An Innovative Non-Pillar Coal-Mining Technology with Automatically Formed Entry: A Case Study

A non-pillar coal-mining technology with an automatically formed entry is proposed,which reduces the waste of coal resources and the underground entry drivage workload.Three key techniques in this technology cooperate to achieve automatic formation and retaining of the gob-side entry,and to realize nonpillar mining.Constant-resistance large deformation(CRLD)support ensures the stability of the entry roof;directional presplitting blasting(DPB)separates the entry roof and the gob roof;and a blockinggangue support system(BGSS)integrates the caved rock material as an effective entry rib.An industrial test was conducted to verify the engineering effects of these key techniques.The field application results showed that the retained entry was under the pressure-relief zone due to the broken-expansion nature of the caved rock mass within the DPB height.After going through a provisional dynamic pressure-bearing zone,the retained entry entered the stability zone.The final stable entry meets the requirements of safety and production.The research results demonstrate the good engineering applicability of this technology.By taking the framework of the technology design principles into consideration and adjusting the measures according to different site conditions,it is expected that the proposed non-pillar coal-mining technology can be popularized on a large scale.

Selenium nanoparticles reduce oxidative stress-induced cardiomyocyte apoptosis in ascites syndrome in broiler chickens via the ATF6-DR5 signaling pathway

Broiler ascites syndrome(AS)is one of the main diseases threatening the health of broilers.It is well documented that myocardial hypertrophy and failure is one of the key mechanisms of broiler ascites syndrome.Therefore,prevention of cardiac hypertrophy and failure would be one goal to reduce broiler ascites syndrome incidence.Myocardial hyper-trophy and failure are closely related to endoplasmic reticulum stress(ERS)in cardiac myocytes,and the endoplasmic reticulum stress signaling system(ATF6-DR5)is one of the important pathways of myocardial apoptosis.Excessive hyper-trophy will affect the heart muscle's normal contraction and diastole function,and the heart will turn from compen-sated to decompensate thus causing myocardial injury.Myocardial apoptosis is a core component of the pathological changes of this myocardial injury.Nano-selenium is a kind of red elemental selenium nanoparticle.Due to its excellent physical,chemical and biological properties,it has attracted extensive academic attention in recent years.It has been proven to have excellent antioxidant,antibacterial,antitumor,antihypertrophic,and antiapoptotic abilties.Herein,nano-selenium(1μmol/L)can inhibit hydrogen peroxide(H_(2)O_(2))-induced oxidative stress in broiler primary cardiomyocytes,and at the same time reduce cardiomyocyte apoptosis.In vivo,nano-selenium can reduce broiler myocardial injury-related enzyme indicators(AST,CK and LDH),and alleviate myocardial injury.It can also activate the antioxidant enzyme system(SOD,GSH-Px and CAT)and reduce MDA,and make the recovery ofT-AOC ability in the organization.Meanwhile,nano-selenium can down-regulate the genes and proteins expression of ATF-6,GRP-78,CHOP and caspase 12 in the ERS-related signaling pathway,and inhibit that of downstream-related caspase 3,Bax and caspase 9,and increase that of the downstream anti-apoptotic Bcl-2,thereby maintaining the homeostasis of the endoplasmic reticulum and alleviating cardiomyocyte apoptosis.It can be seen that nano-selenium can protect the damaged myocardium in the broiler ascites caused by high-salt drinking by regulating the ATF6-DR5 signaling pathway.This study was performed in chickens and cardiomyocyte cells and attempted to demonstrate that selenium nanoparticles can protect the damaged myocar-dium in broiler ascites.This paper provides a new idea for preventing and treating broiler ascites syndrome.

The dopamine receptor D4 regulates the proliferation of pulmonary arteries smooth muscle in broilers by downregulating AT1R

The major cause of pulmonary vascular remodeling in broilers is abnormal proliferation of vascular smooth muscle cells(VSMCs),and one of the main causes of pulmonary hypertension syndrome(PHS)in broilers is pulmonary artery vascular remodeling.Forty Arbor Acres(AA)broilers were randomly divided into four groups(n=10):a control group(deionized water,Og/L NaCl),a freshwater group(FW,deionized water+1 g/L NaCl),highly salinized freshwater group 1(H-SFW-1,deionized water+2.5 g/L NaCl)and highly salinized freshwater group 2(H-SFW-2,deionized water+5 g/L NaCl).The results of in vivo experiments showed that vascular smooth muscle of the broilers could be significantly proliferated by intake of high-salinity fresh water(H-SFW-1&H-SFW-2),which significantly increased the content of angiotensin II(Ang II)and the expression of angiotensin II type 1(AT1)receptor protein.Meanwhile,it significantly decreased the expression of dopamine receptor D4(DRD4)protein.The results of in vitro experiments showed that exogenous Ang II induced the proliferation of primary VSMCs in broilers,which could be significantly inhibited by DRD4 agonists(D4A,HY-101384A)and enhanced by DRD4 inhibitors(D4I;HY-B0965).In addition,the results of immunoblotting and fluorescence quantitative PCR showed that AT1 receptors could be negatively regulated by DRD4 in VSMCs of broilers,either at the transcriptional or translational level.At the same time,the expression of AT1 receptor could be increased by DRD4 inhibition by D4I and decreased by DRD4 activation by D4A.The negative regulatory effect of DRD4 on AT1 receptor occurred in a dose-dependent manner.These results indicate that long-term intake of highly salinized fresh water can cause PHS in broilers,accompanied by varying degrees of proliferation of pulmonary artery smooth muscle.This mechanism may involve response of its receptor being induced by increased Ang II,while DRD4 can negatively regulate it.

Stem cell-derived hepatocyte therapy using versatile biomimetic nanozyme incorporated nanofiber-reinforced decellularized extracellular matrix hydrogels for the treatment of acute liver failure

Reactive oxygen species(ROS)-associated oxidative stress,inflammation storm,and massive hepatocyte necrosis are the typical manifestations of acute liver failure(ALF),therefore specific therapeutic interventions are essential for the devastating disease.Here,we developed a platform consisting of versatile biomimetic copper oxide nanozymes(Cu NZs)-loaded PLGA nanofibers(Cu NZs@PLGA nanofibers)and decellularized extracellular matrix(dECM)hydrogels for delivery of human adipose-derived mesenchymal stem/stromal cells-derived hepatocyte-like cells(hADMSCs-derived HLCs)(HLCs/Cu NZs@fiber/dECM).Cu NZs@PLGA nanofibers could conspicuously scavenge excessive ROS at the early stage of ALF,and reduce the massive accumulation of pro-inflammatory cytokines,herein efficiently preventing the deterioration of hepatocytes necrosis.Moreover,Cu NZs@PLGA nanofibers also exhibited a cytoprotection effect on the transplanted HLCs.Meanwhile,HLCs with hepatic-specific biofunctions and anti-inflammatory activity acted as a promising alternative cell source for ALF therapy.The dECM hydrogels further provided the desirable 3D environment and favorably improved the hepatic functions of HLCs.In addition,the pro-angiogenesis activity of Cu NZs@PLGA nanofibers also facilitated the integration of the whole implant with the host liver.Hence,HLCs/Cu NZs@fiber/dECM performed excellent synergistic therapeutic efficacy on ALF mice.This strategy using Cu NZs@PLGA nanofiber-reinforced dECM hydrogels for HLCs in situ delivery is a promising approach for ALF therapy and shows great potential for clinical translation.

Spatiotemporal control of CRISPR/Cas9 gene editing

The clustered regularly interspaced short palindromic repeats(CRISPRJ/associated protein 9(CRISPR/Cas9)gene editing technology,as a revolutionary breakthrough in genetic engineering,offers a promising platform to improve the treatment of various genetic and infectious diseases because of its simple design and powerful ability to edit different loci simultaneously.However,failure to conduct precise gene editing in specific tissues or cells within a certain time may result in undesirable consequences,such as serious off-target effects,representing a critical challenge for the clinical translation of the technology.Recently,some emerging strategies using genetic regulation,chemical and physical strategies to regulate the activity of CRISPR/Cas9 have shown promising results in the improvement of spatiotemporal controllability.Herein,in this review,we first summarize the latest progress of these advanced strategies involving cell-specific promoters,small-molecule activation and inhibition,bioresponsive delivery carriers,and optical/thermal/ultrasonic/magnetic activation.Next,we highlight the advantages and disadvantages of various strategies and discuss their obstacles and limitations in clinical translation.Finally,we propose viewpoints on directions that can be explored to further improve the spatiotemporal operability of CRISPR/Cas9.

Effect of annealing on the damage threshold and optical properties of HfO2/Ta2O5/SiO2 high-reflection film

The effect of thermal annealing on the optical properties, microstructure, and laser-induced damage threshold(LIDT) of HfO2/Ta2O5/SiO2 HR films has been investigated. The transmission spectra shift to a short wavelength and the X-ray diffraction peaks of monoclinic structure HfO2 are enhanced after thermal annealing. The calculated results of the m(-111) diffraction peak show that the HfO2 grain size is increased, which is conducive to increasing the thermal conductivity. Thermal annealing also reduces the laser absorption of high-reflection films. The improvement of thermal conductivity and the decrease of laser absorption both contribute to the improvement of LIDT. The experimental results show that the highest LIDT of 22.4 J/cm2 is obtained at300°C annealing temperature. With the further increase of annealing temperature, the damage changes from thermal stress damage to thermal explosion damage, resulting in the decrease of LIDT.