Decarboxylation of 6-nitro-5-alkoxybenzisoxazole-3-carboxylate ion (1,OMe and 1,OTD, alkoxy ) MeO, n-C14H29O, respectively) is accelerated by cationic micelles of cetyltrialkylammonium bromide (CTABr, CTEABr, CTPABr, CTBABr, alkyl ) Me, Et, n-Pr, n-Bu respectively). The first-order rate constants kobs for reaction of 1,OMe increase monotonically with [surfactant] and become constant when the substrate is fully bound and kobs ) k′M. The values of kobs for 1,OTD increase sharply with increasing [surfactant] and reach well-defined maxima at [surfactant] at or below the cmc, before decreasing to values corresponding to kobs ) k′M. The magnitude of the rate maxima and the increase in k′M are in the sequence CTABr < CTEABr < CTPABr < CTBABr. The rate maxima are due to formation of premicellar complexes of substrate with one or a few surfactant monomers, but they "dissolve" in micelles at higher [surfactant]. A rationalization is provided for acceleration by very dilute surfactants.
Using data from InCHIANTI, a prospective population-based survey of older persons, we examined the relationship of peroneal nerve conduction velocity (NCV, a measure of nerve myelination) and compound muscle action potential (CMAP, a measure of axonal degeneration) with calf muscle mass and density, two complementary measures of sarcopenia. NCV and CMAP were assessed by surface electroneurography of the right peroneal nerve conducted in 1162 participants, 515 men and 647 women, age 21-96 years, free of major neurological diseases. Cross-sectional muscle area and calf muscle density were measured using peripheral quantitative computerized tomography (pQCT). Both nerve and muscle parameters declined with age although in most cases the decline was not linear. In both sexes, CMAP, but not NCV, was independently and significantly associated with calf muscle density. These findings suggest that intrinsic changes in the muscle tissue are partially caused by a reduction in the number of motor axons.
These findings suggest that older community-dwelling adults with lower plasma carotenoids levels, a marker of poor fruit and vegetable intake, are at a higher risk of decline in skeletal muscle strength over time.
Pre-clinical studies suggest that both omega-6 and omega-3 fatty acids have beneficial effects on peripheral nerve function. Rats feed a diet rich in polyunsaturated fatty acids (PUFAs) showed modification of phospholipid fatty acid composition in nerve membranes and improvement of sciatic nerve conduction velocity (NCV). We tested the hypothesis that baseline plasma omega-6 and omega-3 fatty acids levels predict accelerated decline of peripheral nerve function. Changes between baseline and the 3-year follow-up in peripheral nerve function was assessed by standard surface ENG of the right peroneal nerve in 384 male and 443 female participants of the InCHIANTI study (age range: 24-97 years). Plasma concentrations of selected fatty acids assessed at baseline by gas chromatography. Independent of confounders, plasma omega-6 fatty acids and linoleic acid were significantly correlated with peroneal NCV at enrollment. Lower plasma PUFA, omega-6 fatty acids, linoleic acid, ratio omega-6/omega-3, arachidonic acid and docosahexanoic acid levels were significantly predicted a steeper decline in nerve function parameters over the 3-year follow-up. Low plasma omega-6 and omega-3 fatty acids levels were associated with accelerated decline of peripheral nerve function with aging.
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