PubMed Health⌕ Search

Biomedical subjects

J Burda

Publications and source records attributed to J Burda.

At least 37 records · Page 2Linked to original sources
PubMed1987

Molecular mechanisms of ischemic damage of spinal cord.

Incomplete ischemia of the spinal cord of rabbits was produced by a 40-min occlusion of the abdominal aorta followed by 1 and 4 days of recirculation. Regional evaluation of ATP-induced bioluminescence after 20 min of ischemia revealed ATP depletion mainly in the gray matter of the spinal cord. After 40 min of ischemia, ATP-induced bioluminescence was too faint to expose the photographic film. Within 1 and 4 days of recovery following 40 min of ischemia, restitution of ATP was regionally heterogeneous, reduced predominantly in the anterior horns of gray matter. Polysome profiles remained unaltered during the ischemic period, but a marked disaggregation of polyribosomes occurred after 10 min of recirculation. Protein synthesis in a cell-free system was inhibited by the addition of a postischemic cytosol or protein fraction isolated from cytosols on a DEAE column. The inhibition can be overcome by the addition of each initiation factor 2 (eIF-2), GTP and GDP exchange factor (GEF). Occlusion of abdominal aorta for 40 min results in decrease in monoamine oxidase accumulation in both proximal and distal ligature placed on sciatic nerve. Within 4 days of recovery the transport was progressively depressed to 22 and 21% in the proximal and distal direction, respectively.

Adenosine Triphosphate↗
PubMed1987

Effect of ischaemia on protein synthesis in vitro.

Changes in the incorporation of 14C-amino acids into proteins in vitro were followed under conditions of ischemia induced by abdominal aorta ligature and subsequent recirculation in dogs. Cell saps isolated from L-S spinal cord, spinal ganglia, the sciatic nerve and medulla oblongata were added to the incorporation mixture composed of ribosomes and an enzymatic system from intact brains. Cytosols isolated from ischemic animals affected the rate of in vitro protein synthesis moderately, while repeated ischemia caused a profound decrease in the incorporation of amino acids into proteins. Cytosols from L-S spinal cord and especially from spinal ganglia after three days of recirculation substantially enhanced incorporation thus indicating a massive response of these tissues to ischemic injury. Cell saps from the medulla oblongata increased amino acid incorporation into proteins in vitro in all experimental groups.

Animals↗
PubMed1986

Influence of blood sera from dogs subjected to ischemia and recirculation on incorporation of 14C-amino acids in vitro.

Incomplete ischemia of the spinal cord was produced in dogs by 40 min occlusion of the abdominal aorta that was followed by 5-40 min of recirculation. Amino acid incorporation into ribosomes in vitro in the presence of venous blood sera was estimated. The most significant reduction in incorporation was produced by sera of the dogs following a short recirculation period (5-10 min). No significant changes were observed at the end of the ischemic period nor at longer periods of recirculation. The decrease in incorporation might be the consequence of inactivation or absence of a substance stimulating polypeptide synthesis in vitro, normally present in blood sera of intact dogs, that temporarily loses its activity during recirculation.

Amino Acids↗
PubMed1986

Effect of blood sera from ischaemic and recirculated dogs on protein synthesis in vitro.

A study was made of the effect on polypeptide synthesis in vitro of venous blood sera from dogs in which incomplete ischaemia had been induced by ligating the abdominal aorta and subsequent recirculation. Sera from the ischaemic animals had practically no effect on the incorporation of 14C-amino acids into the proteins, but sera obtained during the first minutes of recirculation reduced proteosynthesis by 24% as compared with the control. During subsequent 40 min recirculation this effect was lost. Separation of the sera on DEAE cellulose showed that the decrease in 14C-amino acid incorporation into protein in vitro was based on the temporary disappearance or inactivation of a substance normally present in the serum of control animals.

Amino Acids↗
PubMed1975

Effect of brain, liver and muscle cytosols on in vitro incorporation of labelled amino acids into the ribosomes of these organs during protein depletion.

The functional state of the rat liver, brain and muscle proteosynthetic apparatus during developing protein depletion was studied, with special reference to the effect of brain cytosols on the synthetic capacity of liver and muscle ribosomes. The results indicate that both stimulant and inhibitory agents (so far unidentified) may be present in brain cytosols during protein depletion.

Adaptation, Physiological↗
PubMed1975

Effect of protein depletion on the RNA content and proteosynthesis level in rat liver and brain.

The authors studied the effect of protein depletion on the RNA content of rat liver and brain and on the incorporation of 14C-leucine into the microsomal and soluble liver and brain fractions. They failed to find a direct relationship between the amount of RNA and the rate of proteosynthesis in the organs in question. The changes found in 14-C-leucine incorporation are discussed in relation to previous studies.

Animals↗