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Biomedical subjects

T Ohno

Publications and source records attributed to T Ohno.

At least 703 records · Page 39Linked to original sources
PubMed1987

16,16-Dimethyl prostaglandin E2 protects gastric mucosal surface epithelial cells from indomethacin-induced damage in rats.

The protective effect of 16,16-dimethyl prostaglandin E2 (dmPGE2) against early damage induced by indomethacin in the rat gastric mucosal surface epithelial cells was studied using a scanning electron microscope. Indomethacin (10 or 25 mg/kg, p.o.) induced a widespread exfoliation of the surface epithelial cells and an exposure of the lamina propria both in the corpus and antrum within 1 hr after the administration. Pretreatment with dmPGE2 (0.3, 3 or 30 micrograms/kg, p.o.) 30 min before indomethacin (25 mg/kg) dose-dependently inhibited these damages. The effects of dmPGE2, at least on the surface epithelial cells in the corpus, appear to be related to the prevention of damage formation itself and is unrelated to the enhancement of reconstitution of once damaged mucosa. Enhanced gastric motility by indomethacin was potently inhibited by pretreatment with 3 and 30 micrograms/kg of dmPGE2, but not with 0.3 micrograms/kg. dmPGE2 pretreatment (30 micrograms/kg) significantly decreased the absorption of indomethacin (25 mg/kg) when determined 10 min after giving indomethacin, but did not affect it when determined 30 and 60 min later. We conclude that dmPGE2 protects gastric mucosal surface epithelial cells from indomethacin injury at an early stage, partly by inhibiting gastric motility.

16,16-Dimethylprostaglandin E2↗
PubMed1987

Effects of 16,16-dimethyl prostaglandin E2 on surface epithelial cell damage in the rat stomach induced by vagal nerve stimulation.

The effect of 16,16-dimethyl prostaglandin E2 (dmPGE2) on gastric surface epithelial cell (SEC) damage induced by vagal nerve stimulation (VS) in urethane-anesthetized rats was studied using scanning electron microscopy. VS (1.25-10 Hz, 0.2 mA, 2 msec, 10 min) resulted in a graded increase in the SEC damage, increased gastric contractions, increased gastric acid secretion, and a decrease in heart rate. Pretreatment with dmPGE2 (0.3-30 micrograms/kg, s.c.) significantly protected the SEC from VS-induced damage, inhibited the increase in gastric contractions and acid secretion, but had no influence on the decrease in heart rate. Atropine (1 mg/kg, s.c.) also protected the SEC from VS-induced damage and inhibited the alterations in response to VS. Timoprazole (30 mg/kg, s.c.) had no protective effects on SEC from VS-induced damage, no effect on increased gastric contractions and heart rate, but did inhibit the increase in gastric acid secretion, in response to VS. These results suggest that: VS-induced SEC damage was caused by increased gastric contractions and not by increased gastric acid secretion, and dmPGE2 protects against SEC damage by inhibiting gastric contractions.

16,16-Dimethylprostaglandin E2↗
PubMed1987

Effect of 16,16-dimethyl prostaglandin E2 on gastric surface epithelial cell damage induced by 20% ethanol in rats.

Prostaglandins protect against the gross damage of gastric mucosa induced by 50-100% ethanol, but do not protect surface epithelial cells (SEC) from necrosis. Since this induced damage to SEC is so severe, we attempted to determine the effects of a prostaglandin on slightly induced SEC damage and gastric potential difference (PD) in response to low concentrations of ethanol. The necrotizing effects of graded concentrations of ethanol (10-50%) to SEC on the rat gastric mucosa were studied by scanning electron and light microscopy. Intragastric instillation of 20% ethanol (v/v, 1 ml/100 g body wt.) to pylorus-ligated rats for 10 min induced slight and reproducible SEC damage consisting mainly of the apical cell membrane erosion of SEC. Pretreatment with 16,16-dimethyl prostaglandin E2 (dmPGE2, 3 or 30 micrograms/kg, p.o. or s.c.) afforded protection of the SEC from 20% ethanol-induced damage. However, the cytoprotective effects of dmPGE2 were abolished when gastric contents were emptied prior to 20% ethanol instillation. Intragastric instillation of ethanol immediately reduced PD in a concentration-related manner. dmPGE2 (3 or 30 micrograms/kg, s.c.) had no effect on the reduction of gastric PD after 20% ethanol treatment and the recovery of reduced PD to normal levels. We conclude that dmPGE2 has no cytoprotective effect on 20% ethanol-induced SEC damage in rat gastric mucosa.

16,16-Dimethylprostaglandin E2↗
PubMed1987

Surface epithelial cell damage induced by restraint and water-immersion stress in rats effects of 16,16-dimethyl prostaglandin E2 on stress-induced gastric lesions.

The time-course of gastric mucosal surface epithelial cell damage and macroscopically visible lesions in response to restraint and water-immersion stress (22 degrees C) in rats was examined, and the effects on it of 16,16-dimethyl prostaglandin E2 (dmPGE2) were compared with those of papaverine, timoprazole and atropine. The stress produced surface epithelial cell damage prior to visible lesion, the former increasing in severity with time and reaching a plateau 60 min later, by which time exfoliation of surface epithelial cells was observable along the mucosal folds. In contrast, macroscopically visible lesions appeared 2 hr after stress, and severity continued to increase with time. Pretreatment injections (s.c.) of dmPGE2 (3, 30 micrograms/kg), papaverine (100 mg/kg) and atropine (1 mg/kg) protected the surface cells against stress (1 hr)-induced damage, and inhibited visible lesion formation after 4 hr stress. Timoprazole (30 mg/kg, s.c.) did not protect the surface cells, but did markedly inhibit visible lesion formation. dmPGE2, papaverine and atropine, but not timoprazole, inhibited stress-induced increases in gastric contractions. dmPGE2, timoprazole and atropine, but not papaverine, inhibited acid secretion in stress-conditions. These results indicated that stress induced damage to the gastric mucosa within 1 hr due to increased gastric contractions, and the surface epithelial cell damage developed into macroscopically visible lesions in the presence of acid, and that dmPGE2 protected the surface epithelium against stress-induced damage probably by inhibiting gastric contractions.

16,16-Dimethylprostaglandin E2↗
PubMed1987

An unsuccessful attempt to isolate human immunodeficiency virus (HIV) from patients with primary immunodeficiency diseases.

Isolation of the human immunodeficiency virus (HIV) was performed in 5 seronegative patients with primary immunodeficiency diseases (IDDs) who had no or little ability to produce antibodies and received a large amount of intravenous gammaglobulin (IVG) for a long period. In this study cultured cells were considered to be infected if the following 2 criteria were met: (1) They produced reverse transcriptase (RT) activity in the supernatant fluid and (2) expressed viral antigens. Under experimental conditions, virus was demonstrated by both RT activity and viral antigen expression detectable by immunofluorescence technique in lymphocyte cultures from 2 seropositive patients with acquired immunodeficiency syndrome-related complex who were examined as controls. There was no evidence of HIV infection in cultures of lymphocytes from all of the 5 patients with primary IDDs and from 2 healthy subjects. The above patients did not show the extremely low numbers of target T4+ cells, which make isolation of the virus in lymphocytes difficult. The present results suggest that current methods of IVG preparation either remove or inactivate HIV.

Adult↗
PubMed1987

Muscle and brown adipose tissue fatty acid profiles in cold-exposed rats.

Effects of cold acclimation and cold exposure for 25 generations on triglyceride (TG)-, total phospholipid (PL)-, and cardiolipin (CL)-fatty acid (FA) compositions were studied in the different types of skeletal muscles (red and white muscles from quadriceps, and soleus) as well as brown adipose tissue (BAT) in rats. TG: in cold-acclimated rats (CA) and rats reared in cold for 25 generations (25G) white muscle showed the decreased saturated FA (SA) and increased polyunsaturated FA (PU). In soleus of 25G, monounsaturated FA (MU) and PU increased, and SA decreased. In BAT, SA increased and MU decreased in CA, and SA and PU decreased, and MU increased in 25G. PL: in red muscle of CA, SA increased and PU decreased. In red muscle of 25G the similar but more marked changes were found accompanied by lowered arachidonic acid and unsaturation index (UI). In BAT, SA, PU, arachidonic acid, and UI increased in CA, and arachidonic acid increased in 25G. CL: in red and white muscles of 25G, oleic acid and MU increased. In BAT, arachidonic acid increased in CA and 25G, and UI increased in 25G. These results suggest that FA unsaturation of CL in the muscles as well as BAT is involved in an enhanced thermogenesis in cold-exposed rats.

Acclimatization↗
PubMed1987

Alkaline bismuth stain as a tracer for Golgi vesicles of plant cells.

An alkaline solution of bismuth subnitrate reacts well with carbohydrate-rich components of Golgi bodies in sections prepared from plant leaves fixed with glutaraldehyde and osmium tetroxide and embedded in Epon. The metal deposits formed are so fine that the stain is appropriate to ultrastructural observation at high magnification. The Golgi vesicles show polarity with respect to the localization of the reactive deposits. Golgi vesicles that had migrated farther from the Golgi cisternae showed greater reactive deposits and higher membrane contrast than those close to the Golgi cisternae. These results indicate that the alkaline bismuth stain is an excellent tracer for Golgi bodies of plant cells.

Bismuth↗
PubMed1987

Inhibitory mechanism of the proliferative responses of resting B cells: feedback regulation by a lymphokine (suppressive B-cell factor) produced by Fc receptor-stimulated B cells.

We investigated the effect of a lymphokine termed 'suppressive B-cell factor' (SBF), which is produced by FcR gamma (Fc receptor for IgG)-stimulated B cells or hybridoma TS4.44, and is known to suppress B-cell responses in vivo and in vitro by inhibiting their proliferation. Small B cells, fractionated by Percoll density gradient, from athymic nude mice (BALB/c) secreted SBF after binding EA (sheep erythrocytes sensitized with IgG mouse anti-sheep erythrocyte antibody), and the proliferation of small but not large B cells was preferentially suppressed by SBF in response to LPS in vitro. Proliferation of purified B cells from BALB/c nu/nu mice, induced by a synergistic interaction between F(ab')2 fragment of goat anti-mouse IgM antibody and B-cell stimulating factor (BSF1), was almost completely abrogated by the co-existence of SBF during the 72-hr culture period. However, the co-culture with SBF for the last 24 or 48 hr, as well as of B cells pretreated with SBF for 1 hr at 37 degrees, partially inhibited the growth response. These findings suggest that SBF operates on resting B cells and holds them in a resting state. This notion would be further supported by the fact that SBF inhibited G0-G1 transition. Taken together, we conclude that SBF acts on the early step of B-cell activation, thereby inhibiting B-cell growth. Arrest of resting B cells in the G0 phase and failure of an increase in functional receptors for BSF1 seem to be responsible for the suppression of B-cell responses.

Animals↗
PubMed1987

Selective IgM deficiency in adults: phenotypically and functionally altered profiles of peripheral blood lymphocytes.

Peripheral blood lymphocytes from four patients with selective IgM deficiency were examined phenotypically and functionally. Although B cell subpopulations determined by surface immunoglobulins were within normal or nearly normal range, T8+ cells were significantly increased and T4/T8 ratios were inverted in three patients. IgM specific hyporesponsiveness in the PWM-driven immunoglobulin production system was observed in all four patients. Ia-like antigen positive T cells were increased in two patients; both had increased Leu2a+ Leu15+ suppressor-effector cells. In addition, Leu3a+ Leu8+ suppressor-inducer cells were increased in one of these two patients. Excessive (either IgM-specific or isotype non-specific) suppressor activity of T cells and IgM specific hyporesponsiveness of non-T cells were observed in these two patients in the recombination plaque assay. Although these results showed the complexity of the pathogenesis of this syndrome, they suggested that suppressor-associated T cells may play a role in some patients with selective IgM deficiency.

Adult↗
PubMed1987

[Superovulation-induced transient hyperprolactinemia in human in vitro fertilization and embryo transfer].

To examine the effects of transient hyperprolactinemia on in vitro fertilization and embryo transfer, 61 cycles in 50 euprolactinemic ovulatory women with irreparable tubal diseases were stimulated with clomiphene (CC) alone or CC and human menopausal gonadotropin followed by human chorionic gonadotropin (hCG). Serum prolactin (PRL) increased after hCG administration with peak values of 45.4 +/- 4.2 ng/ml on the day of laparoscopic oocyte aspiration. The highest serum estradiol (E2) concentration was found on the day before PRL peak and serum progesterone (P) began to increase after hCG injection concomitant with the PRL rise. The group having 50 ng/ml or more of PRL (34 cycles) had significantly higher levels of E2 during preovulatory and early luteal phase compared to those of the group having less than 50 ng/ml of PRL (27 cycles) but there was no significant difference between the P levels in the two groups. In the higher PRL group 72 (62.1%) of 116 collected oocytes were fertilized and 6 (20.0%) conceived. In the lower PRL group 45 oocytes (58.4%) of 77 were fertilized and 3 (12.5%) became pregnant. These data suggest that elevated serum PRL concentrations may have no effect on fertilization of oocytes in vitro or embryonic development.

Adult↗
PubMed1987

Inhibitory mechanism of the proliferative response of B lymphocytes: suppression of the proliferation induced by anti-mu antibody and BSF1 by immune complexes.

We studied the effect of immune complexes (IC) on the responses of polyclonally activated murine B cells. For this, normal resting B cells were stimulated with the F(ab')2 fraction of goat anti-mouse mu-chain antibody and B-cell stimulating factor 1 (BSF1) after preculturing them with IC. Next, the relative membrane potential changes and the subsequent proliferative response were analysed. IC, particularly in antibody excess, inhibited both membrane depolarization and while those in antigen excess did poorly. Neither antigen nor antibody alone was effective. Inhibition was mediated via binding of IC to FcR gamma on B cells in a dose-dependent manner. Kinetic experiments showed that at least 6 hr was necessary for inducing the suppression of B-cell responses after binding of IC. We conclude that IC bound to FcR gamma on B cells regulates B-cell responses by acting on the initial step of activation.

Animals↗