Dynamics of electrons in the quantum Hall bubble phases

In Landau levels N > 1, the ground state of the two-dimensional electron gas (2DEG) in a perpendicular magnetic field evolves from a Wigner crystal for small filling of the partially filled Landau level, into a succession of bubble states with increasing number of guiding centers per bubble as the filling increases, to a modulated stripe state near half filling. In this work, we show that these first-order phase transitions between the bubble states lead to measurable discontinuities in several physical quantities such as the density of states and the magnetization of the 2DEG. We discuss in detail the behavior of the collective excitations of the bubble states and show that their spectra have higher-energy modes besides the pinned phonon mode. The frequencies of these modes, at small wavevector k, have a discontinuous evolution as a function of filling factor that should be measurable in, for example, microwave absorption experiments.Comment: 13 pages, 7 figures. Corrected typos in eqs. (38),(39),(40

Fermion confinement induced by geometry

We consider a five-dimensional model in which fermions are confined in a hypersurface due to an interaction with a purely geometric field. Inspired by the Rubakov-Shaposhnikov field-theoretical model, in which massless fermions can be localized in a domain wall through the interaction of a scalar field, we show that particle confinement may also take place if we endow the five-dimensional bulk with a Weyl integrable geometric structure, or if we assume the existence of a torsion field acting in the bulk. In this picture, the kind of interaction considered in the Rubakov-Shaposhnikov model is replaced by the interaction of fermions with a geometric field, namely a Weyl scalar field or a torsion field. We show that in both cases the confinement is independent of the energy and the mass of the fermionic particle. We generalize these results to the case in which the bulk is an arbitrary n-dimensional curved space.Comment: 8 page

Robustness and Generalization

We derive generalization bounds for learning algorithms based on their robustness: the property that if a testing sample is "similar" to a training sample, then the testing error is close to the training error. This provides a novel approach, different from the complexity or stability arguments, to study generalization of learning algorithms. We further show that a weak notion of robustness is both sufficient and necessary for generalizability, which implies that robustness is a fundamental property for learning algorithms to work

Improving Global Precipitation Product Access at the GES DISC

The NASA Goddard Earth Sciences Data and Information Services Center (GES DISC) has been actively and continually engaged in improving the access to and use of Global Precipitation Measurement (GPM), Tropical Precipitation Measuring Mission (TRMM), and other precipitation data, including the following new services and Ongoing development activities: Updates on GPM products and data services, New features in Giovanni, Ongoing development activities; and Precipitation product and service outreach activities

GPM, TRMM, and Other Global Precipitation Products and Services at NASA GES DISC

Precipitation is a key environmental variable. For example, in agriculture, precipitation, temperature, water (soil moisture), solar radiation, NDVI, etc., are key variables.Rainfed agriculture major farming practices that rely on rainfall for water.Rainfed agriculture: >95% of farmed land (sub-Saharan Africa); 90% (Latin America); 75% (Near East and North Africa); 65% (East Asia); 60% (South Asia).Droughts and floods can cause severe crop loss. The Goddard Earth Sciences (GES) Data and Information Services Center (DISC), one of 12 NASA data centers, is located in Greenbelt, Maryland, USA. The NASA GES DISC is a major data archive center for global precipitation, water & energy cycles, atmospheric composition, and climate variability

The Related Transcriptional Enhancer Factor-1 Isoform, TEAD4216, Can Repress Vascular Endothelial Growth Factor Expression in Mammalian Cells

Increased cellular production of vascular endothelial growth factor (VEGF) is responsible for the development and progression of multiple cancers and other neovascular conditions, and therapies targeting post-translational VEGF products are used in the treatment of these diseases. Development of methods to control and modify the transcription of the VEGF gene is an alternative approach that may have therapeutic potential. We have previously shown that isoforms of the transcriptional enhancer factor 1-related (TEAD4) protein can enhance the production of VEGF. In this study we describe a new TEAD4 isoform, TEAD4216, which represses VEGF promoter activity. The TEAD4216 isoform inhibits human VEGF promoter activity and does not require the presence of the hypoxia responsive element (HRE), which is the sequence critical to hypoxia inducible factor (HIF)-mediated effects. The TEAD4216 protein is localized to the cytoplasm, whereas the enhancer isoforms are found within the nucleus. The TEAD4216 isoform can competitively repress the stimulatory activity of the TEAD4434 and TEAD4148 enhancers. Synthesis of the native VEGF165 protein and cellular proliferation is suppressed by the TEAD4216 isoform. Mutational analysis indicates that nuclear or cytoplasmic localization of any isoform determines whether it acts as an enhancer or repressor, respectively. The TEAD4216 isoform appears to inhibit VEGF production independently of the HRE required activity by HIF, suggesting that this alternatively spliced isoform of TEAD4 may provide a novel approach to treat VEGF-dependent diseases

A rough set-based association rule approach implemented on exploring beverages product spectrum

[[abstract]]When items are classified according to whether they have more or less of a characteristic, the scale used is referred to as an ordinal scale. The main characteristic of the ordinal scale is that the categories have a logical or ordered relationship to each other. Thus, the ordinal scale data processing is very common in marketing, satisfaction and attitudinal research. This study proposes a new data mining method, using a rough set-based association rule, to analyze ordinal scale data, which has the ability to handle uncertainty in the data classification/sorting process. The induction of rough-set rules is presented as method of dealing with data uncertainty, while creating predictive if—then rules that generalize data values, for the beverage market in Taiwan. Empirical evaluation reveals that the proposed Rough Set Associational Rule (RSAR), combined with rough set theory, is superior to existing methods of data classification and can more effectively address the problems associated with ordinal scale data, for exploration of a beverage product spectrum.[[notice]]補正完畢[[incitationindex]]SCI[[booktype]]紙本[[booktype]]電子

Cosmic acceleration and phantom crossing in f(T)f(T)-gravity

In this paper, we propose two new models in $f(T)$ gravity to realize universe acceleration and phantom crossing due to dark torsion in the formalism. The model parameters are constrained and the observational test are discussed. The best fit results favors an accelerating universe with possible phantom crossing in the near past or future followed respectively by matter and radiation dominated era.Comment: 20 pages, 18 figures, Will appear in Astrophys Space Sc

CLEC5A Regulates Japanese Encephalitis Virus-Induced Neuroinflammation and Lethality

CLEC5A/MDL-1, a member of the myeloid C-type lectin family expressed on macrophages and neutrophils, is critical for dengue virus (DV)-induced hemorrhagic fever and shock syndrome in Stat1−/− mice and ConA-treated wild type mice. However, whether CLEC5A is involved in the pathogenesis of viral encephalitis has not yet been investigated. To investigate the role of CLEC5A to regulate JEV-induced neuroinflammation, antagonistic anti-CLEC5A mAb and CLEC5A-deficient mice were generated. We find that Japanese encephalitis virus (JEV) directly interacts with CLEC5A and induces DAP12 phosphorylation in macrophages. In addition, JEV activates macrophages to secrete proinflammatory cytokines and chemokines, which are dramatically reduced in JEV-infected Clec5a−/− macrophages. Although blockade of CLEC5A cannot inhibit JEV infection of neurons and astrocytes, anti-CLEC5A mAb inhibits JEV-induced proinflammatory cytokine release from microglia and prevents bystander damage to neuronal cells. Moreover, JEV causes blood-brain barrier (BBB) disintegrity and lethality in STAT1-deficient (Stat1−/−) mice, whereas peripheral administration of anti-CLEC5A mAb reduces infiltration of virus-harboring leukocytes into the central nervous system (CNS), restores BBB integrity, attenuates neuroinflammation, and protects mice from JEV-induced lethality. Moreover, all surviving mice develop protective humoral and cellular immunity against JEV infection. These observations demonstrate the critical role of CLEC5A in the pathogenesis of Japanese encephalitis, and identify CLEC5A as a target for the development of new treatments to reduce virus-induced brain damage

Non-Steroidal Anti-Inflammatory Drugs and Cognitive Function: Are Prostaglandins at the Heart of Cognitive Impairment in Dementia and Delirium ?

Studies of non-steroidal anti-inflammatory drugs (NSAIDs) in rheumatoid arthritis imply that inflammation is important in the development of Alzheimer’s disease (AD). However, these drugs have not alleviated the symptoms of AD in those who have already developed dementia. This suggests that the primary mediator targeted by these drugs, PGE2, is not actively suppressing memory function in AD. Amyloid-β oligomers appear to be important for the mild cognitive changes seen in AD transgenic mice, yet amyloid immunotherapy has also proven unsuccessful in clinical trials. Collectively, these findings indicate that NSAIDs may target a prodromal process in mice that has already passed in those diagnosed with AD, and that synaptic and neuronal loss are key determinants of cognitive dysfunction in AD. While the role of inflammation has not yet become clear, inflammatory processes definitely have a negative impact on cognitive function during episodes of delirium during dementia. Delirium is an acute and profound impairment of cognitive function frequently occurring in aged and demented patients exposed to systemic inflammatory insults, which is now recognised to contribute to long-term cognitive decline. Recent work in animal models is beginning to shed light on the interactions between systemic inflammation and CNS pathology in these acute exacerbations of dementia. This review will assess the role of prostaglandin synthesis in the memory impairments observed in dementia and delirium and will examine the relative contribution of amyloid, synaptic and neuronal loss. We will also discuss how understanding the role of inflammatory mediators in delirious episodes will have major implications for ameliorating the rate of decline in the demented population