University of Catania

About: University of Catania is a education organization based out in Catania, Italy. It is known for research contribution in the topics: Population & Large Hadron Collider. The organization has 14599 authors who have published 41195 publications receiving 1032705 citations. The organization is also known as: Università degli Studi di Catania & Universita degli Studi di Catania.

Diabetes Mellitus and Sperm Parameters

Abstract: Because of the paucity of studies and inconsistencies regarding the impact of diabetes mellitus (DM) on semen quality, this disease is seldom looked for in the infertile patient. Recently, this view has been challenged by findings showing that DM induces subtle molecular changes that are important for sperm quality and function. This brief review shows the main sperm parameters in patients with DM and presents the mechanisms hypothesized to explain the changes observed in these patients. The data available suggest that DM alters conventional sperm parameters. In addition, DM causes histologic damage of the epididymis, with a negative impact on sperm transit. Various mechanisms may explain the sperm damage observed in patients with DM. These include endocrine disorders, neuropathy, and increased oxidative stress. Many authors suggest that DM decreases serum testosterone levels. This is associated with a steroidogenetic defect in Leydig cells. In addition, diabetic neuropathy seems to cause atonia of seminal vesicles, bladder, and urethra. Furthermore, DM is associated with an increased oxidative stress, which damages sperm nuclear and mitochondrial DNA. Finally, spermatogenesis derangement and germ cell apoptosis in type 1 DM may relate to a local autoimmune damage, whereas insulin resistance, obesity, and other related comorbidities may impair sperm parameters and decrease testosterone serum levels in patients with type 2 DM.

Performance of photon reconstruction and identification with the CMS detector in proton-proton collisions at √s = 8 TeV

Abstract: A description is provided of the performance of the CMS detector for photon reconstruction and identification in proton-proton collisions at a centre-of-mass energy of 8 TeV at the CERN LHC. Details are given on the reconstruction of photons from energy deposits in the electromagnetic calorimeter (ECAL) and the extraction of photon energy estimates. The reconstruction of electron tracks from photons that convert to electrons in the CMS tracker is also described, as is the optimization of the photon energy reconstruction and its accurate modelling in simulation, in the analysis of the Higgs boson decay into two photons. In the barrel section of the ECAL, an energy resolution of about 1% is achieved for unconverted or late-converting photons from H→γγ decays. Different photon identification methods are discussed and their corresponding selection efficiencies in data are compared with those found in simulated events.

Ferulic acid ethyl ester protects neurons against amyloid beta- peptide(1-42)-induced oxidative stress and neurotoxicity: relationship to antioxidant activity.

Abstract: Alzheimer's disease (AD) is neuropathologically characterized by depositions of extracellular amyloid and intracellular neurofibrillary tangles, associated with loss of neurons in the brain. Amyloid β-peptide (Aβ) is the major component of senile plaques and is considered to have a causal role in the development and progress of AD. Several lines of evidence suggest that enhanced oxidative stress and inflammation play important roles in the pathogenesis or progression of AD. The present study aimed to investigate the protective effects of ethyl-4-hydroxy-3-methoxycinnamic acid (FAEE), a phenolic compound which shows antioxidant and anti-inflammatory activity, on Aβ(1–42)-induced oxidative stress and neurotoxicity. We hypothesized that the structure of FAEE would facilitate radical scavenging and may induce protective proteins. Aβ(1–42) decreases cell viability, which was correlated with increased free radical formation, protein oxidation (protein carbonyl, 3-nitrotyrosine), lipid peroxidation (4-hydroxy-2-trans-nonenal) and inducible nitric oxide synthase. Pre-treatment of primary hippocampal cultures with FAEE significantly attenuated Aβ(1–42)-induced cytotoxicity, intracellular reactive oxygen species accumulation, protein oxidation, lipid peroxidation and induction of inducible nitric oxide synthase. Treatment of neurons with Aβ(1–42) increases levels of heme oxygenase-1 and heat shock protein 72. Consistent with a cellular stress response to the Aβ(1–42)-induced oxidative stress, FAEE treatment increases the levels of heme oxygenase-1 and heat shock protein 72, which may be regulated by oxidative stresses in a coordinated manner and play a pivotal role in the cytoprotection of neuronal cells against Aβ(1–42)-induced toxicity. These results suggest that FAEE exerts protective effects against Aβ(1–42) toxicity by modulating oxidative stress directly and by inducing protective genes. These findings suggest that FAEE could potentially be of importance for the treatment of AD and other oxidative stress-related diseases.

Excitation and nonradiative deexcitation processes of Er 3 + in crystalline Si

Abstract: A detailed investigation on the excitation and deexcitation processes of ${\mathrm{Er}}^{3+}$ in Si is reported. In particular, we explored Er pumping through electron-hole pair recombination and Er deexcitation through Auger processes transferring energy to either free or bound electrons and holes. Since Er donor behavior would result in a free-carrier concentration varying along its profile, experiments have been performed by embedding the whole Er profile within previously prepared $n$-doped or $p$-doped regions. Multiple P (B) implants were performed in $n$-type ($p$-type) Czochralski Si samples in order to realize uniform dopant concentrations from $4\ifmmode\times\else\texttimes\fi{}{10}^{16}$ to $1.2\ifmmode\times\else\texttimes\fi{}{10}^{18}/{\mathrm{cm}}^{3}$ at depths between 0.5 and 2.5 \ensuremath{\mu}m below the surface. These samples have been subsequently implanted with 4 MeV $3.3\ifmmode\times\else\texttimes\fi{}{10}^{13}{\mathrm{E}\mathrm{r}/\mathrm{c}\mathrm{m}}^{2}$ and annealed at 900 \ifmmode^\circ\else\textdegree\fi{}C for 30 min. Free electrons or holes concentrations in the region where Er sits were measured by spreading resistance profiling. It has been found that the release of electrons or holes from shallow donors and acceptors, occurring at temperatures between 15 and 100 K, produces a strong reduction of both time decay and luminescence intensity at 1.54 \ensuremath{\mu}m. These phenomena are produced by Auger deexcitation of the ${\mathrm{Er}}^{3+}$ intra-$4f$ electrons with energy transfer to free carriers. The Auger coefficient of this process has been measured to be ${C}_{A}\ensuremath{\sim}5\ifmmode\times\else\texttimes\fi{}{10}^{\ensuremath{-}13}{\mathrm{cm}}^{3}{\mathrm{}\mathrm{s}}^{\mathrm{\ensuremath{-}}1}$ for both free electrons and free holes. Moreover, at 15 K (when the free carriers are frozen and the donor and acceptor levels occupied) the ${\mathrm{Er}}^{3+}$ time decay has been found to depend on the P (or B) concentrations. This is attributed to an impurity Auger deexcitation to electrons (or holes) bound to shallow donors (acceptors): the efficiency of this process has been determined to be two orders of magnitude smaller with respect to the Auger deexcitation with free carriers. Furthermore, at temperatures above 100 K a nonradiative back-transfer decay process, characterized by an activation energy of 0.15 eV, is seen to set in for both $p$-type and $n$-type samples. This suggests that the back-transfer process, which severely limits the high-temperature luminescence efficiency, is always completed by a thermalization of an electron trapped at an Er-related level to the conduction band. Finally, by analysis of the pump power dependence of time decay and luminescence yield at 15 K, we have found that excitation of Er through the recombination of an electron-hole pair is a very efficient process, characterized by an effective cross section of $3\ifmmode\times\else\texttimes\fi{}{10}^{\ensuremath{-}15}{\mathrm{cm}}^{2}$ and able to provide an internal quantum efficiency as high as 10% at low temperatures (15 K) and pump powers (below 1 mW). This efficiency is significantly reduced when, at higher temperatures and/or high pump powers, strong nonradiative decay processes set in. These phenomena are investigated in detail and their impact on device operation perspectives are analyzed and discussed.

Mitochondrial involvement in brain function and dysfunction: relevance to aging, neurodegenerative disorders and longevity.

Abstract: It is becoming increasingly evident that the mitochondrial genome may play a key role in neurodegenerative diseases. Mitochondrial dysfunction is characteristic of several neurodegenerative disorders, and evidence for mitochondria being a site of damage in neurodegenerative disorders is partially based on decreases in respiratory chain complex activities in Parkinson's disease, Alzheimer's disease, and Huntington's disease. Such defects in respiratory complex activities, possibly associated with oxidant/antioxidant balance perturbation, are thought to underlie defects in energy metabolism and induce cellular degeneration. Efficient functioning of maintenance and repair process seems to be crucial for both survival and physical quality of life. This is accomplished by a complex network of the so-called longevity assurance processes, which are composed of genes termed vitagenes. A promising approach for the identification of critical gerontogenic processes is represented by the hormesis-like positive effect of stress. In the present review, we discuss the role of energy thresholds in brain mitochondria and their implications in neurodegeneration. We then review the evidence for the role of oxidative stress in modulating the effects of mitochondrial DNA mutations on brain age-related disorders and also discuss new approaches for investigating the mechanisms of lifetime survival and longevity.