Our present knowledge of body fluid physiology originates with Claude Bernard's concept of a "milieu interieur" of constant composition. (2, 3) This concept, enunciated in 1859, stimulated intensive research, from which several theories have evolved to explain the formation of edema. If today different schools of thought are still opposed with respect to the intrinsic mechanism of edema formation, they at least agree as to its definition. Edema is a condition which is manifested by chronic, progressive accumulation of salt and water in the extra-cellular space, accompanied by an increase of body weight. This definition allows the exclusion of all syndromes in which there is only redistribution of fluid within the body, as in acute pulmonary edema.

A comparative study, emphasizing lung mechanics, was made of the clinical and functional pattern in two groups of emphysematous patients; 8 with and 11 without chronic respiratory failure. Loss of lung elasticity appeared to be the most prominent mechanical abnormality in the group with normal arterial blood gases. Airway obstruction due to expiratory check valving was less marked than in the hypercapnic group where it seemed to be the major difficulty, impairment of lung elasticity being a secondary feature. These and other demonstrated differences, suggested that qualitatively different disease processes were represented in the two groups, possibly centrilobular emphysema in the hypercapnic group as opposed to diffuse emphysema in the group with normal blood gases. In addition, the findings suggested that the chief mechanism producing chronic hypercapnia in emphysema is an inability to compensate for distributional defects by increasing ventilation, due to mechanical restriction of the respiratory bellows.

The importance of tile adrenal cortex in influencing sodium and potassium metabolism is well established. The adrenal cortex secretes a number of steroid hormones which affect sodium and potassium excretion to varying degrees. The hormone which is the most potent in its sodium retaining effect is aldosterone. It promotes the sodium reabsorption for the exchange of potassium or hydrogen ion in the distal tubules of the kidney. There are several problems which are not well understood, e.g. the physiological importance of the rate of secretion of various steroids, the synergistic or antagonistic action of various adrenal cortical hormones on the absorption, distribution and excretion of electrolyte and their interplay with each other.

Acute pancreatitis may be induced by many different types of injuries to the organ. The tissue reaction may vary in severity, but it is believed that it varies little in character, whatever the agent causing the injury may be. For this reason acute pancreatitis is often defined as an acute inflammatory response of the pancreas to injury. In 1842 Classen (1) recognized acute pancreatitis and described its pathological picture. Soon after this, in 1850, Claude Bernard (2) induced the first experimental pancreatitis by injecting oil and bile into the pancreatic duct of animals.

The localization of function of organs of the body by external counting following injection of radio-active isotopes is a new, and rapidly developing field of study. New recording techniques are being introduced every year, and the accuracy of this method increases with improvement in instrumentation. The kidney lends itself well to this technique, as its major job is to concentrate various substances from the blood, and excrete them in the urine. Therefore hippuran, an end product of metabolism, and neohydrin, a foreign compound, are rapidly removed from the circulation, and concentrated in the kidney. "Tagging" these substances with radio-active isotopes, makes the detection of their distribution in the body easy by means of external counting techniques.

The nephrotic syndrome has been defined as “renal loss of albumin resulting in diminished concentration, variably associated with hyperlipoidemia and edema” (1). It has been clear since the time of Richard Bright (2) that some patients with renal disease are edematous and have lipemic serum and marked proteinuria. Association of the nephrotic syndrome with other systemic diseases such as lupus erythematosus (3), diabetes mellitus (4, 5) and amyloidosis (6), and with infections such as syphilis (7, 8) and malaria (9) has been observed.

In-vivo investigations of renal tubular transport of the imino acids and glycine in man and rat have revealed that these compounds may share a common membrane transfer mechanism. However, the locus of "commonness” cannot be resolved by such techniques. In-vitro studies reported in this communication permit the application of Michaelis-Menten formulation to the kinetics of transport of these compounds in rat kidney cortex slices. The data indicate that L-proline, hydroxy-L-proline and glycine cannot be transported by identical mechanisms but that there is some aspect of these systems which is common. The order of affinity for transport in-vitro is proline > hydroxyproline > glycine, confirming in-vivo observations. The relation of these findings to the control of imino acid and glycine transport under certain genetic and maturational conditions in man, is discussed. A proposal as to the locus of commonness in transport generally, and more specifically in the transport of glycine and the imino acids, is discussed.

The most important drawbacks of gastric surgery for peptic ulcer have been: operative mortality, recurrences and the post-gastrectomy syndromes. Technical improvements have diminished the importance of the first two factors, and have focused attention on the post-gastrectomy syndromes. Research in the pathophysiology of the post-gastrectomy syndromes, both by clinical observation and animal experimentation, has served in distinguishing the following distinct entities (1).

The first significant study of biochemical changes which accompany vomiting or gastric succion in animal or man was made by Gamble in 1925 (31). Although a few predecessors had observed the therapeutic effect of sodium chloride infusions in such experimental situations, (37, 38, 51) Gamble first demonstrated that blood alkalosis was a major alteration secondary to loss of gastric juice and studied the corrective effect of acute sodium chloride infusion. His data have been amply confirmed by certain of his contemporaries and a number of subsequent works (35, 43, 3a, 10, 15, 36, 44, 46, 47, 67, 78, 22).

The elusive role of the adrenal cortex in hypertension has recently been depicted in the following analogy: "The adrenal cortex is like a lady who has kept bad company and late hours for so long that, human nature being what it is, she must have sinned. Testimony has been brought against her, however, only by her few suitors who had adrenal hyperplasia or adrenal tumors. Her other friends have refrained from talking. Perhaps this is because they are gentlemen; or perhaps it is only that they do not have much to talk about." [...]