Zobrazeno 1 - 10
of 53
pro vyhledávání: '"S. R. Price"'
Autor:
E. Löfberg, Jonas Bergström, A. Alvestrand, S. R. Price, A. Gutierrez, William E. Mitch, J. Wernerman, Björn Anderstam
Publikováno v:
European Journal of Clinical Investigation. 32:345-353
Background Treatment with glucocorticosteroids causes a negative nitrogen balance, but the kinetic mechanisms responsible for this catabolic effect are controversial. We investigated the effects of 60 mg day−1 prednisolone on protein synthesis and
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::425bed1a5d6e5d77e5e873c1ec233de4
https://doi.org/10.1046/j.1365-2362.2002.00993.x
https://doi.org/10.1046/j.1365-2362.2002.00993.x
Publikováno v:
Scopus-Elsevier
Abstract —Angiotensin II (Ang II) is known to act as a growth factor and may be involved in cardiac remodeling. We have shown that insulin-like growth factor-I (IGF-I) is an autocrine mediator of growth responses to Ang II in vascular smooth muscle
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c69c19edb6d727911198f967fd038a9e
https://doi.org/10.1161/01.hyp.34.5.1053
https://doi.org/10.1161/01.hyp.34.5.1053
Autor:
S. R. Price, X. Wang
Publikováno v:
Mineral and Electrolyte Metabolism. 25:224-227
Metabolic acidosis and glucocorticoids act in concert to stimulate branched-chain amino acid (BCAA) oxidation in adrenalectomized rats. In muscles of normal rats, metabolic acidosis increases the maximal activity of the rate-limiting enzyme, branched
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ecd7909b27eb15cc1d16fd528c15f077
https://doi.org/10.1159/000057452
https://doi.org/10.1159/000057452
Publikováno v:
American Journal of Physiology-Cell Physiology. 272:C2031-C2036
In muscles of rats with metabolic acidosis, branched-chain alpha-ketoacid dehydrogenase (BCKAD) activity is increased. Potential stimulatory signals include acidemia and/or glucocorticoids. It is unclear whether the signal(s) increases BCKAD activity
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9758641af89f93c4bd671fda66cd868e
https://doi.org/10.1152/ajpcell.1997.272.6.c2031
https://doi.org/10.1152/ajpcell.1997.272.6.c2031
Autor:
William E. Mitch, L S Phillips, Xiaonan H. Wang, X Ding, S. R. Price, B K England, C Jurkovitz, James L. Bailey
Publikováno v:
Journal of Clinical Investigation. 98:1703-1708
In normal subjects and diabetic patients, insulin suppresses whole body proteolysis suggesting that the loss of lean body mass and muscle wasting in insulinopenia is related to increased muscle protein degradation. To document how insulinopenia affec
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0d233e214f8a53cc60cd5ca634b19f32
https://doi.org/10.1172/jci118968
https://doi.org/10.1172/jci118968
Autor:
B. K. England, S. R. Price
Publikováno v:
Blood Purification. 13:147-152
Malnutrition and a loss of lean body mass frequently complicate chronic renal failure. Muscle wasting in uremia is caused by increased protein degradation, decreased protein synthesis and increased branched-chain amino acid oxidation. Acidosis and gl
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f3bbb3de9e03d87e2e90ab40223db621
https://doi.org/10.1159/000170197
https://doi.org/10.1159/000170197
Autor:
S. R. Price, William E. Mitch, S Grieber, James L. Bailey, R Medina, R. C. May, B K England, Alfred L. Goldberg
Publikováno v:
Journal of Clinical Investigation. 93:2127-2133
Metabolic acidosis often leads to loss of body protein due mainly to accelerated protein breakdown in muscle. To identify which proteolytic pathway is activated, we measured protein degradation in incubated epitrochlearis muscles from acidotic (NH4Cl
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1eda378f816b66634414017a70d1eac4
https://doi.org/10.1172/jci117208
https://doi.org/10.1172/jci117208
Publikováno v:
American Journal of Physiology-Renal Physiology. 266:F536-F542
We have found abnormalities in Na-K-adenosine-triphosphatase (Na-K-ATPase) function in different tissues of rats with chronic renal failure (CRF). A potential mechanism for these findings is a change in Na-K-ATPase alpha- and/or beta-gene expression.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9f76e7f4994d2c75573ec5ce569ed664
https://doi.org/10.1152/ajprenal.1994.266.4.f536
https://doi.org/10.1152/ajprenal.1994.266.4.f536
Publikováno v:
American Journal of Kidney Diseases. 23:224-228
An early response to metabolic acidosis is an increase in the degradation of muscle protein to provide the nitrogen needed to increase glutamine production so the kidney can excrete acid. In patients with renal insufficiency, this process may represe
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d19b5a3021499873bea0599e09596304
https://doi.org/10.1016/s0272-6386(12)80976-0
https://doi.org/10.1016/s0272-6386(12)80976-0
Publikováno v:
Scopus-Elsevier
ADP-ribosylation factors (ARFs) are approximately 20-kDa guanine nucleotide-binding proteins that serve as GTP-dependent allosteric activators of cholera toxin ADP-ribosyltransferase activity. Four species of mammalian ARF, termed ARF 1-4, have been
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::77d29ce0b3295f0eb93d8c73a36fed2c
https://doi.org/10.1016/s0021-9258(18)49913-9
https://doi.org/10.1016/s0021-9258(18)49913-9