Analytic calculations of trial wave functions of the fractional quantum Hall effect on the sphere

We present a framework for the analytic calculations of the hierarchical wave functions and the composite fermion wave functions in the fractional quantum Hall effect on the sphere by using projective coordinates. Then we calculate the overlaps between these two wave functions at various fillings and small numbers of electrons. We find that the overlaps are all most equal to one. This gives a further evidence that two theories of the fractional quantum Hall effect, the hierarchical theory and the composite fermion theory, are physically equivalent.Comment: 37 pages, revte

Combined In Silico, In Vivo, and In Vitro Studies Shed Insights into the Acute Inflammatory Response in Middle-Aged Mice

We combined in silico, in vivo, and in vitro studies to gain insights into age-dependent changes in acute inflammation in response to bacterial endotoxin (LPS). Time-course cytokine, chemokine, and NO2-/NO3- data from "middle-aged" (6-8 months old) C57BL/6 mice were used to re-parameterize a mechanistic mathematical model of acute inflammation originally calibrated for "young" (2-3 months old) mice. These studies suggested that macrophages from middle-aged mice are more susceptible to cell death, as well as producing higher levels of pro-inflammatory cytokines, vs. macrophages from young mice. In support of the in silico-derived hypotheses, resident peritoneal cells from endotoxemic middle-aged mice exhibited reduced viability and produced elevated levels of TNF-α, IL-6, IL-10, and KC/CXCL1 as compared to cells from young mice. Our studies demonstrate the utility of a combined in silico, in vivo, and in vitro approach to the study of acute inflammation in shock states, and suggest hypotheses with regard to the changes in the cytokine milieu that accompany aging. © 2013 Namas et al

Demonstration of laser pulse amplification by stimulated Brillouin scattering

The energy transfer by stimulated Brillouin backscatter from a long pump pulse (15 ps) to a short seed pulse (1 ps) has been investigated in a proof-of-principle demonstration experiment. The two pulses were both amplified in different beamlines of a Nd:glass laser system, had a central wavelength of 1054 nm and a spectral bandwidth of 2 nm, and crossed each other in an underdense plasma in a counter-propagating geometry, off-set by 10∘. It is shown that the energy transfer and the wavelength of the generated Brillouin peak depend on the plasma density, the intensity of the laser pulses, and the competition between two-plasmon decay and stimulated Raman scatter instabilities. The highest obtained energy transfer from pump to probe pulse is 2.5%, at a plasma density of 0.17ncr, and this energy transfer increases significantly with plasma density. Therefore, our results suggest that much higher efficiencies can be obtained when higher densities (above 0.25ncr) are used

Structure of the Dead Sea Pull-Apart Basin From Gravity Analyses

Analyses and modeling of gravity data in the Dead Sea pull-apart basin reveal the geometry of the basin and constrain models for its evolution. The basin is located within a valley which defines the Dead Sea transform plate boundary between Africa and Arabia. Three hundred kilometers of continuous marine gravity data, collected in a lake occupying the northern part of the basin, were integrated with land gravity data from Israel and Jordan to provide coverage to 30 km either side of the basin. Free-air and variable-density Bouguer anomaly maps, a horizontal first derivative map of the Bouguer anomaly, and gravity models of profiles across and along the basin were used with existing geological and geophysical information to infer the structure of the basin. The basin is a long (132 km), narrow (7-10 km), and deep (≤10 km) full graben which is bounded by subvertical faults along its long sides. The Bouguer anomaly along the axis of the basin decreases gradually from both the northern and southern ends, suggesting that the basin sags toward the center and is not bounded by faults at its narrow ends. The surface expression of the basin is wider at its center (≤16 km) and covers the entire width of the transform valley due to the presence of shallower blocks that dip toward the basin. These blocks are interpreted to represent the widening of the basin by a passive collapse of the valley floor as the full graben deepened. The collapse was probably facilitated by movement along the normal faults that bound the transform valley. We present a model in which the geometry of the Dead Sea basin (i.e., full graben with relative along-axis symmetry) may be controlled by stretching of the entire (brittle and ductile) crust along its long axis. There is no evidence for the participation of the upper mantle in the deformation of the basin, and the Moho is not significantly elevated. The basin is probably close to being isostatically uncompensated, and thermal effects related to stretching are expected to be minimal. The amount of crustal stretching calculated from this model is 21 km and the stretching factor is 1.19. If the rate of crustal stretching is similar to the rate of relative plate motion (6 mm/yr), the basin should be ~3.5 m.y. old, in accord with geological evidence

The Global Burden of Latent Tuberculosis Infection: A Re-estimation Using Mathematical Modelling.

BACKGROUND: The existing estimate of the global burden of latent TB infection (LTBI) as "one-third" of the world population is nearly 20 y old. Given the importance of controlling LTBI as part of the End TB Strategy for eliminating TB by 2050, changes in demography and scientific understanding, and progress in TB control, it is important to re-assess the global burden of LTBI. METHODS AND FINDINGS: We constructed trends in annual risk in infection (ARI) for countries between 1934 and 2014 using a combination of direct estimates of ARI from LTBI surveys (131 surveys from 1950 to 2011) and indirect estimates of ARI calculated from World Health Organisation (WHO) estimates of smear positive TB prevalence from 1990 to 2014. Gaussian process regression was used to generate ARIs for country-years without data and to represent uncertainty. Estimated ARI time-series were applied to the demography in each country to calculate the number and proportions of individuals infected, recently infected (infected within 2 y), and recently infected with isoniazid (INH)-resistant strains. Resulting estimates were aggregated by WHO region. We estimated the contribution of existing infections to TB incidence in 2035 and 2050. In 2014, the global burden of LTBI was 23.0% (95% uncertainty interval [UI]: 20.4%-26.4%), amounting to approximately 1.7 billion people. WHO South-East Asia, Western-Pacific, and Africa regions had the highest prevalence and accounted for around 80% of those with LTBI. Prevalence of recent infection was 0.8% (95% UI: 0.7%-0.9%) of the global population, amounting to 55.5 (95% UI: 48.2-63.8) million individuals currently at high risk of TB disease, of which 10.9% (95% UI:10.2%-11.8%) was isoniazid-resistant. Current LTBI alone, assuming no additional infections from 2015 onwards, would be expected to generate TB incidences in the region of 16.5 per 100,000 per year in 2035 and 8.3 per 100,000 per year in 2050. Limitations included the quantity and methodological heterogeneity of direct ARI data, and limited evidence to inform on potential clearance of LTBI. CONCLUSIONS: We estimate that approximately 1.7 billion individuals were latently infected with Mycobacterium tuberculosis (M.tb) globally in 2014, just under a quarter of the global population. Investment in new tools to improve diagnosis and treatment of those with LTBI at risk of progressing to disease is urgently needed to address this latent reservoir if the 2050 target of eliminating TB is to be reached

Topological states in photonic systems

Optics played a key role in the discovery of geometric phase. It now joins the journey of exploring topological physics, bringing bosonic topological states that equip us with the ability to make perfect photonic devices using imperfect interfaces.National Science Foundation (U.S.) (DMR-1419807)United States. Department of Energy (DE-SC0001299

Light and tree size influence belowground development in yellow birch and sugar maple

The effects of light and tree size on the root architecture and mycorrhiza of yellow birch (Betula alleghaniensis Britton) and sugar maple (Acer saccharum Marsh) growing in the understory of deciduous forests in southern Qu

SHARPIN Is Essential for Cytokine Production, NF-κB Signaling, and Induction of Th1 Differentiation by Dendritic Cells

Spontaneous mutations of the Sharpin (SHANK-associated RH domain-interacting protein, other aliases: Rbckl1, Sipl1) gene in mice result in systemic inflammation that is characterized by chronic proliferative dermatitis and dysregulated secretion of T helper1 (Th1) and Th2 cytokines. The cellular and molecular mechanisms underlying this inflammatory phenotype remain elusive. Dendritic cells may contribute to the initiation and progression of the phenotype of SHARPIN-deficient mice because of their pivotal role in innate and adaptive immunity. Here we show by flow cytometry that SHARPIN- deficiency did not alter the distribution of different DC subtypes in the spleen. In response to TOLL-like receptor (TLR) agonists LPS and poly I:C, cultured bone marrow-derived dendritic cells (BMDC) from WT and mutant mice exhibited similar increases in expression of co-stimulatory molecules CD40, CD80, and CD86. However, stimulated SHARPIN-deficient BMDC had reduced transcription and secretion of pro-inflammatory mediators IL6, IL12P70, GMCSF, and nitric oxide. Mutant BMDC had defective activation of NF-κB signaling, whereas the MAPK1/3 (ERK1/2) and MAPK11/12/13/14 (p38 MAP kinase isoforms) and TBK1 signaling pathways were intact. A mixed lymphocyte reaction showed that mutant BMDC only induced a weak Th1 immune response but stimulated increased Th2 cytokine production from allogeneic naïve CD4+ T cells. In conclusion, loss of Sharpin in mice significantly affects the immune function of DC and this may partially account for the systemic inflammation and Th2-biased immune response