The Design, Building, and Testing of a Constant on Discreet Jammer for the Ieee 802.15.4/ZIGBEE Wireless Communication Protocol

As wireless protocols become easier to implement, more products come with wireless connectivity. This latest push for wireless connectivity has left a gap in the development of the security and the reliability of some protocols. These wireless protocols can be used in the growing field of IoT where wireless sensors are used to share information throughout a network. IoT is being implemented in homes, agriculture, manufactory, and in the medical field. Disrupting a wireless device from proper communication could potentially result in production loss, security issues, and bodily harm. The 802.15.4/ZigBee protocol is used in low power, low data rate, and low cost wireless applications such as medical devices and home automation devices. This protocol uses CSMA-CA (Carrier Sense Multiple Access w/ Collision Avoidance) which allows for multiple ZigBee devices to transmit simultaneousness and allows for wireless coexistence with the existing protocols at the same frequency band. The CSMA-CA MAC layer seems to introduce an unintentional gap in the reliability of the protocol. By creating a 16-tone signal with center frequencies located in the center of the multiple access channels, all channels will appear to be in use and the ZigBee device will be unable to transmit data. The jamming device will be created using the following hardware implementation. An FPGA connected to a high-speed Digital to Analog Converter will be used to create a digital signal synthesizer device that will create the 16-tone signal. The 16-tone signal will then be mixed up to the 2.4 GHz band, amplified, and radiated using a 2.4 GHz up-converter device. The transmitted jamming signal will cause the ZigBee MAC layer to wait indefinitely for the channel to clear. Since the channel will not clear, the MAC layer will not allow any transmission and the ZigBee devices will not communicate

Flexible 1kV thin-film transistor driving out-of-plane dielectric elastomer actuator

This work demonstrates dielectric elastomer actuators controlled by the world's first thin-film transistors on flexible substrate operating at 1kV, thereby enabling locally switching high-voltages on DEAs using a low control voltage. The high voltages required to drive DEAs limit their integration in complex systems, such as high resolution haptic displays and multiple-degree-of-freedom robotics. We report here a top-gate, thin-film transistor (TFT) with coplanar electrodes specifically designed to drive DEAs. The TFTs are fabricated on flexible polyimide, using solution-processed zinc-tin oxide, offset gate and thick dielectric bilayer of Alumina and Parylene. The TFT switches reliably at up to 1kV, outperforming on this metric all published high-voltage TFTs. The on-off current ratio ranges from 20 to 200, the saturation mobility is 0.1cm2/Vs, and the threshold voltage is 10V. Our DEAs are designed for maximal actuation strain at 1kV, to match the maximal voltage of the TFTs. The DEA is a diaphragm actuator: a suspended non-prestretched membrane with electrodes on both sides. The circular electrode has a 5 mm diameter and the silicone membrane is 17um thick. A backpressure of 50mbar is applied to the membrane. The TFT is wired in parallel with the DEA. A change of out-of-plane displacement of 350um is achieved with 30V applied to the gate, for a circuit bias voltage of 1.4kV. The TFT + DEA operate reliably for several weeks

Flexible Zinc-Tin Oxide Thin Film Transistors Operating at 1 kV for Integrated Switching of Dielectric Elastomer Actuators Arrays

Flexible high-voltage thin- lm transistors (HVTFTs) operating at more than 1 kV are integrated with compliant dielectric elastomer actuators (DEA) to create a exible array of 16 independent actuators. To allow for high-voltage operation, the HVTFT implements a zinc–tin oxide channel, a thick dielectric stack, and an offset gate. At a source–drain bias of 1 kV, the HVTFT has a 20 μA on-current at a gate voltage bias of 30 V. Their electrical characteris- tics enable the switching of DEAs which require drive voltages of over 1 kV, making control of an array simpler in comparison to the use of external high-voltage switching. These HVTFTs are integrated in a flexible haptic display consisting of a 4 × 4 matrix of DEAs and HVTFTs. Using a single 1.4 kV supply, each DEA is independently switched by its associated HVTFT, requiring only a 30 V gate voltage for full DEA de ection. The 4 × 4 display operates well even when bent to a 5 mm radius of curvature. By enabling DEA switching at low voltages, flexible metal-oxide HVTFTs enable complex flexible systems with dozens to hundreds of independent DEAs for applications in haptics, Braille displays, and soft robotics

Loss of hepatic DEPTOR alters the metabolic transition to fasting

Objective The mechanistic target of rapamycin (mTOR) is a serine/threonine kinase that functions into distinct protein complexes (mTORC1 and mTORC2) that regulates growth and metabolism. DEP-domain containing mTOR-interacting protein (DEPTOR) is part of these complexes and is known to reduce their activity. Whether DEPTOR loss affects metabolism and organismal growth in vivo has never been tested. Methods We have generated a conditional transgenic mouse allowing the tissue-specific deletion of DEPTOR. This model was crossed with CMV-cre mice or Albumin-cre mice to generate either whole-body or liver-specific DEPTOR knockout (KO) mice. Results Whole-body DEPTOR KO mice are viable, fertile, normal in size, and do not display any gross physical and metabolic abnormalities. To circumvent possible compensatory mechanisms linked to the early and systemic loss of DEPTOR, we have deleted DEPTOR specifically in the liver, a tissue in which DEPTOR protein is expressed and affected in response to mTOR activation. Liver-specific DEPTOR null mice showed a reduction in circulating glucose upon fasting versus control mice. This effect was not associated with change in hepatic gluconeogenesis potential but was linked to a sustained reduction in circulating glucose during insulin tolerance tests. In addition to the reduction in glycemia, liver-specific DEPTOR KO mice had reduced hepatic glycogen content when fasted. We showed that loss of DEPTOR cell-autonomously increased oxidative metabolism in hepatocytes, an effect associated with increased cytochrome c expression but independent of changes in mitochondrial content or in the expression of genes controlling oxidative metabolism. We found that liver-specific DEPTOR KO mice showed sustained mTORC1 activation upon fasting, and that acute treatment with rapamycin was sufficient to normalize glycemia in these mice. Conclusion We propose a model in which hepatic DEPTOR accelerates the inhibition of mTORC1 during the transition to fasting to adjust metabolism to the nutritional status. Keywords: DEPTOR; mTOR; Liver; Glucose; Fastin

The Hepatokine TSK does not affect brown fat thermogenic capacity, body weight gain, and glucose homeostasis

Objectives Hepatokines are proteins secreted by the liver that impact the functions of the liver and various tissues through autocrine, paracrine, and endocrine signaling. Recently, Tsukushi (TSK) was identified as a new hepatokine that is induced by obesity and cold exposure. It was proposed that TSK controls sympathetic innervation and thermogenesis in brown adipose tissue (BAT) and that loss of TSK protects against diet-induced obesity and improves glucose homeostasis. Here we report the impact of deleting and/or overexpressing TSK on BAT thermogenic capacity, body weight regulation, and glucose homeostasis. Methods We measured the expression of thermogenic genes and markers of BAT innervation and activation in TSK-null and TSK-overexpressing mice. Body weight, body temperature, and parameters of glucose homeostasis were also assessed in the context of TSK loss and overexpression. Results The loss of TSK did not affect the thermogenic activation of BAT. We found that TSK-null mice were not protected against the development of obesity and did not show improvement in glucose tolerance. The overexpression of TSK also failed to modulate thermogenesis, body weight gain, and glucose homeostasis in mice

New genetic loci link adipose and insulin biology to body fat distribution.

Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms

Le financement et l'organisation territoriale de la police de l'eau en France

National audienc

Le bilan d'un contrat de rivière: le cas de la Reyssouze

[fre] En vingt ans, le contrat de rivière est devenu populaire auprès des maîtres d'ouvrage locaux. Il vise à responsabiliser les usagers par le biais d'une gestion de l'eau décentralisée, participative et territoriale. Le contrat de rivière Reyssouze (Ain) étudié dans cet article a effectivement facilité la réalisation d'importants travaux (stations d'épuration, réfection d'ouvrages hydrauliques...). Cependant, la rivière demeure dystrophe et, une partie des agents économiques, n'a pas fondamentalement modifié son comportement vis-à-vis du cours d'eau. L'efficacité des contrats de cette nature demeure limitée en raison de l'inapplication du droit de l'eau dans le domaine agricole. [eng] The assessment of a river agreement: the case of the river Reyssouze - For 20 years, "river contracts " have been widely used in France. They aim at making agents aware of their responsabilities via a decentralized water management. The "river contract Reyssouze" (a river in Ain, France) studied in this paper has led to civil engineering (water purification plants, hydraulic structures...). However, this river is still quite polluted (hypertrophication) and many agents have not modified their behaviour regarding the river. We show that the efficiency of this kind of contract is very limited because of a lack of measures to enforce the laws in the farm sector.

Le bilan d'un contrat de rivière : le cas de la Reyssouze dans l'Ain

International audienc

Endotoxin mediated-iNOS induction causes insulin resistance via ONOO⁻ induced tyrosine nitration of IRS-1 in skeletal muscle.

It is believed that the endotoxin lipopolysaccharide (LPS) is implicated in the metabolic perturbations associated with both sepsis and obesity (metabolic endotoxemia). Here we examined the role of inducible nitric oxide synthase (iNOS) in skeletal muscle insulin resistance using LPS challenge in rats and mice as in vivo models of endotoxemia.Pharmacological (aminoguanidine) and genetic strategies (iNOS⁻/⁻ mice) were used to counter iNOS induction in vivo. In vitro studies using peroxynitrite (ONOO⁻) or inhibitors of the iNOS pathway, 1400 W and EGCG were conducted in L6 myocytes to determine the mechanism by which iNOS mediates LPS-dependent insulin resistance. In vivo, both pharmacological and genetic invalidation of iNOS prevented LPS-induced muscle insulin resistance. Inhibition of iNOS also prevented insulin resistance in myocytes exposed to cytokine/LPS while exposure of myocytes to ONOO⁻ fully reproduced the inhibitory effect of cytokine/LPS on both insulin-stimulated glucose uptake and PI3K activity. Importantly, LPS treatment in vivo and iNOS induction and ONOO⁻ treatment in vitro promoted tyrosine nitration of IRS-1 and reduced insulin-dependent tyrosine phosphorylation.Our work demonstrates that iNOS-mediated tyrosine nitration of IRS-1 is a key mechanism of skeletal muscle insulin resistance in endotoxemia, and presents nitrosative modification of insulin signaling proteins as a novel therapeutic target for combating muscle insulin resistance in inflammatory settings