Enhanced generation of reactive oxygen species and photocatalytic activity by Pt-based metallic nanostructures: the composition matters

The modification of semiconductor nanostructures with metallic nanocomponents can promote the separation of electron/hole from photoexited semiconductors by forming heterojunctions, thus exhibit enhanced photocatalytic activities and potential applications. In this study, Pt-based NPs, including Pt, PtCu, and PtCuCo are employed as model co-catalysts to comparatively study their capability to enhance the photocatalytic activity of TiO₂ nanosheets. It was found that each of Pt, PtCu, and PtCuCo can greatly enhance the photocatalytic activity of TiO₂ toward degradation of organic dyes. Using electron spin resonance spectroscopy, we demonstrated that deposition of Pt-based NPs resulted in more production of reactive oxygen species including hydroxyl radicals, superoxide, and singlet oxygen. The enhancing effects of Pt-based NPs on generation of ROS and photocatalytic activity showed same trend: PtCuCo?>?PtCu?>?Pt. The mechanism underlying the enhancement differences in Pt-based NPs may be mainly related to electronic structure change of Pt in alloying with Cu and Co. These results are valuable for designing hybrid nanomaterials with high photocatalytic efficiency for applications in water purification and antibacterial products.     

INAUGURAL ARTICLE by a Recently Elected Academy Member:Functional redundancy of type I and type II receptors in the regulation of skeletal muscle growth by myostatin and activin A

Myostatin (MSTN) is a transforming growth factor-β (TGF-β) family member that normally acts to limit muscle growth. The function of MSTN is partially redundant with that of another TGF-β family member, activin A. MSTN and activin A are capable of signaling through a complex of type II and type I receptors. Here, we investigated the roles of two type II receptors (ACVR2 and ACVR2B) and two type I receptors (ALK4 and ALK5) in the regulation of muscle mass by these ligands by genetically targeting these receptors either alone or in combination specifically in myofibers in mice. We show that targeting signaling in myofibers is sufficient to cause significant increases in muscle mass, showing that myofibers are the direct target for signaling by these ligands in the regulation of muscle growth. Moreover, we show that there is functional redundancy between the two type II receptors as well as between the two type I receptors and that all four type II/type I receptor combinations are utilized in vivo. Targeting signaling specifically in myofibers also led to reductions in overall body fat content and improved glucose metabolism in mice fed either regular chow or a high-fat diet, demonstrating that these metabolic effects are the result of enhanced muscling. We observed no effect, however, on either bone density or muscle regeneration in mice in which signaling was targeted in myofibers. The latter finding implies that MSTN likely signals to other cells, such as satellite cells, in addition to myofibers to regulate muscle homeostasis.

Myostatin (MSTN) is a secreted signaling molecule that normally acts to limit skeletal muscle growth (for review, see ref. 1). Mice lacking MSTN exhibit dramatic increases in muscle mass throughout the body, with individual muscles growing to about twice the normal size (2). MSTN appears to play two distinct roles in regulating muscle size, one to regulate the number of muscle fibers that are formed during development and a second to regulate the growth of those fibers postnatally. The sequence of MSTN has been highly conserved through evolution, with the mature MSTN peptide being identical in species as divergent as humans and turkeys (3). The function of MSTN has also been conserved, and targeted or naturally occurring mutations in MSTN have been shown to cause increased muscling in numerous species, including cattle (3–5), sheep (6), dogs (7), rabbits (8), rats (9), swine (10), goats (11), and humans (12). Numerous pharmaceutical and biotechnology companies have developed biologic agents capable of blocking MSTN activity, and these have been tested in clinical trials for a wide range of indications, including Duchenne and facioscapulohumeral muscular dystrophy, inclusion body myositis, muscle atrophy following falls and hip fracture surgery, age-related sarcopenia, Charcot–Marie–Tooth disease, and cachexia due to chronic obstructive pulmonary disease, end-stage kidney disease, and cancer.The finding that certain inhibitors of MSTN signaling can increase muscle mass even in Mstn^−/− mice revealed that the function of MSTN as a negative regulator of muscle mass is partially redundant with at least one other TGF-β family member (13, 14), and subsequent studies have identified activin A as one of these cooperating ligands (15, 16). MSTN and activin A share many key regulatory and signaling components. For example, the activities of both MSTN and activin A can be modulated extracellularly by naturally occurring inhibitory binding proteins, including follistatin (17, 18) and the follistatin-related protein, FSTL-3 or FLRG (19, 20). Moreover, MSTN and activin A also appear to share receptor components. Based on in vitro studies, MSTN is capable of binding initially to the activin type II receptors, ACVR2 and ACVR2B (also called ActRIIA and ActRIIB) (18) followed by engagement of the type I receptors, ALK4 and ALK5 (21). In previous studies, we presented genetic evidence supporting a role for both ACVR2 and ACVR2B in mediating MSTN signaling and regulating muscle mass in vivo. Specifically, we showed that mice expressing a truncated, dominant-negative form of ACVR2B in skeletal muscle (18) or carrying deletion mutations in Acvr2 and/or Acvr2b (13) have significantly increased muscle mass. One limitation of the latter study, however, was that we could not examine the consequence of complete loss of both receptors using the deletion alleles, as double homozygous mutants die early during embryogenesis (22). Moreover, the roles that the two type I receptors, ALK4 and ALK5, play in regulating MSTN and activin A signaling in muscle in vivo have not yet been documented using genetic approaches. Here, we present the results of studies in which we used floxed alleles for each of the type II and type I receptor genes in order to target these receptors alone and in combination in muscle fibers. We show that these receptors are functionally redundant and that signaling through each of these receptors contributes to the overall control of muscle mass.     

六西格玛在肿瘤标志物质量目标选择上的应用

目的应用6σ理论对肿瘤标志物项目的分析性能进行评价，并初步确定各项目的质量目标。 方法收集本实验室2018年1至12月室内质控数据和国家卫生健康委临床检验中心室间质量评价结果，以生物学变异导出的质量规范和国家室间质量评价标准作为允许总误差(TEa)计算6项肿瘤标志物的σ水平，并依据质量目标选择流程图和肿瘤标志物分析性能验证图评价肿瘤标志物的分析性能，进而为肿瘤标志物选择合适的质量目标。 结果应用不同层级的生物学变异导出的质量规范和国家室间质量评价标准，肿瘤标志物项目的σ水平存在显著差异；依据质量目标选择流程图：选择生物学变异导出的"适当的"质量规范作为CA125项目的质量目标，选择生物学变异导出的"最低的"质量规范作为t-PSA、CEA、AFP、CA199和CA153项目的质量目标。 结论6σ能够客观评价肿瘤标志物的分析性能，并为实验室质量目标的选择提供重要的参考价值。     

Intermittent Internal Fixation With a Locking Plate to Preserve Epiphyseal Growth Function During Limb-Salvage Surgery in a Child With Osteosarcoma of the Distal Femur: A Case Report

Limb shortening is a problem associated with surgery for osteosarcoma of the lower extremity in adolescents, as the tumors frequently occur near the epiphysis. Herein we report the use of a less invasive stabilization system (LISS) and an intermittent fixation method to preserve the growth function of epiphysis in an 11-year-old patient with an osteosarcoma of the distal femur.The 11-year-old male presented with left knee enlargement and pain for 2 weeks, and magnetic resonance imaging (MRI) and biopsy were consistent with osteosarcoma of the left distal femur. After preoperative chemotherapy, en bloc tumor resection was performed with margins based on MRI findings preserving the epiphyseal growth plate, the tumor cavity was filled with inactivated bone and bone cement, and a LISS was used to stabilize the femur. Aggressive postoperative chemotherapy was given. Approximately 105 weeks after surgery radiography showed that the distal end of the plate had moved superior to the epiphysis along with bone growth. Locking screws were placed in the distal part of the LISS plate to stabilize the re-implanted bone, and external fixation was not needed.The patient was able to walk with the crutches 1 week postoperatively, and bear weight on the extremity 6 weeks postoperatively. At 6 years after surgery, the patient''s height had increased 52 cm, shortening of the affected limb was only 1 cm, and the circumference of the affected limb was 2 cm smaller than that of the contralateral limb. There was no significant discomfort in the affected limb, and there was no gait abnormality. The patient could jump and run, and could participate in sports including basketball and badminton to the same degree as his peers.In summary, the novel method of bone reconstruction and fixation provided good results in a child with an osteosarcoma of the distal femur. This fixation method preserves the osteogenic function of the epiphysis and restored bone integrity simultaneously, and provides good functional recovery.     

Exploration of D022-Type Al3TM(TM = Sc,Ti, V,Zr, Nb,Hf, Ta): Elastic Anisotropy,Electronic Structures,Work Function and Experimental Design

The structural properties, elastic anisotropy, electronic structures and work function of D0₂₂-type Al₃TM (TM = Sc, Ti, V, Y, Zr, Nb, La, Hf, Ta) are studied using the first-principles calculations. The results indicate that the obtained formation enthalpy and cohesive energy of these compounds are in accordance with the other calculated values. It is found that the Al₃Zr is the most thermodynamic stable compound. The mechanical property indexes, such as elastic constants, bulk modulus, shear modulus, Young’s modulus, Poisson’s ratio, and Vickers hardness are systematically explored. Moreover, the calculated universal anisotropic index, percent anisotropy and shear anisotropic factors of D0₂₂-type Al₃TM are analyzed carefully. It demonstrates that the shear modulus anisotropy of Al₃La is the strongest, while that of Al₃Ta is the weakest. In particular, the density of states at Fermi level is not zero, suggesting that these phases have metal properties and electrical conductivity. More importantly, the mechanisms of correlation between hardness and Young’s modulus are further explained by the work function. Finally, the experimental design proves that D0₂₂-Al₃Ta has an excellent strengthening effect.     

Role of macrophages in peripheral nerve injury and repair

Resident and inflammatory macrophages are essential effectors of the innate immune system. These cells provide innate immune defenses and regulate tissue and organ homeostasis. In addition to their roles in diseases such as cancer, obesity and osteoarthritis, they play vital roles in tissue repair and disease rehabilitation. Macrophages and other inflammatory cells are recruited to tissue injury sites where they promote changes in the microenvironment. Among the inflammatory cell types, only macrophages have both pro-inflammatory(M1) and anti-inflammatory(M2) actions, and M2 macrophages have four subtypes. The co-action of M1 and M2 subtypes can create a favorable microenvironment, releasing cytokines for damaged tissue repair. In this review, we discuss the activation of macrophages and their roles in severe peripheral nerve injury. We also describe the therapeutic potential of macrophages in nerve tissue engineering treatment and highlight approaches for enhancing M2 cell-mediated nerve repair and regeneration.     

营养风险与腹膜后肿瘤患者住院时间的相关性研究

目的 探讨营养风险与腹膜后肿瘤患者住院时间的相关性。方法 采用回顾性研究，选取2012年1月至2018年12月四川大学华西医院血管外科新入院腹膜后肿瘤患者60例，采用营养风险筛查表评估患者营养风险，收集患者体质指数、围术期血红蛋白和白蛋白水平、住院天数、术后恶心呕吐发生情况、术后排气、排便时间和首次进食时间。采用单因素分析比较不同患者住院时间，采用多重线性逐步回归分析患者住院时间的影响因素。结果 纳入的60例腹膜后肿瘤患者中，40例患者（66.7%）术前存在营养风险，52例患者（86.7%）术后存在营养风险；单因素分析显示，患者术前、术后营养风险 （术前P<0.001，术后P=0.043）、术前白蛋白 （P=0.019）、术后血红蛋白 （P=0.019）、术后白蛋白（P=0.025） 水平以及术后恶心呕吐 （P=0.001） 均会影响患者的住院时间；患者住院时间与围术期营养风险筛查工具评分、术后首次进食时间、术后排气时间和排便时间具有相关性，且相关性强（r=0.759~0.770； P<0.01）；多因素分析显示术前营养风险是腹膜后肿瘤患者住院时间的重要预测因素（β=0.399）。结论 术前营养风险是腹膜后肿瘤患者住院时间的预测因子。