Investigation of the effects of solution composition and container material type on the loss of 11-nor-delta 9-THC-9-carboxylic acid.

The loss of 11-nor-delta 9-tetrahydrocannabinol-9-carboxylic acid (THC-COOH) from solution was studied using fluorescence polarization immunoassay (FPIA) technology and x-ray photoelectron spectroscopy (XPS). Several materials (glass, silylated glass, high density polyethylene, polypropylene, polystyrene, polymethylmethacrylate, Teflon, and Kynar) were studied along with three solvents (water, urine, and Abbott cannabinoids diluent). THC-COOH losses ranging from 0 to 9.7 ng/cm2 and concentration reductions to 46% of starting values were measured. XPS indicated the presence of fluorine-labeled THC-COOH at materials surfaces. A half-life of 10 min was calculated for THC-COOH loss from urine stored in high density polyethylene at room temperature. Sample handling losses during pipetting were determined and ranged from 1.1 to 7.9 ng per aliquot. The effects of sample volume and sample handling on the THC-COOH concentrations of controls were also investigated.

Effects of diabetes mellitus on parathyroid hormone-stimulated protein kinase activity, ferredoxin phosphorylation, and renal 1,25-dihydroxyvitamin D production.

Impairment in the stimulation of renal production of 1,25-dihydroxyvitamin D[1,25 (OH)2D] by parathyroid hormone (PTH) occurs in diabetes. Renal response to PTH in terms of 25-hydroxyvitamin D-1-hydroxylase (1-OHase) stimulation involves increased cyclic adenosine monophosphate (cAMP) production, increased cAMP-dependent protein kinase activity, and dephosphorylation of renal ferredoxin (renoredoxin). To identify the step where diabetes might impair PTH stimulation of 1-OHase, we studied the effects of PTH on 1,25(OH)2D production, cAMP content, cAMP-dependent protein kinase activity, and the phosphorylation state of renoredoxin by using renal slices from diabetic and nondiabetic rats. PTH and forskolin significantly stimulated 1,25(OH)2D production in renal slices from nondiabetic animals but not from diabetic animals. PTH-stimulated cAMP production and cAMP-dependent protein kinase activity in renal slices were not altered by diabetes. However, diabetes significantly impaired the capacity of PTH to dephosphorylate renoredoxin and to increase the activity of the 1-OHase enzyme complex. These results suggest that the decreased capacity of PTH to stimulate 1-OHase activity in diabetic animals may reflect the decreased capacity of PTH to alter the phosphorylation state of renoredoxin in these animals.

Multicenter, comparative study of enoxacin and ceftriaxone for treatment of uncomplicated gonorrhea.

The efficacy of single dose enoxacin, 400 mg was compared to ceftriaxone, 250 mg IM for therapy of uncomplicated gonorrhea in 152 evaluable patients attending sexually transmitted disease clinics in Baltimore, Indianapolis and Seattle. Anogenital gonorrhea was cured in 75 (99%) of 76 patients treated with enoxacin and 73 (97%) of 75 patients treated with ceftriaxone. Three of three patients with pharyngeal gonorrhea were not cured by enoxacin while all three ceftriaxone treated cases of pharyngeal gonorrhea were cured. All cases of anogenital gonorrhea caused by beta-lactamase producing Neisseria gonorrheae (11 patients), gonococci with high-level, plasmid-mediated tetracycline resistance (11 patients), or gonococci with chromosomally mediated penicillin resistance (22 patients) were cured. The IC90 for enoxacin of N. gonorrhoeae isolated in this study was 0.06 microgram/ml. Enoxacin appears to be a well tolerated, efficacious alternative to currently recommended therapy for patients with uncomplicated, anogenital gonorrhea including cases potentially caused by antibiotic resistant N. gonorrhoeae.