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Biomedical subjects

A Funakoshi

Publications and source records attributed to A Funakoshi.

At least 145 records · Page 8Linked to original sources
PubMed1992

Neuropsychological evaluation before and after surgical treatment of temporal lobe epilepsy.

We present the results of pre- and postoperative neuropsychological evaluations of 58 patients with temporal lobe epilepsy who underwent a chronic intracranial EEG monitoring and a subsequent standard anterior temporal lobectomy. Wada's test provided valuable information on the speech dominant side and on the focus localization. Some warning signs as well as verbal automatisms indicated the effect for focus localization and lateralization. The results of interictal neuropsychological tests suggested that each subgroup of TLE performed differently. A postoperative neuropsychological performance has improved in many tests that may be explained by the diminished epileptic bombardment resulting from the resection.

Adolescent↗
PubMed1992

Protective effect of human pancreatic secretory trypsin inhibitor on cerulein-induced acute pancreatitis in rats.

We examined the protective effect of human pancreatic secretory trypsin inhibitor (PSTI), a specific trypsin inhibitor secreted from pancreatic acinar cells into the pancreatic duct, on cerulein-induced acute pancreatitis in conscious rats. The protective effect of human PSTI-RS, an analogue of PSTI with Arg-44 to Ser substitution which has a longer half-life in vitro, was also examined. Intraperitoneal administration of a pharmacological dose of cerulein to conscious rats induced acute pancreatitis, characterized by light microscopy as cellular disorganization of the acini and interstitial edema. Intravenous infusion of human PSTI (10, 50 or 250 micrograms/rat/h) into rats with cerulein-induced acute pancreatitis decreased their pancreatic wet weight and plasma amylase concentration. It also caused a dose-dependent decrease in vacuoles in acinar cells and interstitial edema. Human PSTI-RS, which has a longer half-life in vivo, was more effective than native PSTI at the same dose rate (10 micrograms/rat/h) in reducing pancreatitis. These results suggest that human PSTI may have a beneficial effect on acute pancreatitis.

Animals↗
PubMed1992

[Effect of ursodeoxycholate on pancreatic exocrine secretion in vitro and in vivo study].

In the present study, we examined the effect of ursodeoxycholate (UDCA) and it's taurine conjugate (TUDC) on rat pancreatic exocrine secretion using dispersed pancreatic acini (in vitro) and conscious rats (in vivo). In in vitro study 300 microM UDCA significantly increased 10(-12)-10(-9) M CCK-8 stimulated amylase release and change of intracellular Ca2+ concentration, but TUDC did not have these effects. In in vivo study intraduodenal infusion of UDCA but not TUDC stimulated pancreatic exocrine secretion. Intravenous infusion of secretin antibody decreased bicarbonate output, however, this increase was not prevented by CCK antagonist. Thus, it was suggested that UDCA has direct action on pancreatic acini and UDCA infused intraduodenally stimulates pancreatic secretion, possibly via the release of a secretin-like substance. The taurine conjugate has weak bioactivity on pancreatic exocrine secretion in both in vitro and in vivo.

Amylases↗
PubMed1992

[Effects of UFT and loxiglumide (CR1505) on liver metastasis of human pancreatic cancer cell line, KP-1 N in nude mice].

Effects of caerulein (CCK), 5-FU and CCK antagonist, loxiglumide (CR1505), were studied on the growth of human pancreatic cancer cell line, KP-1 N, in vitro. And effects of UFT and CR 1505 were also studied on liver metastasis in nude mice. The growth of KP-1 N was stimulated approximately 40% by addition of 10(-10) M of CCK in vitro. CR1505 antagonized the action of CCK, that is, the 40% growth rate increase was suppressed by addition of 25 microM of CR1505. Moreover, the growth rate of the cells dose-dependently decreased by the addition of CR1505. 5-FU also dose-dependently inhibited the growth of KP-1 N in culture. 5-FU additionally decreased the growth rate of KP-1 N in combination with CR1505. A number of metastatic nodules were found in the liver of nude mice a month after injections of KP-1 N cells into the spleen CR1505 suppressed the liver metastasis in nude mice which were administered with UFT. These results suggest that CR1505 would be useful for the treatment of human pancreatic cancer in combination with UFT.

Animals↗
PubMed1991

Bile acids in human plasma interfere with cholecystokinin bioassay using dispersed pancreatic acini.

A bioassay using dispersed pancreatic acini was used to measure fasting plasma cholecystokinin (CCK) concentrations in 105 patients with various kinds of gastrointestinal diseases, 17 patients with diabetes mellitus, and 6 healthy volunteers. High plasma CCK bioactivities were observed in patients with obstructive jaundice, choledocolithiasis, and primary biliary cirrhosis. Twenty-three samples with high CCK bioactivities were assayed by the same bioassay after the addition of a specific CCK antagonist and by a CCK radioimmunoassay in order to determine whether the high CCK-like bioactivity was due to circulating CCK or other factors. High CCK bioactivities were partially inhibited by the specific CCK antagonist, CR-1409, but the activities were not totally abolished. The residual bioactivities (not inhibited by CR-1409) correlated with plasma bile acid concentrations. The inhibitable CCK bioactivities correlated with plasma CCK levels obtained by radioimmunoassay. Although the bioassay using dispersed pancreatic acini has several advantages for measuring plasma CCK, this method overestimates CCK bioactivities in patients with high plasma bile acid concentrations.

Animals↗
PubMed1991

Bioactivity of synthetic human cholecystokinin (CCK)-33 in vitro and in vivo.

The relative potencies of synthetic human cholecystokinin (h-CCK)-33, porcine CCK-33 (p-CCK-33) and CCK-8 were examined by measuring pancreatic secretion in the conscious rat (in vivo) and amylase release from rat pancreatic acini using a perifusion study (in vitro). The increments of protein output during an 1-hr infusion of 100 pmol/kg/hr of h-CCK-33, p-CCK-33 and CCK-8 were 27.0 +/- 2.9 mg/hr (M +/- SE), 19.3 +/- 2.8 and 14.0 +/- 1.8 mg/hr, respectively. H-CCK-33 and p-CCK-33 showed significantly higher responses of protein output than CCK-8 in a same molar ratio, in vivo. In vitro, the stimulation with 10(-10) M h-CCK-33, p-CCK-33 and CCK-8 led to a similar biphasic amylase release in a perifusion study. Twenty-five microM CR-1409, an antagonist for CCK receptor, completely inhibited the 10(-10) M h-CCK-33-stimulated amylase release. Although it was found that h-CCK-33 and p-CCK-33 were more potent than CCK-8 in vivo, 10(-10) M CCK-8, h-CCK-33 and p-CCK-33 were equipotent on rat pancreatic acini in vitro. It is suggested that the discrepancy in potencies of the large molecular form and small molecular form of CCK in vivo and in vitro may be attributed to the delay of degradation of the large molecular form of CCK in vivo.

Amylases↗
PubMed1991

7B2, a possible marker for nonfunctioning pancreatic islet cell tumor.

Plasma 7B2 was measured in 13 patients with pancreatic islet cell tumors, 11 with pancreatic adenocarcinoma and 31 normal subjects as a control. The mean (+/- SD) concentrations of plasma 7B2 in the normal subjects and the patients with pancreatic islet cell tumors were 67 +/- 10 and 1041 +/- 1786 pmol/l, respectively, and the value in the patients with pancreatic islet cell tumors was significantly higher than that in the normal subjects (p less than 0.01). Elevation of plasma 7B2 over the normal range, defined as less than the mean + 3SD value of those in the normal subjects, was found in 10 of 13 patients with pancreatic islet cell tumors including 4 with nonfunctioning tumor. Plasma 7B2 dropped into the normal range postoperatively in 3 patients with nonfunctioning tumor. Plasma 7B2 concentrations in the patients with pancreatic adenocarcinoma remained in the normal range. These results raise a possibility that 7B2 is a useful marker for pancreatic islet cell tumors, in particular nonfunctioning tumor.

Adenoma, Islet Cell↗
PubMed1991

Clinical usefulness of serum phospholipase A2 determination in patients with pancreatic diseases.

A new kit for radioimmunoassay of serum phospholipase A2 (PLA2) with monoclonal antibody (S-0932, Shionogi, Osaka, Japan) was used to examine PLA2 levels in patients with various diseases. Patients with acute pancreatitis showed significantly increased serum PLA2 levels. In patients with chronic pancreatitis, significant correlations were observed between the levels of factors evaluated by the secretin test and serum PLA2 levels. In patients with pancreatic cancer, serum PLA2 levels varied with disease severity. Serum PLA2 concentrations were within the normal range in patients with other malignant tumors, diabetes mellitus, and chronic liver diseases but were increased in patients with chronic renal failure. S-Sepharose column analysis of sera showed a small peak of pro-PLA2 and a large peak of PLA2 in sera from patients with severe acute pancreatitis, but a large peak of pro-PLA2 in healthy controls and patients with other diseases. On G-100 gel filtration, high-molecular-weight PLA2 immunoreactivity was detected in sera of patients with chronic renal failure, whereas a single peak of PLA2 immunoreactivity coinciding with that of standard PLA2 was detected in sera of patients with acute pancreatitis. These results suggest that (a) measurement of serum PLA2 is clinically useful for diagnosis and monitoring of pancreatitis, (b) active PLA2 in the circulation is dominant in severe acute pancreatitis, and (c) the kidney may be the main site of PLA2 degradation or excretion.

Acute Disease↗
PubMed1991

Immunohistochemical study of the distribution of pancreastatin in endocrine tumors of the pancreas and in normal pancreatic tissue: analysis of autopsy cases.

Using sixteen cases (sixteen lesions) of endocrine tumor of the pancreas, found in 1,300 consecutive autopsy cases (661 men and 639 women; mean age, 79.0 years), we examined distribution patterns of pancreastatin (PST) in these endocrine tumors and in normal tissues around them, using immunohistochemical staining. In addition, the distribution patterns of PST was compared with those of insulin (INS), glucagon (GLU), somatostatin (SOM), and pancreatic polypeptide (PP), in these tissues. Normal islets of Langerhans were stained completely and evenly for PST. Two endocrine tumors did not stain for PST at all, six were partially stained, and eight were stained as densely as normal islets, or even more densely. Acinar cells were only partially stained for PST in 11 cases and showed scattered staining in three cases. Epithelial cells of ducts or ductuli were partially stained for PST in 10 cases and showed scattered staining in three cases. Distribution patterns of PST coincided with that of INS in 56% (9/16) of cases, GLU in 81% (13/16), SOM in 31% (5/16), and PP in 31% (5/16). In the eight tumors that were stained at least as densely for PST as normal islets, the staining pattern did not coincide with that of INS in any case (0%), coincided with that of GLU in all 8 cases (100%), and coincided with those of SOM and PP in one case each (13%). Therefore, the distribution of GLU-producing cells (A cells) coincided most closely with that of PST. It is concluded that most PST is secreted from A cells in human pancreas.

Adenoma, Islet Cell↗
PubMed1991

Long term inhibitory effects of pancreastatin and diazepam binding inhibitor on pancreatic beta-cell deoxyribonucleic acid replication, polyamine content, and insulin secretion.

The two peptides pancreastatin and diazepam binding inhibitor (DBI) were recently demonstrated in pancreatic islets and were shown to inhibit insulin secretion in short term experiments. In the present study we investigated long term effects of pancreastatin and DBI on the DNA synthesis, polyamine content, and insulin secretion of pancreatic beta-cells in tissue culture. For this purpose fetal rat pancreatic islets enriched in beta-cells were isolated and cultured for 3 days at different concentrations of rat pancreastatin and porcine DBI. It was found that pancreastatin dose-dependently decreased beta-cell DNA synthesis, reaching maximal inhibition at 100 nM. In parallel with this, pancreastatin also decreased insulin secretion and the islet contents of insulin and the polyamines spermidine and spermine. These effects were abolished by a high glucose concentration or addition of GH. Also, DBI evoked a dose-dependent inhibition of beta-cell DNA synthesis but affected neither the islet contents of insulin or polyamines nor insulin secretion. Like pancreastatin, DBI was ineffective in preventing the increased beta-cell DNA synthesis, insulin content, or secretion in response to high glucose or GH. It is concluded that pancreastatin and DBI inhibit beta-cell DNA synthesis and function in vitro. In the case of pancreastatin these inhibitory effects may be mediated by a decrease in islet polyamine content. It is suggested that pancreastatin and DBI may influence beta-cell replication and function in vivo in an autocrine or paracrine fashion.

Animals↗
PubMed1991

Acetylcholine regulates pancreastatin secretion from the human pancreastatin-producing cell line (QGP-1N).

Studies were made of pancreastatin (PST) secretion from a human PST-producing cell line (QGP-1N) in response to various secretagogues. Cells with immunoreactivity for PST were observed in monolayer cultures of QGP-1N cells. Carbachol stimulated PST secretion and the intracellular Ca2+ mobilization concentration dependently in the range of 10(-6)-10(-4) M. The PST secretion and Ca2+ mobilization induced by carbachol were inhibited by atropine. The calcium ionophore (A23187) stimulated PST secretion. However, cholecystokinin and gastrin-releasing peptide did not stimulate either PST secretion or Ca2+ mobilization. Secretin also did not stimulate PST secretion. The glucose concentration in the culture medium had no effect on PST secretion. These results suggest that PST secretion is mainly regulated by acetylcholine through a muscarinic receptor, and that an increase in intracellular Ca2+ plays an important role in stimulus-secretion coupling in QGP-1N cells.

Acetylcholine↗
PubMed1991

Absence of luminal bile increases duodenal content of cholecystokinin in rats.

The effects of the removal of bile from the proximal intestine on pancreas, plasma cholecystokinin (CCK) concentration, and duodenal content of CCK were examined in rats. Bile was excluded from the duodenum and introduced into the distal ileum through a silastic cannula for 7 days. Pancreatic juice was maintained to be normally secreted into the duodenum. After 7-day bile diversion, plasma CCK concentration and duodenal CCK content were significantly increased in bile-diverted rats. Trypsin content in the proximal intestine in bile-diverted rats was one-half that in control. Pancreatic wet weight, protein content, and DNA content in the pancreas were slightly increased, and lipase content was slightly decreased, by bile diversion, but none of these changes was statistically significant. Amylase content significantly decreased and chymotrypsin content significantly increased in bile-diverted rats. Intragastric administration of camostate (trypsin inhibitor) significantly increased plasma CCK concentration in both bile-diverted and control rats, and the net increase was much greater in bile-diverted rats than in control rats. In conclusion, bile diversion increased duodenal CCK content and increased the CCK response to luminal stimulant.

Amylases↗
PubMed1991

A case of transient elevation of the serum carcinoembryonic antigen and associated with severe malnutrition and low T3, T4 syndrome.

A patient with a transient elevation of the serum carcinoembryonic antigen (CEA) associated with a benign disease was reported. The elevation of CEA was noted in the patient with low T3, T4 syndrome associated with malnutrition due to malabsorption syndrome induced by post-gastrectomy and chronic pancreatitis. Mild liver dysfunction and diabetes mellitus were also noted. The CEA level decreased as T3, T4 level and malnutrition were improved by administration of a massive digestive enzyme preparation. This inverse correlation between the serum CEA and serum T3, T4 levels suggested that high levels of the serum CEA can be found in the patient with malnutrition.

Biomarkers, Tumor↗
PubMed1990

Elevated plasma levels of pancreastatin (PST) in patients with non-insulin-dependent diabetes mellitus (NIDDM).

Pancreastatin (PST) is known as the peptide which inhibits first phase of glucose-stimulated insulin secretion. Fasting plasma PST levels and responses of PST after oral glucose ingestion in patients with non-insulin-dependent diabetes mellitus (NIDDM) were studied with human PST-specific radioimmunoassay. Fasting plasma PST in NIDDM patients was not different from healthy controls, although a slightly higher level of PST was observed in patients treated with sulfonylurea among NIDDM patients. No significant increase in plasma PST was observed after a glucose ingestion in healthy controls. In contrast, plasma PST levels in NIDDM patients rose significantly after glucose ingestion. These results suggest a possible pathophysiological role for PST in NIDDM.

Administration, Oral↗