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Biomedical subjects

Y Kawabe

Publications and source records attributed to Y Kawabe.

At least 181 records · Page 10Linked to original sources
PubMed1989

Fluctuation of the mucosal hydroxyproline content in compound 48/80-induced gastric lesions in rats.

Extensive gastric mucosal lesions were observed after i.p. administration of compound 48/80 (0.75 mg/kg) for 3 days to rats. The mucosal hydroxyproline content was significantly increased at 4 h after the last injection of compound 48/80 and subsequently decreased as the lesions were healed. Treatment with cimetidine (50 mg/kg, i.p.) did not prevent compound 48/80-induced gastric lesions. The increase in the mucosal hydroxyproline content was significantly reduced by treatment with cimetidine. This fact suggested that cimetidine might have an inhibitory effect on the regeneration of connective tissue.

Animals↗
PubMed1989

The role of prostaglandin D2 in the genesis of indomethacin-induced gastric lesions in rats.

Four kinds of prostaglandins (PGs), 6-keto-PGF1 alpha, PGF2 alpha, PGE2 and PGD2, in rat gastric mucosa were decreased at 1 or 6 h after oral administration of indomethacin (2 or 12 mg/kg). With 2 mg/kg of indomethacin, the PG levels had slightly recovered 6 h later. Gastric lesions were observed 6 h after administration of indomethacin (12 mg/kg), but not with 2 mg/kg. Omeprazole (20 mg/kg, i.p.) prevented ulcer formation caused by indomethacin, without improvement of the reduced gastric mucosal PG levels. PGD2 (0.5 mg/kg, p.o.) reduced indomethacin-induced gastric lesions and considerable amounts of PGD2 existed in the gastric mucosa. We conclude that H+ is a determining factor in the genesis of indomethacin-induced gastric lesions and persistent decreases in tissue PG levels also participate in ulcer formation.

Animals↗
PubMed1989

[Hyperamylasemia in acute exacerbation in patients with chronic respiratory failure].

Serum amylase level was examined in 129 cases (225 episodes) of chronic respiratory failure at acute exacerbation, and in 59 cases (62 episodes) of pneumonia without respiratory failure as a control. Cases accompanying diseases, such as acute pancreatitis, parotiditis, ileus, and renal dysfunction, which were expected to develop hyperamylasemia were excluded. The 225 episodes were divided according to the cause of acute exacerbation into 4 groups: pneumonia, bronchitis, right heart failure without infection, and others (e.g. hemoptysis). Hyperamylasemia (greater than 400 S-U) was observed in groups of pneumonia (15/40 = 35.5%) and of bronchitis (12/95 = 12.6%) respectively, but not in those of right heart failure without infection (0/73 = 0%) and others (0/17 = 0%). As a result, hyperamylasemia was found only under conditions of inflammation of lung parenchyma and bronchi with acute exacerbation of respiratory failure. On the other hand no hyperamylasemia was observed in 62 episodes of only pneumonia without respiratory failure. It was concluded that both respiratory tract infection and acute respiratory failure are necessary factors for development of hyperamylasemia originating from lung or bronchi.

Aged↗
PubMed1989

Effects of the synthesized prostaglandin E2-analogue arbaprostil on gastric mucosal lesions in rats.

The effects of arbaprostil (CU-83), a newly synthesized prostaglandin (PG) E2 analogue, on gastric lesions were investigated. Experiment 1: The animals were divided into 3 groups: 1. the control group: untreated, 2. 50% ethanol group: rats were given 1 ml of 50% ethanol intragastrically, and 3. arbaprostil + 50% ethanol group: arbaprostil (10 micrograms/kg) was administered p.o. 30 min before 50% ethanol administration. 1 h after ethanol administration, stomachs were isolated, and gastric mucosal lesions were observed. Experiment 2: Rats were divided into 4 groups; 1. the control group; untreated, 2. 6 h stress group; animals were placed in a stress cage and immersed into a water bath (23 degrees C) for 6 h, 3. arbaprostil (10 micrograms/kg) + 6 h stress group, and 4. arbaprostil (100 micrograms/kg) + 6 h stress group; arbaprostil 10 micrograms/kg or 100 micrograms/kg was administered 30 min before 6 h of water immersion stress, respectively. In each experiment, stomachs were isolated and gastric mucosal lesions were observed. Immediately after the observation of lesions, the fundic mucosal layer was separated from the muscle layer, and mucosal PGs levels were measured by high performance liquid chromatography. Four kinds of PGs, i.e., 6-keto-PG F1 alpha, PGF2 alpha, PGE2, and PGD2 were detected in gastric mucosa. Administration of 50% ethanol and water immersion stress induced gastric lesions and decreased all 4 mucosal PGs levels. Arbaprostil, 10 micrograms/kg, reduced ethanol-induced gastric lesions and maintained mucosal PGs levels, concomitantly, however, the same doses of arbaprostil did not show a protective effect against water immersion stress-induced gastric lesions or decreases in PGs levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[Results of radiotherapy in carcinoma of the larynx].

Long-termed treatment results have been analysed in 224 previously untreated patients with a squamous cell carcinoma of the larynx who were given irradiation for curative therapy. The 5-year cumulative local control rates of T1NO and T2NO cases with phonation were 80.9% and 74.1%, respectively and a total laryngectomy was chiefly performed for the recurrent cases. The 5-year cumulative local control rates with of without phonation were 97.0% and 91.8%, respectively. The introduction of a multi-disciplinary treatment was found necessary for the locally advanced cases (T4 or N3 cases), because of a low local control rate (about 25%) from radiotherapy alone.

Adult↗
PubMed1989

Genesis and recovery of ethanol-induced gastric lesions in rats: possible involvement of prostaglandin D2.

We investigated the different effects of administration of high and low concentrations of ethanol (from 3% to 50%) on gastric mucosa in rats in relation to the changes in prostaglandin (PG) levels. Gastric lesions were induced by 50% ethanol, and all kinds of PGs were significantly decreased 1 h after administration, concomitantly. Thirty percent ethanol did not induce gastric lesions and had no effects on PG levels. Five percent ethanol significantly increased 6-keto-PGF1 alpha, PGF2 alpha, and PGE2 levels. Ten percent ethanol increased significantly PGD2 level. Premedication with sucralfate protected significantly gastric mucosa against 50% ethanol, and maintained PG levels, concomitantly. We also investigated the recovery time course of gastric lesions by 50% ethanol. Gastric lesions did not recover significantly after 24 h, recovered considerably after 48 h, and fully after 96 h. Levels of 6-keto-PGF1 alpha, PGF2 alpha, and PGE2 were fully recovered 24 h after exposure to 50% ethanol; however, a significant decrease in PGD2 level still was observed. PGD2 was recovered significantly after 48 h. These results indicate that different concentrations of ethanol induce different effects on gastric mucosal PGs, and that not only PGE2, but also other PGs, especially PGD2, might be linked with the genesis and recovery of gastric lesions by 50% ethanol.

Animals↗
PubMed1988

The effect of a new gastric proton pump inhibitor on serotonin-induced gastric mucosal lesions in rats.

The anti-ulcer effect of NC-1300, a new proton pump inhibitor, and its effect on gastric mucosal blood flow were studied in rats. Acute gastric mucosal lesions were induced by the subcutaneous administration of serotonin, 20 mg/kg. Using the electrolytically generated hydrogen gas clearance technique, it was determined that such gastric ulceration resulted mainly from a decrease in gastric mucosal blood flow. These lesions could be inhibited to a statistically significant extent by the intravenous administration of NC-1300, 20 mg/kg, which markedly inhibited gastric acid secretion. However, the serotonin-induced decrease in gastric mucosal blood flow could not be prevented by pretreatment with 20 mg/kg of NC-1300. It was concluded that protection against serotonin-induced gastric ulceration can be achieved by markedly inhibiting gastric acid secretion.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1988

Natural killer and natural killer-like cell activity of peripheral blood and intrathyroidal mononuclear cells from patients with Graves' disease.

This study was undertaken to investigate the natural killer (NK) and natural killer-like (NK-like) cell cytotoxic activity toward autologous thyrocytes of peripheral blood mononuclear cells (PB-MNC) and thyroid gland mononuclear cells (TG-MNC) from previously hyperthyroid patients with Graves' disease, and the effects of recombinant interleukin-2 on such cytotoxic activity. The average cytotoxicities of PB-MNC from Graves' patients toward K562 cells (NK-sensitive cells), Raji cells (NK-resistant cells), and autologous thyrocytes were 23.9 +/- 10.8 (+/- SD) lytic units (LU), 7.4 +/- 3.8 LU, and 11.7 +/- 4.4 LU, respectively. There were no differences in the NK and NK-like cell activity of PB-MNC between Graves' disease patients and normal subjects. In contrast to PB-MNC from patients with Graves' disease, NK and NK-like cell activity was markedly decreased in TG-MNC (NK cell activity, 2.1 +/- 2.3 LU; NK-like cell activity, 1.5 +/- 1.5 LU). TG-MNC from Graves' patients had no cytotoxic activity against autologous thyrocytes. Using the monoclonal anti-Leu 7 and anti-CD16 antibodies and a two-color immunofluorescence method, the NK cell subsets were examined in PB-MNC and TG-MNC from Graves' patients. The percentage of CD16+ cells was significantly decreased in TG-MNC compared to PB-MNC, whereas there was no significant difference in the percentage of Leu 7+ cells between PB-MNC and TG-MNC. Incubation of TG-MNC with medium only did not increase the NK and NK-like cell activity of these cells. Furthermore, incubation of autologous PB-MNC with supernatants of minced thyroid tissues did not alter their NK and NK-like cell activity. The decreased NK and NK-like cell activity of TG-MNC was augmented when these cells were incubated with recombinant interleukin-2. These results suggest that the reduction of NK cell activity in TG-MNC may allow perpetuation of B-cell activation and lead to excessive production of autoantibody in thyroid tissue.

Adolescent↗
PubMed1988

Phenotypic analyses and concanavalin-A-induced suppressor cell dysfunction of intrathyroidal lymphocytes from patients with Graves' disease.

The expression of phenotypic markers and Concanavalin-A-induced suppressor activity was compared among mononuclear cells isolated from thyroid glands and peripheral blood of thionamide-treated patients with hyperthyroid Graves' disease and peripheral blood from normal subjects. Intrathyroidal lymphocytes were obtained by two different methods (TG-1 and TG-2 cells), gradient centrifugation of supernatants of minced thyroid tissue and overnight culture of thyroid debris after mechanical disaggregation and enzymatic digestion, respectively. The percentages of CD3+ cells (all mature T cells) among peripheral blood and TG-1 and TG-2 cells from Graves' patients were similar, but the percentages of B1+ cells (pan B cells) among the TG-1 and TG-2 cells were markedly increased compared to that in peripheral blood. The percentages of CD4+ cells among the TG-1 and TG-2 cells were significantly less than that in peripheral blood. The percentages of CD4+2H4+ cells among CD4+ cells in TG-1 and TG-2 cells also were significantly less than that in peripheral blood. The percentage of CD4+4B4+ cells among CD4+ cells in thyroid glands was markedly higher than that in peripheral blood. The percentages of CD8+ cells and CD8+CD11b- cells (cytotoxic T cells) in thyroid glands were significantly higher than those in peripheral blood from Graves' patients and peripheral blood from normal subjects. The CD8+CD11b+ cells were subdivided into two subpopulations on the basis of CD8 antigen density. The percentage of dull CD8+CD11b+ cells (natural killer cells) among TG-2 cells was lower than that in peripheral blood, but there was no significant difference in bright CD8+CD11b+ cells (suppressor-effector T cells) between thyroid glands and peripheral blood. The percent suppression induced by Concanavalin-A in both TG-1 and TG-2 cells was significantly decreased compared with that in peripheral blood. These results suggest that impairment of suppressor cell activity and an increased number of B cells exist in thyroid glands of patients with Graves' disease compared to those in peripheral blood. It, thus, appears likely that both B cell hyperactivity and suppressor T cell dysfunction may induce excess production of autoantibodies in the thyroid glands of such patients.

Adolescent↗
PubMed1988

The effects of cytokines, antithyroidal drugs and glucocorticoids on phagocytosis by thyroid cells.

The present study was undertaken to examine whether thyrocytes possess phagocytic activity and whether the phagocytic activity is influenced by cytokines, such as interleukin 1, 2 (IL 1, IL 2) and interferon-alpha, -beta, and -gamma (IFN-alpha, beta, and gamma), and drugs, such as methimazole and dexamethasone. Thyroid glands were obtained from patients with Graves' disease. Thyrocytes were prepared by collagenase digestion. Thyrocytes were pre-incubated in the presence or absence of cytokines and drugs at 37 degrees C for 20 h and were further incubated with fluoresceinated latex beads at 37 degrees C for 60 min. The number of phagocytic thyrocytes was determined by FACS IV. Phagocytosis of latex beads was indeed seen within thyrocytes and gradually increased in a time-dependent manner. The rate of phagocytosis in thyrocytes was extremely slow as compared with that in macrophages. Phagocytic activity was detected in thyrocytes from patients with Graves' disease and from normal thyroid tissue adjacent to thyroid cancer. Phagocytosis was inhibited by IL 1, but was enhanced by IL 2. Although the enhanced phagocytosis with IFN-beta was consistently seen, little effect was detected with IFN-alpha and -gamma. Both methimazole and dexamethasone markedly inhibited phagocytosis. These results indicated that thyrocytes had phagocytic properties and that their phagocytic activity was modulated by cytokines, antithyroidal drugs and dexamethasone.

Antithyroid Agents↗
PubMed1988

Action spectrum for UV erythema and reproduction of the skin lesions in hydroa vacciniforme.

Action spectra for UV erythema and reproduction of the skin lesions in 4 patients with hydroa vacciniforme (HV) were studied. Vesicles were successfully reproduced by repeated daily monochromatic irradiations of 330, 340, 350 and 360 nm for 5, 6 or 7 days. The daily doses were equivalent to global solar radiation for 70-190 min. The vesicles produced were identical to those of HV, macroscopically and histologically. Repeated daily exposures to a small dose of UVA produced vesicles, whereas a large but single exposure to UVA failed to do so. Daily exposures to UVB failed to produce the vesicles. The minimal erythema dose (MED) was lower than the minimum limits of the normal persons in the 290-310 nm range.

Adolescent↗
PubMed1988

Photosensitive lichenoid reaction accompanied by nonphotosensitive subacute prurigo caused by carbamazepine.

A 58-year-old man developed a lichenoid reaction on light-exposed areas and subacute prurigo separate from the sun-exposed areas after receiving 200 mg of carbamazepine daily for one year. The difference action spectrum for erythema with or without ingesting the drug ranged from 250 to 390 nm with peaks at 260 and 290 nm. A positive photoingestion test was obtained after administering 2 mg of carbamazepine orally in one dose. Patch test with carbamazepine was negative, while photopatch test with carbamazepine was positive. Positive intracutaneous test was obtained with an irradiated mixture of human serum albumin and carbamazepine at 24 h and 48 h after injection. This patient appeared to be a case of photosensitive lichenoid reaction accompanied by nonphotosensitive subacute prurigo caused by carbamazepine.

Acute Disease↗
PubMed1988

Synergy in antigen presentation by thyroid epithelial cells and monocytes from patients with Graves' disease.

The present study was undertaken to examine the ability of thyrocytes from Graves' patients to present purified protein derivative (PPD) to autologous peripheral blood T cells. Normal human thyrocytes which were pre-cultured with interferon-gamma were able to induce the proliferation of T cells in response to PPD antigen, but unstimulated thyrocytes failed to do. Thyrocytes from Graves' patients on which HLA-DR antigens were expressed have an ability to induce the proliferation of T cells. Thyrocytes from Graves' patients which were pulsed with PPD antigen for 4 h were capable of stimulating proliferation of the T cells. However, the stimulation index of T cells co-cultured with thyrocytes and PPD were significantly lower than that of T cells co-cultured with monocytes and PPD. Sub-optimal numbers of monocytes which by themselves were unable to support T-cell proliferation synergistically augmented antigen presentation by thyrocytes. These results suggest that cellular interactions among thyrocytes, monocytes and T cells may perpetuate immune or autoimmune responses in thyroid tissues from Graves' patients.

Adolescent↗