High Photocatalytic Hydrogen Production of Ag@TiO2 with Different Sizes by Simple Chemical Synthesis.

The photocatalytic enhancement of sliver-based metals compounded with semiconductor materials has been demonstrated. However, there are relatively few studies on the effect of particle size in the system on photocatalytic performance. In this paper, silver nanoparticles of two different sizes, 25 and 50 nm, were prepared by a wet chemical method and subsequently sintered to obtain a photocatalyst with a core-shell structure. The photocatalyst Ag@TiO2-50/150 prepared in this study has a hydrogen evolution rate as high as 4538.90 µmol·g-1·h-1. It is interesting to find that when the ratio of silver core size to composite size is 1:3, the hydrogen yield is almost not affected by the silver core diameter, and the hydrogen production rate is basically the same. In addition, the rate of hydrogen precipitation in air for 9 months was still more than 9 times those of previous studies. This provides a new idea for the study of the oxidation resistance and stability of photocatalysts.

Study on the mechanism of NOx reduction by NH3-SCR over a ZnXCu1-XFe2O4 catalyst.

Experimental evidence shows that CuFe2O4 exhibits excellent catalytic performance in the SCR reaction. However, there is a lack of in-depth research on its specific reaction mechanism. Our study begins by computing the adsorption model of molecules like NH3 and then goes on to examine the SCR reaction mechanism of NH3 on CuFe2O4 before and after Zn doping. The results indicate that NH3 is chemically adsorbed (-1.26 eV) on the surface and has a strong interaction with the substrate. Importantly, Zn doping provides more favorable reactive sites for NH3 molecules. Subsequent investigation into the NH3 dehydrogenation and SCR reaction processes showed that incorporating Zn can greatly decrease the energy barrier of the most critical step in the reaction (0.58 eV). Additionally, the study also assesses the feasibility of the reaction of adsorbed NO with surface active O atoms to form NO2 (barrier 0.86 eV). Lastly, the sulfur resistance of the catalyst before and after doping is calculated and analyzed, and it is found that Zn doping effectively improves the sulfur resistance. Our study provides valuable theoretical guidance for the development of ferrite spinel and doping modification.

Anisotropic Free-Standing Aerogels Based on Graphene/Silk for Pressure Sensing and Efficient Adsorption.

Compressible, conductive, ultralight, and superhydrophobic graphene aerogels (GAs) are promising for wearable electronics and adsorption applications. However, the unsatisfactory sensing performances and lack of multiscale structural regulation still impede the development of multifunctional GAs. Herein, a multifunctional aerogel based on graphene/silk is reported─a highly ordered three-dimensional (3D) reduced graphene oxide (rGO) conductive network is established by an alkali-induced hydrothermal self-assembly strategy, while silk fibroin (SF) bound to graphene oxide (GO) by electrostatic interactions is uniformly distributed throughout the network. The ultralight rGO/SF aerogel (GSA) has the property that its resistance varies with compression, so it can be used for flexible pressure sensors. A GSA-based sensor can detect compressive stresses down to 0.35 kPa and has a response time of 0.55 s and a recovery time of 0.58 s. It has a good linear response from 0.5 to 30 kPa with sensitivities of 0.54 kPa-1 (0.5-4 kPa) and 0.21 kPa-1 (4-30 kPa), respectively. The GSA-based sensor also has excellent durability, remaining stable after 12,000 cycles. As proof of concept, its applications for health monitoring, speech recognition, and motion capture are shown. Furthermore, the carbonized rGO/SF aerogels (C-GSAs) with superhydrophobicity can adsorb various organic substances (146.7-278.8 g/g) and achieve oil-water separation.

Lipid metabolism characterization in gastric cancer identifies signatures to predict prognostic and therapeutic responses.

Purpose: Increasing evidence has elucidated the significance of lipid metabolism in predicting therapeutic efficacy. Obviously, a systematic analysis of lipid metabolism characterizations of gastric cancer (GC) needs to be reported. Experimental design: Based on two proposed computational algorithms (TCGA-STAD and GSE84437), the lipid metabolism characterization of 367 GC patients and its systematic relationship with genomic characteristics, clinicopathologic features, and clinical outcomes of GC were analyzed in our study. Differentially expressed genes (DEGs) were identified based on the lipid metabolism cluster. At the same time, we applied single-factor Cox regression and random forest to screen signature genes to construct a prognostic model, namely, the lipid metabolism score (LMscore). Next, we deeply explored the predictive value of the LMscore for GC. To verify the specific changes in lipid metabolism, a total of 90 serum, 30 tumor, and non-tumor adjacent tissues from GC patients, were included for pseudotargeted metabolomics analysis via SCIEX triple quad 5500 LC-MS/MS system. Results: Five lipid metabolism signature genes were identified from a total of 3,104 DEGs. The LMscore could be a prognosticator for survival in different clinicopathological GC cohorts. As well, the LMscore was identified as a predictive biomarker for responses to immunotherapy and chemotherapeutic drugs. Additionally, significant changes in sphingolipid metabolism and sphingolipid molecules were discovered in cancer tissue from GC patients by pseudotargeted metabolomics. Conclusion: In conclusion, multivariate analysis revealed that the LMscore was an independent prognostic biomarker of patient survival and therapeutic responses in GC. Depicting a comprehensive landscape of the characteristics of lipid metabolism may help to provide insights into the pathogenesis of GC, interpret the responses of gastric tumors to therapies, and achieve a better outcome in the treatment of GC. In addition, significant alterations of sphingolipid metabolism and increased levels of sphingolipids, in particular, sphingosine (d16:1) and ceramide, were discovered in GC tissue by lipidome pseudotargeted metabolomics, and most of the sphingolipid molecules have the potential to be diagnostic biomarkers for GC.

Significant metabolic alterations in patients with hepatitis B virus replication observed via serum untargeted metabolomics shed new light on hepatitis B virus infection.

Until now, the metabolic effects of hepatitis B virus (HBV) replication on the progression of hepatic diseases (hepatitis, cirrhosis, and liver cancer) and liver functions have remained unexplored. Thus, a total of 199 hepatic disease patients with active and inactive HBV were enrolled in this study to explore serum metabolic characteristics using untargeted metabolomics. Multiple analyses, including principal component analysis (PCA), partial least squares discriminant analysis (PLS-DA), volcano plot and pathway analysis, were used for metabolic data analysis. Additionally, differential metabolites were analysed by commercial databases. A decrease of approximately 0.8-fold in amino acids (L-glutamic acid, D-glutamine and L-tyrosine) and an increase of 2-fold in phosphatidylcholines (PCs) and lysophosphatidylcholines (LPCs) were observed in hepatic disease patients with HBV replication. Moreover, downregulation of arachidonic acid, PC 34:2, sn-glycerol-3-phosphocholine, 1-palmitoylglycerophosphoinositol, and 1-oleoylglycerophosphoinositol by 0.6-fold was also found in the serum of patients with HBV replication. In addition, liver function was significantly different between cirrhosis patients with or without HBV replication (p < .05). In summary, this is the first study to focus on the metabolic changes induced by HBV replication in patients and to compare metabolic alterations in the progression of hepatic disease induced by HBV infection. High levels of amino acid depletion and PC and LPC biosynthesis were primarily observed, which may shed new light on the pathogenesis and treatment of HBV infection.

DFT studies of the CH4-SCR of NO on Fe-doped ZnAl2O4(100) surface under oxygen conditions.

The catalytic reduction performance of NO on the surface of Fe-doped ZnAl2O4 (100) was calculated based on DFT. The adsorption of NO and other molecules, the change of reaction energy of CH4 and C2H4 as reducing agents, and the activation energy barrier of CH4 were studied. It was found that the best adsorption energy of NO is -2.166 eV. Compared with Al and Zn sites, doped Fe atoms are better adsorption catalytic sites. At temperatures of 300 K and 600 K, the molecules will move in the direction of the Fe atoms. O2 adsorption will repel NO, reduce its adsorption energy, and cause NO to lose electrons and be oxidized. The reaction enthalpy with CH4 as the reducing agent is -7.02 eV, and with C2H4 is -3.45 eV. Transition state calculations show that O reduces the dissociation barrier of CH4 by about 2 eV. The smaller adsorption energy and negative reaction enthalpy of the product indicate that the iron-doped ZnAl2O4 has a good catalytic NO potential. This also provides a basis for future research on the catalytic mechanism of different hydrocarbons.

LanCL1 promotes motor neuron survival and extends the lifespan of amyotrophic lateral sclerosis mice.

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by progressive loss of motor neurons. Improving neuronal survival in ALS remains a significant challenge. Previously, we identified Lanthionine synthetase C-like protein 1 (LanCL1) as a neuronal antioxidant defense gene, the genetic deletion of which causes apoptotic neurodegeneration in the brain. Here, we report in vivo data using the transgenic SOD1G93A mouse model of ALS indicating that CNS-specific expression of LanCL1 transgene extends lifespan, delays disease onset, decelerates symptomatic progression, and improves motor performance of SOD1G93A mice. Conversely, CNS-specific deletion of LanCL1 leads to neurodegenerative phenotypes, including motor neuron loss, neuroinflammation, and oxidative damage. Analysis reveals that LanCL1 is a positive regulator of AKT activity, and LanCL1 overexpression restores the impaired AKT activity in ALS model mice. These findings indicate that LanCL1 regulates neuronal survival through an alternative mechanism, and suggest a new therapeutic target in ALS.

Developmental and activity-dependent expression of LanCL1 confers antioxidant activity required for neuronal survival.

Production of reactive oxygen species (ROS) increases with neuronal activity that accompanies synaptic development and function. Transcription-related factors and metabolic enzymes that are expressed in all tissues have been described to counteract neuronal ROS to prevent oxidative damage. Here, we describe the antioxidant gene LanCL1 that is prominently enriched in brain neurons. Its expression is developmentally regulated and induced by neuronal activity, neurotrophic factors implicated in neuronal plasticity and survival, and oxidative stress. Genetic deletion of LanCL1 causes enhanced accumulation of ROS in brain, as well as development-related lipid, protein, and DNA damage; mitochondrial dysfunction; and apoptotic neurodegeneration. LanCL1 transgene protects neurons from ROS. LanCL1 protein purified from eukaryotic cells catalyzes the formation of thioether products similar to glutathione S-transferase. These studies reveal a neuron-specific glutathione defense mechanism that is essential for neuronal function and survival.

Increased callus mass and enhanced strength during fracture healing in mice lacking the sclerostin gene.

Humans with inherited sclerostin deficiency have high bone mass. Targeted deletion of the sclerostin gene in mice (SOST-KO) causes increases in bone formation, bone mass and bone strength. Inhibition of sclerostin by a monoclonal antibody increases bone formation and enhances fracture healing in rodent and primate models. In this study, we describe the temporal progression of femoral fracture healing in SOST-KO mice compared with wild type (WT) control mice to further characterize the role of sclerostin in fracture healing. Sixty-seven male 9-10 week-old SOST-KO (N=37) and WT (N=30) mice underwent a closed femoral fracture. Weekly radiography was used to monitor the progress of healing. Histologic sections were used to characterize callus composition, evaluate callus bridging, and quantify lamellar bone formation on days 14 and 28. Densitometry and biomechanical testing were utilized to characterize bone mass and strength at the fractured and contralateral femurs on day 45. A significant improvement in time to radiographic healing (no discernible fracture line) was observed in SOST-KO mice, which corresponded to an increase in histologic bony bridging at 14 days (38% versus 0% in WT). Both genotypes appeared to be nearly fully bridged at 28 days post-fracture. The increased bridging at 14 days was associated with 97% greater bone area and 40% lower cartilage area in the callus of SOST-KO mice as compared to WT mice. Bone formation-related endpoints were higher in SOST-KO mice at both 14 and 28 days. At 45 days post-fracture, peak load and bone mass were significantly greater in the fractured femurs of SOST-KO mice as compared to WT mice. In conclusion, fractures in mice lacking sclerostin showed accelerated bridging, greater callus maturation, and increased bone formation and strength in the callus.

Dickkopf-1 regulates bone formation in young growing rodents and upon traumatic injury.

The physiological role of Dickkopf-1 (Dkk1) during postnatal bone growth in rodents and in adult rodents was examined utilizing an antibody to Dkk1 (Dkk1-Ab) that blocked Dkk1 binding to both low density lipoprotein receptor-related protein 6 (LRP6) and Kremen2, thereby preventing the Wnt inhibitory activity of Dkk1. Treatment of growing mice and rats with Dkk1-Ab resulted in a significant increase in bone mineral density because of increased bone formation. In contrast, treatment of adult ovariectomized rats did not appreciably impact bone, an effect that was associated with decreased Dkk1 expression in the serum and bone of older rats. Finally, we showed that Dkk1 plays a prominent role in adult bone by mediating fracture healing in adult rodents. These data suggest that, whereas Dkk1 significantly regulates bone formation in younger animals, its role in older animals is limited to pathologies that lead to the induction of Dkk1 expression in bone and/or serum, such as traumatic injury.

Increased RANK ligand in bone marrow of orchiectomized rats and prevention of their bone loss by the RANK ligand inhibitor osteoprotegerin.

Orchiectomized (ORX) rats were used to examine the extent to which their increased bone resorption and decreased bone density might relate to increases in RANKL, an essential cytokine for bone resorption. Serum testosterone declined by >95% in ORX rats 1 and 2 weeks after surgery (p<0.05 versus sham controls), with no observed changes in serum RANKL. In contrast, RANKL in bone marrow plasma and bone marrow cell extracts was significantly increased (by approximately 100%) 1 and 2 weeks after ORX. Regression analyses of ORX and sham controls revealed a significant inverse correlation between testosterone and RANKL levels measured in marrow cell extracts (R=-0.58), while marrow plasma RANKL correlated positively with marrow plasma TRACP-5b, an osteoclast marker (R=0.63). The effects of RANKL inhibition were then studied by treating ORX rats for 6 weeks with OPG-Fc (10 mg/kg, twice/week SC) or with PBS, beginning immediately after surgery. Sham controls were treated with PBS. Vehicle-treated ORX rats showed significant deficits in BMD of the femur/tibia and lower trabecular bone volume in the distal femur (p<0.05 versus sham). OPG-Fc treatment of ORX rats increased femur/tibia BMD and trabecular bone volume to levels that significantly exceeded values for ORX or sham controls. OPG-Fc reduced trabecular osteoclast surfaces in ORX rats by 99%, and OPG-Fc also prevented ORX-related increases in endocortical eroded surface and ORX-related reductions in periosteal bone formation rate. Micro-CT of lumbar vertebrae from OPG-Fc-treated ORX rats demonstrated significantly greater cortical and trabecular bone volume and density versus ORX-vehicle controls. In summary, ORX rats exhibited increased RANKL protein in bone marrow plasma and in bone marrow cells, with no changes in serum RANKL. Data from regression analyses were consistent with a potential role for testosterone in suppressing RANKL production in bone marrow, and also suggested that soluble RANKL in bone marrow might promote bone resorption. RANKL inhibition prevented ORX-related deficits in trabecular BMD, trabecular architecture, and periosteal bone formation while increasing cortical and trabecular bone volume and density. These results support the investigation of RANKL inhibition as a strategy for preventing bone loss associated with androgen ablation or deficiency.

RANKL inhibition with osteoprotegerin increases bone strength by improving cortical and trabecular bone architecture in ovariectomized rats.

INTRODUCTION: Ovariectomy (OVX) results in bone loss caused by increased bone resorption. RANKL is an essential mediator of bone resorption. We examined whether the RANKL inhibitor osteoprotegerin (OPG) would preserve bone volume, density, and strength in OVX rats. MATERIALS AND METHODS: Rats were OVX or sham-operated at 3 mo of age. Sham controls were treated for 6 wk with vehicle (Veh, PBS). OVX rats were treated with Veh or human OPG-Fc (10 mg/kg, 2/wk). Serum RANKL and TRACP5b was measured by ELISA. BMD of lumbar vertebrae (L(1)-L(5)) and distal femur was measured by DXA. Right distal femurs were processed for bone histomorphometry. Left femurs and the fifth lumbar vertebra (L(5)) were analyzed by muCT and biomechanical testing, and L(6) was analyzed for ash weight. RESULTS: OVX was associated with significantly greater serum RANKL and osteoclast surface and with reduced areal and volumetric BMD. OPG markedly reduced osteoclast surface and serum TRACP5b while completely preventing OVX-associated bone loss in the lumbar vertebrae, distal femur, and femur neck. Vertebrae from OPG-treated rats had increased dry and ash weight, with no significant differences in tissue mineralization versus OVX controls. muCT showed that trabecular compartments in OVX-OPG rats had significantly greater bone volume fraction, vBMD, bone area, trabecular thickness, and number, whereas their cortical compartments had significantly greater bone area (p < 0.05 versus OVX-Veh). OPG improved cortical area in L(5) and the femur neck to levels that were significantly greater than OVX or sham controls (p < 0.05). Biomechanical testing of L(5) and femur necks showed significantly greater maximum load values in the OVX-OPG group (p < 0.05 versus OVX-Veh). Bone strength at both sites was linearly correlated with total bone area (r(2) = 0.54-0.74, p < 0.0001), which was also significantly increased by OPG (p < 0.05 versus OVX). CONCLUSIONS: OPG treatment prevented bone loss, preserved trabecular architecture, and increased cortical area and bone strength in OVX rats.