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Biomedical subjects

J Okuda

Publications and source records attributed to J Okuda.

At least 145 records · Page 8Linked to original sources
PubMed1987

Is curative endoscopic treatment of early gastric cancer possible?

Fifty-four lesions found in 51 cases of early gastric cancer were treated with the Nd:YAG laser, N2 dye laser, local injection of ethanol, polypectomy and a combination of these methods between November, 1980 and July, 1986. Among these lesions, 34 were followed for more than one year with the endoscope. In 86% of the lesions treated, no recurrence of cancer was detected during the observation period, nor were there any deaths from gastric cancer. An analysis of the results showed that local cure of early gastric cancer in the mucosal layer could be accomplished with many kinds of endoscopic devices and that the difficulties for curative treatment depended on tumor localization and size. Further, we were able to assess local cure after endoscopic treatment on the basis of the endoscopic features of the tumor; local cure presents as a scarred stage with a smooth surface and with no abnormal granules or irregular redness. At present, endoscopic treatment should however, be limited to inoperable cases, since we cannot definitively diagnose lymph node metastasis or depth of cancer invasion.

Biopsy↗
PubMed1987

Anomeric preference in uptake of D-glucose and of D-galactose by rat lenses.

To determine the anomeric preference of uptake of D-glucose and of D-galactose by rat lenses, we crystallized alpha-, beta-D-[U-14C]glucose (720 microCi/mmol) and alpha-, beta-D-[U-14C]galactose (180 microCi/mmol) by our method and incubated them separately with rat lenses for 1 min, because of the short half-life of mutarotation of alpha-D-glucose (9.6 min) and of alpha-D-galactose (4.6 min) in HEPES medium at 30 degrees C. During aerobic incubation of rat lenses in HEPES medium containing radioactive alpha or beta anomer of D-glucose, there was no significant difference in the rate of uptake between alpha and beta anomers of D-glucose by rat lenses. However, 1.59 times greater incorporation of alpha-D-galactose was observed over that of beta-D-galactose under the same conditions.

Animals↗
PubMed1987

[Transfer of ofloxacin into suction blister fluid after its oral administration].

After oral administration of 300 mg of ofloxacin (OFLX), the concentration of OFLX in serum peaked at 2 hours and reached 2.88 +/- 0.62 micrograms/ml (mean +/- S.D.). In the fluid of dermal blisters produced by suction, the peak value was 1.74 +/- 0.88 micrograms/ml at 4 hours. Pharmacokinetically, Cmax (maximum concentration), Tmax (time of maximum concentration), Ka (absorption rate constant) and AUC0-8hrs. (area under the concentration-time curve) were calculated as 2.65 micrograms/ml, 2.07 hours, 0.79 hr-1 and 14.5 micrograms.hr/ml in serum, and 1.59 micrograms/ml, 4.49 hours, 0.27 hr-1 and 10.1 micrograms.hr/ml, respectively. Therapeutic AUC (area under the curve above minimum effective concentration) were also calculated as 13.3 micrograms.hr/ml (0.14-12.4 hours) in serum, and 11.5 micrograms.hr/ml (0.42-17.3 hours).

Administration, Oral↗
PubMed1986

Glucose transport into human erythrocytes treated with phospholipase A2 or C.

Phospholipase A2 induced crenation of human erythrocytes and decreased glucose transport activity (influx rate) by 40% when 51% of phosphatidylcholine (PC) in the membrane was hydrolyzed. On the other hand, phospholipase C induced invagination of the cells and negligibly affected the glucose transport in the case of 21% hydrolysis of the PC. By altering the pH of the medium for suspending cells treated with phospholipase A2 from 7.4 to 6.0, cell shape was changed from clear crenation to slight invagination, but glucose transport activity was not affected. Cells that were treated with phospholipase A2 and then washed with albumin to remove free fatty acids produced in the cell membrane showed an almost normal cell shape and slightly higher glucose transport activity than did untreated cells. The ratios of beta-D-glucose transport rate to alpha-D-glucose transport rate in untreated cells, cells treated with phospholipase A2 and cells treated with phospholipase C were 1.13, 1.04, and 1.20, respectively. These results demonstrate that the drastic morphological change (invagination or crenation) induced by the treatment with phospholipases bears no clear relationship to the activity of glucose transport and suggest that the increase in the volume of the outer half of the lipid bilayer might reduce the rate of glucose transport across the human erythrocyte membrane and change the anomeric preference of glucose transport.

Biological Transport↗
PubMed1986

Studies on systemic absorption of tobramycin in polyethylene glycol ointment applied to wounds of burn patients.

The penetration of tobramycin ointment (0.2 per cent) through human burn wounds was studied in two patients with superficial dermal burn (SDB) and deep dermal burn (DDB), two patients with DDB, one patient with full thickness burn (FB) and one patient with burn ulcer (BU). After application of the ointment, the absorption of tobramycin occurred promptly with a peak level at 2-6 h in the sera of patients with SDB + DDB and DDB only. In the BU patient it was found at 2 h; while in the FB, at 10-12 h. The excretion of tobramycin into the urine was also studied. The absorption rate constants (ka) of the two SDB + DDB patients were 0.31 and 0.74, of the two DDB patients, 0.079 and 0.18, and those of the DB and the BU patients, 0.053 and 0.95, respectively. The absorption ratios of tobramycin (amount excreted into the urine during 24 h/applied dose) were different, depending on the condition of the burn wound, and ranged from a low of 10.3 per cent (FB) to a high of 44.0 per cent (BU). These results show that the treatment of burn patients with tobramycin ointment to control burn wound infection should be carefully supervised, especially in the case of BU.

Administration, Topical↗
PubMed1986

Auditory extinction to nonverbal and verbal stimuli.

The so-called auditory extinction phenomenon in a verbal dichotic listening test was investigated in seven brain damaged patients from the qualitative standpoint. As the result, it became evident that the phenomenon could result from competition between verbal materials presented to both ears in at least two different levels of auditory processing i.e., sound perception and linguistic recognition. From the present study, we emphasize the following: If Bender's definition is followed, it is advisable to use the term extinction only for the phenomenon at the acoustic level. If the use of the term extinction for the phenomenon is to be continued at the linguistic level, the presence of auditory extinction and/or obscuration to nonverbal stimuli should be noted.

Acoustic Stimulation↗
PubMed1986

Lateralization phenomenon of complex auditory hallucinations.

A case is described of a patient who developed a transient verbal hallucination, lateralized to the right ear, and fluent aphasia after a hemorrhagic infarction in the left superior temporal gyrus. On the basis of this patient and the cases in the literature showing unilateral complex auditory hallucinations, the clinical significance of the lateralization phenomenon of complex auditory hallucinations was investigated. As a result, the lateralization phenomenon of complex auditory hallucinations could be considered a significant clinical sign indicating the existence of a lesion in the superior temporal gyrus opposite the hallucination side.

Aphasia↗
PubMed1986

Effect of exogenous lipids incorporated into the membrane of human erythrocytes on its glucose transport activity.

Addition of a phosphatidylcholine (dilinoleoyl), lysophosphatidylcholine (palmitoyl), saturated or unsaturated long-chain fatty acid (stearic or oleic) into human erythrocyte suspension caused both dose-dependent incorporation of the lipid into the membrane and inhibition of the glucose transport across the membrane. Loading to or partial removal of cholesterol from the membrane increased or decreased the transport rate, respectively. There was no correlation between the changes in the transport activity and those in cell shape caused by such alterations in the membrane lipid composition.

Blood Glucose↗
PubMed1986

Anomeric preference of glucose phosphorylation and glycolysis in human erythrocytes.

Lactate output from the alpha and beta anomers of glucose was measured in intact human erythrocytes at 37 degrees C; and glucose anomer phosphorylation, in human erythrocyte homogenates. The rates of both glucose metabolism (lactate output) and phosphorylation were higher in the presence of beta-D-glucose as distinct from alpha-D-glucose at three glucose concentrations used (2, 5, and 10 mM). Thus, the v beta/v alpha ratios of metabolism and phosphorylation of glucose at 2 mM were 1.24 and 1.22, respectively. The results indicate that the beta preference of hexokinase, a rate-limiting enzyme in glycolysis, is reflected in beta-preferential glycolysis.

Blood Glucose↗
PubMed1985

Inhibition of glucose-stimulated insulin release by pseudo-alpha-DL-glucose as a glucokinase inhibitor.

Pseudo-alpha- and pseudo-beta-DL-glucose, the isomers of 5-hydroxymethyl-1,2,3,4-cyclohexanetetrol with alpha-gluco and beta-gluco configurations, were used as synthetic analogs of glucose anomers to study the mechanism of glucose-stimulated insulin release by pancreatic islets. Neither isomer was phosphorylated by liver glucokinase nor stimulated insulin release from islets. Incubation of islets with pseudo-alpha-DL-glucose resulted in a considerable accumulation of the glucose analog, probably the D form, in islets. The alpha-isomer, but not the beta-isomer, inhibited both glucose-stimulated insulin release (44% inhibition at 20 mM) and islet glucokinase activity (36% inhibition at 20 mM) in a concentration-dependent manner and to a comparable degree. These results strongly suggest that the inhibition of glucose-stimulated insulin release by pseudo-alpha-DL-glucose is due to the inhibition of islet glucokinase by the glucose analog, providing additional evidence for the essential role of islet glucokinase in glucose-stimulated insulin release.

Animals↗