Biomedical subjects

S Tani

Publications and source records attributed to S Tani.

At least 109 records · Page 6Linked to original sources

PubMed1990

Direct inhibition of pepsinogen secretion from rat gastric chief cells by somatostatin.

Effects of somatostatin on pepsinogen secretion was investigated in the rat in vivo and in vitro. In the perfused rat stomach, somatostatin inhibited secretagogue-induced acid secretion in dose-dependent manner. However, effects of somatostatin on secretagogue-induced pepsinogen secretion were obscure. To clarify the effects of somatostatin on the chief cells, gastric mucosal cells were isolated by a proteolytic enzyme. Somatostatin inhibited carbachol- and cholecystokinin octapeptide-induced pepsinogen secretion from dispersed gastric mucosal cells in a dose-dependent manner. Histamine-induced pepsinogen secretion, which was recovered by culturing, was also inhibited by somatostatin. These results suggest that somatostatin inhibits secretagogue-induced pepsinogen secretion directly.

Animals↗

PubMed1990

[Spread of surgical indication for hepatoma with postoperative transcatheter arterial infusion].

UNLABELLED: We evaluated the reduction surgery and the postoperative TAI for unresectable hepato-cellular carcinoma (HCC). Eight patients underwent reduction surgery and postoperative TAI (group I). Twenty-five patients underwent combination therapy with TAI, TAE, EI, hyperthermia and irradiation, who had not undergone reduction surgery (group II). Nine patients underwent a relative noncurative operation (group III). We studied the prognosis of these three groups. RESULTS: The one-year survival rates were 85.7% in group I, 38.6% in group II and 55.5% in group III. The three-year survival rates were 42.9% in group I, 10.7% in group II and 55.5% in group III. There was a significant difference of prognosis between group I and group II (p less than 0.05, generalized Wilcoxon). These results suggest that reduction surgery and post operative TAI for unresectable HCC improve the prognosis.

Antineoplastic Agents↗

PubMed1990

Overproduction and crystallization of tryptophanase from recombinant cells of Escherichia coli.

We have cloned the tryptophanase structural gene from Escherichia coli B/1t7-A into E. coli K-12 MD55 with a vector plasmid, pBR322. The cloned cells produced a large amount of the enzyme corresponding to more than 30% of the total soluble protein. With the enzyme obtained by this overproduction system, we have prepared three different crystals of tryptophanase, apo-enzyme, holo-enzyme, and a complex of holo-enzyme and L-alanine, by using polyethylene glycol 4000 or potassium phosphate as a precipitant and the hanging drop method. These single crystals appeared to be suitable for X-ray diffraction analysis.

Alanine↗

PubMed1990

An evaluation of the agar plate method for the detection of Strongyloides stercoralis in northern Thailand.

An examination of the stools from school-children in northern Thailand was performed in order to compare the efficacy of a new method--the agar plate method--for the detection of Strongyloides stercoralis with traditional methods. Twenty-three positive specimens (15.5%) from a total of 148 specimens were detected as follows: 18 cases by the agar plate method, 13 cases by direct stool smear, 11 cases by filter paper culture, and four cases by the formalin-ether method (MGL). On the basis of the above results, the agar plate method appeared to be more efficient than traditional methods for detecting Strongyloides in human stool samples. Other positive factors in its favour were ease of manipulation and low cost. There were some problems with using this method. Five cases shown to be positive by traditional methods were negative in the agar plate method, and it was necessary to discriminate Strongyloides microscopically from other similar nematode larvae, especially in an area, such as northern Thailand, with a high prevalence of hookworms.

Animals↗

PubMed1989

Kinetic approach with ab initio MO method on ionic selectivity and size in sodium channel.

Three kinds of models for ionic selectivity and size of the filter in sodium channel have been treated by using ab initio molecular orbital (MO) calculations with MINI-3 and MIDI-3* basis sets. A three-components system, HCO2M-H2O (M = Li+, Na+ or K+), is acceptable for describing experimental facts well. Thermochemical parameters obtained from harmonic vibrational analysis with MINI-3 basis sets, for the translocation of the permeant metal cations in the HCO2M-H2O system, are that the activation enthalpies for Li+, Na+ and K+ are 7.0, 6.4 and 23.4 kJ/mol, and also the free energies of activation are 10.6, 1.5 and 19.0 kJ/mol, respectively. These results are qualitatively in good correspondence with experimental facts of the ion selectivity of the channel. One of water molecule was found to have a key role in the translocation of the permeant cations.

Animals↗

PubMed1989

[Effects of neuromedin B and neuromedin C on insulin release from isolated perfused rat pancreas].

Neuromedin B and neuromedin C are novel decapeptides that have recently been isolated from porcine spinal cord and canine intestinal mucosa. We have studied the effects of neuromedin B and neuromedin C on insulin release from the isolated perfused rat pancreas. The effect of neuromedin B was detectable at a concentration of 10mM, and that of neuromedin C was detectable at a concentration of 1nM. Further increase in the concentration of neuromedin B and neuromedin C resulted in dose-dependent increases in insulin secretion. The effectiveness of neuromedin B and neuromedin C as insulinotropic agents depended on the glucose concentration; both were more effective at a higher concentration of glucose. However, insulinotropic effects of these peptides in the presence of 8.3mM glucose were limited to the first 3 min of a 20-min perfusion. These results, coupled with a recent study demonstrating bombesin-like immunoreactivity in nerves in the pancreas, suggest that neuromedin B and neuromedin C exert a direct local action on insulin secretion in the pancreas.

Amino Acid Sequence↗

PubMed1989

[Atrial natriuretic factor: an epidemiological study. Preliminary results].

We performed an epidemiological study on the atrial natriuretic factor pattern in a young population. Subjects were recruited in the Ospedale Militare Principale of Rome among young men liable to conscription, whose hospitalization was due either to essential hypertension or to other pathologies (not influencing our study, such as headache etc.). The recruitment lead to the formation of three different groups: normotensives, normotensives with family history of hypertension (mother and/or father) and hypertensives. On the morning of the study (after 7 days of pharmacological wash-out, under a diet containing 120 mEq of Na+/die), blood samples were taken. Plasma atrial natriuretic factor, renin activity and aldosterone were assayed by RIA. Digoxin-like immunoreactive substance was assayed by a solid-phase radioimmunoassay, following the extraction of plasma. Serum creatinine, sodium, potassium and urinary sodium and potassium (24 h before the study) were assayed by standard methods. Urinary kallikrein was assayed by chromogenic substrate S-2266. So far, we have studied 60 subjects (26 hypertensives, 21 normotensives and 13 normotensives with family history) and we wish to discuss in this article the preliminary results concerning the atrial natriuretic factor and its relationship with renin activity, aldosterone and blood pressure. Our results show that the mean plasma levels of atrial natriuretic factor in the hypertensive group were higher, although not significantly, than those of the other two groups and that the normotensives with family history had slightly higher levels as compared to normotensives (Delta % = + 7.4).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Effect of a new cholinergic agonist, aclatonium napadisilate, on exocrine and endocrine rat pancreas.

The effect of aclatonium napadisilate, a choline sulfonate derivative, on exocrine and endocrine pancreatic functions was compared with that of carbamylcholine in both isolated pancreatic acini and the isolated perfused pancreas of rats. In the isolated acini, aclatonium napadisilate and carbamylcholine stimulated amylase release. While the relative efficacy of aclatonium napadisilate was the same as that of carbamylcholine, aclatonium napadisilate was about 20-fold less potent. In the isolated perfused pancreas, 0.1 microM or higher concentrations of aclatonium napadisilate elicited a significant insulin release in the presence of 8.3 mM glucose, whereas an appreciable increase in pancreatic exocrine secretion was obtained with a 10 times higher concentration (1.0 microM). In contrast, carbamylcholine did not stimulate insulin release at a dose (0.1 microM) that stimulated pancreatic exocrine secretion. The insulin-releasing effect of aclatonium napadisilate depended on the glucose concentration. These stimulatory effects of aclatonium napadisilate on endocrine and exocrine pancreatic secretion were inhibited by the muscarinic receptor antagonist pirenzepine but were not affected by the cholecystokinin receptor antagonist proglumide. These results indicate that aclatonium napadisilate stimulates both endocrine and exocrine pancreatic secretion via muscarinic receptors and that its action on B cells is more potent than on the exocrine pancreas.

Acetylcholine↗

PubMed1989

Loxiglumide. A new proglumide analog with potent cholecystokinin antagonistic activity in the rat pancreas.

D,L-4-(3,4-dichlorobenzoylamino)-5-(N-3-methoxypropyl-pentylami no)-5- oxopentanoic acid (CR 1505; loxiglumide) is a newly developed analog of proglumide. We examined the inhibitory effects of loxiglumide on pancreatic exocrine function in the isolated pancreatic acini and the isolated perfused pancreata of rats. Loxiglumide inhibited cholecystokinin octapeptide (CCK-8)-stimulated amylase release and, similarly, binding of [125I]CCK-8 to isolated rat pancreatic acini. Loxiglumide was about 3000 times more potent than the reference substance proglumide, but was about 1000 times less potent than L-364,718, another new CCK antagonist having benzodiazepine ring, in inhibiting CCK-8-stimulated amylase release. The inhibitory effect of loxiglumide displayed competitive kinetics and was specific for CCK in that the effects of other receptor secretagogues or agents bypassing receptors were not altered. The inhibitory effect of loxiglumide was fully reversible in isolated acini. However, the pancreata perfused with 10 microM loxiglumide for 20 min did not respond to CCK-8 for more than 20 min even after the removal of loxiglumide infusion. In contrast, an immediate increase in pancreatic exocrine secretion was observed after proglumide removal. Loxiglumide appeared to be bound to the receptors on acinar cells in a slowly dissociating state. These results indicate that loxiglumide acts as a potent, competitive, and specific CCK antagonist on the exocrine pancreas and, because of its prolonged inhibitory action, may be useful as a therapeutic agent in pancreatic disease.

Amylases↗

PubMed1989

Effect of a new cholecystokinin receptor antagonist CR 1392 on caerulein-induced acute pancreatitis in rats.

The effects of cholecystokinin receptor antagonist CR 1392 was studied in a model of mild acute pancreatitis induced in rats by four subcutaneous injections of the secretagogue caerulein. A single subcutaneous injection of 50 mg/kg body weight of CR 1392 caused a dramatic reduction in serum amylase concentration and pancreatic wet weight as well as histologic improvement of the caerulein-induced acute pancreatitis when given 30 min before the first caerulein injection. CR 1392 was also effective in reducing the elevated serum amylase activity, pancreatic weight, and histologic alterations even when administered after the pancreatitis had been induced. These present observations suggest that CR 1392 remains active for more than 3 h and blocks the action of caerulein on the pancreas.

Acute Disease↗

PubMed1989

Hydrocortisone treatment increases the sensitivity and responsiveness to cholecystokinin in rat pancreas.

The effects of hydrocortisone treatment on the secretory abilities of pancreatic acini to various secretagogues were studied. Rats were given subcutaneous injections of hydrocortisone at doses of 1.25, 2.5, or 5.0 mg/kg body wt once daily for 7 days. Hydrocortisone led to a small dose-dependent increase in pancreatic wet weight per 100 g body wt, which was associated with an increase in both total protein and DNA contents. In acini prepared from hydrocortisone-treated rats, both the responsiveness and the sensitivity to cholecystokinin octapeptide (CCK-8) was increased. The concentration dependence of cellular Ca2+ mobilization in response to CCK-8 was also shifted to lower concentrations in acini from hydrocortisone-treated rats compared with control rat acini. In vivo administration of hydrocortisone caused a significant increase in the affinity of 125I-CCK-8 binding to high-affinity receptors. The secretory responsiveness to carbamylcholine and bombesin, but not to secretin, was also increased but without any change in the sensitivity. Moreover, the hydrocortisone treatment increased the secretory responsiveness of acini to the Ca2+ ionophore A23187 and the phorbol ester 12-O-tetradecanoylphorbol-13-acetate but did not to an adenosine 3',5'-cyclic monophosphate analogue, 8-bromoadenosine 3',5'-cyclic monophosphate. The present observations suggest that in vivo glucocorticoid administration affects both the CCK receptors and a postreceptor loci.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1989

Effects of a new proglumide analogue CR 1392 on pancreatic exocrine secretion in the rat.

The effects of proglumide analogue. CR 1392, on pancreatic exocrine secretion were studied in the isolated pancreatic acini and the isolated perfused pancreata of rats. In the isolated acini, CR 1392 caused a parallel rightward shift of the dose-response curve for amylase secretion stimulated by cholecystokinin octapeptide (CCK-8). CR 1392 inhibited maximally stimulated amylase release by CCK-8 (100 pM) in a concentration-dependent manner, with a half maximal inhibition (ID50) at 8.0 +/- 0.6 microM. CR 1409, another proglumide analogue, also caused a concentration-dependent inhibition (ID50: 3.2 +/- 0.4 microM). Although CR 1409 was about 2.5-fold more potent than CR 1392 in inhibiting the stimulated amylase release, 1 mM CR 1409 caused 107.4 +/- 0.9% increase in amylase release, suggesting acinar cell damage. CR 1392 (1 mM) also caused 19.9 +/- 2.3% increase in amylase release, but was less toxic than CR 1409. The antagonism produced by CR 1392 was selective for CCK and had no effect on amylase release stimulated by other receptor secretagogues or by agents bypassing receptors. CR 1392 added 20 min after the CCK-8 stimulation rapidly abolished pancreatic exocrine secretion in both isolated acini and isolated perfused pancreas. Although the inhibitory effect of CR 1392 was fully reversible in the isolated acini, the pancreata perfused with 100 microM CR 1392 for 20 min did not respond to the subsequent stimulation with CCK-8 for more than 20 min. These results indicate that CR 1392 is a potent, competitive, specific and long acting antagonist of CCK in rat pancreas.

Amylases↗

PubMed1989

Pepsinogen secretion from cultured rat gastric mucosal cells.

Rat gastric mucosal cells were isolated with the aid of 0.1% collagenase and Dispase. Pepsinogen secretion from these cells was stimulated by carbachol, cholecystokinin octapeptide (CCK(S)-8) and pentagastrin, but not by histamine. Attempts to obtain a sufficient number of cells using a higher concentration of Dispase resulted in disappearance of the responses to secretagogues. However, when gastric mucosal cells thus prepared were cultured for 24 h in a CO2 incubator, they were found to respond not only to carbachol, CCK(S)-8 and pentagastrin, but also to histamine, resulting in an increase in pepsinogen secretion. The secretagogue-induced pepsinogen secretion was inhibited by its antagonist in a dose-dependent manner. These results suggest that the receptor present in chief cells for pepsinogen secretion was destroyed during the isolation procedure and regenerated during culture.

Animals↗

PubMed1989

Increased beta-cell secretory responsiveness to ceruletide and TPA in streptozocin-induced mildly diabetic rats.

We examined the effects of various stimuli on immunoreactive insulin (IRI) and glucagon (IRG) release from perfused pancreases isolated from control and streptozocin-induced diabetic (STZ-D) rats. Diabetes was induced by injecting 30 mg/kg STZ into rats fasted for 16-18 h 12-17 days before our experiments. Glucose (11.1 mM) caused a distinct biphasic pattern of IRI release from the control pancreas, whereas the first phase was marginal and the second phase was absent in the diabetic pancreas. Arginine (20 mM)-induced IRI release was similar in both groups, whereas IRG release was greater in the control rats than in the diabetic rats. Thus, this model of STZ-D simulates a certain class of non-insulin-dependent diabetes mellitus (NIDDM). In these diabetic animals, the cholecystokinin (CCK) analogue ceruletide (620 pM) caused a significantly greater increase in IRI release in the presence of 5.6 mM glucose than in the control rats, but ceruletide caused a similar IRG release in both groups. Because CCK and ceruletide stimulate phosphoinositide turnover in pancreatic islets, we examined the effects of carbachol and phorbol ester TPA on IRI release in the presence of 5.6 mM glucose. Carbachol (10 microM), which is thought to generate similar second messengers as ceruletide, induced greater IRI release in diabetic than in control rats. TPA (100 nM) caused a significantly greater increase in IRI release from the diabetic than the control pancreas. Our results demonstrate that the insulin-releasing mechanism involved in protein kinase C activation is enhanced in this model of NIDDM.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

[Inhibitory effect of a new proglumide derivative, loxiglumide, on CCK action in isolated rat pancreatic acini].

The effect of a new proglumide derivative, loxiglumide (DL-4-(3,4-dichloro-benzoyl-amino)-5-(N-3-methoxy-propyl-pentylamino+ ++)-5-oxo-pentanic acid; CR 1505), on binding of 125I-CCK-8 and amylase release stimulated by CCK-8 was investigated in isolated rat pancreatic acini. Loxiglumide inhibited CCK-8-stimulated amylase release and binding of 125I-CCK-8 to rat pancreatic acini in a dose-dependent manner. Loxiglumide caused a concentration-dependent rightward shift of the dose-response curve for CCK-8-stimulated amylase release without altering the maximal response. Schild plots showed a slope of 0.82 and pA2 value of 7.05. The inhibitory effect of loxiglumide on amylase release was reversible. Loxiglumide significantly inhibited amylase release in response to CCK-8, caerulein and gastrin-I. However, loxiglumide had no effect on amylase release stimulated by other receptor secretagogues (bombesin, carbamylcholine, secretion and vasoactive intestinal polypeptide) or by agents bypassing receptors (A23187 and TPA). These results indicate that loxiglumide acts as a potent, competitive and specific CCK antagonist on the pancreatic acini.

Amylases↗

PubMed1989

Bioassay of plasma cholecystokinin in rat and human: inhibition of protein synthesis prevents the decrease in the sensitivity and responsiveness of isolated rat pancreatic acini to CCK-8.

Isolated rat pancreatic acini were most sensitive and responsive when stimulated directly with cholecystokinin octapeptide (CCK-8) without preincubation. Both the responsiveness and sensitivity of acini to CCK-8 decreased time dependently with prolonged preincubation. When acini were stimulated with CCK-8 following pulse labeling with radioactive leucine, old protein was discharged together with newly synthesized (labeled) protein. However, the sensitivity and responsiveness of these acini for release of labeled protein were primarily reduced with preincubation, indicating that newly synthesized protein was contributing to the time-dependent loss of sensitivity and responsiveness. Then isolated acini were treated with 300 microM cycloheximide for 2 h. This treatment prevented the decreases in the sensitivity and responsiveness of amylase release to CCK-8 stimulation and made these alterations in one series of experiments negligible. Using these acini, a sensitive and specific bioassay for the measurement of CCK in human and rat plasma was developed.

Amylases↗

PubMed1989

[Plasma cholecystokinin concentration in patients with chronic pancreatitis measured by bioassay].

We developed a specific and sensitive bioassay for measuring plasma cholecystokinin (CCK) in human and investigated CCK response after a test meal in patients with chronic pancreatitis. Treatment with cycloheximide increased the sensitivity and responsiveness of isolated rat pancreatic acini to CCK-octapeptide (CCK-8) and thus plasma levels of CCK-8 as low was 0.17 pM were detectable. Fasting plasma CCK levels in normal subjects as CCK-8 equivalents were 0.75 +/- 0.25 pM and rose to a peak of 6.2 +/- 0.68 pM at 45 min after a test meal consisting of 400 ml milk and 2 boiled eggs. Basal and stimulated plasma levels of CCK-8 in patients with non-calcified chronic pancreatitis were significantly higher than those in normal subjects. In contrast, postprandial responses of plasma CCK-8 in patients with calcified chronic pancreatitis was significantly low compared to those in control subjects, although basal plasma levels were not significantly different from those in controls.

Amylases↗

PubMed1989

Morphology on spontaneous regression of the autochthonous colon carcinoma in WF Osaka rat strain.

In order to study the spontaneous regression of the colon cancers of WF Osaka strain rats, laparotomies were carried on 701 rats in sequence at the age of four months. Among them, 260 cases were found having colon cancers at the laparotomy. 107 out of them showed spontaneous regression of the colon cancer in the ascending colon. Most of the cases which spontaneously regressed were rather the early stage (stage 1 and 2) of the colon cancer, though 26 cases of advanced cancer also showed spontaneous regression. Grossly the lesions of the spontaneous regression were those of thickened, elongated ascending colon, with occasional dilation. Some cases showed the cystic formation at the portion of former lesions. There was a case which showed normal appearance of the ascending colon with regional lymph node metastasis measuring 1.5 x 1.5 centimeters. Histological appearance was varied showing reconstruction of the muscular layer and mucularis mucosae. Mucosal epithelium was almost normal looking, but glandular arrangement showed cystic dilation. The ectopic existence of glandular composition was seen in the restored lesion in the muscular layer. Macrophage infiltration was indispensably main histological reaction with central necrosis of formerly existed cancer cells, which was considered to be cellular immunity against cancer cells, or exogenous substances, such as viruses in cancer cells.

Animals↗