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Biomedical subjects

Y Yasuda

Publications and source records attributed to Y Yasuda.

At least 289 records · Page 16Linked to original sources
PubMed1987

[The effect of glucagon on hepatic blood flow and ICG excretion].

Loading of glucagon on mongrel dogs was performed and the following results were obtained: The effects of glucagon on hemodynamics were decrease in the vascular resistance and increase in the blood flow in the superior mesenteric artery. Therefore, the blood flow of the portal vein was also increased. In the hepatic artery, glucagon also decreased the vascular resistance, when the blood flow was initially increased and then decreased. This might be attributable to the difference in sensitivity between the vascular resistance by glucagon. While administration of glucagon increased the blood flow of the portal vein, it had less effect on the vascular resistance. Though the blood flow of the hepatic tissues by hydrogen gas clearance method correlated favorably with the hepatic inflow measured with electromagnetic flowmeter, local blood flow in the hepatic tissues was not always constant in the liver and had some difference. Concerning change in local blood flow in the hepatic tissues, in low perfusion area, the blood flow was increased by low concentration of glucagon. This change in distribution of the blood flow was presumed to be caused by the portal flow. After simultaneous loading of glucagon and ICG, glucagon accelerated excretion of ICG. After simultaneous loading of glucagon and ICG on cirrhotic and control patients, accelerated excretion of ICG with time course was observed in control group. On the other hand, slightly accelerated excretion was seen in cirrhotics. It was suggested that simultaneous loading test of glucagon and ICG may be useful as a test for dynamic ability of hepatic circulation which can not be obtained by ICG loading test.

Animals↗
PubMed1986

Leydig cell hyperplasia in fetal mice treated transplacentally with ethinyl estradiol.

Pregnant female mice were given ethinyl estradiol on days 11 through 17 of gestation. On day 18 the dams were killed and the male fetuses were examined for testicular differentiation. Three of 12 males from dams treated with the highest dose of ethinyl estradiol showed cryptorchid testes with uterine tubes. Light and electron microscopic evaluation of the testes, both cryptorchid and normal, demonstrated foci of hyperplasia of Leydig cells showing cytoplasmic and nuclear pleomorphism, increase in lipid droplets, and decrease in smooth endoplasmic reticulum and ribosomes when compared to testes from control fetal mice. Morphometric determinations of the testes indicated that the number of Leydig cells in a unit area (mm2) in the interstitial tissue showed a dose-response relationship to ethinyl estradiol in the normal testes. The number of Leydig cells in the testes exposed to the highest dose of estrogen showed a significant difference between cryptorchid and normal testes: the former had fewer Leydig cells than the latter. These morphological observations indicate that hyperplasia of Leydig cells of fetal mouse testis at term can be induced by transplacental treatment with ethinyl estradiol and suggest that a malignant transformation into a Leydig cell tumor is possible.

Animals↗
PubMed1986

Developmental anomalies induced by all-trans retinoic acid in fetal mice: I. Macroscopic findings.

The administration of a single dose of all-trans retinoic acid on day 8 of gestation to pregnant mice, ICR strain, led to malformed fetuses in all of the litters. All-trans retinoic acid (RA) was dissolved in olive oil and given in doses of 60 or 40 mg/kg of body weight. The control mice were given vehicle alone. Examination on day 18 of gestation of the fetuses exposed to 60 mg/kg showed various malformations, such as exencephaly, exophthalmus, micrognathia, agnathia, cleft palate, cleft lower lip, spina bifida, atresia ani, tail anomalies, agenesis of the kidneys, or hydronephrosis. In the fetuses exposed to 40 mg/kg, isolated cleft palate was much more common than in those exposed to 60 mg/kg. Double-stained preparations of bone and cartilage showed cranio-facial anomalies and axial skeletal anomalies: a- or hypogenesis of palatine or maxillary bones, tympanic ring, squamosal temporal bone or otic ossicles in cartilage, and fusion of basioccipital to basisphenoid and maxilla, zygomatic and mandibular bones; a- or hypogenesis of caudal vertebrae and supernumerary thoracic and lumbar vertebrae. These results indicate that anomalies comparable to those seen in the infants of mothers treated with isotretinoin, 13-cis retinoic acid, during pregnancy can also be induced in mice and suggest that the site affected by RA may be neural crest cells, including those in the cephalic and caudal regions, and cells committed to somitic mesoderm in the trunk region.

Abnormalities, Drug-Induced↗
PubMed1986

Pig mitochondrial DNA: polymorphism, restriction map orientation, and sequence data.

Restriction endonuclease cleavage patterns of mitochondrial DNA (mtDNA) in pigs were analyzed using 18 enzymes which recognize six nucleotides and 1 four-nucleotide-recognizing enzyme. Pigs including Taiwan native breeds and miniature strains maintained in Japan were examined in this study; four commercial breeds of pigs and Japanese wild boars have been investigated earlier [Watanabe, T., et al. (1985). Biochem. Genet. 23:105]. mtDNA polymorphisms were observed in the cleavage patterns of five restriction enzymes, Bg1II, EcoRV, ScaI, StuI, and TaqI. The results support the previous hypothesis that pigs must be derived from two different maternal origins, European and Asian wild boars, and that a breed, Large White, arises from both European and Asian pigs. Two HindIII cleavage fragments were cloned into the HindIII site of M13mp10 and were partially sequenced by the dideoxynucleotide-chain termination method. Furthermore, DraI and StuI cleavage sites were newly determined on the restriction endonuclease map. On the basis of these results, the restriction endonuclease cleavage map of pig mtDNA was rewritten. Comparing sequence data of pig mtDNA at 237 positions with those of cow, human, mouse, and rat mtDNA, the sequence difference, silent and replacement changes, and transitions and transversions among mammalian species were estimated. The relationships among them are discussed.

Animals↗
PubMed1986

Accelerated differentiation in seminiferous tubules of fetal mice prenatally exposed to ethinyl estradiol.

Ethinyl estradiol (EE) in olive oil (0.02, 0.2, or 2.0 mg/kg) administered to pregnant mice on days 11 to 17 of pregnancy induced abnormal differentiation of gonocytes and fetal Sertoli cells in male fetuses on day 18 of gestation. Light and electron microscopic examination of the testes showed fewer darkly stained prospermatogonia and more lightly stained prospermatogonia in the experimental than in the control fetuses. Widespread degeneration and lysis of gonocytes were seen only in the experimental mice. No spermatogonia type A could be detected. In spite of comparable mitotic rates in the Sertoli cells of the experimental and control mice and more dark Sertoli cells with well developed smooth endoplasmic reticulum (SER) in the experimental mice, one of the functions of fetal Sertoli cells was suppressed: there were fewer dark slender Sertoli cells with long processes extending to the centers of tubules and more contact areas with gonocytes, phenomena which may play a role in the migration of gonocytes towards the periphery of the tubules. More Sertoli cells were detected in the undescended than the descended testes exposed to the highest dose of EE. These morphological findings indicate that prenatal exposure to EE induces acceleration of prespermatogenesis and disturbances in the initiation of spermatogenesis and in the mechanical function of Sertoli cells.

Animals↗
PubMed1986

The kinetic study on cell surface antigens of a hybridoma between human B cells and a mouse B-cell line.

Human B cells obtained from tonsils were fused with a mutant clone of a murine B-cell line in the presence of polyethylene glycol and dimethyl sulfoxide. THT12.58, a subclone of the human-mouse B-cell hybridoma, was shown to express human B-cell surface antigens on the cell membrane, namely B1, B2, I2, human IgM and IgD derived from human B cells by analysis of flow microfluorometry (FMF), as well as murine B-cell markers; the amount of these human B-cell markers on THT12.58 did not change for more than 1 year after establishment. Interestingly, the expression of the human B-cell antigens significantly decreased after treatment of the cells with B-cell stimulatory factors (BSF) obtained from the supernatant of the culture of PHA-P activated T cells; this was followed by significant enlargement in cell size compared with the control. A marked decrease in the amount of each antigen on the hybrid was observed when treated with Staphylococcus aureus Cowan I strain (SAC) in addition to BSF. In contrast, the expression of these markers on the cells increased after exposure of the cells to recombinant human interferon-gamma (rINF-gamma). Additionally, the effect of BSF on the generation of IgM-secreting cells by human B cells markedly decreased after absorption of BSF with the hybrid cells. These results suggest that THT12.58 may possess a receptor for BSF on the cell surface, and be capable of differentiating into much more mature stage of B-cell lineage after exposure to BSF. Thus, this kind of a human-mouse B-cell hybridoma with human B-cell differentiation antigens can be a good model to investigate the kinetics of cell surface antigens and characterization of a receptor for BSF on human B cells.

Animals↗
PubMed1986

Discordances in the temporal pattern of the ACTH/beta-endorphin releasing effects of synthetic CRFs and partially purified bovine CRF in a superfusion system.

Temporal characteristics of ACTH and beta-endorphin secretion induced by bovine hypothalamic CRF-A (void volume) and CRF-B (Kav = 0.583) separated by Sephadex G-100 were compared to those of synthetic ovine or rat CRF, sauvagine and vasopressin. Dispersed cells or minced fragments of rat adenohypophyses perifused in a column were exposed to various secretagogues, and ACTH and/or beta-endorphin concentrations of the effluent were measured by radioimmunoassays. CRF-A or CRF-B induced an immediate brisk rise of ACTH and beta-endorphin within 1 min after initiation of CRF perifusion. The maximum rate of ACTH or beta-endorphin secretion was reached 1-2 min later. Hormone secretion persisted throughout a 10-min exposure to these secretagogues. More than 80% of the total ACTH or beta-endorphin secretion induced by 10-min perifusion with bovine CRF occurred during exposure to CRF. With 10-min perifusion with 300 ng/ml ovine or rat CRF, the onset of the major CRF-stimulated ACTH or beta-endorphin secretion was markedly delayed compared to that following bovine CRF. During perifusion with ovine or rat CRF, a modest slow increase in ACTH or beta-endorphin secretion was observed. More than 60-70% of the total ACTH or beta-endorphin secretion induced by 10-min perifusion with rat or ovine CRF occurred after CRF withdrawal. The ACTH secretory patterns for sauvagine were very similar to those for synthetic rat or ovine CRF. These results suggest some qualitative differences between partially purified bovine CRF and synthetic ovine or rat CRF.

Adrenocorticotropic Hormone↗