A Prediction based Energy-Efficient Tracking Method in Sensor Networks

I. INTRODUCTION Recently, an increasing interest in deploying wireless sensor networks (WSNs) for real-life applications. OTSN is mainly used to track certain objects in a monitored area and to report their position to the application's users. Object tracking, which is also called target tracking, is a major field of research in WSNs and has many real-life applications such as wild life monitoring, security applications for buildings and compounds to avoid interference or trespassing, and international border monitoring for prohibited crossings. Additionally, object tracking is measured one of the most challenging applications in WSNs due to its application requirements, which place a heavy load on the network resources, mainly energy consumption. The main task of an object tracking sensor network (OTSN) is to track a moving object and to report its latest location in the monitored area to the application in an acceptable timely manner, and this dynamic process of sensing and reporting keeps the network's resources under heavy pressure. However, there has been a very limited focus on the energy lost by the computing components, which are referred to as microcontroller unit (MCU) and the sensing components OTSN is considered as one of the most energy-consuming applications of WSNs. Due to this fact, there is a necessity to develop energy-efficient techniques that adhere to the application requirements of an objecttracking system, which reduce the total energy consumption of the OTSN while maintaining a tolerable missing rate level

Group I Metabotropic Glutamate Receptors Modulate Motility and Enteric Neural Activity in the Mouse Colon

Glutamate is the major excitatory neurotransmitter in the central nervous system, and there is evidence that Group-I metabotropic glutamate receptors (mGlu1 and mGlu5) have established roles in excitatory neurotransmission and synaptic plasticity. While glutamate is abundantly present in the gut, it plays a smaller role in neurotransmission in the enteric nervous system. In this study, we examined the roles of Group-I mGlu receptors in gastrointestinal function. We investigated the expression of Grm1 (mGlu1) and Grm5 (mGlu5) in the mouse myenteric plexus using RNAscope in situ hybridization. Live calcium imaging and motility analysis were performed on ex vivo preparations of the mouse colon. mGlu5 was found to play a role in excitatory enteric neurotransmission, as electrically-evoked calcium transients were sensitive to the mGlu5 antagonist MPEP. However, inhibition of mGlu5 activity did not affect colonic motor complexes (CMCs). Instead, inhibition of mGlu1 using BAY 36-7620 reduced CMC frequency but did not affect enteric neurotransmission. These data highlight complex roles for Group-I mGlu receptors in myenteric neuron activity and colonic function

Kif1bp loss in mice leads to defects in the peripheral and central nervous system and perinatal death

Abstract Goldberg-Shprintzen syndrome is a poorly understood condition characterized by learning difficulties, facial dysmorphism, microcephaly, and Hirschsprung disease. GOSHS is due to recessive mutations in KIAA1279, which encodes kinesin family member 1 binding protein (KIF1BP, also known as KBP). We examined the effects of inactivation of Kif1bp in mice. Mice lacking Kif1bp died shortly after birth, and exhibited smaller brains, olfactory bulbs and anterior commissures, and defects in the vagal and sympathetic innervation of the gut. Kif1bp was found to interact with Ret to regulate the development of the vagal innervation of the stomach. Although newborn Kif1bp −/− mice had neurons along the entire bowel, the colonization of the gut by neural crest-derived cells was delayed. The data show an essential in vivo role for KIF1BP in axon extension from some neurons, and the reduced size of the olfactory bulb also suggests additional roles for KIF1BP. Our mouse model provides a valuable resource to understand GOSHS