Adaptive real-time routing protocol for (M,k)-firm in industrial wireless multimedia sensor networks

© 2020 by the authors. Licensee MDPI, Basel, Switzerland. Many applications are able to obtain enriched information by employing a wireless multimedia sensor network (WMSN) in industrial environments, which consists of nodes that are capable of processing multimedia data. However, as many aspects of WMSNs still need to be refined, this remains a potential research area. An efficient application needs the ability to capture and store the latest information about an object or event, which requires real-time multimedia data to be delivered to the sink timely. Motivated to achieve this goal, we developed a new adaptive QoS routing protocol based on the (m,k)-firm model. The proposed model processes captured information by employing a multimedia stream in the (m,k)-firm format. In addition, the model includes a new adaptive real-time protocol and traffic handling scheme to transmit event information by selecting the next hop according to the flow status as well as the requirement of the (m,k)-firm model. Different from the previous approach, two level adjustment in routing protocol and traffic management are able to increase the number of successful packets within the deadline as well as path setup schemes along the previous route is able to reduce the packet loss until a new path is established. Our simulation results demonstrate that the proposed schemes are able to improve the stream dynamic success ratio and network lifetime compared to previous work by meeting the requirement of the (m,k)-firm model regardless of the amount of traffic

An enhanced mobility and temperature aware routing protocol through multi-criteria decision making method in wireless body area networks

© 2018 by the authors. In wireless body area networks, temperature-aware routing plays an important role in preventing damage of surrounding body tissues caused by the temperature rise of the nodes. However, existing temperature-aware routing protocols tend to choose the next hop according to the temperature metric without considering transmission delay and data loss caused by human posture. To address this problem, multiple research efforts exploit different metrics such as temperature, hop count and link quality. Because their approaches are fundamentally based on simple computation through weighted factor for each metric, it is rarely feasible to obtain reasonable weight value through experiments. To solve this problem, we propose an enhanced mobility and temperature-aware routing protocol based on the multi-criteria decision making method. The proposed protocol adopts the analytical hierarchy process and simple additive weighting method to assign suitable weight factors and choose the next hop while considering multiple routing criteria. Simulation results are presented to demonstrate that the proposed protocol can efficiently improve transmission delay and data loss better than existing protocols by preventing the temperature rise on the node

Sepsis-Like Systemic Inflammation Induced by Nano-Sized Extracellular Vesicles From Feces

Nano-sized extracellular vesicles (EVs), including exosomes, microvesicles, and other types of vesicles, are released by most mammalian cells and bacteria. We here ask whether feces contain EVs of mammalian and/or bacterial origin, and whether these EVs induce systemic inflammation. Fecal extracellular vesicles (fEVs) were isolated from mice and humans. The presence of EVs from Gram-negative and Gram-positive bacteria was detected by enzyme-linked immunosorbent assay using anti-lipid A and anti-lipoteichoic acid antibodies, whereas Western blot using anti-beta-actin antibody was employed to detect host-derived EVs in the fEVs. Further, fEVs were administered into mice by intraperitoneal injection, and inflammatory responses were investigated in the peritoneum, blood, and lungs. The role of TLR2 and TLR4 were studied using knockout mice. Significant quantities of EVs were present in feces from mice as well as humans, and derived from Gram-negative and Gram-positive bacteria, as well as the host. Bacteria-free fEVs introduced into the peritoneum induced local and systemic inflammation (including in the lungs), but fEVs from germ-free animals had weaker effects. This pronounced local and systemic inflammatory responses seemed to be induced by EVs from both Gram-negative and Gram-positive bacteria, and was attenuated in mice lacking TLR2 or TLR4. Our findings show that fEVs cause sepsis-like systemic inflammation, when introduced intraperitoneally, a process regulated by TLR2 and TLR4.11Ysciescopu

Superparamagnetic Iron Oxide Nanoparticles Coated with Galactose-Carrying Polymer for Hepatocyte Targeting

Our goal is to develop the functionalized superparamagnetic iron oxide nanoparticles (SPIONs) demonstrating the capacities to be delivered in liver specifically and to be dispersed in physiological environment stably. For this purpose, SPIONs were coated with polyvinylbenzyl-O-β-D-galactopyranosyl-D-gluconamide (PVLA) having galactose moieties to be recognized by asialoglycoprotein receptors (ASGP-R) on hepatocytes. For use as a control, we also prepared SPIONs coordinated with 2-pyrrolidone. The sizes, size distribution, structure, and coating of the nanoparticles were characterized by transmission electron microscopy (TEM), electrophoretic light scattering spectrophotometer (ELS), X-ray diffractometer (XRD), and Fourier transform infrared (FT-IR), respectively. Intracellular uptake of the PVLA-coated SPIONs was visualized by confocal laser scanning microscopy, and their hepatocyte-specific delivery was also investigated through magnetic resonance (MR) images of rat liver. MRI experimental results indicated that the PVLA-coated SPIONs possess the more specific accumulation property in liver compared with control, which suggests their potential utility as liver-targeting MRI contrast agent

Autism-like behavior caused by deletion of vaccinia-related kinase 3 is improved by TrkB stimulation

Vaccinia-related kinases (VRKs) are multifaceted serine/threonine kinases that play essential roles in various aspects of cell signaling, cell cycle progression, apoptosis, and neuronal development and differentiation. However, the neuronal function of VRK3 is still unknown despite its etiological potential in human autism spectrum disorder (ASD). Here, we report that VRK3-deficient mice exhibit typical symptoms of autism-like behavior, including hyperactivity, stereotyped behaviors, reduced social interaction, and impaired context-dependent spatial memory. A significant decrease in dendritic spine number and arborization were identified in the hippocampus CA1 of VRK3-deficient mice. These mice also exhibited a reduced rectification of AMPA receptor-mediated current and changes in expression of synaptic and signaling proteins, including tyrosine receptor kinase B (TrkB), Arc, and CaMKII alpha. Notably, TrkB stimulation with 7,8-dihydroxyflavone reversed the altered synaptic structure and function and successfully restored autism-like behavior in VRK3-deficient mice. These results reveal that VRK3 plays a critical role in neurodevelopmental disorders and suggest a potential therapeutic strategy for ASD.112Ysciescopu

Non-Dioxin-Like Polychlorinated Biphenyls Inhibit G-Protein Coupled Receptor-Mediated Ca2+ Signaling by Blocking Store-Operated Ca2+ Entry

Polychlorinated biphenyls (PCBs) are ubiquitous pollutants which accumulate in the food chain. Recently, several molecular mechanisms by which non-dioxin-like (NDL) PCBs mediate neurodevelopmental and neurobehavioral toxicity have been elucidated. However, although the G-protein coupled receptor (GPCR) is a significant target for neurobehavioral disturbance, our understanding of the effects of PCBs on GPCR signaling remains unclear. In this study, we investigated the effects of NDL-PCBs on GPCR-mediated Ca2+ signaling in PC12 cells. We found that ortho-substituted 2,2', 6-trichlorinated biphenyl (PCB19) caused a rapid decline in the Ca2+ signaling of bradykinin, a typical Gq-and phospholipase C beta-coupled GPCR, without any effect on its inositol 1,4,5-trisphosphate production. PCB19 reduced thapsigargin-induced sustained cytosolic Ca2+ levels, suggesting that PCB19 inhibits SOCE. The abilities of other NDL-PCBs to inhibit store-operated Ca2+ entry (SOCE) were also examined and found to be of similar potencies to that of PCB19. PCB19 also showed a manner equivalent to that of known SOCE inhibitors. PCB19-mediated SOCE inhibition was confirmed by demonstrating the ability of PCB19 to inhibit the SOCE current and thapsigargin-induced Mn2+ influx. These results imply that one of the molecular mechanism by which NDL-PCBs cause neurobehavioral disturbances involves NDL-PCB-mediated inhibition of SOCE, thereby interfering with GPCR-mediated Ca2+ signaling.1142Ysciescopu

A Protein Profile of Visceral Adipose Tissues Linked to Early Pathogenesis of Type 2 Diabetes Mellitus

Adipose tissue is increasingly recognized as an endocrine organ playing important pathophysiological roles in metabolic abnormalities, such as obesity, cardiovascular disease, and type 2 diabetes mellitus (T2DM). In particular, visceral adipose tissue (VAT), as opposed to subcutaneous adipose tissue, is closely linked to the pathogenesis of insulin resistance and T2DM. Despite the importance of VAT, its molecular signatures related to the pathogenesis of T2DM have not been systematically explored. Here, we present comprehensive proteomic analysis of VATs in drug-naïve early T2DM patients and subjects with normal glucose tolerance. A total of 4,707 proteins were identified in LC-MS/MS experiments. Among them, 444 increased in abundance in T2DM and 328 decreased. They are involved in T2DM-related processes including inflammatory responses, peroxisome proliferator-activated receptor signaling, oxidative phosphorylation, fatty acid oxidation, and glucose metabolism. Of these proteins, we selected 11 VAT proteins that can represent alteration in early T2DM patients. Among them, up-regulation of FABP4, C1QA, S100A8, and SORBS1 and down-regulation of ACADL and PLIN4 were confirmed in VAT samples of independent early T2DM patients using Western blot. In summary, our profiling provided a comprehensive basis for understanding the link of a protein profile of VAT to early pathogenesis of T2DM. © 2014 by The American Society for Biochemistry and Molecular Biology, Inc.1

Bacteriological investigation of ground water sources in selected urban areas of district Mardan, Khyber Pakhtunkhwa, Pakistan

Microbial contamination of ground water sources is a common problem in all the big cities, which endangers health and impairs quality of living . To assess this, 39 water samples were collected from highly populated 13 union councils from the urban area of district Mardan. Faecal coliform and Escherichia coli were investigated both qualitatively and quantitatively. Qualitative study showed that faecal coliform was found in 90% samples and E. coli in 56% samples. Quantitatively, faecal coliform most probable number (MPN) was ranging from 1601 to 2400 for about 28% samples, followed by 551 to 1600 and 201 to 550 for 20% samples each, 40 to 200 for 18% samples and less than 40 for about 13% samples. The major cause of the bacteriological contamination was found to be the extent of susceptibility of the water sources to intrusions from the nearest contamination source.Keywords: Mardan, urban area, microbial contamination, faecal coliform, ground water, Escherichia col

Activation of PERK Signaling Attenuates Aβ-Mediated ER Stress

Alzheimer's disease (AD) is characterized by the deposition of aggregated beta-amyloid (Aβ), which triggers a cellular stress response called the unfolded protein response (UPR). The UPR signaling pathway is a cellular defense system for dealing with the accumulation of misfolded proteins but switches to apoptosis when endoplasmic reticulum (ER) stress is prolonged. ER stress is involved in neurodegenerative diseases including AD, but the molecular mechanisms of ER stress-mediated Aβ neurotoxicity still remain unknown. Here, we show that treatment of Aβ triggers the UPR in the SK-N-SH human neuroblastoma cells. Aβ mediated UPR pathway accompanies the activation of protective pathways such as Grp78/Bip and PERK-eIF2α pathway, as well as the apoptotic pathways of the UPR such as CHOP and caspase-4. Knockdown of PERK enhances Aβ neurotoxicity through reducing the activation of eIF2α and Grp8/Bip in neurons. Salubrinal, an activator of the eIF2α pathway, significantly increased the Grp78/Bip ER chaperone resulted in attenuating caspase-4 dependent apoptosis in Aβ treated neurons. These results indicate that PERK-eIF2α pathway is a potential target for therapeutic applications in neurodegenerative diseases including AD