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Biomedical subjects

R Saito

Publications and source records attributed to R Saito.

At least 289 records · Page 16Linked to original sources
PubMed1985

Effect of photooxidation on catalytic and regulatory properties of NAD-linked malic enzyme from Escherichia coli.

In an aim to elucidate the structure-function relationship of NAD-linked malic enzyme [EC 1.1.1.38] from Escherichia coli W, the effect of chemical modification on the catalytic and regulatory properties of the enzyme was studied. Upon photooxidation of the enzyme in the presence of methylene blue, a time-dependent inactivation occurred following pseudo-first order kinetics. The pH-dependence of the inactivation rate exhibited a pK value of 6.1. L-Malate, NAD+, and Mn2+ markedly protected the enzyme against the inactivation. Prior masking of the catalytically essential sulfhydryl groups with p-mercuribenzoate did not result in a retardation of the rate of photoinactivation. This excluded the possibility of an involvement of sulfhydryl group modification in the photoinactivation. Although the Km values for L-malate and NAD+ were not affected by photooxidation, the S0.5 value and the Hill coefficient for Mn2+ were considerably altered, and the cooperative nature of the saturation profile for Mn2+ in the native enzyme was completely abolished. The activating effect of L-aspartate on the native enzyme was completely abolished upon photooxidation, and the inhibitory effect of CoA was also diminished to a marked extent upon the treatment. The oxaloacetate decarboxylating activity of the enzyme was lost in parallel with the loss of the activity for oxidative decarboxylation of L-malate. These results suggest a possible involvement of histidyl residue(s) in the catalytic and regulatory functions of the enzyme.

Escherichia coli↗
PubMed1985

Non-Hodgkin's lymphoma of the esophagus.

A case of non-Hodgkin's lymphoma of the esophagus in a 82-year-old woman is presented. the esophageal lesion revealed a variety of macroscopic manifestations including giant rugae, submucosal nodules, multiple erosions, and craters. The patient died 7 months after diagnosis. The esophageal involvement was considered to be primary.

Aged↗
PubMed1984

Adenosquamous carcinoma of the prostate.

An unusual adenosquamous carcinoma originating in the prostate of a 70-year-old man is described. Four years prior to the development of this lesion, a diagnosis of adenocarcinoma had been established by needle biopsy and the patient had been treated with radiation. Light microscopic examination revealed a pattern of adenocarcinoma predominant in the periurethral region and squamous cell carcinoma at the periphery. The latter neoplastic component involved the bladder and rectum and extended to the pelvic wall. Immunoperoxidase staining for prostatic acid phosphatase occurred in both cellular components, and electron microscopic examination confirmed the squamous differentiation of tumor cells.

Adenocarcinoma↗
PubMed1984

Bile salt stimulation of colonic epithelial proliferation. Evidence for involvement of lipoxygenase products.

Prostaglandin E2 (PGE2) and several other prostaglandins synthesized by colon suppress the proliferative activity of colonic epithelium. However, bile salts stimulate colonic epithelial proliferation despite the actions of bile salts to enhance the release of arachidonate and consequent colonic synthesis of PGE2. The current study was conducted to assess whether bile salt-induced increases in colonic formation of arachidonate metabolites other than PGE2 were linked to the stimulation of the proliferative activity of colonic epithelium. Within 10 min of addition, deoxycholate markedly stimulated the in vitro release of [14C]arachidonate from prelabeled rat colon. When given in vivo by intracolonic instillation deoxycholate (10 mumol) increased colonic accumulation of immunoreactive prostaglandin E (PGE), thromboxane B2 (TXB2), and the lipoxygenase product 12-hydroxyeicosatetraenoic acid (12-HETE) by two to fourfold over control in 30 min. This effect of intracolonic deoxycholate was followed by a ninefold increase in mucosal ornithine decarboxylase activity (4 h), and a subsequent two to threefold increase in [3H]thymidine [( 3H]Thd) incorporation into DNA of either mucosal scrapings or isolated pools of proliferative colonic epithelial cells (24 h). Intracolonic instillation of indomethacin (50 mumol) suppressed to low or undetectable levels both basal colonic accumulation of PGE and TXB2 and the increases in each parameter induced by subsequent instillation of deoxycholate. By contrast, indomethacin enhanced accumulation of 12-HETE in both control colons and those subsequently exposed to deoxycholate. The increases in 12-HETE induced by indomethacin alone were correlated with stimulation of mucosal ornithine decarboxylase activity and [3H]Thd incorporation into mucosal DNA. Indomethacin also enhanced the increases in these parameters induced by deoxycholate. Intracolonic instillation of phenidone (25-100 mumol) suppressed accumulation of PGE, TXB2, and 12-HETE in control colons and the increases in these parameters induced by a subsequent instillation of deoxycholate. Phenidone alone did not alter mucosal ornithine decarboxylase activity or [3H]thymidine incorporation into mucosal DNA. However, phenidone suppressed or abolished increases in these parameters induced by a subsequent instillation of deoxycholate. 4-(2-[IH-imidazol-1-yl]ethoxy) benzoic acid hydrochloride UK 37,248, which selectively reduced colonic TXB2 to undetectable levels without altering PGE or 12-HETE, had no effect on control or deoxycholate-induced increases in mucosal ornithine decarboxylase activity or [3H]Thd incorporation into DNA. Neither indomethacin nor phenidone altered the increases in [(14)C]arachidonate release induced in vitro by deoxycholate. Chenodeoxycholate and cholate also stimulated [(14)C]arachidonate release from colon in vitro within 10 min, and increased colonic 12-HETE (30 min) and mucosal ornithine decarboxylase activity (4 h) upon intracolonic installation. Prior installation of phenidone inhibited the increases in both 12-HETE and ornithine decarboxylase activity induced by these bile salts. The results support a role for bile salt-induced increases in colonic accumulation of lipoxygenase products, as reflected by 12-HETE, in the subsequent stimulation of the proliferative activity of colonic epithelium.

Animals↗
PubMed1984

A ten-year experience with surgical resection for patients with metastatic lung tumors.

Removal of metastatic lung tumor was performed for 27 patients in a period from January, 1972 to December, 1981. They included 22 carcinomas and 5 sarcomas. Diagnosis as having lung metastasis was made after removal of the primary tumor in 18 patients and at the time of the first detection of the primary tumor in 4 patients. In 5 patients the operation for the metastatic tumor preceded that for the primary malignancy. Metastatic tumors were localized in one lobe in 13 patients. Thirteen of the 27 patients underwent lobectomy and 14 received other types of operation, with or without hilar and/or mediastinal lymphnode dissection. Four patients underwent bilateral thoracotomy. Survival rates at 3 and 5 postoperative years of the group of patients who underwent the operation for primary malignancy first were both 49 percent. The number of lesions removed or the type of operation did not seem to have correlations with the survival rate. Patients whose tumor-free interval was more than 40 months tended to survive longer than those who had an interval less than 40 months. The group with a tumor doubling time of more than 50 days showed a higher survival rate than the group with a doubling time of less than 50 days. Of the 4 patients thoracotomized bilaterally 2 are alive for 20 and 34 months postoperatively, while the other 2 died at 20 and 65 months after the operation. In the selected patients with metastatic lung tumors, surgical treatment can be conducted with a reasonably good result, even though the metastatic malignancy is multiple or bilateral.

Carcinoma↗
PubMed1984

Rejection monitoring by lymphocyte blastogenesis assay in canine lung allotransplantation.

Seventy-seven adult mongrel dogs underwent left lung transplantation to study the immunological detection of posttransplant rejection response using the lymphocyte blastogenesis assay. Experimental animals were divied into 3 groups; control autotransplantation (4 dogs), control allotransplantation (32 dogs) and immunosuppressed allotransplantation (41 dogs). The lymphocyte blastogenesis assay included mixed lymphocyte reaction (MLR), lymphocyte reactivity to lectins (PHA, ConA and PWM) and spontaneous blastogenesis in peripheral lymphocyte culture methods. The latter two tests were performed in serial blood samples up to the 38th posttransplant day. In the control autotransplant group there were no particular changes in posttransplant PHA reactivities. In the animals with lung allograft, results of preoperative MLR between donor and recipient showed no particular relationships to posttransplant rejection response. The recipient, however, showed a decreased response to PHA and an increased spontaneous blastogenesis at the period undergoing rejection which were confirmed by blood samples taken within 2 days before sacrifice of animals whose transplant specimens showed apparent histologic findings of rejection. In the immunosuppressed allotransplantation group, those findings of PHA response and spontaneous blastogenesis had often preceded the rejection episode detected on chest x-ray films, whereas there were no particular changes in both parameters of dogs bearing enhanced allografts. The serial detection of spontaneous blastogenesis and PHA reactivity in peripheral lymphocyte may be one of the useful methods for early prediction of rejection episode in lung transplantation.

Animals↗
PubMed1983

Forskolin-induced cyclic AMP production and gastric acid secretion in dispersed rabbit parietal cells: novel evidence for a major role of cyclic AMP in acid release.

Forskolin, a unique diterpine which is a direct activator of cyclic AMP-generating systems, stimulated both cyclic AMP and acid production in dispersed rabbit parietal cells. This agent was also capable of augmenting the action of histamine on both cyclic AMP and acid production at a low concentration. These findings provided novel evidence for a major role of cyclic AMP in gastric acid secretion.

Animals↗
PubMed1983

Effect of acid perfusion of the terminal ileum on plasma immunoreactive secretin and pancreatic secretion in the rat.

The distribution of immunoreactive secretin in acid extracts of the alimentary tract of the rat was determined. It was found to be contained in higher concentrations in the duodenum and in the terminal ileum than in other parts of the intestine. To elucidate the possible role of secretin contained in the terminal ileum, this part of the intestine was perfused with hydrochloric acid, a potent secretin secretagogue, and changes in plasma immunoreactive secretin levels and in pancreatic secretion were investigated in anaesthetized rats. Plasma immunoreactive secretin was increased from 65 +/- 5 pg/ml to 108 +/- 13 pg/ml during a 10 minutes perfusion with hydrochloric acid. This was significantly higher than that of saline perfusion but significantly lower than that of duodenal perfusion with hydrochloric acid. Acid perfusion of the terminal ileum also caused a three-fold increase in pancreatic flow rate and a twofold increase in bicarbonate concentration. These results suggest that the terminal ileum, through release of secretin, might play a role in regulating the pancreatic secretion of water and bicarbonate in response to changes in intraluminal fluids in the distal intestine in the rat.

Animals↗
PubMed1983

Role of local prostaglandin synthesis in the modulation of proliferative activity of rat colonic epithelium.

The role of local prostaglandin (PG) synthesis in the modulation of the proliferative activity of colonic epithelium was examined in rat colon. Experimental rats were given either indomethacin (5 mg/kg s.c. every 8 h for three doses) or aspirin (0.5 g/100 g diet for 3 d). In rats treated with indomethacin or aspirin, the incorporation of [3H]thymidine (dThd) into DNA in vivo was increased approximately twofold over control in mucosal scrapings from distal colon, and approximately threefold over control in the proliferating pool of epithelial cells isolated from distal colon. [3H]dThd incorporation into DNA was also examined ex vivo immediately after distal colonic resection. It was approximately twofold higher in mucosa of colonic segments (1-h incubation) from rats treated with indomethacin or aspirin in vivo, compared with corresponding values of segments from control rats. Immunoreactive (i) prostaglandin E (PGE), the dominant PG product of colon segment incubates by high-performance liquid chromatography analysis of [14C]arachidonate metabolites, was markedly (95%) reduced in the media of 1-h colon incubates from indomethacin- or aspirin-treated rats, compared with control rats. Moreover, the cyclic (c)AMP content of mucosa of segments from indomethacin- or aspirin-treated rats was significantly lower than that of control rats. Prolonged incubation (4-24 h) of colonic segments from indomethacin-treated rats, in the absence of indomethacin in vitro, led to an eventual return of [3H]dThd incorporation into DNA, iPGE, and mucosal cAMP to control values. Conversely, inclusion of indomethacin (0.25 mM) in the incubations (6 h) of colonic segments from indomethacin-treated rats resulted in persistent suppression of iPGE and mucosal cAMP, as well as persistent enhancement of [3H]dThd incorporation into mucosal DNA. However, incubation of colonic segments from control rats (no in vivo drug exposure) with indomethacin or aspirin in vitro for periods up to 24 h failed to alter DNA synthesis, despite marked reduction in media iPGE and lower mucosal cAMP. The latter observations suggested that additional in vivo factors initiated the enhancement of DNA synthesis in indomethacin- or aspirin-treated rats. Exogenous PGE2, D2, I2, or F2 alpha, each of which increased the endogenous mucosal cAMP content of incubated colonic segments from control, indomethacin- or aspirin-treated rats, all suppressed [3H]dThd incorporation into mucosal DNA in vitro. Dibutyryl cAMP, but not dibutyryl cGMP, had an analogous suppressive effect on in vitro [3H]dThd incorporation into DNA. Thus, the present observations are consistent with an inhibitory action of endogenous colonic PG synthesis on the proliferative activity of colonic epithelium. This action may be mediated through cAMP.

Animals↗