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Biomedical subjects

H Ueda

Publications and source records attributed to H Ueda.

At least 811 records · Page 45Linked to original sources
PubMed1985

Involvement of gonadotrophin and steroid hormones in spermiation in the amago salmon, Oncorhynchus rhodurus, and goldfish, Carassius auratus.

Effects of intraperitoneal injections of chum salmon gonadotrophin (SGA) and various steroid hormones (17 alpha, 20 beta-dihydroxy-4-pregnen-3-one; 17 alpha,20 beta-diOHprog, 17 alpha-hydroxy-progesterone, testosterone, 11-ketotestosterone) on the induction of in vivo spermiation were examined in nonspermiating amago salmon (Oncorhynchus rhodurus) and goldfish (Carassius auratus). A single injection of SGA to amago salmon and two successive injections to goldfish induced strong spermiation responses. Similarly two successive injections of 17 alpha,20 beta-diOHprog caused precocious spermiation in both species; however, the response to 17 alpha,20 beta-diOHprog was of lesser magnitude than that to SGA. The spermiation response of goldfish to 17 alpha-hydroxyprogesterone was similar to that of 17 alpha,20 beta-diOHprog. Neither testosterone nor 11-ketotestosterone were effective in inducing spermiation in amago salmon, but these steroids were found to be slightly effective in goldfish. Effects of a single injection of SGA on changes in serum levels of 17 alpha,20 beta-diOHprog and 11-ketotestosterone were also examined in nonspermiating amago salmon. Serum levels of 17 alpha,20 beta-diOHprog dramatically increased after treatment and peaked on Day 2 and thereafter declined quickly. Similarly, 11-ketotestosterone peaked on Day 2, but the levels remained high throughout the experimental period. Considered together, these findings are consistent with the suggestion that 17 alpha, 20 beta-diOHprog is involved in the process of spermiation in teleosts. It is further suggested that this hormone is a testicular steroidal mediator of gonadotrophin-induced spermiation in amago salmon.

Animals↗
PubMed1985

Immunoelectron microscopic localization of growth hormone in the pituitary glands of two teleosts, tilapia (Sarotherodon mossambicus) and amago salmon (Oncorhynchus rhodurus).

Growth hormone (GH) cells were investigated with the protein A-gold technique on the pituitary glands of tilapia (Sarotherodon mossambicus) and amago salmon (Oncorhynchus rhodurus). By the use of specific antiserum against tilapia GH to both species, the immunoreactive gold particles were demonstrated to be preferentially located on the secretory granules of the GH cells. Specimens fixed only with periodate-lysine-paraformaldehyde (PLP) preserved the hormonal antigenicity well. Osmium postfixation, although considerably reducing the antigenicity and thus resulting in a decrease in number of the gold particles on the GH cells, gave much more satisfactory ultrastructural preservation and immunoreactive localization of immunoreactive material. This investigation demonstrated that, after combined fixation with PLP and PLP-osmium, we could determine the function of a given cell type in various endocrine organs as well as the precise antigenic sites in such cells.

Animals↗
PubMed1985

How is kyotorphin (Tyr-Arg) generated in the brain?

Kyotorphin (Tyr-Arg) was rapidly degraded in the brain homogenates and purified membrane-bound aminopeptidase from monkey brains. The degradation of kyotorphin by these preparations was effectively inhibited by bestatin. When brain homogenates or slices were incubated with bestatin, kyotorphin was accumulated time-dependently in a rate of 1.0 or 2.1 pmol/mg protein/hr, respectively. The bestatin-induced kyotorphin accumulation was inhibited by leupeptin, p-chloromercuribenzoate, but not phenylmethylsulfonylfluoride or diisopropylphosphate. The kyotorphin accumulation was concentrated in the P2 (crude mitochondrial) fraction, particularly in the particulate or synaptosomal fraction. These findings suggest that kyotorphin may be generated in vitro from precursor proteins by membrane-bound, leupeptin-sensitive "kyotorphin converting enzymes" in close vicinity to membrane-bound aminopeptidase which rapidly degrades kyotorphin generated.

Animals↗
PubMed1985

Sequence polymorphisms around the 5'-end of the silkworm fibroin H-chain gene suggesting the occurrence of crossing-over between heteromorphic alleles.

Nucleotide sequences around the 5'-ends of the silkworm fibroin H-chain genes of the three strains, Nd(2), J-139, and F1(Gunka X Hoshun), of Bombyx mori were determined. Comparison of the sequences among these strains and the sequences reported previously for the two other strains, F1(Gunpo X Shugyoku) and Daizo, indicates that polymorphisms are present in the 5'-flanking and intron regions and that each region has at least two sequence variants independent of each other. These results suggest that crossing over between the heteromorphic H-chain alleles has occurred during the breeding of these strains.

Alleles↗
PubMed1985

Effect of respiratory acidosis on ventricular shunt flow and hemodynamics in dogs with ventricular septal defect.

The effects of respiratory acidosis on ventricular shunt flow and hemodynamics were studied in 20 anesthetized dogs with a ventricular septal defect and a normal pulmonary vascular bed. The interventricular shunt flow was measured directly by using a specially designed electromagnetic flow probe. Respiratory acidosis was produced by hypoventilation and tachypnea with constant minute volume. Hypoxemia was also induced by hypoventilation, but not by tachypnea with constant minute volume. Systemic vascular resistance was increased in severe hypoventilation at 100 and 50 ml of tidal volume, and tachypnea at 100 ml of tidal volume. However the increase of pulmonary vascular resistance was observed in only severe hypoventilation: arterial pH 6.9, PaO2 24 mmHg, and PaCO2 88 mmHg. Left to right ventricular shunt flow and pulmonary blood flow were increased significantly with no change of systemic blood flow in both conditions of respiratory acidosis. The diastolic fraction of shunt flow was increased significantly. These findings indicate that the increase of left to right shunt flow in respiratory acidosis might be one of the risk factors of congestive heart failure for the patients with ventricular septal defect.

Acidosis, Respiratory↗
PubMed1985

Involvement of epinephrine in the presynaptic beta adrenoceptor mechanism of norepinephrine release from rat hypothalamic slices.

Using high-performance liquid chromatography with electro-chemical detector, we measured field impulse (5 or 2 Hz)- and high K+ (20 mM)-evoked release of endogenous norepinephrine from rat hypothalamic slices. Release by impulses at 5 Hz was tetrodotoxin-sensitive and both types of release were Ca++-dependent. Isoproterenol (10(-10) to 10(-8) M) dose-dependently facilitated impulse-evoked release and l-propranolol (10(-8) M) shifted dose-effect curve of isoproterenol to the right. Atenolol (10(-8) to 10(-6) M) or butoxamine (10(-9) to 10(-8) M), beta-1 and beta-2-antagonist, respectively, dose-dependently antagonized the facilitatory effect of isoproterenol (10(-8) M). Tazolol (10(-8) to 10(-7) M), beta-1-agonist, and salbutamol (10(-10) to 10(-8) M), beta-2-agonist, dose-dependently increased impulse-evoked release. Epinephrine (10(-9) M) also facilitated impulse-evoked release and the action was antagonized by l-propranolol (10(-8) M). Isoproterenol (10(-8) M) also facilitated high K+-evoked release in the presence of tetrodotoxin (3 X 10(-7) M) to exclude possible involvement of axonal conduction or neuronal loops. This facilitatory effect was antagonized by l-propranolol (10(-8) M). l-Propranolol (3 X 10(-7) M) alone decreased release by impulses at 2 Hz, but the d-isomer produced no effect. When rats were pretreated with 2,3-dichloro-alpha-methylbenzylamine, an inhibitor of phenylethanolamine N-methyltransferase, the enzyme catalyzing the formation of epinephrine from norepinephrine, 80 mg/kg i.p. before decapitation, the l-propranolol-induced decrease was abolished completely.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Isolation of retinoic acid-resistant clones from human breast cancer cell line MCF-7 with altered activity of cellular retinoic acid-binding protein.

After ethyl methane sulfonate mutagenesis of the mammary carcinoma cell line, MCF-7, we have isolated three clones, U-2, U-3, and U-9, resistant to retinoic acid. These three clones showed more than a 1000-fold higher level of resistance to retinoic acid than the parental MCF-7 cells when assayed by colony formation in monolayer culture system or by growth curves. The three resistant clones showed a 200-fold higher resistance to 13-cis-retinoic acid, about 10-fold higher resistance to retinol, and about 2-fold higher resistance to retinyl acetate, respectively, than MCF-7. Binding of [3H]retinoic acid or [3H]-retinol to a cellular fraction in situ showed apparent decrease of the specific binding of retinoic acid in U-2, but there was no such specific fraction bound to retinol in U-2 and MCF-7. Sucrose gradient analysis with cytoplasmic fraction showed little, if any, cellular retinoic acid-binding protein in U-2, but a significant amount of the cellular retinoic acid-binding protein could be found in MCF-7. By contrast, there was no activity of cellular retinol-binding protein in both MCF-7 and U-2. The sensitivity or resistance of mammalian cells in culture to retinoic acid is discussed in relation with cellular binding activity for vitamin A.

Breast Neoplasms↗
PubMed1985

Presynaptic inhibitory dopamine receptors on noradrenergic nerve terminals: analysis of biphasic actions of dopamine and apomorphine on the release of endogenous norepinephrine in rat hypothalamic slices.

Electrical field stimulation (5 Hz)- or high K+ (20 mM)-evoked release of endogenous norepinephrine from superfused rat hypothalamic slices in the presence of cocaine (20 microM) was measured by high-performance liquid chromatography with an electrochemical detector. Apomorphine (10-1000 nM) dose-dependently facilitated the electrically evoked release. Apomorphine (1 microM)-induced facilitation was abolished by pretreatment with yohimbine (100 nM), was converted to inhibition by yohimbine (1 microM), but was not antagonized by propranolol (300 nM). Epinephrine (100 nM) decreased the electrically evoked release and the decrease was antagonized by yohimbine (100 nM) and by apomorphine (100 nM), but not by S-sulpiride (100 nM). In the presence of yohimbine (1 microM), apomorphine (10-1000 nM) dose-dependently inhibited the electrically evoked release. Furthermore, in the presence of tetrodotoxin (300 nM), apomorphine (100 nM) also decreased the high K+-evoked release and this decrease was antagonized by S-sulpiride (100 nM). Dopamine produced biphasic actions on the electrically evoked release, a dose-dependent decrease at 30 and 100 nM and an increase at 300 and 1000 nM. Dopamine (300 nM)-induced increase was antagonized by propranolol (300 nM) but not by yohimbine (100 nM). The dopamine (100 nM)-induced decrease was antagonized by S-sulpiride (1 nM), but not by the R-isomer. S-sulpiride (10 to 100 nM) alone dose-dependently increased the electrically evoked release, whereas the R-isomer had no effect. Haloperidol (100 nM) also increased the electrically evoked release.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

[Immunological studies on renal transplantation in rats. Effects of pretransplant blood transfusion on renal graft survival].

An attempt was made to search the mechanism underlying the beneficial effect of blood transfusion effects using the rat renal transplantation model. The mean survival time of (Sprague-Dawley (SD X Wistar)) F1 renal grafts in untreated SD recipients was 11.3 days. Treatment to SD recipients with 1 ml of Wistar whole blood 7 to 21 days prior to transplantation prolonged the mean survival time of (SD X Wistar) F1 renal grafts and maximum effect of prolongation (greater than 81.3 days) was seen when renal transplantation was performed on the 9th day after the treatment. Treatment with Wistar bone marrow cells, red blood cells and platelets 9 days before transplantation prolonged the mean survival time to greater than 41.0 days, greater than 39.3 days and greater than 46.9 days, respectively, whereas no significant effect was observed in the SD recipients pretreated with Wistar thymocytes or with Wistar plasma. Third party blood transfusion also had moderate effects on the prolongation of renal graft survival, but maximum effects of blood transfusion were obtained by donor specific blood transfusion. Sera taken from SD rats at various times after the treatment with Wistar whole blood were assayed for their ability to suppress the mixed leukocyte reaction (MLR) of SD responder and (SD X Wistar) F1 stimulator cells. Suppressor activity rapidly increased with time up to 7 days after blood transfusion. Potent suppression of the MLR was observed with sera obtained between 7 and 15 days after the treatment. Thereafter, suppressor activity gradually decreased but sera obtained even 21 days after the treatment still suppressed the MLR by more than 50%. The experimental results suggest that MLR suppressor factor(s) generated in the recipients by blood transfusion may play an important role in preventing renal graft rejection. Furthermore, not only class II antigens but also class I antigens in the transfusate may be relevant to the immune response which causes a beneficial effect by pretransplant blood transfusion.

Animals↗
PubMed1985

Potentiation by vitamin A of the action of anticancer agents against murine tumors.

Combinations of retinol palmitate (RP) and six different anticancer agents were examined to determine their effects on the life-span of mice bearing ascites sarcoma 180 or P388 leukemia. With ascites sarcoma 180, administration of a fixed dose of RP (3.3 mg/kg) considerably enhanced the antitumor effects of 5-fluorouracil (5-FU) (5 mg/kg, or 20 mg/kg), methotrexate (MTX) (0.5 mg/kg, or 1 mg/kg) and 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea (ACNU) (12.5 mg/kg), when given by intraperitoneal injection. However RP failed to potentiate the antitumor effects of adriamycin (ADM) and 6-mercaptopurine (6-MP) against sarcoma 180. With P388 leukemia, RP (167 mg/kg, or 333 mg/kg) enhanced the antitumor effects of 6-MP (25 mg/kg, or 50 mg/kg), MTX (1 mg/kg, or 2 mg/kg), ADM (0.2 mg/kg), ACNU (5 mg/kg) and cis-dichlorodiammine-platinum (CDDP) (1 mg/kg) to a considerable extent, but it did not potentiate the antitumor effect of 5-FU. The combination of RP with ACNU or CDDP was particularly effective against P388 leukemia.

Animals↗
PubMed1985

[A case of giant hydronephrosis and a review of 324 cases in the literature].

A case of giant hydronephrosis due to ureteropelvic junction obstruction in an 18-year-old boy is reported. The patient had been told to undergo an operation for the left hydronephrosis at 2 years of age. However, he stayed away from hospital until he presented at our clinic with nausea caused by a large abdominal mass. Radiological evaluation revealed a left giant hydronephrosis with no function and slight compensatory hypertrophy in the right kidney. Left nephrectomy was performed and the pelvic capacity was approximately 7,700 ml. Histopathological examination showed muscular hyperplasia at the ureteropelvic junction. The term giant hydronephrosis may be defined as a hydronephrosis the contents of which are greater than 1,000 ml. Three hundred twenty four cases of giant hydronephrosis in the literature are reviewed and the age, sex, side involved, pelvic capacity, etiology, and relation to hypertension are discussed.

Adolescent↗