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G Tamura

Publications and source records attributed to G Tamura.

324 records · Page 18Linked to original sources

Substructure of the cytoplasmic membrane of Bacillus megaterium. I. Method for the fractionation of "Ghosts".

A method of fractionation of "ghosts" was devised to identify the chemical components of the cytoplasmic membrane. The method consists of dialyzing the "ghosts" against distilled water, and then dissolving the ghosts in dilute alkali. The ghosts were fractionated into four fractions by use of differential centrifugation. The components of each fraction were analyzed in detail. The ratio of lipid to protein and content of carbohydrate were found to be different for the four fractions. The main two fractions (fractions 2 and 3) contained several types of materials. Fraction 2, which is soluble in alkali and sedimentable at 105,000 x g, contained protein and lipid in the ratio of 2:1; ribonucleic acid was not detectable. Under the electron microscope, the ghosts appeared to have released the cell's cytoplasmic contents, but many small dense particles (about 100 A in diameter) remained adherent to the membrane surface. On the other hand, fraction 2 appeared to be made up only of a membrane structure. No 100 A particles were visible in this fraction. From these results, fraction 2 seemed to be pure membrane material.

Bacillus megaterium↗

Kluyveromyces lactis killer toxin inhibits adenylate cyclase of sensitive yeast cells.

K1 killer toxin secreted by the K1 strain of Saccharomyces cerevisiae, has been well characterized. It is a simple protein of molecular weight (MW) 11,470 (ref. 3), encoded by a double-stranded, linear RNA plasmid, called M RNA, of MW 1.1-1.7 x 10(6) (refs 4-6). It is lethal to sensitive Saccharomyces cerevisiae which does not carry M RNA. Leakage of K+ and ATP is the first distinct response in sensitive cells, and the toxic action is thought to be due to its action as a protonophore or K+ ionophore. Recently, a further killer toxin has been found in Kluyveromyces lactis IFO 1267, and it is associated with the presence of the double-stranded linear DNA plasmids, pGK1-1 (MW 5.4 x 10(6)) and pGK1-2 (MW 8.4 x 10(6)). It has been shown, by curing pGK1-1 or deletion mapping, that the structural gene for the killer toxin and immunity-determining gene reside on the smaller plasmid. Moreover, the plasmids could be transferred from K. lactis to S. cerevisiae by protoplast fusion and protoplast transformation. As the K. lactis toxin is encoded by a DNA plasmid and has a relatively wider action spectrum than K1 killer toxin, the mode of action of the toxin is highly interesting. Here we report that K. lactis toxin inhibits adenylate cyclase in sensitive yeast cells and brings about arrest of the cells at the G1 stage.

1-Methyl-3-isobutylxanthine↗

Familial occurrence of telangiectatic osteosarcoma: cousin cases.

Familial occurrence of osteosarcoma is rare. We report cousin cases, an 11-year-old girl and an 8-year-old boy with telangiectatic osteosarcoma. The tumors occurred in the metaphysis of the distal tibia and the lamina of thoracic vertebra. The local behaviors appeared aggressive, but the clinical courses were relatively indolent in both cases. The histologic features were similar, showing anaplastic tumor cells producing osteoid and proliferation of blood cavities. Clustering of malignancies within a family suggests the presence of a genetic factor.

Bone Neoplasms↗

Allelic loss on chromosomes 3p, 5q and 17p in renal cell carcinomas.

Loss-of-heterozygosity (LOH) has been studied on 3p (von Hippel-Lindau gene locus), 5q and 17p (p53 gene locus) by a polymerase chain reaction (PCR)-based strategy in 42 sporadic renal cell carcinomas (RCC). LOH at seven microsatellite loci on 5q was investigated because a tumor suppressor gene on 5q involved in the development and/or progression of RCC has not yet been identified. LOH was found in seven (17%) RCC at single or multiple loci on 5q, 38% (11/29 informative cases) on 3p, and 6% (2/35 informative cases) on 17p. Replication error (RER) was present in 10% (4/42) RCC at single or multiple loci. The minimum region of deletion on 5q to account for LOH was mapped to 5q31.1 (interferon regulatory factor-1; IRF-1 locus), where LOH was detected in 23% (6/26 informative cases). LOH on 3p and 5q occurred in both stage 2 and more advanced (stage 3 and 4) tumors at similar incidences (41 and 33% on 3p; and 24 and 22% on 5q, respectively), suggesting that LOH on these chromosomes is an early genetic event. All RCC exhibiting LOH on 3p or 5q (IRF-1 locus) were the clear cell or the mixed clear and granular cell types. These findings suggest that LOH on 3p and 5q plays an important role in the genesis of clear cell RCC. In addition, only one tumor exhibited LOH on both 3p and 5q, which suggests that LOH occurs not sequentially but independently.

Carcinoma, Renal Cell↗

Establishment and characterization of a new human extrahepatic bile duct carcinoma cell line (ICBD-1).

A new human extrahepatic bile duct carcinoma cell line (ICBD-1) was established from surgically resected tumor of a 71-year-old Japanese male patient. ICBD-1 cells proliferate in a layer with a population doubling time of 31.5 h and secrete tissue polypeptide antigen. ICBD-1 cells have a tetraploid pattern with a DNA index of 1.83 and chromosome counts showed equally distribution in a range from 65 to 69. IC50 values for ICBD-1 cells were 200 ng/ml for adriamycin, 400 ng/ml for mitomycin C, 2 microg/ml for cisplatin and 300 ng/ml for 5-fluorouracil. ICBD-1 cells were successfully transplanted to male nude mice, inducing progressive tumor growth. Histologically, nude mouse tumors were less differentiated than the original human tumor. Tumor cells showed alveolar structures with thin fibrous stroma, classified as poorly-differentiated adenocarcinoma. ICBD-1 is the fourth established cell line that originate from extrahepatic bile duct carcinoma and it will be applicable for the experimental studies of this disease.

Adenocarcinoma↗

Bronchial responses to enalapril in asthmatic, hypertensive patients.

The subjects, six asthmatic patients with mild essential hypertension, were aged 48 to 63 years and each was being treated with theophylline. Five patients received 10 mg of enalapril daily for two weeks and one received 5 mg for four weeks. Their bronchial responses to inhaled methacholine were measured with a modification of the 3-Hz oscillation method before and after the enalapril treatment. The patients' mean blood pressures decreased significantly from 180.7/100.3 to 152.0/93.3 mmHg after treatment. No treatment-associated changes in the frequency of coughing, the number of asthmatic attacks, or use of antiasthmatic drugs were noted. The results of the bronchial provocation tests revealed no changes in bronchial sensitivity or reactivity during treatment. Serum substance P levels were 61.3 pg/ml before treatment and 60.2 pg/ml after treatment. It is concluded that therapeutic doses of enalapril did not exacerbate asthmatic attacks or increase bronchial hypersensitivity in these asthmatic, hypertensive patients.

Asthma↗