Cyclic cocycles on twisted convolution algebras

We give a construction of cyclic cocycles on convolution algebras twisted by gerbes over discrete translation groupoids. For proper \'etale groupoids, Tu and Xu provide a map between the periodic cyclic cohomology of a gerbe-twisted convolution algebra and twisted cohomology groups which is similar to a construction of Mathai and Stevenson. When the groupoid is not proper, we cannot construct an invariant connection on the gerbe; therefore to study this algebra, we instead develop simplicial techniques to construct a simplicial curvature 3-form representing the class of the gerbe. Then by using a JLO formula we define a morphism from a simplicial complex twisted by this simplicial curvature 3-form to the mixed bicomplex computing the periodic cyclic cohomology of the twisted convolution algebras. The results in this article were originally published in the author's Ph.D. thesis.Comment: 39 page

Arthropod Pest Management in Organic Vegetable Greenhouses

We present a comprehensive discussion of pest management in organic greenhouse vegetable production. Greenhouse structures and production practices vary greatly in different regions of the world. In northern Europe and North America, they are closed heated structures because of the long periods of cold weather and biological control is highly developed. In Israel, commercial greenhouses are made of netting or plastic, are not heated because the winters are generally mild in comparison with northern climes and hot in the summers, and biological control is used almost exclusively on some crops. In South America, greenhouses are simple structures covered with plastic material without nets or heating/cooling systems. We limit our discussion to properly closed and ventilated greenhouses, exclusive of structures that are opened for any period during the day or season. Our discussion covers greenhouse structure; the first line of defense, regulatory, and phytosanitary measures; various management methods; and finally specific management of primary pest groups, mites, thrips, hemipterans (aphids, mealybugs, and whiteflies), and small Lepidoptera.EEA ConcordiaFil: Weintraub, Phyllis G. Agricultural Research Organization. Gilat Research Center; IsraelFil: Recht, Eitan. Plant Protection and Inspection Services; IsraelFil: Mondaca, Lilach Lily. Sapir Academic Collage; IsraelFil: Harari, Ally R. Agricultural Research Organization. Volcani Center; IsraelFil: Diaz, Beatriz Maria. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Concordia; ArgentinaFil: Bennison, Jude. ADAS Boxworth; Reino Unid

Mu-Metal Enhancement of Effects in Electromagnetic Fields Over Single Emitters Near Topological Insulators

We focus on the transmission and reflection coefficients of light in systems involving of topological insulators (TI). Due to the electro-magnetic coupling in TIs, new mixing coefficients emerge leading to new components of the electromagnetic fields of propagating waves. We have discovered a simple heterostructure that provides a 100-fold enhancement of the mixing coefficients for TI materials. Such effect increases with the TI's wave impedance. We also predict a transverse deviation of the Poynting vector due to these mixed coefficients contributing to the radiative electromagnetic field of an electric dipole. Given an optimal configuration of the dipole-TI system, this deviation could amount to $0.18\%$ of the Poynting vector due to emission near not topological materials, making this effect detectable

Pancreatic polypeptide inhibits somatostatin secretion

AbstractPancreatic polypeptide (PP) is a major agonist for neuropeptide Y4 receptors (NPY4R). While NPY4R has been identified in various tissues, the cells on which it is expressed and its function in those cells has not been clearly delineated. Here we report that NPY4R is present in all somatostatin-containing cells of tissues that we tested, including pancreatic islets, duodenum, hippocampus, and hypothalamus. Its agonism by PP decreases somatostatin secretion from human islets. Mouse embryonic hippocampal (mHippo E18) cells expressed NPY4Rs and their activation by PP consistently decreased somatostatin secretion. Furthermore, central injection of PP in mice induced c-Fos immunoreactivity in somatostatin-containing cells in the hippocampus compared with PBS-injected mice. In sum, our results identify PP as a pivotal modulator of somatostatin secretion

Amplification of the Angiogenic Signal through the Activation of the TSC/mTOR/HIF Axis by the KSHV vGPCR in Kaposi's Sarcoma

Background: Kaposi’s sarcoma (KS) is a vascular neoplasm characterized by the dysregulated expression of angiogenic and inflammatory cytokines. The driving force of the KS lesion, the KSHV-infected spindle cell, secretes elevated levels of vascular endothelial growth factor (VEGF), essential for KS development. However, the origin of VEGF in this tumor remains unclear. Methodology/Principal Findings: Here we report that the KSHV G protein-coupled receptor (vGPCR) upregulates VEGF in KS through an intricate paracrine mechanism. The cytokines secreted by the few vGPCR-expressing tumor cells activate in neighboring cells multiple pathways (including AKT, ERK, p38 and IKK$\beta$) that, in turn, converge on TSC1/2, promoting mTOR activation, HIF upregulation, and VEGF secretion. Conditioned media from vGPCR-expressing cells lead to an mTORdependent increase in HIF-1$\alpha$ and HIF-2$\alpha$ protein levels and VEGF upregulation. In a mouse allograft model for KS, specific inhibition of the paracrine activation of mTOR in non-vGPCR-expressing cells was sufficient to inhibit HIF upregulation in these cells, and abolished the ability of the vGPCR-expressing cells to promote tumor formation $in$ $vivo$. Similarly, pharmacologic inhibition of HIF in this model blocked VEGF secretion and also lead to tumor regression. Conclusions/Significance: Our findings provide a compelling explanation for how the few tumor cells expressing vGPCR can contribute to the dramatic amplification of VEGF secretion in KS, and further provide a molecular mechanism for how cytokine dysregulation in KS fuels angiogenesis and tumor development. These data further suggest that activation of HIF by vGPCR may be a vulnerable target for the treatment of patients with KS