PubMed · 8753506
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T Shimizu. 1995. [Acetate].. https://pubmed.ncbi.nlm.nih.gov/8753506/
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A noninvasive method to determine the carboxyl content in oxidized celluloses, using solid-state carbon-13 cross-polarization-magic angle spinning nuclear magnetic resonance (13C CP/MAS NMR) spectroscopy, has been developed. Standard samples containing 0, 4, 8, 12, 16, and 20% carboxyl content were prepared by mixing appropriate amounts of powdered cellulose, a non-oxidized cellulose standard prepared from cotton linter by ball-milling for 96 h, and a commercial oxidized cellulose sample that had a 20% carboxyl content. Standard curves were constructed by plotting the percent carboxyl content against the peak area at 171 ppm, normalized with (i) a peak area at 104 ppm and (ii) the sum of peak areas at 171, 62, and 65 ppm. The regression analysis of the curves yielded a linear relationship with correlation coefficient (R2) values of 0.9868 and 0.9863, respectively. To validate the methods, five new samples of oxidized cellulose were prepared and analyzed. The values obtained were comparable to those determined by the calcium acetate method described in the United States Pharmacopoeia (USP), indicating that the solid-state 13C CP/MAS NMR can be used to analyze carboxyl content in oxidized celluloses.
Colonic mucosal wounds are repaired, in part, by epithelial migration. Signaling mechanisms regulating this migration are poorly characterized. This study aimed to examine the role that the epidermal growth factor (EGF) receptor (EGF-R) and its ligands, EGF and transforming growth factor-alpha (TGF-alpha), play in migration in wounded in vitro models of colonic epithelium. Migration was assessed over 24 h in circular wounds made in confluent monolayers of LIM1215 human colon cancer cells. EGF and TGF-alpha stimulated migration twofold from 4 h after wounding. Basal migration and the motogenic effects of short chain fatty acids and hepatocyte growth factor were mediated through enhanced binding of TGF-alpha to EGF-R, while trefoil peptide-mediated motogenesis required EGF-R activation independently of TGF-alpha binding. Activation of protein kinase C (PKC) stimulated migration, an effect more potent than, and independent of, EGF-R activation. However, neither inhibition of PKC by Ro 31-8220 nor depletion of PKC by pretreatement with phorbol myristate acetate attenuated EGF-R-mediated motogenesis. In conclusion, EGF-R activation via TGF-alpha binding, or intracellularly, mediates basal LIM1215 migration and the effects of several motogens, with the exception of PKC activators. Since EGF-R and PKC have physiological activators in vivo, they may control colonic mucosal repair processes following injury.
OBJECTIVE: To determine the ability of montelukast, a leukotriene receptor antagonist, to allow tapering of inhaled corticosteroids in clinically stable asthmatic patients. DESIGN: Double blind, randomised, placebo controlled, parallel group study. After a single blind placebo run in period, during which (at most) two inhaled corticosteroids dose decreases occurred, qualifying, clinically stable patients were allocated randomly to receive montelukast (10 mg tablet) or matching placebo once daily at bedtime for up to 12 weeks. SETTING: 23 academic asthma centres in United States, Canada, and Europe. PARTICIPANTS: 226 clinically stable patients with chronic asthma receiving high doses of inhaled corticosteroids (113 randomised to montelukast and 113 to placebo). INTERVENTIONS: Every 2 weeks, the inhaled corticosteroids dose was tapered, maintained, or increased (rescue) based on a standardised clinical score. MAIN OUTCOME MEASURES: Last tolerated dose of inhaled corticosteroids. RESULTS: Compared with placebo, montelukast allowed significant (P=0. 046) reduction in the inhaled corticosteroid dose (montelukast 47% v placebo 30%; least square mean difference 17.6%, 95% confidence interval 0.3 to 34.8). Fewer patients on montelukast (18 (16%) v 34 (30%) placebo, P=0.01) required discontinuation because of failed rescue. CONCLUSIONS: Montelukast reduces the need for inhaled corticosteroids among patients requiring moderate to high doses of corticosteroid to maintain asthma control.