When an animal receives one or more parenteral injection of certain foreign materials - proteins, red blood cells, tissue extracts from another species, bacteria or bacterial products - there generally appears in the serum, within a few days, a substance which possesses the unique property of reacting with the material injected (1). This serum component is termed antibody and the material which stimulated its production is called antigen. The animal which has formed antibodies is said (by convention) to be immunized. The presence of antibodies in the serum of immunized animals may be recognized by the occurrence of certain characteristic reactions such as precipitation, agglutination, and complement fixation.

Investigations of the participation of non-endocrine organs in steroid transformations are gaining equal prominence with those studies in which end products of overall steroid metabolism are sought in the excretia. Although the liver probably plays an important role in this regard, the importance of extrahepatic tissues in steroid metabolism is becoming increasingly apparent. In 1948 Werthessen and collaborators (1, 2, 3) reported that incubation of estrone in blood resulted in destruction of the 17-keto function of the steroid accompanied by a loss of biological activity. On the other hand, Bischoff and associates (4, 5) incubated the red cells of rabbit or man with estrone and observed a marked increase in the biological activity of the added steroid. The discrepancy in the two sets of data was ascribed at the time to differences either in assay techniques or in experimental conditions.

Jaundice is the clinical manifestation of increased levels of serum bilirubin, and is evident when this level rises above 2 mg%. Jaundice results from a breakdown in either uptake, conjugation or excretion or bilirubin by the liver, and the origin or the symptom can usually be determined by the type of pigment present in the serum. About 50% of all newborn infants exhibit some degree of jaundice, which seldom exceeds 10 mg% and is maximal between the third and fourth days of life. This is generally referred to as “icterus neonatorum” or physiological jaundice. Superimposed on this "icterus neonatorum” are the more severe cases of jaundice for which there is a known cause. These include blood group incompatability between mother and child (erythroblastosis fetalis), septicemia, hepatitis and congenital obliteration of the bile duct.

The suppression of the formation of corticosterone by the rat adrenal tissue in vivo and in vitro by androgens is reported. There is some evidence that androgens can be converted to more polar compounds by the incubated glands. Two such metabolites of 17α-methyl-Δ5-androstene-3β, 17β-diol (MAD) have been investigated. One is methyltestosterone, probably formed by the oxidation of MAD by the enzyme, 3β-hydroxydehydrogenase. The other may, in addition, contain one or more extra hydroxyl groups. Even more polar compounds have been observed. Whether these originate from the exogenous androgens or arise as a consequence of diversion of corticoid synthesis from corticosterone is not known.

Although the presence of phosphorus in phosphoproteins, phospholipids and nucleic acids has long been known, one of the significant advances in biochemistry in the past few decades has been the increasing realization of its central role in the metabolism of living organisms. In particular, it is now recognized that its function in the stepwise degradation reaction through which energy is harnessed and integrated with the synthetic processes, is essential for the maintenance of life.

In the living animal, brain often swells greatly following trauma. There are two types of brain swelling: 1. One occurs very rapidly and is probably due to a dilatation of blood vessels or an increase in the cerebrospinal fluid volume or both. This is what Elliott and Jasper have referred to as 'inflation' (Elliott and Jasper, 1949). 2. The other is more chronic and is brought about by an increase in the water content of the cerebral tissues. Many experimental studies of cerebral edema have been published yet little is known about the basic mechanisms responsible for its production. At the same time there is a great need to gain some understanding of the beneficial effects of cortisone which has been used on an empirical basis to relieve the symptoms commonly attributed to cerebral edema (Galicich and French, 1961; Rasmussen and Gulati, 1962).

The nephrotic syndrome bas been defined as a "pathological state of divergent etiologies, characterized by hyperlipemia, proteinuria, hypoalbuminemia and edema." (1) The primary site of the disease process is in the glomerulus and under the light microscope thickened, frayed glomerular basement membranes can be seen. (2)Electron microscopy on the other band, reveals that the lesion is chiefly due to an alteration of the epithelial layers of the basement membrane, there is a fusion or smudginess of the podocytes to form broad plaques of epithelial cytoplasm. Several etiological agents have been known to induce a nephrotic syndrome: systemic diseases such as diabetes mellitus, lupus erythematous, amyloidosis; infectious diseases, syphillis, malaria; chemical agents, trimethadione, paradione, gold salts, penicillamine; allergic reactions to bee stings, poison oak; renal diseases, chronic glomerulonephritis, acute poststreptococcal glomerulonephritis and renal vein thrombosis.

Acetylcholine (ACh) was first synthesized by Bayer (1867), but its pharmacological action vas not realised until Hunt and Traveau (1906) illustrated its depressor activity on the nervous system, an action which could be abolished by atropine. Dixon (1906) noted that muscarine mimicked vagal stimulation and later restated the possibility of humoral mediation by chemicals (Dixon and Hamill, 1909), an idea first put forward by Elliott (1904) with regard to the possible mode of action of adrenalin. The first indication that ACh was a naturally occurring substance came with its isolation from some extracts of ergot which had been observed to have pressor effects (Ewins, 1914).

A large number of 17-ketosteroids have been found in the urine since the first one vas isolated almost thirty-five years ago. Butenandt and his co-workers in 1931 (1) first isolated a crystalline steroid with androgenic activity from a chloroform extract of normal male urine which had been hydrolysed with acid and subsequently identified it as androsterone in 1934 (2). In the same year, these authors described the isolation of dehydroisoandrosterone from urine. (3) In 1938 Butler and Marrian (4) reported the isolation of two other 17-ketosteroids, etiocholanolone and isoandrosterone, from a large quantity of unhydrolysed urine excreted by a woman with an adrenocortical tumour. The isolation of etiocholanolone from the urine of a normal male subject was reported by Callow (5) in 1939.

Since the beginning of this century, a large amount of evidence has accumulated indicating that antibody can be partially digested by enzymes without loss of activity. As will be indicated in the following review, much of this work was undertaken primarily to eliminate the occurrence of serum sickness, a syndrome due to the intravascular interaction between passively administered heterologous antitoxic antisera and the antibodies formed to these antisera in the recipient. Enzymatic treatment of antitoxins was used in an attempt to reduce their antigenicity and hence their ability to elicit an immune responce, with its possibly disastrous sequelae. The early work on enzymatic degradation of antibodies was conducted almost exclusively with antitoxins produced in the horse, since this species has been the favoured source of antisera for clinical use.