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This article presents abstracts of research articles on finance. The paper "The Demand for Money in Denmark: 1921-62" is a study of the demand for money in Denmark using the aggregate stock of money, net national income and the rate of interest as the main variables. The method applied is single-equation regression analysis, and the relations are estimated for different periods and with various combinations of the variables. The article "Stochastic Reserve Losses" is concerned with the Orr-Mellon thesis which introduced the notion of uncertainty into the well-known comparative static analysis of bank credit expansion. The paper "The Impact of Monetary Stringency on Business Investment" utilizes the unique potential provided by the OBE-SEC surveys of the capital outlays of non-farm business to develop quantitative estimates of the reductions in both plant and equipment and inventory investment which resulted from the unusually severe credit stringency in 1966. An attempt is made to distinguish the direct effects, operating through the high cost of funds from accelerator or expectational effects, operating through reductions in actual or expected sales attributed to the impact of credit conditions on the firm's customers.

A patient with the Zollinger-Ellison syndrome was followed with multiple gastric secretion tests and serum gastrin analyses for six years. During this period cimetidine requirement increased to a daily dose of 8 g, but it reversed spontaneously after two years. The altered cimetidine effectiveness was not associated with reduced oral bioavailability and serum calcium was unchanged. Total serum gastrin was very high at all times, and fractionation of gastrins in serum by gel filtration showed varying proportion of big to small gastrins, but not in a mode which explained the parietal cell resistance to cimetidine. [ABSTRACT FROM PUBLISHER]

In a double-blind, parallel-group clinical trial of 195 patients with duodenal ulcers who after a short-term study had relief of pain and healed ulcers proved endoscopically, 65 were randomized to receive 20 mg omeprazole 3 days a week (once in the morning from Friday to Sunday), 64 to receive 10 mg omeprazole once daily in the morning, and 66 to receive placebo for up to 6 months. The patients underwent repeat endoscopy with biopsy of the gastric fundic mucosa (qualitative assessment of argyrophilic cell population), assessment of symptoms, and laboratory screening with measurement of basal serum gastrin concentrations at 3 and 6 months or more often if indicated by recurrence of symptoms. At 3 months, endoscopically proved ulcer relapse occurred in 16% receiving 20 mg omeprazole 3 days a week; 21% receiving 10 mg omeprazole daily; and 50% receiving placebo. At 6 months, corresponding rates were 23%, 27%, and 67% with 95% confidence intervals of difference between the placebo group and omeprazole groups of 28%-60% and 24%-56% (P less than 0.00001), respectively, and between omeprazole groups of -19%-11% (NS). No major clinical or laboratory side effects were noted. Thus both omeprazole regimens are effective and safe in preventing duodenal ulcer relapse.

The concentration of the NH2-terminal fragment of gastrin-17 in serum was determined by radioimmunochemistry. Two antisera were used, one specific for the COOH-terminus and the other for the NH2-terminus of gastrin-17. The NH2-terminal gastrin-17 immunoreactivity in unfractionated serum correlated well with the amount of fragment found after gel filtration of the same sera (p less than 0.001). In healthy subjects (no. = 100), the NH2- and COOH-terminal gastrin immunoreactivity was 8 +/- 1 and 20 +/- 1 pmol/l (mean +/- SEM), respectively. In patients with acute duodenal ulcer (no. = 30) and acute gastritis (no. = 10) the NH2-terminal immunoreactivity was fourfold increased compared with in healthy subjects (p less than 0.001), whereas the COOH-terminal was identical, the NH2- and COOH-terminal concentrations being 33 +/- 7 and 22 +/- 2 pmol/l in duodenal ulcer and 35 +/- 6 and 21 +/- 1 pmol/l in acute gastritis. Other groups of patients had NH2- and COOH-terminal gastrin concentrations in serum similar to those measured in healthy subjects. The results suggest that gastrin cells process gastrin-17 abnormally during the acute phase of duodenal ulcer and gastritis.

Molecular heterogeneity is a fundamental feature of ribosomally synthesized proteins and polypeptides. The heterogeneity reflects gene duplications with subsequent differences in mutation of the genes, different post-transcriptional and post-translational processings and different amino acid modifications. Gut hormones are also heterogeneous, but the degree of heterogeneity reported so far for each hormone has varied. The most extensively studied (i.e. cholecystokinins, gastrins, opioid peptides and glucagons) have displayed a high degree off heterogeneity. Similar degrees will probably emerge for the remaining gut hormones when they have been studied in greater detail. In accordance with the nature of the molecular difference, a distinction between macro- and microheterogeneity is proposed. Macroheterogeneity is caused by variations in peptide chain length; microheterogeneity by derivatizations or substitutions in single amino acid residues. The molecular heterogeneity has profound implications for measurement and study of a gut hormone. Thus, measurement in biological fluids requires careful evaluation of the number and affinity of different molecular forms. Understanding of the function and pathophysiology of gut hormones requires full clarification of their molecular heterogeneity.

The effect of sulfuric acid esterification of Tyr-12 in gastrin-17 on immunoreactivity was evaluated by the ability of seventeen antisera raised against non-sulfated gastrin-17 to bind sulfated gastrins in extracts of gastrinoma and antral tissue. Using non-sulfated Tyr-12 iodinated gastrin as tracer, and non-sulfated gastrin-17 as standard the antisera showed three different patterns of reactivity: Three antisera (Nos. 2602, 2605 and 4562) bound sulfated gastrins with low (4-23%) potency; four antisera (Nos. 2604, 2720, 4710 and 4713) measured sulfated gastrins with a potency similar to that of non-sulfated gastrins (81-100% crossreactivity); whereas ten antisera (Nos. 2601, 2606, 2609, 2716, 2717, 2718, 4556, 4559, 4560 and 4563) displayed enhanced reactivity with sulfated gastrins (130-373% crossreactivity). Using Gly-2 iodinated gastrin as tracer, the latter type of antisera reacted almost equally with sulfated and non-sulfated gastrins, suggesting that the apparent increase in binding of sulfated gastrins rather is due to increased displacement of Tyr-12 iodinated gastrin. The results show that derivatization of amino acid residues greatly influences antibody binding.

We compared serum concentrations of cathodic trypsin-like immunoreactivity, pancreatic lipase, and pancreatic isoamylase as diagnostic tests of chronic pancreatitis (and of pancreatic steatorrhea in the 41 patients with steatorrhea) in 105 patients (57 men, 48 women) consecutively investigated because of clinical suspicion of chronic pancreatitis. Chronic pancreatitis (36 patients), pancreatic steatorrhea (24 patients), and other diseases were diagnosed without knowledge of the serum levels of the three enzymes. When evaluated by means of receiver operating characteristic curves, no differences were found in diagnostic performance of the enzymes with regard to chronic pancreatitis or pancreatic steatorrhea. The sensitivity and specificity for recognition of chronic pancreatitis ranged from 0.306 to 0.444 and from 0.942 to 0.986 when the discrimination values were chosen to give highest efficiencies. The similar ranges for pancreatic steatorrhea were 0.500-0.708 and 0.882-0.941. In conclusion, none of the three enzymes had any advantage over the others as diagnostic tests of chronic pancreatitis or of pancreatic steatorrhea. Only positive test results have clinical importance because of the low sensitivities of the three enzymes.

The degree of tyrosine sulfation and the distribution between gastrin-17- and gastrin-34-like immunoreactivity (LI) were studied in the antra of ten mammalian species. Specific radioimmunoassays, gel-, and ion-exchange chromatography as well as enzymatic cleavage with trypsin and arylsulfatase were used. The percentage of sulfation varied from 24.4 +/- 4.2 (mean +/- SEM) in dogs to 80.1 +/- 2.6 in sheep, 46.8 +/- 3.3 in humans, 50.1 +/- 3.2 in cows, 55.9 +/- 2.3 in rats, 57.4 +/- 3.1 in pigs, 61.3 +/- 2.2 in guinea pigs, 64.1 +/- 4.7 in cats, 64.8 +/- 2.1 in mice and 68.2 +/- 2.8 in rabbits. Gastrin-34-LI in antral extracts could be converted to gastrin-17-LI by trypsin in all species. Five percent of antral gastrins eluted as gastrin-34-LI in all species. We conclude that while the ratio of gastrin-34-LI to gastrin-17-LI varies little in mammals, large differences occur in the degree of sulfation.

We found small amounts of cholecystokinin in the normal human adenohypophysis and therefore examined pituitary tumors from 87 patients with acromegaly, Cushing's disease, Nelson's syndrome, prolactinoma, or inactive pituitary adenomas. Five adenomas associated with Nelson's syndrome contained increased amounts of cholecystokinin, the concentrations being extremely high in two: 8281 and 13,453 pmol per gram as compared with less than 30 pmol per gram in normal pituitary glands. The cholecystokinin concentrations were moderately increased in adenomas from another 12 patients, of whom 5 had Cushing's disease and 7 acromegaly with adenomas containing ACTH. The cholecystokinin peptides from the tumors were smaller and less sulfated than cholecystokinin from normal pituitary glands. We conclude that ACTH-producing pituitary cells may also produce an altered form of cholecystokinin.

We examined whether parietal cell vagotomy (PCV) changed the distribution between the different molecular forms of gastrin. Serum, antrum, and duodenum from PCV patients, unoperated duodenal ulcer (DU) patients and control subjects were studied. PCV was followed by a twofold increase in the serum gastrin concentration, while the distribution between small and large gastrins were unaffected. However, sulfation of antral gastrins was reduced from 45 percent in unoperated DU patients to 34 percent in PCV patients (p less than 0.01). We conclude that gastrin sulfation is diminished after PCV. Diminished sulfation seems to be correlated to hypergastrinaemia of antral origin and not to specific diseases.

The sulfation of gastrin in serum, antrum and duodenum was studied in 22 normo- and 20 hypergastrinemic patients. The ratio between gastrin-17 and gastrin-34 was measured in antrum and duodenum. The degree of sulfation was reduced in the antrum of hypergastrinemic patients (35.3 +/- 1.3%, mean +/- SEM) compared with 48.0 +/- 2.1% in normo-gastrinemic patients (p less than 0.001). The degree of sulfation in serum and duodenum was similar to that of the antral gastrins in all patients. The percentage of gastrin-34 in antrum was increased (7.3 +/- 0.7%) in hypergastrinemic compared with 4.9 +/- 0.3% in normogastrinemic patients (p less than 0.01). In the duodenum the percentage of gastrin-34 was similar in normo- and hypergastrinemia. When classified according to clinical diagnosis, sulfation of antral gastrin was normal in duodenal ulcer (47.6 +/- 4.5%) but decreased in gastric ulcer (36.7 +/- 1.6%, p less than 0.01) and pernicious anemia (31.3 +/- 1.9%, p less than 0.001) compared with 48.2 +/- 2.2% in control patients. In pernicious anemia a larger proportion of antral gastrins occurred as gastrin-34 (8.2 +/- 0.9%) compared with 4.8 +/- 0.4% in control patients (p less than 0.01). Our study suggests that both sulfation and proteolytic processing of the gastrin precursor is diminished in hypergastrinemia of antral origin.

The degree of tyrosine-O-sulfation and the ratio between large (gastrin-34 and component I) and small (gastrin-17 and -14) molecular forms of gastrin were studied in extracts of human fetal (n = 14) and adult (n = 9) antrum, duodenum, jejunum and pancreas. Boiled water extracts were applied to gel- and ion-exchange chromatography before and after treatment with trypsin and arylsulfatase. The fractions were monitored with sequence-specific radioimmunoassays that distinguish sulfated from non-sulfated gastrins. In antrum and duodenum about half the gastrins were sulfated at all stages of development. In the fetal jejunum gastrin occurred in sulfated form only while in the adult 72% (range, 64-88%) of the jejunal gastrins were sulfated. The larger molecular forms of gastrin predominated in the fetal compared with the adult antrum. In duodenum and jejunum, however, the ratio between small and large forms was the same in fetus and adult. Gastrin was undetectable in both fetal and adult pancreas. The results show that the degree of sulfation of gastrin varies substantially in the different parts of the gut at different stages of development. The differences may have functional significance, since sulfation increases the pancreozyminic and cholecystokinetic potency of gastrin.

Sulfated gastrins were quantitated in sera from 15 patients with the Zollinger--Ellison syndrome (ZES) by specific radioimmunoassays. The total concentration of gastrin varied from 174 to 285 000 pmol/l. Sulfated gastrins constituted 44.8 +/- 5.5% (mean +/- S.E.M.) of the gastrins in ZES sera compared with 37.7 +/- 1.9% in sera from 100 control subjects (P greater than 0.1). There was no correlation between gastrin concentration and sulfation (r = 0.40). Gel and ion-exchange chromatography showed that up to 90% of the gastrins could be in the sulfated form. The highest degree of sulfation was found in sera where the small gastrin components dominated. Thus, the percentage of small gastrins (G-17 and G-14) correlated with the degree of sulfation (N = 15, r = 0.75, P less than 0.01). We suggest therefore that proteolytic processing of the gastrin precursor and sulfation of tyrosyl are associated.

Glucose tolerance and B cell function were assessed in 30 consecutive chronic alcoholic patients without overt diabetes mellitus. Plasma glucose, insulin, and C peptide concentrations were measured during an oral glucose tolerance test. All patients underwent a liver biopsy and an exocrine pancreatic function test (Lundh test). Compared with the controls, the three groups of alcoholic patients (those with histologically normal livers, n = 12; those with steatosis, n = 10; and those with cirrhosis, n = 8) all had a two-fold increase in plasma concentrations of insulin as well as C peptide in the fasting state, despite normal fasting levels of glucose. After oral glucose all groups of patients had elevated plasma levels of glucose, insulin, and C peptide compared with the controls. The C peptide/insulin ratio was similar to that in the controls in all groups of alcoholics. Patients with decreased exocrine pancreatic function (n = 7) had a significantly lower insulin and C peptide response to glucose than the patients with normal exocrine pancreatic function. It is concluded that (1) chronic alcoholics even with histologically normal livers have endogenous insulin resistance, and (2) associated damage to the exocrine pancreas is more common than previously recognized and decompensation of B cell function could be demonstrated in patients with decreased exocrine pancreatic secretion.

Fourteen patients with verified pancreatic cysts were examined by both preoperative endoscopic retrograde pancreatography (ERP) and ultrasonic scanning. ERP showed filling of a cyst in 4 patients and raised suspicion of a cyst in 8. In two patients it was not possible to visualize the pancreatic duct. Ultrasonic scanning showed a cyst in 12 patients. There were two false negative ultrasonic diagnoses. These two were correctly diagnosed by ERP. Ultrasonically guided percutaneous puncture was carried out on 19 occasions in 8 patients. Cysts down to 2 cm in diameter were punctured without difficulty. There were no clinically significant complications due to the punctures. One patient was followed for 20 months without ultrasonically demonstrable recurrence of a large cyst aspirated, showing that definite therapy is possible by this method. Puncture can be used to verify the diagnosis and as treatment in patients where surgery is contraindicated.

A radioimmunochemical procedure which distinguishes sulfated from non-sulfated gastrins has been developed. Two antisera raised against synthetic non-sulfated human hexadecapeptide gastrin were used. No. 2604 binds sulfated and non-sulfated gastrins with equimolar potency, whereas No. 2605 reacts poorly with sulfated gastrin (ID50 for non-sulfated gastrin: ID50 for sulfated gastrin = 0.06). Both antisera bind gastrins of different molecular length with equimolar potency using monoiodinated human gastrin-17 as tracer. The method was validated by fractionating gastrins in serum and in tissue extracts, and by recovery experiments. We found that Component I of gastrin--like the smaller gastrin components--was present in both, sulfated and non-sulfated form. In serum from normal fasting subjects the concentration of non-sulfated gastrin was 12.5 +/- 0.8 pmol/l (mean +/- SEM) with a total range of 0-44 pmol/l and the corresponding values for sulfated gastrin were 7.5 +/- 0.5 pmol/l (range 0-20 pmol/l). Sulfated gastrin accounted for more than half of the gastrins in only 21% of normal subjects. There was a parallel rise and fall in sulfated and non-sulfated gastrins after a meal and after stimulation with adrenaline.

The basal concentrations of sulfated and non-sulfated gastrins in serum were measured radioimmunochemically in healthy subjects and in normo- and hyper-gastrinemic diseases. The degree of sulfation in patients with duodenal and gastric ulcer, chronic pancreatitis, gallstone disease, and chronic renal failure were similar to that of healthy controls, in whom 37.7 +/- 1.9% (mean +/- SEM) of serum gastrins were sulfated. In eight patients with the Zollinger-Ellison syndrome 57 +/- 5.4% of the gastrins were sulfated (p less than 0.005, compared with controls). In patients with pernicious anemia (no. = 20) only 24.4 +/- 2.0% of the gastrins were sulfated (p less than 0.005, compared with controls). An inverse correlation (r = -0.63, p less than 0.01) was found between the degree of sulfation and the total gastrin concentration in pernicious anemia but not in gastrinoma patients. The results indicate that diseases with increased synthesis of gastrin are accompanied by an abnormal degree of sulfation.

The exocrine pancreatic function was studied in 460 patients suffering from dyspepsia (defined as abdominal pain, chronic diarrhoea, and/or weight loss) by measuring the duodenal concentrations of amylase and lipase after a test meal (Lundh test). In 159 of the patients (35 per cent) a reduced pancreatic function was found. In 143 out of these a diagnosis of possible or verified chronic pancreatitis was made. In about half of these 143 patients, the diagnosis chronic pancreatitis was clinically unexpected. Consequently, chronic pancreatitis is to be suspected as a cause of dyspepsia when more usual causes have been excluded.

Postanaesthetic arousal time was studied in elderly patients given either glycopyrrolate 0.01 mg kg-1 or atropine 0.02 mg kg-1 before antagonism of neuromuscular blockade. Forty patients (age greater than or equal to 65 yr) undergoing elective hip replacement were included in a double-blind study. Arousal was scored for 2 h after recovery using a modified scoring system. No difference in arousal time was found between the two groups.

Only a decade ago surgery was the preferred treatment of recurrent peptic ulcer. With the introduction of cimetidine in 1976 effective and safe medical treatment could be offered to the patient. H2-receptor antagonists are still the basic drugs in ulcer healing, but in recent years mucosa protective agents as sucralfate and colloidal bismuth have been increasingly used. Complete inhibition of acid secretion may be achieved by the new proton pump inhibitor omeprazole. In ulcer resistant to treatment with H2-receptor antagonists either a mucosa protective agent, as colloidal bismuth or a potent acid inhibitor (omeprazole) may be used. In recurrent duodenal ulcer a systematic and prolonged maintenance therapy with H2-receptor antagonists is indicated. This treatment is safe and it reduces the incidence of a relapse to one third compared with placebo. Surgery is no longer indicated in the majority of patients with uncomplicated recurrent peptic ulcer. In most patients this disease can now be controlled by effective and cheap anti-ulcer drugs. Although medical treatment of peptic ulcer has been used for centuries, surgery was still the main treatment of recurrent peptic ulcer in the nineteen seventies. Up to that time the surgical management of ulcer disease had made major progress, while medical treatment had failed to offer effective cure. Thus, as late as in 1975 the medical treatment of peptic ulcer consisted of antacids, bed rest and carbenoxolone. With the important side effects of carbenoxolone in mind, it is no wonder that medical treatment was no alternative to surgery in patients suffering from recurrent peptic ulcer.(ABSTRACT TRUNCATED AT 250 WORDS)

The efficiency of immunoreactive trypsin (IRT), pancreatic polypeptide (PP), and pancreatic isoamylase (PI) in the diagnosis of chronic pancreatitis was studied in 80 consecutive patients clinically suspected of having chronic pancreatitis. Twenty-five patients had chronic pancreatitis, and of these, 17 had pancreatic insufficiency. IRT, PP, and PI were of no value in the diagnosis of chronic pancreatitis without insufficiency. The three tests were of equal but limited value in diagnosing pancreatic insufficiency (nosographic sensitivities, 0.53 to 0.59, and predictive values of a negative test, 0.88 to 0.90). The combination of IRT, PP, and PI did not increase the diagnostic efficiency compared with each of the three tests alone. We conclude that IRT, PP, and PI are of similar but limited value as diagnostic tests for pancreatic insufficiency.