start-ver=1.4 cd-journal=joma no-vol=35 cd-vols= no-issue=4 article-no= start-page=273 end-page=277 dt-received= dt-revised= dt-accepted= dt-pub-year=1981 dt-pub=198110 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Insulin binding to erythrocytes in diabetes mellitus. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Insulin binding to erythrocytes was studied in diabetic patients. Insulin binding was lower in untreated diabetics and diabetic patients treated with diet or insulin than in normal subjects. Binding variation was mainly due to decreased binding site concentration in untreated and insulin-treated patients, and to lowered insulin binding site affinity in diet-treated patients. Several patients treated with hypoglycemic agents showed higher insulin binding due to increased binding site concentration. Insulin binding to erythrocytes may not always reflect the insulin binding status of insulin sensitive tissues.

en-copyright= kn-copyright= en-aut-name=OkadaYoshio en-aut-sei=Okada en-aut-mei=Yoshio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=ArimaTerukatsu en-aut-sei=Arima en-aut-mei=Terukatsu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=OkazakiSatoru en-aut-sei=Okazaki en-aut-mei=Satoru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=NakataKen-ichi en-aut-sei=Nakata en-aut-mei=Ken-ichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=YamabukiTakahiro en-aut-sei=Yamabuki en-aut-mei=Takahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=NagashimaHideo en-aut-sei=Nagashima en-aut-mei=Hideo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil= kn-affil=Fred Hutchison Cancer Research Center affil-num=2 en-affil= kn-affil=Okayama University Medical School and Health Research Center affil-num=3 en-affil= kn-affil=Okayama University Medical School and Health Research Center affil-num=4 en-affil= kn-affil=Okayama University Medical School and Health Research Center affil-num=5 en-affil= kn-affil=Okayama University affil-num=6 en-affil= kn-affil=Okayama University Medical School and Health Research Center en-keyword=insulin binding kn-keyword=insulin binding en-keyword=diabetes mellitus kn-keyword=diabetes mellitus en-keyword= erythrocyte. kn-keyword= erythrocyte. END start-ver=1.4 cd-journal=joma no-vol=35 cd-vols= no-issue=4 article-no= start-page=289 end-page=291 dt-received= dt-revised= dt-accepted= dt-pub-year=1981 dt-pub=198110 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Effects of L-glutamate on cyclic AMP levels in slices from different areas of rat cerebral cortex with a chronic iron-induced focus. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

The effect of L-glutamate of cyclic AMP levels in different areas of rat cerebral cortex was examined during the development of an iron-induced focus in the left sensorimotor cortex. The addition of L-glutamate resulted in increased cyclic AMP levels in slices from the quarter of cortex with the iron-induced focus. The levels lowered in slices from the quarter of cortex most remote from the focus. Thus L-glutamate showed stimulatory and inhibitory effects on the accumulation of cyclic AMP.

en-copyright= kn-copyright= en-aut-name=HattoriYukiko en-aut-sei=Hattori en-aut-mei=Yukiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=InabaKozo en-aut-sei=Inaba en-aut-mei=Kozo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=HoriYasuo en-aut-sei=Hori en-aut-mei=Yasuo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University en-keyword=rat cerebral cortex kn-keyword=rat cerebral cortex en-keyword=cyclic AMP kn-keyword=cyclic AMP en-keyword= L-glutamate kn-keyword= L-glutamate en-keyword= iron-induced focus. kn-keyword= iron-induced focus. END start-ver=1.4 cd-journal=joma no-vol=35 cd-vols= no-issue=4 article-no= start-page=221 end-page=234 dt-received= dt-revised= dt-accepted= dt-pub-year=1981 dt-pub=198110 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Movement of plasma membrane proteins of Ehrlich ascites tumor cells in relation to cap formation induced by concanavalin A: a study on the non-capped areas. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

In order to get precise information about the movement of plasma membrane proteins in cap formation, cyto- and bio-chemical analyses were made of the plasma membranes from non-capped areas of Ehrlich ascites tumor cells (EATCs) exposed to concanavalin A (Con A). Blebs formed by treatment with cytochalasin B (CB) of the non-capped areas of cells having a cap were isolated and used as the plasma membranes from non-capped areas (ConA-CB-bleb fraction). This bleb fraction was compared with a bleb fraction prepared from cells without ConA-treatment (CB-bleb fraction). Cytochemical analysis of ConA-CB-bleb fraction revealed a decreased in conA binding sites (ConA-BS) compared to the CB-bleb fraction. SDS polyacrylamide slab gel electrophoresis also revealed a decrease in the major components of ConA-BS of the ConA-CB-bleb fraction. The minor components of ConA-BS showed no distinct quantitative difference between the ConA-CB-bleb and CB-bleb fractions. NA+ K+-adenosine triphosphatase (ATPase), 5' nucleotidase (5'ND) and gamma-glutamyl transpeptidase (gamma-GTP) did not show any decrease in activity in the ConA-CB-bleb fraction, but the activity of D+-stimulated phosphatase (K-Pase) was decreased. The findings indicate that there are two types of plasma membrane glycoproteins in EATCs; one includes those participating in cap formation due to ConA, e.g. the major components of ConA-BS and K-Pase, and the other, those not participating in such cap formation, e.g. some minor components of ConA-BS, ATPase, 5'ND and gamma-GTP, which keep their places without moving.

en-copyright= kn-copyright= en-aut-name=NakamotoShu en-aut-sei=Nakamoto en-aut-mei=Shu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=Okayama University en-keyword=concanavalin A kn-keyword=concanavalin A en-keyword=cytochalasin B kn-keyword=cytochalasin B en-keyword=capping kn-keyword=capping en-keyword=bleb kn-keyword=bleb en-keyword= biochemical analysis. kn-keyword= biochemical analysis. END start-ver=1.4 cd-journal=joma no-vol=35 cd-vols= no-issue=4 article-no= start-page=263 end-page=272 dt-received= dt-revised= dt-accepted= dt-pub-year=1981 dt-pub=198110 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=A case of angio-immunoblastic lymphadenopathy with dysproteinemia related to allopurinol. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

A 63-year-old man developed generalized lymphadenopathy with skin rashes, fever, hepatomegaly and polyclonal hypergammaglobulinemia, twice, in February 1972 and in June 1979, after taking allopurinol for gout. Cervical lymph node biopsy, performed each time, showed the presence of immunoblasts and plasma cells, effaced nodal structure with involvement of the pericapsular tissue, rich vascularity and numerous mitoses, indicative of angio-immunoblastic lymphadenopathy with dysproteinemia (Frizzera, Moran and Rappaport). The existence of hypersensitivity to drugs, in particular, allopurinol in certain patients was emphasized, and induction of immunoblastic lymphadenopathy with various other therapeutic agents was briefly discussed.

en-copyright= kn-copyright= en-aut-name=IrinoShoxo en-aut-sei=Irino en-aut-mei=Shoxo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SanadaHiroshi en-aut-sei=Sanada en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MaesakoNaohisa en-aut-sei=Maesako en-aut-mei=Naohisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TanakaToshio en-aut-sei=Tanaka en-aut-mei=Toshio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil= kn-affil=Kagawa Medical School affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Matsue Red Cross Hospital affil-num=4 en-affil= kn-affil=Okayama University en-keyword=angio-immunoblastic lymphadenopathy kn-keyword=angio-immunoblastic lymphadenopathy en-keyword= allopurinol. kn-keyword= allopurinol. END start-ver=1.4 cd-journal=joma no-vol=35 cd-vols= no-issue=4 article-no= start-page=247 end-page=261 dt-received= dt-revised= dt-accepted= dt-pub-year=1981 dt-pub=198110 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Concomitant presence of anti-tumor effector cells and suppressor cells in the spleen of tumor-bearing mice : the nature of suppressor cells. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

In order to investigate the immunological responsiveness of tumor-bearing hosts to tumor cells, splenic suppressor cells from Ehrlich tumor-bearing mice that inhibited anti-tumor effector cell activity were characterized. In vitro cell-mediated cytoxicity and cytostasis assays were performed to test for the existence of anti-tumor immunity. suppressive activity assayed by cell mixture experiments became apparent with decline of anti-tumor immunity and progressive tumor growth. The cells mediating the suppression were found to be nylon wool column adherent T cells and inhibited T cell dependent cytotoxicity rather than non-T cell dependent cytostasis. In vivo cell transfer experiments demonstrated that intravenous injection of suppressor cells to a host already inoculated with tumor cells mixed with antitumor effector cells resulted in significant enhancement of tumor growth. This inhibition of in vivo neutralization assay be suppressor cells was found in not only allogeneic but also syngeneic tumor system. Splenectomy at the time of tumor resection endowed the host with stronger resistance against subsequent reinoculated tumor than sham-splenectomy did, reflected by prolonged survival times. These results suggest that splenectomy combined with surgical removal of the tumor is a useful treatment of clinical malignancies.

en-copyright= kn-copyright= en-aut-name=HizutaAkio en-aut-sei=Hizuta en-aut-mei=Akio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=Okayama University en-keyword=suppressor T cell kn-keyword=suppressor T cell en-keyword=nylon wool columu fractionation kn-keyword=nylon wool columu fractionation en-keyword=tumor enhancement kn-keyword=tumor enhancement en-keyword=splenectomy kn-keyword=splenectomy en-keyword= tumor-bearing mice. kn-keyword= tumor-bearing mice. END start-ver=1.4 cd-journal=joma no-vol=35 cd-vols= no-issue=4 article-no= start-page=293 end-page=306 dt-received= dt-revised= dt-accepted= dt-pub-year=1981 dt-pub=198110 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Present status and history of the mouse colony of Okayama University Medical School. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

The present status and the history of inbred strains of mice in the Experimental Animal Center, Okayama University Medical School, otherwise known as gThe Colony of Okayama University Medical Schoolh are described.

en-copyright= kn-copyright= en-aut-name=OhmoriMasaki en-aut-sei=Ohmori en-aut-mei=Masaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=Kagawa Medical School en-keyword=inbred strain kn-keyword=inbred strain en-keyword=mouse colocy kn-keyword=mouse colocy en-keyword= Okayama University Medical School. kn-keyword= Okayama University Medical School. END start-ver=1.4 cd-journal=joma no-vol=35 cd-vols= no-issue=4 article-no= start-page=235 end-page=245 dt-received= dt-revised= dt-accepted= dt-pub-year=1981 dt-pub=198110 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Antigen-induced and non-antigen-induced histamine release from rat mast cells sensitized with mouse antiserum. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Marked IgE-mediated histamine release from rat mast cells sensitized in vitro with mouse antiserum occurs in the presence of added Ca++ and phosphatidylserine (PS), although a considerable degree of antigen-induced histamine release which may utilize intracellular or cell-bound calcium is also observed. The decay in the responsiveness to Ca++ of the sensitized cells stimulated by antigen in Ca++-free medium in the presence of PS is relatively slow, and maximum release is produced by Ca++ added 1 min after antigen. Histamine release also occurs when Ca++ is added after PS in the absence of antigen to the sensitized cells suspended in Ca++-free medium. Unlike the antigen-induced release, the intensity of this non-antigen-induced release varies depending on both mast-cell and antiserum pools. A heat-labile factor(s), which is different from antigen-specific IgE antibody and is also contained in normal mouse serum, is involved in this reaction. In the antigen-nondependent (PS + Ca++)-induced release, no decay in the responsiveness to Ca++ is observed after PS addition. Both the antigen-induced and non-antigen-induced release are completed fairly rapidly and are dependent of temperature, pH and energy.

en-copyright= kn-copyright= en-aut-name=KuroseMasao en-aut-sei=Kurose en-aut-mei=Masao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=Okayama University en-keyword=histamine release kn-keyword=histamine release en-keyword=rat peritoneal mast cells kn-keyword=rat peritoneal mast cells en-keyword=mouse lgE kn-keyword=mouse lgE en-keyword= phosphatidylserine. kn-keyword= phosphatidylserine. END start-ver=1.4 cd-journal=joma no-vol=35 cd-vols= no-issue=4 article-no= start-page=285 end-page=287 dt-received= dt-revised= dt-accepted= dt-pub-year=1981 dt-pub=198110 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=14q12 translocation in a non-Burkitt lymphoma. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Chromosome analysis was performed on cells from a patient of null cell lymphoma, well-differentiated type. A 14q12 translocation was observed in all the banded cells. In addition, there were multiple chromosome abnormalities. This case will be useful in considering the significance of the 14q1(1-3) translocation in malignant lymphoma disease.

en-copyright= kn-copyright= en-aut-name=MiyamotoKanji en-aut-sei=Miyamoto en-aut-mei=Kanji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HayashiKyoichi en-aut-sei=Hayashi en-aut-mei=Kyoichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TsubotaTeruhiko en-aut-sei=Tsubota en-aut-mei=Teruhiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TanakaToshio en-aut-sei=Tanaka en-aut-mei=Toshio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University en-keyword=malignant lymphoma kn-keyword=malignant lymphoma en-keyword=chromosome analysis kn-keyword=chromosome analysis en-keyword= 14q12 translocation. kn-keyword= 14q12 translocation. END start-ver=1.4 cd-journal=joma no-vol=35 cd-vols= no-issue=4 article-no= start-page=279 end-page=284 dt-received= dt-revised= dt-accepted= dt-pub-year=1981 dt-pub=198110 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Influence of liver injury on testosterone 5 alpha-reductase activity in the rat diencephalon. en-subtitle= kn-subtitle= en-abstract= kn-abstract=Diencephalon testosterone 5 alpha-reductase activity and plasma testosterone level were measured in the rat with liver injury caused by i.p. administration of CCl4. Testosterone levels in plasma were decreased after CCl4 injection in both group I (0.1ml/150g B.W./once a day for 2 days) and group II (0.01ml/150g B.W./twice a week for three weeks). 5 alpha-Reductase activity in the diencephalon was decreased both on the 7th day after administration in group I and in group II, while being transiently increased on the 1st day after administration in group I. These results suggest that testosterone metabolism in the brain is inhibited during liver disorders. en-copyright= kn-copyright= en-aut-name=KaneyukiTakao en-aut-sei=Kaneyuki en-aut-mei=Takao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=ShohmoriToshikiyo en-aut-sei=Shohmori en-aut-mei=Toshikiyo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= affil-num=1 en-affil= kn-affil=Okayama Prefectural Junior College affil-num=2 en-affil= kn-affil=Okayama University en-keyword=liver injury kn-keyword=liver injury en-keyword=CCI4 kn-keyword=CCI4 en-keyword=testosterone 5-reductase kn-keyword=testosterone 5-reductase en-keyword=testosterone kn-keyword=testosterone en-keyword=estradiol-17 kn-keyword=estradiol-17 END