A novel mobile communication system using Pulse Position based Chirp Spread Spectrum modulation

The paper presents a new mobile communication system based on Chirp Spread Spectrum (CSS) transmission. The downlink modulation scheme is extended with Pulse Position Modulation (PPM) to carry data for multiple mobile terminals simultaneously. The described novel mechanism ensures reliable and robust communication between the parties, especially for terminals moving with high speeds or at long range. Furthermore, the proposed system take care of the uplink communication as well, where Closed-Loop Power Control (CLPC) is applied to handle the near-far problem and improve the performance of the system. Based on the attributes of the proposed system the application area covers sensor networks, IoT applications and Industry 4.0 as general field of LPWAN, however, mobility of terminals also considered.Analytical investigations for downlink communication are described focusing on the instantaneous symbol-error rate and average SER in Rayleigh fading channel. The results show that the proposed Pulse Position based Chirp Spread Spectrum technique for Multiple Access (shortly PP-CSS-MA) allows higher data rates that is used for the multiple access feature. In addition, numerical results are presented as well, and they point out the benefits of the applied CLPC mechanism. Finally, considerations regarding to the implementation of the proposed communication system are described

A novel mobile communication system using Pulse Position based Chirp Spread Spectrum modulation

The paper presents a new mobile communication system based on Chirp Spread Spectrum (CSS) transmission. The downlink modulation scheme is extended with Pulse Position Modulation (PPM) to carry data for multiple mobile terminals simultaneously. The described novel mechanism ensures reliable and robust communication between the parties, especially for terminals moving with high speeds or at long range. Furthermore, the proposed system take care of the uplink communication as well, where Closed-Loop Power Control (CLPC) is applied to handle the near-far problem and improve the performance of the system. Based on the attributes of the proposed system the application area covers sensor networks, IoT applications and Industry 4.0 as general field of LPWAN, however, mobility of terminals also considered.Analytical investigations for downlink communication are described focusing on the instantaneous symbol-error rate and average SER in Rayleigh fading channel. The results show that the proposed Pulse Position based Chirp Spread Spectrum technique for Multiple Access (shortly PP-CSS-MA) allows higher data rates that is used for the multiple access feature. In addition, numerical results are presented as well, and they point out the benefits of the applied CLPC mechanism. Finally, considerations regarding to the implementation of the proposed communication system are described

PPARγ controls CD1d expression by turning on retinoic acid synthesis in developing human dendritic cells

Dendritic cells (DCs) expressing CD1d, a molecule responsible for lipid antigen presentation, are capable of enhancing natural killer T (iNKT) cell proliferation. The signals controlling CD1 expression and lipid antigen presentation are poorly defined. We have shown previously that stimulation of the lipid-activated transcription factor, peroxisome proliferator-activated receptor (PPAR)γ, indirectly regulates CD1d expression. Here we demonstrate that PPARγ, turns on retinoic acid synthesis by inducing the expression of retinol and retinal metabolizing enzymes such as retinol dehydrogenase 10 and retinaldehyde dehydrogenase type 2 (RALDH2). PPARγ-regulated expression of these enzymes leads to an increase in the intracellular generation of all-trans retinoic acid (ATRA) from retinol. ATRA regulates gene expression via the activation of the retinoic acid receptor (RAR)α in human DCs, and RARα acutely regulates CD1d expression. The retinoic acid–induced elevated expression of CD1d is coupled to enhanced iNKT cell activation. Furthermore, in vivo relevant lipids such as oxidized low-density lipoprotein can also elicit retinoid signaling leading to CD1d up-regulation. These data show that regulation of retinoid metabolism and signaling is part of the PPARγ-controlled transcriptional events in DCs. The uncovered mechanisms allow the DCs to respond to altered lipid homeostasis by changing CD1 gene expression

LXR Nuclear receptors are transcriptional regulators of dendritic cell chemotaxis

The liver X receptors (LXRs) are ligand-activated nuclear receptors with established roles in the maintenance of lipid homeostasis in multiple tissues. LXRs exert additional biological functions as negative regulators of inflammation, particularly in macrophages. However, the transcriptional responses controlled by LXRs in other myeloid cells, such as dendritic cells (DCs), are still poorly understood. Here we used gain- and loss-of-function models to characterize the impact of LXR deficiency on DC activation programs. Our results identified an LXR-dependent pathway that is important for DC chemotaxis. LXR-deficient mature DCs are defective in stimulus-induced migration in vitro and in vivo. Mechanistically, we show that LXRs facilitate DC chemotactic signaling by regulating the expression of CD38, an ectoenzyme important for leukocyte trafficking. Pharmacological or genetic inactivation of CD38 activity abolished the LXR-dependent induction of DC chemotaxis. Using the low-density lipoprotein receptor-deficient (LDLR−/−) LDLR−/− mouse model of atherosclerosis, we also demonstrated that hematopoietic CD38 expression is important for the accumulation of lipid-laden myeloid cells in lesions, suggesting that CD38 is a key factor in leukocyte migration during atherogenesis. Collectively, our results demonstrate that LXRs are required for the efficient emigration of DCs in response to chemotactic signals during inflammation

Varga et al.: Macrophage PPARγ, a Lipid Activated Transcription Factor Controls the Growth Factor GDF3 and Skeletal Muscle Regeneration Immunity. 2016 Nov 15;45(5):1038-1051. doi: 10.1016/j.immuni.2016.10.016.

Tissue regeneration requires inflammatory and reparatory activity of macrophages. Macrophages detect and eliminate the damaged tissue and subsequently promote regeneration. This dichotomy requires the switch of effector functions of macrophages coordinated with other cell types inside the injured tissue. The gene regulatory events supporting the sensory and effector functions of macrophages involved in tissue repair are not well understood. Here we show that the lipid activated transcription factor, PPARγ, is required for proper skeletal muscle regeneration, acting in repair macrophages. PPARγ controls the expression of the transforming growth factor-β (TGF-β) family member, GDF3, which in turn regulates the restoration of skeletal muscle integrity by promoting muscle progenitor cell fusion. This work establishes PPARγ as a required metabolic sensor and transcriptional regulator of repair macrophages. Moreover, this work also establishes GDF3 as a secreted extrinsic effector protein acting on myoblasts and serving as an exclusively macrophage-derived regeneration factor in tissue repair

Assessing the Effects of Climate on Host-Parasite Interactions: A Comparative Study of European Birds and Their Parasites

[Background] Climate change potentially has important effects on distribution, abundance, transmission and virulence of parasites in wild populations of animals. [Methodology/Principal Finding] Here we analyzed paired information on 89 parasite populations for 24 species of bird hosts some years ago and again in 2010 with an average interval of 10 years. The parasite taxa included protozoa, feather parasites, diptera, ticks, mites and fleas. We investigated whether change in abundance and prevalence of parasites was related to change in body condition, reproduction and population size of hosts. We conducted analyses based on the entire dataset, but also on a restricted dataset with intervals between study years being 5–15 years. Parasite abundance increased over time when restricting the analyses to datasets with an interval of 5–15 years, with no significant effect of changes in temperature at the time of breeding among study sites. Changes in host body condition and clutch size were related to change in temperature between first and second study year. In addition, changes in clutch size, brood size and body condition of hosts were correlated with change in abundance of parasites. Finally, changes in population size of hosts were not significantly related to changes in abundance of parasites or their prevalence. [Conclusions/Significance] Climate change is associated with a general increase in parasite abundance. Variation in laying date depended on locality and was associated with latitude while body condition of hosts was associated with a change in temperature. Because clutch size, brood size and body condition were associated with change in parasitism, these results suggest that parasites, perhaps mediated through the indirect effects of temperature, may affect fecundity and condition of their hosts. The conclusions were particularly in accordance with predictions when the restricted dataset with intervals of 5–15 years was used, suggesting that short intervals may bias findings.The Academy of Finland is acknowledged for a grant to TE (project 8119367) and EK (project 250709). PLP was supported by a research grant (TE_291/2010) offered by the Romanian Ministry of Education and Science. T. Szép received funding from OTKA K69068 and JT from OTKA 75618. JMP was supported by a JAE grant from Consejo Superior de Investigaciones Científicas. SM-JM, FdL-AM, JF, JJS and FV were respectively supported by projects CGL2009-09439, CGL2012-36665, CGL2009- 11445, CGL2010-19233-C03-01 and CGL2008-00562 by the Spanish Ministry of Science and Innovation and FEDER and project EVITAR by the Spanish Ministry of Health. FV was also supported by the European Regional Development Fund. MACT was funded by a predoctoral FPU grant from the Spanish Ministry of Education (AP20043713). PM was supported by grant from the Polish Ministry of Science and Higher Education (project 2P04F07030), and the Foundation for Polish Science