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Biomedical subjects

R Saito

Publications and source records attributed to R Saito.

At least 271 records · Page 15Linked to original sources
PubMed1986

Relationship between loss of rat colonic surface epithelium induced by deoxycholate and initiation of the subsequent proliferative response.

Bile acids increase the proliferative activity of rat colonic epithelium. However, the mechanisms responsible are unknown. The present study examined the relationships between deoxycholate (DOC) induced surface cell sloughing, as measured by loss of DNA into the lumen and by light microscopy, and the subsequent increases in mucosal ornithine decarboxylase activity and [3H]thymidine (dThd) incorporation into mucosal DNA induced by deoxycholate. Intracolonic instillation of DOC (10 mumol; 5 mM) resulted in a progressive increase in luminal DNA content which was significant by 1 min and maximal by 1 h. No further increase in luminal DNA occurred between 1 and 4 h after DOC. Similarly, light microscopy demonstrated a progressive loss of surface epithelium between 10 min and 1 h after DOC instillation. By 4 h after DOC, the colonic mucosal surface was normal histologically. The rapid repair of the epithelial surface occurred without a detectable increase in [3H]dThd incorporation into DNA within 4 h. The latter finding thus suggested that upward migration of nondividing crypt epithelial cells rather than the rapid initiation of new DNA synthesis and new mitotic activity was responsible for surface repair. Enhanced proliferative activity of colonic mucosa, as measured by increased [3H]dThd incorporation into DNA, did occur subsequently (12 to 24 h) after instillation of DOC. The dose response of early surface cell loss and the subsequent proliferative response to DOC were identical, consistent with a link between these two DOC mediated events. However, two observations suggested that surface epithelial loss alone was not sufficient to trigger the proliferative response to DOC: intracolonic instillation of DOC followed by removal of the DOC solution at 1 h, at which time surface epithelial loss was maximal, did not result in an increase in ornithine decarboxylase activity or [3H]dThd incorporation into DNA when these parameters were assessed at 4 h or 12 to 48 h, respectively; phenidone, an antioxidant and radical scavenger, and bis[(3,5-diisopropyl-salicylato) (O,O) copper(II), a lipophilic agent with superoxide dismutase activity, abolished the DOC mediated proliferative response but did not prevent the early loss of surface cells. The results imply that events other than or in addition to surface cell loss are necessary for the expression of the action of DOC to stimulate the proliferative activity of colonic epithelium.

Animals↗
PubMed1986

The microvascular architecture of the vestibule and the endolymphatic duct and sac of the rat in vascular corrosion casts.

The blood vessels of the vestibule and the endolymphatic duct and sac (ES) of the rat were reproduced with methacrylate casting medium and observed under a scanning electron microscope. Dense capillary networks of the macula utriculi and the macula sacculi were observed. The collecting venules from the vestibule emptied into the vein of the vestibular aqueduct (VVAQ). The plexus of the vessels in the ES was triangular in shape and had anastomoses with vessels of the bone and dura and drained into the VVAQ. The posterior meningeal artery (PMA) gave off two branches to the ES. These findings supported the similarity of the vascularization of the vestibule and the ES between the human and the rat.

Animals↗
PubMed1985

Role of the central muscarinic receptor of prostaglandin I2 in cardiovascular function in rat.

The effects of injection of prostaglandin (PG) I2 into the cerebral ventricle on cardiovascular responses and their modification by intracerebroventricular (i.c.v.) pretreatment with several drugs were studied in male Wistar rats under urethane anesthesia. When injected into the ventricle, PG I2 (50 nmol/kg) caused a decrease in blood pressure and an increase in heart rate which were of short duration and were significantly inhibited by i.c.v. pretreatment with drugs, such as atropine (0.4 mumol/kg) and diphenhydramine (1 mumol/kg), having an anticholinergic effect. The similar effects induced by intravenous (i.v.) injection of PG I2 (5 nmol/kg) were not inhibited by i.v. pretreatment with these drugs. These results suggest that PG I2 play a role in regulation of cardiovascular function through central muscarinic acetylcholine receptors.

Animals↗
PubMed1985

16,16-Dimethyl prostaglandin E2 suppresses the increases in the proliferative activity of rat colonic epithelium induced by indomethacin and aspirin.

Treatment of rats with indomethacin rapidly increased ornithine decarboxylase (4 h) of colonic mucosa and [3H]thymidine incorporation into colonic mucosal deoxyribonucleic acid (DNA) (1 or 5 days) when this parameter was examined in vivo and ex vivo. The changes in colonic mucosal ornithine decarboxylase and DNA synthesis induced by indomethacin were correlated temporally with suppression of colonic prostaglandin synthesis, as assessed from ex vivo colonic production of prostaglandin E, the dominant prostaglandin product of colon. Autoradiographic studies indicated that the enhancement of proliferative activity of colonic epithelium after treatment with indomethacin for 1 day was confined to the lower third of the colonic crypt (normal proliferative zone). After 5 days of indomethacin treatment, however, there was an extension of the proliferative zone to the upper third of the colonic crypts. Concurrent treatment of rats with the stable prostaglandin E2 analogue, 16,16-dimethyl prostaglandin E2, suppressed indomethacin-induced increases in colonic mucosal ornithine decarboxylase and DNA synthesis. Concurrent administration of 16,16-dimethyl prostaglandin E2 also prevented the extension of the proliferative zone of colonic epithelium induced by 5 days of indomethacin administration. 16,16-Dimethyl prostaglandin E2 alone for 1-5 days had no detectable effects on colonic mucosal ornithine decarboxylase and DNA synthesis compared with corresponding control values. Increases in colonic mucosal DNA synthesis were also induced by treatment of rats for 5 days with aspirin (ASA). The stimulation of colonic mucosal DNA synthesis induced by ASA was significantly suppressed by concurrent administration of 16,16-dimethyl prostaglandin E2 and was also correlated with the inhibition of colonic prostaglandin synthesis by ASA. The colons of rats treated with indomethacin for 1 day or ASA for 5 days appeared normal by light microscopy. However, treatment of rats for 5 days with indomethacin resulted in mild to moderate inflammation of the lamina propria and some goblet cell depletion at the mucosal surface, but no loss of surface epithelium. The ultrastructure of the surface epithelium of the colons of rats treated with indomethacin or ASA was normal as assessed by electron microscopy. The results thus demonstrate that inhibition of local colonic prostaglandin synthesis is associated with increases in the proliferative activity of colonic epithelium, and that these increases are suppressed by administration of 16,16-dimethyl prostaglandin E2.(ABSTRACT TRUNCATED AT 400 WORDS)

16,16-Dimethylprostaglandin E2↗
PubMed1985

Recurrence of carcinoma of the oral cavity, oropharynx and maxillary sinus after radical neck dissection.

Cervical recurrence was studied in 63 patients who had undergone radical neck dissection for the treatment of carcinoma of the oral cavity, oropharynx and maxillary sinus. Over the whole series, recurrence occurred in 17 patients (27%). The rate of recurrence did not decrease in patients who remained free of carcinoma at the primary site, but was significantly lower in patients in whom elective neck dissection was performed than in those who were treated by therapeutic or secondary neck dissection. With the exception of two patients, cervical recurrence was associated with the presence of metastatic lymph nodes. Although the rate of recurrence was not affected by the number of metastatic lymph nodes, it was very high (80%) in patients having metastatic lymph nodes with histological evidence of extra-nodal spread. The results indicate that elective treatment by irradiation or surgery may be needed to reduce cervical recurrence because of a high tendency of carcinoma of the oral cavity and adjacent regions to metastasize.

Carcinoma, Squamous Cell↗
PubMed1985

Treatment of juvenile laryngeal papilloma with a combination of laser surgery and interferon.

The therapeutic results obtained from the treatment of juvenile laryngeal papillomas with combined laser surgery and alpha-type IFN treatment are reported. Three cases of papilloma occurring under four years of age were found to be of the fulminant type with a strong tendency for recurrence. The results were complete remission of papilloma in two cases and a residual trace in one case. Thus, at present, control of the disease has been successful. A combination of several modes of treatment may be necessary for a more lasting therapeutic effect. Currently, no single method has been used to treat the disease. Laser surgery and IFN are both powerful therapies for this tenacious disease.

Child, Preschool↗
PubMed1985

Temporal bone pathology in congenital anomalies of the oval window and the facial nerve.

Temporal bones of six infants with congenital ear anomalies were examined for abnormalities of the oval window and facial nerve. These temporal bones were classified into two groups according to the degree of malformation: group A, those with atresia or absence of the oval window; and, group B, those with hypoplasia of the stapes and annular ligament. Group A, consisting of five ears, were associated with severe middle ear anomalies such as the abnormal course of the facial nerve and absence of the stapes. In group B, consisting of seven ears, the stapes were present and the facial nerve presented minor anomalies such as obtuse angulation at the first genu, central migration of the geniculate ganglion cells, ectopic muscles and a wide bony dehiscence of the facial canal around the oval window. Probable origin of the anomalies in group A could mainly be due to maldevelopment of the facial nerve during an earlier embryonal period while that of group B could have developed after the ninth week of the fetal period and are mostly localized along the second branchial arch.

Abnormalities, Multiple↗