Testing a quintessence model with CMBR peaks locations

We show that a model of quintessence with exponential potential, which allows to obtain general exact solutions, can generate location of CMBR peaks which are fully compatible with present observational data

Testing a quintessence model with CMBR peaks location

We show that a model of quintessence with exponential potential, which allows to obtain general exact solutions, can generate locations of CMBR peaks which are fully compatible with present observational dataComment: 7 pages, no figure

A large sample study of spin relaxation and magnetometric sensitivity of paraffin-coated Cs vapor cells

We have manufactured more than 250 nominally identical paraffin-coated Cs vapor cells (30 mm diameter bulbs) for multi-channel atomic magnetometer applications. We describe our dedicated cell characterization apparatus. For each cell we have determined the intrinsic longitudinal, \sGamma{01}, and transverse, \sGamma{02}, relaxation rates. Our best cell shows \sGamma{01}/2\pi\approx 0.5 Hz, and \sGamma{02}/2\pi\approx 2 Hz. We find a strong correlation of both relaxation rates which we explain in terms of reservoir and spin exchange relaxation. For each cell we have determined the optimal combination of rf and laser powers which yield the highest sensitivity to magnetic field changes. Out of all produced cells, 90% are found to have magnetometric sensitivities in the range of 9 to 30 fTHz. Noise analysis shows that the magnetometers operated with such cells have a sensitivity close to the fundamental photon shot noise limit

oxidative stress and proteostasis network culprit and casualty of alzheimer s like neurodegeneration

Free radical-mediated damage to proteins is particularly important in aging and age-related neurodegenerative diseases, because in the majority of cases it is a non-reversible phenomenon that requires clearance systems for removal. Major consequences of protein oxidation are loss of protein function and the formation of large protein aggregates, which are often toxic to cells if allowed to accumulate. Deposition of aggregated, misfolded, and oxidized proteins may also result from the impairment of protein quality control (PQC) system, including protein unfolded response, proteasome, and autophagy. Perturbations of such components of the proteostasis network that provides a critical protective role against stress conditions are emerging as relevant factor in triggering neuronal death. In this outlook paper, we discuss the role of protein oxidation as a major contributing factor for the impairment of the PQC regulating protein folding, surveillance, and degradation. Recent studies from our group and from others aim to better understand the link between Down syndrome and Alzheimer's disease neuropathology. We propose oxidative stress and alteration of proteostasis network as a possible unifying mechanism triggering neurodegeneration

Intranasal rapamycin ameliorates Alzheimer-like cognitive decline in a mouse model of Down syndrome

Background: Down syndrome (DS) individuals, by the age of 40s, are at increased risk to develop Alzheimer-like dementia, with deposition in brain of senile plaques and neurofibrillary tangles. Our laboratory recently demonstrated the disturbance of PI3K/AKT/mTOR axis in DS brain, prior and after the development of Alzheimer Disease (AD). The aberrant modulation of the mTOR signalling in DS and AD age-related cognitive decline affects crucial neuronal pathways, including insulin signaling and autophagy, involved in pathology onset and progression. Within this context, the therapeutic use of mTOR-inhibitors may prevent/attenuate the neurodegenerative phenomena. By our work we aimed to rescue mTOR signalling in DS mice by a novel rapamycin intranasal administration protocol (InRapa) that maximizes brain delivery and reduce systemic side effects. Methods: Ts65Dn mice were administered with InRapa for 12 weeks, starting at 6 months of age demonstrating, at the end of the treatment by radial arms maze and novel object recognition testing, rescued cognition. Results: The analysis of mTOR signalling, after InRapa, demonstrated in Ts65Dn mice hippocampus the inhibition of mTOR (reduced to physiological levels), which led, through the rescue of autophagy and insulin signalling, to reduced APP levels, APP processing and APP metabolites production, as well as, to reduced tau hyperphosphorylation. In addition, a reduction of oxidative stress markers was also observed. Discussion: These findings demonstrate that chronic InRapa administration is able to exert a neuroprotective effect on Ts65Dn hippocampus by reducing AD pathological hallmarks and by restoring protein homeostasis, thus ultimately resulting in improved cognition. Results are discussed in term of a potential novel targeted therapeutic approach to reduce cognitive decline and AD-like neuropathology in DS individuals

Network Sensitivity of Systemic Risk

A growing body of studies on systemic risk in financial markets has emphasized the key importance of taking into consideration the complex interconnections among financial institutions. Much effort has been put in modeling the contagion dynamics of financial shocks, and to assess the resilience of specific financial markets - either using real network data, reconstruction techniques or simple toy networks. Here we address the more general problem of how shock propagation dynamics depends on the topological details of the underlying network. To this end we consider different realistic network topologies, all consistent with balance sheets information obtained from real data on financial institutions. In particular, we consider networks of varying density and with different block structures, and diversify as well in the details of the shock propagation dynamics. We confirm that the systemic risk properties of a financial network are extremely sensitive to its network features. Our results can aid in the design of regulatory policies to improve the robustness of financial markets

Polar distortions in hydrogen bonded organic ferroelectrics

Although ferroelectric compounds containing hydrogen bonds were among the first to be discovered, organic ferroelectrics are relatively rare. The discovery of high polarization at room temperature in croconic acid [Nature \textbf{463}, 789 (2010)] has led to a renewed interest in organic ferroelectrics. We present an ab-initio study of two ferroelectric organic molecular crystals, 1-cyclobutene-1,2-dicarboxylic acid (CBDC) and 2-phenylmalondialdehyde (PhMDA). By using a distortion-mode analysis we shed light on the microscopic mechanisms contributing to the polarization, which we find to be as large as 14.3 and 7.0\,$\mu$C/cm$^{2}$ for CBDC and PhMDA respectively. These results suggest that it may be fruitful to search among known but poorly characterized organic compounds for organic ferroelectrics with enhanced polar properties suitable for device applications.Comment: Submitte

It Is All About (U)biquitin: Role of Altered Ubiquitin-Proteasome System and UCHL1 in Alzheimer Disease

Free radical-mediated damage to macromolecules and the resulting oxidative modification of different cellular components are a common feature of aging, and this process becomes much more pronounced in age-associated pathologies, including Alzheimer disease (AD). In particular, proteins are particularly sensitive to oxidative stress-induced damage and these irreversible modifications lead to the alteration of protein structure and function. In order to maintain cell homeostasis, these oxidized/damaged proteins have to be removed in order to prevent their toxic accumulation. It is generally accepted that the age-related accumulation of “aberrant” proteins results from both the increased occurrence of damage and the decreased efficiency of degradative systems. One of the most important cellular proteolytic systems responsible for the removal of oxidized proteins in the cytosol and in the nucleus is the proteasomal system. Several studies have demonstrated the impairment of the proteasome in AD thus suggesting a direct link between accumulation of oxidized/misfolded proteins and reduction of this clearance system. In this review we discuss the impairment of the proteasome system as a consequence of oxidative stress and how this contributes to AD neuropathology. Further, we focus the attention on the oxidative modifications of a key component of the ubiquitin-proteasome pathway, UCHL1, which lead to the impairment of its activity