Theoretical Analysis of a Large Momentum Beamsplitter using Bloch Oscillations

In this paper, we present the implementation of Bloch oscillations in an atomic interferometer to increase the separation of the two interfering paths. A numerical model, in very good agreement with the experiment, is developed. The contrast of the interferometer and its sensitivity to phase fluctuations and to intensity fluctuations are also calculated. We demonstrate that the sensitivity to phase fluctuations can be significantly reduced by using a suitable arrangement of Bloch oscillations pulses

Vascular and blood-brain barrier-related changes underlie stress responses and resilience in female mice and depression in human tissue

Prevalence, symptoms, and treatment of depression suggest that major depressive disorders (MDD) present sex differences. Social stress-induced neurovascular pathology is associated with depressive symptoms in male mice; however, this association is unclear in females. Here, we report that chronic social and subchronic variable stress promotes blood-brain barrier (BBB) alterations in mood-related brain regions of female mice. Targeted disruption of the BBB in the female prefrontal cortex (PFC) induces anxiety- and depression-like behaviours. By comparing the endothelium cell-specific transcriptomic profiling of the mouse male and female PFC, we identify several pathways and genes involved in maladaptive stress responses and resilience to stress. Furthermore, we confirm that the BBB in the PFC of stressed female mice is leaky. Then, we identify circulating vascular biomarkers of chronic stress, such as soluble E-selectin. Similar changes in circulating soluble E-selectin, BBB gene expression and morphology can be found in blood serum and postmortem brain samples from women diagnosed with MDD. Altogether, we propose that BBB dysfunction plays an important role in modulating stress responses in female mice and possibly MDD

Proposal for new experimental schemes to realize the Avogadro constant

We propose two experimental schemes to determine and so to realize the Avogadro constant $N\_{A}$ at the level of 10$^{-7}$ or better with a watt balance experiment and a cold atom experiment measuring $h/m(X)$ (where $h$ is the Planck constant and $m(X)$ the mass of the atom $X$). We give some prospects about achievable uncertainties and we discuss the opportunity to test the existence of possible unknown correction factors for the Josephson effect and quantum Hall effect

Testing new physics with the electron g-2

We argue that the anomalous magnetic moment of the electron (a_e) can be used to probe new physics. We show that the present bound on new-physics contributions to a_e is 8*10^-13, but the sensitivity can be improved by about an order of magnitude with new measurements of a_e and more refined determinations of alpha in atomic-physics experiments. Tests on new-physics effects in a_e can play a crucial role in the interpretation of the observed discrepancy in the anomalous magnetic moment of the muon (a_mu). In a large class of models, new contributions to magnetic moments scale with the square of lepton masses and thus the anomaly in a_mu suggests a new-physics effect in a_e of (0.7 +- 0.2)*10^-13. We also present examples of new-physics theories in which this scaling is violated and larger effects in a_e are expected. In such models the value of a_e is correlated with specific predictions for processes with violation of lepton number or lepton universality, and with the electric dipole moment of the electron.Comment: 34 pages, 7 figures. Minor changes and references adde

Charged-Lepton Flavour Physics

This writeup of a talk at the 2011 Lepton-Photon symposium in Mumbai, India, summarises recent results in the charged-lepton flavour sector. I review searches for charged-lepton flavour violation, lepton electric dipole moments and flavour-conserving CP violation. I also discuss recent progress in tau-lepton physics and in the Standard Model prediction of the muon anomalous magnetic moment.Comment: Presented at Lepton-Photon 2011, Mumbai, India; 23 pages, 14 figure

Long-Range Bidirectional Strand Asymmetries Originate at CpG Islands in the Human Genome

In the human genome, CpG islands (CGIs), which are GC- and CpG-rich sequences, are associated with transcription starting sites (TSSs); in addition, there is evidence that CGIs harbor origins of bidirectional replication (OBRs) and are preferred sites for heteroduplex formation during recombination. Transcription, replication, and recombination processes are known to induce specific mutational patterns in various genomes, and therefore, these patterns are expected to be found around CGIs. We use triple alignments of human, chimp, and macaque to compute the rates of nucleotide substitutions in up to 1 Mbps long intergenic regions on both sides of CGIs. Our analysis revealed that around a CGI there is an asymmetry between complementary substitution rates that is similar to the one that found around the OBR in bacteria. We hypothesize that these asymmetries are induced by differences in the replication of the leading and lagging strand and that a significant number of CGIs overlap OBRs. Within CGIs, we observed a mutational signature of GC-biased gene conversion that is associated with recombination. We suggest that recombination has played a major role in the creation of CGIs

Same-Sex Parents Negotiating the Law in Italy: Between Claims of Recognition and Practices of Exclusion

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Epidemiology and heritability of Major Depressive Disorder, stratified by age of onset, sex, and illness course in Generation Scotland:Scottish Family Health Study (GS:SFHS)

The heritability of Major Depressive Disorder (MDD) has been estimated at 37% based largely on twin studies that rely on contested assumptions. More recently, the heritability of MDD has been estimated on large populations from registries such as the Swedish, Finnish, and Chinese cohorts. Family-based designs utilise a number of different relationships and provide an alternative means of estimating heritability. Generation Scotland: Scottish Family Health Study (GS:SFHS) is a large (n = 20,198), family-based population study designed to identify the genetic determinants of common diseases, including Major Depressive Disorder. Two thousand seven hundred and six individuals were SCID diagnosed with MDD, 13.5% of the cohort, from which we inferred a population prevalence of 12.2% (95% credible interval: 11.4% to 13.1%). Increased risk of MDD was associated with being female, unemployed due to a disability, current smokers, former drinkers, and living in areas of greater social deprivation. The heritability of MDD in GS:SFHS was between 28% and 44%, estimated from a pedigree model. The genetic correlation of MDD between sexes, age of onset, and illness course were examined and showed strong genetic correlations. The genetic correlation between males and females with MDD was 0.75 (0.43 to 0.99); between earlier (≤ age 40) and later (> age 40) onset was 0.85 (0.66 to 0.98); and between single and recurrent episodic illness course was 0.87 (0.72 to 0.98). We found that the heritability of recurrent MDD illness course was significantly greater than the heritability of single MDD illness course. The study confirms a moderate genetic contribution to depression, with a small contribution of the common family environment (variance proportion = 0.07, CI: 0.01 to 0.15), and supports the relationship of MDD with previously identified risk factors. This study did not find robust support for genetic differences in MDD due to sex, age of onset, or illness course. However, we found an intriguing difference in heritability between recurrent and single MDD illness course. These findings establish GS:SFHS as a valuable cohort for the genetic investigation of MDD

Glutamine depletion by crisantaspase hinders the growth of human hepatocellular carcinoma xenografts

Background: A subset of human hepatocellular carcinomas (HCC) exhibit mutations of β-catenin gene CTNNB1 and overexpress Glutamine synthetase (GS). The CTNNB1-mutated HCC cell line HepG2 is sensitive to glutamine starvation induced in vitro with the antileukemic drug Crisantaspase and the GS inhibitor methionine-L-sulfoximine (MSO). Methods: Immunodeficient mice with subcutaneous xenografts of the CTNNB1-mutated HCC cell lines HepG2 and HC-AFW1 were treated with Crisantaspase and/or MSO, and tumour growth was monitored. At the end of treatment, tumour weight and histology were assessed. Serum and tissue amino acids were determined by HPLC. Gene and protein expression were estimated with RT-PCR and western blot and GS activity with a colorimetric method. mTOR activity was evaluated from the phosphorylation of p70S6K1. Results: Crisantaspase and MSO depleted serum glutamine, lowered glutamine in liver and tumour tissue, and inhibited liver GS activity. HepG2 tumour growth was significantly reduced by either Crisantaspase or MSO, and completely suppressed by the combined treatment. The combined treatment was also effective against xenografts of the HC-AFW1 cell line, which is Crisantaspase resistant in vitro. Conclusions: The combination of Crisantaspase and MSO reduces glutamine supply to CTNNB1-mutated HCC xenografts and hinders their growth