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Biomedical subjects

Y Kiuchi

Publications and source records attributed to Y Kiuchi.

At least 127 records · Page 7Linked to original sources

Casein and histone kinases of a rat ascites hepatoma as compared with those of rat liver.

Seryl/threonyl-protein kinases in cytosolic and particulate fractions from rat liver and AH-13, a rat ascites hepatoma, have been studied by chromatographing these fractions on DEAE-cellulose and assaying the eluates with casein, phosvitin, histone and protamine as substrates. Liver cytosolic fraction contains a group of well-characterized seryl/threonyl-protein kinases, namely, casein kinases I and II and histone kinases I and II. Liver particulate fraction, on the other hand, is almost totally devoid of casein kinase I and histone kinase I but contains an additional peak of casein kinase tentatively designated casein kinase III. In AH-13, cytosolic casein kinase I is markedly increased and particulate-associated casein kinases II and III are moderately increased as compared with liver. Moreover, it was found that in AH-13, the histone kinase I level is high in the particulate fraction but markedly decreased in the cytosolic fraction. It is suggested that particulate-associated histone kinase I may be of cytosolic origin.

Animals↗

Genetic regulation of GM2 (NeuGc) expression in liver of mouse.

GM2 containing NeuGc was a major ganglioside in mouse liver of inbred strains such as DBA/2, BALB/c, C57BL/10 and C3H/He, which are commonly used for biochemical and immunological studies. On the other hand, the liver of WHT/Ht, an inbred strain, contained GM3 (NeuGc) as a major ganglioside and lacked GM2 (NeuGc). We report here that the GM2 (NeuGc) expression was analyzed in the liver of the progeny between WHT/Ht and DBA/2 and the positive expression of GM2 (NeuGc) was proved to be a dominant trait regulated by an autosomal single gene. Moreover, the N-acetylgalactosaminyltransferase activity to convert GM3 (NeuGc) to GM2 (NeuGc) was measured in the liver microsomal fraction of WHT/Ht, BALB/c and their F1. F1 expressed almost half of the activity in BALB/c and WHT/Ht did not express a detectable amount of activity. The backcross of F1 to WHT/Ht segregated into two groups. One expressed both GM2 (NeuGc) and the transferase activity and the other expressed neither of them. There was no exceptional individual which was not grouped into either of these two groups. These results indicate that GM2 (NeuGc) expression is directly regulated by the N -acetylgalactosaminyltregated into two groups. One expressed both GM2 (NeuGc) and the transferase activity and the other expressed neither of them. There was no exceptional individual which was not grouped into either of these two groups. These results indicate that GM2 (NeuGc) expression is directly regulated by the N-acetylgalactosaminyltransferase activity, the expression of the enzyme activity is regulated by an autosomal single gene and WHT/Ht is a mutant of the recessive homozygote which cannot express the enzyme activity in its liver. WHT/Ht does not develop any neurological symptoms but grows and breeds well. The brain ganglioside composition was proved to be identical to those in BALB/c brain. The result suggests that WHT/Ht has N-acetylgalactosaminyltransferase to convert GM3 (NeuAc) to GM2 (NeuAc) in its brain. It is a subject for further study to elucidate what kind of defect is involved in the GM2 (NeuGc) biosynthesis of WHT/Ht liver.

Animals↗

Genetically regulated expression of UDP-N-acetylgalactosamine: GM3(NeuGc) N-acetylgalactosaminyltransferase [EC 2.4.1.92] activity in mouse liver.

GM2 containing NeuGc was a major ganglioside in the liver of mouse strains such as BALB/c, DBA/2, C3H/He, and C57BL/10, whereas WHT/Ht mouse liver did not contain GM2(NeuGc) but contained GM3(NeuGc) as a major ganglioside. Since GM3(NeuGc) is a biosynthetic precursor of GM2(NeuGc), WHT/Ht liver was considered to lack the ability to synthesize GM2(NeuGc) from GM3(NeuGc) (Hashimoto, Y., et al. (1983) J. Biochem. 93, 895-901). In this study we measured the activity of UDP-N-acetylgalactosamine : GM3(NeuGc) N-acetylgalactosaminyltransferase in the liver of BALB/c, WHT/Ht, and their progeny. The transferase activity in the microsomal fraction of BALB/c liver was 2.10 +/- 0.32 X 10(-5) units/mg protein (means +/- S.D.), whereas no activity was detected in that of WHT/Ht liver, F1 hybrids between BALB/c and WHT/Ht expressed GM2(NeuGc) as well as the enzyme activity, the level of which was almost half that in BALB/c liver 1.10 +/- 0.12 X 10(-5) units/mg protein). The backcross generation of F1 to WHT/Ht segregated into two groups with respect to expression of GM2(NeuGc) and the transferase activity: 11 of the 21 mice analyzed expressed both GM2(NeuGc) and the transferase activity (1.28 +/- 0.18 X 10(-5) units/mg protein), whereas the rest expressed neither. These results suggest that the expression of GM2(NeuGc) is directly regulated by the activity of UDP-N-acetylgalactosamine: GM3(NeuGc) N-acetylgalactosaminyltransferase in mouse liver.

Animals↗

The kinetics of interferon clearance in mice: comparison of mouse and human interferon.

Mice were injected with three kinds of interferon, i.e., mouse, human leucocyte and human fibroblast interferon, and the kinetics of their clearance from the blood was compared. After intravenous injection, mouse interferon was cleared very rapidly with an initial half life to two to three minutes, while both types of human interferon were cleared rather slowly with a corresponding value of about 20 minutes. When mouse interferon was injected intramuscularly or intraperitoneally, only very low levels of interferon activity were detected in the serum, and the recovery did not exceed 1% at any time. In contrast, both types of human interferon gave appreciable levels of activity in the serum upon injection by the same routes, and the levels remained stable during the observation period. The recovery of human interferon in the blood was about 10-fold that of mouse interferon. Mouse interferon was not inactivated in vitro by incubation with normal mouse serum. Our results suggest the validity of using homologous interferon for studies on the kinetics of interferon clearance in experimental animals.

Animals↗

Strain differences in the production of mouse interferon.

Studies were conducted to compare the interferon (IFN) production of four strains of mice when injected with Newcastle disease virus (NDV), polyinosinic-polycytidylic acid (poly I. C), lipopolysaccharide (LPS) or purified protein derivative (PPD). When injected with NDV, C57BL/6 and DDD mice generated higher levels of IFN than BALB/c and C3H/He mice. Upon injection with poly I. C or LPS, C57BL/6 and C3H/He mice produced higher levels of IFN than BALB/c and DDD mice. Differences in IFN production were also observed among BCG-sensitized mice of all four strains upon injection with PPD, C57BL/6 mice engendered the highest levels of IFN, while the C3H/He and DDD mice were intermediate in their response, with the BALB/c mice producing the least amount of IFN.

Animals↗

Generalized glycogen storage disease in Japanese quail (Coturnix coturnix japonica).

Two Japanese quail which were incapable of wing movement and three normal quail were examined by histological and ultrastructural methods. The diseased birds had glycogen deposits in their skeletal muscle, cardiac muscle, smooth muscle, and nerve cells of the brain and spinal cord. According to the distribution of the lesions and the characteristics of the deposited glycogen, the diseased birds had glycogenosis which was analogous to type II found in man. The usefulness of this disease as a model for glycogenosis in man is discussed.

Adult↗

Drug sensitivity of rat bladder cancer in syngeneic hosts and athymic nude mice.

The effects of chemotherapeutic agents on BC-47 rat bladder cancer were investigated in nude mice and syngenetic hosts to clarify the influence of host factors on chemotherapy. The BC-47 cancer was rich in stroma and lacked central necrosis in syngeneic ACI/N rats. In contrast, in nude mice it had little stroma and underwent necrosis in the center, and cancer cells proliferated primarily at the periphery in contact with the normal host tissue. The cancer showed similar patterns of sensitivity to bleomycin, 1,3-bis (2-chloroethyl)-1-nitro-sourea, 5-fluorouracil, and mitomycin C in both hosts. In contrast, adriamycin and pyranyl secalonic acid D (pyranyl secalonic acid) had different effects in the two hosts, being significantly effective in rats, but ineffective in nude mice.

Animals↗

Difference in response to mouse hepatitis virus among susceptible mouse strains.

After intraperitoneal inoculation with a high-virulent mouse hepatitis virus (MHV) a significant difference was seen in survival time between DDD and CDF1 (BALB/c X DDD) mice, while 50% lethal doses were not significantly different. With 3 X 10(3) PFU of the virus CDF1 and DDD mice died in 45 and 120 hr, respectively, on the average. This difference of susceptibility between DDD and CDF1 mice was first demonstrable at the age of 1 week and was more pronounced at the age of 4 weeks but showed no dependence of the sex. Virus titers ran 2 to 3 log higher in the liver and blood of CDF1 than in those of DDD mice, while being only 1 log higher in the spleen. At an early stage of infection viral antigen was demonstrable by immunofluorescence in sinusoidal lining cells of the liver more prominently in VDF1 than in DDD mice. Interferon production occurring in parallel with virus growth was significantly higher in CDF1 than in DDD mice. In DDD mice, liver lesions were rather focal with some accumulation of round cells, while they were confluent with poor cellular response in CDF1 mice. Viral growth in cultured peritoneal macrophages from CDF1 mice was 1 log higher than in those from DDD mice. The results suggest that the divergence in response to MHV among susceptible mice greatly depends upon the susceptibility of macrophages and reticuloendothelial cells which constitute primary targets of the virus.

Animals↗

Transmissible enterocolitis in hamsters caused by Tyzzer's organism.

An outbreak of enteric form of Tyzzer's disease occurred in a golden hamster colony, and 60% of diseased animals examined were found to have severe enterocolitis without hepatic lesions. Organisms were detected within mucosal epithelial cells, especially in the lower ileum, cecum and colon showing degenerative and necrotic changes, and in some cases organisms were also detected in the smooth muscle layer. Infiltration of neutrophils and mononuclear cells in the lamina propria and submucosa was observed. Hamsters either having been cage-mates with diseased ones or given perorally cecal contents from affected animals, suffered from severe diarrhea and were shown to have necrotic foci in the liver. By intravenous inoculation with affected hamster liver homogenate into cortisone-treated mice, hepatic lesions characteristic of Tyzzer's disease were produced. Moreover, such infected mouse liver was found to cause severe diarrhea in hamsters when administered perorally.

Animals↗

Enzyme properties of monoamine oxidase in the frontal cortex and liver of the gerbil (Meriones unguiculatus).

1. Enzyme properties of monoamine oxidase (MAO) in the frontal cortex and liver of the gerbil were investigated using 5-hydroxytryptamine (5-HT), benzylamine (Bz) and tyramine (Tyr) as substrates. 2. The Km values of MAO towards the three substrates were almost similar to the values in other species. The Vmax value of MAO towards Bz was much lower than the value towards 5-HT. 3. In the inhibition studies with selective MAO-A and MAO-B inhibitors, clorgyline and deprenyl, deamination of 5-HT, Bz and Tyr in both tissues was induced by MAO-A alone, MAO-B alone and both forms of the enzyme, respectively, indicating the same substrate specificity as that in rats. 4. The apparent proportion of MAO-A to MAO-B activities in the gerbil liver was approximately 6:4, whereas MAO-A in the frontal cortex of the gerbil was exclusively predominant, consistent with the previous data in the golden hamster which belongs to the same family as the gerbil.

Animals↗