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The quality of vanadium–titanium magnetite sinters is poor. The high-pellet operation of the blast furnace ironmaking process is a feasible method for utilization of the High-chromium Vanadium–titanium magnetite (HVTM). To ensure the basicity of the burden, flux pellets need to be investigated. In this study, HVTM concentrate and CaCO3 were used to prepare flux pellets. The phase transition and oxidation induration mechanism of flux pellets were studied separately and analyzed by scanning electron microscopy and energy dispersive spectroscopy. Solid-phase and solid–liquid-phase experiments were used to verify the phase transition behavior. The results indicated that the basicity (CaO/SiO2) increased from 0.4 to 1.4, and the compressive strength of HVTM concentrate flux pellets first increased to 4916 N and then decreased to 2399 N at 1523 K for 20 minute. The porosity of the pellets increased from 8.236 to 20.734 pct. Perovskite produced due to increasing basicity reduced the slag content and had a low bonding strength, which reduced the overall compressive strength of the pellets. The increasing basicity was conducive to the solid solution of Ti forming an iron-titanium solid solution. The addition of CaCO3 increased the porosity of the pellets. The oxidation induration of the pellets changed from oxide-bonded to slag-bonded.

Toe formation is a phenomenon resulting from unconnected cracks between blastholes, which occurred during blasting excavation of the abutment slot at Baihetan hydropower station. Analysis of crack development has tended not to focus on the high in-situ stress environment at the slope corner. Therefore, this study aimed to explore the toe formation process through theoretical analysis and numerical simulation. Firstly, a three-blasthole model was established to analyze the effects of blasting load and in-situ stress on crack extension. Then, a finite-element model of the abutment slot was built to simulate crack propagation under different in-situ stress environment. Finally, optimization measures for avoiding toe were proposed. The results demonstrate that cracks grow preferentially in the direction of the maximum tangential tensile stress and are influenced by the blasting load and in-situ stress. On the lateral side of the abutment slot, the crack initiation and extension occur far from the centerline due to the deviation of the maximum tangential tensile stress. The deviation increased as the in-situ stress. Consequently, cracks between blastholes not being able to connect with each other results in toe formation. Increment of the linear density of the charge and optimization of the excavated profile are both effective in reducing the impact of the stress concentration caused by in-situ stress and preventing toe formation.

Extracellular matrix (ECM) is a non-cellular three-dimensional macromolecular network that not only provides mechanical support but also transduces essential molecular signals in organ functions. ECM is constantly remodeled to control tissue homeostasis, responsible for cell adhesion, cell migration, cell-to-cell communication, and cell differentiation, etc. The dysregulation of ECM components contributes to various diseases, including cardiovascular diseases, fibrosis, cancer, and neurodegenerative diseases, etc. Aberrant ECM remodeling is initiated by various stress, such as oxidative stress, inflammation, ischemia, and mechanical stress, etc. Hydrogen sulfide (H2S) is a gasotransmitter that exhibits a wide variety of cytoprotective and physiological functions through its anti-oxidative and anti-inflammatory actions. Amounting research shows that H2S can attenuate aberrant ECM remodeling. In this review, we discussed the implications and mechanisms of H2S in the regulation of ECM remodeling in cardiovascular diseases, and highlighted the potential of H2S in the prevention and treatment of cardiovascular diseases through attenuating adverse ECM remodeling.

Hydrogen sulphide (H2S), a newly identified gasotransmitter, can be endogenously produced by cystathionine gamma-lyase (CSE) in the cardiovascular system. This study investigated the role of the CSE/H2S system on lipid overload-induced lipotoxicity and cardiac senescence. Lipid overload in rat cardiomyocyte cells (H9C2) promoted intracellular accumulation of lipid, oxidative stress, mitochondrial dysfunctions, lipid peroxidation and inhibited cell viability, all of which could be reversed by exogenously applied H2S. Further data revealed that H2S protected H9C2 cells from lipid overload-induced senescence by altering the expressions of lipid metabolism-related genes and inhibiting cellular acetyl-CoA and global protein acetylation. Enhancement of protein acetylation abolished the protective role of H2S on cardiac senescence. In vivo, knockout of the CSE gene strengthened cardiac lipid accumulation, protein acetylation, and cellular ageing in high fat diet-fed mice. Taken together, the CSE/H2S system is capable of maintaining lipid homeostasis and cellular senescence in heart cells under lipid overload.

Hydrogen sulfide (H2 S) is a gasotransmitter that regulates both physiological and pathophysiological processes in mammalian cells. Recent studies have demonstrated that H2 S promotes aerobic energy production in the mitochondria in response to hypoxia, but its effect on anaerobic energy production has yet to be established. Glycolysis is the anaerobic process by which ATP is produced through the metabolism of glucose. Mammalian red blood cells (RBCs) extrude mitochondria and nucleus during erythropoiesis. These cells would serve as a unique model to observe the effect of H2 S on glycolysis-mediated energy production. The purpose of this study was to determine the effect of H2 S on glycolysis-mediated energy production in mitochondria-free mouse RBCs. Western blot analysis showed that the only H2 S-generating enzyme expressed in mouse RBCs is 3-mercaptopyruvate sulfurtransferase (MST). Supplement of the substrate for MST stimulated, but the inhibition of the same suppressed, the endogenous production of H2 S. Both exogenously administered H2 S salt and MST-derived endogenous H2 S stimulated glycolysis-mediated ATP production. The effect of NaHS on ATP levels was not affected by oxygenation status. On the contrary, hypoxia increased intracellular H2 S levels and MST activity in mouse RBCs. The mitochondria-targeted H2 S donor, AP39, did not affect ATP levels of mouse RBCs. NaHS at low concentrations (3-100 μM) increased ATP levels and decreased cell viability after 3 days of incubation in vitro. Higher NaHS concentrations (300-1000 μM) lowered ATP levels, but prolonged cell viability. H2 S may offer a cytoprotective effect in mammalian RBCs to maintain oxygen-independent energy production.

Sulforaphane (SF) is a potential secondary metabolite with anticancer activity and its metabolic pathway has been revealed in the model plant Arabidopsis thaliana. Generally, the SF extraction cycle from broccoli is long and the yield is low, which means that it no longer meets cancer treatment requirements. Therefore, the SF content needs to be urgently improved. In this study, MAM1, FMOGS–OX2, and Myrosinase, which are required for SF biosynthesis, were introduced into broccoli by Agrobacterium tumefaciens-mediated transformation. To obtain plants with a higher SF content, broccoli was transformed using Myrosinase-FMOGS–OX2-MAM1 (M-F-A) triple genes in tandem and by adding each of the genes on their own. The results showed that the SF contents in the MAM1, FMOGS–OX2, or Myrosinase transgenic plants improved by 1.7–3.4, 1.6–2.7, and 3.7-fold compared to the wild type (WT), respectively, However, the SF contents in transgenic plants with all three genes improved by 1.86–5.5fold. Furthermore, we examined the anticancer effect of the SF extracts from transgenic plants via cell viability detection of HCT116 colon cancer cells. The results showed that SF extracts from transgenic plants had more obvious anticancer activity than SF extracts from WT, and the SF extracts from the multiple genes plants had stronger anticancer activity than the single gene plants. In summary, the multiple genes transformation increased the SF content in broccoli more than single gene introductions. The aim of this research was to improve sulforaphane content by introducing FMOGS–OX2, MAM1, and Myrosinase genes, and Myrosinase-FMOGS–OX2-MAM1 (M-F-A) serial triple genes into broccoli.

Both estrogen and hydrogen sulfide (H2S) inhibit the proliferation of vascular smooth muscle cells (SMCs) and development of atherosclerosis. In the absence of endogenous H2S as occurred in CSE-knockout (KO) mouse, however, estrogen stimulates the proliferation of vascular SMCs. The underlying mechanisms for this seemingly controversial vascular effect of estrogen are unclear. In the present study, we demonstrated that the stimulatory effect of estrogen on the proliferation of CSE-KO SMCs was suppressed by the inhibitor of insulin-like growth factor-1 receptor (IGF-1R) or knockdown of IGF-1R protein expression. Estrogen downregulated the expression of insulin-like growth factor-1 (IGF-1) and IGF-1R in aortic tissues or aortic SMCs isolated from WT and CSE-KO mice. Furthermore, endogenous H2S downregulated IGF-1R, but upregulated estrogen receptor (ER)-α, in aortic tissues or SMCs. ER-α and IGF-1R were co-located in SMCs and co-immunoprecipitated, which was decreased by H2S. Finally, both endogenous and exogenous H2S induced the S-sulfhydration of IGF-1R, but not ER-α, in WT-SMCs and CSE-KO SMCs, which underlies the decreased formation of IGF-1R/ER-α hybrid in the presence of H2S. Thus, the absence of H2S favors the interaction of estrogen with IGF-1R/ER-α hybrid to stimulate SMCs proliferation. The appreciation of a critical role of H2S in preventing estrogen-induced SMCs proliferation will help better understand the regulation of complex vascular effects of estrogen and sex-related cardiovascular diseases.

The outbreak of COVID-19 pneumonia caused by a new coronavirus (severe acute respiratory syndrome coronavirus 2, SARS-CoV-2) is posing a global health emergency and has led to more than 380,000 deaths worldwide. The cell entry of SARS-CoV-2 depends on two host proteins angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2). There is currently no vaccine available and also no effective drug for the treatment of COVID-19. Hydrogen sulfide (H2S) as a novel gasotransmitter has been shown to protect against lung damage via its anti-inflammation, antioxidative stress, antiviral, prosurvival, and antiaging effects. In light of the research advances on H2S signaling in biology and medicine, this review proposed H2S as a potential defense against COVID-19. It is suggested that H2S may block SARS-CoV-2 entry into host cells by interfering with ACE2 and TMPRSS2, inhibit SARS-CoV-2 replication by attenuating virus assembly/release, and protect SARS-CoV-2-induced lung damage by suppressing immune response and inflammation development. Preclinical studies and clinical trials with slow-releasing H2S donor(s) or the activators of endogenous H2S-generating enzymes should be considered as a preventative treatment or therapy for COVID-19.

Hydrogen sulfide (H

Aims: The physiological and pathological importance of hydrogen sulfide (H2S) as a novel gasotransmitter has been widely recognized. Cystathionine gamma-lyase (CSE) is one of the major H2S-producing enzymes and it regulates diverse functions in connection with intracellular calcium (Ca2+). The aim of this study is to examine the role of H2S in Golgi stress-related cell injury and skeletal muscle disorders. Results: Golgi stressors (brefeldin A [BFA] and monensin) decreased the expression of GM130 and ATP2C1 (two markers of Golgi stress response), induced Golgi apparatus fragmentation, and caused a higher level of oxidative stress and cell apoptosis in mouse myoblast cells. In addition, Golgi stressors upregulated CSE expression and endogenous H2S generation, and exogenously applied H2S was able to protect but inhibition of CSE/H2S system deteriorated Golgi stress response. Activating transcription factor 4 (ATF4) acted as an upstream molecule to increase CSE expression on Golgi stress response. Mechanically, Golgi stressors induced intracellular level of Ca2+, and chelating cellular Ca2+ markedly attenuated Golgi stress response, indicating the key role of Ca2+ in initiating Golgi stress and cell apoptosis. Further, administration of either angiotensin II or BFA initiated Golgi stress response and induced skeletal muscle atrophy in mice, which was further deteriorated by CSE deficiency but rescued by exogenously applied sodium hydrosulfide (NaHS). Innovation and Conclusion: The activation of the CSE/H2S pathway and the decrease of intracellular Ca2+ are two cellular protective mechanisms against Golgi stress, and the CSE/H2S system would be a target for preventing skeletal muscle dysfunctions.

Hydrogen sulfide (H2S), a multifunctional gasotransmitter, participates in a wide range of cellular signal transduction and pathophysiological processes. Cystathionine gamma-lyase (CSE) acts as a major H2S-generating enzyme in peripheral organs and tissues. As a cysteine-rich and heavy metal-binding protein, metallothionein-1 (MT-1) is known to protect cells from various environmental stresses. Here we demonstrated that exposure of cadmium (Cd) induced oxidative stress, depleted intracellular thiols, and stimulated apoptotic cell death in mouse myoblast cells. CSE expression and H2S production were significantly enhanced by Cd treatment. NaHS, a well-known H2S donor, at physiologically relevant concentration significantly alleviated Cd-induced damage in both myoblasts and mouse skeletal muscles. In contrast, down-regulation of CSE/H2S system deteriorated Cd-stimulated oxidative stress and cell death. Exposure of the cells to Cd lead to increased expressions of metal regulatory transcription factor 1 and MT-1, while siRNA-mediated MT-1 knockdown alleviated Cd-induced CSE expression and caused more oxidative stress and cell death. In addition, H2S post-translationally modified MT-1 by S-sulfhydration and stabilized zinc-protein complex. Taken together, these data suggest that CSE/H2S system would protect myoblasts and skeletal muscles from Cd-induced damage by S-sufhydrating MT-1.

Hydrogen sulphide (H

Cystathionine gamma-lyase (CSE)-derived hydrogen sulfide (H

Disulfiram (DSF), a sulfur-containing compound, has been used to treat chronic alcoholism and cancer for decades by inactivating aldehyde dehydrogenase (ALDH). Hydrogen sulfide (H

Hydrogen sulfide (H2 S) can be endogenously produced and belongs to the class of signaling molecules known as gasotransmitters. Cystathionine gamma-lyase (CSE)-derived H2 S is implicated in the regulation of cell differentiation and the aging process, but the involvements of the CSE/H2 S system in myogenesis upon aging and injury have not been explored. In this study, we demonstrated that CSE acts as a major H2 S-generating enzyme in skeletal muscles and is significantly down-regulated in aged skeletal muscles in mice. CSE deficiency exacerbated the age-dependent sarcopenia and cardiotoxin-induced injury/regeneration in mouse skeletal muscle, possibly attributed to inefficient myogenesis. In contrast, supplement of NaHS (an H2 S donor) induced the expressions of myogenic genes and promoted muscle regeneration in mice. In vitro, incubation of myoblast cells (C2C12) with H2 S promoted myogenesis, as evidenced by the inhibition of cell cycle progression and migration, altered expressions of myogenic markers, elongation of myoblasts, and formation of multinucleated myotubes. Myogenesis was also found to upregulate CSE expression, while blockage of CSE/H2 S signaling resulted in a suppression of myogenesis. Mechanically, H2 S significantly induced the heterodimer formation between MEF2c and MRF4 and promoted the binding of MEF2c/MRF4 to myogenin promoter. MEF2c was S-sulfhydrated at both cysteine 361 and 420 in the C-terminal transactivation domain, and blockage of MEF2c S-sulfhydration abolished the stimulatory role of H2 S on MEF2c/MRF4 heterodimer formation. These findings support an essential role for H2 S in maintaining myogenesis, presenting it as a potential candidate for the prevention of age-related sarcopenia and treatment of muscle injury.

Hydrogen sulfide (H

Reinforced concrete (RC) is one of the most commonly used construction materials. However, impact and blast loads could completely destroy RC structures, causing tremendous casualties and property losses. Therefore, analyzing the damage mechanism and dynamic behaviour of RC structures under blast loading is significant. This paper presents a study on the behaviour of RC slabs subjected to air and underwater contact detonation. Two RC slabs were tested under real blast loads. One was tested under air contact explosion of 210 g TNT, the other was tested subjected to underwater contact explosion of 6 g TNT. Damage evolution and damage mechanism of the RC slabs subjected to the air and underwater contact explosions are investigated by using high-fidelity numerical models. The damage patterns obtained from the numerical models match well with those of the tests. The effect of experimental environments on the structural behaviour of the slabs subjected to the underwater explosions is also discussed. The different response of the RC slabs subjected air and underwater explosions with identical charge mass are analyzed contrastively by employing the validated coupled method. The results show that the present model can give a reliable prediction of damage characteristics for RC structures under various blast scenarios. The experimental environments have important influence on the structural response and bubble development. The damage of the RC slabs induced by underwater contact explosion is significantly larger than that caused by air contact blast with equal charge mass.

Columns are the key load-bearing elements in infrastructures. Common cross-section shapes of columns are square and circle. Those columns may be subjected to various blasting scenarios. This paper investigates the effects of cross-section shape on the anti-knock performance of RC columns subjected to air and underwater blast loads. The reliability of the fully coupled Lagrangian-Eulerian numerical model is verified by comparing with the results of the field blast test. The damage characteristics and dynamic response of the RC column with different cross-section shapes subjected to contact and close-in air explosions are investigated. The anti-knock performance of the RC column with different cross-section shapes subjected to contact and close-in underwater explosion is also studied. Nonlinear dynamic response behavior and damage mechanism of the RC column subjected to contact and close-in explosion are compared. The improvement effects of the reinforcement ratio and ultra-high performance concrete on the blast resistance of the underwater RC column are investigated. The results show that the cross-section shape has an important influence on the anti-knock performance of the column, whether subjected to air or underwater explosions. Employing circular cross-section can effectively improve the blast resistance of the column.

Hydrogen sulfide (H(2)S) is the most recently recognized gasotransmitter, influencing a wide range of physiological processes. As a critical regulator of metabolism, H(2)S has been suggested to be involved in the pathology of many diseases, particularly obesity, diabetes and cardiovascular disorders. Its involvement in liver health has been brought to light more recently, particularly through knockout animal models, which show severe hepatic lipid accumulation upon ablation of H(2)S metabolic pathways. A complex relationship between H(2)S and lipid metabolism in the liver is emerging, which has significant implications for liver disease establishment and/or progression, regardless of the disease‐causing agent. In this review, we discuss the critical importance of H(2)S in hepatic lipid metabolism. We then describe the animal models so far related with H(2)S and lipid‐associated liver disease, as well as H(2)S‐based treatments available. Finally, we highlight important considerations for future studies and identify areas in which much still remains to be determined. LINKED ARTICLES: This article is part of a themed section on Hydrogen Sulfide in Biology & Medicine. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v177.4/issuetoc

This paper is aim to investigate the damage characteristics of a shallow-buried water diversion box culvert subjected to a surface explosion. For this purpose, the soil model is verified by comparing with the analytical formulas of the Technical Manual (TM5-855-1), and the accuracy of the reinforced concrete model is validated with a previous explosion test. Subsequently, a three-dimensional (3D) numerical model of the water diversion culvert is established. A fully coupled Eulerian and Lagrangian (CEL) approach is presented to model the soil-structure-water interaction. The shock wave propagation characteristics in the soil, culvert and water medium are captured. The dynamic responses and damage processes of the shallow-buried box culvert in design water diversion condition (i.e. unconfined full flow) subjected to surface explosion are investigated. Other three water diversion conditions (i.e. pressure flow, free flow and no water) are employed to evaluate the influence of the water diversion condition on the antiknock performance of the culvert. The effects of the burial depth and charge weight on the dynamic behavior of the culvert to surface explosion are also discussed. The results show that the surface blast loads will cause a great threat to the whole security of the shallow-buried water diversion box culvert. The water diversion condition has a significant influence on the dynamic behavior of the culvert when subjected to a surface explosion.

Hydrogen sulfide (H2S) is a gaseous signaling molecule that participates in multiple physiological processes in both animals and plants. Mitogen-activated protein kinase (MAPK) is important signaling molecule that links the growth and developmental signals and environment stimuli to cellular responses. In the current study we explored the relationship between H2S and MAPK in drought stress resistance in Arabidopsis. The quantitative real-time (qRT)-PCR, root tip bending experiment and stomatal aperture assay were used in this paper. Drought stress activated both H2S biosynthesis and gene expression of MAPKs. The increase in MAPK expression was depressed in lcd/des1, a double mutant of H2S synthesis. Then we selected MPK4 as our target and used mpk4 mutants for further studies. H2S was able to alleviate the drought stress in wild-type (WT) Arabidopsis but not in mpk4 mutants. Meanwhile, H2S-induced stomatal movement was impaired in mpk4 mutants. We then examined the role of H2S and MPK4 in stomatal movements in response to abscisic acid (ABA) and hydrogen peroxide (H2O2). ABA- and H2O2- mediated stomatal movements were impaired in lcd/des1 and mpk4 mutants, and H2S-induced stomatal closure was impaired in slac1–3 mutants. Our results suggested that MPK4 is important downstream of H2S in the drought stress response and in stomatal movement, and that the H2S-MPK4 cascade is involved in ABA-mediated stomatal movement to regulate the drought stress.

Aims Hydrogen sulfide (H2S), an important gasotransmitter, is involved in a variety of cellular functions and pathophysiologic processes. Drug resistance due to alterations in drug trafficking and metabolism severely limits the effectiveness of cancer therapy. This study examined the role of H2S in drug resistance in liver cancer cells. Materials and methods Human primary hepatocellular carcinoma cell line (HepG2) and doxorubicin (Dox)-resistant cells were used in this study. Cell survival was analyzed by MTT, Annexin V-FITC/propidium iodide staining and clonogenic assay. Western blotting was used for analysis of protein expression, and immunoprecipitation was used to determine interactions of LXR/RXR. Key findings The expression of H2S-generating enzyme cystathionine gamma-lyase (CSE) was inhibited by doxorubicin treatment in HepG2 cells, and H2S sensitized Dox-inhibited cell survival and colony formation. In addition, H2S promoted cellular retention of Dox by suppressing the expressions of ABCA1 and ABCG8. H2S significantly blocked Dox-induced heterodimer formation between LXRα and RXRβ and attenuated the binding of LXRα/RXRβ to the promoters of ABCA1 and ABCG8 genes. RXRβ but not LXRα was S-sulfhydrated by H2S, and blockage of RXRβ S-sulfhydration abolished the inhibitory role of H2S on LXRα/RXRβ heterodimer formation. CSE expression was reduced in Dox-resistant cells in comparison with their parental cells, while H2S could reverse drug resistance in Dox-resistant cells. Significance Our study provides a novel solution for reversing drug resistance in cancer cells by targeting H2S signalling.