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John B. Anderson

Other affiliations: Howard Hughes Medical Institute
Bio: John B. Anderson is an academic researcher from Harvard University. The author has contributed to research in topics: Toad & Hypoglycemia. The author has an hindex of 4, co-authored 4 publications receiving 706 citations. Previous affiliations of John B. Anderson include Howard Hughes Medical Institute.

Papers
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Journal ArticleDOI
TL;DR: The short-circuit current of the isolated toad bladder was regularly stimulated with pure oxytocin and vasopressin when applied to the serosal surface under aerobic and anaerobic conditions.
Abstract: Studies were made of the active ion transport by the isolated urinary bladder of the European toad, Bufo bufo, and the large American toad, Bufo marinus. The urinary bladder of the toad is a thin membrane consisting of a single layer of mucosal cells supported on a small amount of connective tissue. The bladder exhibits a characteristic transmembrane potential with the serosal surface electrically positive to the mucosal surface. Active sodium transport was demonstrated by the isolated bladder under both aerobic and anaerobic conditions. Aerobically the mean net sodium flux across the bladder wall measured with radioactive isotopes, Na(24) and Na(22), just equalled the simultaneous short-circuit current in 42 periods each of 1 hour's duration. The electrical phenomenon exhibited by the isolated membrane was thus quantitatively accounted for solely by active transport of sodium. Anaerobically the mean net sodium flux was found to be slightly less than the short-circuit current in 21 periods of observation. The cause of this discrepancy is not known. The short-circuit current of the isolated toad bladder was regularly stimulated with pure oxytocin and vasopressin when applied to the serosal surface under aerobic and anaerobic conditions. Adrenaline failed to stimulate the short-circuit current of the toad bladder.

308 citations

Journal ArticleDOI
TL;DR: In 1941, Brown and Harvey described hypoglycemia after alcoholic debauch in six chronic alcoholics from the Baltimore area, and in 1942, Tucker and Porter noted four cases among chronicalcoholics from Richmond, Virginia.
Abstract: In 1941, Brown and Harvey described hypoglycemia after alcoholic debauch in six chronic alcoholics from the Baltimore area (1). In 1942, Tucker and Porter noted four cases among chronic alcoholics from Richmond, Virginia (2). Since then, fewer than 100 instances of alcoholism associated with hypoglycemia have been reported, and most of these accounts have appeared in the foreign literature (3-12). Certain summary statements about \"alcohol hypoglycemia\" are justified. First, although the condition was originally ascribed to \"smoke,\" or more specifically, denatured alcohol solvents (\"Solox\") 1 (1, 2), later reports have excluded methanol, ethyl acetate, gasoline, or methyl isobutyl ketone (3, 4, 7, 9-12). Second, well-documented pediatric cases indicate that the addiction of the chronic alcoholic is not mandatory (4, 7, 9-

209 citations

Journal ArticleDOI
01 Jun 1965-Diabetes
TL;DR: It has been proposed that the effects of alcohol upon gluconeogenesis by cellular preparation may be conditioned by the alternative pathways available for reoxidizing the cytoplasmic NADH2 which is generated during alcohol oxidation.
Abstract: Attempts to characterize the hypoglycemia that may follow alcohol ingestion have disclosed the following: The hypoglycemia can be reproduced with pure ethanol and it occurs at blood alcohol levels which do not exceed the range of mild intoxication. It is not attended by plasma changes characteristicof liver damage or peripheral “insulin-like” actions. Circulating immunologically-reactive insulin does not increase and pancreatic responsiveness to islet cell secretogogues such as glucose and tolbutamide is preserved. The hypoglycemia cannot be terminated by glucagon. From infusion experiments, it cannot be ascribed to enhanced peripheral utilization of glucose. In normal humans or dogs, induction of experimental alcohol hypoglycemia with alcohol requires several days of preliminary fasting; in patients with diminished gluconeogenic reserve, regardless of etiology, lesser dietary deprivation is required. Ethanol can also attenuate the prevailing hyperglycemia in fasted “juvenile” diabetics from whom insulin has been withheld to the point of early ketoacidosis. In vitro studies have corroboratedthat at least some of the blood sugar lowering actions of alcohol may be ascribed to a direct impairment in the endogenous formation of glucose from smaller precursors. Oxidative-decarboxylation of added substrates by slices of human, rabbit or rat liver is invariably reduced in the presence of alcohol.Under appropriate conditions, a concomitant inhibition of gluconeogenesis isobserved. It has been proposed that the effects of alcohol upon gluconeogenesis by cellular preparation may be conditioned by the alternative pathways available for reoxidizing the cytoplasmic NADH 2 which is generatedduring alcohol oxidation. A pivotal role has been assigned to the prevailing intrahepatic availability and turnover of pyruvate.

104 citations

Journal ArticleDOI
TL;DR: Tissue studies were performed on the isolated urinary bladder of the toad, Bujo marinus, and small intestine, stomach, heart, ventral abdominal skin, and skeletal muscle were used for the study of the oxygen consumption of various toad tissues.

85 citations


Cited by
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Journal ArticleDOI
05 Jan 1972-Nature
TL;DR: “Tight junctions” between cells in some epithelia actually provide the main route of passive ion permeation and the degree of junctional tightness may underlie important functional differences between different epithelias.
Abstract: “Tight junctions” between cells in some epithelia actually provide the main route of passive ion permeation. The degree of junctional tightness may underlie important functional differences between different epithelia.

742 citations

Journal ArticleDOI
Philip Felig1
TL;DR: A glucose-alanine cycle in which alanine is formed peripherally by transamination of glucose-derived pyruvate and transported to the liver where its carbon skeleton is reconverted to glucose is suggested.
Abstract: Alanine is quantitatively the primary amino acid released by muscle and extracted by the splanchnic bed in postabsorptive as well as prolonged fasted man. The hepatic capacity for conversion of alanine to glucose exceeds that of all other amino acids. Insulin inhibits gluconeogenesis by reducing hepatic alanine uptake. In contrast, in diabetes, an increase in hepatic alanine extraction is observed in the face of diminished circulating substrate. In prolonged fasting, diminished alanine release is the mechanism whereby gluconeogenesis is reduced. In circumstances in which alanine is deficient, such as pregnancy and ketotic hypoglycemia of infancy, fasting hypoglycemia is accentuated. Augmented glucose utilization in exercise and hyperpyruvicemia consequent to inborn enzymatic defects are accompanied by increased circulating levels of alanine. These data thus suggest the existence of a glucose-alanine cycle in which alanine is formed peripherally by transamination of glucose-derived pyruvate and transported to the liver where its carbon skeleton is reconverted to glucose. The rate of recycling of glucose carbon skeletons in this pathway appears to occur at approximately 50% of that observed for the Cori (lactate) cycle.

694 citations

Book ChapterDOI
01 Jan 1992
TL;DR: Whereas deaths from other causes such as cardiovascular diseases decreased in the period from 1950 to 1974 by 2% in the United States, deaths from cirrhosis climbed 71.7%.
Abstract: The mortality rates for cirrhosis vary greatly from country to country. For example, in 1972 the World Health Organization reported mortality rates of 7.5/100,000 in Finland and 57.2/100,000 in France. The corresponding per-capita alcohol consumptions were 5.1 and 16.8 liters of absolute alcohol (International Statistics on Alcoholic Beverages: Production Trade and Consumption 1950–1972, 1977). Whereas deaths from other causes such as cardiovascular diseases decreased in the period from 1950 to 1974 by 2% in the United States, deaths from cirrhosis climbed 71.7%. Since then, mortality from cirrhosis has leveled off or even decreased in the United States. The reduction, however, pertains primarily to nonalcoholic cirrhosis (Liver Cirrhosis Mortality in the United States, 1988). In Canada, cirrhosis has been the most rapidly increasing cause of death in the population over 25 years of age, followed by lung and bronchial cancer and suicide (Schmidt, 1977), and it is now the fifth major cause of death for men in the productive years from 25 to 64 (Rankin, 1977). The concentration of mortality of alcoholic cirrhosis to a rather young population group also occurs in the United States. In Baltimore, it was the fifth leading cause of death for persons 25 to 44 years of age (Kuller et al., 1969) and the fourth leading cause of death for those 25 to 64 years of age in New York City (New York City; Summary of Vital Statistics, 1984).

461 citations

Journal ArticleDOI
TL;DR: The effect of vasopressin and cyclic 3’,5’-AMP on the permeability to water and urea of the isolated perfused rabbit collecting tubule was measured and permeability was not significantly altered despite simultaneous increases in water permeability.
Abstract: GRANTHAM, JARED J., AND MAURICE B. BURG. Effect ofuasopressin and cyclic AMP on permeability of isolated collecting tubules. Am. J. Physiol. 21 I (I) : 255-259. rg66.-The effect of vasopressin and cyclic 3’,5’-AMP on the permeability to water and urea of the isolated perfused rabbit collecting tubule was measured. When added to the solution bathing the outside of the tubule, these agents regularly increased both net water absorption along an osmotic gradient and the diffusional permeability to water as measured with THO in the absence of an osmotic gradient. When added only to the solution bathing the luminal border of the cells, vasopressin was ineffective. Urea permeability was not significantly altered by either vasopressin or cyclic 3’) $-AMP despite simultaneous increases in water permeability.

424 citations

Journal ArticleDOI
TL;DR: The physiology of thermoregulation is important in light of recent advances in therapy using core rewarming, and pathophysiology, etiology and management of the hypothermia syndrome are reviewed.
Abstract: Hypothermia, defined as a core temperature less than 35 degrees C, is frequently not recognized, in part because of the inadequacy of standard thermometers. This entity has multiple causes and unique pathophysiologic consequences that complicate diagnosis and treatment. Understanding of the physiology of thermoregulation is important in light of recent advances in therapy using core rewarming. Pathophysiology, etiology and management of the hypothermia syndrome are reviewed.

399 citations