Fiber guiding at the Dirac frequency beyond photonic bandgaps

Light trapping within waveguides is a key practice of modern optics, both scientifically and technologically. Photonic crystal fibers traditionally rely on total internal reflection (index-guiding fibers) or a photonic bandgap (photonic-bandgap fibers) to achieve field confinement. Here, we report the discovery of a new light trapping within fibers by the so-called Dirac point of photonic band structures. Our analysis reveals that the Dirac point can establish suppression of radiation losses and consequently a novel guided mode for propagation in photonic crystal fibers. What is known as the Dirac point is a conical singularity of a photonic band structure where wave motion obeys the famous Dirac equation. We find the unexpected phenomenon of wave localization at this point beyond photonic bandgaps. This guiding relies on the Dirac point rather than total internal reflection or photonic bandgaps, thus providing a sort of advancement in conceptual understanding over the traditional fiber guiding. The result presented here demonstrates the discovery of a new type of photonic crystal fibers, with unique characteristics that could lead to new applications in fiber sensors and lasers. The Dirac equation is a special symbol of relativistic quantum mechanics. Because of the similarity between band structures of a solid and a photonic crystal, the discovery of the Dirac-point-induced wave trapping in photonic crystals could provide novel insights into many relativistic quantum effects of the transport phenomena of photons, phonons, and electrons

Two Bee-Pollinated Plant Species Show Higher Seed Production when Grown in Gardens Compared to Arable Farmland

Background Insect pollinator abundance, in particular that of bees, has been shown to be high where there is a super-abundance of floral resources; for example in association with mass-flowering crops and also in gardens where flowering plants are often densely planted. Since land management affects pollinator numbers, it is also likely to affect the resultant pollination of plants growing in these habitats. We hypothesised that the seed or fruit set of two plant species, typically pollinated by bumblebees and/or honeybees might respond in one of two ways: 1) pollination success could be reduced when growing in a floriferous environment, via competition for pollinators, or 2) pollination success could be enhanced because of increased pollinator abundance in the vicinity. Methodology/Principal Findings We compared the pollination success of experimental plants of Glechoma hederacea L. and Lotus corniculatus L. growing in gardens and arable farmland. On the farms, the plants were placed either next to a mass-flowering crop (oilseed rape, Brassica napus L. or field beans, Vicia faba L.) or next to a cereal crop (wheat, Triticum spp.). Seed set of G. hederacea and fruit set of L. corniculatus were significantly higher in gardens compared to arable farmland. There was no significant difference in pollination success of G. hederacea when grown next to different crops, but for L. corniculatus, fruit set was higher in the plants growing next to oilseed rape when the crop was in flower. Conclusions/Significance The results show that pollination services can limit fruit set of wild plants in arable farmland, but there is some evidence that the presence of a flowering crop can facilitate their pollination (depending on species and season). We have also demonstrated that gardens are not only beneficial to pollinators, but also to the process of pollination

Evidence for a novel Kit adhesion domain mediating human mast cell adhesion to structural airway cells

Background: Human lung mast cells (HLMCs) infiltrate the airway epithelium and airway smooth muscle (ASM) in asthmatic airways. The mechanism of HLMC adhesion to both cell types is only partly defined, and adhesion is not inhibited by function-blocking anti-Kit and anti-stem cell factor (SCF) antibodies. Our aim was to identify adhesion molecules expressed by human mast cells that mediate adhesion to human ASM cells (HASMCs) and human airway epithelial cells. Methods: We used phage-display to isolate single chain Fv (scFv) antibodies with adhesion-blocking properties from rabbits immunised with HLMC and HMC-1 membrane proteins. Results: Post-immune rabbit serum labelled HLMCs in flow cytometry and inhibited their adhesion to human BEAS-2B epithelial cells. Mast cell-specific scFvs were identified which labelled mast cells but not Jurkat cells by flow cytometry. Of these, one scFv (A1) consistently inhibited mast cell adhesion to HASMCs and BEAS-2B epithelial cells by about 30 %. A1 immunoprecipitated Kit (CD117) from HMC-1 lysates and bound to a human Kit-expressing mouse mast cell line, but did not interfere with SCF-dependent Kit signalling. Conclusion: Kit contributes to human mast cell adhesion to human airway epithelial cells and HASMCs, but may utilise a previously unidentified adhesion domain that lies outside the SCF binding site. Targeting this adhesion pathway might offer a novel approach for the inhibition of mast cell interactions with structural airway cells, without detrimental effects on Kit signalling in other tissues

Stimulated optomechanical excitation of surface acoustic waves in a microdevice

Stimulated Brillouin interaction between sound and light, known to be the strongest optical nonlinearity common to all amorphous and crystalline dielectrics, has been widely studied in fibers and bulk materials but rarely in optical microresonators. The possibility of experimentally extending this principle to excite mechanical resonances in photonic microsystems, for sensing and frequency reference applications, has remained largely unexplored. The challenge lies in the fact that microresonators inherently have large free spectral range, while the phase matching considerations for the Brillouin process require optical modes of nearby frequencies but with different wavevectors. We rely on high-order transverse optical modes to relax this limitation. Here we report on the experimental excitation of mechanical resonances ranging from 49 to 1400 MHz by using forward Brillouin scattering. These natural mechanical resonances are excited in ~100 um silica microspheres, and are of a surface-acoustic whispering-gallery type

Cardiac fibrosis can be attenuated by blocking the activity of transglutaminase 2 using a selective small-molecule inhibitor

Cardiac fibrosis is implicit in all forms of heart disease but there are no effective treatments. In this report, we investigate the role of the multi-functional enzyme Transglutaminase 2 (TG2) in cardiac fibrosis and assess its potential as a therapeutic target. Here we describe the use a highly selective TG2 small-molecule inhibitor to test the efficacy of TG2 inhibition as an anti-fibrotic therapy for heart failure employing two different in vivo models of cardiac fibrosis: Progressively induced interstitial cardiac fibrosis by pressure overload using angiotensin II infusion: Acutely induced focal cardiac fibrosis through myocardial infarction by ligation of the left anterior descending coronary artery (AMI model). In the AMI model, in vivo MRI showed that the TG2 inhibitor 1–155 significantly reduced infarct size by over 50% and reduced post-infarct remodelling at 20 days post insult. In both models, Sirius red staining for collagen deposition and levels of the TG2-mediated protein crosslink ε(γ-glutamyl)lysine were significantly reduced. No cardiac rupture or obvious signs of toxicity were observed. To provide a molecular mechanism for TG2 involvement in cardiac fibrosis, we show that both TGFβ1-induced transition of cardiofibroblasts into myofibroblast-like cells and TGFβ1- induced EndMT, together with matrix deposition, can be attenuated by the TG2 selective inhibitor 1–155, suggesting a new role for TG2 in regulating TGFβ1 signalling in addition to its role in latent TGFβ1 activation. In conclusion, TG2 has a role in cardiac fibrosis through activation of myofibroblasts and matrix deposition. TG2 inhibition using a selective small-molecule inhibitor can attenuate cardiac fibrosis

Systematic Analysis of Pleiotropy in C. elegans Early Embryogenesis

Pleiotropy refers to the phenomenon in which a single gene controls several distinct, and seemingly unrelated, phenotypic effects. We use C. elegans early embryogenesis as a model to conduct systematic studies of pleiotropy. We analyze high-throughput RNA interference (RNAi) data from C. elegans and identify “phenotypic signatures”, which are sets of cellular defects indicative of certain biological functions. By matching phenotypic profiles to our identified signatures, we assign genes with complex phenotypic profiles to multiple functional classes. Overall, we observe that pleiotropy occurs extensively among genes involved in early embryogenesis, and a small proportion of these genes are highly pleiotropic. We hypothesize that genes involved in early embryogenesis are organized into partially overlapping functional modules, and that pleiotropic genes represent “connectors” between these modules. In support of this hypothesis, we find that highly pleiotropic genes tend to reside in central positions in protein-protein interaction networks, suggesting that pleiotropic genes act as connecting points between different protein complexes or pathways

Systematic Analysis of Pleiotropy in C. elegans Early Embryogenesis

Pleiotropy refers to the phenomenon in which a single gene controls several distinct, and seemingly unrelated, phenotypic effects. We use C. elegans early embryogenesis as a model to conduct systematic studies of pleiotropy. We analyze high-throughput RNA interference (RNAi) data from C. elegans and identify “phenotypic signatures”, which are sets of cellular defects indicative of certain biological functions. By matching phenotypic profiles to our identified signatures, we assign genes with complex phenotypic profiles to multiple functional classes. Overall, we observe that pleiotropy occurs extensively among genes involved in early embryogenesis, and a small proportion of these genes are highly pleiotropic. We hypothesize that genes involved in early embryogenesis are organized into partially overlapping functional modules, and that pleiotropic genes represent “connectors” between these modules. In support of this hypothesis, we find that highly pleiotropic genes tend to reside in central positions in protein-protein interaction networks, suggesting that pleiotropic genes act as connecting points between different protein complexes or pathways

Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as ‘accidental cell death’ (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. ‘Regulated cell death’ (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death

Phenotypic alterations in type II alveolar epithelial cells in CD4+ T cell mediated lung inflammation

<p>Abstract</p> <p>Background</p> <p>Although the contribution of alveolar type II epithelial cell (AEC II) activities in various aspects of respiratory immune regulation has become increasingly appreciated, our understanding of the contribution of AEC II transcriptosome in immunopathologic lung injury remains poorly understood. We have previously established a mouse model for chronic T cell-mediated pulmonary inflammation in which influenza hemagglutinin (HA) is expressed as a transgene in AEC II, in mice expressing a transgenic T cell receptor specific for a class II-restricted epitope of HA. Pulmonary inflammation in these mice occurs as a result of CD4⁺T cell recognition of alveolar antigen. This model was utilized to assess the profile of inflammatory mediators expressed by alveolar epithelial target cells triggered by antigen-specific recognition in CD4⁺T cell-mediated lung inflammation.</p> <p>Methods</p> <p>We established a method that allows the flow cytometric negative selection and isolation of primary AEC II of high viability and purity. Genome wide transcriptional profiling was performed on mRNA isolated from AEC II isolated from healthy mice and from mice with acute and chronic CD4⁺T cell-mediated pulmonary inflammation.</p> <p>Results</p> <p>T cell-mediated inflammation was associated with expression of a broad array of cytokine and chemokine genes by AEC II cell, indicating a potential contribution of epithelial-derived chemoattractants to the inflammatory cell parenchymal infiltration. Morphologically, there was an increase in the size of activated epithelial cells, and on the molecular level, comparative transcriptome analyses of AEC II from inflamed versus normal lungs provide a detailed characterization of the specific inflammatory genes expressed in AEC II induced in the context of CD4⁺T cell-mediated pneumonitis.</p> <p>Conclusion</p> <p>An important contribution of AEC II gene expression to the orchestration and regulation of interstitial pneumonitis is suggested by the panoply of inflammatory genes expressed by this cell population, and this may provide insight into the molecular pathogenesis of pulmonary inflammatory states. CD4⁺T cell recognition of antigen presented by AEC II cells appears to be a potent trigger for activation of the alveolar cell inflammatory transcriptosome.</p