[County physician Christian Lintrup's work in the Norwegian county Hedemark 1800-1831].

Background: The first decades after 1800 were dominated by war, bad crops and epidemics and the few existing public physicians worked under difficult conditions.

Material And Methods: A review of medical reports from the period 1804-31 and county physician Christian Lintrup's (1768-1844) correspondence with other public physicians in the county of Hedmark (Hedemarken at the time) and the county official (their administrative leader).

Results: Lintrup was born in Denmark, took his medical university degree in 1798 in Copenhagen and was appointed county physician in Hedemarken in 1799.

[Botulism in Osterdalen in 1831].

The earliest report we have had of an outbreak of botulism in Norway is from 1934, of five cases caused by contaminated salted and dried ham. All patients survived. This paper describes an early outbreak of botulism in the county of Hedmark in 1831 on the basis of a previously unknown report to the county governor from district public health officer Peter Heiberg (1778-1849).

[The introduction of the Public Health Act of 1860].

The Public Health Act of 1860 introduced modern health legislation in Norway. The act was a consequence of the industrial revolution and was influenced by the European hygienic movement and the English Public Health Act of 1848. The act placed the responsibility for public health measures on the local authorities in accordance with contemporary political philosophy.

[Growth and stagnation--development of health services during the 20th century].

The health services of Norway have changed over the last century in tune with the development of society. The health services are not only the result of scientific and technological progress, but also a product of changes in prevailing political and social conditions and ideologies. Quality assessment and concern for the ethical basis of the health services ought to be given priority in the years to come.

Improved assay for fecal calprotectin.

Fecal calprotectin is a marker of inflammatory and neoplastic disease in the lower gastrointestinal tract. A new fecal sample preparation procedure for the measurement of calprotectin has been developed, with higher calprotectin yield and lower contamination risk. Changes in the new method compared to the original [Roseth AG, Fagerhol MK, Aadland E, Schonsby H.

[13C-urea breath test as diagnostic method in Helicobacter pylori infection].

We have evaluated a 13C-urea breath test for the diagnosis of Helicobacter pylori infection. The 13C-test was analyzed with isotope-selective nondispersive infrared spectrometry and compared with a 14C-urea breath test and the urease test in gastric mucosal biopsies. 46 patients were analyzed with breath tests; 23 patients were negative and 22 patients were positive with both methods.

Fecal calprotectin concentration in patients with colorectal carcinoma.

Purpose: The study contained herein was undertaken to investigate fecal calprotectin excretion in a series of patients with colorectal carcinoma and to determine whether the excretion was influenced by localization or stage of the tumor. Furthermore, the effect of surgical treatment on the concentrations was studied. Fecal calprotectin was also compared with plasma concentrations of calprotectin, carcinoembryonic antigen, and C-reactive protein.

Faecal calprotectin: a novel test for the diagnosis of colorectal cancer?

Calprotectin, a prominent cytosol protein in neutrophil granulocytes, was present in increased concentrations in stools from 50 of 53 patients with colorectal cancer, 32 of 40 patients with colorectal polyps, and all of 18 patients with gastric cancer. After radical surgery, faecal calprotectin levels reverted to the normal range in all but one patient with colorectal cancer. Calprotectin determinations are simplified by the stability of this protein in stools.

Assessment of the neutrophil dominating protein calprotectin in feces. A methodologic study.

This study describes methods for extraction and quantification of calprotectin (L1 protein) in feces by enzyme immunoassay. This protein is a prominent antimicrobial component of neutrophils, monocytes, macrophages, and squamous epithelia. Calprotectin was stable in feces during storage for 7 days at room temperature.

The inhibitory effect of bile on the binding of vitamin B12 to intrinsic factor. An in vivo study in rats.

To investigate whether bile reduces the amount of vitamin B12 bound by intrinsic factor (IF) in the intestinal juice in vivo, choledochocolic fistulae were made in 9 rats, and 10 rats were sham-operated. Small-intestinal juice was collected 1 h after gastric instillation of 57CoB12. The percentage of 57CoB12 bound by IF in the intestinal juice was markedly increased in fistula rats (median, 86%; range, 75-91%) as compared with sham-operated rats (35%; 12-50%) (p less than 0.

Effect of calcium deficiency on vitamin B12 absorption in rats.

The influence of calcium on vitamin B12 absorption was investigated in two experiments. In the first we investigated whether B12 malabsorption in rats with biliary diversion through choledochocolic fistula is caused by deficiency of calcium in the small intestine. Calcium concentrations were measured in 10 fistula- and 10 sham-operated rats.

[Hydrogen breath tests in the diagnosis of primary lactase deficiency].

The H2 breath test as an indirect method of detecting lactase deficiency was evaluated in 55 patients referred because of abdominal complaints. The patients underwent both jejunal biopsy with determination of enzyme activities and the H2 breath test. 19 patients had lactase deficiency defined as a lactase/sucrase ratio less than 0.

Is vitamin B12 malabsorption in bile fistula rats due to bacterial overgrowth? A study of bacterial metabolic activity in the small bowel.

To investigate whether vitamin B12 malabsorption in rats with choledochocolic fistulae is caused by bacterial overgrowth, we studied intestinal bacterial metabolic activity in choledochocolic fistula-operated rats, self-filling blind-loop-operated rats, and sham-operated rats. Fistula-operated rats had a moderate indicanuria compared with sham-operated ones, whereas the faecal excretion of nitrogen was unchanged. There was no difference in the amounts of radioactivity recovered in sediments of intestinal contents after an oral dose of 57CoB12, indicating unaltered bacterial uptake of vitamin B12 in fistula rats.

Effect of gastric anacidity on the release of cobalamins from food and their subsequent binding to R-protein.

Rabbit liver homogenate, labelled in vivo with 57Co, was used to investigate the effect of anacid gastric juice on the release of cobalamins from food and on the cobalamin binding to proteins in humans. The cobalamin release was investigated in vitro by incubating the liver homogenate with native and neutralized gastric juice. The cobalamin release and the amount of cobalamins bound to R-protein were significantly higher with native than with neutralized gastric juice.

Intestinal epithelial function and villus surface area in rats with bile fistulae.

We have previously found reduced absorption of vitamin B12 in rats with choledochocolic fistulae. To investigate whether the reduction is caused by epithelial dysfunction or mucosal hypoplasia, choledochocolic fistulae were made in 11 rats, whereas 10 rats were sham-operated. The epithelial function was evaluated 9 days later by measuring the uptake of 57CoB12 and glucose in perfused intestinal segments and by determining the activities of 11 mucosal enzymes.

The effect of omeprazole on gastric acidity and the absorption of liver cobalamins.

The effect of gastric anacidity on the absorption of food-bound cobalamins is uncertain. Omeprazole, an inhibitor of the enzyme H-K-ATPase in the parietal cell, is the most potent inhibitor of gastric acidity known so far. In 17 healthy male volunteers the absorption of liver-bound cobalamins was assessed after a single intravenous dose of omeprazole (80 mg) or placebo in a double-blind, crossover manner.

Local disodium cromoglycate is ineffective in ulcerative proctosigmoiditis.

Conflicting results have emerged from studies using oral and rectal disodium cromoglycate (DSCG) in inflammatory bowel disease. In the present double-blind study, 43 patients with active ulcerative proctosigmoiditis received either placebo (n = 22) or 600 mg DSCG (n = 21) rectally as enemas for eight weeks. Assessment was made from clinical investigations, endoscopy, laboratory tests, biopsies, and diary cards.