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Biomedical subjects

S Ota

Publications and source records attributed to S Ota.

At least 217 records · Page 12Linked to original sources
PubMed1989

[Studies of children with acute lymphoblastic leukemia (ALL) who relapsed. Relationship of site of relapse, time and prognosis].

One hundred and forty patients out of 511 children with ALL who were entered in the study of the Children's Cancer & Leukemia Study Group from 1981 through March 1988 had relapsed by August 1988. The sites of relapse were BM (including concurrent CNS relapse) in 96 cases (70%), CNS in 36 cases (25%), and testicles in 8 cases (5%). A second complete remission was induced in 57 of the 75 patients (76%) with ALL in the first BM relapse. The projected disease-free survival (DFS) for those in the second BM remission was 26.0% at 2 years and the length of the first remission was correlated with the outcome. In the patients in early marrow relapse within 12 months after diagnosis, the probability of maintaining a second remission at 2 years was 6.7% compared to 29.8% in those in intermediate marrow relapse. All patients in late relapse after more than 48 months from diagnosis are surviving with no evidence of disease. The outcome of the patients with isolated extra-marrow relapse was so favorable that the probability of maintaining a second remission for those in CNS relapse was 41.4% at 3 years, and 57.1% in patients in testicular relapse. These data suggest that 20-30% of patients relapsing after more than 12 months from diagnosis may be salvaged, but those who relapsed during active therapy within the first 12 months after diagnosis, other types of treatment should by considered.

Bone Marrow↗
PubMed1988

Cytoprotective effect of acetaminophen against taurocholate-induced damage to rat gastric monolayer cultures.

Acetaminophen has recently been reported to protect against drug damage to gastric mucosa in vivo. The present study tested acetaminophen protection in cultured rat gastric mucous cells against sodium taurocholate-induced damage and assessed the role of endogenous prostaglandins. Cell damage was assessed by phase-contrast microscopy and quantitated by Chromium-51 release assay which positively correlated with the trypan blue dye exclusion test (r = 0.98). The effect of acetaminophen on the production of PGE2 and 6-keto-prostaglandin F1a (6KF) was also studied. Sodium taurocholate caused cell death in a dose-dependent manner as indicated by increased 51Cr release. Preincubation with 5 mM acetaminophen significantly reduced 51Cr release caused by 5 mM sodium taurocholate, producing a 40% increase in cell survival. This cytoprotection was not blocked by indomethacin. PGE2 and 6KF of the media did not change after preincubation with nondamaging concentrations of acetaminophen or taurocholate. These results indicate that: (1) acetaminophen exerts a direct protective effect on gastric mucous cells cultured in vitro independent of indirect factors such as blood flow and (2) this protection is not associated with increased prostaglandin production.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Prostaglandin E2 output by isolated rat gastric parietal cells and non-parietal epithelial cells.

Prostaglandins have acid antisecretory and cytoprotective effects in gastric mucosa when given exogenously. This study's purpose was to isolate preparations of parietal and non-parietal cells from rat stomachs and to compare prostaglandin output by these cells. Gastric epithelial cells were isolated from rat stomachs using pronase. Cells from different incubation times were collected separately and enriched by discontinuous Percoll gradient. Cell types were identified by hematoxylin and eosin stain, succinic dehydrogenase activity (parietal cells), periodic acid Schiff staining (mucous cells), Bowie staining (chief cells) and electron microscopy. Prostaglandin E2 activity was measured by radio-immunoassay. Parietal cells were purified to over 90% while the non-parietal preparation contained 67% chief cells and over 31% mucous cells. By electron-microscopy, cell integrity was seen to be maintained. The parietal cell enriched fraction contained two and one-half times the amount of prostaglandin E2 that the non-parietal chief cell enriched fraction did, p less than 0.01. These results raise the question as to whether output of PGE2 by parietal cells could play a role in modulating gastric acid secretion directly by parietal cells as well as in protecting the deeper layers of gastric mucosa against damaging agents in-vivo.

Animals↗
PubMed1988

Salicylate effects on a monolayer culture of gastric mucous cells from adult rats.

Aspirin, acetyl salicylic acid, damages gastric mucosal cells. This effect is considered related to its inhibition of prostaglandin synthesis. On the other hand, sodium salicylate has been reported to be cytoprotective against drug damage to gastric mucosa in vivo. One reason for this difference is that salicylic acid, unlike acetyl salicylic acid does not inhibit prostaglandin synthesis by gastric mucosa in vivo. Previous studies on tissue culture cells from our laboratory have required gastric mucosa from fetal rats; this was time consuming and expensive. The purpose of this study was to develop a primary cell culture of adult rat fundic epithelial cells and to test the effect of sodium salicylate on: (1) prostaglandin (PGE2) production, (2) cell viability, (3) reducing cell damage by sodium taurocholate. Gastric epithelial cells were isolated from adult rat stomachs and cultured on collagen gel. Cells reached confluency on day 4 at which stage fibroblasts were rarely seen (less than 1%). Autoradiographic study showed that cultured cells incorporated [3-H] thymidine into nuclei. In histochemical studies, 94% of the cells contained PAS positive granules (mucous cells). Mucous granules were observed in the cytoplasm of the majority of cells by electronmicroscopy. These cells synthesised prostaglandin E2 as determined by radioimmunoassay. Indomethacin 10(-4) M strongly suppressed PGE2 production after 30 minutes while 10(-3) and 10(-4)M sodium salicylate had no effect. Pharmacologic concentrations of 10 mM sodium salicylate had no effect on PGE2 production at 30 minutes and only weakly inhibited production after one hour incubation. Sodium salicylate up to 30 mM had no effect on cell viability, a concentration of 50 mM being necessary to produce significant cell damage. Sodium salicylate 10 mM significantly protected cells against damage induced by 10 mM sodium taurocholate. We conclude: (i) adult rat gastric mucous epithelial cells can be successfully cultured in vitro; (ii) prostaglandin synthesis is inhibited by indomethacin but not by low doses of sodium salicylate; (iii) sodium salicylate does not damage gastric mucosal cells except at very high concentrations; (iv) sodium salicylate protects against damage to cells induced by sodium taurocholate.

Animals↗
PubMed1988

A quantitative cytologic study of sputum in early squamous cell bronchogenic carcinoma.

The abnormal cells (atypical squamous cells and cancer cells) in the sputum of 12 in situ and 20 early invasive squamous cell carcinomas were studied quantitatively and compared with the cells in 12 borderline cases and 11 frankly invasive squamous cell carcinomas, In in situ and early invasive squamous cell carcinomas, the mean nuclear diameters were larger and multinucleated cells and distinct nucleoli were more frequent than in borderline cases. Furthermore, the mean cellular diameters and the number of abnormal cells per slide were smaller, the distinct nucleoli were less frequent and acidophilic cytoplasms were more frequent than in frankly invasive squamous cell carcinomas. The results indicate that (1) in situ and early invasive squamous cell carcinomas are generally distinguishable cytologically from borderline cases and from frankly invasive squamous cell carcinomas and (2) the cytologic differentiation between in situ and early invasive squamous cell carcinomas is quantitatively insufficient.

Carcinoma, Bronchogenic↗
PubMed1988

[Mass screening for early lung cancer by the Miyagi method].

Mass screening for early detection of lung cancer has been in practice from 1982. Up to 1985, 583,549 persons-years have been screened. Screening was done by examining miniature X-rays taken of the chest for all those tested, and by sputum cytology for those thought to be high-risk, 34,044 persons-years. Heavy smokers over 50 years of age comprised much of the high-risk cases and persons evidencing hemoptysis. In a total of 207 detected cases of lung cancer, 120 cases were found by chest X-ray only, 69 cases were uncovered by sputum cytology only, and 18 cases were discovered by both X-ray and cytology. In one hundred and forty-four cases the cancers were resected and in 69 cases the cancers were determined to be in an early stage.

Female↗
PubMed1987

Arachidonic acid stimulation of mucus production by rat gastric cultured cells.

The effect of arachidonic acid (AA) on mucus production (synthesis and secretion) by rat gastric monolayer-cultured cells was investigated. For the study of mucus synthesis, the rate of incorporation of [3H]glucosamine into the cultured cells was measured. The rate of release of glycoprotein into the culture media from the cells, which were incubated in the medium containing [3H]glucosamine for 24 hr in advance, was determined for the study of mucus secretion. Prostaglandins in the medium were measured by radioimmunoassay. AA (10(-4) M) significantly increased mucus synthesis and secretion by the cultured cells (P less than 0.01). PG (E2 and I2) synthesis by the cultured cells was significantly enhanced by AA (10(-4) M) (P less than 0.05). An addition of indomethacin to the culture medium abolished this effect of AA. These results suggested that gastric mucus production was enhanced by AA in vitro and that this effect may be mediated by endogenous PG production.

Animals↗
PubMed1987

Arachidonic acid does not protect against sodium taurocholate damage to rat gastric epithelial cell cultures.

Arachidonic acid is cytoprotective against ethanol damage in vivo. Stimulation of production of endogenous prostaglandin has been postulated as a mechanism of this protection. The current study assessed the ability of arachidonic acid to protect gastric mucosal cells directly and the effect of arachidonic acid on prostaglandin production. To determine cytoprotection, sodium taurocholate was used as a damaging agent and cell viability was assayed by 51Cr release in vitro. By the dose response curve, 5 mM sodium taurocholate was chosen for the protective study. Cells were preincubated with arachidonic acid (0.1-10 micrograms/ml) and then incubated with 5 mM sodium taurocholate. The synthetic activity of prostaglandins by cultured cells was assessed using 14C arachidonic acid prelabeled cells. Media content of prostaglandin E2 was assayed by radioimmunoassay. Cell viability was assayed by 51Cr release. Our results showed that arachidonic acid did not significantly protect cultured gastric cells against sodium taurocholate damage, while larger doses of arachidonic acid produced cell damage. Furthermore, cultured gastric cells produced mainly prostaglandin E2 and prostaglandin I2 and arachidonic acid stimulated prostaglandin E2 production dose-dependently (p less than 0.01). In conclusion, arachidonic acid does not directly protect gastric mucosal cells in vitro. In vivo protection by arachidonic acid must be based on indirect factors such as preservation of microvasculature.

Animals↗
PubMed1987

Prostaglandin protects against taurocholate-induced damage to rat gastric mucosal cell culture.

Prostaglandins protect gastric mucosa against noxious agents, but it is unknown whether this protection includes a direct action on the cells themselves, this action is limited to damaging agents that inhibit prostaglandin synthesis, or cellular cyclic adenosine monophosphate is the mediator. The present study tested these questions in cultured gastric mucous epithelial cells. The effect of 16,16-dimethyl prostaglandin E2 on cellular cyclic adenosine monophosphate level and the effect of 16,16-dimethyl prostaglandin E2, dibutyryl cyclic adenosine monophosphate, and isobutyl methyl xanthine on taurocholate-induced damage to cultured rat gastric mucosal cells was determined. As parameters of cell damage, the trypan blue dye exclusion test and 51Cr-release were employed. Taurocholate significantly increased 51Cr-release in a dose-dependent manner and decreased the number of viable cells. 16,16-Dimethyl prostaglandin E2 (1.0 microM) diminished the cell damage caused by 10 mM taurocholate (p less than 0.01) and increased cyclic adenosine monophosphate levels. Prostaglandin F2 alpha but not prostaglandin I2 was also cytoprotective. Addition of dibutyryl cyclic adenosine monophosphate (1.0 mM) and isobutyl methyl xanthine while significantly increasing cyclic adenosine monophosphate levels did not significantly reduce taurocholate-induced cell damage. Thus, in vitro 16,16-dimethyl prostaglandin E2 directly protects gastric mucous cells against taurocholate-induced injury, direct prostaglandin cytoprotection is not limited to damaging agents that inhibit prostaglandin synthesis, and cyclic adenosine monophosphate levels do not correlate with gastric mucosal cell damage and may not be involved in the direct protective effect of prostaglandins.

16,16-Dimethylprostaglandin E2↗
PubMed1987

Primary structures of M6 and M7 of mugiline beta (Mugil japonicus).

Mugiline beta isolated from mature sperm nuclei of the Formosan grey mullet, belonging to Perciformes, was fractionated into seven components (M1-M7), by chromatography on CM-Sephadex C-25. The amino acid sequences of the two major components (M6 and M7) were then determined. M6 contained 33 amino acid residues per molecule: Arg, 21; Thr, 1; Ser, 1; Glu, 1; Pro, 3; Ala, 2; Val, 2; Met, 0.3 and Ile, 1.7. The amino acid sequence of M6 is: Pro-Arg-Arg-Arg-Arg-Glu-Thr-Ser-Arg-Pro-Ile-Arg-Arg-Arg-Arg-Arg-Ala-Pro- Ile (Met)-Arg-Arg-Arg-Arg-Arg-Val-Val-Arg-Arg-Arg-Arg. Isoleucine at position 22 is partially replaced by methionine. M7 had an amino acid sequence similar to that of M6 except that glutamic acid at position 6 of M6 was replaced by glutamine. A high degree of homology in the sequences was found between mugiline beta from mullet and thynnine from tuna fish, which also belongs to Perciformes.

Amino Acid Sequence↗
PubMed1987

Oxygen metabolite-induced cytotoxicity to cultured rat gastric mucosal cells.

Reactive oxygen metabolites have been reported to be responsible for the pathogenesis of ischemia-induced gastric mucosal lesions. We have investigated the possible protective effect of specific enzymes and oxygen radical scavenging agents on oxygen metabolite-induced injury to cultured gastric mucosal cells. Oxygen-reactive metabolites were generated by 1 mM xanthine and 10-100 mU/ml xanthine oxidase. Cytotoxicity was quantified by measuring 51Cr release from prelabeled cells. Xanthine oxidase caused a dose-dependent increase of 51Cr release in the presence of 1 mM xanthine. Catalase (an enzyme that reduces hydrogen peroxide) diminished xanthine-xanthine oxidase-induced 51Cr release in a dose-dependent manner. Superoxide dismutase (a scavenger of superoxide radical) failed to affect the amounts of 51Cr release induced by xanthine plus xanthine oxidase. Pretreatment with diethyl maleate, which depletes intracellular glutathione, potentiated oxygen radical-mediated 51Cr release dose dependently. The presence of ferrous ion or ethylenediaminetetraacetic acid-chelated iron, which promote the formation of hydroxyl radical, did not alter xanthine-xanthine oxidase-induced cellular injury. Furthermore, agents that inactivate hydroxyl radical also failed to protect the cells from oxygen metabolite-induced injury. We conclude that in vitro oxygen metabolites, extracellularly generated, have a direct toxic effect on gastric mucosal cells; hydrogen peroxide is a major mediator of oxygen metabolite-induced gastric cell injury; the oxygen-derived superoxide and hydroxyl radicals are less toxic to gastric mucosal cells than hydrogen peroxide; and intracellular glutathione, which detoxifies hydrogen peroxide, may be involved in antioxidant defense mechanisms.

Animals↗
PubMed1987

Prevention of exercise-induced bronchospasm in asthmatic children. Effect of aerosol and oral procaterol hydrochloride.

This double-blind crossover study compared the therapeutic value of bronchodilator procaterol hydrochloride at 5 micrograms per puff by aerosol inhalation using a metered-dose inhaler and at 25 micrograms by oral administration using tablets with respective inert placebos in preventing exercise-induced bronchospasm (EIB) in 10 children with bronchial asthma. The two active dosage formulations produced a significant EIB inhibitory effect compared with the placebos. In a comparison of the two active preparations, the aerosol was more efficacious than the tablet in improving all respiratory parameters examined, and statistical significance was obtained in FEV1, MMEF, PEFR, V50, and V25 5 minutes after exercise. Further, the aerosol was beneficial in all subjects, while the tablet was beneficial in seven of 10.

Administration, Oral↗