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Biomedical subjects

T Shimada

Publications and source records attributed to T Shimada.

At least 937 records · Page 52Linked to original sources
PubMed1983

Radiation therapy of carcinoma of the extrahepatic bile ducts.

Carcinoma of the extrahepatic bile ducts was treated in 25 patients by radiation therapy between 1974 and 1981. Seventeen patients were men and eight were women, and the average age was 59.2 years. Cobalt-60 beam or 10 MV x ray was used for radiation therapy, with the total dose ranging from 10 Gy to 60 Gy. Twenty-one patients received 40 Gy or more. Twenty-two patients underwent surgical procedures such as percutaneous transhepatic drainage or T-tube drainage before radiation therapy. Total bilirubin level decreased after radiation therapy in 21 patients. Side effects included loss of appetite, nausea, vomiting, general fatigue, and duodenal ulcer. The mean survival of all patients was 9.2 months after completion of radiation therapy. The longest survival has been for 6.5 years, and the patient is alive and well as of this writing. Radiation therapy proved effective in treatment of carcinoma of the extrahepatic bile ducts in terms of palliation and prognosis.

Bile Duct Neoplasms↗
PubMed1983

Ultrastructural changes during the enhancement of cellular 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase in a Chinese hamster cell mutant resistant to compactin (ML 236B).

Chinese hamster V79 cell mutants resistant to compactin (ML236B) were isolated. A resistant clone, MF-2, grown in the presence of 2 micrograms/ml of ML236B for 1 week showed a 30-fold increase in 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-Co A) reductase activity compared to MF-2 grown in the absence of ML236B, and cells grown for 4 weeks showed a 53-fold increase. Apparent ultrastructural changes in thin sections of the MF-2 cells were observed after growth in ML236B: dilated cisternae in the rough endoplasmic reticulum had or did not have flocculated contents; there was significant distension of perinuclear space; and vesicular inclusion bodies were present in nuclei.

Animals↗
PubMed1983

Long-term evaluation of ultra-early operation for hypertensive intracerebral hemorrhage in 100 cases.

In the past 10 years, the authors performed microsurgical evacuation of hypertensive intracerebral hematoma in 100 cases during the ultra-early stage (within 7 hours) after the apoplectic attack. Operative indications were the presence of obvious hemiplegia and disturbed consciousness (from stupor to semicoma). Functional outcomes at 6 months postoperatively were as follows: 15 patients had returned to a full social life, 35 were capable of self-care at home, 33 required partial care at home, two were bedridden and in a vegetative state, and seven had died.

Aged↗
PubMed1983

Serological studies on Vibrio fluvialis.

The serology of 138 strains of Vibrio fluvialis was studied. Eighteen O-antigenic groups were defined among them and it was shown that the H antigens of all the strains were identical regardless of the biovar. The presence of mucoid antigen, which inhibits O agglutination, was found in some strains. As all O antisera for V. fluvialis contained some R antibody, all diagnostic O sera must be absorbed with R organisms before use. Some O antigens of V. fluvialis were identical with those of certain Vibrio cholerae serovars.

Africa↗
PubMed1983

Role of HMW kininogen in surface-mediated activation of Factor XII.

We have shown that bovine HMW kininogen remarkably accelerates the activation of Factor XII and prekallikrein in the presence of kaolin, adsorbing on kaolin through the fragment 1.2 region and forming a complex with prekallikrein through the light chain region (Sugo et al., 1980; Ikari et al., 1981). The present study was undertaken to examine the role of HMW kininogen in the activation of Factor XII and prekallikrein with other negatively-charged surfaces. The activation system used here was as follows; (1) Activation of prekallikrein by Factor XII, (2) Activation of Factor XII by plasma kallikrein and (3) Activation of prekallikrein by Factor XIIa. Among a variety of foreign surfaces, amylose sulfate and sulfatide were the most efficient in the activation reaction of Factor XII and prekallikrein. Bovene HMW kininogen accelerated all the three reactions triggered by these surfaces. However, the accelerating effect of HMW kininogen on the activation of Factor XII by plasma kallikrein was very weak, when amylose sulfate or sulfatide was used as surface. The three reactions were highly dependent on the amounts of HMW kininogen and surfaces contained in the reaction mixtures. Excess amount of them inhibited these reactions. Among the various fragments, which were prepared from HMW kininogen digests with plasma and urinary kallikreins (Sugo et al., 1980), a large fragment consisting of fragment 1.2 and light chain accelerated the reactions. Thus both fragment 1.2 and the light chain region in HMW kininogen were essential for these activation reactions.

Amylose↗
PubMed1983

Effect of nicotinamide administration to rats on the liver microsomal drug metabolizing enzymes.

A single injection or 3 successive injections of nicotinamide (500 mg/kg body wt) increased NADPH-cytochrome c reductase and aniline hydroxylase activities of rat liver microsomes without changing cytochrome P-450 content. Oral administration of nicotinamide for 2 weeks resulted in significant increase in cytochrome P-450, indicating that nicotinamide was an inducer of cytochrome P-450 though its potency was weak. A kinetic study indicated that microsomes isolated from control rats contained only high affinity (low Km) form of aniline hydroxylase while microsomes isolated from nicotinamide-treated rats contained more high affinity form and a newly appeared-low affinity (high Km) form. These results suggest that there exist at least 2 different cytochrome P-450s participating in aniline hydroxylation in rat liver microsomes and nicotinamide induces the high Km form. Ethanol or nicotinamide consumption for 2 weeks resulted in enhancement of high affinity form and appearance of low affinity form but with slightly different Km values.

Aminopyrine N-Demethylase↗
PubMed1983

Mechanism of surface-mediated activation of bovine Factor XII and prekallikrein.

The mechanism of kaolin-mediated activation of bovine Factor XII was studied in the presence of prekallikrein and HMW kininogen. The activated enzymes were assayed using fluorogenic peptides, Boc-Glu (OBzl)-Gly-Arg-4-methylcoumaryl-7-amide (MCA) for Factor XIIa and Z-Phe-Arg-MCA for plasma kallikrein. The rates of activation of the zymogens were separately measured by blocking either of the active enzymes with specific inhibitors, corn inhibitor for Factor XIIa (Ki = 6.7 nM) and Trasylol for plasma kallikrein (Ki = 3.9 nM). The result was as follows: (1) At the early stage of the activation reaction, kallikrein activity was first generated after short lag time, and then Factor XIIa activity was generated with a sigmoidal curve. In the presence of corn inhibitor, the activation of prekallikrein was observed, but in the presence of Trasylol, the activation of Factor XII was not observed. In the presence of high concentration of Ala-Phe-Arg-Ch2Cl, which inactivates immediately both of the active enzymes, the cleavage of a single chain prekallikrein into the two chain form by Factor XII was shown by SDS-PAGE, using nonlabelled and tritiated prekallikrein. (2) The incubation of Factor XII alone in a quartz cuvette or in the presence of kaolin and HMW kininogen did not result in the activation of Factor XII. The concave upward curve due to an autocatalytic activation was not observed even after the addition of Factor XIIa to Factor XII preparation. Moreover, no structural change of Factor XII during the incubation with kaolin and HMW kininogen was shown by SDS-PAGE, using 3H-Factor XII. (3) The rates of activation of prekallikrein by Factor XII and by Factor XIIa were approximately the same at higher concentration of prekallikrein. However, at lower concentration of prekallikrein the rate of activation of prekallikrein by Factor XII was shown to be a sigmoidal curve and slower than that by Factor XIIa. These results indicate that the activation of bovine Factor XII is initiated by the attack of Factor XII on prekallikrein, followed by the reciprocal activation of Factor XII by plasma kallikrein generated. The autocatalytic activation of bovine Factor XII by Factor XIIa was not demonstrated.

Amino Acid Chloromethyl Ketones↗
PubMed1983

Induction of transformation by six classes of chemical carcinogens in adult rat liver epithelial cells.

A transformation assay system using two clonal strains of adult rat liver epithelial cells is described. The carcinogens N-methyl-N'-nitro-N-nitrosoguanidine, methylmethanesulfonate, N-2-fluorenylacetamide, aflatoxin B1, benzo(a)pyrene, dimethylnitrosamine, nitrosopyrrolidine, and dimethyl-4-aminoazobenzene induced anchorage independency in one or both clonal strains, whereas noncarcinogenic analogues were inactive. In the absence of carcinogen exposure, the cell strains exhibited no spontaneous transformation to anchorage independency. These results demonstrate the reliability of anchorage independency as an in vitro end point and the specific responsiveness of adult rat liver epithelial cells to a wide range of carcinogens. Thus, the assay of transformation in adult rat liver epithelial cells is potentially useful for detection of chemical carcinogens and the study of their mechanisms of action.

Animals↗
PubMed1983

Isolation of chloroquine-resistant Chinese hamster V79 cell variants that are also resistant to ammonium chloride.

Chloroquine-resistant (CQr) clones (CQ-21 and CQ-22) have been isolated from mutagenized hamster lung V79 cells by exposing the cells to a high dose of chloroquine. CQ-21 and CQ-22 showed about 3-fold higher resistance to chloroquine than the parental V79 cells, and they showed specific cross-resistance to another amine, NH4Cl, which is also concentrated in lysosomes. CQr clone showed no cross-resistance to other unrelated agents. Chloroquine-induced inhibition of [125I]ricin internalization was observed in both cell lines at neutral pH, but the inhibition of uptake was less in the variant. Also, the degradation of endogenous protein was slowed in the mutant; further, treatment of cells with 30 micrograms/ml of chloroquine inhibited the degradation of endogenous proteins in the parental V79, but not in CQ-22 cells. Similar levels of acid phosphatase, beta-glucuronidase and cathepsin D were observed in V79 and CQ-22 cells, but the level of cathepsin B was lower in the mutant. Electron microscopy showed an increased number of electron-dense bodies, possibly autophagosomes/lysosomes, in the mutant cells grown for 4 days with 5 micrograms/ml of chloroquine. Similar aberrant structures were observed in the parental V79 cells treated for only 3 h with 5 micrograms/ml of chloroquine.

Ammonium Chloride↗