Energy consumption is the core issue in wireless sensor networks (WSN). To generate a node energy model that can accurately reveal the energy consumption of sensor nodes is an extremely important part of protocol development, system design and performance evaluation in WSNs. In this paper, by studying component energy consumption in different node states and within state transitions, the authors present the energy models of the node core components, including processors, RF modules and sensors. Furthermore, this paper reveals the energy correlations between node components, and then establishes the node energy model based on the event-trigger mechanism. Finally, the authors simulate the energy models of node components and then evaluate the energy consumption of network protocols based on this node energy model. The proposed model can be used to analyze the WSNs energy consumption, to evaluate communication protocols, to deploy nodes and then to construct WSN applications
Traumatic brain injury (TBI) is one of the leading causes of neurological disability in young adults. Edaravone, a novel synthetic small-molecule free-radical scavenger, has been shown to have a neuroprotective effect in both animal models of cerebral ischemia and stroke patients; however, the underlying mechanism is poorly understood. In this report, we investigated the potential mechanisms of edaravone treatment in a rat model of TBI. TBI was induced in the right cerebral cortex of male adult rats using Feeney's weight-drop method. Edaravone (0.75, 1.5, or 3 mg/kg) or vehicle (normal saline) was intravenously administered at 2 and 12 h after TBI. Edaravone treatment significantly decreased hippocampal CA3 neuron loss, reduced oxidative stress, and decreased neuronal programmed cell death compared to vehicle treatment. The protective effects of edaravone treatment were also related to the pathology of TBI on non-neuronal cells, as edaravone decreased astrocyte and glial activation. Lastly, edaravone treatment significantly reduced the presence of inflammatory cytokines, cerebral edema, blood-brain barrier (BBB) permeability, and, importantly, neurological deficits following TBI. Our results suggest that edaravone exerts a neuroprotective effect in the rat model of TBI. The likely mechanism is via inhibiting oxidative stress, leading to a decreased inflammatory response and glial activation, and thereby reducing neuronal death and improving neurological function.
The effects of melatonin on the mitochondrial DNA (mtDNA) damage induced by 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridine ion (MPP(+)) were investigated both in vivo and in vitro. MPTP (24 mg/kg, s.c.) induced a rapid increase in the immunoreactivity of 8-hydroxyguanine (8-oxoG), a common biomarker of DNA oxidative damage, in the cytoplasm of neurons in the Substantia Nigra Compact of mouse brain. Melatonin preinjection (7.5, 15 or 30 mg/kg, i.p.) dose-dependently prevented MPTP-induced DNA oxidative damage. In SH-SY5Y cells, MPP(+) (1 mm) increased the immunoreactivity of 8-oxoG in the mitochondria at 1 hr and in the nucleus at 3 hr after treatment. Melatonin (200 microm) preincubation significantly attenuated MPP(+)-induced mtDNA oxidative damage. Furthermore, MPP(+) time-dependently increased the accumulation of mitochondrial oxygen free radicals (mtOFR) from 1 to 24 hr and gradually decreased the mitochondrial membrane potential (Psim) from 18 to 36 hr after incubation. At 72 hr after incubation, MPP(+) caused cell death in 49% of the control. However, melatonin prevented MPP(+)-induced mtOFR generation and Psim collapse, and later cell death. The present results suggest that cytoprotection of melatonin against MPTP/MPP(+)-induced cell death may be associated with the attenuation of mtDNA oxidative damage via inhibition of mtOFR generation and the prevention of Psim collapse.
Owing to the wide use of novel nanoparticles (NPs) such as zinc oxide (ZnO) in all aspects of life, toxicological research on ZnO NPs is receiving increasing attention in these days. In this study, the toxicity of ZnO NPs in a human pulmonary adenocarcinoma cell line LTEP-a-2 was tested in vitro. Log-phase cells were exposed to different levels of ZnO NPs for hours, followed by colorimetric cell viability assay using tetrazolium salt and cell survival rate assay using trypan blue dye. Cell morphological changes were observed by Giemsa staining and light microscopy. Apoptosis was detected by using fluorescence microscopy and caspase-3 activity assay. Both intracellular reactive oxygen species (ROS) and reduced glutathione (GSH) were examined by a microplate-reader method. Results showed that ZnO NPs (≥0.01 μg/mL) significantly inhibited proliferation (P < 0.05) and induced substantial apoptosis in LTEP-a-2 cells after 4 h of exposure. The intracellular ROS level rose up to 30–40% corresponding to significant depletion (approximately 70–80%) in GSH content in LTEP-a-2 cells (P < 0.05), suggesting that ZnO NPs induced apoptosis mainly through increased ROS production. This study elucidates the toxicological mechanism of ZnO NPs in human pulmonary adenocarcinoma cells and provides reference data for application of nanomaterials in the environment.
This paper takes 516 households who planted wheat in Heyang County, Shaanxi Province in 2018, as samples to construct three policy environments: Technological guidance for planting, subsidies for organic fertilizer application, and agricultural tailwater discharge standards. The experimental choice method was used to empirically analyze policy preferences during the process of fertilizer reduction. The results indicate that households show different preferences for the three policy settings: The fertilizer application rate is reduced by 6.98% if providing full technological guidance for farmers throughout the wheat planting process and is reduced by 5.18% under the background of providing appropriate organic fertilizer subsidies. The agricultural tailwater discharge standards have the least impact on the reducing level of chemical fertilizer application, with decreasing amounts of only 1.85% and 0.77% under the second-level and the first-level agricultural tailwater discharge standards, respectively. These results indicate that households in Heyang County, Shaanxi Province, demonstrate a low willingness to accept the agricultural tailwater discharge standards in order to cut down on the amount of chemical fertilizer application and the agricultural non-point source pollution. Therefore, compared with a compounded annual growth rate (CAGR) of 1% of fertilizer usage nationwide according to the Chinese Ministry of Agriculture, given the current planting environment and policies design, providing comprehensive technological guidance as well as price subsidies for the organic fertilizer can significantly and robustly reduce the excessive application of fertilizer in Heyang County, Shaanxi Province, under the best scenario, thereby further alleviating agricultural non-point source pollution.
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