This is the third of a series of papers on three-loop computation of renormalization constants for Lattice QCD. Our main points of interest are results for the regularization defined by the Iwasaki ...gauge action and
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Wilson fermions. Our results for quark bilinears renormalized according to the RI’-MOM scheme can be compared to non-perturbative results. The latter are available for twisted mass QCD: being defined in the chiral limit, the renormalization constants must be the same. We also address more general problems. In particular, we discuss a few methodological issues connected to summing the perturbative series such as the effectiveness of boosted perturbation theory and the disentanglement of irrelevant and finite-volume contributions. Discussing these issues we consider not only the new results of this paper, but also those for the regularization defined by the tree-level Symanzik improved gauge action and
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Wilson fermions, which we presented in a recent paper of ours. We finally comment on the extent to which the techniques we put at work in the NSPT context can provide a fresher look into the lattice version of the RI’-MOM scheme.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Pores for order: Particles of silica gel can be transformed into MCM‐41 without losing their size and shape by a low‐temperature hydrothermal treatment (see electron micrographs). This method allows ...easy preparation of custom‐tailored materials for chromatography and separation.
To identify the transductional mechanisms responsible for the neuroprotective effect of nitric oxide (NO) during ischemic preconditioning (IPC), we investigated the effects of this gaseous mediator ...on mitochondrial Mn-superoxide dismutase (Mn-SOD) expression and activity. In addition, the possible involvement of Ras/extracellular-regulated kinase (ERK) ERK1/2 pathway in preserving cortical neurons exposed to oxygen and glucose deprivation (OGD) followed by reoxygenation was also examined. Ischemic preconditioning was obtained by exposing neurons to a 30-min sublethal OGD (95% N₂ and 5% CO₂). Then, after a 24-h interval, neurons were exposed to 3 h of OGD followed by 24 h of reoxygenation (OGD/Rx). Our results revealed that IPC reduced cytochrome c (cyt c) release into the cytosol, improved mitochondrial function, and decreased free radical production. Moreover, it induced an increase in nNOS expression and NO production and promoted ERK1/2 activation. These effects were paralleled by an increase in Mn-SOD expression and activity that persisted throughout the following OGD phase. When the neurons were treated with L-NAME, a well known NOS inhibitor, the increase in Mn-SOD expression occurring during IPC was reduced and, as a result, IPC-induced neuroprotection was prevented. Similarly, when ERK1/2 was inhibited by its selective inhibitor PD98059, the increase in Mn-SOD expression observed during IPC was almost completely abolished. As a result, its neuroprotective effect on cellular survival was thwarted. The present findings indicate that during IPC the increase in Mn-SOD expression and activity are paralleled by NO production. This suggests that NO neuroprotective role occurs through the stimulation of Mn-SOD expression and activity. In particular, NO via Ras activation stimulates downstream ERK1/2 cascade. This pathway, in turn, post-transcriptionally activates Mn-SOD expression and activity, thus promoting neuroprotection during preconditioning.
Micelle‐templated silicas (MTSs) such as MCM‐41 and MCM‐48 feature unique textural properties owing to their uniform distribution of mesopores with tunable sizes. MTS synthesis is relevant to unique ...self‐assembly processes between surfactants and inorganic matter. The properties of MTSs have been explored in view of applications in fields as diverse as catalysis, chromatography, sensing, photonics, optics, drug delivery, etc. The aim of this contribution is to review, and to highlight by new results, a synthesis strategy we have developed since 2002 to control the particle morphology of MTSs at the micro‐ to millimeter scale, a key step for transferring these materials from the status of beautiful artworks to applicable products. It is based on the concept of pseudomorphic synthesis. Pseudomorphism is well known in the mineral world. It allows preparation of a mineral with a morphology that is not related to its crystallographic symmetry group. The resulting mineral assumes the outward crystal habit of a different mineral. This principle occurs at a nonconstant matter content by using a mineralization solution that exchanges anions (or cations) with an existing (preshaped) solid body, and allows the new structure to precipitate while maintaining the existing morphology. The concept of pseudomorphic transformation is now applied to amorphous preshaped silica particles to produce MTSs with the same morphology, using an alkaline solution to dissolve the silica and reprecipitate it around surfactant micelles into the ordered MTS structures. MTSs with hexagonal and cubic symmetry, different pore sizes, and controlled morphology have been synthesized. The new pseudomorphs have been successfully used as supports in chromatography, a very demanding application in terms of particle size and morphology.
A strategy for engineering the particle size and morphology of ordered mesoporous silicas (see figure) at the micro‐ to millimeter scales is presented. It is based on the controlled dissolution/reprecipitation of preshaped amorphous silicas in the presence of surfactants. This pseudomorphic synthesis could be applied to other material morphologies (monoliths, thin films), opening new perspectives in the preparation and applications of hierarchically porous materials.
The aim of the present study was to investigate whether K V 3.4 channel subunits are involved in neuronal death induced by neurotoxic β-amyloid peptides (Aβ). In particular, to test
this ...hypothesis, three main questions were addressed: 1) whether the Aβ peptide can up-regulate both the transcription/translation
and activity of K V 3.4 channel subunit and its accessory subunit, MinK-related peptide 2 (MIRP2); 2) whether the increase in K V 3.4 expression and activity can be mediated by the nuclear factor-κB (NF-κB) family of transcriptional factors; and 3) whether
the specific inhibition of K V 3.4 channel subunit reverts the Aβ peptide-induced neurodegeneration in hippocampal neurons and nerve growth factor (NGF)-differentiated
PC-12 cells. We found that Aβ 1â42 treatment induced an increase in K V 3.4 and MIRP2 transcripts and proteins, detected by reverse transcription-polymerase chain reaction and Western blot analysis,
respectively, in NGF-differentiated PC-12 cells and hippocampal neurons. Patch-clamp experiments performed in whole-cell configuration
revealed that the Aβ peptide caused an increase in I A current amplitude carried by K V 3.4 channel subunits, as revealed by their specific blockade with blood depressing substance-I (BDS-I) in both hippocampal
neurons and NGF-differentiated PC-12 cells. The inhibition of NF-κB nuclear translocation with the cell membrane-permeable
peptide SN-50 prevented the increase in K V 3.4 protein and transcript expression. In addition, the SN-50 peptide was able to block Aβ 1â42 -induced increase in K V 3.4 K + currents and to prevent cell death caused by Aβ 1â42 exposure. Finally, BDS-I produced a similar neuroprotective effect by inhibiting the increase in K V 3.4 expression. As a whole, our data indicate that K V 3.4 channels could be a novel target for Alzheimer's disease pharmacological therapy.
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