Early Detection of Pipeline Natural Gas Leakage from Hyperspectral Imaging by Vegetation Indicators and Deep Neural Networks.

The timely detection of underground natural gas (NG) leaks in pipeline transmission systems presents a promising opportunity for reducing the potential greenhouse gas (GHG) emission. However, existing techniques face notable limitations for prompt detection. This study explores the utility of Vegetation Indicators (VIs) to reflect vegetation health deterioration, thereby representing leak-induced stress. Despite the acknowledged potential of VIs, their sensitivity and separability remain understudied. In this study, we employed ground vegetation as biosensors for detecting methane emissions from underground pipelines. Hyperspectral imaging from vegetation was collected weekly at both plant and leaf scales over two months to facilitate stress detection using VIs and Deep Neural Networks (DNNs). Our findings revealed that plant pigment-related VIs, modified chlorophyll absorption reflectance index (MCARI), exhibit commendable sensitivity but limited separability in discerning stressed grasses. A NG-specialized VI, the optimized soil-adjusted vegetation index (OSAVI), demonstrates higher sensitivity and separability in early detection of methane leaks. Notably, the OSAVI proved capable of discriminating vegetation stress 21 days after methane exposure initiation. DNNs identified the methane leaks following a 3-week methane treatment with an accuracy of 98.2%. DNN results indicated an increase in visible (VIS) and a decrease in near-infrared (NIR) in spectra due to methane exposure.

Extracorporeal Carbon Dioxide Removal in Patients with Acute Respiratory Distress Syndrome or Chronic Obstructive Pulmonary Disease: A Systematic Review and Meta-Analysis.

BACKGROUND: Extracorporeal carbon dioxide removal (ECCO2R) was used to prevent invasive mechanical ventilation and associated mechanical damage in patients with acute respiratory distress syndrome (ARDS). OBJECTIVES: This study aimed to investigate the efficacy and safety of ECCO2R treatment in patients with ARDS or chronic obstructive pulmonary disease (COPD). METHODS: MEDLINE, EMBASE, and the Cochrane Library were systematically searched for relevant studies that reported patient prognosis, blood gas parameters, and ECCO2R-related adverse events (AEs) published as of September 2020. Odds ratios (ORs), weighted mean differences (WMDs), and their corresponding 95% confidence intervals (CIs) were used to compare the outcomes. RESULTS: Fifteen studies involving 532 ARDS or COPD patients were included. Compared with controls, ECCO2R did not influence the 28-day mortality (OR = 0.73, 95% CI: 0.28-1.87, p = 0.51), the length of hospital stay (WMD = 3.34, 95% CI: -5.22 to 11.90, p = 0.444), and the length of intensive care unit stay (WMD = -0.39, 95% CI: -8.76 to 7.99, p = 0.928). Compared with baseline values, partial pressure of carbon dioxide (PaCO2) in the ECCO2R group was significantly reduced, while the ratio of arterial oxygen partial pressure to fractional inspired oxygen (PaO2/FiO2) and pH increased. The overall rate of ECCO2R-related AEs was 35% (95% CI: 17-53%, p < 0.001), and bleeding was the most common AE with a rate of 22% (95% CI: 13-31%, p = 0.002). The rate of ECCO2R-related deaths was low. CONCLUSIONS: In conclusion, there was no statistically significant difference in the prognosis of patients with and without ECCO2R treatment. ECCO2R significantly reduced PaCO2 and improved PaO2/FiO2 and pH values in patients with ARDS or COPD. Bleeding was the most common ECCO2R-related AE.

Clinical and Epidemiological Characteristics of Rhabdomyolysis: A Retrospective Study.

Background: Rhabdomyolysis (RM) refers to a clinical syndrome in which muscle cells are damaged by various causes and the clinical manifestations are mainly muscle pain, weakness, and dark urine. Acute kidney injury (AKI) is a serious complication of RM with complex mechanisms and high mortality. Therefore, understanding the pathogenesis and clinical manifestations, early diagnosis and treatment of RM are crucial to improve its prognosis. Method: Analysis of medical records of RM patients admitted to Tianjin Medical University General Hospital from October 2019 to October 2022. Statistical software SPSS 25.0 was used to analyze the data. The risk factors of RM-complicated AKI were analyzed by logistic regression. The receiver operating characteristic (ROC) curve was plotted, the area under the curve (AUC) was calculated, and the optimal cutoff value was determined by the Youden index. P < 0.05 indicates a statistically significant difference between the groups. Result: Among the 71 patients, the median age of the patients was 53.0 (30.0, 71.0) years and was 2.5 times higher in men than in women. Infection was the most common etiology. History of alcohol consumption, CK, and creatinine were independent influencing factors for AKI due to RM. Logistic regression analysis showed that CK combined with creatinine had a better predictive value than the single index. Conclusion: Our study revealed the clinical and laboratory characteristics of RM in the population attending the Tianjin Medical University General Hospital in the last three years, which is a reference for future multicenter, prospective studies.

4-Methylcytosine distribution follows the power function in Geobacter sulfurreducens genome.

Single-molecule real-time DNA sequencing revealed that 4-methylcytosine (m4C) commonly exists in bacterial genomes. In this work, samples with different m4C methylation patterns were studied. Results reveal that m4C modification is a biochemical reaction with distance effect, and its distribution follows the power function in the positive, negative, and double strands of genomic DNA sequences of Geobacter sulfurreducens. Furthermore, the value of regression coefficient in the fitting formula for double strands was the sum of those in the fitting formulae for positive and negative strands. Meanwhile, the value of exponent coefficient was the average, implicating an interesting mathematical phenomenon about power function. Considering the potent role of m4C in gene expression and the present results being obtained from the same genomic DNA sequence, this work suggests that the patterns of m4C distribution may be served as a signal for G. sulfurreducens to rapidly identify the genes to respond to environmental stresses or signals. This study opens a new avenue to extend our knowledge about the modification mechanisms and the epigenetic information of m4C modification in prokaryotes.

Methylome and Metabolome Analyses Reveal Adaptive Mechanisms in Geobacter sulfurreducens Grown on Different Terminal Electron Acceptors.

The Geobacter species evolved respiratory versatility to utilize a wide range of terminal electron acceptors. To explore this adaptive mechanism, Fe(III) citrate, hydrous ferric oxide, and fumarate were selected as electron acceptors, and the methylome and metabolome of Geobacter sulfurreducens PCA grown on each electron acceptor were investigated via third-generation, single-molecule real-time DNA sequencing and gas chromatography/time-of-flight mass spectrometry-based metabolomics, respectively. Results showed that the patterns of 4-methylcytosine (m4C) and 6-methyladenine (m6A) modification, the concentrations of fatty acids (e.g., caprylic acid, capric acid, and squalene), and the activity of antioxidant enzymes (e.g., superoxide dismutase, catalase, and glutathione reductase) were all varied in different electron acceptor cultures. Moreover, genes (e.g., GSU0466 and GSU1467) with low expression levels generally had high methylation levels. These findings suggest that m4C and m6A modifications, fatty acids, and antioxidant enzymes all play a role in the adaptation of G. sulfurreducens to diverse electron acceptors, and DNA methylation may be involved in the adaptation mainly via gene expression regulation.

Transcriptomic analysis reveals the molecular mechanism of Alzheimer-related neuropathology induced by sevoflurane in mice.

Anesthetics could induce cognitive dysfunctions, such as Alzheimer's disease in humans or mice. However, the precise molecular mechanism is unclear. Sevoflurane is a common anesthetic widely used in clinical practice. Here, we demonstrated the induction of cognitive dysfunction induced by Sev in mice to corroborate the signaling pathway and the differentially expressed genes (DEGs) followed by analyzing their functions. The cognitive function of mice was measured by the Morris water maze test. Transcriptomic data were annotated with Illumina HiSeq. 2000. Further, the changes in related proteins or genes were analyzed by western blotting and real-time quantitative polymerase chain reaction. Our results showed that Sev could cause a decline in cognitive competence in mice. The transcriptomic data indicated that adding up to 566 genes were upregulated and 1073 genes were downregulated. The genes of Plin4, Lcn2, Lrg1, Foxf1, and Ctla2a were significantly upregulated, while the genes of Arc, Npas4, Egr2, Hes5, and Cdh9 were downregulated dramatically. The Gene Ontology term with the highest enrichment of DEGs are involved in the regulation of cellular and macromolecule metabolism and cation and nucleic acid binding, respectively. The Kyoto encyclopedia of genes and genomes analysis indicated that the mitogen-activated protein kinases (MAPK) pathway was one of the most important metabolic pathways. In addition, the metabolic pathways related to cognitive function, such as the nervous system and neurodegenerative disease showed significant changes. Furthermore, we found that p38, c-Jun N-terminal kinase, and extracellular signal-regulated kinase of the MAPK signaling pathway played important roles in this process. In conclusion, these results provide the first important clues for identifying the DEGs and signaling pathways in the hippocampus due to a Sev-induced cognitive deficiency in mice.

Geobacter sulfurreducens-inoculated bioelectrochemical system reveals the potential of metabolic current in defining the effect of extremely low-frequency electromagnetic field on living cells.

The effect of extremely low-frequency electromagnetic fields (ELF-EMFs) on human health has become a worldwide concern, and no molecule/factor has been established as a measurable indicator of this effect. Diseases related to ELF-EMF are generally accompanied with energy metabolic dysfunction, and the energy in metabolism often flows in terms of electrons in all living cells. Hence, this study specifically investigated the relationship between metabolic current and ELF-EMF. By applying 0-128 Gauss ELF-EMFs to Geobacter sulfurreducens-inoculated bioelectrochemical systems, we found that metabolic current was increased and oscillated in ELF-EMF-exposed G. sulfurreducens. All effects were exposure dose dependent. Moreover, the oscillation amplitude varied linearly with the ELF-EMF strength. These results reveal that metabolic current can be used as a dosimetric indicator of the effect of ELF-EMF on living organisms, including human beings.

Lipidomic alteration and stress-defense mechanism of soil nematode Caenorhabditis elegans in response to extremely low-frequency electromagnetic field exposure.

To assess the impacts of man-made extremely low-frequency electromagnetic field (ELF-EMF) on soil ecosystems, the soil nematode was applied as a biological indicator to characterize ecotoxicity of ELF-EMF. In this paper, a soil-living model organism, Caenorhabditis elegans (C. elegans) was exposed to 50 Hz, 3 mT ELF-EMF. The integrated lipidome, proteome and transcriptome analysis were applied to elucidate physiological acclimations. Lipidomic analysis showed that ELF-EMF exposure induced significant alterations of 64 lipids, including significant elevation of triacylglycerols (TGs). Proteome results implied 157 changed protein expressions under ELF-EMF exposure. By transcriptomic analysis, 456 differently expressed genes were identified. Gene Ontology (GO) function and pathway analyses showed lipidomic alteration, mitochondrial dysfunction and the stress defense responses following ELF-EMF exposure in C. elegans. Conjoint analysis of proteome and transcriptome data showed that a higher expression of genes (sip-1, mtl-1 and rpl-11.1, etc.) were involved in stress defense responses to ELF-EMF exposure. These results indicated that ELF-EMF can induce effects on soil nematodes, mainly through disturbing lipid metabolism such as increasing TGs content, and eliciting stress defense responses. This study provided a new understanding in ELF-EMF exposure effects on soil nematodes and suggested a potential way of interpreting ELF-EMF influences on soil ecosystems.

[Extremely low frequency electromagnetic radiation enhanced energy metabolism and induced oxidative stress in Caenorhabditis elegans].

The aim of this study was to determine the effects of extremely low frequency electromagnetic field (ELF-EMF) on energy metabolism and oxidative stress in Caenorhabditis elegans (C. elegans). Worms in three adult stages (young adult stage, egg-laying stage and peak egg-laying stage) were investigated under 50 Hz, 3 mT ELF-EMF exposure. ATP levels, ATP synthase activity in vivo, reactive oxygen species (ROS) content, and changes of total antioxidant capacity (TAC) were detected, and worms' oxidative stress responses were also evaluated under ELF-EMF exposure. The results showed that ATP levels were significantly increased under this ELF-EMF exposure, and mitochondrial ATP synthase activity was upregulated simultaneously. In young adult stage, worms' ROS level was significantly elevated, together with upregulated TAC but with a decreased ROS-TAC score indicated by principal component analysis. ROS level and TAC of worms had no significant changes in egg-laying and peak egg-laying stages. Based on these results, we concluded that ELF-EMF can enhance worm energy metabolism and elicit oxidative stress, mainly manifesting as ATP and ROS level elevation together with ATP synthase upregulation and ROS-TAC score decrease in young adult C. elegans.

Resveratrol Attenuates Cognitive Deficits of Traumatic Brain Injury by Activating p38 Signaling in the Brain.

BACKGROUND Traumatic brain injury (TBI) is characterized by cognitive deficits, which was associated with brain oxidative stress and apoptosis. Resveratrol (RSV) is an anti-apoptotic and anti-oxidative. This study aimed to investigate neuroprotective effects and involved molecular mechanisms in TBI. MATERIAL AND METHODS RSV and p38 inhibitor were administrated to TBI rats. Cognitive deficits were evaluated by Morris water maze assay. Reactive oxygen species (ROS) and apoptosis were detected in rat brains by fluorescent staining. Western blotting was used to assess the phosphorylation of p38 and the expression levels of Nrf2, HO1, and activated caspase-3. RESULTS RSV administration attenuated cognitive deficits of TBI rats. The ROS generation and apoptosis in the brain of TBI rats were suppressed by RSV treatment. Moreover, RSV treatment recovered activation of p38/Nrf2/HO1 signaling pathway. The co-administration of p38 inhibitor impaired RSV's attenuating effects on cognitive deficits, brain apoptosis, and ROS generation. CONCLUSIONS RSV attenuated cognitive deficits of TBI by inhibiting oxidative stress-mediated apoptosis via targeting p38/Nrf2 signaling.

Mimicking a Natural Enzyme System: Cytochrome c Oxidase-Like Activity of Cu2O Nanoparticles by Receiving Electrons from Cytochrome c.

Inorganic nanomaterials-based artificial enzymes (nanozymes) have received considerable attention over the past years. However, the substrates studied for nanozymes have so far been limited to small organic molecules. The catalytic oxidation of biomacromolecules, such as proteins, by nanozymes has not yet been reported to date. In this study, we report that cuprous oxide nanoparticles (Cu2O NPs) possess cytochrome c oxidase (CcO)-like activity and catalyze the oxidation of cytochrome c (Cyt c), converting it from the ferrous state to the ferric state under atmospheric oxygen conditions. Furthermore, the CcO-like activity of Cu2O NPs is pH- and size-dependent. The lower the solution pH and the smaller the particle size, the higher the CcO-like activity. The artificial Cyt c-Cu2O NPs system closely mimics the native Cyt c-CcO enzyme system, which opens new vistas in enzyme construction and potential applications.

Mitochondrial ferritin, a new target for inhibiting neuronal tumor cell proliferation.

Mitochondrial ferritin (FtMt) has a significant effect on the regulation of cytosolic and mitochondrial iron levels. However, because of the deficiency of iron regulatory elements (IRE) in FtMt's gene sequence, the exact function of FtMt remains unclear. In the present study, we found that FtMt dramatically inhibited SH-SY5Y cell proliferation and tumor growth in nude mice. Interestingly, excess FtMt did not adversely affect the development of drosophila. Additionally, we found that the expression of FtMt in human normal brain tissue was significantly higher than that of neuroblastoma, but not higher than that of neurospongioma. However, the expression of transferrin receptor 1 is completely opposite. We therefore hypothesized that increased expression of FtMt may negatively affect the vitality of neuronal tumor cells. Therefore, we further investigated the underlying mechanisms of FtMt's inhibitory effects on neuronal tumor cell proliferation. As expected, FtMt overexpression disturbed the iron homeostasis of tumor cells and significantly downregulated the expression of proliferating cell nuclear antigen. Moreover, FtMt affected cell cycle, causing G1/S arrest by modifying the expression of cyclinD1, cyclinE, Cdk2, Cdk4 and p21. Remarkably, FtMt strongly upregulated the expression of the tumor suppressors, p53 and N-myc downstream-regulated gene-1 (NDRG1), but dramatically decreased C-myc, N-myc and p-Rb levels. This study demonstrates for the first time a new role and mechanism for FtMt in the regulation of cell cycle. We thus propose FtMt as a new candidate target for inhibiting neuronal tumor cell proliferation. Appropriate regulation of FtMt expression may prevent tumor cell growth. Our study may provide a new strategy for neuronal cancer therapy.

The effect of anti-inflammatory properties of ferritin light chain on lipopolysaccharide-induced inflammatory response in murine macrophages.

Ferritin light chain (FTL) reduces the free iron concentration by forming ferritin complexes with ferritin heavy chain (FTH). Thus, FTL competes with the Fenton reaction by acting as an antioxidant. In the present study, we determined that FTL influences the lipopolysaccharide (LPS)-induced inflammatory response. FTL protein expression was regulated by LPS stimulation in RAW264.7 cells. To investigate the role of FTL in LPS-activated murine macrophages, we established stable FTL-expressing cells and used shRNA to silence FTL expression in RAW264.7 cells. Overexpression of FTL significantly decreased the LPS-induced production of tumor necrosis factor alpha (TNF-α), interleukin 1ß (IL-1ß), nitric oxide (NO) and prostaglandin E2 (PGE2). Additionally, overexpression of FTL decreased the LPS-induced increase of the intracellular labile iron pool (LIP) and reactive oxygen species (ROS). Moreover, FTL overexpression suppressed the LPS-induced activation of MAPKs and nuclear factor-κB (NF-κB). In contrast, knockdown of FTL by shRNA showed the reverse effects. Therefore, our results indicate that FTL plays an anti-inflammatory role in response to LPS in murine macrophages and may have therapeutic potential for treating inflammatory diseases.

Airborne ultraviolet imaging system for oil slick surveillance: oil-seawater contrast, imaging concept, signal-to-noise ratio, optical design, and optomechanical model.

The airborne ultraviolet imaging system, which assesses oil slick areas better than visible and infrared optical systems, was designed to monitor and track oil slicks in coastal regions. A model was built to achieve the upwelling radiance distribution of oil-covered sea and clean seawater, based on the radiance transfer software. With this model, the oil-seawater contrast, which affects the detection of oil-covered coastal areas, was obtained. The oil-seawater contrast, fundamental imaging concept, analog calculation of SNR, optical design, and optomechanical configuration of the airborne ultraviolet imaging system are illustrated in this paper. The study of an airborne ultraviolet imaging system with F-number 3.4 and a 40° field of view (FOV) in near ultraviolet channel (0.32-0.38 µm) was illustrated and better imaging quality was achieved. The ground sample distance (GSD) is from 0.35 to 0.7 m with flight height ranges from 0.5 to 1 km. Comparisons of detailed characteristics of the airborne ultraviolet imaging system with the corresponding characteristics of previous ultraviolet systems were tabulated, and these comparisons showed that this system can achieve a wide FOV and a relative high SNR. A virtual mechanical prototype and tolerances analysis are illustrated in this paper to verify the performance of fabrication and assembly of the ultraviolet system.

Successful treatment of a severely injured victim from 8.12 Tianjin Port Explosion, China.

A male patient, 55 years old, was found from a container yard 65 h later following a chemical warehouse explosion in Tianjin, China on August 12, 2015. He was about 50 m away from the explosion center. He was subjected to compound multiple trauma, multi-viscera function damage, multiple fractures, hemothorax, traumatic wet lung, respiratory failure I, hypovolemic shock and impaired liver and kidney functions. After a series of successful treatments, he was rescued and recovered well.

Sevoflurane causes cognitive impairment by inducing iron deficiency and inhibiting the proliferation of neural precursor cells in infant mice.

AIMS: Numerous studies on animals have shown that exposure to general anesthetics in infant stage may cause neurocognitive impairment. However, the exact mechanism is not clear. The dysfunction of iron metabolism can cause neurodevelopmental disorders. Therefore, we investigated the effect of iron metabolism disorder induced by sevoflurane (Sev) on cognitive function and the proliferation of neural precursor cells (NPCs) and neural stem cells (NSCs) in infant mice. METHODS: C57BL/6 mice of postnatal day 14 and neural stem cells NE4C were treated with 2% Sev for 6 h. We used the Morris water maze (MWM) to test the cognitive function of infant mice. The proliferation of NPCs was measured using bromodeoxyuridine (BrdU) label and their markers Ki67 and Pax6 in infant brain tissues 12 h after anesthesia. Meanwhile, we used immunohistochemical stain, immunofluorescence assay, western blot, and flow cytometer to evaluate the myelinogenesis, iron levels, and cell proliferation in cortex and hippocampus or in NE4C cells. RESULTS: The results showed that Sev significantly caused cognitive deficiency in infant mice. Further, we found that Sev inhibited oligodendrocytes proliferation and myelinogenesis by decreasing MBP and CC-1 expression and iron levels. Meanwhile, Sev also induced the iron deficiency in neurons and NSCs by downregulating FtH and FtL expression and upregulating the TfR1 expression in the cortex and hippocampus, which dramatically suppressed the proliferation of NSCs and NPCs as indicated by decreasing the colocalization of Pax6+ and BrdU+ cells, and caused the decrease in the number of neurons. Interestingly, iron supplementation before anesthesia significantly improved iron deficiency in cortex and hippocampus and cognitive deficiency induced by Sev in infant mice. Iron therapy inhibited the decrease of MBP expression, iron levels in neurons and oligodendrocytes, and DNA synthesis of Pax6+ cells in hippocampus induced by Sev. Meanwhile, the number of neurons was partially recovered in hippocampus. CONCLUSION: The results from the present study demonstrated that Sev-induced iron deficiency might be a new mechanism of cognitive impairment caused by inhaled anesthetics in infant mice. Iron supplementation before anesthesia is an effective strategy to prevent cognitive impairment caused by Sev in infants.

Amelioration of nitroglycerin-induced migraine in mice via Wuzhuyu decoction: Inhibition of the MZF1/PGK1 pathway and activation of NRF2 antioxidant response.

ETHNOPHARMACOLOGICAL RELEVANCE: Migraine, a chronic and intricate disorder, manifests as recurrent episodic headaches accompanied by various neurological symptoms. Wuzhuyu Decoction (WZYD) is a traditional Chinese medical formula with promising effects in treating migraines; however, its underlying mechanisms have not yet been clarified. AIM OF STUDY: The study aimed to evaluate WZYD's effectiveness in migraine treatment and investigate the potential mechanism of WZYD's effects on migraine and oxidative stress. MATERIALS AND METHODS: Behavior tests and immunofluorescence assay for the intensity of migraine markers to assess the migraine-relieving effect of WZYD after chronic migraine model induced by nitroglycerin in mice. The impacts of WZYD on oxidative stress-related markers, including reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), nuclear factor erythroid 2-related factor 2 (NRF2), heme oxygenase 1 (HO1), and NAD (P)H quinone oxidoreductase 1 (NQO1) in brain tissue were examined. In addition, protein expression or mRNA levels of the MZF1/PGK1 were detected using Western blot or PCR, respectively. Finally, the MZF1 overexpression vector was constructed to the higher level of MZF1. The MZF1/PGK1 signaling pathway expression was evaluated by markers of oxidative stress including NRF2 and others in this series of experiments. RESULTS: Through murine model experimentation, we observed that WZYD effectively alleviates migraine symptoms, signifying its therapeutic efficacy. Mechanistically, WZYD emerges as a potent activator of the NRF2, acting as a robust defense against oxidative stress. In vitro investigations demonstrated that WZYD combats oxidative stress and curbs cell apoptosis induced by these detrimental conditions. Furthermore, by suppressing the transcriptional expression of PGK1, an influential player in the NRF2 pathway, WZYD effectively activates NRF2 signaling. Intriguingly, we have identified MZF1 as the mediator orchestrating the regulation of the PGK1/NRF2 pathway by WZYD. CONCLUSION: The study confirms the effectiveness of WZYD in alleviating migraine symptoms. Mechanistically, WZYD activated the NRF2 signaling pathway; moreover, the action of WZYD involved the down-regulation of PGK1 mediated by MZF1, which promoted the activation of the NRF2 pathway. This study advances our understanding of the intricate mechanisms driving WZYD's efficacy, paving the way for novel treatments in migraine management.

Transmembrane serine protease 6, a novel target for inhibition of neuronal tumor growth.

Transmembrane serine protease 6 (Tmprss6) has been correlated with the occurrence and progression of tumors, but any specific molecular mechanism linking the enzyme to oncogenesis has remained elusive thus far. In the present study, we found that Tmprss6 markedly inhibited mouse neuroblastoma N2a (neuro-2a) cell proliferation and tumor growth in nude mice. Tmprss6 inhibits Smad1/5/8 phosphorylation by cleaving the bone morphogenetic protein (BMP) co-receptor, hemojuvelin (HJV). Ordinarily, phosphorylated Smad1/5/8 binds to Smad4 for nuclear translocation, which stimulates the expression of hepcidin, ultimately decreasing the export of iron through ferroportin 1 (FPN1). The decrease in cellular iron levels in neuro-2a cells with elevated Tmprss6 expression limited the availability of the metal forribo nucleotide reductase activity, thereby arresting the cell cycle prior to S phase. Interestingly, Smad4 promoted nuclear translocation of activating transcription factor 3 (ATF3) to activate the p38 mitogen-activated protein kinases signaling pathway by binding to ATF3, inducing apoptosis of neuro-2a cells and inhibiting tumor growth. Disruption of ATF3 expression significantly decreased apoptosis in Tmprss6 overexpressed neuro-2a cells. Our study describes a mechanism whereby Tmprss6 regulates the cell cycle and apoptosis. Thus, we propose Tmprss6 as a candidate target for inhibiting neuronal tumor growth.

Effect of extremely low frequency electromagnetic field on the pathogenicity of Magnaporthe oryzae.

Numerous works have reported that extremely low frequency electromagnetic fields (ELF-EMFs) were associated with human health; however, little is known about their effects on the occurrence of agricultural diseases. In this study, Magnaporthe oryzae was used as a model organism, and its pathogenicity under 50 Hz, 3 mT ELF-EMF was studied. Our results showed that the pathogenicity, growth rate, and conidia generation of M. oryzae were enhanced under ELF-EMF exposure. In addition, M. oryzae exposed to ELF-EMF showed enhanced tolerance to cell wall-perturbing agents sodium lauryl sulphate, and increased expression of cell wall integrity-related genes, including RAC1, CDC42, RHO2, and NOX2. In addition, the level of reactive oxygen species (ROS) and the expression level of ROS scavenger system-related gene MoAP1 increased in ELF-EMF-exposed samples, whereas the total antioxidant capacity and the activities of superoxide dismutase and catalase did not change. Results of our study demonstrated that exposure to 50 Hz, 3 mT ELF-EMF enhanced the infection ability of M. oryzae, which present new important challenges for understanding the effect of ELF-EMF exposure on farmland ecology, especially on agricultural diseases.

Effect of Bi Content on the Microstructure, Mechanical and Tribological Properties of Cu-Sn Alloy.

To reduce the use of the toxic Pb element in the Cu-Sn alloy with high friction performance, Cu-xBi-10Sn alloys with different Bi contents were prepared by gravity casting, and the effect of Bi content on the microstructure, mechanical properties and wear property of Cu-Sn alloys were studied. The results showed that the Bi element was distributed in bands or long strips on the dendritic arms and did not form compounds with other elements. With the increase in Bi content, the hardness and tensile strength of Cu-xBi-10Sn alloys present a trend of increasing first and then decreasing. When the Bi content was 7 wt.%, the maximum hardness value was obtained, and the ultimate tensile strength was close to that of Cu-10Pb-10Sn alloy. Compared with Cu-10Pb-10Sn alloy, Cu-7Bi-10Sn alloy also possessed better friction reduction and wear resistance under the oil lubrication condition.