Hasil untuk "Physiology"

Rebecca E. Koch, A. Kavazis, D. Hasselquist et al.

Dietary carotenoids have been proposed to boost immune system and antioxidant functions in vertebrate animals, but studies aimed at testing these physiological functions of carotenoids have often failed to find support. Here we subject yellow canaries (Serinus canaria), which possess high levels of carotenoids in their tissue, and white recessive canaries, which possess a knockdown mutation that results in very low levels of tissue carotenoids, to oxidative and pathogen challenges. Across diverse measures of physiological performance, we detect no differences between carotenoid-rich yellow and carotenoid-deficient white canaries. These results add further challenge to the assumption that carotenoids are directly involved in supporting physiological function in vertebrate animals. While some dietary carotenoids provide indirect benefits as retinoid precursors, our observations suggest that carotenoids themselves may play little to no direct role in key physiological processes in birds. Dietary carotenoids have been proposed to have physiological benefits in addition to contributing to coloration. Here, Koch et al. compare immune and antioxidant functions in yellow, carotenoid-rich vs. white, carotenoid-deficient canaries and find no difference, suggesting a limited physiological role of carotenoids.

Rui Wang

T. Finkel

Although historically viewed as purely harmful, recent evidence suggests that reactive oxygen species (ROS) function as important physiological regulators of intracellular signaling pathways. The specific effects of ROS are modulated in large part through the covalent modification of specific cysteine residues found within redox-sensitive target proteins. Oxidation of these specific and reactive cysteine residues in turn can lead to the reversible modification of enzymatic activity. Emerging evidence suggests that ROS regulate diverse physiological parameters ranging from the response to growth factor stimulation to the generation of the inflammatory response, and that dysregulated ROS signaling may contribute to a host of human diseases.

R. Medzhitov

M. Valko, D. Leibfritz, J. Moncol’ et al.

John Allen

A. Craig

R. Sapolsky, L. Romero, A. Munck

B. McEwen

W. Dröge

R. Ulrich, R. Simons, B. D. Losito et al.

John F. R. Kerr, A. Wyllie, R. Alastair et al.

The term apoptosis is proposed for a hitherto little recognized mechanism of controlled cell deletion, which appears to play a complementary but opposite role to mitosis in the regulation of animal cell populations. Its morphological features suggest that it is an active, inherently programmed phenomenon, and it has been shown that it can be initiated or inhibited by a variety of environmental stimuli, both physiological and pathological.The structural changes take place in two discrete stages. The first comprises nuclear and cytoplasmic condensation and breaking up of the cell into a number of membrane-bound, ultrastructurally well-preserved fragments. In the second stage these apoptotic bodies are shed from epithelial-lined surfaces or are taken up by other cells, where they undergo a series of changes resembling in vitro autolysis within phagosomes, and are rapidly degraded by lysosomal enzymes derived from the ingesting cells.Apoptosis seems to be involved in cell turnover in many healthy adult tissues and is responsible for focal elimination of cells during normal embryonic development. It occurs spontaneously in untreated malignant neoplasms, and participates in at least some types of therapeutically induced tumour regression. It is implicated in both physiological involution and atrophy of various tissues and organs. It can also be triggered by noxious agents, both in the embryo and adult animal.

Marek Malik, J. Bigger, A. J. Camm et al.

S. Gordon, P. Taylor

A. Goldberger, L. A. N. Amaral, Leon Glass et al.

P. Basser, C. Pierpaoli

Madalena Costa, A. Goldberger, Chung-Kang Peng

G. Pearson, Fred L Robinson, T. Gibson et al.

W. Knaus, E. Draper, D. Wagner et al.

J. Friedman, J. Halaas