Growth hormone signaling is necessary for lifespan extension by dietary methionine

Growth hormone significantly impacts lifespan in mammals. Mouse longevity is extended when growth hormone (GH) signaling is interrupted but markedly shortened with high‐plasma hormone levels. Methionine metabolism is enhanced in growth hormone deficiency, for example, in the Ames dwarf, but suppressed in GH transgenic mice. Methionine intake affects also lifespan, and thus, GH mutant mice and respective wild‐type littermates were fed 0.16%, 0.43%, or 1.3% methionine to evaluate the interaction between hormone status and methionine. All wild‐type and GH transgenic mice lived longer when fed 0.16% methionine but not when fed higher levels. In contrast, animals without growth hormone signaling due to hormone deficiency or resistance did not respond to altered levels of methionine in terms of lifespan, body weight, or food consumption. Taken together, our results suggest that the presence of growth hormone is necessary to sense dietary methionine changes, thus strongly linking growth and lifespan to amino acid availability.     

Biochemical alterations in acute human poliomyelitis electrolyte patterns and trends

Pronounced alterations occur in the biochemical findings in acute poliomyelitis. These are derived from three major mechanisms: (a) inefficient pulmonary gaseous exchange, resulting in respiratory acidosis; (b) profound changes in nitrogen metabolism, resulting in decreased serum albumin, tissue destruction, and increased urinary nitrogen; (c) losses of electrolytes through extrarenal channels such as lung and tracheal secretions, sweating, and gastrointestinal disturbances. The extent of these alterations may be defined by appropriate serum and urinary biochemical determinations. These determinations are valuable both from a therapeutic and a prognostic standpoint. They also contribute to further understanding of physiologic and pathologic conditions in acute poliomyelitis.