The hepatitis A virus (HAV), a picornavirus, is a common cause of hepatitis worldwide. Spread of infection is generally person to person or by oral intake after fecal contamination of skin or mucous membranes; less commonly, there is fecal contamination of food or water. Hepatitis A is endemic in developing countries, and most residents are exposed in childhood. In contrast, the adult population in developed countries demonstrates falling rates of exposure with improvements in hygiene and sanitation. The export of food that cannot be sterilized, from countries of high endemicity to areas with low rates of infection, is a potentially important source of infection. After ingestion and uptake from the gastrointestinal tract, the virus replicates in the liver and is excreted into the bile. Cellular immune responses to the virus lead to destruction of infected hepatocytes with consequent development of symptoms and signs of disease. Humoral immune responses are the basis for diagnostic serologic assays. Acute HAV infection is clinically indistinguishable from other causes of acute viral hepatitis. In young children the disease is often asymptomatic, whereas in older children and adults there may be a range of clinical manifestations from mild, anicteric infection to fulminant hepatic failure. Clinical variants include prolonged, relapsing, and cholestatic forms. Management of the acute illness is supportive, and complete recovery without sequelae is the usual outcome. Research efforts during World War II led to the development of passive immunoprophylaxis. Pooled immune serum globulin is efficacious in the prevention and attenuation of disease in exposed individuals. More recently, active immunoprophylaxis by vaccination has been accomplished. Future eradication of this disease can now be contemplated.

Hepatitis A: Old and New

General Pharmacology and Neuropharmacology of Benzodiazepine Derivatives

Temporomandibular joint pain referred from muscles of the head and neck

Publisher Summary Isoenzyme refers to a biochemically distinct class of catalytically active proteins with the same specificity of bond cleavage or alteration, which can occupy several zones following electrophoresis. The chapter focuses on the mechanism of catalysis and uncompetitive inhibition and provides analyses of studies reporting distinctive immunochemical properties as well as physical properties of enzymes prepared from several organs. In the case of alkaline phosphatase, the studies rely on a combination of organ source, biochemical properties, and electrophoretic distinctions as guidelines for working in this field. Placental alkaline phosphatase is an isoenzyme of alkaline phosphatase, which can be distinguished from other alkaline phosphatases by biochemical means. The different molecular forms of this isoenzyme, which can be produced and separated by physical means, are referred as variants of placental alkaline phosphatase. Hyperphosphatasemia in diseases of liver and bone has made the serum alkaline phosphatase determination the most frequently demanded enzyme assay.

Isoenzymes of Human Alkaline Phosphatase

Summary

Researches of the past ten years bearing on the physiological significance of the common acid and alkaline phosphomonoesterases may be summarized in the following facts and concepts, (i) The alkaline phos-phomonoesterase appears to be a salt-soluble, the acid a water-soluble, substance; both consist of a metallic coenzyme and a protein-like carrier. Neither depends oh sulphydryl groups for activity, but the alkaline phosphatase seems to require amine and phenolic hydroxy! groups; it is affected only by strong oxidizing agents. There is not yet any incontestable evidence that alkaline phosphomonoesterases of different sources are not identical. (2) Phosphatases probably catalyse only hydrolyses, not syntheses. (3) The content of both phosphatases in the blood serum is characteristic of age and physiological state, and is used in the diagnosis of bone and liver disorders; biliary obstruction results in elevation of serum alkaline phosphatase probably because phosphatase is normally excreted by way of liver and gut, but other explanations are possible. Diet influences serum alkaline phosphatase level. (4) The study of phosphatase function has been advanced by the development of techniques for the histochemical demonstration of acid and alkaline phosphatases. (5) It is certain that alkaline phosphatase is indispensable in normal ossification; it is generally instrumental in abnormal calcifications, but in a few cases calcification occurs without it. (6) Glycolysis seems to accompany normal bone formation, but this fact does not clarify all the unsolved problems of ossification. (7) Hormones and vitamins influence both alkaline phosphatase activity and bone formation. (8) In kidney tubules alkaline phosphatase probably functions in dephosphorylating sugar molecules that are removed from the tubular fluid by phosphorylation. The enzyme is present at other sites where it might serve in a similar manner. (9) Phosphatases are commonly found in the cytoplasm of growing, regenerating, and secreting cells in which protein synthesis is being carried on; there appears to be a correlation in such cells between content of pentosenucleic acid and of phosphatase. In dividing nuclei, phosphatase parallels desoxyribonucleic acid. (10) Acid phosphatase is found in seminal fluid, and may help to nourish the sperm. (11) The occurrence of two common phosphomonoesterases with widely different pH optima may indicate a mechanism for allowing two dephosphorylating steps to go on simultaneously in a single cell. In tissues which carry on much traffic in glycogen, acid phosphatase is possibly provided to prevent bone formation. (12) The actual role which the phosphatases play in the physiology of the organism will be understood only with elucidation of the complete enzyme systems of which the phosphatases are a part.

The physiological significance of the phosphomonoesterases

Pharmacology in medicine

SummaryAn experiment on the transmission of infectious hepatitis has been carried out among 19 volunteers at 2 institutions. At one of the institutions 3 different samples of serum containing the icterogenic agent were inoculated intracutaneously into 5 human subjects, and the disease was produced in 3 after incubation periods of 56 to 70 (avg 64) days.At another institution other samples of serum and also specimens of feces (and urine) were fed to 9 human subjects, and the disease was produced in 5 after an incubation period of 20 to 84 (avg 37) days by both of these materials.One case of “naturally acquired” hepatitis has appeared among the institutional personnel 51 days after the beginning of the experiment and 31 days after the appearance of the first experimental case.

Experimental Production of Hepatitis by Feeding Icterogenic Materials.

The problem of water retention in liver disease has been approached through both clinical and animal studies. In clinical studies Aldersberg and Fox (1943) found an abnormal retention of water when water tolerance tests were performed on patients with severe parenchymatous liver disease and recently Ralli et al. (1945) have demonstrated antidiuretic activity in urines from patients with hepatic cirrhosis and ascites. With respect to animal studies Aldersberg and Fox (1943) observed abnormal water tolerance tests in dogs when the liver was injured by phosphorus and histamine. Shay, Kolm, and Fels (1945) also reported the occurrence of abnormal water tolerance tests in rats fed a high fat diet. Leslie and Ralli (1947) have recently found that rats fed a high fat-low protein diet showed a decreased urine output during water tolerance tests, and they observed that the urines from such rats had antidiuretic activity.

Renal excretion of water and antidiuretic substances in patients with hepatic cirrhosis and rats with dietary liver injury.

THERE is some indirect evidence in the literature indicating that the conversion of carotene to vitamin A may be impaired during experimental hypothyroidism (Drill, 1943). In 1926 Kunde noted the appearance of xerophthalmia in rabbits 8 to 12 months after thyroidectomy, even though the diet was adequate for normal (unoperated) animals. Other studies on carotene and vitamin A excretion in the milk of thyroidectomized animals also lead to the conclusion that the thyroid gland was necessary for the conversion of carotene to vitamin A (Fellenberger and Greuter, 1932; Fasold and Heidemann, 1933). These papers suggest strongly that the conversion of carotene to vitamin A is not normal in the thyroidectomized animal.

Effect of thyroidectomy on the conversion of carotene to vitamin a1

IT IS KNOWN that estrogenic substances can be inactivated by the liver (Zondek, 1935; Israel, Meranze and Johnston, 1937; Golden and Sevringhaus, 1938; Biskind, 1941). When pellets of estrcne are implanted intrasplenically in castrated female rats, vaginal cornification will not occur if a normal diet is fed. This is interpreted as being due to the inactivation of estrone by the liver. However, if a diet deficient in the whole vitamin B complex is fed vaginal cornification will occur (Biskind and Biskind, 1942). When yeast was added to the deficient diet the liver regained its ability to inactivate estrone as judged by the return of the vaginal smear to an anestrous condition. Similar studies were made by Segaloff and Segaloff (1944). They injected estrogens intrasplenically into castrate female rats and noted the per cent showing estrus. They concluded that a deficiency of the vitamin B complex decreased the ability of the liver to inactivate estrone and a-estradiol, and that the addition of thiamine and...

Effect of vitamin b complex deficiency, controlled inanition and methionine on inactivation of estrogen by the liver

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