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Biomedical subjects

K Onodera

Publications and source records attributed to K Onodera.

At least 307 records · Page 17Linked to original sources
PubMed1988

Influence of the deprivation of a single amino acid on cellular proliferation and survival in rat 3Y1 fibroblasts and their derivatives transformed by a wide variety of agents.

We compared proliferation and survival of various syngeneic transformed cell lines under conditions of depletion of 15 amino acids in Dulbecco-Eagle's medium. We used a normal fibroblast line 3Y1 and 22 transformed sublines of 3Y1 which had been induced by one of seven transforming agents--simian virus 40, mouse polyomavirus, adenovirus type 12, E1A gene of adenovirus type 12, cDNA of Harvey murine sarcoma virus, Rous sarcoma virus, or N-methyl-N'-nitro-N-nitrosoguanidine. Unlike other untransformed cells examined (mouse BALB/c-3T3 line, mouse NIH-3T3 line, and primary Fischer rat embryo fibroblasts), 3Y1 ceased to proliferate and accumulated in a viable state with a G1-phase DNA content under 14 singular deprivations of amino acid. None of the transformed 3Y1 lines completely arrested in the G1 phase of the cell cycle and each showed different levels of survival, depending on each transforming agent. As for transformed 3Y1 cells induced by a given virus or a given transforming gene, any one of the three sublines shared the same trend with respect to proliferation and survival. Transformed derivatives induced by N-methyl-N'-nitro-N-nitrosoguanidine showed almost the same trend in proliferation, but the patterns of survival were not uniform. Our observations suggest that the unique responses of 3Y1 to amino acid depletion are differently modified by different transforming agents.

Adenoviridae↗
PubMed1988

A study of liver regeneration using fetal rat liver tissue transplanted into the spleen.

The liver morphology of fetal hepatic tissue transplanted into an ectopic location was investigated over one year period. Fetal liver fragments prepared from a maternal rat on the 18th or 19th day of pregnancy were injected into the splenic parenchyma of syngeneic rats using a 21 gauge needle. Histologically, the fetal liver did not essentially show any apparent lobular architecture or cord structure. The transplanted fetal hepatic tissues survived and formed hepatic cords in the spleen instead of undergoing degeneration and necrosis. Three characteristic features became complete during the 4 weeks following transplantation, namely; clumps of hepatocytes with obvious hepatic cords and sinusoids, markedly proliferating bile ducts and proliferating individual hepatocytes. Macroscopic nodules of the hepatocytes on the spleen were seen at about 6 months after transplantation. When the differentiation of the transplanted fetal hepatic tissue was compared with the development of a normal neonatal liver after birth, it was delayed by only about one week, while there was no proliferation of bile ducts in the normal neonatal liver. This experimental model provides a useful system for investigating liver regeneration and the mechanism of cell growth.

Animals↗
PubMed1988

IgA nephropathy and Henoch-Schönlein purpura nephritis with anterior uveitis.

Two patients with IgA nephropathy and a patient with Henoch-Schönlein purpura nephritis each associated with anterior uveitis are described. As anterior uveitis accompanying IgA nephropathy improved, renal manifestations were relieved. The patient with Henoch-Schönlein purpura nephritis suffered from not only anterior uveitis but also keratitis. It is suggested that immune mechanisms which induce IgA nephropathy may play a role in the development of anterior uveitis and keratitis.

Adolescent↗
PubMed1988

Regional changes in brain histamine levels following dietary-induced thiamine deficiency in rats.

Histamine levels in thiamine deficient rats were significantly lower in the hippocampus, amygdala, olfactory bulb, thalamus and pons-medulla oblongata than those of normal and pair-fed groups. In the case of the hypothalamus, thiamine deficiency produced a significant increase in histamine levels. These changes observed in the thiamine deficient group were reversed to the normal levels by supplying the normal diet. These data present a new finding that thiamine deficiency affects the central histaminergic neuron system as well as other monoaminergic systems.

Animals↗
PubMed1987

Effect of chlorpheniramine on muricide induced by thiamine deficiency: pharmacokinetic and behavioral studies.

Chlorpheniramine (5-10 mg/kg) showed a dose-dependent suppressive effect on muricide induced by thiamine deficiency at 1 hr after oral administration. The ED50 value for muricidal suppression was about 7.1 mg/kg (95% confidence limits, 5.4-9.3 mg/kg). The maximum effect of muricidal suppression lasted for 1-2 hr after oral dosage (10 mg/kg). Chlorpheniramine was detectable at 10 min in the blood and brain of thiamine deficient killer-rats by using a high-performance liquid chromatographic method. Maximum brain and blood levels of chlorpheniramine appeared at 45 and 60 min, respectively. In terms of regional distribution, the highest levels were measured in the limbic system, especially in the hippocampus. Although neither blood nor brain levels of chlorpheniramine reflect its pharmacological activity, it can easily enter the brain and suppress muricide more potently than imipramine.

Aggression↗
PubMed1987

Comparison among lipid constituents in native LDL, ultra-water-soluble LDL, and vessel wall, and their significance in arteriosclerosis.

The lipid constituents in native low-density lipoproteins (LDL), ultra-water-soluble LDL (UWS-LDL), and aortic intimal tissues were compared. These lipoproteins were obtained from healthy persons and patients with atherosclerotic diseases. Also, aortic intimas were separated from arterial walls obtained within 5 hr after the donor's death. (1) From the native LDL, cholesterol esters (CE), triglycerides (TG), small amounts of free fatty cid (FFA), free cholesterol (CF), and phospholipids (PL) were demonstrable by iodine vapor on TLC, but from UWS-LDL the above lipids plus a new lipid (spot X) were observed between TG and FFA on TLC. And also, an unknown spot with the same Rf value as spot X was recognized on TLC of lipid extract from the atherosclerotic lesion, but not from the normal intima. (2) The production of spot X in UWS-LDL is probably related to the oxidation of lipids in native LDL. Also, the spot X in UWS-LDL and the spot X in the atherosclerotic lesions are probably related to the oxidation of CE in these lipids. (3) The existence of UWS-LDL is important to the initiation and probably the progression of atherosclerosis.

Aorta↗
PubMed1987

Muricidal suppression by chlorpheniramine and changes in brain levels following dietary-induced thiamine deficiency in rats.

The effects of thiamine deficiency on pharmacological and pharmacokinetic activities of chlorpheniramine were investigated in rats. Chlorpheniramine (5-10 mg/kg) showed a dose-dependent suppressive effect on muricide induced by thiamine deficiency. The ED50 value for muricidal suppression at 1 hr was approximately 7.1 mg/kg (95% confidence limits, 5.4-9.3 mg/kg) after oral administration. Using a high-performance liquid chromatographic (HPLC) method, chlorpheniramine was detectable at 10 min in the blood and brain of rats. The present pharmacokinetic data suggest that chlorpheniramine can easily pass through the blood-brain barrier (B.B.B.) and enter the brain. It is stored therein and is later slowly released and excreted. In thiamine deficient rats, chlorpheniramine entered the brain in much higher concentrations than in normal and pair-fed rats, and significantly higher levels were maintained for a period of 1.5 hr. These results suggest that thiamine deficiency affects pharmacological and pharmacokinetic activities in rats, and support the view that there is a malfunction of the B.B.B. in thiamine deficient rats. These factors should be taken into consideration in clinical usage and dosage.

Aggression↗
PubMed1987

Effects of decarboxylase inhibitors on muricidal suppression by L-dopa in thiamine deficient rats.

Male Wistar rats maintained on a thiamine deficient diet showed mouse-killing behavior (muricide). On the 30th day of experimental feeding, the incidence of the muricide was 70%. Intraperitoneal (i.p.) injection of 3-(3,4-dihydroxyphenyl)-l-alanine (l-dopa) suppressed the muricide in a dose-dependent manner. This suppressive effect was potentiated with carbidopa, but was quite reduced by pretreatment with alpha-monofluoromethyldopa or FLA-63. These results indicated that the effect of l-dopa was dependent on its decarboxylation, and its conversion to noradrenaline (NA) essential for muricidal suppression in the brain. The NA precursors, l-dopa, l-threo-dops or maprotiline and Y-8894, which can increase the availability of synaptic catecholamines (CA), also showed muricidal suppression. CA depletors (alpha-methyl-p-tyrosine, FLA-63 and alpha-monofluoromethyl-p-tyrosine) did not significantly increase the incidence of muricide induced by thiamine deficiency nor decrease the number of killer-rats. These findings suggest that brain CA may not participate in the mediation of muricide induced by thiamine deficiency in this experiment, but such muricide can be pharmacologically characterized by the effects which are brought about by catecholaminergic agents.

Aggression↗