Homotherapy for heteropathy: Interleukin-41 and its biological functions.

Interleukin-41 (IL-41) is a newly discovered cytokine, named Cometin, Subfatin, meteorin-like transcription (Metrnl), and so forth. It is widely expressed in animals and can exert its biological roles through autocrine and paracrine forms. It has functions such as anti-inflammatory, improving body metabolism, regulating immunity, regulating fat metabolism and participates in the process of autoimmune disease or inflammatory injury. It plays an important role in psoriasis, diabetes, Crohn's disease (CD), osteoarthritis, Kawasaki disease (KD), Graves' disease, autoimmune hepatitis, infertility, obesity, sepsis, cardiovascular diseases and respiratory diseases. This paper reviews the biological functions of IL-41, the relationship between IL-41 and diseases, the effects of IL-41 in the cytokine network and the possible signalling pathways. In order to explore the same target or the same drug for the treatment of different diseases from the perspective of homotherapy for heteropathy, cytokine strategies based on IL-41 have been put forward for the precise treatment of immune diseases and inflammatory diseases. It is worth noting that IL-41 related preparations for lung protection and smoking cessation are interesting research fields.

Heterogeneous optical network and power allocation scheme for inter-CubeSat communication.

In this Letter, the problems of achieving inter-CubeSat communication through radio frequency (RF) and lasers are explained, and the feasibility of using visible light communication to replace RF and lasers is investigated. On this basis, a novel, to the best of our knowledge, heterogeneous optical network with high flexibility is proposed, in which CubeSats are divided into clusters in pairs. CubeSats in each cluster utilize different optical modulation methods to achieve a compromise between optical power efficiency and spectral efficiency, as well as avoid inter-CubeSat interference. Furthermore, under the maximum power and minimum capacity constraints, a closed-form optical power allocation solution minimizing an overall bit error rate (BER) is investigated. Simulation results show that our proposed scheme is more preferred in practical systems and can achieve 3.8 dB gains compared to the conventional power allocation scheme at a BER of 10-4.

Current trends and possibilities of typical microbial protein production approaches: a review.

Global population growth and demographic restructuring are driving the food and agriculture sectors to provide greater quantities and varieties of food, of which protein resources are particularly important. Traditional animal-source proteins are becoming increasingly difficult to meet the demand of the current consumer market, and the search for alternative protein sources is urgent. Microbial proteins are biomass obtained from nonpathogenic single-celled organisms, such as bacteria, fungi, and microalgae. They contain large amounts of proteins and essential amino acids as well as a variety of other nutritive substances, which are considered to be promising sustainable alternatives to traditional proteins. In this review, typical approaches to microbial protein synthesis processes were highlighted and the characteristics and applications of different types of microbial proteins were described. Bacteria, fungi, and microalgae can be individually or co-cultured to obtain protein-rich biomass using starch-based raw materials, organic wastes, and one-carbon compounds as fermentation substrates. Microbial proteins have been gradually used in practical applications as foods, nutritional supplements, flavor modifiers, and animal feeds. However, further development and application of microbial proteins require more advanced biotechnological support, screening of good strains, and safety considerations. This review contributes to accelerating the practical application of microbial proteins as a promising alternative protein resource and provides a sustainable solution to the food crisis facing the world.

Nutrient-rich hydrothermal carbon production by exogenous nutrients combined with seaweed internal water.

As a product of hydrothermal carbonization (HTC) technology, hydrothermal carbon has shown excellent application potential in soil improvement, greenhouse gas reduction and pollution remediation. Since a large amount of water and biomass are directly used as reaction media, hydrothermal carbon produced by traditional HTC possesses poor nutrient properties and accompanied by the generation of toxic and hazardous wastewater. Here, a versatile and easily scalable strategy has been demonstrated for the one-step production of industrial nutrient-rich hydrothermal carbon (NRHC) by combining the exogenous nutrients with seaweed internal water. During the reaction process, exogenous nutrients (NH4H2PO3, KNO3, CO(NH2)2) participated in the HTC reaction and were uniformly distributed on the surface of hydrothermal carbon through surface complexation precipitation, ion exchange, and electrostatic interactions. Simulations based on density functional theory revealed that NRHC produced in presence of exogenous nutrients possessed more active sites and surface charges. Moreover, the adsorbent and adsorbate were simultaneously affected by intermolecular forces, electrostatic forces, and internal energy of the system, and the thermodynamics of adsorption process was more stable. Compared with no exogenous nutrient involvement, NRHC produced by exogenous nutrients showed 2.12, 18.56, and 25.69 times increase in the N, P, and K content. The length of the seed germination root system increased by 4.3-5.9 times, which met the standards set for agricultural fertilizer. Due to increased yield per unit volume and reduced wastewater generation, the cost of NRHC production reduced by 47.83-58.23 per cent and profit enhanced by 1.56-1.68 times, as compared to traditional HTC. This low-cost streamlined process provides a new strategy for large-scale production and direct application of hydrothermal carbon.

Effect of Ginkgo biloba leaves on the removal efficiency of Cr(VI) in soil and its underlying mechanism.

Cr(VI) is a toxic, teratogenic, and carcinogenic heavy metal element in soil that poses major ecological and human health risks. In this study, microcosm tests combined with X-ray absorption near-edge spectra (XANES) and 16Sr DNA amplification techniques were used to explore the effect of Ginkgo biloba leaves on the removal efficiency of Cr(VI) in soil and its underlying mechanism. Ginkgo biloba leaves had a favorable remediation effect on soil varying in Cr(VI) contamination levels, and the optimal effect was observed when 5% Ginkgo biloba leaves were added. The occurrence state of Cr(VI) in soil before and after the addition of Ginkgo biloba leaves was analyzed by XANES, which revealed that Cr(VI) was fully converted to the more biologically innocuous Cr(III), and the hydroxyl-containing quercetin in Ginkgo biloba leaves was one of the primary components mediating this reduction reaction. The Cr(VI) content was significantly lower in non-sterilized soil than in sterilized soil, suggesting that soil microorganisms play a key role in the remediation process. The addition of Ginkgo biloba leaves decreased the α-diversity and altered the ß-diversity of the soil bacterial community. Actinobacteria was the dominant phylum in the soil remediated by Ginkgo biloba leaves; four genera of Cr(VI)-reducing bacteria were also enriched, including Agrococcus, Klebsiella, Streptomyces, and Microbacterium. Functional gene abundances predicted by PICRUST indicated that the expression of glutathione synthesis genes was substantially up-regulated, which might be the main metabolic pathway underlying the mitigation of Cr(VI) toxicity in soil by Cr(VI)-reducing bacteria. In sum, Ginkgo biloba leaves can effectively remove soil Cr(VI) and reduce Cr(VI) to Cr(III) via quercetin in soil, which also functions as a carbon source to drive the production of glutathione via Cr(VI)-reducing bacteria and mitigate Cr(VI) toxicity. The findings of this study elucidate the chemical and microbial mechanisms of Cr(VI) removal in soil by Ginkgo biloba leaves and provide insights that could be used to enhance the remediation of Cr(VI)-contaminated soil.

Increase in hnRNPA1 Expression Suffices to Kill Motor Neurons in Transgenic Rats.

A dominant mutation in hnRNPA1 causes amyotrophic lateral sclerosis (ALS), but it is not known whether this mutation leads to motor neuron death through increased or decreased function. To elucidate the relationship between pathogenic hnRNPA1 mutation and its native function, we created novel transgenic rats that overexpressed wildtype rat hnRNPA1 exclusively in motor neurons. This targeted expression of wildtype hnRNPA1 caused severe motor neuron loss and subsequent denervation muscle atrophy in transgenic rats that recapitulated the characteristics of ALS. These findings demonstrate that the augmentation of hnRNPA1 expression suffices to trigger motor neuron degeneration and the manifestation of ALS-like phenotypes. It is reasonable to infer that an amplification of an as-yet undetermined hnRNPA1 function plays a pivotal role in the pathogenesis of familial ALS caused by pathogenic hnRNPA1 mutation.

Effect of prophylactic use of hydrolyzed protein formula on gastrointestinal diseases and physical growth in preterm infants: a Meta analysis. / é¢„é˜²æ€§ä½¿ç”¨æ°´è§£è›‹ç™½é æ–¹å¥¶å¯¹æ—©äº§å„¿èƒƒè‚ é“ç–¾ç— åŠä½“æ ¼ç”Ÿé•¿å½±å“çš„Meta分析.

OBJECTIVES: To systematically evaluate the effect of prophylactic use of hydrolyzed protein formula on gastrointestinal diseases and physical development in preterm infants. METHODS: A computerized search was performed in the databases including China National Knowledge Infrastructure, Wanfang Data, Weipu, PubMed, Embase, and the Cochrane Library to identify randomized controlled trials of the effect of prophylactic use of hydrolyzed protein formula on gastrointestinal diseases and physical growth in preterm infants. RevMan 5.3 software was used to perform a Meta analysis for the included studies. RESULTS: A total of 7 randomized controlled studies were included. The results of Meta analysis showed that compared with the whole protein formula, the prophylactic use of hydrolyzed protein formula could reduce the risk of neonatal necrotizing enterocolitis (RR=0.40, P=0.04) and feeding intolerance (RR=0.40, P=0.005), and had no significant effect on the growth of weight, length and head circumference (P>0.05). CONCLUSIONS: Compared with the whole protein formula, the prophylactic use of hydrolyzed protein formula in preterm infants may reduce the occurrence of necrotizing enterocolitis and feeding intolerance, and can meet the nutrient requirement of physical development. However, the evidence is limited, and the results of this study cannot support the routine prophylactic use of hydrolyzed protein formula in preterm infants.

Detergent-insoluble inclusion constitutes the first pathology in PFN1 transgenic rats.

Mutation of profilin 1 (PFN1) can cause amyotrophic lateral sclerosis (ALS). To assess how PFN1 mutation causes the disease, we created transgenic rats with human genomic DNA that harbors both the coding and the regulatory sequences of the human PFN1 gene. Selected transgenic lines expressed human PFN1 with or without the pathogenic mutation C71G at a moderate and a comparable level and in the similar pattern of spatial and temporal expression to rat endogenous PFN1. The artificial effects of arbitrary transgene expression commonly observed in cDNA transgenic animals were minimized in PFN1 transgenic rats. Expression of the mutant, but not the wild type, human PFN1 in rats recapitulated the cardinal features of ALS including the progressive loss of motor neurons and the subsequent denervation atrophy of skeletal muscles. Detergent-insoluble PFN1 inclusions were detected as the first pathology in otherwise asymptomatic transgenic rats expressing mutant human PFN1. The findings suggest that protein aggregation is involved in the neurodegeneration of ALS associated with PFN1 mutation. The resulting rat model is useful to mechanistic study on the ALS.

Retracted: Ferruginol Diterpenoid Selectively Inhibits Human Thyroid Cancer Growth by Inducing Mitochondrial Dependent Apoptosis, Endogenous Reactive Oxygen Species (ROS) Production, Mitochondrial Membrane Potential Loss and Suppression of Mitogen-Activated Protein Kinase (MAPK) and PI3K/AKT Signaling Pathways.

An editorial decision has been made to retract this manuscript due to breach of publishing guidelines, following the identification of non-original and manipulated figures. Reference: Guoqing Luo, Jingjing Zhou, Guanjie Li, Ningdong Hu, Xu Xia, Haibo Zhou: Ferruginol Diterpenoid Selectively Inhibits Human Thyroid Cancer Growth by Inducing Mitochondrial Dependent Apoptosis, Endogenous Reactive Oxygen Species (ROS) Production, Mitochondrial Membrane Potential Loss and Suppression of Mitogen-Activated Protein Kinase (MAPK) and PI3K/AKT Signaling Pathways.  Med Sci Monit 2019; 25:2935-2942. 10.12659/MSM.914348.

One-Dimensional Quasiperiodic Mosaic Lattice with Exact Mobility Edges.

The mobility edges (MEs) in energy that separate extended and localized states are a central concept in understanding the localization physics. In one-dimensional (1D) quasiperiodic systems, while MEs may exist for certain cases, the analytic results that allow for an exact understanding are rare. Here we uncover a class of exactly solvable 1D models with MEs in the spectra, where quasiperiodic on-site potentials are inlaid in the lattice with equally spaced sites. The analytical solutions provide the exact results not only for the MEs, but also for the localization and extended features of all states in the spectra, as derived through computing the Lyapunov exponents from Avila's global theory and also numerically verified by calculating the fractal dimension. We further propose a novel scheme with experimental feasibility to realize our model based on an optical Raman lattice, which paves the way for experimental exploration of the predicted exact ME physics.

Biogenic FeS promotes dechlorination and thus de-cytotoxity of trichloroethylene.

Abiotic iron monosulfide (FeS) has attracted growing interests in dechlorinating trichloroethylene (TCE) in anoxic groundwater, but it is still unclear how biogenic FeS affects the dechlorination and thus the cytotoxity of TCE. In this work, a biogenic FeS was synthesized by Shewanella oneidensis MR-1 with addition of ferrihydrite and S0, and it was used for dechlorination of TCE in alkaline environment and the de-cytotoxicity was evaluated by the growth of Synechocystis sp. PCC6803. The results show that the biogenic FeS was of mackinawite, with a loose flower-like mosaic structure. The dechlorination of TCE by the biogenic FeS was accelerated by 6 times than that by abiotic FeS. TCE was dechlorinated mainly by hydrogenolysis to form dichloroethane (C2H2Cl2), vinyl chloride (C2H3Cl), and finally ethylene, accompanied with transformation of both Fe2+ to Fe3+ and monosulfide to disulfide and polysulfide on the biogenic FeS surface. The concentration for 50% of maximal inhibition effect (EC50) of TCE to Synechocystis was 486 mg/L and the inhibition to Synechocystis under the EC50 was relieved more significantly on addition of the biogenic FeS than that of abiotic FeS. These results indicate that the biogenic FeS promoted the dechlorination and thus de-cytotoxity of TCE.

[Efficacy and safety of fluconazole in prophylaxis of invasive fungal infections in very low birth weight infants: a Meta analysis].

OBJECTIVE: To assess the efficacy and safety of fluconazole in the prophylaxis of invasive fungal infection in very low birth weight (VLBW) infants. METHODS: Databases including PubMed, Embase, the Cochrane Library, Wanfang Data, Weipu, and CNKI were searched for randomized controlled trials (RCTs) of prophylactic fluconazole in VLBW infants. Review Manager 5.3 software was used to perform a Meta analysis of the included studies. RESULTS: A total of 12 RCTs were included, involving 1 679 VLBW infants. The Meta analysis showed that prophylactic fluconazole significantly reduced the incidence of invasive fungal infection (RR=0.44, 95%CI: 0.27-0.71, P<0.001), the incidence of fungal colonization (RR=0.31, 95%CI: 0.24-0.40, P<0.001), and the mortality during hospitalization (RR=0.74, 95%CI: 0.58-0.94, P=0.01) compared with the control group. There were no significant differences between VLBW infants using different doses of fluconazole in the incidence of invasive fungal infection and fungal colonization (P>0.05). No significant differences were found in the incidence of fluconazole resistance and complications between the fluconazole and control groups (P>0.05). CONCLUSIONS: Prophylactic fluconazole can effectively and safely prevent invasive fungal infection in VLBW infants, even at a small dose.

Ferruginol Diterpenoid Selectively Inhibits Human Thyroid Cancer Growth by Inducing Mitochondrial Dependent Apoptosis, Endogenous Reactive Oxygen Species (ROS) Production, Mitochondrial Membrane Potential Loss and Suppression of Mitogen-Activated Protein Kinase (MAPK) and PI3K/AKT Signaling Pathways.

BACKGROUND Thyroid cancer causes considerable mortality and morbidity across the globe. Owing to the unavailability of biomarkers and the adverse effects of existing drugs, there is an urgent need to develop efficient chemotherapy for the treatment of thyroid cancers. Plants have served as exceptional source of drugs for the treatment of lethal diseases. The purpose of this study was to evaluate the anticancer effects of ferruginol against thyroid cancer cells. MATERIAL AND METHODS We monitored the cell proliferation rate using 3-(4,5-dimethylthiazol-2-Yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Apoptosis was detected using 4',6-diamidino-2-phenylindole (DAPI), acridine orange/ethidium bromide (AO/EB), and annexin V/propidium iodide (PI) staining. Reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) levels were examined by fluorescence microscopy. Protein expressed was examined by western blotting. RESULTS We found that ferruginol exerted potent antiproliferative action against thyroid cancer cells, and an IC50 of 12 µM was observed for ferruginol against the MDA-T32 cell line. The toxic effects of ferruginol were less pronounced against normal cells. The anticancer effects of ferruginol were likely due to the induction of apoptosis which was also associated with upregulation of Bax and downregulation of Bcl-2. Ferruginol also caused ROS mediated alterations in the MMP of MDA-T32 cells. In MDA-T32 cells, ferruginol might also block the MAPK and PI3K/AKT signaling pathway, which is believed to be an important therapeutic target of anticancer drugs. CONCLUSIONS In conclusion, in view of the results of this study, it might be suggested that ferruginol might serve as an essential lead molecule for the treatment of thyroid cancer provided further in-depth studies especially studying ferruginol toxicological as well as in vivo studies are needed.

Expression of ALS-linked TDP-43 mutant in astrocytes causes non-cell-autonomous motor neuron death in rats.

Mutation of Tar DNA-binding protein 43 (TDP-43) is linked to amyotrophic lateral sclerosis. Although astrocytes have important roles in neuron function and survival, their potential contribution to TDP-43 pathogenesis is unclear. Here, we created novel lines of transgenic rats that express a mutant form of human TDP-43 (M337V substitution) restricted to astrocytes. Selective expression of mutant TDP-43 in astrocytes caused a progressive loss of motor neurons and the denervation atrophy of skeletal muscles, resulting in progressive paralysis. The spinal cord of transgenic rats also exhibited a progressive depletion of the astroglial glutamate transporters GLT-1 and GLAST. Astrocytic expression of mutant TDP-43 led to activation of astrocytes and microglia, with an induction of the neurotoxic factor Lcn2 in reactive astrocytes that was independent of TDP-43 expression. These results indicate that mutant TDP-43 in astrocytes is sufficient to cause non-cell-autonomous death of motor neurons. This motor neuron death likely involves deficiency in neuroprotective genes and induction of neurotoxic genes in astrocytes.

Ionomic and metabolic responses to neutral salt or alkaline salt stresses in maize (Zea mays L.) seedlings.

BACKGROUND: Soil salinity and alkalinity present a serious threat to global agriculture. However, most of the studies have focused on neutral salt stress, and the information on the metabolic responses of plants to alkaline salt stress is limited. This investigation aimed at determining the influence of neutral salt and alkaline salt stresses on the content of metal elements and metabolites in maize plant tissues, by using mixtures of various proportions of NaCl, NaHCO3, Na2SO4, and Na2CO3. RESULTS: We found that alkaline salt stress suppressed more pronouncedly the photosynthesis and growth of maize plants than salinity stress. Under alkaline salt stress conditions, metal ions formed massive precipitates, which ultimately reduced plant nutrient availability. On the other hand, high neutral salt stress induced metabolic changes in the direction of gluconeogenesis leading to the enhanced formation of sugars as a reaction contributing to the mitigation of osmotic stress. Thus, the active synthesis of sugars in shoots was essential to the development of salt tolerance. However, the alkaline salt stress conditions characterized by elevated pH values suppressed substantially the levels of photosynthesis, N metabolism, glycolysis, and the production of sugars and amino acids. CONCLUSIONS: These results indicate the presence of different defensive mechanisms responsible for the plant responses to neutral salt and alkaline salt stresses. In addition, the increased concentration of organic acids and enhanced metabolic energy might be potential major factors that can contribute to the maintenance intracellular ion balance in maize plants and counteract the negative effects of high pH under alkaline salt stress.

Increased Ubqln2 expression causes neuron death in transgenic rats.

Pathogenic mutation of ubiquilin 2 (UBQLN2) causes neurodegeneration in amyotrophic lateral sclerosis and frontotemporal lobar degeneration. How UBQLN2 mutations cause the diseases is not clear. While over-expression of UBQLN2 with pathogenic mutation causes neuron death in rodent models, deletion of the Ubqln2 in rats has no effect on neuronal function. Previous findings in animal models suggest that UBQLN2 mutations cause the diseases mainly through a gain rather than a loss of functions. To examine whether the toxic gain in UBQLN2 mutation is related to the enhancement of UBQLN2 functions, we created new transgenic rats over-expressing wild-type human UBQLN2. Considering that human UBQLN2 may not function properly in the rat genome, we also created transgenic rats over-expressing rat's own Ubqln2. When over-expressed in rats, both human and rat wild-type Ubqln2 caused neuronal death and spatial learning deficits, the pathologies that were indistinguishable from those observed in mutant UBQLN2 transgenic rats. Over-expressed wild-type UBQLN2 formed protein inclusions attracting the autophagy substrate sequestosome-1 and the proteasome component 26S proteasome regulatory subunit 7. These findings suggest that excess UBQLN2 is toxic rather than protective to neurons and that the enhancement of UBQLN2 functions is involved in UBQLN2 pathogenesis. Pathogenic mutation in ubiquilin 2 (UBQLN2) causes neurodegeneration in ALS and FTLD. Studies in rodent models suggest a gain of toxic function in mutant UBQLN2. We created new transgenic rats as a relevant model and examined whether enhancing wild-type UBQLN2 expression is implicated in the pathogenesis of mutant UBQLN2. We observed that over-expression of human or rat wild-type Ubqln2 caused protein aggregation and neuronal death in transgenic rats. Our findings suggest that excess UBQLN2 is toxic rather than protective to neurons and that uncontrolled enhancement of UBQLN2 function is involved in UBQLN2 pathogenesis. Read the Editorial Highlight for this article on page 159.

Visible-Light-Driven Photocatalytic Activation of Inert Sulfur Ylides for 3-Acyl Oxindole Synthesis.

Bicarbonyl-substituted sulfur ylide is a useful, but inert reagent in organic synthesis. Usually, harsh reaction conditions are required for its transformation. For the first time, it was demonstrated that a new, visible-light photoredox catalytic annulation of sulfur ylides under extremely mild conditions, permits the synthesis of oxindole derivatives in high selectivities and efficiencies. The key to its success is the photocatalytic single-electron-transfer (SET) oxidation of the inert amide and acyl-stabilized sulfur ylides to reactive radical cations, which easily proceeds with intramolecular C-H functionalization to give the final products.

The Antitumor Effect of DYC-279 on Human Hepatocellular Carcinoma HepG2 Cells.

DYC-279 is a newly synthesized compound. In this study, we revealed that DYC-279 could inhibit the proliferation of HepG2 cells in a dose- and time-dependent manner using the CCK-8 test. FACS showed that DYC-279 induced a G2/M arrest and apoptosis in a dose-dependent manner. Western blot demonstrated that DYC-279-induced G2/M arrest effect was correlated with the inhibition of cyclin-dependent kinase 1 activity, including a concomitant downregulation of cyclinD1 and cdc2 and upregulation of cyclinB1 in HepG2 cells. DYC-279 also significantly increased the ratio of Bax/Bcl-2, and stimulated the released of cytochrome c into cytosol and also activated caspase-9 and caspase-3, suggesting DYC-279 induced apoptosis via mitochondrial apoptotic pathway. These data support that DYC-279 has anticancer properties in HepG2 cells and may be used as a novel effective reagent in the treatment of human liver cancer.

Reactive astrocytes secrete lcn2 to promote neuron death.

Glial reaction is a common feature of neurodegenerative diseases. Recent studies have suggested that reactive astrocytes gain neurotoxic properties, but exactly how reactive astrocytes contribute to neurotoxicity remains to be determined. Here, we identify lipocalin 2 (lcn2) as an inducible factor that is secreted by reactive astrocytes and that is selectively toxic to neurons. We show that lcn2 is induced in reactive astrocytes in transgenic rats with neuronal expression of mutant human TAR DNA-binding protein 43 (TDP-43) or RNA-binding protein fused in sarcoma (FUS). Therefore, lcn2 is induced in activated astrocytes in response to neurodegeneration, but its induction is independent of TDP-43 or FUS expression in astrocytes. We found that synthetic lcn2 is cytotoxic to primary neurons in a dose-dependent manner, but is innocuous to astrocytes, microglia, and oligodendrocytes. Lcn2 toxicity is increased in neurons that express a disease gene, such as mutant FUS or TDP-43. Conditioned medium from rat brain slice cultures with neuronal expression of mutant TDP-43 contains abundant lcn2 and is toxic to primary neurons as well as neurons in cultured brain slice from WT rats. Partial depletion of lcn2 by immunoprecipitation reduced conditioned medium-mediated neurotoxicity. Our data indicate that reactive astrocytes secrete lcn2, which is a potent neurotoxic mediator.

A Routing Protocol for Multisink Wireless Sensor Networks in Underground Coalmine Tunnels.

Traditional underground coalmine monitoring systems are mainly based on the use of wired transmission. However, when cables are damaged during an accident, it is difficult to obtain relevant data on environmental parameters and the emergency situation underground. To address this problem, the use of wireless sensor networks (WSNs) has been proposed. However, the shape of coalmine tunnels is not conducive to the deployment of WSNs as they are long and narrow. Therefore, issues with the network arise, such as extremely large energy consumption, very weak connectivity, long time delays, and a short lifetime. To solve these problems, in this study, a new routing protocol algorithm for multisink WSNs based on transmission power control is proposed. First, a transmission power control algorithm is used to negotiate the optimal communication radius and transmission power of each sink. Second, the non-uniform clustering idea is adopted to optimize the cluster head selection. Simulation results are subsequently compared to the Centroid of the Nodes in a Partition (CNP) strategy and show that the new algorithm delivers a good performance: power efficiency is increased by approximately 70%, connectivity is increased by approximately 15%, the cluster interference is diminished by approximately 50%, the network lifetime is increased by approximately 6%, and the delay is reduced with an increase in the number of sinks.