LIM domain only 7 negatively controls nonalcoholic steatohepatitis in the setting of hyperlipidemia.

BACKGROUND AND AIMS: Hyperlipidemia has been extensively recognized as a high-risk factor for NASH; however, clinical susceptibility to NASH is highly heterogeneous. The key controller(s) of NASH susceptibility in patients with hyperlipidemia has not yet been elucidated. Here, we aimed to reveal the key regulators of NASH in patients with hyperlipidemia and to explore its role and underlying mechanisms. APPROACH AND RESULTS: To identify the predominant suppressors of NASH in the setting of hyperlipidemia, we collected liver biopsy samples from patients with hyperlipidemia, with or without NASH, and performed RNA-sequencing analysis. Notably, decreased Lineage specific Interacting Motif domain only 7 (LMO7) expression robustly correlated with the occurrence and severity of NASH. Although overexpression of LMO7 effectively blocked hepatic lipid accumulation and inflammation, LMO7 deficiency in hepatocytes greatly exacerbated diet-induced NASH progression. Mechanistically, lysine 48 (K48)-linked ubiquitin-mediated proteasomal degradation of tripartite motif-containing 47 (TRIM47) and subsequent inactivation of the c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (MAPK) cascade are required for the protective function of LMO7 in NASH. CONCLUSIONS: These findings provide proof-of-concept evidence supporting LMO7 as a robust suppressor of NASH in the context of hyperlipidemia, indicating that targeting the LMO7-TRIM47 axis is a promising therapeutic strategy for NASH.

Room-Temperature Two-Dimensional InSe Plasmonic Laser.

Two-dimensional (2D) semiconductors, owing to their strong excitonic emission, are emerging as efficient gain media for constructing the ultimate nanolaser. The further integration of 2D semiconductors with plasmonic devices holds promise for realizing the thinnest laser. However, the implementation of 2D semiconductor plasmonic lasing is severely hindered by the limited cavity feedback and low gain resulting from insufficient plasmon-exciton interactions. Here, we report the realization of a room-temperature 2D semiconductor plasmonic laser by embedding an InSe nanoflake into a plasmonic Fabry-Perot (F-P) cavity. This plasmonic F-P cavity shows an exceptional ability to recycle the leaked dark surface plasmon, resulting in >2-fold enhancement of feedback compared to that of conventional metal-insulator-semiconductor nanolasers. Moreover, via combination of field enhancement and orientation matching, this cavity facilitates optimized plasmon-exciton coupling to ensure sufficient gain for sustaining room-temperature lasing. Our work may open up the possibilities for multifunctional photonic devices based on 2D materials.

TMEM100 acts as a TAK1 receptor that prevents pathological cardiac hypertrophy progression.

Pathological cardiac hypertrophy is the primary cause of heart failure, yet its underlying mechanisms remain incompletely understood. Transmembrane protein 100 (TMEM100) plays a role in various disorders, such as nervous system disease, pain and tumorigenesis, but its function in pathological cardiac hypertrophy is still unknown. In this study, we observed that TMEM100 is upregulated in cardiac hypertrophy. Functional investigations have shown that adeno-associated virus 9 (AAV9) mediated-TMEM100 overexpression mice attenuates transverse aortic constriction (TAC)-induced cardiac hypertrophy, including cardiomyocyte enlargement, cardiac fibrosis, and impaired heart structure and function. We subsequently demonstrated that adenoviral TMEM100 (AdTMEM100) mitigates phenylephrine (PE)-induced cardiomyocyte hypertrophy and downregulates the expression of cardiac hypertrophic markers in vitro, whereas TMEM100 knockdown exacerbates cardiomyocyte hypertrophy. The RNA sequences of the AdTMEM100 group and control group revealed that TMEM100 was involved in oxidative stress and the MAPK signaling pathway after PE stimulation. Mechanistically, we revealed that the transmembrane domain of TMEM100 (amino acids 53-75 and 85-107) directly interacts with the C-terminal region of TAK1 (amino acids 1-300) and inhibits the phosphorylation of TAK1 and its downstream molecules JNK and p38. TAK1-binding-defective TMEM100 failed to inhibit the activation of the TAK1-JNK/p38 pathway. Finally, the application of a TAK1 inhibitor (iTAK1) revealed that TAK1 is necessary for TMEM100-mediated cardiac hypertrophy. In summary, TMEM100 protects against pathological cardiac hypertrophy through the TAK1-JNK/p38 pathway and may serve as a promising target for the treatment of cardiac hypertrophy.

Prediction of high thermal rectification behavior in carbon/C3N heteronanotubes based on nonequilibrium molecular dynamics simulations.

Carbon/C3N heteronanotubes (CC3NNTs) have garnered significant interest for their distinctive performance and versatility across various applications. However, the understanding of interfacial heat transport within these heterostructures remains limited. This study aims to enrich the field by constructing models of CC3NNTs through the bonding of CNTs and C3NNTs, and employs nonequilibrium molecular dynamics (NEMD) simulations to predict their heat flux and thermal rectification (TR) effects. Placing the heat source in the CNT region induces a stronger heat flux compared to the C3NNT region, thus demonstrating a pronounced TR effect. This effect can be attributed to the mismatch in phonon spectra, as evidenced by the cumulative correlation factor derived from the phonon density of states (phonon DOS). Using this approach, we predict that the TR ratio for zigzag CC3NNTs (ZCC3NNT) significantly exceeds that of armchair CC3NNTs (ACC3NNT). Notably, in contrast to ACC3NNT, ZCC3NNT exhibits the phenomenon of negative differential thermal resistance in the backward heat flux with a temperature difference of Δ = 120 K. This phenomenon can be attributed to a lower phonon participation ratio at Δ = 120 K compared to other values of Δ. Subsequently, given that ZCC3NNT demonstrates the most pronounced TR ratio at room temperature, we explored how stress-strain, system size, defect density, and interface position impact the TR ratio. These insights are invaluable for guiding the design of thermal rectifiers, smart thermal management systems, and microelectronic processor coolers.

UGCG modulates heart hypertrophy through B4GalT5-mediated mitochondrial oxidative stress and the ERK signaling pathway.

Mechanical pressure overload and other stimuli often contribute to heart hypertrophy, a significant factor in the induction of heart failure. The UDP-glucose ceramide glycosyltransferase (UGCG) enzyme plays a crucial role in the metabolism of sphingolipids through the production of glucosylceramide. However, its role in heart hypertrophy remains unknown. In this study, UGCG was induced in response to pressure overload in vivo and phenylephrine stimulation in vitro. Additionally, UGCG downregulation ameliorated cardiomyocyte hypertrophy, improved cardiomyocyte mitochondrial oxidative stress, and reduced the ERK signaling pathway. Conversely, UGCG overexpression in cardiomyocytes promoted heart hypertrophy development, aggravated mitochondrial oxidative stress, and stimulated ERK signaling. Furthermore, the interaction between beta-1,4-galactosyltransferase 5 (B4GalT5), which catalyses the synthesis of lactosylceramide, and UGCG was identified, which also functions as a synergistic molecule of UGCG. Notably, limiting the expression of B4GalT5 impaired the capacity of UGCG to promote myocardial hypertrophy, suggesting that B4GalT5 acts as an intermediary for UGCG. Overall, this study highlights the potential of UGCG as a modulator of heart hypertrophy, rendering it a potential target for combating heart hypertrophy.

ING5 overexpression upregulates miR-34c-5p/Snail1 to inhibit EMT and invasion of lung cancer cells.

ING5 belongs to the inhibitor of growth (ING) candidate tumor suppressor family, which is involved in multiple cellular functions, such as cell cycle regulation, apoptosis, and chromatin remodelling. Previously, we reported that ING5 overexpression inhibits EMT by regulating EMT-related molecules, including Snail1, at the mRNA and protein levels. However, the mechanisms remain unclear. In the current study, we identify that ING5 overexpression induces the upregulation of miR-34c-5p. The expression levels of both ING5 and miR-34c-5p in NSCLC tissues from the TCGA database are decreased compared with that in adjacent tissues. Higher expression levels of both ING5 and miR-34c-5p predict longer overall survival (OS). Snail1 is the target gene of miR-34c-5p, as predicted by an online database, which is further verified by a dual-luciferase reporter assay. The expression level of Snail1 in NSCLC cells is markedly reduced following miR-34c-5p overexpression, leading to the inactivation of the Snail1 downstream TGF-ß/Smad3 signaling pathway. The TGF-ß signaling-specific inhibitor LY2157299 reverses the enhanced EMT, proliferation, migration, and invasion abilities induced by the miR-34c-5p inhibitor. Furthermore, tail vein injection of miR-34c-5p agomir inhibits xenografted tumor metastasis. Overall, this study concludes that miR-34c-5p, induced by ING5 overexpression, is a tumor suppressor that targets Snail1 and mediates the inhibitory effects of ING5 on the EMT and invasion of NSCLC cells. These results provide a novel mechanism mediating the antitumor effects of ING5.

Integrating a Nanowire Laser in an on-Chip Photonic Waveguide.

We report a simple and facile integration strategy of a laser source in passive photonic integrated circuits (PICs) by deterministically embedding semiconductor nanowires (NWs) in waveguides. InP NWs laid on a SiN slab are buried by a polymer layer which also acts as an electron-beam resist. With electron-beam lithography, hybrid polymer-SiN waveguides are formed with precisely embedded NWs. The lasing behavior of the waveguide-embedded NWs is confirmed, and more importantly, the NW lasing mode couples into the hybrid waveguide and forms an in-plane guiding mode. Multiple waveguide-embedded NW lasers are further integrated in complex photonic structures to illustrate that the waveguiding mode supplied by the NW lasers could be manipulated for on-chip signal processing, including power splitting and wavelength-division multiplexing. This integration strategy of an on-chip laser is applicable to other PIC platforms, such as silicon and lithium niobate, and the top cladding layer could be changed by depositing SiN or SiO2, promising its CMOS compatibility.

FGF5 protects heart from sepsis injury by attenuating cardiomyocyte pyroptosis through inhibiting CaMKII/NFκB signaling.

Sepsis accompanied by myocardial injury is an important cause of multiple organ dysfunction, and its underlying molecular mechanism is not fully clear. Although diverse effects of fibroblast growth factor (FGF) in heart have been discovered till now, the specific role of FGF5 in heart remains unclear. Therefore, our study aims to explore the possible impacts of FGF5 on sepsis-induced cardiac injury. Sepsis-induced cardiac injury was established through administration of lipopolysaccharide (LPS). The expression level of FGF5 in sepsis heart was decreased, and injection of FGF5-overexpressing adenovirus attenuated cardiac injury reflected by echocardiographic and pathological findings. Besides, FGF5 overexpression, not only in vivo heart but also in vitro cardiomyocytes, reduced the levels of oxidative stress and pyroptosis resulted from LPS. In addition, overexpression of FGF5 reduced LPS-activated the levels of phosphorylated CaMKII (p-CaMKII), p-NFκB, NLRP3, caspase-1, IL-1ß and IL-18. Furthermore, KN93, the inhibitor of CaMKII, exerted the similarly protective effects on LPS-induced pyroptosis. In summary, our study implied the beneficial effects of FGF5 on LPS-induced cardiac injury, which was at least partially attributed to the inhibition of CaMKII-mediated pyroptotic signaling.

Propagation characteristics of terahertz wave in inductively coupled plasma.

Firstly, the electron density distribution of inductively coupled plasma (ICP) is measured by laser Thomson scattering (TS) method and the features of the ICP under the same experimental conditions are simulated by finite element method (FEM). The simulated results are in good agreement with the experimental results, which verifies the accuracy of the ICP generation simulation model. Secondly, the propagation characteristics of terahertz wave in ICP are measured by terahertz time domain spectroscopy (THz-TDS) and calculated by FEM according to the electron density distribution of ICP simulated in the first step above. The high consistency between the experimental and simulation results of terahertz wave propagation characteristics in ICP further proves the accuracy of terahertz wave transmission model in plasma and the feasibility of joint simulation with ICP generation simulation model.

Coptisine Attenuates Diabetes-Associated Endothelial Dysfunction through Inhibition of Endoplasmic Reticulum Stress and Oxidative Stress.

Coptisine is the major bioactive protoberberine alkaloid found in Rhizoma Coptidis. Coptisine reduces inflammatory responses and improves glucose tolerance; nevertheless, whether coptisine has vasoprotective effect in diabetes is not fully characterized. Conduit arteries including aortas and carotid arteries were obtained from male C57BL/6J mice for ex vivo treatment with risk factors (high glucose or tunicamycin) and coptisine. Some arterial rings were obtained from diabetic mice, which were induced by high-fat diet (45% kcal% fat) feeding for 6 weeks combined with a low-dose intraperitoneal injection of streptozotocin (120 mg/kg). Functional studies showed that coptisine protected endothelium-dependent relaxation in aortas against risk factors and from diabetic mice. Coptisine increased phosphorylations of AMPK and eNOS and downregulated the endoplasmic reticulum (ER) stress markers as determined by Western blotting. Coptisine elevates NO bioavailability and decreases reactive oxygen species level. The results indicate that coptisine improves vascular function in diabetes through suppression of ER stress and oxidative stress, implying the therapeutic potential of coptisine to treat diabetic vasculopathy.

A long-acting isomer of Ac-SDKP attenuates pulmonary fibrosis through SRPK1-mediated PI3K/AKT and Smad2 pathway inhibition.

Idiopathic pulmonary fibrosis (IPF) is a progressive, life-threatening lung disease with a poor prognosis. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a critical negative regulator of fibrosis development. However, it's extremely short half-life greatly limits its applications. Previously, we reported an Ac-SDKP analog peptide in which Asp and Lys residues were replaced with D-amino acids (Ac-SDD KD P). Ac-SDD KD P exhibits better resistance to angiotensin-1-converting enzyme (ACE)-mediated degradation and a longer half-life than Ac-SDKP in rat and human sera. The objective of this study was to explore the potential application of Ac-SDD KD P for the treatment of IPF and to clarify the underlying mechanisms. We found that Ac-SDD KD P exerted similar antifibrotic effects as Ac-SDKP on human fetal lung fibroblast-1 (HFL-1) proliferation, α-smooth muscle actin (α-SMA), collagen I and collagen III expression, and Smad-2 phosphorylation in vitro. In vivo, Ac-SDD KD P exhibited significantly greater protective effects against bleomycin-induced pulmonary fibrosis than Ac-SDKP in mice. α-SMA, CD45, collagen I and collagen III expression, and Smad-2 phosphorylation were significantly decreased in the lungs of Ac-SDD KD P-treated but not Ac-SDKP-treated mice. Furthermore, a pull-down experiment was used to screen for molecules that interact with Ac-SDKP. Co-immunoprecipitation (Co-IP) and computer-based molecular docking experiments demonstrated an interaction between Ac-SDKP or Ac-SDD KD P (Ac-SDKP/Ac-SDD KD P) and serine/arginine-rich protein-specific kinase 1 (SRPK1) that caused inhibition SRPK1-mediated phosphatidylinositol-3 kinase/ serine/threonine kinase (PIK3/AKT) signaling pathway activation and Smad2 phosphorylation and thereby attenuated lung fibrosis. Our data suggest that long-acting Ac-SDD KD P may potentially be an effective drug for the treatment of pulmonary fibrosis. The interacting molecule and antifibrotic mechanism of Ac-SDKP/Ac-SDD KD P were also identified, providing an experimental and theoretical foundation for the clinical application of the drug.

d-amino acid modification protects N-Acetyl-seryl-aspartyl-lysyl-proline from physiological hydroxylation and increases its antifibrotic effects on hepatic fibrosis.

N-Acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a critical negative regulator of fibrosis development in the liver. However, its extremely short half-life in vivo greatly compromises its potential applications. Here, we report an Ac-SDKP analog peptide with d-amino acid replacement (Ac-SDD KD P). The stability of Ac-SDD KD P and its prevention of liver fibrosis were investigated in vitro and in vivo. The stabilities of Ac-SDKP and Ac-SDD KD P exposed to angiotensin-1-converting enzyme (ACE) and their half-lives in rats and human sera were determined by high-performance liquid chromatography. The inhibitory effects of Ac-SDKP and Ac-SDD KD P on the proliferation and activation of hepatic stellate cells (HSC-T6) were evaluated using the Cell Counting Kit-8, Western blotting, reverse transcription quantitative polymerase chain reaction, and immunofluorescence assays. Finally, the protective effects of Ac-SDKP and Ac-SDD KD P on carbon tetrachloride (CCl4 )-induced liver fibrosis in rats were compared. d-Amino acid replacement significantly enhanced the stability of the peptide to ACE and prolonged the half-life of Ac-SDKP in rats and human sera. The Ac-SDKP-mediated inhibition of HSC-T6 cell proliferation was well preserved, and Ac-SDD KD P exerted inhibitory effects comparable to Ac-SDKP on α-smooth muscle actin (α-SMA), collagen I and III expression, and phosphorylated-Smad-2 expression. After intraperitoneal (i.p.) administration, Ac-SDD KD P exhibited significantly greater protection than Ac-SDKP against CCl4 -induced liver fibrosis in rats. The serum alanine aminotransferase, aspartate aminotransferase, albumin, and total protein levels of the Ac-SDD KD P-treated rats were significantly lower than those of the Ac-SDKP-treated rats. α-SMA, CD45, and collagen I and III expression, as well as Smad-2 phosphorylation were significantly attenuated in the livers of the Ac-SDD KD P-treated rats compared to those of the Ac-SDKP-treated rats. Furthermore, we showed that the Ac-SDD KD P concentration in the rat liver increased to a physiological level of 60 min after i.p. administration, although i.p. administration of Ac-SDKP failed to enhance the peptide concentration in the rat liver. Our findings indicate that d-amino acid replacement is a simple and effective method to enhance the stability of Ac-SDKP. Ac-SDD KD P represents potential application of Ac-SDKP in fibrosis treatment and provides a new potential treatment strategy for liver fibrosis. © 2019 IUBMB Life, 71(9):1302-1312, 2019.

Self-Assembly Growth of In-Rich InGaAs Core-Shell Structured Nanowires with Remarkable Near-Infrared Photoresponsivity.

Understanding the compositional distribution of ternary nanowires is essential to build the connection between nanowire structures and their potential applications. In this study, we grew epitaxial ternary InGaAs nanowires with high In concentration on GaAs {111}B substrates. Our detailed electron microscopy characterizations suggest that the grown ternary InGaAs nanowires have an extraordinary core-shell structure with In-rich cores and Ga-enriched shells, in which both nanowire cores and shells showed compositional gradient. It was found that In-rich nanowire cores are formed due to the Ga-limited growth environment, caused by the competition with the spontaneous InGaAs planar layer growth on the substrate that consumes more Ga than the nominal Ga concentration during the growth. Moreover, the composition gradient in the nanowires cores and shells is a result of strain relaxation between them. Our optoelectronic property measurements from prototype nanowire devices show a remarkable photoresponsivity under the near-infrared illumination. This study provides a new approach for designing and realizing complex nanowire heterostructures for high-efficiency nanowire-based systems and devices.

Visible Light-Assisted High-Performance Mid-Infrared Photodetectors Based on Single InAs Nanowire.

One-dimensional InAs nanowires (NWs) have been widely researched in recent years. Features of high mobility and narrow bandgap reveal its great potential of optoelectronic applications. However, most reported work about InAs NW-based photodetectors is limited to the visible waveband. Although some work shows certain response for near-infrared light, the problems of large dark current and small light on/off ratio are unsolved, thus significantly restricting the detectivity. Here in this work, a novel "visible light-assisted dark-current suppressing method" is proposed for the first time to reduce the dark current and enhance the infrared photodetection of single InAs NW photodetectors. This method effectively increases the barrier height of the metal-semiconductor contact, thus significantly making the device a metal-semiconductor-metal (MSM) photodiode. These MSM photodiodes demonstrate broadband detection from less than 1 µm to more than 3 µm and a fast response of tens of microseconds. A high detectivity of ∼1012 Jones has been achieved for the wavelength of 2000 nm at a low bias voltage of 0.1 V with corresponding responsivity of as much as 40 A/W. Even for the incident wavelength of 3113 nm, a detectivity of ∼1010 Jones and a responsivity of 0.6 A/W have been obtained. Our work has achieved an extended detection waveband for single InAs NW photodetector from visible and near-infrared to mid-infrared. The excellent performance for infrared detection demonstrated the great potential of narrow bandgap NWs for future infrared optoelectronic applications.

Paris Saponin VII Inhibits the Migration and Invasion in Human A549 Lung Cancer Cells.

Metastasis is the main cause of death in lung cancer. Targeting the process of metastasis is a strategy to lung cancer treatment. Trillium tschonoskii Maxim., a traditional Chinese medicine, has been used for treatment of many diseases, including cancer. This study aims to determine the anti-metastatic effect of paris saponin VII (PS VII) which was extracted from T. tschonoskii Maxim. by using human lung cancer cell line A549 cells. Our results showed that PS VII could significantly suppress the viability as well as cell migration and invasion abilities of A549 cells in a concentration-dependent manner. PS VII reduced the activity of matrix metalloproteinase-2 (MMP-2) and MMP-9 by elevating the expression of TIMP1/2. These data indicated that PS VII could reduce the metastatic capability of A549 cells, probably through up-regulating the expression of TIMP1/2. These findings demonstrated a new therapeutic potential for PS VII in anti-metastatic therapy of lung cancer. Copyright © 2015 John Wiley & Sons, Ltd.

Experimental study on mechanical and hydraulic properties of xanthan gum improved low liquid limit silty soil.

The low liquid limit silty soil in the North China plain area is generally unsuitable for direct use as roadbed and slope soil. In order to improve the performance of low liquid limit silty soil, xanthan gum was used as an improver. Through a series of tests, the improvement effect of xanthan gum on low liquid limit silty soil was studied. The test results showed that Xanthan gum as an improver could significantly improve the unconfined compressive strength of silty soil. With the increase in dosage and curing age, the unconfined compressive strength of improved silty soil continued to improve and eventually tended to stabilize. The optimal dosage and curing period were 2% and 7 days, respectively. In addition, Xanthan gum could greatly improve the permeability and disintegration of low liquid limit silty soil. The permeability coefficient of improved silty soil with a content of 0.75% Xanthan gum and a 7-day curing period was 4.73 × 10-4 m·s-1, which was only 1.10% of that of plain silty soil at the same curing period. After immersion in water for 12 h, the soil only experienced slight disintegration. The scanning electron microscope image showed that the gel generated by the hydration reaction of Xanthan gum could improve the compactness and integrity of the soil by filling the voids, thus significantly improving the mechanical and hydraulic properties of the low liquid limit silty soil.

Experimental study on axial tensile properties of basalt fibre reinforced recycled aggregate concrete.

In order to investigate the tensile properties of basalt fibre reinforced recycled aggregate concrete (BFRAC), the axial tensile tests were carried out on BFRAC specimens using the concrete axial tensile testing device. The effects of basalt fibre (BF) content and recycled aggregate replacement rate on the tensile properties of BFRAC were quantitatively investigated, and the tensile damage mechanism of BFRAC was analysed. The following conclusions were drawn: The volume fraction of BF had the most prominent effect on the axial tensile properties of BFRAC. The axial tensile strength and peak tensile strain of BFRAC both showed the change rule of first increasing and then decreasing with the increase of BF volume fraction. The replacement rate of recycled aggregate is negatively correlated with the tensile properties of BFRAC. The larger the replacement rate, the worse the tensile properties of BFRAC. When the replacement rate of recycled aggregate is 30 % and the volume fraction of BF is 0.3 %, the tensile properties of BFRAC are better, as well as its economic and environmental performance. The axial tensile strength and peak tensile strain were 2.08 MPa and 114 × 10-6, respectively. BFRAC exhibits the toughening and crack arresting effect of BF, and the crack development is relatively slow, showing more obvious plastic damage characteristics.

Experimental study on direct tensile fatigue performance of basalt fiber reinforced concrete.

Conducting research on the fatigue performance of concrete materials is of great significance for the anti fatigue design of concrete structures. Currently, indirect tensile or compressive strength tests are commonly used to study the fatigue performance of basalt fiber reinforced concrete, but there is little research on its fatigue performance under direct tensile conditions. Using a fatigue testing machine and a self-developed concrete axial tensile device, direct tensile fatigue tests of basalt fiber reinforced concrete were conducted under different fiber content and stress levels. Based on fatigue test data, the entire fatigue tensile process of basalt fiber reinforced concrete was analyzed, and the effects of fiber content and stress level on the fatigue life of concrete specimens were explored. Strain fatigue life curves of concrete with different fiber content were plotted. The experimental results indicate that the failure mode of basalt fiber reinforced concrete under cyclic loading is brittle failure; with the increase of basalt fiber content, the fatigue life of concrete first increases and then decreases. When the fiber content is 0.3%, the fatigue life of basalt fiber concrete is the highest compared to the benchmark concrete. When the fiber content is the same, the fatigue life of concrete decreases with the increase of stress level. The fatigue deformation process of basalt fiber reinforced concrete can be divided into three stages: the stage of fast strain growth, the stage of uniform strain growth, and the stage of rapid strain growth.

Step by step and combined supporting technique with allowable deformation + limiting shape for soft rock roadway.

Aiming at the difficult problems of the large deformation in weakly cemented soft rock roadways, the reasons of large deformation are analyzed for roadways in Hongqingliang coal mine. On this basis, the principle of step by step combined support technology based on allowable deformation + limiting shape for weakly cemented soft rock roadway is proposed, and the optimal support parameters of step by step combined technology are determined by FLAC3D. Step by step combined support technology includes the primary support of anchor bolt + anchor cable + initial shotcrete and the secondary support of U-shaped steel shed + filling flexible material behind shed + control of key parts. The comparative analysis on the site shows that the deformation rate and final deformation amount of the surrounding rock after the step by step combined support are less than those of the primary support, and the deformation of the surrounding rock can be controlled effectively after the secondary support is added. Step by step combined support is superior to the traditional bolt + anchor cable combined repair in terms of economy and efficiency. The optimal construction period of each working procedure of the step by step combined technology is 28 days after the completion of the first support, and the step by step combined support based on allowable deformation + limiting shape is an effective way to control the surrounding rock of soft rock roadway.