The patriarch of experimental pancreas research is REIGNIER DE GRAAF (1641-1673). He carried out the first experiments with dogs in order to ob tain fistular secretion (1664). But only few years later, the just arisen interest in the physiology of the pancreas was severely set back by remarks of CONRAD BRUNNER. In 1682, BRUNNER expressed his belief that on the basis of experi ments he had carried out the pancreas was a vitally unimportant organ. He overlooked that after ligation of the main duct (discovered in the turkey by HOFMAN in 1641 and in a human cadaver by WIRSUNG in 1642), in the dog an accessory duct (described by SANTORINI in 1724) usually maintains an adequate flow of secretion. EBERLE in his monograph (1834) confirmed the emulsifying capacity of the pancreatic juice which had already been suggested by SYLVIUS (FRAN CISCUS DE LE BOE, 1614-1672) and he dealt with the essential enzymatic functions of the pancreatic juice such as amylolysis, lipolysis and proteolysis. Since HEIDENHAIN (1875), we know that for example trypsin (largely isolated by KUHNE in 1867) is situated in the acinar epithelial cells as zymogen in inactive form; it is thought that the action of "acid" on the glandular tissue is needed for inducing the "enzymatic activity." According to what we know now about the central role of acidosis in the activation of zymogen this topic is, of course, of topical interest."

Toxoplasmosis is a ubiquitous infection, contracted by at least a third of the population in most areas of the globe. Clinical disease arises rarely, usually unexpectedly, but sometimes with disastrous effects on the patient. Humans, pets, farm and zoo animals may contract toxoplasmosis, possibly involving any clinical laboratory in its diagnosis. Pathologists must ponder the clinical significance of a hyperplastic l. ymph node, a cyst found at autopsy, or a serologic titer. Serving as scientific physicians, pathologists are asked: How is toxoplasmosis diagnosed? 'What is the treatment for ocular toxoplasmosis, for congenital infection, or for toxoplasmosis in the immunologically compromised host? vVhy does disease develop in as diverse areas as the eye, lymph nodes and placenta? How is Toxoplasma transmitted? This review proposes to survey recent advances, providing a scientific background to diagnose and manage the clinical problems of toxoplasmosis. Reviews are available which emphasize other aspects, such as serologic pro cedures, resistance and immunity (REMINGTON, 1970), the clinical syndromes (DESMONTS, '1969; FELDMAN, 1968) and comprehensive presentations (JACOBS, 1967; FRENI{EL, '1970). Transmission and Prevalence The recent discovery of the coccidian stages of Toxoplasma in the cat intestine and the Toxoplasma oocyst excreted in cat feces, considerably broadens our understanding of Toxoplasma and its transmission (FRENKEL, DUBEY and MILLER, 1970)."

wurden 150-280 mg% genannt). Entsprechend lag auch der Serumcholesterinwert mit 22 mg %, der Serumphosphorlipidwert mit 45 mg % und der Gesamtlipidwert mit 80 mg% extrem niedrig. Carotinoide konnten uberhaupt nicht nachgewiesen werden, und der Vitamin A-Gehalt war mindestens auf 1/ der Norm herabgesetzt. 5 Die Autoren brachten ihre Beobachtung mit der Beschreibung von vier weiteren Fallen von Acanthocytose und Hypocholesterinamie (37-60 mg%) in Zusammenhang, bei welchen zwar auf A-ss-Lipoproteidamie nicht untersucht worden war, die aber durch die grosse AEhnlichkeit der Symptome als gleiche Krankheit imponierten. Bei allen vier Personen war Konsanguinitat bei Eltern oder Grosseltern vorhanden. Von groesster Bedeutung waren Verlaufsbeobach tungen uber mehrere Jahre!, welche Schlusse auf die Entwicklung, also auch auf die Folgen des ss-Lipoproteidmangels, erlaubten. Alle Kranken, auch der von SALT beobachtete Fall, zeigten coeliakieahnliche Symptome: Durchfallperioden, Fett stuhle und roentgenologisch weite Dunndarmlumina. Die alteren Patienten litten an einer atypischen Retinitis pigmentosa und an einer Ataxie vom Typ Friedreich 2. Bei einem vom 13. bis 19. Lebensjahr beobachteten Knaben entwickelte sich in 3 dieser Zeit die Retinitis, und es verstarkten sich die neurologischen Symptome * Daraus ergab sich der naheliegende Schluss, dass die Progredienz des Leidens ihre Ursache in einem durch Transport- bzw. Vehikelinsuffizienz fortwirkenden spezifisch lokalisierten Mangelzustand haben kann. Ob der Mangel an Blut lipiden oder an in Lipiden geloesten Vitaminen und Wirkstoffen (etwa Vitamin A oder Carotinoid) bedeutungsvoller ist, das kann noch nicht naher bestimmt werden.

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