Establishment of a hepatocyte line for studying biosynthesis of long-chain polyunsaturated fatty acids from a marine teleost, the white-spotted spinefoot Siganus canaliculatus.

A hepatocyte line was established from the liver of white-spotted spinefoot Siganus canaliculatus to study the biosynthesis of long-chain polyunsaturated fatty acids (LC-PUFA). The cells from the line, designated S. canaliculatus hepatocyte line (SCHL), grew and multiplied well in Dulbecco's modified Eagle's medium (DMEM)-F12 medium supplemented with 20 mM 4-(2-hydroxyethyl) piperazine-1-ethanesulphonic acid (HEPES), 10% foetal bovine serum (FBS) and 0·5% rainbow trout Oncorhychus mykiss serum at 28° C, showing an epithelial-like morphology and the normal chromosome number of 48 (2n) and have been subcultured for over 60 passages. The identity of the hepatocytes was confirmed by periodic acid Schiff (PAS) staining. The mRNA expression of all genes encoding the key enzymes for LC-PUFA biosynthesis including two desaturases (Δ4 Fad and Δ6-Δ5 Fad) and two elongases (Elovl4 and Elovl5), were detected in all cells from passages 5 to 60 and their expression levels became stable after passage 35 and showed responses to various PUFA incubation. This is similar to the situation determined in the liver of S. canaliculatus that were fed diets containing different fatty acids. These results indicated that SCHL was successfully established and can provide an in vitro tool to investigate lipid metabolism and regulatory mechanisms of LC-PUFA biosynthesis in teleosts, especially marine species.

Validation of the Korean version of the EORTC QLQ-C30.

This study evaluated the Korean version of the EORTC QLQ-C30 (version 3.0) in terms of psychometric properties and its validation. One hundred and seventy patients completed three questionnaires EORTC QLQ-C30, the Beck depression inventory (BDI), and a brief pain inventory (BPI). Multitrait scaling analyses demonstrated that all scales met multidimensional conceptualization criteria, in terms of convergence and discrimination validity. Cronbach's alpha coefficients for eight multiple-item scales were greater than 0.70, with the exception of cognitive functioning. All interscale correlations were statistically significant in the expected direction (p < 0.01). Multivariate analyses showed that physical and emotional functioning were significant explanatory variables for the global quality-of-life (QOL) scale (regression coefficients: 0.36, p < 0.001; and 0.37, p < 0.001; respectively). All scales were significantly associated with pain severity and interference of the BPI, and with the cognitive-affective and somatic scales of the BDI. The emotional-functioning scale was substantially correlated with the cognitive-affective scale and somatic scale of the BDI. These results demonstrate that the Korean version of the EORTC QLQ-C30 is a valid instrument for evaluating Korean-speaking patients with cancer, and can be used to distinguish clearly between subgroups of patients of differing performance status.

Anaerobic digestion of polyelectrolyte flocculated waste activated sludge.

This work examined how adding one of three polyelectrolyte flocculants (T3052: cationic, T2000: non-ionic, and T1052: anionic) affected the anaerobic digestion of wastewater sludge. Methane production, floc characteristics (morphology and zeta-potential) and process parameters (soluble chemical oxygen demands (SCODs) and reductive potentials) were monitored along the digestion tests. The digestion rates of T2000- and T1052-conditioned sludge resembled that for original sludge. The T3052-flocculated sludge generated methane at a higher rate during the first 6 days of digestion than did the original one. In the following stage, the digestion rate of sludge flocculated with T3052 at dosage exceeding 15 g/kg dried solids declined. For example, at 40 days of digestion the methane production amounts for original, 15 g/kg DS flocculated, and 40 g/kg flocculated sludge were of 136, 105, and 85 g/kg DS, respectively. The role of flocculants could change in different stages of digestion. The dosed polymers had no apparent toxicity to the inoculum used. The changes in SCOD, adenosintriphosphate concentrations, oxidative and reductive potential, and zeta-potentials did not correlate with the noted hindered digestion for T3052-conditioned sludge. Microphotographic observation revealed that the flocs of T3052-conditioned sludge were not only of a large size, but also were resistant to structural deterioration during digestion. Therefore, mass transfer resistance was proposed to account for the hindered digestion efficiency observed for T3052-conditioned sludge.

Relationship between Helicobacter pylori and rosacea: it may be a myth.

Although it is debatable whether Helicobacter pylori may play a role in the pathogenesis of rosacea, some authors suggested that the treatment of H. pylori might have a beneficial effect. The aim of this investigation was to compare the prevalence of H. pylori between rosacea patients and controls, and to evaluate an effect of H. pylori eradication on rosecea by a 2-week triple therapy that was composed of amoxicillin, clarithromycin and omeprazole. H. pylori was detected by using gastroscopic biopsy with Warthin-Starry stain. Forty-two (84%) of 50 patients with rosacea and 39 (78%) of 50 controls had H. pylori, showing no significant difference in prevalence. The cure rates of H. pylori in rosacea patients and controls were 80% (16/20) and 85% (17/20), respectively. There was no significant decrease in the intensity of erythema in active treatment and placebo groups both during and after the treatment. Temporary improvement in papulopustules exclusively during the treatment (within 2 weeks) could be independent of H. pylori eradication. Overall, no significant reduction in the number of papulopustules was observed in active treatment and placebo groups after the treatment (in 2 months). Taken together, our study found no significant lessening of rosacea lesions by treating H. pylori infection, which conclusively does not concur with a view that H. pylori may be related to rosacea.

Ulcerogenic tumor syndrome of the pancreas associated with a nongastrin acid secretagogue.

Among 30 patients with islet cell neoplasms or hyperplasia who exhibited marked gastric acid hypersecretion and peptic ulceration and/or diarrhea, fasting plasma gastrin concentrations were less than 150 pg/ml in 11 patients, whereas the remaining 19 patients had hypergastrinemia. Plasma extracts from seven of these 11 patients were assayed for acid secretagogue activity in rats. All seven plasma extracts had secretagogue activity that was not found in the plasma extracts of ten patients with ordinary duodenal ulcer disease. Each of the tumor or pancreatic tissue extracts obtained from nine patients exhibited secretagogue activity in rats even though tissue gastrin content was 101.9 pmol (213.8 ng).g-1 or less. The secretagogue activity of the tumor extracts was confirmed in conscious gastric fistula dogs. The tumors' secretagogue activity, in contrast to gastrin, was destroyed by trypsin. It was eluted between porcine motilin and human gastrin I from a Sephadex G-50 (Pharmacia LKB Biotechnology, Inc., Piscataway, NJ) superfine column and was not retained by CM-cellulose, at pH 8.5. Its retention time during reverse phase HPLC on a C18 column also differed from those of G17 and G34. Thus, this secretagogue activity appeared mediated by a small, acidic peptide with a molecular size of about 2000 to 3000 daltons. The present study indicates that plasma and tumor extracts of these 11 patients contain a gastric acid secretagogue activity mediated by a nongastrin peptide. We suggest that what may be a distinct clinical entity associated with endocrine neoplasms of the pancreas should be considered in the face of excessive acid hypersecretion without fasting hypergastrinemia.

Atropine abolishes the potentiation effect of secretin and cholecystokinin-octapeptide on exocrine pancreatic secretion in humans.

Potentiating action between secretin and cholecystokinin on exocrine pancreatic secretion of bicarbonate has been well recognized. In the present study, we studied the effect of atropine on potentiating action on pancreatic exocrine secretion stimulated by exogenous secretin in physiologic dose and cholecystokinin-octapeptide in humans. Using a dye-dilution technique and a duodenal triple-lumen tube, pancreatic secretion of both bicarbonate and trypsin was determined while gastric juice was completely aspirated. Secretin given i.v. in a dose of 2.7 pmol/kg/h, which was known to achieve a similar plasma concentration of secretin after meal in humans, and cholecystokinin-octapeptide 26.2 pmol/kg/h potentiated pancreatic secretion of bicarbonate but not the pancreatic trypsin output. Atropine given i.v. in a dose of 1 mg/h abolished the potentiation effect of the two hormones on pancreatic bicarbonate output. Since the inhibitory effect of atropine on the secretin-stimulated bicarbonate output was statistically significant, the major inhibitory effect of atropine on the potentiation of pancreatic bicarbonate secretion appears to be its effect on the action of secretin.

Secretin is an enterogastrone in humans.

We studied in humans the effect of exogenous secretin in a physiological dose on gastric acid secretion stimulated by pentagastrin and postprandial plasma gastrin concentration. Two doses of pentagastrin, 80 and 160 pmol/kg/hr were used to stimulate gastric acid secretion. Secretin in two doses, 2.8 and 5.6 pmol/kg/hr were tried to study the response on stimulated gastric acid secretion. Intravenous secretin in a dose of 5.6 pmol/kg/hr significantly inhibited the gastric acid output stimulated by intravenous pentagastrin in a dose of 160 pmol/kg/hr, from 11.25 +/- 1.5 to 5.99 +/- 1.34 meq/hr while lower dose of intravenous secretin (2.8 pmol/kg/hr) failed to inhibit the gastric acid output stimulated by the same dose of pentagastrin. However, the lower dose of intravenous secretin (2.8 pmol/kg/hr) inhibited the gastric acid output significantly from 8.78 +/- 1.21 to 6.37 +/- 1.62 meq/hr when gastric secretion was stimulated by the lower dose of pentagastrin (80 pmol/kg/hr). The plasma concentrations of secretin during intravenous secretin in a dose of 2.8 pmol/kg/hr was similar to postprandial plasma concentrations of secretin as previously reported. Doubling the dose of intravenous secretin resulted in almost twofold higher plasma concentrations than postprandial plasma concentrations. In addition, the low dose of secretin (2.8 pmol/kg/hr) suppressed the integrated postprandial gastrin response from 13.9 +/- 3.7 to 11.2 +/- 2.8 ng/min/ml (P = 0.05) when endogenous release of secretin was blocked by intravenous cimetidine. Since the dose of pentagastrin and secretin employed in this study fell in a physiologic range, the inhibitory effect of secretin on stimulated gastric acid secretion appears to be a physiologic action in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

Release of cholecystokinin and exocrine pancreatic secretion in response to an elemental diet in human subjects.

We investigated in human volunteers the effects of an elemental diet (ED) containing amino acids on release of endogenous cholecystokinin (CCK) using a highly sensitive and specific radioimmunoassay of CCK and exocrine pancreatic secretion using a dye dilution technique with polyethylene glycol 4000 as a nonabsorbable marker. Intrajejunal administration of ED at three different infusion rates (12.5, 25, and 50 ml/30 min) resulted in a significant increase in plasma CCK concentration in a dose-related manner. Plasma concentrations of gastrin or secretin, however, did not change. Pancreatic secretion of protein, amylase, and bicarbonate also increased significantly. The change in pancreatic secretion of protein, amylase, and bicarbonate output paralleled that of the circulating CCK level but not that of plasma secretin. Thus, the dose of amino acid contained in ED recommended for clinical use can significantly stimulate the release of CCK from the upper small intestine, raising the plasma concentration of CCK. This level can evoke a significant increase in exocrine pancreatic secretion.

Non-gastrin secretogogue in ulcerogenic tumors of the pancreas.

In 18 patients with hypersecretion of acid, severe ulcer diathesis, and pancreatic islet cell tumor or hyperplasia, 14 had hypergastrinemia and 4 had normal plasma gastrin concentration. The neoplasms contained several gut peptides beside gastrin. The immunoreactive gastrin in the tumor extracts measured less than 7 ng/g, less than the amount previously reported. The extracts of each patient's tumor also contained a secretogogue other than gastrin that stimulated gastric acid secretion in rats. In addition, the plasma extracts of 2 patients also contained a secretogogue that stimulated acid secretion. After surgical resection of a recurrent metastatic tumor in 1 patient, basal acid secretion decreased from 13.9 to less than 1 meq/h, and the bioactivity of the plasma disappeared. These observations suggest the existence of a secretogogue that appears to be a protein in the pancreatic tumors of some patients with severe ulcer diathesis and hypersecretion.

Study of electromechanical activity of the stomach in humans and in dogs with particular attention to tachygastria.

The relationship between electric and mechanical activities of the gastric antrum was investigated in both humans and dogs. In 2 patients, in whom platinum monopolar electrodes were implanted on the serosal surface of the antrum and a perfused manometric tube was placed in the stomach, the number of gastric contractions detected by manometry was only less than 50% of the pacesetter potentials accompanied by action potentials or second potentials. No contraction of the stomach was recorded by manometry when pacesetter potentials occurred without action potentials or second potentials. The relationship was further investigated in 11 anesthetized dogs prepared with implanted electrodes and sensitive ministrain gauges implanted on the serosal surface of the stomach and an intragastric manometric tube. In these dogs, phasic contractions were always recorded by the method using ministrain gauges although the electrical activity showed only PSPs without action potentials or second potentials. The manometry, however, could not recognize these phasic contractions. When the stomach was stimulated by bethanechol infusion through the splenic artery, as in the human stomach, the manometry detected less than 50% of gastric contractions detected by the strain gauge recording. The gastric dysrhythmia including tachygastria, tachyarrhythmia, and bradygastria was induced in 10 dogs by epinephrine, 100 micrograms X kg-1 X h-1, infused via the splenic artery. During the period of gastric dysrhythmia, the phasic contractions disappeared and no contraction associated with action potential could be observed. The phasic contractions reappeared as long as the PSPs occurred regularly in a frequency of 4-5 cycles/min during either the control period or during the period of epinephrine infusion. The epinephrine-induced gastric dysrhythmia was blocked or reversed to normal pacesetter potentials by intraarterial infusion of phentolamine. Our study suggests the following: (1) the pacesetter potentials not only pace and direct gastric contraction, but they may also play a role in the genesis of phasic contractions of the stomach, and (2) gastric contractions detected by sensitive strain gauges are not always recorded by the intraluminal manometry and, thus, gastric dysrhythmia may not be detected by the manometry in humans.

Potentiation effect of cholecystokinin-octapeptide on pancreatic bicarbonate secretion stimulated by a physiologic dose of secretin in humans.

We studied the potentiation effect of cholecystokinin-octapeptide and secretin on pancreatic secretion of bicarbonate and trypsin in humans. The pancreatic bicarbonate and trypsin outputs were determined by using a triple-lumen duodenal tube and indicator dilution technique while gastric juice was completely aspirated. When cholecystokinin-octapeptide in varied doses, 2.6, 5.3, 10.9, 26.3, 52.6, and 109.4 pmol . kg-1 . h-1, was added to i.v. infusion of secretin in a physiologic dose, 0.03 clinical units (CU) . kg-1 . h-1, the bicarbonate outputs were significantly greater than those achieved by secretin or cholecystokinin-octapeptide alone or the sum of the bicarbonate outputs produced by each hormone. The potentiation effect of cholecystokinin-octapeptide occurred at the dose of 10.9 pmol . kg-1 . h-1. No further further augmentation on the bicarbonate output occurred when the dose of cholecystokinin-octapeptide was increased in the dose range greater than 10.9 pmol . mg-1 . h-1. No potentiation on pancreatic secretion of trypsin was apparent when the two hormones were given simultaneously. Thus, cholecystokinin-octapeptide in a relatively small dose range potentiated the pancreatic bicarbonate secretion stimulated by a physiologic dose of secretin. The pancreatic enzyme secretion does not appear to be potentiated by two hormones.

Effects of atropine on the action and release of secretin in humans.

Using two groups of volunteers, we investigated the effects of atropine on pancreatic secretion of bicarbonate, protein, and trypsin stimulated by secretin. Secretin given intravenously in graded doses of 0.03, 0.06, and 0.125 clinical units.kg-1.h-1 produced significant increases in pancreatic secretion of bicarbonate in a dose-related manner. Pancreatic secretion of bicarbonate and protein was significantly suppressed by intravenous atropine, despite the dose of secretin infused. Intrajejunal perfusion of HCl at a rate of 3.3 mM/h, producing plasma secretin concentration comparable with that of the postprandial state, resulted in significant increases in the pancreatic secretion of bicarbonate. The increase in the pancreatic secretion of bicarbonate and trypsin was significantly suppressed by atropine. However, atropine did not affect the increase in the plasma secretin concentration produced by jejunal acidification or intravenous secretin. These studies indicate that atropine inhibits the pancreatic effect but not the intestinal release of secretin.

Gastric and small intestinal myoelectric dysrhythmia associated with chronic intractable nausea and vomiting.

We describe a patient with symptoms of severe nausea, vomiting, epigastric bloating and pain, and marked weight loss due to a gastrointestinal motility disturbance. Motility abnormalities were characterized by uncoordinated high pressure (as high as 300 mm Hg) contractions and uncoordinated interdigestive motor complexes in the duodenum and small intestine, and tachygastria often associated with tachyarrhythmia in the gastric myoelectric activity recordings. Uncoordinated interdigestive myoelectric complexes again were found in the duodenum and small intestine. These abnormal myoelectric activities observed in the in-vivo study were confirmed in the in-vitro study. After distal hemigastrectomy and gastrojejunostomy, the symptoms of nausea, vomiting, and epigastric pain decreased considerably. Thus, the motility abnormality found in the study appears to be responsible for the symptoms described. This is probably a new clinical entity. The importance of manometric and myoelectric study of a gastrointestinal motility for unexplained nausea and vomiting is emphasized.

Electrogastrographic study of patients with unexplained nausea, bloating, and vomiting.

A method of recording gastric myoelectric activity with a peroral suction electrode was evaluated, and the recording was compared with that obtained by implanted electrodes on the serosal surface of the stomach of laparotomized humans. In a group of patients with unexplained nausea, epigastric bloating, and vomiting, abnormal antral myoelectric activities were found by a peroral electrode, in contrast to a regular pacesetter potential (frequency: 3-4/min) in control subjects. These abnormalities were confirmed by the recordings from the implanted electrodes in the same subjects. The study indicates that peroral recording of gastric myoelectric activity is a useful diagnostic method for the detection of gastric myoelectric activity abnormalities in humans.