DD-dimensions Dirac fermions BEC-BCS cross-over thermodynamics

An effective Proca Lagrangian action is used to address the vector condensation Lorentz violation effects on the equation of state of the strongly interacting fermions system. The interior quantum fluctuation effects are incorporated as an external field approximation indirectly through a fictive generalized Thomson Problem counterterm background. The general analytical formulas for the $d$-dimensions thermodynamics are given near the unitary limit region. In the non-relativistic limit for $d=3$, the universal dimensionless coefficient $\xi ={4}/{9}$ and energy gap $\Delta/\epsilon_f ={5}/{18}$ are reasonably consistent with the existed theoretical and experimental results. In the unitary limit for $d=2$ and T=0, the universal coefficient can even approach the extreme occasion $\xi=0$ corresponding to the infinite effective fermion mass $m^*=\infty$ which can be mapped to the strongly coupled two-dimensions electrons and is quite similar to the three-dimensions Bose-Einstein Condensation of ideal boson gas. Instead, for $d=1$, the universal coefficient $\xi$ is negative, implying the non-existence of phase transition from superfluidity to normal state. The solutions manifest the quantum Ising universal class characteristic of the strongly coupled unitary fermions gas.Comment: Improved versio

Effect of the desorption process on photoluminescence excitation spectra of porous silicon

Photoluminescence (PL), photoluminescence excitation (PLE) and FTIR methods were used to study the PL excitation mechanism in porous silicon (PS). Two types of PLE spectra were observed, consisting of two (visible and ultraviolet) and one (only ultraviolet) bands. The intensities of each PLE band depend differently on the anodization conditions during aging and thermal treatment. Two excitation channels were shown to exist in PS. The visible PLE band at 300 K was attributed to light absorption of some species on the surface of Si wires.Досліджено механізм збудження фотолюмінесценції пористого кремміго методами фотолюмінесценції та інфрачервоного поглинання. Показано, що існує два типі спектрів збудження, які містять або дві смуги (видиму та ультрафіолетову), або тільки одну (ультрафіолетову) смугу. Вивчено залежності інтенсивностей кожної смуги від режимів електрохімічного травлення, а також їх поведінка у процесі старіння та термічного оброблення пористих шарів. Показано, що існують два канали збудження фотолюмінесценції. Видима смуга у спектрі збудження при 300 К пов.язується з поглинанням світла у речовинах, які адсорбовані на поверхні кремнієвих ниток.Исследован механизм возбуждении фотолюминесценции пористого кремнии методами фотолюминесценции и инфракрасного поглощения. Показано, что существуют два типа спектров возбуждения, которые содержат либо две полосы (видимую и ультрафиолетовую), либо только одну (ультрафиолетовую) полосу. Изучены зависимости ингенсивностей каждой полосы возбуждения от режимов электрохимического травления, а также их поведение в процессе старения и термических обработок пористых слоев. Показано, что существуют два канала возбуждения фотолюминесценции. Видимая полоса в спектре возбуждения при 300 К связывается с поглощением света веществами, адсорбированными на поверхности кремниевых нитей

Paraoxonase 2 protein is spatially expressed in the human placenta and selectively reduced in labour

Humans parturition involves interaction of hormonal, neurological, mechanical stretch and inflammatory pathways and the placenta plays a crucial role. The paraoxonases (PONs 1–3) protect against oxidative damage and lipid peroxidation, modulation of endoplasmic reticulum stress and regulation of apoptosis. Nothing is known about the role of PON2 in the placenta and labour. Since PON2 plays a role in oxidative stress and inflammation, both features of labour, we hypothesised that placental PON2 expression would alter during labour. PON2 was examined in placentas obtained from women who delivered by cesarean section and were not in labour and compared to the equivalent zone of placentas obtained from women who delivered vaginally following an uncomplicated labour. Samples were obtained from 12 sites within each placenta: 4 equally spaced apart pieces were sampled from the inner, middle and outer placental regions. PON2 expression was investigated by Western blotting and real time PCR. Two PON2 forms, one at 62 kDa and one at 43 kDa were found in all samples. No difference in protein expression of either isoform was found between the three sites in either the labour or non-labour group. At the middle site there was a highly significant decrease in PON2 expression in the labour group when compared to the non-labour group for both the 62 kDa form (p = 0.02) and the 43 kDa form (p = 0.006). No spatial differences were found within placentas at the mRNA level in either labour or non-labour. There was, paradoxically, an increase in PON2 mRNA in the labour group at the middle site only. This is the first report to describe changes in PON2 in the placenta in labour. The physiological and pathological significance of these remains to be elucidated but since PON2 is anti-inflammatory further studies are warranted to understand its role

Chiral bosonization for non-commutative fields

A model of chiral bosons on a non-commutative field space is constructed and new generalized bosonization (fermionization) rules for these fields are given. The conformal structure of the theory is characterized by a level of the Kac-Moody algebra equal to $(1+ \theta^2)$ where $\theta$ is the non-commutativity parameter and chiral bosons living in a non-commutative fields space are described by a rational conformal field theory with the central charge of the Virasoro algebra equal to 1. The non-commutative chiral bosons are shown to correspond to a free fermion moving with a speed equal to $c^{\prime} = c \sqrt{1+\theta^2}$ where $c$ is the speed of light. Lorentz invariance remains intact if $c$ is rescaled by $c \to c^{\prime}$. The dispersion relation for bosons and fermions, in this case, is given by $\omega = c^{\prime} | k|$.Comment: 16 pages, JHEP style, version published in JHE

BGWM as Second Constituent of Complex Matrix Model

Earlier we explained that partition functions of various matrix models can be constructed from that of the cubic Kontsevich model, which, therefore, becomes a basic elementary building block in "M-theory" of matrix models. However, the less topical complex matrix model appeared to be an exception: its decomposition involved not only the Kontsevich tau-function but also another constituent, which we now identify as the Brezin-Gross-Witten (BGW) partition function. The BGW tau-function can be represented either as a generating function of all unitary-matrix integrals or as a Kontsevich-Penner model with potential 1/X (instead of X^3 in the cubic Kontsevich model).Comment: 42 page

VEGF binding to NRP1 is essential for VEGF stimulation of endothelial cell migration, complex formation between NRP1 and VEGFR2, and signaling via FAK Tyr407 phosphorylation

In endothelial cells, neuropilin-1 (NRP1) binds vascular endothelial growth factor (VEGF)-A and is thought to act as a coreceptor for kinase insert domain-containing receptor (KDR) by associating with KDR and enhancing VEGF signaling. Here we report mutations in the NRP1 b1 domain (Y297A and D320A), which result in complete loss of VEGF binding. Overexpression of Y297A and D320A NRP1 in human umbilical vein endothelial cells reduced high-affinity VEGF binding and migration toward a VEGF gradient, and markedly inhibited VEGF-induced angiogenesis in a coculture cell model. The Y297A NRP1 mutant also disrupted complexation between NRP1 and KDR and decreased VEGF-dependent phosphorylation of focal adhesion kinase at Tyr407, but had little effect on other signaling pathways. Y297A NRP1, however, heterodimerized with wild-type NRP1 and NRP2 indicating that nonbinding NRP1 mutants can act in a dominant-negative manner through formation of NRP1 dimers with reduced binding affinity for VEGF. These findings indicate that VEGF binding to NRP1 has specific effects on endothelial cell signaling and is important for endothelial cell migration and angiogenesis mediated via complex formation between NRP1 and KDR and increased signaling to focal adhesions. Identification of key residues essential for VEGF binding and biological functions provides the basis for a rational design of antagonists of VEGF binding to NRP1

Establishing an infrastructure for collaboration in primate cognition research

Inferring the evolutionary history of cognitive abilities requires large and diverse samples. However, such samples are often beyond the reach of individual researchers or institutions, and studies are often limited to small numbers of species. Consequently, methodological and site-specific-differences across studies can limit comparisons between species. Here we introduce the ManyPrimates project, which addresses these challenges by providing a large-scale collaborative framework for comparative studies in primate cognition. To demonstrate the viability of the project we conducted a case study of short-term memory. In this initial study, we were able to include 176 individuals from 12 primate species housed at 11 sites across Africa, Asia, North America and Europe. All subjects were tested in a delayed-response task using consistent methodology across sites. Individuals could access food rewards by remembering the position of the hidden reward after a 0, 15, or 30-second delay. Overall, individuals performed better with shorter delays, as predicted by previous studies. Phylogenetic analysis revealed a strong phylogenetic signal for short-term memory. Although, with only 12 species, the validity of this analysis is limited, our initial results demonstrate the feasibility of a large, collaborative open-science project. We present the ManyPrimates project as an exciting opportunity to address open questions in primate cognition and behaviour with large, diverse datasets

Enhanced Lifetime Of Excitons In Nonepitaxial Au/cds Core/shell Nanocrystals

The ability of metal nanoparticles to capture light through plasmon excitations offers an opportunity for enhancing the optical absorption of plasmon-coupled semiconductor materials via energy transfer. This process, however, requires that the semiconductor component is electrically insulated to prevent a backward charge flow into metal and interfacial states, which causes a premature dissociation of excitons. Here we demonstrate that such an energy exchange can be achieved on the nanoscale by using nonepitaxial Au/CdS core/shell nanocomposites. These materials are fabricated via a multistep cation exchange reaction, which decouples metal and semiconductor phases leading to fewer interfacial defects. Ultrafast transient absorption measurements confirm that the lifetime of excitons in the CdS shell (tau approximate to 300 ps) is much longer than lifetimes of excitons in conventional, reduction-grown Au/CdS heteronanostructures. As a result, the energy of metal nanoparticles can be efficiently utilized by the semiconductor component without undergoing significant nonradiative energy losses, an important property for catalytic or photovoltaic applications. The reduced rate of exciton dissociation in the CdS domain of Au/CdS nanocomposites was attributed to the nonepitaxial nature of Au/CdS interfaces associated with low defect density and a high potential barrier of the interstitial phase

Abnormalities in Oxygen Sensing Define Early and Late Onset Preeclampsia as Distinct Pathologies

BACKGROUND: The pathogenesis of preeclampsia, a serious pregnancy disorder, is still elusive and its treatment empirical. Hypoxia Inducible Factor-1 (HIF-1) is crucial for placental development and early detection of aberrant regulatory mechanisms of HIF-1 could impact on the diagnosis and management of preeclampsia. HIF-1α stability is controlled by O(2)-sensing enzymes including prolyl hydroxylases (PHDs), Factor Inhibiting HIF (FIH), and E3 ligases Seven In Absentia Homologues (SIAHs). Here we investigated early- (E-PE) and late-onset (L-PE) human preeclamptic placentae and their ability to sense changes in oxygen tension occurring during normal placental development. METHODS AND FINDINGS: Expression of PHD2, FIH and SIAHs were significantly down-regulated in E-PE compared to control and L-PE placentae, while HIF-1α levels were increased. PHD3 expression was increased due to decreased FIH levels as demonstrated by siRNA FIH knockdown experiments in trophoblastic JEG-3 cells. E-PE tissues had markedly diminished HIF-1α hydroxylation at proline residues 402 and 564 as assessed with monoclonal antibodies raised against hydroxylated HIF-1α P402 or P564, suggesting regulation by PHD2 and not PHD3. Culturing villous explants under varying oxygen tensions revealed that E-PE, but not L-PE, placentae were unable to regulate HIF-1α levels because PHD2, FIH and SIAHs did not sense a hypoxic environment. CONCLUSION: Disruption of oxygen sensing in E-PE vs. L-PE and control placentae is the first molecular evidence of the existence of two distinct preeclamptic diseases and the unique molecular O(2)-sensing signature of E-PE placentae may be of diagnostic value when assessing high risk pregnancies and their severity

Myc-regulated microRNAs attenuate embryonic stem cell differentiation

Myc proteins are known to have an important function in stem cell maintenance. As Myc has been shown earlier to regulate microRNAs (miRNAs) involved in proliferation, we sought to determine whether c-Myc also affects embryonic stem (ES) cell maintenance and differentiation through miRNAs. Using a quantitative primer-extension PCR assay we identified miRNAs, including, miR-141, miR-200, and miR-429 whose expression is regulated by c-Myc in ES cells, but not in the differentiated and tumourigenic derivatives of ES cells. Chromatin immunoprecipitation analyses indicate that in ES cells c-Myc binds proximal to genomic regions encoding the induced miRNAs. We used expression profiling and seed homology to identify genes specifically downregulated both by these miRNAs and by c-Myc. We further show that the introduction of c-Myc-induced miRNAs into murine ES cells significantly attenuates the downregulation of pluripotency markers on induction of differentiation after withdrawal of the ES cell maintenance factor LIF. In contrast, knockdown of the endogenous miRNAs accelerate differentiation. Our data show that in ES cells c-Myc acts, in part, through a subset of miRNAs to attenuate differentiation