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Biomedical subjects

Y Fujii

Publications and source records attributed to Y Fujii.

At least 955 records · Page 53Linked to original sources
PubMed1988

Cell-mediated immunity induced in mice after vaccination with a protease activation mutant, TR-2, of Sendai virus.

Our previous study has shown that, although a trypsin-resistant mutant of Sendai virus, TR-2, replicates only in a single cycle in mouse lung with a negligible lesion, the animal acquires a strong immunity against lethal infection with wild-type Sendai virus, suggesting that TR-2 could be used as a new type of live vaccine (M. Tashiro and M. Homma, J. Virol. 53:228-234, 1985). In the present study, we investigated the immunological response elicited in TR-2-infected mice, particularly with respect to cell-mediated immunity. Analyses of cytotoxic activities of spleen cells with 51Cr release assays revealed that Sendai virus-specific T lymphocytes (CTL), in addition to natural killer activity and antiviral antibodies, were induced in DBA/2 and C3H/He mice infected intranasally with TR-2. Proteolytic activation of the fusion glycoprotein F was required for the primary induction of CTL, though not necessarily for stimulation of natural killer and antibody responses. Memory of the CTL induced by TR-2 was long-lasting and was recalled in vivo immediately after challenge with wild-type Sendai virus. In contrast to TR-2, immunization with inactive split vaccine failed to induce the CTL response, but it elicited a high titer of serum antibody and a low level of natural killer activity.

Animals↗
PubMed1988

Renal metabolism of atrial natriuretic peptide in the rat.

The purpose of this study was to identify the nephron and cell sites involved in the renal metabolism of alpha-rat atrial natriuretic peptide (alpha-rANP) and to examine the degradation products of the peptide. In micro-dissected nephrons 125I-labeled ANP degradation rate was highest in proximal convoluted (PCT) and straight tubules and lowest in glomeruli and papillary collecting tubules, indicating that the sites of ANP degradation and of the receptors that mediate its biological activity in the nephron do not coincide. Among subcellular fractions of cortical homogenates, the luminal membranes were the most active in metabolizing ANP. In contrast, ANP degradation by isolated basolateral membranes was negligible, and the basolateral uptake route in intact tubules did not contribute significantly to its catabolism. Cortical homogenates, luminal membranes, and isolated PCT degraded ANP without evidence of saturation up to pharmacological concentrations (10(-6) M) of the peptide. A major intermediate metabolite was rapidly formed by luminal membranes and was identified with use of a sequence and compositional analysis. This metabolite had the same amino acid sequence as ANP with a cleavage at position Cys7-Phe8, and the disulfide bridge was preserved. These results demonstrate a rapid degradation of ANP by kidney tissue and suggest that the luminal membrane of the proximal tubule is a major nephron site of ANP catabolism.

Animals↗
PubMed1988

Hypoxic contractile response in isolated human pulmonary artery: role of calcium ion.

The mechanism for hypoxic pulmonary vasoconstriction (HPVC) was investigated in human pulmonary arterial strips. Hypoxia in the presence of histamine (10(-6) M) caused marked pulmonary arterial contraction, which was reversed by O2. The hypoxic contraction in the presence of histamine was inhibited by diphenhydramine, but not by cimetidine. The hypoxic histamine-mediated contraction was attenuated but still present in the absence of extracellular Ca2+, or by the inhibitors of voltage-dependent Ca2+ influx. However, it was inhibited significantly by a further depletion of intracellular Ca2+, or by HA 1004, an intracellular calcium antagonist. A low concentration (10(-7) M) of a calcium ionophore, A23187, enhanced the hypoxic contraction in the presence of histamine, whereas procaine completely inhibited it. W-7, a calmodulin inhibitor, significantly decreased the hypoxic histamine-mediated contraction, but 12-O-tetradecanoylphorbol-13-acetate (TPA), a C-kinase promotor, had no effect. The hypoxic contractile response was also observed in the presence of both A23187 and KCl instead of histamine, but the hypoxia-induced contraction with KCl alone was much smaller than that. These results indicate that hypoxia in the presence of certain other vasoactive agents has a potent contractile effect on the human pulmonary artery and that the response is dependent on Ca2+. Enhancement of both Ca2+ influx and Ca2+ release from intracellular storage sites by hypoxia, which interacts with calmodulin, were suggested to be involved in the mechanism of HPVC.

Aged↗
PubMed1988

New canine model of chronic pancreatitis due to chronic ischemia with incomplete pancreatic duct obstruction.

A new experimental model of chronic pancreatitis was produced by a combination of chronic ischemia and incomplete obstruction of the pancreatic duct. Ischemia was induced by ligation and separation of branches flowing into the left pancreatic lobe from the splenic artery. Incomplete ductal obstruction was achieved by ligation and separation of the minor pancreatic duct and placement of a polyethylene tube in the major pancreatic duct. Macroscopic examination at 6 months after model preparation showed that the pancreas was hard, with severe inflammatory change. In the secretin test, the flow rate of pancreatic juice, amylase output and bicarbonate concentration were significantly reduced as compared with the controls. Pancreatography revealed dilatation and meandering of the major pancreatic duct and poor visualization of its secondary and tertiary bifurcations. The histopathological findings consisted of a decrease in the pancreatic parenchyma, replacement of fat, severe inflammatory cell infiltration, extensive fibrosis and tubular complexes. This model most closely resembles human chronic pancreatitis, and is a very useful instrument.

Animals↗
PubMed1988

Production of interleukin-1 alpha and a parathyroid hormone-like factor by a squamous cell carcinoma of the esophagus (EC-GI) derived from a patient with hypercalcemia.

To determine the pathogenesis of humoral hypercalcemia associated with esophageal carcinoma in a 65-yr-old patient, clonal cell lines (EC-GI) were established from the tumor. The EC-GI cells produced bone-resorbing activity which eluted from a Sephadex G-75 column in a broad peak, with an apparent mol wt of 10,000-50,000. In addition to PTH-like factor(s), the EC-GI cells produced a factor with thymocyte proliferation-stimulating activity which had an apparent mol wt of 15,000-20,000. This interleukin-1 (IL-1)-like factor(s) with acidic pI (4.8 and 5.2) exactly coeluted with the bone-resorbing activity upon DEAE-Sepharose ion exchange chromatography. Both bone-resorbing and thymocyte proliferation-stimulating activities were completely inhibited by anti-IL-1 alpha antiserum, but not by anti-IL-1 beta antiserum. Northern blot hybridization studies revealed that EC-GI cells produced exclusively mRNA for IL-1 alpha. Furthermore, fractions containing IL-1-like activity and PTH-like activity synergistically stimulated bone resorption in vitro, and transplantation of EC-GI cells into nude mice caused hypercalcemia in vivo. These findings suggest that IL-1 alpha and PTH-like factor produced by this squamous cell carcinoma synergistically stimulate bone resorption and are related to humoral hypercalcemia in tumor-bearing nude mice and in the patient.

Aged↗
PubMed1988

[Effects of TJ-41 (Tsumura Hochu-ekki-to) on spermatogenic disorders in mice under current treatment with adriamycin].

Experiments were performed to investigate the effects of TJ-41 on spermatogenic disorders under current treatment with adriamycin (ADR). Male ICR mice were intraperitoneally injected with ADR at the dose of 0.15 mg/kg, twice a week for 5 weeks. Simultaneously, these mice were orally administered TJ-41 at the dose of 1, 2 or 4 g/kg for 12 weeks. The effects of TJ-41 were evaluated by histological analysis of germ cells in the testis at 7 weeks after the last injection of ADR. TJ-41 at a dose of 4 g/kg significantly inhibited the decrease of testis weight in mice treated with ADR. TJ-41 at doses of 1 and 4 g/kg significantly decreased the proportion of seminiferous tubules without germ cells as compared with the ADR-treated group. On the other hand, TJ-41 at doses of 1 and 4 g/kg significantly increased the proportion of normal seminiferous tubules and the Sertoli cell ratio of spermatocytes as compared with the ADR-treated group. These results indicate that TJ-41 may qualitatively and quantitatively protect against the decrease of germ cells in the testis of mice treated with ADR.

Animals↗
PubMed1988

3,3',5'-Triiodothyronine inhibits ontogenetic development of iodothyronine-5'-deiodinase in the liver of the neonatal mouse.

To elucidate the effect of rT3 on iodothyronine-5'-deiodinating activity (I-5'-DA) in the liver of neonatal mice, rT3 was injected sc on the 5-8th day after birth and I-5'-DA in the liver was determined. A single injection of rT3 (0.01-1 microgram/g) inhibited the ontogenetically developing I-5'-DA in a dose- and time-dependent manner. The inhibitory effect was reversible and specific for I-5'-DA. Lineweaver-Burk analysis revealed that the time- and dose-dependent decrease in the enzyme activity was due to a decrease in Vmax with no alteration in Km values (5 x 10(-8) mol/l). The maximal inhibitory effect was observed at a dose of 1 microgram rT3/g, whereas the inhibitory effect was diminished at greater doses (4-10 micrograms/g), probably owing to a contamination with T4 of the rT3 preparation administered. Furthermore, consistent with our previous in vitro findings, rT3 inhibited the I-5'-DA induced by T3 in the liver of neonatal mice. These findings suggest that rT3 inhibited I-5'-DA in the liver of neonatal mice by decreasing the amount of enzyme available to the substrate and that rT3 also elicited an antagonistic effect against T3 in the induction of I-5'-DA in vivo.

Animals↗
PubMed1988

Apolipoprotein E phenotypes of normo- and hyperlipoproteinemia in Japanese.

Apolipoprotein E phenotypes of normo- and hyperlipoproteinemia in Japanese were examined by the disc gel isoelectric focusing technique, which was modified according to the method of Kashyap et al. (1981). Apoprotein E isoproteins were clearly separated by this method. Six phenotypes (E2/2, E3/3, E4/4, E2/3, E2/4 and E3/4) were determined in 107 cases of normolipoproteinemia and 75 cases of hyperlipoproteinemia. In normolipoproteinemia, apoE phenotype frequencies were similar to those of the Japanese and Caucasian populations which were reported previously. In hyperlipoproteinemia, a higher frequency of phenotype E2/2 and a lower frequency of E3/3 were observed. The apo E phenotypes of type IIa and IIb were distributed similarly to that of normal subjects. In contrast, only 27.8% of type IV patients had E3/3 phenotype. Among type V patients 64.3% was homozygous or heterozygous for E-4, and only 14.3% was homozygous for E-3 (E3/3). The results suggest that the apolipoprotein E phenotypes are similarly distributed among different human races and the apolipoprotein E phenotypes could be one of the etiological factors associated with some types of hyperlipoproteinemia.

Adult↗
PubMed1988

Abdominal surgery in patients over 80 years of age.

Out of 179 surgical admissions in 1987, 8 (4.5%) were over 80 years old; of these, 7 had malignant disease. Careful clinical assessment indicated that the benefits of operation outweighed the surgical risks. Surgery was performed under general anesthesia. All 8 patients recovered, despite numerous complications, and were symptom- free up to 11 months after treatment. Provided that such patients are in the care of an experienced, skilled surgical team, major operative procedures should be carried out more frequently in the elderly, especially when the patient anticipates a successful outcome.

Abdomen↗
PubMed1988

[The clinical significance of murine monoclonal antibody (1H1) prepared against human pancreatic cancer cell line BxPC-3].

A new murine monoclonal antibody (1H1) was prepared by immunizing mice i.p. with human pancreatic cancer cell line (BxPC-3). The antibody reacted with 8 of 48 cultured cell lines that were all adenocarcinoma. Thin sections of normal and cancerous tissues were examined by immunoperoxidase staining. Thirty-nine of 48 (81%) pancreatic cancers, 11 of 23 (48%) gastric cancers, 12 of 18 (67%) colorectal cancers, 9 of 19 (48%) breast cancers, 2 of 5 (40%) lung cancers and 2 of 2 (100%) duodenal cancers were stained positively, but 5 islet cell tumors, 3 esophageal cancers and 2 hepatomas were not stained positively. Normal gastro-intestinal tract of adult or fetus was stained weakly or hardly stained. SDS-PAGE showed that 1H1 antigen recognized by 1H1 Mab had a relative molecular weight of over 400 K. Da. Immunoelectron microscopical study has shown that the antigen recognized by 1H1 antibody was localized in the cell membranes of the BxPC-3 cells. 1H1 antigen was found to be present in culture-spent medium of BxPC-3 cells by ELISA. Thus, 1H1 antibody may be useful for early detection of pancreatic cancers.

Adenocarcinoma↗
PubMed1988

Stimulation of alkaline phosphatase activity by thyroid hormone in mouse osteoblast-like cells (MC3T3-E1): a possible mechanism of hyperalkaline phosphatasia in hyperthyroidism.

In order to elucidate the mechanism of increased alkaline phosphatase (AI-P) activity of bone origin in serum of patients with hyperthyroidism, the effects of thyroid hormone on mouse osteoblast-like cells (MC3T3-E1) were studied in vitro. Triiodo-L-thyronine (T3) and thyroxine (T4) produced a dose-dependent increase in AI-P activity in the cells at minimum concentrations of 10(-10)M T3 (free T3, 5 x 10(-12) M) and 10(-8) M T4 (free T4, 8 x 10(-11) M), respectively. Scatchard analysis revealed that MC3T3-E1 cells contained nuclear binding sites specific for T3 with an apparent Kd of 120 pM (maximum number of binding sites, approximately 2500 per cell). When cells were cultured with T3 in alpha-minimal essential medium (alpha-MEM) for a prolonged period, AI-P activity also became detectable in the conditioned medium. In contrast to rat osteosarcoma cells (ROS 17/2.8), MC3T3-E1 cell growth was inhibited by T4 in a concentration-dependent manner. These findings suggest that thyroid hormone inhibits proliferation and stimulates differentiation of mouse osteoblast-like cells. Since T3 and T4 stimulate AI-P activity not only in the cells but also in the medium, we speculate that the hyper-alkaline phosphatasia frequently seen in patients with hyperthyroid Graves' disease is partly due to a direct effect of thyroid hormone on osteoblasts or osteoblast-like cells.

Alkaline Phosphatase↗