Pancreatic elastase-1-producing B-cell lymphoma.
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Humans↗
Biomedical subjects
A Jimi
Publications and source records attributed to A Jimi.
Acetylcholine regulates glucagon secretion from human glucagonoma cells.
Human glucagonoma cells were isolated and maintained in vitro. Incubation experiments showed that carbachol (Cch) induced the simultaneous release of glucagon, VIP (vasoactive intestinal polypeptide), and pancreatic polypeptide (PP) at levels significantly higher than basal levels. Atropine abolished the stimulatory effect of Cch on glucagon, VIP, and PP release. An immunohistological study of the tumor tissues revealed that the cells contained glucagon, VIP, and PP. These findings demonstrate, for the first time, the in vitro release of glucagon from glucagonoma cells by Cch stimulation.
Carbachol↗
Lack of effect of cholecystokinin receptor antagonist (CR1505) on recovery of experimental pancreatitis after pancreatic duct occlusion in rats.
The effect of long term administration of a synthetic cholecystokinin (CCK) receptor antagonist CR1505 (loxiglumide) on pancreatitis was examined in rats after pancreatic duct ligation (PL) with an internal bile fistula. All rats were given both 6 mg/day of CR1505 continuously infused intraduodenally with an osmotic pump and 32 mg/day introduced into the stomach with an orogastric tube. Rats were killed 7, 14, and 28 days after PL, and changes of body weight, pancreatic wet weight, daily food intake, pancreatic protein content, and histology, plasma amylase concentration, and both plasma and duodenal CCK concentrations were examined. Administration of CR1505 for 7 days from immediately after PL, resulted in decrease of body weight, increase of daily food intake, and significant increases of intestinal CCK concentration and the level of CCK mRNA. However, its administration from day 7 to day 14 or 28 did not improve any of the parameters examined except inflammatory infiltration of the pancreas on the 14th postoperative day. These results suggest that CR1505 may have a beneficial effect on recovery from pancreatitis when administered during the early stage, but not when administered during a later stage.
Animals↗
Gene expression of erythropoietin in hepatocellular carcinoma.
A 68-year-old man with hepatocellular carcinoma complicated by erythrocytosis showed an increased plasma level of immunoreactive erythropoietin (EPO). Northern blot analysis and RT-PCR (reverse transcriptase and polymerase chain reaction) of EPO mRNA extracted from a surgical specimen indicated high expression of EPO mRNA in the tumor tissue. Histological and immunocytochemical examination showed that the tumor was a hepatocellular carcinoma with predominant immunostaining for EPO. The erythrocytosis improved and the high serum EPO level decreased after resection of the tumor. This is the first demonstration of EPO mRNA expression in hepatocellular carcinoma tissue by RT-PCR.
Aged↗
In vitro release of vasoactive intestinal polypeptide and pancreatic polypeptide from human VIPoma cells and its inhibition by somatostatin analogue (SMS 201-995).
BACKGROUND: The purpose of the present study was to determine whether vasoactive intestinal polypeptide (VIP) is released from the tumor cells of VIPoma and if so then to attempt to show how its release is regulated by cultured human VIPoma cells. METHODS: A resected specimen of a pancreatic tumor from a patient with watery diarrhea, hypokalemia, and achrohydria syndrome was examined. The dissociated cells were obtained by collagenase digestion of the tumor tissue and were cultured in vitro. RESULTS: The extraction of tumor cells disclosed that the cells contained VIP and pancreatic polypeptide (PP). Neither insulin, glucagon, somatostatin nor pancreastatin was detected. Immunohistochemically, 40% to 60% of the cells in the tumor stained positively for VIP and 1% to 5% stained positively for PP. The dissociated cells became reaggregated in the culture (50 to 300 microns) and could be maintained in vitro. Incubation experiments revealed a simultaneous in vitro release of VIP and PP with a significant increase by either carbachol or phorbol myristate acetate but not by theophylline or caerulein. Atropine completely abolished the stimulatory effects of carbachol on VIP and PP release. Octreotide (somatostatin analogue [SMS 201-995]) significantly inhibited the carbachol and phorbol myristate acetate-stimulated VIP and PP release. CONCLUSIONS: These findings show the in vitro release of VIP and PP from the VIPoma cells and also provide evidence for the direct inhibitory effect of somatostatin analogue on both the VIP and PP release from the tumor cells.
Adult↗
The increasing prevalence of benign proliferative breast lesions in Japanese women.
BACKGROUND: Although the increasing incidence of breast cancer in Japan has been well-documented, the possibility that there also has been an increase in the frequency of benign proliferative breast disease in Japanese women has not been previously studied. METHODS: The authors compared the histologic findings in a series of 266 consecutive benign breast biopsy specimens from 1974 to 1975 (Group I) to those in a series of 266 similar biopsy specimens accessioned at the same institution in Japan one decade later (i.e., 1984 to 1985; Group II). The extent of sampling was similar in both groups. The specimens were categorized as showing nonproliferative lesions, proliferative lesions without atypia, or atypical hyperplasia using the criteria of Dupont and Page. RESULTS: Proliferative lesions without atypia were significantly more common in biopsy specimens from Group II than those from Group I (16.2% versus 9%; P = 0.01). Although atypical hyperplasias were twice as common in Group II as in Group I, these lesions were uncommon in both groups (2% in Group II versus 1% in Group I, p = NS). The differences in pathologic findings between the two groups were most evident in younger women. For patients younger than 40 years of age, the prevalence of proliferative lesions (with or without atypia) was 18% for Group II and 6% for Group I (P = 0.003). For patients 40 years of age or older, proliferative lesions were seen in 17% of patients in Group II and 13% in Group I (P value, not significant). CONCLUSIONS: The frequency of benign proliferative breast lesions in Japanese women, particularly among women younger than 40 years of age, is increasing. These observations are consistent with the results of previous studies in North America that have demonstrated a relationship between benign proliferative breast lesions and the development of breast cancer.
Adolescent↗
Parallel secretion of pancreastatin and somatostatin from human pancreastatin producing cell line (QGP-1N).
In this investigation we studied pancreastatin (PST) secretion from a human PST producing cell line (QGP-1N) in response to various secretagogues. Immunocytochemical study revealed the immunoreactivity of PST and somatostatin (SMT) in the same cells of a monolayer culture. Ki-ras DNA point mutation on codon 12 was found. Carbachol stimulated secretion of PST and SMT and intracellular Ca2+ mobilization in the range of 10(-6)-10(-4) M. The secretion and Ca2+ mobilization were inhibited by atropine, a muscarinic receptor antagonist. Phorbol ester and calcium ionophore (A23187) stimulated secretion of PST and SMT. The removal of extracellular calcium suppressed both secretions throughout stimulation with 10(-5) M carbachol. Fluoride, a well-known activator of guanine nucleotide binding (G) protein, stimulated intracellular Ca2+ mobilization and secretion of PST and SMT in a dose-dependent manner in the range of 5-40 mM. Also, 10(-5) M carbachol and 20 mM fluoride stimulated inositol 1,4,5-triphosphate production. However, cholecystokinin and gastrin-releasing peptide did not stimulate Ca2+ mobilization or secretion of the two peptides. These results suggest that secretion of PST and SMT from QGP-1N cells is regulated mainly by acetylcholine in a parallel fashion through muscarinic receptors coupled to the activation of polyphosphoinositide breakdown by a G-protein and that increases in intracellular Ca2+ and protein kinase C play an important role in stimulus-secretion coupling.
Adenoma, Islet Cell↗
Changes in plasma and duodenal cholecystokinin concentrations after pancreatic duct occlusion in rats.
The changes in plasma and duodenal cholecystokinin (CCK) concentrations after pancreatic duct occlusion were examined in rats. The rats were sacrificed 1, 3, 7, 10, 14, and 30 days after occlusion of the duct. Histological examination showed acute inflammation on days 1 and 3 after duct occlusion, interstitial fibrosis and regenerative changes on days 7, 10, and 14, and pancreatic atrophy on day 30. The plasma CCK concentration increased from 0.45 pM to 2.0 pM after the occlusion and then remained high throughout the observation period. In contrast to the stable increase in plasma CCK concentration, the CCK content in the duodenum increased on days 1 and 3, decreased on day 7, increased on day 10, reaching over the control level on day 14, and then returned to the control level on day 30. Administration of boiled and 10-fold concentrated rat pancreatic juice or human pancreatic secretory trypsin inhibitor for seven days after pancreatic duct occlusion reversed the decrease in duodenal CCK content. The major molecular forms of duodenal CCK were CCK-8, -33, and -58. These results indicate that (1) basal plasma CCK concentration did not reflect the duodenal CCK content, (2) duodenal CCK content was well correlated with a decrease in inflammation in the pancreas, and (3) a nonenzymatic component in the pancreatic juice reversed the decrease in duodenal CCK content and body weight caused by pancreatic duct occlusion.
Acute Disease↗
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↗
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↗
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↗
Xanthogranulomatous pyelonephritis, perinephric type--a case report.
A 46 year-old woman with perinephric type of xanthogranulomatous pyelonephritis is described. She had a fever and pain with a palpable mass in her right flank. The blood analysis revealed anemia, leucocytosis, gamma-globulinemia, but no hyperlipidemia. The urine analysis showed nothing abnormal, but enterobacter was present in the urine. An intravenous pyelogram demonstrated a right non-functioning kidney. The diagnosis of a perinephric abscess was made from the x-ray and ultrasonogram, and a right nephrectomy was performed. The resected kidney had a tumor-like lump covered with Gerota's fascia at the postero-lateral side of the kidney. The cut surface of the kidney revealed an area of hemorrhage, blood clotting, abscess and a brownish yellow area in the perinephric fat tissue. The calyx and pelvis were normal. Histologically, the brownish yellow area was a granuloma with foam cell infiltration. The foam cells contained lipids. The renal parenchyma showed a non-specific chronic pyelonephritis.
Female↗
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↗
Isolation and characterization of a tumor-derived human protein related to chromogranin A and its in vitro conversion to human pancreastatin-48.
A protein with pancreastatin-like immunoreactivity has been isolated and purified from liver metastasis of a patient with insulinoma. NH2-terminal residue analysis, in conjunction with the use of antibodies that are specific for the C-terminal amide peptide of porcine pancreastatin, identified this protein as a 186-amino-acid protein corresponding to human chromogranin A-116-301 (the fragment corresponding to the positions from 116 to 301 of human chromogranin A). Digestion of this protein with trypsin yielded a 48-amino-acid peptide with the retention of full pancreastatin activity. Serum from patient with insulinoma contains a peptide specie(s) that comigrates with the 48-amino-acid pancreastatin, suggesting that this peptide might be a physiologically important circulation form of pancreastatin in humans. A sensitive radioimmunoassay was established using antibody developed against a synthetic 29-amino-acid peptide amide of pancreastatin. Immunocytochemical staining revealed that a major population of human pancreatic islet cells were immunoreactive to the antiserum but with varying intensity of staining. Pancreastatin-like immunoreactivity was not observed in exocrine acinar cells.
Adenoma, Islet Cell↗
Pancreastatin producing cell line from human pancreatic islet cell tumor.
It has been characterized that cell line QGP-1 derived from human non-functioning pancreatic islet cell tumor produces human pancreastatin. Exponentially growing cultures produced 5.7 fmol of pancreastatin/10(6) cells/hr. Human pancreastatin immunoreactivities in plasma and tumor after xenografting with QGP-1 into nude mouse were 92.7 fmol/ml and 160.2 pmol/g wet weight, respectively. Immunocytochemical study revealed both chromogranin A and pancreastatin immunoreactive cells in the tumor. Gel filtrations of culture medium and tumor extract identified heterogenous molecular forms of PST-LI which eluted as large and smaller molecular species. These results suggest that plasma pancreastatin levels may be useful as a tumor marker of endocrine tumor of the pancreas, and the pancreastatin producing cell line may be useful for studies of the mechanism of secretions and processing of chromogranin A and pancreastatin.
Adenoma, Islet Cell↗
[A comparative study of HBV-associated liver diseases between Korea and western part of Japan].
Overall positive rate of HBsAg in both serum and liver tissue was the highest in Pusan, followed by Kitakyushu and Osaka. HBsAg positive rate among patients with liver cirrhosis and hepatocellular carcinoma (HCC) was higher in Pusan than in Kitakyushu. Primary liver cancers, most of which were HCCs, were more frequently (3.4%) found in all inpatients of Kosin University, Pusan, than in those of UOEH (Kitakyushu), 1.9%. HCCs in Pusan were younger, less associated with cirrhosis and rather poorly differentiated than those in Kitakyushu and Osaka, Japan, and they might be related to a higher rate of HBsAg carriers in the former.
Carcinoma, Hepatocellular↗
Bioactivity of human pancreastatin and its localization in pancreas.
Synthetic human pancreastatin and its C-terminal fragment were first evaluated with respect to the biological activity on the insulin secretion in the isolated rat islets. Both these pancreastatins inhibited glucose-stimulated insulin secretion at a concentration of 100 nM. The relative molar potency of human pancreastatin compared to that of porcine pancreastatin was equivalent. The pancreastatin-reactive cells were widely located in the islets of Langerhans, and not observed in exocrine acinar cells by immunocytochemistry using human pancreastatin C-terminal specific antibody. These results suggest that human pancreastatin may modulate endocrine function of the pancreas, especially insulin secretion.
Amino Acid Sequence↗
High plasma pancreastatinlike immunoreactivity in a patient with malignant insulinoma.
High levels of pancreastatinlike immunoreactivity were detected in the plasma (2.9 pmol/ml, greater than 200-fold the normal level), pancreas (2.9 nmol/g wet wt, greater than 450-fold the normal level), and liver (1.6 nmol/g wet wt) of a patient with pancreatic insulinoma with metastasis to the liver by a sensitive and specific radioimmunoassay for human pancreastatin. Antiserum was produced against the C-terminal fragment of human pancreastatin-(24-52), which was synthesized according to the sequence of human chromogranin A corresponding to that of pancreastatin. With the antiserum, intense immunocytochemical staining was detected in the tumors. Sephadex G-50 gel filtration showed that the tumors and plasma contained two molecular forms of pancreastatinlike immunoreactivity--a molecular form coeluted with synthetic human pancreastatin-52 and a larger molecular form (Mr approximately 12,000-15,000). The smaller form eluted in the same position as synthetic human pancreastatin-52 on reverse-phase high-performance liquid chromatography.
Adenoma, Islet Cell↗