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Biomedical subjects

N Papadakis

Publications and source records attributed to N Papadakis.

At least 37 records · Page 2Linked to original sources
PubMed1977

Fluorescent derivatives of the pyruvate dehydrogenase component of the Escherichia coli pyruvate dehydrogenase complex.

One sulfhydryl group per polypeptide chain of the pyruvate dehydrogenase component of the pyruvate dehydrogenase multienzyme complex from Escherichia coli was selectively labeled with N-[P-(2-benzoxazoyl)phenyl]-maleimide (NBM), 4-dimethylamino-4-magnitude of-maleimidostilbene (NSM), and N-(4-dimethylamino-3,5-dinitrophenyl)maleimide (DDPM) in 0.05 M potassium phosphate (pH 7). Modification of the sulfhydryl group did not alter the enzymatic activity or the binding of 8-anilino-1-naphthalenesulfonate (ANS) or thiochrome diphosphate to the enzyme. The fluorescence of the NBM or NSM coupled to the sulfhydryl group on the enzyme was quenched by binding to the enzyme of the substrate pyruvate the coenzyme thiamine diphosphate, the coenzyme analogue thiochrome diphosphate, the regulatory ligands acetyl-CoA, GTP, and phosphoenolpyruvate, and the acetyl-CoA analogue, ANS. Fluorescence energy transfer measurements were carried out for the enzyme-bound donor-acceptor pairs NBM-ANS, NBM-thiochrome diphosphate ANS-DDPM, and thiochrome diphosphate-DDM. The results indicate that the modified sulfhydryl group is more than 40 A from the active site and approximately 49 A from the acetyl-CoA regulatory site. Thus, a conformational change must accompany the binding of ligands to the regulatory and catalytic sites. Anisotropy depolarization measurements with ANS bound on the isolated pyruvate dehydrogenase in 0.05 M potassium phosphate (pH 7.0) suggest that under these conditions the enzyme is dimeric.

Anilino Naphthalenesulfonates↗
PubMed1977

A new method of cranioplasty. Technical note.

A new method of cranioplasty is described. The skull defect is exposed, and an impression is taken which is used for the construction of a plaster of Paris model of the defect. Methyl methacrylate is molded to the model and thus an accurate reproduction of the skull defect is produced. The technique has the main advantage of good cosmetic appearance and strength.

Humans↗
PubMed1976

Fluorescence energy-transfer measurements between coenzyme A and flavin adenine dinucleotide binding sites of the Escherichia coli pyruvate dehydrogenase multienzyme complex.

The interaction of the pyruvate dehydrogenase multienzyme complex from Escherichia coli with 1,N6-etheno-CoA (epsilonCoA) and coenzyme A (CoA) has been investigated using equilibrium binding, steady-state fluorescence, and fluorescence lifetime measurements. A procedure for the resolution of the pyruvate dehydrogenase multienzyme complex into the pyruvate dehydrogenase enzyme and the transacetylase-flavoprotein subcomplex also is given. Direct binding studies with epsilonCoA indicate that 25 bound epsilonCoA molecules/multienzyme complex can be readily displaced by CoA, while approximately 21 bound epsilonCoA molecules/transacetylase-flavoprotein subcomplex can be displaced by CoA. The dissociation constant for the CoA displaceable epsilonCoA is 57.8 muM for the complex and 126 muM for the subcomplex in 0.02 M potassium phosphate (pH 7.0) at 5 degrees C. The kinetic behavior of epsilonCoA as a substrate was investigated and compared with that of CoA under a variety of conditions; the apparent Michaelis constants for epsilonCoA are considerably larger than those for CoA, while the corresponding maximal velocities are smaller. Fluorescence energy transfer measurements between bound epsilonCoA on the dihydrolipoyl transacetylase enzyme and flavin adenine dinucleotide on the dihydrolipoyl dehydrogenase enzyme either in the complex or subcomplex indicate, assuming the emission and absorption dipoles are randomly oriented, that these two probes must be at least 50 A apart.

Apoenzymes↗
PubMed1976

Retained intracranial metallic foreign bodies. Report of two cases.

The authors discuss two examples of extensive migration of retained metallic foreign bodies. The potential for further neurological injury from migration, formation of neurotoxic breakdown products, and the danger of infection are factors to be assessed when considering the removal of retained intracranial metallic foreign bodies.

Adolescent↗
PubMedDate not supplied

Reversal of experimental acute cerebral vasospasm by angiotensin converting enzyme inhibition.

We tested the hypothesis that cerebral arteriospasm developing after rupture of a subarachnoid aneurysm may be due to the vasoconstrictor effect of locally generated angiotensin II. Ten dogs had subarachnoid hemorrhage simulated by intracisternal introduction of 2 ml autologous blood, and were followed by cineangiography. Thirty minutes later, when acute arteriospasm was established, seven dogs received injection of the angiotensin converting enzyme inhibitor teprotide and 3 control dogs received normal saline. Repeat angiography at 30 and 90 minutes after injection, showed total or partial release of spasm in the experimental dogs and no change or further intensification of spasm in the control animals. We concluded that angiotensin converting enzyme inhibition may be a potentially useful approach for the reversal or prevention of cerebral arteriospasm after subarachnoid hemorrhage.

Acute Disease↗
PubMedDate not supplied

PH changes on the surface of brain and in cisternal fluid in dogs in cardiac arrest.

We measured brain surface pH and cisternal cerebrospinal fluid (CSF) acid-base variables in Na-pentobarbital anesthetized dogs during KCl induced cardiac arrest. Electrocardiographically, an agonal rhythm occurred within seconds, presumably resulting in rapid fall in cerebral blood flow. The mean arterial blood pressure fell from 125 +/- 22 (mean +/- 1 SD) to 35 +/- 28 mm Hg at 30 seconds and to 19 +/- 3 mm Hg at 60 seconds after KCl injection. The mean brain surface pH (n = 8) dropped abruptly from 7.30 to 6.80 within 3 minutes after induction of cardiac arrest. Changes in cisternal CSF pH, however, occurred slowly with the mean pH falling from 7.33 to 7.27 at 4 minutes and to 6.99 at 10 minutes after induction of cardiac arrest. The fall in cisternal CSF pH was due to a rise in CSF concentration of organic acids as well as a rise in CSF Pco2; the mean cisternal CSF [HCO3-] fell 3.6 mEq/l while the mean cisternal CSF lactate concentration and the mean CSF Pco2 rose, respectively, 2.1 mEq/l and 37.8 mm Hg 10 minutes after induction of cardiac arrest. We conclude that during acute ischemic anoxia gross pH disequilibria develop between brain extracellular fluid and cisternal CSF; analyses of the latter fluid provide unreliable information about brain metabolic status and its acid-base balance even up to ten minutes after induction of cardiac arrest.

Acidosis↗