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Selective photocatalytic oxidation of 1-phenyl ethanol to acetophenone using titanium dioxide (TiO2) raw and doped with Fe or V, prepared by flame aerosol deposition method, was investigated. The effects of metal doping on crystal phase and morphology of the synthesized nanostructured TiO2 were analyzed using XRD, TEM, Raman spectroscopy, and BET nitrogen adsorbed surface area measurement. The increase in the concentration of V and Fe reduced the crystalline structure and the anatase-to-rutile ratios of the synthesized TiO2. Synthesized TiO2 became fine amorphous powder as the Fe and V concentrations were increased to 3 and 5%, respectively. Doping V and Fe to TiO2 synthesized by the flame aerosol increased photocatalytic activity by 6 folds and 2.5 folds, respectively, compared to that of pure TiO2. It was found that an optimal doping concentration for Fe and V were 0.5% and 3%, respectively. The type and concentration of the metal dopants and the method used to add the dopant to the TiO2 are critical parameters for enhancing the activity of the resulting photocatalyst. The effects of solvents on the photocatalytic reaction were also investigated by using both water and acetonitrile as the reaction medium. [ABSTRACT FROM AUTHOR] more...

Ca2+ release from the sarcoplasmic reticulum (SR) into the cytosol is a crucial part of excitation–contraction (E-C) coupling. Excitation–contraction uncoupling, a deficit in Ca2+ release from the SR, is thought to be responsible for at least some of the loss in specific force observed in aging skeletal muscle. Excitation–contraction uncoupling may be caused by alterations in expression of the voltage-dependent calcium channel α1s (CaV1.1) and β1a (CaVβ1a) subunits, both of which are necessary for E-C coupling to occur. While previous studies have found CaV1.1 expression declines in old rodents, CaVβ1a expression has not been previously examined in aging models. Western blot analysis shows a substantial increase of CaVβ1a expression over the full lifespan of Friend Virus B (FVB) mice. To examine the specific effects of CaVβ1a overexpression, a CaVβ1a-YFP plasmid was electroporated in vivo into young animals. The resulting increase in expression of CaVβ1a corresponded to decline of CaV1.1 over the same time period. YFP fluorescence, used as a measure of CaVβ1a-YFP expression in individual fibers, also showed an inverse relationship with charge movement, measured using the whole-cell patch-clamp technique. Specific force was significantly reduced in young CaVβ1a-YFP electroporated muscle fibers compared with sham-electroporated, age-matched controls. siRNA interference of CaVβ1a in young muscles reduced charge movement, while charge movement in old was restored to young control levels. These studies imply CaVβ1a serves as both a positive and negative regulator CaV1.1 expression, and that endogenous overexpression of CaVβ1a during old age may play a role in the loss of specific force. [ABSTRACT FROM AUTHOR] more...

In this work we hypothesized that denervation in flexor digitorum brevis (FDB) muscle from ageing mice is more extensive than predicted by standard functional and structural assays used in the past. In addition, we asked whether denervation is a fully or partially developed process. Despite the reported alteration in skeletal muscle innervation, the quantification of the extension and magnitude of denervation in ageing rodents has remained elusive. To address these two questions we utilized a combination of electrophysiological and immunohistochemical assays directed to detecting the expression of tetrodotoxin (TTX)-resistant sodium channels (Nav1.5) in FDB muscles from young-adult and senescent mice. Sodium current density measured with the macropatch cell-attached technique did not show significant differences between FDB fibres from young and old mice. The TTX dose–response curve, using the whole cell voltage-clamp technique, showed three populations of fibres in senescent mice, one similar to fibres from young mice (TTX sensitive), another one similar to fibres from experimentally denervated muscle (TTX resistant), and a third group intermediate between these two. Partially and fully denervated fibres added up to approximately 50% of the total number of fibres tested, a number that concurs with the percentage of fibres positive for the Nav1.5 channel by specific immunostaining. [ABSTRACT FROM AUTHOR] more...

In the present work, we investigate whether changes in excitation-contraction (EC) coupling mode occur in skeletal muscles from ageing mammals by examining the dependence of EC coupling on extracellular Ca2+. Single intact muscle fibres from flexor digitorum brevis muscles from young (2-6 months) and old (23-30 months) mice were subjected to tetanic contractile protocols in the presence and absence of external Ca2+. Contractile experiments in the absence of external Ca2+ show that about half of muscle fibres from old mice are dependent upon external Ca2+ for maintaining maximal tetanic force output, while young fibres are not. Decreased force in the absence of external Ca2+ was not due to changes in charge movement as revealed by whole-cell patch-clamp experiments. Ca2+ transients, measured by fluo-4 fluorescence, declined in voltage-clamped fibres from old mice in the absence of external Ca2+. Similarly, Ca2+ transients declined in parallel with tetanic contractile force in single intact fibres. Examination of inward Ca2+ current and of mRNA and protein assays suggest that these changes in EC coupling mode are not due to shifts in dihydropyridine receptor (DHPR) and/or ryanodine receptor (RyR) isoforms. These results indicate that a change in EC coupling mode occurs in a population of fibres in ageing skeletal muscle, and is responsible for the age-related dependence on extracellular Ca2+. [ABSTRACT FROM AUTHOR] more...

Despite the multiple effects on mammals during development, the effectiveness of the insulin-like growth factor-1 (IGF-1) to sustain cell function and structure in the brain of senescent mammals is almost completely unknown. To address this issue, we investigated whether the effects of IGF-1 on specific targets are preserved at later stages of life. Voltage-gated Ca&sup2+; channels (VGCC) are well-characterized targets of IGF-1. VGCC regulate membrane excitability and gene transcription along with other functions that have been found to be impaired in the brain of senescent rodents. As the voluntary control of movement has been reported to be altered in the elderly, we investigated the expression, function and responsiveness of high (HVA)- and low-voltage-activated (LVA) Ca&sup2+; channels to IGF-1, using the whole-cell configuration of the patch-clamp and RT-PCR in the specific region of the rat motor cortex that controls hindlimb muscle movement. We detected the expression of α[sub1A], α[sub1B] and α[sub1E] genes encoding the HVA Ca&sup2+; channels P/Q, N and R, respectively, but not α[sub1C], α[sub1D], α[sub1S] encoding the L-type Ca&sup2+; channel in this region of the brain cortex. IGF-1 enhanced Ca&sup2+; channel currents through P/Q- and N-type channels but not significantly through the R-type or LVA channels. IGF-1 enhanced the amplitude but did not modify the voltage dependence of Ca&sup2+; channel currents in young (2- to 4-week-old), young adult (7-month-old) and senescent (28- to 29-month-old) rats. These results support the concept that despite the reported decrease in circulating (liver) and local (central nervous system) production of IGF-1 with ageing, key neuronal targets such as the VGCC remain responsive to the growth factor throughout life. [ABSTRACT FROM AUTHOR] more...