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1) In electively immuno-induced carcinomas of the exocrine pancrease in Mice, where A (glucagon) and B (insulin) endocrine cells persist, cells with a pancreatic polypeptide immunoreactivity are also detected, even in late evolution stages. These cells, like D cells, containing somatostatin, are localized only in the pancreatic remains surrounding the anaplasic carcinomatous tissue: islets, adenomatous parenchyma, and ductular epithelium. Ultrastructure of these cells shows their active elaboration of numerous chracteristic secretion granules. (2) Immunocytoenzymatic detection of gastrin is negative in the exocrine and endocrine pancreatic tissues. However one of the anti-gastrin sera used gives a positive reaction, in some carinomatous cells only. Does this immunoreactivity characterize a polypeptide specific to the pancreatic carcinomatous cell?

Peculiar cytoplasmic inclusions with crystalline pattern are described in the obese hyperglycaemic mouse pancreas acinar cells. They are generally associated with filamentous structures. However, crystalline and filamentous inclusions have also been observed in isolated forms. These inclusions are not digested by pronase. Since they have also been encountered in normal mice, it seems that the hyperglycaemic syndrome does not play a role in inducing their formation.

Pancreatic A cells of the lizard Varanus niloticus are characterized by the presence of two types of mitochondria: (a) normal, small mitochondria (about 0.4 X 1 micron), and (b) giant mitochondria, measuring up to 9 micron in length and 1 micron in diameter. Giant mitochondria show various shapes. Their matrix is filled with tubules, filaments, and dense granules. Transverse sections of tubules are polygonal in shape and about 20 nm in diameter. They are grouped in bundles. The filaments, about 9-10 nm in diameter, are arranged in parallel layers crossing each other at a 57 degree angle. In a closely related species, Varanus exanthematicus, pancreatic A cells do not show these peculiar features.

The injection of bile under low pressure led in 21 dogs out of 30 to a process of acute pancreatitis and to the reproduction of the different histopathological types of pancreatitis seen in man. This represents a weighty argument in favour of the concept of oedematous pancreatitis, interstitial pancreatitis with sometimes major cytosteatonecrosis and necrosing pancreatitis as different manifestations of the same disease, which is not universally accepted. Our research has once again emphasized the fact that the interstitial phenomena and in particular fatty necrosis precede parenchymatous necrosis. Morphological studies were used to attempt to define the link between fat necrosis and acinar necrosis. Light microscopy showed that there was no topographic evidence of direct involvement of the acinar cell in contact with fat necrosis. By contrast, ultrastructural studies revealed initial involvement of the basal pole of the acinar cell. This would emphasize the responsibility of interstitial phenomena in the maintenance, if not the induction, of acinar necrosis. It cannot be excluded that fat necrosis could indirectly, via the liberation of factors carried by oedema, play a role in these phenomena of acinar necrosis. In addition, it was noted that the apical poles of the acinar cells did not seem to be damaged, the acinar lumina were dilated and there was loss of the intercellular junctions. This would hence indicate the possible passage into the interstitium of a toxic substance (bile salts, enzymes liberated in excess) coming directly from the acinar lumina.

Using the optical and electron microscope, the authors studied the effects in the rate of cathetersiation of the pancreatic ducts after laparotomy. 62 rats underwent operation, 42 of which received an injection of 30 p.cent urinary radioselectan, 10 an injection of simple isotonic saline and in 10 of which simple catheterisation without injection was carried out. With injection under high pressure, regardless of the substance used, lesions of acute pancreatitis occurred in almost all cases in the short term and in the long term lesions of localised chronic pancreatitis were fairly common. For these reasons, the authors feel that routine parenchymography is contraindicated and that only opacification of the main pancreatic ducts is permissible.

Pancreatic Polypeptide (PP) was first described in birds by Kimmel et al. (1968). It was later isolated from the pancreas of several mammalian species by Chance and Jones (1974). It has been demonstrated in the islets of many animal species by immunocytochemical methods. PP levels are assayable in plasma and rise sharply after food intake. The pharmacological properties and physiological role of PP are still ill defined. It appears to have a spectrum of actions peculiar to each species. Recent research on this subject is reviewed in this article. High levels of circulating PP have been demonstrated in juvenile and maturity-onset diabetics, as well as in some patients with islet cell tumors. However no definite clinical syndrome due to hypersecretion of PP as been identified as yet. It remains a matter of speculation that a deficiency of PP might be responsible for some types of obesity. PP-cells are rare in the pancreas of healthy young individuals. Hyperplasia of PP-cells has been observed in a wide variety of pathological conditions, but is most prominent in the pancreas of chronic insulin dependent diabetics. Histologic evidence strongly suggests that PP-cell hyperplasia represents an atypical form of islet regeneration. It is always focal in distribution and is most remarkable in those lobules that have lost the capacity to reproduce islets of normal cytologic composition.

Different techniques have been used to realise organ culture of larval pancreas of Alytes obstetricans Laur. Some methods allow to get satisfaction results. The general aspect of the explant is described, as also the ultrastructure of the different parts of the pancreas. The results allow to consider the experimental study of the in vitro metamorphosis under the influence of thyroxine.

Isometric virus particles, 60 nm in diameter, have been isolated from diseased scorpions. The virus is pathogenic after ingestion. Its morphogenesis occurs in the cytoplasm of hepatopancreas cells which are totally destroyed at the end of the disease.

The study of the pancreas development in Pleurodeles waltlii Michah (amphibian urodele) shows the following characteristics: 1) The dorsal rudiment is formed the first, even before the irrigation of the tree producing branchial buds (end of stage 30). This rudiment is formed by isolation of cells rich in vitellus from the dorsal wall of the archenteron. The ventral rudiment, which is massive and more developed on the right side than on the left, appears only a few hours later. The two rudiments fuse at the eclosion time (after stage 35). (2) The elements of the exocrine pancreas, which are the first formed, take place little before the eclosion (stage 33b). They come from the transformation of the cells rich in vitellus, with embryonic character. Solid masses of these cells are first formed and then hollowed in tubules which secondarily join the central pancreatic canal of rudiments. (3) The endocrine elements, which are as rare in the larva as in the adult, appear only after the eclosion. The B cells are formed first (stage 35).

After intraperitoneal inoculation with mouse hepatitis virus (MHv) into mice, the excretory cells of the pancreas showed a marked vacuolar degeneration concomitantly with hepatitis. MHV-specific antigen was evidenced in the cytoplasm of infected cells. Electron microscopy revealed a number of virions within the matrix, spaces of the endoplasmic reticulum and areas of focal cytoplasmic necrosis. The virus titer of the pancreas was equal or superior to that of the liver at least in early stage of infection.

Light- and electronmicroscopical observations are made on the pancreas of 18 rats after 4 weeks of B1-avitaminosis. The B1-avitaminotic animals show a definite decrease in bodyweight and in the weight of their pancreas. The mitochondria of the acinar cells are swollen and invaded by numerous vacuoles. Single cells die by eosinoplilic necrosis. The islets of Langerhans demonstrate a definite hyperplasia (polynesis) and hypertrophy (macronesis). The mitochondria are swollen and also transformed into vacuoles. There is a lysosomial granulolysis. Only occasional lesions are observed in the A1 and A2 cells of the islets.