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Biomedical subjects

K Fujiwara

Publications and source records attributed to K Fujiwara.

At least 649 records · Page 36Linked to original sources
PubMed1988

Enhancing effect of phenobarbital sodium on Tyzzer's disease in mice.

Tyzzer's disease in mice was aggravated by phenobarbital sodium (PB) given consecutively after bacterial inoculation. In PB-treated mice, mortality rate and severity of liver lesions were higher with more prominent bacterial propagation in hepatocytes as compared with non-treated ones, suggesting that PB had an enhancing effect on metabolic activities of host hepatocytes resulting in increased intracellular growth of bacteria.

Animals↗
PubMed1988

Glucagon and insulin for the treatment of hepatic failure in dimethylnitrosamine-intoxicated rats.

When rats received dimethylnitrosamine every 24 h until death, plus hormone treatment after the first 24 h, the survival was enhanced between 100 and 140 h compared with the control rats, with attenuated derangements of prothrombin time and serum albumin levels at 120 h. In rats given a single dose of dimethylnitrosamine, hepatic DNA synthesis peaked at 48 h. The synthesis was increased after hormone treatment when started immediately, but not when delayed for 24 h. Hormone treatment for 3 days starting 24 h after a single dose of dimethylnitrosamine produced a rapid normalization of decreased hepatic protein content on day 9, although hepatic DNA content was not affected. These results suggest that this treatment is effective for hepatic failure, and the promotion of restoration of liver function is a contributing factor to its effect, in addition to the stimulation of hepatocyte proliferation.

Animals↗
PubMed1988

A two-site solid phase enzyme immunoassay for rat epidermal growth factor.

A sensitive and simple two-site enzyme immunoassay was developed for rat epidermal growth factor (rEGF), which was purified from male rat submaxillary glands. This system is based on the sandwiching of the antigen between anti-rat EGF IgG antibody coated on a polystyrene bead and anti-rat EGF Fab' antibody-linked peroxidase, whose activity was stable at 4 degrees C for 6 months. In this system, the rat EGF was detectable at a concentration of 2 pg/tube. No interference was observed by addition of human plasma. There was no cross-reactivity with mouse EGF, human EGF, or other substances with similar chemical structures.

Animals↗
PubMed1988

Formation of the tooth enamel rod pattern and the cytoskeletal organization in secretory ameloblasts of the rat incisor.

The localization of actin, myosin, tropomyosin, alpha-actinin, vinculin, and desmoplakin I/II was visualized by immunofluorescence microscopy. Antibodies against myosin, tropomyosin, and alpha-actinin and rhodamine-phalloidin labeled strongly the proximal and distal terminal webs which ultrastructurally consist of dense microfilament bundles. In the distal terminal web, the staining by these reagents occurred mostly perpendicular to the long axis of the incisor. Antivinculin stained the general area where the distal terminal web is located in the ameloblast. Anti-desmoplakin I/II labeled the junctional area associated with the proximal and distal terminal webs. The anti-desmoplakin staining was stronger along the cell border perpendicular to the long axis of the incisor. Comparison of the rhodamine-phalloidin staining pattern of the distal terminal web and the enamel secretion pattern by ameloblasts revealed that a change in the distal terminal web staining pattern preceded a change in the secretion pattern. These observations suggest that the cytoskeletal organization in the ameloblast is involved in the formation of the enamel matrix pattern in the rat incisor.

Actins↗
PubMed1988

Evidence for potentiation of lipid peroxidation in the rat liver after chronic ethanol feeding.

Hepatic steatosis was induced in rats by feeding nutritionally adequate liquid diet containing ethanol as 36% of energy for 4-5 weeks. After 24 h fasting and withdrawal from ethanol, liver ischaemia for 30 min followed by 2 h reperfusion resulted in a significant increase in microsomal lipid peroxide content and a decrease in reduced glutathione content as well as in protein synthesis with a rapid accumulation of triglyceride in the liver. In rats fed a non-ethanol diet or those fed a high-cholesterol diet with hepatic steatosis, however, similar phenomena were not found. These findings suggest that chronic ethanol feeding potentiates hepatic lipid peroxidation.

Animals↗
PubMed1988

[Pharmacokinetics of carboplatin (CBDCA) and tissue concentration of platinum in gynecologic organs].

A pharmacokinetics and platinum concentration in the gynecologic organs were measured following the intravenous drip infusion of 375 mg/m2 of CBDCA. Total platinum (TP) in plasma decreased biphasically and free platinum (FP) was almost monophasically eliminated. The t 1/2 of FP was about 51 min. and the percentage of FP out of TP at four hours after administration was more than 92%, which was much higher proportion compared with that of cisplatin (CDDP). A cumulative excretion of platinum in the urine within 24 hours was 69%. The platinum concentration in the benign part of portio and endocervix were higher than that of malignant portion, although there were no significant differences in other pelvic organs such as ovary and tubes. However, pelvic lymph-nodes showed less platinum concentration both in metastatic and non-metastatic tissues. Platinum concentration in the tissue did not change significantly with lapse of time. Bone marrow suppression was observed especially in the patients who had received chemotherapy or radiotherapy. No renal toxicity was observed even without any hydration and gastro-intestinal toxicity was much milder than that of CDDP.

Antineoplastic Agents↗
PubMed1988

Contribution of hepatic reticuloendothelial system to glomerular IgA deposition in rat liver injury.

Liver damage was induced in rats by a single dose of dimethylnitrosamine or D-galactosamine. In the dimethylnitrosamine model, marked glomerular IgA deposition occurred between Days 4 and 28, with its peak at Day 14. Serum IgA levels were significantly increased at Days 2 and 4, then gradually decreased, and normalized at Day 14. In the D-galactosamine model, however, no such deposition was observed, though serum IgA levels similarly increased on Days 2 and 4. IgA content in high molecular weight fraction from serum increased at Day 3 in both models. This increment remained at Day 7 only in the dimethylnitrosamine model, in which carbon clearance from the circulation was significantly decreased at Day 3. These data suggest that dysfunction of the hepatic reticuloendothelial system is a factor contributing to glomerular IgA deposition occurring in liver injury.

Alanine Transaminase↗