[The use of thermal desorption in the evaluation of activated charcoal dosimeters].
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Air Pollutants↗
Biomedical subjects
P Nguyen
Publications and source records attributed to P Nguyen.
A re-evaluation of the HSA-piroxicam interaction.
Piroxicam binding to HSA was studied using equilibrium dialysis and fluorescence methods. It was shown that this drug, like its analogs isoxicam and tenoxicam, binds to the apazone locus (site I area) and to a lesser extent to the diazepam site (site II). The piroxicam binding to HSA can be modulated by various specific ligands--apazone, warfarin, diazepam, ibuprofen--and these drug interactions have to be considered not only as potential displacement from the HSA binding sites but also in terms of induced allosteric effects.
Apazone↗
Selective cyclooxygenase 2 inhibition lowers spinal cord prostaglandin concentrations after injury.
BACKGROUND CONTEXT: Prostaglandin E2 (PGE2) and thromboxane B2 (TxB2) concentrations are elevated in the injured spinal cord for hours to days after injury. Treatment of animals with a selective cyclooxygenase-2 (COX-2) inhibitor has been shown to improve functional outcome in an animal model. PURPOSE: We sought to characterize the effects of COX-2 inhibition on prostaglandin concentrations in the spinal cord after injury. STUDY DESIGN/SETTING: A drug study was performed using 76 male Long Evans rats. OUTCOME MEASURES: PGE2 and TxB2 concentrations were measured by enzyme immune assay. METHODS: Fifty-six rats were subject to spinal cord injury, and 4 rats served as sham controls. Twenty eight rats received 3 mg/kg of celebocid by means of an orogastric tube within 20 minutes after injury, and 28 received vehicle alone. The animals were sacrificed at time points between 2 and 72 hours after injury, and PGE2 and TxB2 levels were measured. A second study was performed using transcardiac saline perfusion in order to reduce intragroup variance in measured PGE2 and TxB2 levels. Sixteen animals underwent spinal cord injury. Animals were sacrificed at 4 and 24 hours after injury, and PGE2 and TxB2 levels were measured. RESULTS: PGE2 and TxB2 concentrations were elevated after injury in all animals. Administration of celebocid resulted in a delayed reduction of PGE2 and TxB2 concentrations in the initial drug study. These results were not statistically significant. Transcardiac perfusion with normal saline reduced the intragroup variance. Using this technique, administration of celebocid resulted in a statistically significant reduction in PGE2 and TxB2 concentrations in the injured cord segment 4 and 24 hours after injury. CONCLUSION: Administration of a selective COX-2 inhibitor after injury results in a decrease of PGE2 and TxB2 concentrations in the injured spinal cord. Transcardiac perfusion after sacrifice reduces measured variance, probably through reducing the contribution of blood-borne prostaglandins.
Animals↗
Regional and temporal changes in prostaglandin E2 and thromboxane B2 concentrations after spinal cord injury.
BACKGROUND CONTEXT: Inflammatory metabolites of arachidonic acid likely play a significant role in secondary injury after spinal cord trauma. PURPOSE: We sought to characterize the regional and temporal alterations in prostaglandin concentrations after injury in a rat model. STUDY DESIGN/SETTING: Prostaglandin E2 (PGE2) and thromboxane B2 (TxB2) concentrations were measured in cerebrospinal fluid (CSF) and in different parts of the injured spinal cord at various time points after spinal cord injury. OUTCOME MEASURES: PGE2 and TxB2 levels were measured by means of an enzyme immune assay. METHODS: Forty-six adult Long Evans rats were subject to spinal cord injury using the NYU impactor. Animals were divided into three groups. Fourteen animals were used in a pilot study to determine the timing and location of PGE2 production after spinal cord injury. These animals were sacrificed, and samples of injured cord, rostral cord and CSF were assayed for PGE2 concentration. The remaining 32 animals were used to establish the time course of prostaglandin production. Twenty-eight animals were subjected to a spinal cord injury, and four animals served as sham-operated controls. These animals were sacrificed at predetermined time points 2 to 72 hours after injury, and the injured segments of spinal cord were harvested. RESULTS: Both PGE2 and TxB2 concentrations increased immediately after injury in the injured segment. PGE2 concentrations increased faster and more dramatically in the injured segment of spinal cord than in CSF or noninjured segments. Elevations in PGE2 and TxB2 concentrations were persistent for 72 hours after injury. CONCLUSION: Elevated concentrations of arachidonic acid metabolites can be detected in the injured segment of the spinal cord for at least 72 hours after injury. Concentration changes are detected earlier and are more dramatic in the injured cord segment than in rostral segments or the CSF.
Animals↗
Stability of thiamin in parenteral nutrition solutions.
Since the vitamin thiamin is sensitive to degradation in the presence of stoichiometric concentrations of sulfite ions, the stability of thiamin in parenteral nutrition solutions containing sulfite as an antioxidant and preservative has been questioned. The usual clinical practice of mixing amino acids, dextrose, and other solutions for administration in total parenteral nutrition significantly dilutes the concentration of sulfite. We have measured the thiamin concentration in total parenteral nutrition solutions sampled from containers after administration to patients. We have also determined the time course of thiamin degradation in solutions containing two concentrations of sulfite. Thiamin content exceeded labeled amounts in total parenteral nutrition bags containing amino acid, dextrose, and multivitamin solutions. However, when multivitamins were added directly to amino acid solutions containing 0.1% (9.6 mM) sulfite, significant degradation occurred by 5 hr. Thiamin was stable for at least 22 hr when added to total parenteral nutrition solutions containing less than 0.05% (4.8 mM) sulfite.
Antioxidants↗
Chronic lymphocytic leukemia with portal hypertension and without liver involvement: a case report underlining the roles of increased spleno-portal blood flow and "protective" sinusoidal vasoconstriction.
We report the case of a 72-year-old woman with well-controlled chronic lymphocytic leukemia (CLL) and splenomegaly who developed portal hypertension with bleeding oesophageal varices in the absence of liver fibrosis or regenerative nodular hyperplasia at surgical wedge liver biopsy. The hepatic venous pressure gradient (HVPG) was elevated and splenectomy resulted in both its normalisation and the regression of oesophageal varices. This case shows the potential for an increased spleno-poral flow to generate severe portal hypertension likely through a "protective" sinusoidal vasoconstriction.
Aged↗