INTERNET OF VEHICLES-BASED REAL-TIME VEHICLE TRACKING

The leading-edge vehicle tracking and scanning system based on embedded board is intended and executed to observe any vehicle from different locations. Every year, many numbers of vehicles are stolen. To prohibit thievery, a phenomenal type of negator is preowned, like padlock, disk break lock and more which is a defensive motion, but it is not safe for all designs. The main impartial is to initiate a control entity that shows the locale spot of a vehicle proving by global position system (GPS) to find the position. Here, global system for mobile (GSM) is accepting for communicating with the vehicle that easily finding a steal. The entity is built for trying out the mastery of the locale spot that transmits to the user when the motion is in exciting direction and stable in the city and some other areas. This whole entity is built by bringing together a Raspberry Pi with GPS, general packetradio service (GPRS), and GSM. The preferred entity makes better use of unique automation that based on the Raspberry Pi. This entity works on the GPS and GSM SIM 900A modules which consists all the three things for communication. GPS and GPRS circulate the chasing information to the server to transmit the message to the mobile number which is saved in this sector for communicating through GSM. This preferred entity also acquires the traveler's protection by testing liquefied petroleum gas effused gas sensor MQ135 and temperature DS18B20 sensor.Â

Brainstem and Spinal Cord Circuitry Regulating REM Sleep and Muscle Atonia

Previous work has suggested, but not demonstrated directly, a critical role for both glutamatergic and GABAergic neurons of the pontine tegmentum in the regulation of rapid eye movement (REM) sleep.To determine the in vivo roles of these fast-acting neurotransmitters in putative REM pontine circuits, we injected an adeno-associated viral vector expressing Cre recombinase (AAV-Cre) into mice harboring lox-P modified alleles of either the vesicular glutamate transporter 2 (VGLUT2) or vesicular GABA-glycine transporter (VGAT) genes. Our results show that glutamatergic neurons of the sublaterodorsal nucleus (SLD) and glycinergic/GABAergic interneurons of the spinal ventral horn contribute to REM atonia, whereas a separate population of glutamatergic neurons in the caudal laterodorsal tegmental nucleus (cLDT) and SLD are important for REM sleep generation. Our results further suggest that presynaptic GABA release in the cLDT-SLD, ventrolateral periaqueductal gray matter (vlPAG) and lateral pontine tegmentum (LPT) are not critically involved in REM sleep control.These findings reveal the critical and divergent in vivo role of pontine glutamate and spinal cord GABA/glycine in the regulation of REM sleep and atonia and suggest a possible etiological basis for REM sleep behavior disorder (RBD)

Mitochondrial ROS regulate thermogenic energy expenditure and sulfenylation of UCP1

Brown adipose tissue (BAT) can dissipate chemical energy as heat through thermogenic respiration, which requires uncoupling protein 1 (UCP1)1,2. Thermogenesis from BAT and beige adipose can combat obesity and diabetes3, encouraging investigation of factors that control UCP1-dependent respiration in vivo. Herein we show that acutely activated BAT thermogenesis is defined by a substantial increase in mitochondrial reactive oxygen species (ROS) levels. Remarkably, this process supports in vivo BAT thermogenesis, as pharmacological depletion of mitochondrial ROS results in hypothermia upon cold exposure, and inhibits UCP1-dependent increases in whole body energy expenditure. We further establish that thermogenic ROS alter BAT cysteine thiol redox status to drive increased respiration, and Cys253 of UCP1 is a key target. UCP1 Cys253 is sulfenylated during thermogenesis, while mutation of this site desensitizes the purine nucleotide inhibited state of the carrier to adrenergic activation and uncoupling. These studies identify BAT mitochondrial ROS induction as a mechanism that drives UCP1-dependent thermogenesis and whole body energy expenditure, which opens the way to develop improved therapeutic strategies for combating metabolic disorders

Balancing emergency message dissemination and network lifetime in wireless body area network using ant colony optimization and Bayesian game formulation

Nowadays, Wireless Body Area Network (WBAN) is emerging very fast and so many new methods and algorithms are coming up for finding the optimal path for disseminating emergency messages. Ant Colony Optimization (ACO) is one of the cultural algorithms for solving many hard problems such as Travelling Salesman Problem (TSP). ACO is a natural behaviour of ants, which work stochastically with the help of pheromone trails deposited in the shortest route to find their food. This optimization procedure involves adapting, positive feedback and inherent parallelism. Each ant will deposit certain amount of pheromone in the tour construction it makes searching for food. This type of communication is known as stigmetric communication. In addition, if a dense WBAN environment prevails, such as hospital, i.e. in the environment of overlapping WBAN, game formulation was introduced for analyzing the mixed strategy behaviour of WBAN. In this paper, the ant colony optimization approach to the travelling salesman problem was applied to the WBAN to determine the shortest route for sending emergency message to the doctor via sensor nodes; and also a static Bayesian game formulation with mixed strategy was analysed to enhance the network lifetime. Whenever the patient needs any critical care or any other medical issue arises, emergency messages will be created by the WBAN and sent to the doctor's destination. All the modes of communication were realized in a simulation environment using OMNet++. The authors investigated a balanced model of emergency message dissemination and network lifetime in WBAN using ACO and Bayesian game formulation. Keywords: Wireless body area network, Ant colony optimization, Bayesian game model, Sensor network, Message latency, Network lifetim

Wavelet Based Contourlet Transform for Image Compression

Wavelet transforms are not capable of reconstructing curved images perfectly, hence we go for this new concept, called Contourlet Transform. It is a multiresolution and directional decomposition of a signal using a combination of Laplacian Pyramid (LP) and a Directional Filter Bank (DFB). The Contourlet transform has good approximation properties for smooth 2D functions and finds a direct discrete-space construction, and is therefore computationally efficient. Recently introduced the wavelet-based contourlet transform (WBCT), it is a non-redundant version of the contourlet transform, and appropriately used this transform for image coding. In this work, we start with a discretedomain construction and then investigate its convergence to an expansion in the continuous-domain. This construction results in a flexible multiresolution, local, and directional image expansion using contour segments, and thus it is named the contourlet transform. Furthermore, a precise link between the developed filter bank and the associated continuous – domain contourlet expansion via a directional multiresolution analysis framework is established. Our simulation results also show that this new coding approach is competitive to the wavelet coder and is visually superior to the wavelet coder for the mentioned images. The original Contourlet Transform has high redundancy, in order to reduce that we have used wavelet transform followed by Directional Filter Bank

Evaluation of electronic properties, molecular profiling, bioactivity score, anti-microbial activity and quantum computational studies on methyl (2E)-2-{[N-(2-formylphenyl)(4-methylbenzene)sulfonamide]methyl}-3-[4-(propan-2-yl)phenyl]prop-2-enoate

This analysis was conducted to evaluate the electronic properties and biological significance of the headline molecule. By means of DFT method, geometrical, vibrational and biological properties of the headline molecule were evaluated which is an efficient means of determining structure and has a wide range of applications in the field of biological vibrational spectroscopy. Calculating the interaction energy and electron density is carried out via NBO, while determining the energetic site of the molecule is done via Molecular Electrostatic Potential (MEP) and HOMO-LUMO analysis. In this work, calculated the biological activity and drug similarity parameters of the headline compound to design new molecules with good pharmacological characteristics and this investigation will provide leading information

Recurring circadian disruption alters circadian clock sensitivity to resetting

A single phase advance of the light:dark (LD) cycle can temporarily disrupt synchrony of neural circadian rhythms within the suprachiasmatic nucleus (SCN) and between the SCN and peripheral tissues. Compounding this, modern life can involve repeated disruptive light conditions. To model chronic disruption to the circadian system, we exposed male mice to more than a month of a 20 h light cycle (LD10:10), which mice typically cannot entrain to. Control animals were housed under LD12:12. We measured locomotor activity and body temperature rhythms in vivo, and rhythms of PER2::LUC bioluminescence in SCN and peripheral tissues ex vivo. Unexpectedly, we discovered strong effects of the time of dissection on circadian phase of PER2::LUC bioluminescent rhythms, which varied across tissues. White adipose tissue was strongly reset by dissection, while thymus phase appeared independent of dissection timing. Prior light exposure impacted the SCN, resulting in strong resetting of SCN phase by dissection for mice housed under LD10:10, and weak phase shifts by time of dissection in SCN from control LD12:12 mice. These findings suggest that exposure to circadian disruption may desynchronize SCN neurons, increasing network sensitivity to perturbations. We propose that tissues with a weakened circadian network, such as the SCN under disruptive light conditions, or with little to no coupling, e.g., some peripheral tissues, will show increased resetting effects. In particular, exposure to light at inconsistent circadian times on a recurring weekly basis disrupts circadian rhythms and alters sensitivity of the SCN neural pacemaker to dissection time

Activation of the GABAergic Parafacial Zone Maintains Sleep and Counteracts the Wake-Promoting Action of the Psychostimulants Armodafinil and Caffeine

We previously reported that acute and selective activation of GABA-releasing parafacial zone (PZVgat) neurons in behaving mice produces slow-wave-sleep (SWS), even in the absence of sleep deficit, suggesting that these neurons may represent, at least in part, a key cellular substrate underlying sleep drive. It remains, however, to be determined if PZVgat neurons actively maintain, as oppose to simply gate, SWS. To begin to experimentally address this knowledge gap, we asked whether activation of PZVgat neurons could attenuate or block the wake-promoting effects of two widely used wake-promoting psychostimulants, armodafinil or caffeine. We found that activation of PZVgat neurons completely blocked the behavioral and electrocortical wake-promoting action of armodafinil. In some contrast, activation of PZVgat neurons inhibited the behavioral, but not electrocortical, arousal response to caffeine. These results suggest that: (1) PZVgat neurons actively maintain, as oppose to simply gate, SWS and cortical slow-wave-activity; (2) armodafinil cannot exert its wake-promoting effects when PZVgat neurons are activated, intimating a possible shared circuit/molecular basis for mechanism of action; (3) caffeine can continue to exert potent cortical desynchronizing, but not behavioral, effects when PZVgat neurons are activated, inferring a shared and divergent circuit/molecular basis for mechanism of action; and 4) PZVgat neurons represent a key cell population for SWS induction and maintenance