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Biomedical subjects

F Ueda

Publications and source records attributed to F Ueda.

At least 55 records · Page 3Linked to original sources
PubMed1992

Development of gap junctions between gastric surface mucous cells during cell maturation in rats.

The development of gap junctions in rat gastric surface mucous cells during their maturation were examined by indirect immunofluorescence and freeze-fracture methods. Monoclonal antibody against liver gap junction protein stained in large spots along the intercellular junctions between mature gastric surface mucous cells. On the other hand, relatively small fluorescent spots were present over the immature surface mucous cells. The freeze-fracture method showed many large irregular gap junctions between mature surface mucous cells. In immature surface mucous cells, the gap junctions were less developed than those of mature cells, and small gap junctions were occasionally associated with tight junctional strands. Quantitatively, the gap junctions in mature cells were larger and more numerous than those in immature cells. These findings show that gap junctions develop during the maturation of surface mucous cells and suggest that the intercellular communication mediated by gap junctions between gastric surface mucous cells plays an important role in the regulation of cell differentiation and in tissue homeostasis.

Animals↗
PubMed1992

Gadolinium-DTPA enhancement of dural structures on MRI after surgery.

Gadolinium-DTPA enhanced MRI was examined before and after surgery in 14 patients with particular attention to the enhancement of falx cerebri, tentorium cerebelli and dura mater. A marked enhancement was observed in 2 falx and 2 tentorium before surgery, whereas it was observed in 7 falx, 9 tentorium and 11 dura after surgery. Among 6 falx, 7 tentorium and 12 dura showing increased enhancement after surgery, 2 falx, 3 tentorium and 8 dura showed marked enhancement which was not observed before surgery. A small amount of subdural haemorrhage during surgery is known to heal as subdural neomembrane with capillaries. An increased enhancement of dural structures conceivably derives from the extravasation of Gd-DTPA through capillaries involved in the subdural neomembrane. In the postoperative MRI, the enhancement of dural structures should be taken into consideration.

Adolescent↗
PubMed1992

Post-irradiation protective effect of irsogladine maleate on intestinal crypt stem cells in mice.

Radioprotective effect of irsogladine maleate, an anti-ulcer drug, on the intestinal crypt stem cell survival was studied in mice using a crypt microcolony assay. Irsogladine maleate was injected intraperitoneally immediately after irradiation and then, daily for three days. A successive administration of the drug following 10 Gy of irradiation increased the survival of intestinal stem cells with a clear dose-related trend. In order to estimate the D0, survival curves were determined for X-ray plus placebo and X-ray plus 10 mg/kg of irsogladine maleate. The D0, for X-ray plus the drug was 2.2 Gy while it was 1.9 Gy for X-ray plus placebo. These findings suggest that isogladine maleate can be applied for the alleviation of intestinal damages in heavily irradiated people by radiation accidents.

Animals↗
PubMed1991

4'-galactooligosaccharide affects sodium and potassium metabolism in rats.

The effect of different levels (0, 10 and 20%) of O-beta-D-galactopyranosyl-(1-4)-O-beta-D-galactopyranosyl-(1-4)-D- glucose (4'-GL) on the bioavailability of sodium and potassium was studied in 18 male rats. Three 3-d metabolic balance studies were conducted during the 62-d feeding trial. These were between d 30 and 32 (first period), 45 and 47 (second period) and 60 and 62 (third period). Growth and food intake were not significantly different (P less than 0.05) between the control group and the 4'-GL-fed groups. In rats fed 10 and 20% 4'-GL diet, the fecal sodium excretion was significantly greater (P less than 0.05) in all three balance periods. Fecal potassium excretion was significantly greater (P less than 0.05) in the 10% 4'-GL-fed group in the second balance period and the 20% 4'-GL-fed group in all balance periods relative to the control group. Although not statistically significant, rats in the 4'-GL-fed groups exhibited a tendency for lower sodium retention and higher potassium retention compared with the control group. The cecal weight of rats in both 4'-GL-fed groups was significantly heavier (P less than 0.05) than that of the control group at the end of study. Sodium concentration in the cecum was significantly lower (P less than 0.05) in the 20% 4'-GL-fed group relative to the other groups.

Animals↗
PubMed1991

Release kinetics of nicotinamide from fatty acid-nicotinamide equimolar complexes. II. Activation thermodynamic quantities.

The rates of release of nicotinamide (NAA) from fatty acid (FA)-NAA complexes, FA-NAA, were determined at various temperatures, and the thermodynamic quantities for the release of NAA were estimated. The results were compared with the previous results obtained for FA-thiamine disulfide (TDS) complexes, (FA)6(TDS). The values of activation enthalpy (delta H ++) and activation entropy (delta S ++) for the release of NAA from FA-NAA were positive and negative, respectively, indicating that the release of NAA is disadvantageous from not only enthalpic but also entropic viewpoints. The plots of delta H++ against the carbon number (n) in the constituent FA showed a zig-zag line with an upward convex at an odd-numbered position and the plots of the absolute values of (-delta S++) showed a zig-zag line with a downward convex at an odd-numbered position, though the positive value of delta H++ increases and the negative value of delta S++ decreases with an increasing n for either even-numbered or odd-numbered FA. It was found that the release of NAA from FA-NAA formed with odd-numbered FA is more disadvantageous enthalpically but more advantageous entropically as compared with that from FA-NAA formed with even-numbered FA. This phenomenon was similar to that observed for (FA)6(TDS). Furthermore, it is suggested that FA-NAA is formed at least by van der Waals forces and hydrophobic interactions and that van der Waals forces are dominant for the formation of FA-NAA formed with odd-numbered FA and that hydrophobic interactions are dominant for the formation of FA-NAA formed with even-numbered FA.

Fatty Acids↗
PubMed1991

Changes in cyclic AMP content of rat gastric mucosa induced by ulcerogenic stimuli--in relation to the antiulcer activity of irsogladine maleate.

Changes in the cyclic AMP (cAMP) content of the gastric mucosa induced by ulcerogenic stimuli were investigated in rats. Ligation of the pylorus for 5 hr produced no glandular mucosal lesion, but increased the cAMP content in the fundus and antrum. Aspirin produced glandular mucosal lesions in the pylorus-ligated rats and caused an increase of the cAMP content in the fundus and a decrease in the antrum. Irsogladine maleate (IM), an antiulcer agent, inhibited both the changes in the cAMP content and the mucosal damage induced by aspirin. IM increased the cAMP content in both regions, especially the antrum, in normal rats. Dibutyryl cAMP (dbcAMP) given orally prevented the gastric mucosal lesions induced by aspirin without affecting gastric secretion. These results suggest that 1) the changes in the cAMP content of the fundus and antrum induced by aspirin may be associated with the formation of glandular mucosal damage, 2) the antiulcer activity of IM may be related to an increase of the cAMP content in mucous cells, and 3) dbcAMP given orally may penetrate into the surface mucous cells and activate defensive functions. Thus, cAMP in the mucous cells may protect the gastric mucosa.

Animals↗
PubMed1991

Intercellular communication in cultured rabbit gastric epithelial cells.

The effects of drugs related to cyclic AMP and a tumor promoter, phorbol ester, on intercellular communications via gap junctions were investigated by the Lucifer Yellow-transfer method in cultured rabbit gastric epithelial cells. Cells were in contact with each drug for 4 hr before the microinjection of the dye into a cell. Dye transfer capacity was significantly increased by dibutyryl cyclic AMP (10(-3) M), theophylline (10(-3) M), 3-isobutyl-1-methylxanthine (10(-4) M), forskolin (10(-6) M) and irsogladine (10(-4) M); and it was inhibited by 12-O-tetradecanoyl-phorbol-13-acetate (100 ng/ml). These results suggest that the intercellular communication between cultured rabbit gastric epithelial cells is upregulated by cyclic AMP.

Animals↗
PubMed1991

Pharmacological properties of the new non-steroidal anti-inflammatory agent etodolac.

The anti-inflammatory, analgesic, antipyretic and ulcerogenic activities of etodolac (CAS 41340-25-4), a new nonsteroidal anti-inflammatory agent, were compared with those of indometacin and other anti-inflammatory drugs in experimental animals. Etodolac had a remarkable anti-inflammatory effect in various experimental models: ultraviolet erythema, carrageenin-induced edema and swelling of adjuvant arthritis. In these models, the effective dose of etodolac was several fold that of indometacin. Etodolac inhibited prostaglandin E2 formation in a concentration-dependent manner, and its inhibitory potency was about 1/5 of that of indometacin. Etodolac also caused marked inhibition of granuloma formation and leucocyte functions such as chemotaxis, lysosomal enzyme release and active oxygen generation. These effects of etodolac were observed at similar doses of indometacin. Etodolac suppressed inflammatory pain but not non-inflammatory pain, and had an antipyretic effect but did not lower normal rectal temperature. Etodolac had no effect on delayed hypersensitivity reactions and was much less ulcerogenic than indometacin. These results indicate that etodolac is a low ulcerogenic anti-inflammatory agent with suppressing activities on leucocyte functions to the same extent as indometacin and prostaglandin biosynthesis.

Animals↗
PubMed1991

Mechanism of anti-inflammatory action of etodolac.

The effect of etodolac (CAS 41340-25-4) on the inflammatory reactions induced by histamine and bradykinin was compared with that of indomethacin and other nonsteroidal anti-inflammatory drugs. Etodolac (50 mg/kg p.o.), indomethacin (20 mg/kg p.o.), diclofenac Na (20 mg/kg p.o.) and acetylsalicylic acid (200 mg/kg p.o.) had no effect on the increase of vascular permeability induced by histamine or bradykinin and on passive cutaneous anaphylaxis in rats. Etodolac (5, 10 and 20 mg/kg p.o.) suppressed concanavalin A-induced paw edema in rats. Etodolac (10 mg/kg p.o.) and bromelain (10 mg/kg i.v.) significantly suppressed the heat-induced elevation of bradykinin in perfusates of rat paws, but indomethacin (20 mg/kg p.o.) and diclofenac Na (20 mg/kg p.o.) did not. Etodolac inhibited bradykinin-forming enzyme activity in a concentration-dependent manner (IC50 = 1.5 x 10[-4) mol/l). These results suggest that etodolac is a unique nonsteroidal anti-inflammatory drug which can inhibit bradykinin formation, unlike indomethacin or diclofenac Na.

Animals↗
PubMed1990

Microwave irradiation is effective in the rapid fixation of gastric mucosa for determination of the prostaglandin content.

The gastric mucosal content of prostaglandin (PG) E2, 6-keto PGF1 alpha, and thromboxane (TX) B2 was determined by radioimmunoassay in unfed rats. The stomach was removed, and gastric mucosal specimens were prepared by microwave irradiation of the 1) intact stomach, 2) frozen stomach, 3) separated frozen glandular portion, 4) frozen gastric mucosa separated from the stomach wall, and 5) separation of frozen gastric mucosa with no microwave irradiation. Procedure 1 resulted in PGE2, TXB2, and 6-keto PGF1 alpha levels of 0.75, 2.33, and 3.04 ng/g tissue in the fundus, and 0.33, 1.92, and 1.76 ng/g tissue in the antrum, respectively. In procedures 2-4 these values were much higher, indicating that the PG content of the gastric mucosa is liable to be changed by various artificial procedures, such as freezing and surgical and mechanical handling. In procedure 5, values of PG contents were quite unreliable. These results suggest that microwave irradiation immediately after removal of the stomach may be the most reliable procedure for the accurate determination of the PG content of the gastric mucosa in vivo.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Effects of extracellular calcium and sodium on cadmium uptake in guinea-pig and rabbit aorta.

1. Effects of Na+ and Ca2+ on Cd2+ uptake in the guinea-pig and rabbit aorta were investigated. 2. The Cd2+ fraction can be divided with EDTA and Zn2+. The EDTA fraction may be intracellular fraction and the Zn2+ fraction may be loosely bound to surface membrane. 3. In Na+ deficient solution the Zn2+ fraction was markedly increased and the EDTA fraction also increased while the external Ca2+ concentrations scarcely affect the Cd2+ contents in both fractions. 4. Cd2+ did not affect the cellular Na+ and K+ contents. 5. These results suggest that Na+ strongly relates with these fractions but Na+ pump does not contribute to these phenomena.

Animals↗
PubMed1989

Effects of inhaled cadmium on breathing in the mouse.

Effects of intranasally administered cadmium (3.67 micrograms Cd approximately 36.7 mg per mouse) on breathing were investigated in mice under pentobarbital anesthesia. Cd levels found in the respiratory tract were dependent on the amount administered. Cd mainly caused degeneration and desquamation of the bronchial epithelium and pulmonary congestion, while the carrier solvent had no effects. On the other hand, the carrier solvent decreased respiratory frequency and enhanced its amplitude. These effects were absent 24 h later. However, Cd strongly affected respiration; frequency and amplitude were decreased and recovery at 24 h was not complete at the higher concentrations. These effects by Cd on respiration were dependent on the concentration of administered Cd and the Cd level in lung. Therefore, these results suggest that intranasally administered Cd has inhibitory effects on mouse respiration, perhaps owing to its acute toxicity to pulmonary tissues.

Administration, Inhalation↗
PubMed1989

[Synergistic effect of irsogladine maleate and histamine H2-receptor antagonists on experimental gastric ulcers in rats].

Effects of irsogladine maleate (IM), in combination with histamine H2-receptor antagonists or a muscarinic receptor antagonist, on the formation of stress ulcer were investigated in rats. The ED50 of IM and that of cimetidine for suppressing stress ulceration were remarkably reduced when these drugs were used in combination. ED50s in this case were less than the theoretical values calculated on the basis of additive action, thereby suggesting the synergistic effect of IM and cimetidine. The synergistic effect of IM and ranitidine or famotidine in suppressing stress ulceration was also observed, while IM and pirenzepine did not always produce a synergistic effect. In addition, for acetic acid-induced gastric ulcers, combined administration of IM and cimetidine also markedly potentiated ulcer healing. The marked synergistic potentiation of IM and histamine H2-receptor antagonists may be due to compensatory coordination of both drugs on the gastric secretion and mucosal microcirculation. These results suggest that the combination of IM and histamine H2-receptor antagonists may be beneficial in clinical gastric ulcer therapy.

Animals↗
PubMed1989

Inhibition of H+,K+-ATPase by methyl(E)-2-(3,4-dimethoxystyryl)-benzimidazole-4-carboxylate (ALE-36).

ALE-36, as well as omeprazole and SCH 28080, markedly inhibited the [14C]aminopyrine (AP) accumulation induced by dibutyryl cyclic AMP (dbcAMP) and H+,K+-ATPase activity in a concentration-dependent manner. The inhibitory effect of omeprazole on the dbcAMP-induced [14C]AP accumulation was reversed by treatment with beta-mercaptoethanol, but those of ALE-36 and SCH 28080 were not. ALE-36 and SCH 28080 did not inhibit dog renal Na+,K+-ATPase activity, while omeprazole and ouabain did inhibit this enzyme activity. These results suggest that the inhibitory action of ALE-36 on acid secretion is due to the specific inhibition of gastric H+,K+-ATPase, the manner being different from in the case of omeprazole.

Adenosine Triphosphatases↗
PubMed1989

Effects of ALE-36 on gastric secretion, and gastric and duodenal ulcers induced in rats.

We examined the antisecretory and anti-ulcer effects of ALE-36 in rats. ALE-36 (3-30 mg/kg) dose-dependently inhibited gastric acid secretion in pylorus-ligated rats. However, the agent apparently increased the volume of gastric juice, and the Na+ and Cl- ion outputs. These changes were almost completely prevented by pretreatment with indomethacin, suggesting that endogenous prostaglandins in the gastric mucosa mediated the changes. Pretreatment with ALE-36 (3-30 mg/kg) inhibited the development of stress-, aspirin-, and indomethacin-induced gastric lesions, and mepirizole-induced duodenal ulcers. Repeated administration of ALE-36 significantly accelerated the healing of gastric ulcers induced by thermocautery.

Animals↗
PubMed1988

Effects of zinc and EDTA on tissue cadmium in various smooth muscles in rabbit and guinea-pig.

1. The effects of zinc (Zn2+) and ethylenediaminetetra-acetic acid (EDTA) on tissue cadmium (Cd2+) were investigated in the smooth muscles of rabbit trachea, taenia coli, aorta and guinea-pig taenia coli. 2. After an Cd uptake in high-K2+ solution, samples were rinsed with cold high-K2+, cold Zn2+ or cold EDTA solution without Cd2+ and the results were quantitatively different from each other. 3. Concentration-response curves were obtained with each treatment of cold solution. 4. It is suggested that tissue Cd2+ can be divided into 3 fractions in the surface membrane and there is another fraction in cellular space.

Animals↗
PubMed1987

[Protective effect of dicloguamine maleate (MN-1695) on HCl-induced gastric mucosal damage in rats--histologic studies].

Effect of MN-1695, a new cytoprotective antiulcer agent, on 0.2 N HCl-induced gastric surface epithelial cell damage was investigated by optical and transmission electron microscopy in rats. Tissue examination after five minutes exposure to 0.2 N HCl showed extensive damage of the surface epithelial cells: dilatation of intercellular spaces including marked edema of lamina propria. It was found that MN-1695 (3 mg/kg) pretreatment prevented such 0.2 N HCl-induced damage of the surface epithelial cells, and it reduced the percentage of damaged mucosa, but not significantly.

Animals↗