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SUMMARY Three infants, in whom the malabsorption syndrome, small intestinal. mucosal damage and clinical cow's milk intolerance were found, were challenged with cow's milk after initial treatment with breast milk. The small intestinal mucosa was investigated with light and electron microscopy both before and after provocation. Clinically one patient reacted rapidly in a few hours and showed round cell infiltration in the surface epithelium and lamina propria 20 hours after a single challenge. Electron microscopy showed short microvilli, abnormal nuclei and thickened basement lamina in the surface epithelium. Two patients reacted slowly. One of them showed similar changes 4 days after commencement of the provocations, but the changes were much more evident 38 days later, when symptoms were also apparent. At this time large accumulations of lysosomes in the apical part of the surface epithelial cell and marked thickening of the basal lamina with accumulations of whirly collagen fibres were detected. The third patient reacted in a milder way, both clinically and morphologically. This study indicates that cow's milk, apparently through its protein fraction, may damage the surface epithelium of the small intestinal mucosa. These alterations during provocation periods resemble those found in coe-liac disease during gluten provocation.

Der Einflus einer induzierten Hypercalcamie auf die Serumgastrinspiegel und die Magensekretion wurde bei Normalpersonen, Patienten mit Ulcus duodeni und Patienten mit Zollinger-Ellison-Syndrom untersucht. Bei allen Patientengruppen kommt es wahrend der Calciumgluconatinfusion zu einem signifikanten Anstieg der Serumgastrinspiegel. Patienten mit Ulcus duodeni schutten jedoch 2–3mal soviel Gastrin wahrend einer Hypercalcamie aus wie Normal-personen, wahrend die Gastrinausschuttung bei Patienten mit Zollinger-Ellison-Syndrom ein Vielfaches der von Ulcus duodeni-Patienten betragt. Die integrierte Saureausschuttung wahrend Hypercalcamie ist bei Ulcus duodeni-Patienten ca. 5fach hoher als bei Kontrollpersonen. Diese Untersuchungen zeigen, das die Calcium-induzierte Magensekretion, zumindestens teilweise, durch eine Gastrinfreisetzung hervorgerufen wird.

To study the genetic control of adult lactose malabsorption (L.M.) 252 relatives of 11 probands over 20 years old and 101 spouses of these relatives and probands were examined. A lactose-tolerance test with ethanol administration was used for diagnosis of L.M. General malabsorption was excluded by a glucose-galactose tolerance test with ethanol. Genetic analysis of family series gave strong support for the inheritance of adult L.M. by a single recessive autosomal gene. The number of affected persons observed in different relative groups of probands also supported this idea.

Folsch, U. R. & Wormsley. K. G. The pancreatic secretion of enzymes in rats treated with soybean diet. Scand. J. Gastroent. 1974, 9, 679–683.The secretory response to CCK-PZ and secretin has been s...

Wahrend einer zweistundigen Inkubation (37°C) in autologem Plasma unter reinem Sauerstoff mit einem Druck von 2,2–2,5 atu weist das Magenepithel von direkt vor der Inkubation entnommenen Magenschleimhautbiopsien dasselbe Wachstumsverhalten auf wiein vivo. Das konnte an Biopsien von Rattenmagen durch Untersuchung der DNS-Syntheserate im Verlauf der Inkubation und durch vergleichendein vitro- undin vivo-Bestimmungen der Zahl der DNS-synthetisierenden Magenepithelzellen gezeigt werden.

Rasanen, T. AND E. Taskinen. The count of mast cells, tissue eosinophils, and epithelial mitoses of rat gastrointestinal mucosa after aspirin treatment. Acta, physiol. scand. 1973.89. 182–186. Mucosal mast cells, tissue eosinophils and epithelial mitoses were counted in the gastrointestinal tract of rats given 1, 3 and 5 times 10 nig of aspirin in 5 ml of water at 12 h intervals by cannulation into the stomach. The mast cell count of the gastric and duodenal mucosa ot rats receiving aspirin fell sharply. No significant change was observed in tissue eosinophilia. The mitotic count in the epithelium of stomach declined clearly, but no decrease occurred in the mitoses of the epithelial cells in the mucosa of the duodenum, jejunum and colon. The results seem to indicate that the injurious action of aspirin is transmitted so that the gastric mucosal mast cells possibly participate in it directly: the heparin contained in the mast cell granules inhibits in the phase of liberation the mitotic activity, especially in the gastric epithelium, and the blood coagulation mechanism locally. The histamine and liliydroxy-tryptamine liberation associated with the release of heparin results in the stimulation of secretion and in vascular reactions of the gastric mucosa.

In 6 dogs with innervated antral pouches (3 with vagally innervated fundic pouches and 3 with vagally denervated fundic pouches) gastric secretion was stimulated by a range of submaximal doses of pentagastrin, each infused intravenously for a period of 6 hours. During the three consecutive 2-hour collection periods of each test the antral pouch was perfused with isotonic saline of pH 7 0, 1.0 and 7.0 respectively at a rate of I ml/min. Neither acid nor pepsin secretion was inhibited by antral acidification. When the antral perfusion rate was increased to 3 ml/min there was still no inhibition of acid secretion from either type of fundic pouch. In each dog the acid response of the fundic pouch to perfusion of the innervated antral pouch with 0–5 per cent acetylcholine was significantly reduced when the pH of the perfusate was lowered from 7.0 to 1.0. The results provide no support for the existence of either an antral inhibitory hormone or inhibitory neural reflex active against pentagastrin-stimulated gastric secretion in the dog. It would seem that antral inhibition of gastric secretion is the result of a diminished release or formation of endogenous gastrin.

Estrogen metabolism in recurrent jaundice of pregnancy (RJP) and pruritus gravidarum (PG) was studied by determining 12 different estrogens in bile and urine. A uniformly marked fall in the biliary concentrations of all estrogens was observed in RJP. This would suggest that the enterohepatic circulation of these steroids is impaired and offers an explanation for the abnormal pattern of urinary estrogens observed in the two related syndromes. The relative excretion (= percentage of total estrogens) of estriol6 and 16-epiestriol in urine was diminished, whereas that of their respective precursors, 16α-hydroxyestrone and 16β-hydroxyestrone was increased. Rather small or insignificant changes were seen in the urinary excretion of other estrogens. Hence the main alterations occurred in the 16-hydroxylation pathways and included decreased conversion of 16α-hydroxyestrone to estriol and of 16β-hydroxyestrone to 16-epiestriol. The primary cause of these alterations is most likely the decreased biliary ex...

Parietal cell and intrinsic factor antibodies were studied in the sera of 156 inhabitants of Pornainen. Parietal cell antibodies were found in 8 per cent of the ‘random sample’, consisting of 135 subjects, and in 34 per cent of the ‘high risk group’ consisting of 29 subjects with decreased gastric secretion. Intrinsic factor antibodies were found in 3 cases in the ‘high risk group’. Two of these had manifest and one latent pernicious anaemia. It seemed that the determination of gastric antibodies may be of some value in screening for severe atrophic gastritis and pernicious anaemia.

In 6 dogs with innervated antral pouches (4 with vagally innervated fundic pouches and 2 with vagally denervated fundic pouches) the effect of irrigating the antral pouches with acid on the pentagastrin-induced secretion from the fundic pouches was assessed. A range of doses of pentagastrin (0.25–8.0 μg. per kg. body-weight per hour) was given by intravenous infusion for 3 hours at a constant rate, each dose being given on six occasions in separate experiments carried out on separate days. No consistent inhibition of secretion was observed in either preparation. The results do not support the concept of either an inhibitory hormone or an inhibitory neural reflex of antral origin active against pentagastrin-stimulated acid secretion.

Images Figs. 1-4 Figs. 5-7,9 Figs. 8,10-12

The ulcerating effects of reserpinisation in the gastric mucosa of rats were studied by special observation of the function of the gastric mucosal mast cells and the changes in mitotic activity of the epithelial cells. The significance of degranulation of the mucosal mast cells for the ulcerating effect of reserpine was also studied after the pretreatment of rats with dexamethasone. Immediately after the dexamethasone treatment there was a pronounced decrease in mitotic count of the gastric mucosal epithelium which 2—3 days later when the mast cells of the gastric mocusa were almost completely degranulated was followed by a 2—3 fold increase in mitotic activity as compared with controls. 10 and 20 days later the mitotic count in the gastric mucosal epithelium decreased below the controls values, the mucosal mast cells being re-granulated over the control values. The changes in mitotic count in the epithelium of duodenum. ileum and colon under the same conditions were scanty. The degranulation of the mast cells was markedly slighter in the intestinal than in the gastric mucosa. In the reserpinized rats the number of mitoses in the gastric epithelium decreased simultaneously with the degranulation of the mast cells. The degranulation of the mast cells in the duodenal mucosa was slighter and no changes in mitotic activity occurred in the duodenal epithelium. Lesions appeared during reserpinisation in the ventricular mucosa. Reserpinisation after the dexamethasone treatment did not cause ulcer formation in the gastric mucosa, nor did it in this phase cause inhibition in the mitotic activity, typical of which was an overshooting 2—3 days after dexamethasone treatment. The mechanism of gastric mucosal ulceration is discussed.

Urinarycoproporphyrin isomerdistributionwasstudiedin 13 patientssufferingfrom the Dubin-Johnson syndrome and severalcontrolgroups.In patientswith the DubinJohnsonsyndromethe isomerdistributionwas quite the reverseto that of normal persons.The urinaryisomerdistributionwas in the normalrange in patientswith Gilbert’s syndrome,hemolyticjaundice, and fatty liver. In many patients with different acute and chronicliver diseases, a clear deviationfrom the normalurinary isomerdistributionwas seen.There was, however,no overlapping with the DubinJohnsonsyndrome.Eventhe fecal coproporphyrin isomerdistributiondeviatedsignificantlyfrom the normalin favorof IsomerI. IT HAS BEEN KNOWN since the end of the last century that an increased porphyrin excretion is a common finding in liver diseases (1). The increase of porphyrin excretion was later shown to be mainly due to coproporphyrin (2). A clear deviation from the normal distribution of urinary coproporphyrin Isomers I and III in many cases of liver cirrhosis, obstructive jaundice, and chiorpromazine jaundice has also been noted (3). The purpose of this preliminary report is to demonstrate the value of urinary coproporphyrin isomer analysis when the syndrome described by Dubin and Johnson (4) is to be differentiated from other liver diseases and diseases which may cause intermittent jaundice.

In extracts of human gastric biopsies gastrin has been estimated with an immunochemical method. In the same biopsies G-cells have been localized with an immunohistological method using peroxidase-labelled antibodies and the endocrine cells investigated electron-microscopically. Gastrin and G-cells could be found regularly in the antral mucosa and only in insignificant amounts or not at all in the fundic mucosa of six normal persons. With the same methods gastrin and G-cells could be demonstrated in the antral mucosa of rats and guinea-pigs. The gastrin content of the antral mucosa of six patients with pernicious anaemia and achlorhydria with elevated serum gastrin levels was more than 20 times higher than in the controls and the G-cells were significantly more numerous. Besides hyperplasia of the G-cells, increased secretory activity was found electron-microscopically. The gastrin release from the G-cells seems to take place mainly via intracellular dissolution of the granule content within the membranous sacs. Although the number of other endocrine cells was increased in pernicious anaemia the ultrastructural identity of the G-cells could be established by comparison with the cells of a Zollinger-Ellison tumour. This tumour contained gastrin and gave a positive immunohistological reaction for this hormone. Also, the fundic mucosa of patients with pernicious anaemia contained gastrin and G-cells, but considerably less than the antral mucosa. Hyperplasia of G-cells was found in six cases of acromegaly, four of which also had a significantly increased gastrin content of the antral mucosa. This finding suggests a trophic function of the hypophysis, especially growth hormone, on the G-cells. Hyperplasia of the G-cells in the antral mucosa of three patients with primary hyperparathyroidism and increased gastrin content in two of the three cases also suggest a trophic function of the serum calcium level on the G-cells.

Malabsorption syndromes include primary and secondary intestinal syndromes and malabsorption of gastric, pancreatic or hepatic origin.Nontropical sprue is more common than the secondary forms and should be considered before other possible causes for the malabsorptive state.Roentgenographic examination of gastrointestinal tract or biopsy of small intestine or mesenteric lymph nodes may help toward diagnosis.Principal treatment includes dietary correction of deficiency states and replacement of vitamins and minerals.

A simple one-point lactose tolerance test to detect lactose malabsorption is described. Based on previous epidemiological studies, alcohol and lactose are given orally and the blood galactose is determined 40 min later. The specificity of the method is between 89 and 97% and the sensitivity from 96 to 100%. The screening method gives nearly as good results as a four-point lactose tolerance test with ethanol and better results than can be obtained by observing the symptoms following an oral lactose load.

In einer tierexperimentellen Untersuchungsreihe an Hunden wurde der Versuch unternommen, den Wirkungsmechanismus der Fundoplicatio mit Hilfe manometrischer Untersuchungsverfahren zu analysieren. Dazu wurde die Funktion dieser Fundusmanschette an drei verschiedenen Modellen untersucht Dabei konnten folgende Ergebnisse ermittelt werden: Die Fundoplicatio verhindert zuverlassig den gastrooesophagealen Reflux. Die Fundusmanschette selbst baut eine manometrisch erfasbare eigene Druckzone auf, die ahnlichen hormonellen Regulationen unterliegt, wie der UOS selbst. Fur die Funktion dieser Manschette ist es von Wichtigkeit, das sie aus der kardianahen Fundusvorderwand gebildet wird, da nur in diesem Bereich eine dem UOS vergleichbare Reaktionsbereitschaft vorliegt. Der Wirkungsmechanismus der Fundoplicatio scheint nach diesen Untersuchungen darin zu liegen, das der Sphincterdruck durch die manschettenbedingte Druckzone wieder auf ein hoheres Niveau gehoben wird und so wieder Druckwerte entstehen, die den gastrooesophagealen Verschlus gewahrleisten. Daneben mussen auch zusatzlich mechanische Faktoren diskutiert werden. Diese tierexperimentellen Ergebnisse finden ihre Bestatigung in den Nachuntersuchungen an mit einer Fundoplicatio versorgten Patienten.

Summary The histochemical properties of EC, the EC number, and the 5-HT content in the various parts of the human intestinal tract were examined from surgically removed biopsies. The fluorescent reaction was the most suitable for demonstrating EC, whereas among the staining reactions only the argyrophil method was able to color all of the EC. The 5-HT content and the EC number were highest in the duodenum, and both quantities decreased in the caudal direction of the intestinal tract. The correlation of the EC number and the 5-HT content and the location of the intestinal 5-HT in the enterochromaffln system were discussed.

In order to assess the reliability of the oral lactose tolerance test with ethanol (LTTE), the jejunal lactase activity and the curves of blood glucose and galactose after an oral load of 50 g lactose were estimated in 75 patients. The galactose metabolism was inhibited by an oral ethanol dosis (300 mg per kg body weight). The reproducibility of the maximum rise in blood glucose was good and that in galactose satisfactory in the 11 patients tested. The maximum rise of blood galactose correlated very well with the jejunal lactase activity in patients with normal histology of the small intestine.

The injection of lysolecithin into the rat pancreas is followed by severe pancreatic necrosis and extensive fat necrosis throughout the abdominal cavity. Phospholipase A, dissolved in a low-concentrated solution of bile acids and injected into the rat pancreas, has the same necrotizing effect. The injected phospholipase A splits the lecithin and the cephalin of the pancreatic tissue into their lysocompounds. The phospholipase A activity of the human pancreas is 10–30 times higher than that found in the pig, ox, or rat pancreas. The lecithin of bile is split into lysolecithin, in mixtures of human bile and human pancreatic juice. Normal human pancreatic tissue has only a low content of lysolecithin. In the necrotic pancreatic tissue of three patients who died of acute pancreatitis, there was a reversal of the normal phospholipid spectrum. Lysolecithin was the main phospholipid fraction in all cases, whereas the lecithin and cephalin were markedly reduced. It is concluded from these results that the intrapa...

Total vagotomy was carried out on rats through laparotomy. and the peripheral end of the vagus was electrically stimulated for one hour after closing the ventricle with a Shay ligature. after the stimulation, the gastric fluid was collected, its volume, pH and concentration of free HCI were measured. Free HCl was secreted significantly less in the ventricles of rats whose mucosal mast cells had been degranulated by dexamethasone before the vagus stimulation, than in the rats not treated with dexamethasone. The importance of the synthesis and accumulation of histamine in the mast cells of the gnstrir mucosa as a peripheral link in the stimulatory chain of gastric secretion is discussed.

Increased bile salt loss was a rare phenomenon in patients subjected to total colectomy and ileostomy for ulcerative colitis, provided the remaining terminal ileum was intact. Ileostomy discharge was increased by enhanced bile salt output. Apart from deconjugation of bile salts, bacterial action on ileostomal acidic and neutral steroids was negligible or absent. Fat content of dejecta was frequently elevated and correlated with vitamin B12 absorption but not with neutral sterol or bile salt elimination. Absence of a bile salt deficiency was indicated by a normal jejunal bile salt concentration and normal micellar phase lipids during fat absorption; the oil phase was expanded, however. Serum cholesterol was normal and serum methyl sterols correlated with sterol balance data, indicating that augmented loss of cholesterol as bile acids was balanced sufficiently by increased cholesterol synthesis.

Kalima, T. V. & Collan, Y. 1970. Intestinal Villus in Experimental Lymphatic Obstruction. Correlation of Light and Electron Microscopic Findings with Clinical Diseases. Scand. J. Gastroent. 5, 497-...

The research described in the following monograph is the result of seven years' work. In 1926 I attempted to introduce psychological methods of treatment into the out-patient department of the First Medical Clinic of the Charité, Berlin. It soon became evident that there was a widespread demand for the application of such methods within the field of the medical clinic. In the course of years, hundreds of patients with psychoneuroses linked to organs passed through our hands. A selection of specially instructive cases is given below. Our researches were performed on patients and collaborators who readily placed themselves at our disposal for our experiments. In grateful remembrance I wish to thank my esteemed former chief, the late Geh. Med.-Rat Prof. Dr. W. His, for the interest he took in my line of work and for the support he extended to it. My work in Germany came to a sudden end in March, 1933, but thanks to the kindness of Dr. F. L. Golla I was able to continue my studies at the Central Pathological Laboratory, London. Furthermore, I owe special thanks to the Professional Committee which, by the grant of a scholarship, enabled me to continue and complete this work.

An mit Chloralose narkotisierten Hunden wurde die direkte Wirkung einiger Genusgifte auf die Gallenentleerung (durch Beeinflussung des Sphincter Oddi) sowie ihre Wirkung auf Tonus und Motilitat des Darmes gepruft. Nicotin und Weckamine hemmen die Darmmotilitat und losen den Tonus des Sphincter Oddi. Die lokale Einwirkung von Alkohol auf die Duodenalschleimhaut fuhrt zu einer Sperrung der Gallenentleerung. Coffein zeigt wechselnde, moglicherweise von der vegetativen Tonuslage abhangige Wirkungen. Diese Befunde konnen nicht ohne Berucksichtigung der zentralnervosen Genusgiftwirkungen fur die Beurteilung der Indikation und Kontraindikation verwertet werden.

Summary A study has been made of the disaccharidase activities and histology of duodenal mucosa in two infants with typical congenital lactose malabsorption. The mucosal samples were taken by means of peroral intestinal biopsy. At the time Of biopsy, the patients were 2½ and 4½ months old and they had been on lactose free diet 39 days and 3 ½ months respectively. Both patients demonstrated a typical clinical picture of lactose and cellobiose malabsorption. In the mucosal samples, lactase and cellobiase activities were almost absent in both patients, whereas other disaccharidase activities were within the normal range. The histological picture of the mucosa was normal in one patient, and slight, partial villous atrophy was seen in the other. This study confirms that the cause of congenital lactose malabsorbtion is an enzyme defect of the intestinal mucosa which histologically may appear normal.

Haikonen. hf. and T. Rasanen. Hjdmgen ion concentration in the gstiic juice after pylurus ligation in dexamethason-treated rot. Acta physiol. scand. 1963. 65. 378–382. — Rats were injected with dexaniethasone 3 × 1 mg at 12-hr intervals before ligation of the pylorus. The hydrogen ion concentration of the gastric secreta. the volume of secretion and the amount of free HCI were measured 2 hrs after tying the ligature. The administration of dexaniethasone for 2 days before ligation of the pylorus inhibited gastric secretion during the ligation and elevated the pH of the secreta. No free HCl was demonstrated in it. Secretion was restored by histamine injected into the rats in connection with the application of the ligature. A single dose of dexamethasone 2 hrs before the application of the ligature caused elevation of gastric secretion. It is suggested that the degranulation of the mast cells of the gastric Iiiucosa during dexamethasone therapy leads to inhibition of gastric secretion with the mucosa losing the histamine needed for its stimulation. This loss may he compensated by exogenous histamine. On the other hand. the histamine-liberating property of dexamethasone enhances secretion when the de-granulation of the mast cdls begins.

Intravenous galactose tolerance tests with and without an alcohol load have been used to study the liver function of fifteen healthy persons and twelve chronic alcoholics whose diet has for long periods been inadequate. The results are related to other liver function tests and to the microscopic appearance of liver biopsy specimens. In patients with normal liver function the T 1/2 value for galactose without ethanol averages 12.7 minutes, with a standard deviation of ± 2.5 minutes. The mean prolongation of the T 1/2 value induced by ethanol was 28.5 ± 5.0 (S.D.) minutes.All but one of the alcoholics had typical fatty infiltration of the liver. The breakdown of galactose without ethanol was equal to that of normal persons. In sharp contrast to the controls, however, the previous ethanol load did not influence the galactose elimination rate in these patients with fatty livers. It is concluded that fatty liver should always be suspected when the ethanol-induced prolongation of the T 1/2 value for galactose r...

The number of mast cells in the mucosa of the glandular stomach of the rat decreased on account of degranulation 2–4 hours after histamine and insulin injections and after ingestion of food. Re-granulation of the mast cells occurred in a later phase. Morphological changes were established in the mast cell granules during gastric stimulation. Tissue eosinophilia of the lamina propria of the glandular stomach increased at the beginning of the stimulation, decreasing in a later phase. Lethal insulin shock caused an increase in the tissue eosinophilia of the glandular stomach. The role of the heparin and histamine contained in the mucosal mast cell granules during the stimulation of the gastric mucosa, in the phase in which the ion changes and local heparinemia in the mucosal lamina propria perhaps provoke inhibition of eosinolysis, is suggested.

Crohn's disease is increasing in frequency, mainly in urban areas. Small bowel disease is 4 times more common than transmural inflammation of the large bowel. A history of colicky abdominal pain, diarrhoea and weight loss should always arouse the suspicion of Crohn's disease, especially when the patient is a young woman. In more than half the patients no mass can be felt. Large bowel disease is relatively commoner in older patients. Crohn's disease must be considered in the differential diagnosis of gynaecological complaints, and may cause symptoms referrable to the spine and hip joints. Barium enema is the most useful confirmatory investigation provided reflux into the terminal ileum is obtained.

Faeces from patients with dystrophia myotonica and controls were incubated aerobically for 20-24 hours with L-histidine, L-carnosine, histamine diphosphate, N-acetylhistamine, and N-acetyl-L-histid...

Of 100 patients with atrophic gastritis, 49 were re-examined 10-15 years after the first and 5-8 years after the second examination, 18 patients answered a questionnaire but declined the re-examina...

The responses of the gastric mucosal mast cells and the subcutaneous mast cells of the abdominal skin of the rat after administration of ACTH, heparin, and asbestos, were studied. The superficial part of the gastric mucosa contained roughly 5 times as many mast cells as the subcutaneous connective tissue. About three-fourths of the gastric mucosal mast cells were degranulated under the influence of ACTH, but the subcutaneous mast cells showed no changes in number and granulation. The observed difference indicates possibly that mast cells in the gastric mucosa and in the epidermis may have important special, but clearly differing, functions. In the gastric mucosa the sensitiveness of mast cells is possibly connected with their function as a peripheral mediator of stimulation of gastric secretion.

Our opinion of the present state of jejunoileal shunt in the treatment of obesity may be summarized as follows: (1) A jejunoileal shunt is of distinct benefit in selected patients for whom the obese state has become a hazard to health. (2) It is not the procedure one does because an obese patient is 25 to 50 pounds overweight. (3) Inasmuch as a high degree of cooperation is essential, a relationship of mutual respect, trust, and responsibility must be present between the physician and patient. A hostile attitude on the part of the patient cannot be tolerated. (4) Although long-range benefits from the control of factors leading to aggravation of cardiovascular disorders may be expected, it may be dangerous to subject patients with well established cardiovascular disease to this procedure. (5) A jejunocolic shunt should not be used for control of obesity. (6) A jejunoileal shunt should definitely be considered as an investigative procedure, for the present, and should not be undertaken unless facilities are available to handle complications and to conduct significant research into the mechanism of obesity and its attendant complications over a long period of time.

SUMMARY Two newborn infants are described, both of whom had a slight omphalocelic anomaly. In both an ectopic lobe was completely detached from the liver itself and located outside the abdominal cavity. In the first case the hepatic lobe had apparently become detached at an early embryonal stage, since the histological picture of the liver was extremely primitive. In the second case the hepatic lobe was perhaps detached in a late intrauterine stage, as its histological picture was characteristic of the mature liver.