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Perovskites with flexible structures and excellent redox properties have attracted considerable attention in industry, and their denitration activities can be further improved with metal substitution.

Probable surface NH3-SCR reaction mechanism over CuCe/TiO2-ZrO2 catalyst is proposed to follow the E–R mechanism and the L–H mechanism, while the E–R mechanism dominates in the reaction and the oxidation of NO closes the catalytic cycle.

The severe electric and thermal environments may cause localized deterioration of the contact behavior of thermoelectric devices. The contact responses of the thermoelectricity under the joint effect of the finite size and the friction are analyzed. The law of the Coulomb friction is adopted. The obtained Fredholm kernel functions reveal the influence of the thickness and the friction. The known Jacobi polynomials are employed to discretize the obtained singular integral equation. The effects of the thermoelectric loadings (the total electric current and the total energy flux), friction coefficient, the thermoelectric strip thickness, and the elastic and thermoelectric material constants on the distribution of the normal traction and the surface in-plane stress are demonstrated in detail. The smaller thermal expansion coefficient and shear modulus will contribute to the lower stress concentration at both contact edges. The surface in-plane tensile stress behind the trailing edge can be alleviated as the thermoelectric strip becomes thinner.

A theoretical frictional contact model of thermoelectric materials with nonlinear thermoelectric coupling loaded by a sliding punch is considered in which the punch is also assumed to be an electrical and thermal conductor. For the electric fields and the temperature fields, some analytical results are obtained by Fourier transform technique, such as the full field closed-form formulas of the electrochemical potential, the temperature, the electric current density and the energy flux. The distributions of normal electric current density and normal energy flux at subsurface are graphically given. For the elastic fields, the thermoelastic contact problem is reduced to a singular integral equation of the second kind in which thermoelectric effects are reflected in the right end of the resulting equation. The present results demonstrate that the normal electric current density, the normal energy flux and the contact pressure on the contact surface of thermoelectric materials exhibit high singularity in the vicinity of the edges of the punch. Furthermore, the effects of the friction coefficient and the thermoelectric loads on the critical stresses, the electric current density intensity factor, the energy flux intensity factor and the stress intensity factor are provided. The finding of the presented model is helpful for accessing the surface wear resistance of thermoelectric materials.

Neuron-restrictive silencer factor (NRSF) is a zinc finger protein that acts as a negative transcriptional regulator by recruiting histone deacetylases and other co-factors. It plays a crucial role in nervous system development and is recently reported to be involved in tumorigenesis in a tumor type-dependent manner; however, the role of NRSF in hepatocellular carcinoma (HCC) tumorigenesis remains unclear. Here, we found that NRSF expression was up-regulated in 27 of 49 human HCC tissue samples examined. Additionally, mice with conditional NRSF-knockout in the liver exhibited a higher tolerance against diethylnitrosamine (DEN)-induced acute liver injury and were less sensitive to DEN-induced HCC initiation. Our results showed that silencing NRSF in HepG2 cells using RNAi technology significantly inhibited HepG2 cell proliferation and severely hindered their migration and invasion potentials. Our results demonstrated that NRSF plays a pivotal role in promoting DEN-induced HCC initiation via a mechanism related to the STAT3 and AKT signaling pathways. Thus, NRSF could be a potential therapeutic target for treating human HCC.

Successful wound healing depends on the reconstruction of proper tissue homeostasis, particularly in the posttraumatic inflammatory tissue microenvironment. Diabetes jeopardizes tissues’ immune homeostasis in cutaneous wounds, causing persistent chronic inflammation and cytokine dysfunction. Previously, we developed an autologous regeneration factor (ARF) technology to extract the cytokine composite from autologous tissue to restore immune homeostasis and promote wound healing. However, treatment efficacy was significantly compromised in diabetic conditions. Therefore, we proposed that a combination of melatonin and ARF, which is beneficial for proper immune homeostasis reconstruction, could be an effective treatment for diabetic wounds. Our research showed that the utilization of melatonin-mediated ARF biogel (AM gel) promoted diabetic wound regeneration at a more rapid healing rate. RNA-Seq analysis showed that AM gel treatment could restore more favorable immune tissue homeostasis with unique inflammatory patterning as a result of the diminished intensity of acute and chronic inflammation. Currently, AM gel could be a novel and promising therapeutic strategy for diabetic wounds in clinical practice through favorable immune homeostatic reconstructions in the tissue microenvironment and proper posttraumatic inflammation patterning.

RILP (Rab-interacting lysosomal protein) is a key regulator of lysosomal transport and a potential tumor suppressor. However, the role of RILP in prostate cancer and the underlying mechanism of RILP in regulating the proliferation, migration, and invasion of prostate cancer cells remain to be studied. In this study, we confirmed RalGDS (Ral guanine nucleotide dissociation stimulator) as the interaction partner of RILP in PC3 prostate cancer cells. Immunofluorescence microscopy showed that RILP recruits RalGDS to the lysosomal compartment. We found that RILP inhibits the activation of RalA and downstream effector RalBP1, and negatively regulates the downstream molecular phosphorylation of Ras. We showed that RILP inhibits the proliferation, migration, and invasion of PC3 prostate cancer cells, which may give rise to novel ideas for cancer treatment.

This study aims to investigate the enhanced low temperature denitration activity and promotional mechanism of a cerium-based catalyst through copper modification. In this paper, copper and cerium oxides were supported on TiO

Myocardial damage due to dysfunctional myocardium has been increasing, and the prognosis of pharmacological and device-based therapies remain poor. Isl1-expressing cells were thought to be progenitor cells for cardiomyocyte proliferation after specific stimuli. However, the true origin of the proliferating myocardiac cells and the role of Isl1 in adult mammals remain unresolved. In this study, Isl1-CreERT2 knock-in mouse model was constructed using CRISPR/Cas9 technology. Using tamoxifen-inducible Isl1-CreERT/Rosa26R-LacZ system, Isl1+cells and their progeny were permanently marked by lacZ-expression. X-gal staining, immunostaining, and quantitative PCR were then used to reveal the fate of Isl1+cells under physiological and exercise conditions in mouse hearts from embryonic stage to adulthood. Isl1+cells were found to localize to the sinoatrial node, atrioventricular node, cardiac ganglia, aortic arch, and pulmonary roots in adult mice heart. However, they did not act as cardiac progenitor cells under physiological and exercise conditions. Although Isl1+cells showed progenitor cell properties in early mouse embryos (E7.5), this ability was lost by E9.5. Furthermore, although the proliferation and regeneration of heart cell was observed in response to exercise, the cells associated were not Isl1 positive.

Most of the world’s large molybdenum (Mo) deposits are genetically related to magmas that underwent significant fractional crystallization and fluid exsolution, and the residual silicate melts are commonly peralkaline. To understand the relationship between melt compositions and the genesis of porphyry Mo mineralization, the partition coefficients of molybdenum (DMo) between fluid and felsic melt were determined at 850 °C, 900 °C, and 100 MPa with various values of A/NK [molar Al2O3/ (Na2O + K2O) in the melt] under an oxygen fugacity around the Ni–NiO (NNO) buffer. The results show that DMo decreases from 4.23 to 0.4 with increasing A/NK from 0.75 to 1.36 in the carbon dioxide series (fluid composed of X CO 2 = 0.096 [molar CO2/(CO2 + H2O)] and 17.5 wt% NaCl). A similar trend was observed in pure water, with A/NK varying from 0.72 to 1.23, DMo decreases from 0.54 to 0.15. Significantly, DMo in peralkaline melt is consistently higher than that in peraluminous melt, even with the same NBO/T (the ratio of non-bridge oxygen and tetrahedron ion). Our study therefore reveals that Mo is easily distributed into fluids that exsolved from peralkaline magmas. This finding explains why highly fractionated magmas are critical for porphyry Mo mineralization.

Successful wound healing relies on reconstructing proper tissue homeostasis, particularly the post-traumatic inflammatory tissue microenvironment. Nevertheless, diabetes jeopardizes tissue’s immune homeostasis of cutaneous wounds, characterized by the accumulation of reactive oxygen species (ROS), causing persistent chronic inflammation and cytokine dysfunction. Previously, we have developed an autologous regeneration factors (ARFs) technology to extract the cytokine composite from autologous tissue to restore the immune homeostasis and promote wound healing. However, treatment efficacy was significantly compromised in diabetic conditions. Therefore, we proposed the combinational use of melatonin and ARF could be an effective treatment for diabetic wounds, considering the melatonin can scavenge ROS, which is beneficial for the proper immune homeostasis reconstruction. Our research showed that the utilization of melatonin-mediated ARF biogel (AM gel) promoted diabetic wound regeneration at a more rapid healing rate. Furthermore, RNA-seq analysis showed that the AM gel treatment could restore more favorable immune tissue homeostasis with unique inflammatory patterning by the dramatically diminished intensity of acute and chronic inflammation. Currently, AM gel could be a novel and promising therapeutic strategy for diabetic wounds in clinical scenarios by reconstructing more favorable immune homeostasis in tissue microenvironment by orchestrating a proper post-traumatic inflammation patterning.# Funding: This work was supported by the National Natural Science Foundation of China (NSFC) (Nos. 81772354, 81902189, 82072409), Clinical Innovation Research Program of Guangzhou Regenerative Medicine and Health Guangdong Laboratory (2018GZR0201001), Science Technology Project of Guangzhou City (201804010185), Natural Science Foundation of Guangdong Province (2019A1515012020), Science and Technology Innovation Project of Foshan City (1920001000025), and National Young Thousand-Talent Scheme to Zhang Zhi-Yong. Declaration of Interest: The authors declare that they have no potential conflict of interest in relation to the study in this paper. Ethical Approval: All animal experiments were approved by the Animal Ethics Committee of Guangdong Medical Laboratory Animal Center.

Correction for ‘Promotional mechanism of enhanced denitration activity with Cu modification in a Ce/TiO2–ZrO2 catalyst for a low temperature NH3-SCR system’ by Wei Zhang et al., RSC Adv., 2022, 12, 378–388, DOI: 10.1039/d1ra06325a

Exercise and resveratrol supplementation exhibit anti-obesity functions in the long term but have not been fully investigated yet in terms of their early potential effectiveness. Mice fed with high-fat diet were categorized into control (Cont), exercise (Ex), resveratrol supplementation (Res), and exercise combined with resveratrol supplementation (Ex ＋ Res) groups. In the four-week period of weight loss, exercise combined with resveratrol supplementation exerted no additional effects on body weight loss but significantly improved whole-body glucose and lipid homeostasis. The combined treatment significantly decreased intrahepatic lipid content but did not affect intramyocellular lipid content. Moreover, the treatment significantly increased the contents of mtDNA and cytochrome c, the expression levels of peroxisome proliferator-activated receptor gamma coactivator-1 alpha and its downstream transcription factors, and the activities of ATPase and citrate synthase. However, exercise, resveratrol, and their combination did not promote myofiber specification toward slow-twitch type. The effects of exercise combined with resveratrol supplementation on weight loss could be partly due to enhanced mitochondrial biogenesis and not to fiber-type shift in skeletal muscle tissues. [BMB Reports 2018; 51(4): 200-205].

Several studies have associated reduced expression of synaptosomal-associated protein of 25 kDa (SNAP-25) with schizophrenia, yet little is known about its role in the illness. In this paper, a forebrain glutamatergic neuron-specific SNAP-25 knockout mouse model was constructed and studied to explore the possible pathogenetic role of SNAP-25 in schizophrenia. We showed that SNAP-25 conditional knockout (cKO) mice exhibited typical schizophrenia-like phenotype. A significantly elevated extracellular glutamate level was detected in the cerebral cortex of the mouse model. Compared with Ctrls, SNAP-25 was dramatically reduced by about 60% both in cytoplasm and in membrane fractions of cerebral cortex of cKOs, while the other two core members of SNARE complex: Syntaxin-1 (increased ~80%) and Vamp2 (increased ~96%) were significantly increased in cell membrane part. Riluzole, a glutamate release inhibitor, significantly attenuated the locomotor hyperactivity deficits in cKO mice. Our findings provide in vivo functional evidence showing a critical role of SNAP-25 dysfunction on synaptic transmission, which contributes to the developmental of schizophrenia. It is suggested that a SNAP-25 cKO mouse, a valuable model for schizophrenia, could address questions regarding presynaptic alterations that contribute to the etiopathophysiology of SZ and help to consummate the pre- and postsynaptic glutamatergic pathogenesis of the illness.

The mechanism for different susceptibilities to obesity after short-term high-fat diet (HFD) feeding is largely unknown. Given the close association between obesity occurrence and mitochondrial dysfunction, the early events in skeletal muscle mitochondrial adaptations between HFD-induced obesity (DIO) and HFD-induced obesity resistant (DIO-R) lean phenotype under excess nutritional environment were explored.ICR/JCL male mice were randomly divided into 2 groups, as follows: low-fat diet (LFD) and HFD groups. After 6 weeks on HFD, HFD-fed mice were classified as DIO or DIO-R according to their body weight gain. Serum parameters, oxidative stress biomarkers, the activation of AMPK/ACC axis, and the expression profiles of mitochondrial biogenesis were measured by using corresponding methods among the LFD control, DIO, and DIO-R groups. Serum glucose, total cholesterol, low-density lipoprotein, and high-density lipoprotein levels were significantly increased in DIO and DIO-R mice compared with LFD controls. However, DIO-R mice had significantly higher MDA levels and exhibited a significantly higher level of AMP-activated protein kinase (AMPK) activation and acetyl-CoA carboxylase (ACC) inactivation than DIO mice. Furthermore, the transcript and protein levels of transcriptional coactivator peroxisome proliferator-activated receptor γ (PPARγ) coactivator 1α (PGC-1α) and estrogen-related receptor-α (ERRα) in DIO-R mice were significantly up-regulated compared with the DIO mice. Although the body weight gain differed, the DIO and DIO-R mice had similar metabolic disturbance of glucose and lipids after short-term HFD consumption. The diverse alterations on fatty acid oxidation and mitochondrial biogenesis pathway induced by AMPK activation might be involved in different susceptibilities to obesity when consuming HFD.

Resveratrol (RSV) has various pharmacological effects, however, few studies have directly addressed the possible antifatigue effects of long-term endurance exercise. The clinical use of RSV is limited by its poor water solubility and extremely short plasma half-life. Solid lipid nanoparticles (SLNs) are considered as reasonable drug delivery systems to overcome some of these drawbacks and expand its applications. In this study, RSV-SLNs were successfully prepared through emulsification and low-temperature solidification. Results showed that RSV-SLN supplementation effectively enhanced endurance performance. RSV-SLN supplementation might enhance mitochondrial function by ameliorating mitochondrial quality control (QC), which was superior to RSV application. These results revealed an unexpected role of RSV-SLN compared with RSV in terms of linking nutrient deprivation to mitochondrial oxidant production through mitochondrial QC. A mitochondrion-mediated pathway was likely involved in RSV-SLN, thereby improving endurance performance. Overall, this study highlighted new possibilities for anti-physical-fatigue strategies.

Corrigendum: RILP interacts with HOPS complex via VPS41 subunit to regulate endocytic trafficking

The HOPS complex serves as a tethering complex with GEF activity for Ypt7p in yeast to regulate late endosomal membrane maturation. While the role of HOPS complex is well established in yeast cells, its functional and mechanistic aspects in mammalian cells are less well defined. In this study, we report that RILP, a downstream effector of Rab7, interacts with HOPS complex and recruits HOPS subunits to the late endosomal compartment. Structurally, the amino-terminal portion of RILP interacts with HOPS complex. Unexpectedly, this interaction is independent of Rab7. VPS41 subunit of HOPS complex was defined to be the major partner for interacting with RILP. The carboxyl-terminal region of VPS41 was mapped to be responsible for the interaction. Functionally, either depletion of VPS41 by shRNA or overexpression of VPS41 C-terminal half retarded EGF-induced degradation of EGFR. These results suggest that interaction of RILP with HOPS complex via VPS41 plays a role in endocytic trafficking of EGFR.

Rab29 (also referred as Rab7L1) is a novel Rab protein, and is recently demonstrated to regulate phagocytosis and traffic from the Golgi to the lysosome. However, its roles in membrane trafficking have not been investigated extensively. Our results in this study revealed that Rab29 is associated with the trans-Golgi network (TGN), and is essential for maintaining the integrity of the TGN, because inhibition of the activity of Rab29 or depletion of Rab29 resulted in fragmentation of the TGN marked by TGN46. Expression of the dominant negative form Rab29T21N or shRNA-Rab29 also altered the distribution of mannose-6-phosphate receptor (M6PR), and interrupted the retrograde trafficking of M6PR through monitoring the endocytosis of CD8-tagged calcium dependent M6PR (cdM6PR) or calcium independent M6PR (ciM6PR), but without significant effects on the anterograde trafficking of vesicular stomatitis virus G protein (VSV-G). Our results suggest that Rab29 is essential for the integrity of the TGN and participates in the retrograde trafficking of M6PRs.

The subcellular location and cell biological function of small GTPase Rab40c in mammalian cells have not been investigated in detail. In this study, we demonstrated that the exogenously expressed GFP-Rab40c associates with lipid droplets marked by neutral lipid specific dye Oil red or Nile red, but not with the Golgi or endosomal markers. Further examination demonstrated that Rab40c is also associated with ERGIC-53 containing structures, especially under the serum starvation condition. Rab40c is increasingly recruited to the surface of lipid droplets during lipid droplets formation and maturation in HepG2 cells. Rab40c knockdown moderately decreases the size of lipid droplets, suggesting that Rab40c is involved in the biogenesis of lipid droplets. Stimulation for adipocyte differentiation increases the expression of Rab40c in 3T3-L1 cells. Rab40c interacts with TIP47, and is appositionally associated with TIP47-labeled lipid droplets. In addition, over-expression of Rab40c causes the clustering of lipid droplets independent of its GTPase activity, but completely dependent of the intact SOCS box domain of Rab40c. In addition, Rab40c displayed self-interaction as well as interaction with TIP47 and the SOCS box is essential for its ability to induce clustering of lipid droplets. Our results suggest that Rab40c is a novel Rab protein associated with lipid droplets, and is likely involved in modulating the biogenesis of lipid droplets.

Adolescent idiopathic scoliosis(AIS) is present in 2 to 4 percent of children between 10 and 16 years of age, which seriously affects the mental and physical health of young people while is defined as a lateral curvature of the spine greater than 10 degrees accompanied by vertebral rotation. The main risk factors for curve progression are a large curve magnitude, skeletal immaturity and female gender. Previous studies have suggested a possible direct relationship between calmodulin and curve progression, and the expression of Calmodulin in the articular process of AIS patients is low, suggesting that it plays a role in the development and progression of AIS. Calmodulin is the calcium binding receptor protein which can bind to and regulate a multitude of different protein targets. Thereby it could affect many different cellular functions, such as inflammation, metabolism, apoptosis, muscle contraction, intracellular movement, short-term and long-term memory, nerve growth and the immune response. Strong claims have been made about the possible adverse effects of Endocrine Disrupting Chemicals (EDCs) on growth, reproduction and development in both humans and animals, and some papers investigate the interaction of EDCs with cell-signaling pathways, such as Ca+ and Calmodulin, to understand how these chemicals disturb development of the endocrine system and of the organs that respond to endocrine signals in organisms indirectly exposed during prenatal and/or early postnatal life. Calmodulin are substances which may interfere with normal function of the endocrine (hormone) system of humans. Some source water and tap water in China have been contaminated by EDCs, and they can not be removed completely by drinking water treatment system of city. Humans are exposed daily to EDCs in water which have potential endocrine disrupting activity. So we suggest that the EDCs in water could affect AIS through various interacting with Ca+ and Calmodulin in signaling pathways. Further research would be carried out to find much more details, but the most important thing is that human should improve water treatment system to reduce EDCs in water and lower the effect on AIS.

Lili Qin,1,* Wenrui Wang,2,* Songhui You,1 Jingmei Dong,1 Yunhe Zhou,1 Jibing Wang1 1Department of Physical Education, 2School of Life Science and Technology, Tongji University, Shanghai, People’s Republic of China *These authors contributed equally to this work Abstract: Folic acid antioxidants were successfully intercalated into layered double hydroxides (LDH) nanoparticles according to a previous method with minor modification. The resultant folic acid-LDH constructs were then characterized by X-ray powder diffraction and transmission electron microscopy. The in vitro antioxidant activities, cytotoxicity effect, and in vivo anti­fatigue were examined by a series of assays. The results showed that folic acid-LDH antioxidant system can scavenge 1,1-diphenyl-2-picrylhydrazyl and hydroxyl free radicals and chelate pro-oxidative Cu2+. The in vitro cytotoxicity assays indicated that folic acid-LDH antioxidant system had no significant cytotoxic effect or obvious toxicity to normal cells. It also prolonged the forced swimming time of the mice by 32% and 51% compared to folic acid and control groups, respectively. It had an obvious effect on decreasing the blood urea nitrogen and blood lactic acid, while increasing muscle and hepatic glycogen levels. Therefore, folic acid-LDH might be used as a novel antioxidant and antifatigue nutritional supplement. Keywords: antioxidant supplementation, free radicals, biomaterials, drug delivery