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Erroneous quotations in the literature and Cohnheim's statement, in his Lectures on General Pathology, that the Wolffian body or mesonephros is the first anlage of the urogenital system prompted this description of the growth of our knowledge of the early development of the kidney. Some of the pertinent older literature is reviewed, and the concept of the holonephros, as opposed to the trinephric view of kidney development, is discussed. Emphasis is placed on the decreasing functional significance of the pronephros with evolutionary development, to the extent that the role of the pronephros in the human is questioned. Cohnheim's seemingly erroneous reference to the development of the kidney is shown to be merely a reflection of the views current at his time.

Although cystic fibrosis of the pancreas is now one of the most widely studied diseases of childhood, the association of this disease with ulceration of the duodenum has only infrequently been reported. On theoretical grounds, such an association would, however, be expected, since the development of ulcers of the duodenum following the diversion of pancreatic juice from this part of the intestine has been clearly demonstrated in the experimental animal by such early observers as Mann and Williamson,1 Elman,2 and Dragstedt.3More recently, Poth and Fromm4 have similarly implicated the deficient neutralization of acid in the duodenum because of pancreatic insufficiency as a factor in the causation of peptic ulceration. It may be of interest in this connection to draw attention to the findings of Shwachman and Leubner5 who noted that, in a large proportion of cases of cystic fibrosis of the pancreas studied by

THE OBSERVATION that rats given cortisone for a prolonged period of time became "exophthalmic"1 prompted several questions. Was it, first of all, justifiable to consider the changed appearance as being due to classical exophthalmos, i. e., the undue protrusion of eyeballs normal in size and shape owing to changes in the retrobulbar tissues of the orbit; or was this appearance caused by a hormonally induced enlargement of the eyeballs, so that the latter no longer could be accommodated by the orbit? The second possibility was not considered likely on anatomical grounds. On the other hand, Jackson2 had observed that the eyeballs in chronically undernourished rats continued to grow, although any gain in body weight was prevented by the restriction of food intake. Since the prolonged administration of cortisone produces in rats a state not unlike chronic inanition, it was decided to examine the effect of this hormone on

Giant cell hepatitis of infancy (for some of the other terms used for this condition see Fienberg1), one of the causes of jaundice in early life, is a disorder of unknown etiology which has attracted much attention in recent years. It is characterized by the presence, in the liver chiefly of young infants, of varying numbers of multinucleated giant cells of hepatocellular origin and by the absence of any other demonstrable pathological condition which could be held responsible for either the jaundice, when present, or for the development of the characteristic giant cells. This definition, however, probably covers only one, perhaps the most obvious, group of cases, as will be shown later in this paper, since it excludes, on the one hand, those undoubted cases of viral hepatitis in young infants where no giant cells have been seen2-19 and, on the other, certain pathological conditions of the infant's

The widely held view that exophthalmos is caused by the excessive production of the thyroid stimulating hormone (T. S. H.) of the adenohypophysis fails to account for some of the best known features of Graves' disease. If an excess of T. S. H. is present in the patient in whom malignant exophthalmos develops without a preceding thyroid disturbance, why, for example, does the basal metabolic rate (B. M. R.) remain at a low or normal level? Why, on the other hand, can marked ocular protrusion be encountered without any demonstrable increase in the level of circulating T. S. H. (Purves & Griesbach 1949, d'Angelo et al. 1951)? How can one reconcile the fact that exophthalmos is not usually a feature of congenital or acquired primary thyroid insufficiency (Purves & Griesbach 1949, Friedgood 1941, Brain 1938, Marine & Rosen 1936, Means 1946, Engel 1939), with the repeatedly confirmed observation that in

Current views about the part played by the thyroid-stimulating hormone of the adenohypophysis (T. S. H.) in the etiology of exophthalmos are based (a) on the well known association of this sign with past or present thyroid disease; (b) on the demonstration of the thyroid-stimulating substance in the blood or urine of some patients with progressive exophthalmos (Hertz, Means & Williams 1941, Rawson 1944, Robertis 1948, Purves & Griesbach 1949, d'Angelo 1949, d'Angelo, Gordon, Paschkis & Cantarow 1949, Dobyns 1950, d'Angelo, Paschkis, Gordon & Cantarow 1951 a, b); (c) on the experimental production of ocular proptosis by anterior pituitary lobe extracts containing T. S. H. (Schockaert 1931, Albert 1945); (d) and on the failure of some workers (Aird 1940, 1941, Albert 1945, Jefferies 1949 c, Smelser & Ozanics 1951) to induce it by anterior pituitary hormones other than T. S. H. Some investigators have, however, questioned the causal role of

It has recently been stated that »Cortisone behaves like a hormone with spermatogenetic activity« (Leroy, 1953 b). In a series of experiments designed to study the effect of cortisone on the male reproductive tract of rats, hamsters and domestic birds, Leroy & Domm(1952) and Leroy(1951, 1952 a, b, 1953 a, b) concluded that the effect of cortisone was determined not only by the type of experimental animal used, but also by the stage of sexual development which it had reached. Cortisone, which for instance precipitated or accelerated testicular development in the prepuberal Leghorn chick, had no stimulating effect on the spermatogenesis of the mature hamster or rat, in fact it produced severe damage of the seminiferous tubules in the immature rat. Yet in mature rats which had been hypophysectomised and adrenalectomised, cortisone was able to maintain complete spermatogenesis (Leroy, 1953 b). In this »spermatogenetic« effect of cortisone therefore