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Biomedical subjects

T Oshima

Publications and source records attributed to T Oshima.

At least 433 records · Page 24Linked to original sources
PubMed1989

[Esophago-bronchial fistulas in adult].

Esophago-bronchial fistulas in adult are rare and for the most part are due to a malignant tumor. The authors present two cases of benign Esophago-bronchial fistula which were discovered accidentally by esophagography. One case was considered to be congenital. Esophagography is the most useful for diagnosis of this disease.

Bronchial Fistula↗
PubMed1989

Factors determining sodium chloride sensitivity of patients with essential hypertension: evaluation by multivariate analysis.

Factors which determine sodium chloride sensitivity, defined as the difference between the mean blood pressure after 1 week of a low sodium chloride diet (3 g/day) and that after 1 week of a high sodium chloride diet (20 g/day), were studied in 60 inpatients with essential hypertension using a multivariate analysis. The sodium chloride sensitivity was independently correlated with the change in erythrocyte sodium concentration (r = 0.47) and with the change in plasma renin activity (r = 0.29); but it was not related to basal blood pressure, the change in plasma volume of the change in plasma norepinephrine concentration. These data suggest that both intracellular sodium accumulation and inadequate suppression of the renin-angiotensin system may be independently involved in the elevation of blood pressure after sodium chloride loading. We could not find the independent importance of volume retention, hyperadrenergic activity or basal blood pressure in the sodium chloride sensitivity.

Blood Pressure↗
PubMed1989

[Multi-modal treatment of patients with multiple liver metastases caused by sigmoid cancer].

A case of sigmoid cancer with multiple liver metastases (S2PON3 + H3) who was treated by multi-modal treatment was reported. The multi-modal treatment is including intra-arterial administration of anti-cancer drugs as a pre-surgery treatment, intra-arterial infusion chemotherapy lasting for three to five weeks (three times), hyperthermia treatment combined with intra-arterial administration of anti-cancer drugs and intra-arterial expandable metalic stent. The patients lived for 2 years and 4 months in good condition.

Aged↗
PubMed1988

Possible induction of fatty acid cyclooxygenase in mouse osteoblastic cells (MC3T3-E1) by cAMP.

Prostaglandin E2 (PGE2), a bone-resorption factor, was essentially the sole arachidonate metabolite in an osteoblastic cell line cloned from mouse calvaria (MC3T3-E1). When the cells were cultured in the presence of 2% newborn bovine serum, 1 microM epinephrine markedly stimulated PGE2 synthesis from endogenous arachidonic acid. The PGE2 synthesis commenced after a lag phase of 1-2 h, and reached a maximum at about 3 h after the addition of epinephrine. The effect of epinephrine was inhibited by propranolol, and epinephrine could be replaced by isoproterenol, suggesting beta-adrenergic stimulation of PGE2 production. A rapid increase in intracellular cAMP was observed upon the addition of epinephrine. When the intracellular cAMP level was raised using cholera toxin or forskolin, the PGE2 synthesis was also stimulated. The enhanced PGE2 synthesis was attributed to an increased level of cyclooxygenase, which was shown by immunoprecipitation of the enzyme using anti-cyclooxygenase antibody. Inhibitors of transcription and translation suppressed the epinephrine-dependent increase in cyclooxygenase activity. These findings suggest induction of cyclooxygenase involving cAMP via an as yet unclarified mechanism.

Animals↗
PubMed1988

Molecular cloning of the beta-subunit of a possible non-F0F1 type ATP synthase from the acidothermophilic archaebacterium, Sulfolobus acidocaldarius.

The gene which encodes the beta subunit of the novel membrane-associated ATPase has been identified and characterized. The beta subunit, which is most likely the soluble part of the non-F0F1 type H+-ATPase, was obtained from the archaebacterium, Sulfolobus acidocaldarius. In terms of its location, it follows just after the gene for its alpha subunit. It is comprised of 1398 nucleotides, corresponding to a protein of 465 amino acids, and the consensus sequence in the nucleotide binding proteins is poorly conserved. Together with previously described results, the distant homology of the S. acidocaldarius ATPase alpha and beta subunits when compared to those of F0F1-ATPases indicates that this archaebacterial ATPase belongs to an ion-translocating ATPase family uniquely different than F0F1-ATPases even if S. acidocaldarius ATPase and F0F1-ATPases have been derived from a common ancestral ATPase.

Amino Acid Sequence↗
PubMed1988

RS-5186, a novel thromboxane synthetase inhibitor with a potent and extended duration of action.

RS-5186, sodium 6-[2-[1-(1H)-imidazolyl]methyl-4,5-dihydrobenzo[b]thiophene]- carboxylate, inhibited platelet thromboxane A2 (TXA2) synthetase with IC50 values of 6 nM and 13 nM for human and rabbit microsomes, respectively. It had a selectivity for TXA2 synthetase 10(5)-fold greater than that for cyclooxygenase, PGI2 synthetase, 5-lipoxygenase and phospholipase A2. When administered orally or intravenously to dogs at 1 mg/kg, RS-5186 suppressed serum TXB2 levels almost completely with sustained duration of action: the suppression during 0.5 hr to 8 hr after dosing was more than 90%, and was 70-80% at 24 hr. Similar suppression of serum TXB2 levels was observed in rats and rabbits. Such suppression by RS-5186 was more potent than that by OKY-046 and CV-4151. Serial administration of RS-5186 (0.1 mg/kg/day p.o.) to dogs for 7 days decreased the serum TXB2 levels constantly during the medication, and no rebound phenomenon was observed after the medication was stopped. In a thrombotic model induced by sodium arachidonate injection in rabbits, RS-5186 at 1 mg/kg p.o. completely protected against sudden death (ED50 = 0.12 mg/kg, 1 hr after dosing) and this protective effect extended over 8 hr. All these results show that RS-5186 is a potent and highly selective TXA2 synthetase inhibitor with a long duration of action, and suggest that the compound could be useful in diseases where TXA2 is involved.

Animals↗
PubMed1988

A single amino acid substitution converts cytochrome P450(14DM) to an inactive form, cytochrome P450SG1: complete primary structures deduced from cloned DNAS.

Genes for lanosterol 14-demethylase, cytochrome P450(14DM), and a mutated inactive cytochrome P450SG1 were cloned from S. cerevisiae strains D587 and SG1, respectively. A single nucleotide change resulting in substitution of Asp for Gly-310 of cytochrome P450(14DM) was found to have occurred in cytochrome P450SG1. In this protein the 6th ligand to heme iron is a histidine residue instead of a water molecule, which may be the ligand for the active cytochrome P450(14DM). Molecular models of the active sites of the cytochrome P450(14DM) and cytochrome P450SG1 were built by computer modeling on the basis of the known structure of that of cytochrome P450CAM whose crystallographic data are available. The mechanisms which may cause a histidine residue to gain access to the heme iron are discussed.

Amino Acid Sequence↗
PubMed1988

The membrane-associated ATPase from Sulfolobus acidocaldarius is distantly related to F1-ATPase as assessed from the primary structure of its alpha-subunit.

Isolation of novel membrane-associated ATPases, presumably soluble parts of the H+-ATPases, from archaebacteria has been recently reported, and their properties were found to be significantly different from the usual F1-ATPase. In order to assess the relationship of the archaebacterial ATPases to the F1-ATPases and other known ATPases, the amino acid sequence of the alpha subunit of the ATPase from Sulfolobus acidocaldarius, an acidothermophilic archaebacterium, was compared with the sequences of other ATPases. The gene encoding its alpha subunit was cloned from the genomic library of S. acidocaldarius, and the nucleotide sequence was determined. The 591-amino acid sequence deduced from the nucleotide sequence contains a small number of short stretches that shows sequence similarity to the alpha and beta subunits of F1-ATPase. However, the overall similarity is too weak to consider it to be a typical member of the F1-ATPase family when the highly conserved sequences of the F1-ATPase subunits among various organisms are taken into account. Moreover, most of these stretches overlap the consensus sequences that are commonly found in some nucleotide-binding proteins. There is no significant sequence similarity to the ion-translocating ATPases, which form phosphorylated intermediates, such as animal Na+,K+-ATPases. Thus, the S. acidocaldarius ATPase and probably other archaebacterial ATPases also appear to belong to a new group of ion-translocating ATPases that has only a distant relationship to F1-ATPase.

Adenosine Triphosphatases↗
PubMed1988

Characteristic structures of actin gels induced with hepatic actinogelin or with chicken gizzard alpha-actinin: implication for their function.

We studied the properties of actinogelin, a Ca2+-regulated actin cross-linking protein isolated from Ehrlich tumor cells or rat liver. Chicken gizzard alpha-actinin was used as a Ca2+-insensitive control. Actinogelin, which has very high gelation activity under low Ca2+ conditions, was found using electron microscopic or fluorescence studies to induce formation of a characteristic structure in which actin filaments and bundles radiate to (or converge from) all directions from spot-like core structures. A similar structure was induced with actinogelin, even in the presence of 0.7 saturation of tropomyosin. No such structure was detected with actinogelin under high Ca2+ conditions, and only a few were found with gizzard alpha-actinin. Because reconstituted structures are similar to those observed intracellularly, actinogelin may be important in the formation of similar microfilament organization in the cells. It seems also important that these structures are reconstituted with only two purified protein components, i.e., actinogelin and actin. Immunocompetition studies showed that actinogelin and gizzard alpha-actinin partially shared antigenicity, and their molecular shape and peptide maps were similar. Their amino acid compositions [Kuo et al., 1982], subunit and domain structures, and binding sites on actin [Mimura and Asano, 1987] are also very similar. Therefore, it is concluded that actinogelin belongs to alpha-actinin superfamily proteins. Furthermore, the presence of functionally different subfamilies concerned with Ca2+ sensitivity, gelation-efficiency, and others is discussed. Actinogelin, which induces networks of actin filaments, may be classified as high gelation type.

Actinin↗
PubMed1988

Localization of the regulatory subunit of cAMP-dependent protein kinase in Saccharomyces cerevisiae.

The subcellular distribution of the regulatory subunit of cAMP-dependent protein kinase in Saccharomyces cerevisiae cells was determined by subcellular fractionation and indirect immunofluorescence microscopy using the bcy1 mutant deficient in the regulatory subunit as control. The regulatory subunit of cAMP-dependent protein kinase showing cAMP-binding activity was identified as a single protein of 50 kDa by photoaffinity labeling and immunoblotting. The regulatory subunit was concentrated in a nuclear fraction in addition to a cytoplasmic fraction. By comparison of the regulatory subunit distribution with the DNA localization, the area detected by the indirect immunofluorescence was identified as the nucleus.

Carrier Proteins↗
PubMed1988

Relationship of cellular calcium to salt sensitivity in patients with essential hypertension.

The significance of cellular calcium metabolism and systemic calcium balance in sodium chloride sensitivity was studied in 16 patients with essential hypertension and in 13 normotensive subjects. With changes in sodium chloride intake from 3 to 20 g/day, mean blood pressure, lymphocyte [Ca2+]i and the acute hypotensive response to nifedipine were increased in the hypertensive patients, but not in the normotensive subjects. Serum calcium concentration was decreased and urinary calcium excretion was increased in both groups. In the hypertensive patients, elevation of mean blood pressure was positively correlated with the increase in lymphocyte [Ca2+]i and with the enhancement of the hypotensive response to nifedipine, but it was not related to the change in serum or urinary calcium. These results suggest that enhancement of cellular-calcium-dependent vasoconstriction may lead to increased blood pressure following sodium chloride loading in patients with essential hypertension.

Calcium↗