld mice to clarify that the extratubular environment of these mice was intact or not. Type A spermatogonia in the transplanted tubules normally differentiated into spermatids, suggesting that the extratubular environment is intact in both WBB6F1-W/Wv and WCB6F1-Sl/Sld mice.

Animals↗
PubMed1989

Inhibitory effect of progesterone on cell death of mouse uterine epithelium.

The protective effect of progesterone against cell death of mouse uterine epithelium was evaluated by examining the retention of 5'-[125I]iodo-2'-deoxyuridine [( 125I]IdUrd) incorporated into the whole uterus and the apoptotic index (percentage of apoptotic cells in total cells), which is a good index of physiological cell death. Castrated adult female mice were given a daily injection of oestradiol-17 beta for 3 days, and then an injection of [125I]IdUrd. They were then divided into 4 groups, which received a daily injection of vehicle only, oestradiol-17 beta (E), progesterone (P), or both oestradiol-17 beta and progesterone (EP), and were killed at intervals during these treatments for determination of 125I radioactivity retained in the whole uterus. On treatment with vehicle only, the 125I radioactivity retained in the uterus decreased rapidly, but treatment with E, P or EP reduced the loss of 125I radioactivity significantly. Progesterone did not antagonize the effect of oestradiol-17 beta on the 125I radioactivity retained in the uterus. The apoptotic index of uterine cells was examined by a similar experimental protocol, but without injection of [125I]IdUrd. In the group treated with vehicle only, the apoptotic indices of both luminal and glandular epithelia increased markedly, but the injection of E, P or EP suppressed these increases significantly. Progesterone did not antagonize the effect of oestradiol-17 beta on the apoptotic index. The apoptotic index of stroma was not affected by the injection of E, P or EP. On the other hand, progesterone completely inhibited the increase in the mitotic index of uterine epithelia induced by oestradiol-17 beta. These results show that progesterone alone or in combination with oestrogen reduced cell death in mouse uterine epithelium and that the effects of oestrogen and progesterone on uterine cell death were independent of their actions on cell division.

Animals↗
PubMed1989

Acceleration of a murine T-cell leukemia associated with loss of interleukin-3 producing activity.

L-8313 is a murine T-cell leukemia cell line the cells of which constitutively produce interleukin-3 (IL-3). S2-8313 is a unique subline of L-8313 which has lost IL-3 producing activity. Although the growth of S2-8313 cells in the bone marrow is comparable to that of L-8313 cells, the survival time of C3H mice grafted with S2-8313 cells is significantly shorter than that of C3H mice grafted with L-8313 cells. The accelerated death observed in C3H mice bearing S2-8313 cells is attributable to early development of granulocytopenia and thrombocytopenia, which resulted from the loss of the IL-3 producing activity.

Animals↗
PubMed1989

Age- and diabetes-accelerated glycation in the human aorta.

The extent of glycation in pieces of human aorta was estimated by determining the content of furosine, which is derived from fructose-lysine through acid hydrolysis. Glycation of human aorta was found to increase with advancing age. A significant positive correlation was found between the degree of atherosclerosis and the furosine level in the aorta in subjects over 60 years of age. Furthermore, the furosine level in the aortae of diabetic patients was significantly higher than that in normal subjects of the same age. These results suggest not only that glycation in the aorta may increase with aging and with the development of arteriosclerosis, but also that diabetes may be related as well to premature aging as to arteriosclerosis.

Adult↗
PubMed1989

Ontogenesis of alpha 2-adrenoceptor coupling with GTP-binding proteins in the rat telencephalon.

The ontogenesis of alpha 2-adrenoceptors and GTP-binding proteins and their coupling activity were investigated in telencephalon membranes of developing rats. The manganese-induced elevation of [3H]clonidine binding was increased in an age-dependent manner but the guanosine 5'-O-(3-thio)triphosphate-induced decrease in binding did not change. The extent of the binding of [3H]clonidine at 15 nM (saturable concentration) increased in an age-dependent manner and reached the adult level at 4 days after birth. Cholera toxin and pertussis toxin catalyzed ADP-ribosylation of proteins of 46 and 41/39 kilodaltons (kDa) in solubilized cholate extracts of the membranes. The 41/39-kDa proteins ADP-ribosylated by pertussis toxin (Gi alpha + Go alpha) were increased with age and reached the adult level at day 12, whereas the 46-kDa protein (Gs alpha) reached its peak on day 12 and then decreased to the fetal level at the adult stage. The immunoblot experiments of the homogenates with antiserum (specific antibody against alpha- and beta-subunit of GTP-binding proteins) demonstrated that the 39-kDa alpha-subunit of (Go alpha) and the 36-kDa beta-subunit of GTP-binding protein (beta 36) increased with postnatal age. In contrast, 35-kDa beta-subunit (beta 35) did not change. From these results, it is suggested that the coupling activity of alpha 2-adrenoceptor with GTP-binding protein gradually develops in a manner parallel with the increase of alpha 2-adrenoceptor and pertussis toxin sensitive GTP-binding proteins, Gi, and that alpha 39 beta 36 gamma may be related to the differentiation and/or growth of nerve cells in rat telencephalon.

Adenosine Diphosphate Ribose↗
PubMed1989

Noradrenaline release enhanced by cholera toxin and pertussis toxin in rat cerebral cortical slices.

The effects of cholera and pertussis toxin on the release of noradrenaline (NA) were studied in the rat cerebral cortex. The cerebral cortical slices were incubated with cholera or pertussis toxin for 2 h, subsequently loaded with 1-[3H]NA and superfused continuously. The pretreatment with cholera toxin significantly (p less than 0.05) enhanced the 20 mM KCl-evoked [3H]NA release. In contrast to a significant (p less than 0.05) increase in [3H]NA release by pertussis toxin, neither A-protomer nor B-oligomer of the toxin could affect the release. These results suggest that cholera and pertussis toxin-substrates, probably guanosine triphosphate-binding proteins, could be involved in the NA release in the central nervous system.

Adenosine Diphosphate Ribose↗
PubMed1989

[Clinical research on congenital hydronephrosis--significance and indication of the preliminary nephrostomy].

Clinical data of 31 patients (34 renal units) with severe congenital hydronephrosis who had received preliminary nephrostomy were reviewed to survey functional recovery of the kidneys and the significance of preliminary nephrostomy. The results were as follows: 1. In most cases, the renal function based on Ccr and 99mTc-DMSA renal scintigraphy after nephrostomy could not improve beyond preoperative one. 2. A close linear correction was found between the thickness of renal parenchyma before preliminary nephrostomy and the renal function after the nephrostomy. 3. Preliminary nephrostomy is indicated for severe hydronephrosis in neonates and infants, obstruction of the lower ureter, and serious general condition, which need accurate split renal function, and for patients without accurate diagnosis.

Adolescent↗
PubMed1989

[Regulatory mechanisms of mast cell differentiation].

Mast cells are a progeny of the multipotential hematopoietic stem cell. Most of progenies of the stem cell complete their differentiation within the bone marrow, but precursors of mast cells leave the bone marrow, migrate in blood, and invade into tissues. After the invasion, precursors proliferate and differentiate into mast cells. An appreciable proportion of mast cells retain proliferative potential after differentiation, and even after degranulation, some mast cells can proliferate and recover the original morphology. Proliferation of mast cells are regulated by both T cell-derived factors (i.e., IL-3 and IL-4) and fibroblast-derived factor(s). Mice of either W/Wv or Sl/Sld genotype lack mast cells, but mast cells do develop when bone marrow cells of W/Wv or Sl/Sld mice were cultured in the presence of T cell-derived factors. Mast cells derived from W/Wv mice cannot respond fibroblast-derived factor(s) and fibroblasts derived from Sl/Sld mice cannot support mast cells of normal mouse origin. Phenotypes of mast cells are determined by the environment in which the mast cells differentiated. However, when mast cells are transplanted into a new environment which is different from the original one, the mast cells acquire the phenotype which are dependent on the second environment.

Animals↗
PubMed1989

Skin blood flow in diabetic patients during cold loading.

We measured periflux blood flow (PBF) in people's fingers and its response to cold loading with a laser Doppler flowmeter. As an index in the cold loading test we used cold recovery time (CRT). Among normal people, CRT increased with age. Diabetics had significantly longer CRTs than did age-matched controls. CRT seems to be useful for evaluating the skin microcirculation in diabetics and the aged.

Adolescent↗
PubMed1989

[Intraarterial chemotherapy of experimentally metastasized liver carcinoma with anticancer emulsion containing surface-active agent].

The w/o Emulsion (w/o) of 0.3% adriamycin (ADR) in the mixture of a water-soluble contrast medium, 60% urografin, and an oily contrast medium, lipiodol, at the ratio of 1 : 4 was combined with 0.5% lecithin. This combination could stabilize the micelles and make the emulsion desirably slow releasing form. ADR emulsion was injected into the hepatic artery of rabbit with metastatic liver carcinoma 7 days after intraportal transplantation of VX2 tumor. The examination at day 5 revealed good accumulation and retention of ADR in tumor. This emulsion was histologically confirmed to be effective in suppressing the growth of metastatic lesion, and it was considered that this ADR emulsion would have a great possibility for clinical application in the treatment of hepatic metastasis of gastrointestinal carcinomas.

Animals↗
PubMed1989

Effect of 5-fluorouracil on "primitive" hematopoietic stem cells that reconstitute whole erythropoiesis of genetically anemic W/Wv mice.

The potential to reconstitute the whole erythropoiesis of a genetically anemic (WB X C57BL/6)F1-W/Wv (WBB6F1-W/Wv) mouse for at least 8 weeks was compared between 5-fluorouracil (5FU)-treated and nontreated bone marrow cells. C57BL/6-Pgk-1b/Pgk-1a female mice, in which each stem cell had either A-type or B-type phosphoglycerate kinase (PGK) owing to the random inactivation of one of two X chromosomes, were used as donors. As a marker of the reconstitution, electrophoretic pattern of hemoglobin was used. The concentration of the stem cells that reconstitute the whole erythropoiesis of WBB6F1-W/Wv mouse was higher in the marrow of donors that had received an injection of 5FU two days previously (two-day 5FU-treated) than in the marrow of nontreated donors. In the marrow of four-day 5FU-treated mice, however, the concentration was comparable to that of nontreated mice. The PGK electrophoretic pattern of WBB6F1-W/Wv mice reconstituted by nontreated marrow cells was comparable to the PGK pattern of WBB6F1-W/Wv mice reconstituted by four-day 5FU-treated marrow cells. Thus, a single stem cell with extensive proliferative potential rather than multiple spleen colony-forming units appeared to be responsible for the erythropoietic reconstitution in the transplantation of nontreated healthy marrow cells as well as 5FU-treated marrow cells.

Anemia↗
PubMed1989

Lymphoid differentiation of the hematopoietic stem cell that reconstitutes total erythropoiesis of a genetically anemic W/Wv mouse.

We investigated whether the stem cell that reconstitutes total erythropoiesis of a WBB6F1-W/Wv mouse differentiates into lymphoid lineage. The electrophoretic pattern of hemoglobin was used as a marker of the reconstitution; 3-phosphoglycerate kinase (PGK), an X chromosome-linked enzyme was used as a tool for estimating clonality. We injected 10(5) bone marrow cells of 5-FU treated C57BL/6-Pgk-1b/Pgk-1a female mice, in which each stem cell had either A-type PGK or B-type PGK due to random inactivation of one of two X chromosomes, into genetically anemic (WB x C57BL/6)F1-W/Wv (hereafter WBB6F1-W/Wv) mice that contained only B-type PGK. The recipient WBB6F1-W/Wv mice, in which erythropoiesis was reconstituted with donor cells for a long term, were killed and the PGK patterns of bone marrows, thymus, lymph nodes, and Peyer's patches were examined. A considerable amount of A-type PGK was detected in the lymphoid organs of the WBB6F1-W/Wv mice in which erythrocytes showed only A-type PGK when killed. In contrast, A-type PGK was scarcely detectable in the lymphoid organs of the WBB6F1-W/Wv mice in which erythrocytes showed only B-type PGK when killed. The present results suggest that the hematopoietic stem cells estimated by the erythropoiesis reconstituting assay differentiate into lymphoid lineage and that the long-term erythropoiesis reconstitution assay is useful for detecting the true primitive hematopoietic stem cells.

Anemia↗
PubMed1989

[A case report of bronchial rupture with a polyvinylchloride (PVC) double-lumen tube].

The patient is a 58-year-old man with a 3-months history of painful swallowing. Endoscopy and biopsy demonstrated squamous cell carcinoma of the middle one third of the esophagus. On Sept. 13, 1987, the patient underwent surgery. The patient was intubated with the PVC double-lumen tube. After the resection of esophagus, when lymphadenectomy was performed, we noticed the herniation of a bronchial cuff through the left main bronchial tear. Surgical repair of the lesion was accomplished with a continuous suture with 3-0 vicryl. Subsequent course of the patient was uneventful. Tracheobronchial rupture is rare complication of intubation with PVC double-lumen tube. This complication results from measures such as using an inadequate tube size, malpositioning the tip of the tube, or insufflating the balloon too rapidly, which dose not allow adaptation of the balloon to the tracheobronchial wall. In our case, overinflation of the bronchial balloon was probably the etiology of rupture. This was probably secondary to diffusion of nitrous oxide, rather than initial over-distension. Meticulous cares must be emphasized to avoid such complication.

Bronchi↗
PubMed1989

Beige rat: a new animal model of Chediak-Higashi syndrome.

Although Chediak-Higashi syndrome (CHS) has been found in various mammalian species, it has not been described in rats. Since giant granules characterizing CHS are easily recognizable in mast cells of beige (CHS) mice, we screened mast-cell granules in the auricle of some mutant rats, of which coat color was diluted by mutation. Giant granules of mast cells were found in a mutant trait that occurred in the inbred colony of the DA strain rat maintained in Hamamatsu University School of Medicine. Giant granules were also observed in neutrophils and pigment cells of the eye. In this mutant, either spontaneous migration or chemotaxis of neutrophils was impaired, and the bleeding time was prolonged. Blood serotonin level of the mutant was about one tenth that of the normal congenic rat, and injection of serotonin normalized the bleeding time of the mutant. Moreover, the natural killer activity of the mutant was significantly impaired. These results indicated that this mutation was comparable to CHS of humans and mice, and we designated it as "beige." Since rats are more favorable than mice for some types of experiments, the beige rat is potentially useful as an animal model of CHS.

Animals↗
PubMed1989

Hepatoprotective effects of cystathionine against acetaminophen-induced necrosis.

The hepatoprotective effects of cystathionine, as a prodrug of cysteine release, were examined in rodents. When cystathionine (100 mg/kg) was administered i.p. in rats, it was eliminated from rat serum with a biological half-life of 1.19 +/- 0.23 hr. Subsequent to the decrease of serum cystathionine, the concentration of cyst(e)ine increased up to 14.5 +/- 1.2 mg/l, and then decreased with a half-life of 4.12 +/- 0.82 hr. The concomitant administration of taurine (100 mg/kg) did not change the half-life of cystathionine (1.42 +/- 0.33 hr), but significantly increased the half-life of cyst(e)ine (19.1 +/- 0.56 hr). This effect of taurine was also observed when cysteine (100 mg/kg) was administered to rats. The liver injury was induced by the i.p. injection of acetaminophen (5.0 mmol/kg). The mortality rates, serum alanine and aspartate aminotransferase activities and the histological analysis of the livers, which were obtained from living mice, were examined 22 hr after the injections. Two administrations of cystathionine (5.0 mmol/kg x 2), one at 20 min before and one 20 min after the acetaminophen injection, prevented the acetaminophen-induced hepatic necrosis, completely. The coadministration of taurine increased the hepatoprotective activity of cystathionine, even at the low dosages (0.18 and 0.55 mmol/kg x 2). Moreover, the treatments using cystathionine, with and without taurine, restored the hepatic glutathione levels to 2.27 +/- 0.23 and 1.80 +/- 0.27 mumol/g, respectively. These levels had been depleted by acetaminophen injection to 0.96 +/- 0.18 mumol/g, 2 hr after the injection. Propargylglycine, an inhibitor of cystathionase, abolished the hepatoprotective effects of cystathionine, although it could not affect the action of cysteine.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaminophen↗