[Incorporation in vitro of 1-14Codium palmitate in lipid fractions of rat liver (slices and isolated liver cells)].
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Biomedical subjects
Publications and source records attributed to J Koenig.
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We have previously demonstrated that 2D 1H NMR is suitable for studying cerebral metabolism. The same technique was used to study the hind leg muscle of normal (C57BL10) and dystrophic (mdx) mice. The results were compared to preliminary results for cultured muscle cells to determine the origin of fatty acid signals.
This work compares the efficacy of varying the concentrations of cryoprotectants when freezing samples of rat muscles for later use in tissue culture. The best yields were obtained with DMSO associated with glycerol and sucrose; before plating, the best results indicated 45% of cells with respect to controls, and delayed (24-36 h) myotube maturation. Maturation was studied by analysing the molecular forms of acetylcholinesterase and the ability of myotubes to form synapses in the presence of neurons, in fresh and frozen muscle.
Synapses obtained in vitro in a system of co-culture of muscle cells and neurons are of embryonic type. We prepared a monoclonal antibody (6.17) which recognizes a molecule synthesized by Schwann cells and used it to show that the main characteristics of maturity (decrease in number of synapses, appearance of junctional folds, and suppression of butyrylcholinesterase expression) are under the control of Schwann cells. In addition, Schwann cells have the capacity to aggregate the acetylcholine receptors in myotube cultures.
Cyclobenzaprine and its major metabolite, norcyclobenzaprine, differ from amitriptyline and nortriptyline only by the presence of a double bond in the cycloheptane ring. Three patients developed sufficient levels of cyclobenzaprine and norcyclobenzaprine because of either rapid or long-term ingestion of cyclobenzaprine to cause positive interferences in both a Syva EMIT assay and a high-performance liquid chromatographic (HPLC) assay for identification and quantitation of tricyclic antidepressants in serum. Cyclobenzaprine coeluted with amitriptyline, and norcyclobenzaprine eluted slightly earlier than, but was poorly resolved from, nortriptyline in this HPLC assay. We found that cyclobenzaprine could be distinguished from amitriptyline and that norcyclobenzaprine could be distinguished from nortriptyline on the basis of gas chromatographic retention times upon gas chromatographic-mass spectrometric analyses after derivatization with trifluoroacetic anhydride. The compounds were also distinguishable by mass spectrometric criteria.
Volatile organic compounds (VOCs) have been implicated as causative agents in asthma and building-related illness. To determine whether a mixture of VOCs could impair lung function or cause airway inflammation among subjects without bronchial hyperresponsiveness, the authors conducted a randomized, crossover-design trial of controlled human exposures to filtered air for four hours, VOCs at 25 mg/m(3) for four hours, and VOCs at 50 mg/m(3) for four hours, using a VOC mixture based on sampling of indoor environments. VOC exposures caused dose-related increases in lower respiratory, upper respiratory, and non-respiratory symptoms, with no significant change in lung function (FEV(1);, FVC, or FEF(25-75), nasal lavage cellularity or differential cell counts, induced sputum cellularity or differential cell counts, or biomarkers of airway inflammation, including IL-8, LTB(4), or albumin in nasal lavage or induced sputum samples. Atopic individuals had significantly reduced FEE(25-75 following exposure to VOCs at 50 mg/m(3), suggesting that these individuals may be more sensitive to the health effects of VOCs. The authors conclude that reductions in levels of VOCs to substantially less than 25 mg/m(3) are required if a "non-irritating" work environment is desired.
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S-sulfonate levels were measured in the nasal lavage (NAL) fluid of humans exposed to sulfur dioxide as a potential biological marker of exposure. These levels were determined by treating NAL fluid protein with cyanide to cleave the S-S linkage and release the sulfite. The cyanolytically released sulfite was measured by ion chromatography. In two experiments, humans were exposed to air or 1 ppm SO2 for 10 minute, and to air or 7 ppm SO2 for 20 minutes and lavaged immediately after exposure. Releasable sulfite levels in NAL fluid were 1.06 +/- 0.24 and 2.61 +/- 0.55 micrograms SO=3/mg protein, respectively (mean +/- SE, n = 5), for the first experiment, and 1.16 +/- 0.37 and 4.91 +/- 0.76 micrograms SO=3/mg protein, respectively (mean +/- SE, n = 8), for the second. The subjects in the former study were persons with asthma. In both experiments, S-sulfonate levels were statistically elevated in the exposed group compared with the control groups (p < 0.05, paired t-test). The same individuals in the second experiment received five additional 20-minute exposures to 7 ppm SO2 every other day, for a total of six exposures. NAL fluid taken at the conclusion of the final exposure had releasable sulfite levels of 4.99 +/- 1.36 micrograms SO=3/mg protein; these levels were statistically elevated relative to controls but were not elevated relative to the 1-day exposure (mean +/- SE, n = 8). The lack of accumulation of S-sulfonates after 6 days of short-term exposure suggests clearance of these compounds from the nasal passages within 24 hours. The levels of S-sulfonates observed in NAL fluid in this study are almost three orders of magnitude higher than those measured in plasma following similar SO2 exposures. Measurement of S-sulfonates in the nasal passage may be an effective short-term biomarker of exposure to SO2.
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