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Univariate and multivariable Cox regression analysis of overall survival (n=95)

Establishment of the FAM135B transgenic mouse model

Supplementary Table S2 Metabolic gene with CNV larger than 20%.

Metabolic activities are often accompanied by cell-cycle progression, yet known connections between these two processes remain limited. Here, we identified the isocitrate dehydrogenase 3β (IDH3β) as a novel substrate of anaphase-promoting complex/cyclosome (APC/C)-CDH1 and an important regulator of the cell cycle. In esophageal squamous cell carcinoma (ESCC), IDH3β was posttranslationally upregulated in late G1 phase, and overexpression of IDH3β accelerated G1–S transition, contributing to the promotion of cell proliferation in vitro and in vivo. α-Ketoglutarate (α-KG), a crucial metabolite in tricarboxylic acid (TCA) cycle, was dependent on IDH3β level and partially accounted for IDH3β-mediated cell growth. IDH3β expression increased PFKFB3 protein levels and enhanced glucose uptake, and high expression of IDH3β correlated with poor survival in patients with ESCC, suggesting a potential application of IDH3β in prognosis. Overall, our results highlight a new molecular connection between cell-cycle regulation and the TCA cycle in ESCC.Significance:These findings show that IDH3β is an APC/C-CDH1 substrate and is expressed in a cell-cycle–dependent manner, highlighting novel molecular cross-talk between the TCA cycle and cell cycle in cancer cells.

Esophageal squamous cell carcinoma (ESCC) is one of the most common and deadly diseases. In our previous comprehensive genomics study, we found that family with sequence similarity 135 member B (FAM135B) was a novel cancer-related gene, yet its biological functions and molecular mechanisms remain unclear. In this study, we demonstrate that the protein levels of FAM135B are significantly higher in ESCC tissues than in precancerous tissues, and high expression of FAM135B correlates with poorer clinical prognosis. Ectopic expression of FAM135B promoted ESCC cell proliferation in vitro and in vivo, likely through its direct interaction with growth factor GRN, thus forming a feedforward loop with AKT/mTOR signaling. Patients with ESCC with overexpression of both FAM135B and GRN had worse prognosis; multivariate Cox model analysis indicated that high expression of both FAM135B and GRN was an independent prognostic factor for patients with ESCC. FAM135B transgenic mice bore heavier tumor burden than wild-type mice and survived a relatively shorter lifespan after 4-nitroquinoline 1-oxide treatment. In addition, serum level of GRN in transgenic mice was higher than in wild-type mice, suggesting that serum GRN levels might provide diagnostic discrimination for patients with ESCC. These findings suggest that the interaction between FAM135B and GRN plays critical roles in the regulation of ESCC progression and both FAM135B and GRN might be potential therapeutic targets and prognostic factors in ESCC.Significance:These findings investigate the mechanisms of FAM135B in promoting ESCC progression and suggest new potential prognostic biomarkers and therapeutic targets in patients with ESCC.

Fig S1. The changing trend of α-KG, fumarate and malate were significantly correlated with S phase.Fig S2. IDH3β accumulated in late G1 phase and CDC20 was not the regulator of IDH3β. Fig S3. The interaction of IDH3β and CDH1 was strong in G1 and weak in G2/M. Fig .S4 IDH3β regulated the G1/S transition and cell proliferation. Fig .S5 Xenograft tumor formation of stable IDH3β overexpressed KYSE410 cells and control cells.Fig .S6 IDH3α, IDH3β and IDH3γ contribute to oxidative metabolism in TCA cycle.Fig .S7 IDH3β-dependent α-KG generation accounts for improving cell proliferation. Fig .S8 IDH3β enhances cytoplasmic PFKFB3 level in IDH3β overexpressed cell.

Quantitative real-time PCR analysis，Proliferation assay and colony formation assay，Cell cycle analysis，Metabolite measurement.

Background: Efficient and accurate methods are needed to automatically segmenting organs-at-risk (OAR) to accelerate the radiotherapy workflow and decrease the treatment wait time. We developed and evaluated the use of a fused model Dense V-Network for its ability to accurately segment pelvic OAR. Material and methods: We combined two network models, Dense Net and V-Net, to establish the Dense V-Network algorithm. For the training model, we adopted 100 kV computed tomography (CT) images of patients with cervical cancer, including 80 randomly selected as training sets, by which to adjust parameters of the automatic segmentation model, and the remaining 20 as test sets to evaluate the performance of the convolutional neural network model. Three representative parameters were used to evaluate the segmentation results quantitatively. Results: Clinical results revealed that Dice similarity coefficient values of the bladder, small intestine, rectum, femoral head and spinal cord were all above 0.87 mm; and Jaccard distance was within 2.3 mm. Except for the small intestine, the Hausdorff distance of other organs was less than 9.0 mm. Comparison of our approaches with those of the Atlas and other studies demonstrated that the Dense V-Network had more accurate and efficient performance and faster speed. Conclusions: The Dense V-Network algorithm can be used to automatically segment pelvic OARs accurately and efficiently, while shortening patients’ waiting time and accelerating radiotherapy workflow.

Abnormal metabolism is recognized as an oncogenic hallmark that is correlated with tumor progression and therapeutic resistance. Here, we used multi-omics, including phosphoproteomics, untargeted metabolomics and lipidomics to demonstrate that the cancer-associated fibroblasts (CAFs)-derived AKT2/choline-phosphate cytidylytransferase α (CCTα)/phosphatidylcholines (PCs) axis mediated the resistance of focal adhesion kinase (FAK) inhibitor-defactinib in esophageal squamous cell carcinoma (ESCC) treatment. We first identified extremely low levels of FAK Tyr397 expression in CAFs, which might possibly provide no available target for defactinib exerting its anti-growth effect in CAFs. Consequently, defactinib upregulated the intracellular concentration of Ca2+ in CAFs, and facilitated the formation of AKT2/CCTα protein complex to phosphorylate CCTα Ser315/319/323 sites, and finally enhanced the production of stromal PCs, which activated intratumoral Janus kinase 2 (JAK2)/Signal transducer and activator of transcription 3 (STAT3) pathway to induce resistance of FAK inhibition. Analysis of clinical samples showed that stromal pAKT2 Ser128 and pCCTα Ser315/319/323 were associated with the tumor malignancy and reduced patient survival. Pseuo-targeted lipidomics and further validation cohort quantitatively demonstrated that plasma PCs allow to distinguish the malignant extent of ESCC patients. Overall, inhibition of stroma-derived PCs and related pathway might be used as potential therapeutic strategies for tumor treatment.

Nanochitin whisker (NC) is an advanced nanobiomaterial with novel physicochemical and biological properties. Fusarium pseudograminearum (Fpg) is an important pathogenic fungus causing wheat crown rot disease. This study explored the mode of action of NC against Fpg as a target microorganism. The effects of different treatments and concentrations of NC on the fungal growth and conidial germination were investigated by in vitro bioassay. The impacts of NC on cell structure integrity, membrane permeability, pathogenesis related key enzymes activity, and the mycotoxin production were examined by electron microscopy, fluorescence spectroscopy, IR spectroscopy, conductometry, and spectrophotometry, respectively. The results showed that NC significantly reduced hyphal growth, and the spore germination rate of Fpg declined by 33.0 % and 23.2 % when Fpg was treated with 30 and 300 μg/mL of NC, respectively. NC vigorously influenced structural stability of cell wall by destroying dextran structure, and strongly stimulated ergosterol production altering membrane integrity of the fungus. It reduced the activities of enzymes related to energy-supply like nicotinamide adenine dinucleotide oxidase and succinate dehydrogenase remarkably. The production of fungal mycotoxin deoxynivalenol was also decreased by NC. These findings provide an important basis for fully understanding the mechanism of nanobiomaterial in plant fungal disease control.

Tumor cell dependence on activated oncogenes is considered a therapeutic target, but protumorigenic microenvironment-mediated cellular addiction to specific oncogenic signaling molecules remains to be further defined. Here, we showed that tumor-associated macrophages (TAMs) produced an abundance of C-C motif chemokine 22 (CCL22), whose expression in the tumor stroma was positively associated with the level of intratumoral phospho-focal adhesion kinase (pFAK Tyr397), tumor metastasis and reduced patient survival. Functionally, CCL22-stimulated hyperactivation of FAK was correlated with increased malignant progression of cancer cells. CCL22-induced addiction to FAK was demonstrated by the persistent suppression of tumor progression upon FAK-specific inhibition. Mechanistically, we identified that diacylglycerol kinase α (DGKα) acted as a signaling adaptor to link the CCL22 receptor C-C motif chemokine receptor 4 (CCR4) and FAK and promoted CCL22-induced activation of the FAK/AKT pathway. CCL22/CCR4 signaling activated the intracellular Ca2+/phospholipase C-γ1 (PLC-γ1) axis to stimulate the phosphorylation of DGKα at a tyrosine residue (Tyr335) and promoted the translocation of DGKα to the plasma membrane to assemble the DGKα/FAK signalosome, which critically contributed to regulating sensitivity to FAK inhibitors in cancer cells. The identification of TAM-driven intratumoral FAK addiction provides opportunities for utilizing the tumor-promoting microenvironment to achieve striking anticancer effects.

Long noncoding RNAs (lncRNAs) are dysregulated in many cancers. Here, we identified the molecular mechanisms of lncRNA Cancer Susceptibility Candidate 8 (CASC8) in promoting the malignancy of esophageal squamous cell carcinoma (ESCC). CASC8 was highly overexpressed in ESCC tissues and upregulation of CASC8 predicted poor prognosis in ESCC patients. Moreover, CASC8 decreased the cisplatin sensitivity of ESCC cells and promoted ESCC tumor growth

BACKGROUND Targeted arterial infusion of verapamil combined with chemotherapy (TVCC) is an effective clinical interventional therapy for esophageal squamous cell carcinoma (ESCC), but multidrug resistance (MDR) remains the major cause of relapse or poor prognosis, and the underlying molecular mechanisms of MDR, temporal intratumoral heterogeneity, and clonal evolutionary processes of resistance have not been determined. METHODS To elucidate the roles of genetic and epigenetic alterations in the evolution of acquired resistance during therapies, we performed whole-exome sequencing on 16 serial specimens from 7 patients with ESCC at every cycle of therapeutic intervention from 3 groups, complete response, partial response, and progressive disease, and we performed whole-genome bisulfite sequencing for 3 of these 7 patients, 1 patient from each group. RESULTS Patients with progressive disease exhibited a substantially higher genomic and epigenomic temporal heterogeneity. Subclonal expansions driven by the beneficial new mutations were observed during combined therapies, which explained the emergence of MDR. Notably, SLC7A8 was identified as a potentially novel MDR gene, and functional assays demonstrated that mutant SLC7A8 promoted the resistance phenotypes of ESCC cell lines. Promoter methylation dynamics during treatments revealed 8 drug resistance protein-coding genes characterized by hypomethylation in promoter regions. Intriguingly, promoter hypomethylation of SLC8A3 and mutant SLC7A8 were enriched in an identical pathway, protein digestion and absorption, indicating a potentially novel MDR mechanism during treatments. CONCLUSION Our integrated multiomics investigations revealed the dynamics of temporal genetic and epigenetic inter- and intratumoral heterogeneity, clonal evolutionary processes, and epigenomic changes, providing potential MDR therapeutic targets in treatment-resistant patients with ESCC during combined therapies. FUNDING National Natural Science Foundation of China, Science Foundation of Peking University Cancer Hospital, CAMS Innovation Fund for Medical Sciences, Major Program of Shenzhen Bay Laboratory, Guangdong Basic and Applied Basic Research Foundation, and the third round of public welfare development and reform pilot projects of Beijing Municipal Medical Research Institutes.

A functionalized carbon nanotube (FCNT)/Ni(HCO3)2-Ni nanostructures were synthesized by decorating nanoflaky and mesoporous Ni(HCO3)2 onto FCNT along with in situ formed reduced metallic Ni for the...

A well-structured anode nanomaterial, which can ensure electron and ion transport and avoid excessive pulverization, is of crucial importance to achieve high capacity with superior cycling stability for both sodium- and lithium-ion batteries (SIBs and LIBs). For the purpose of a superior rate performance, this work here has designed and successfully synthesized a new Na+/Li+ storage nanomaterial of SCS/Sn2Fe@GO through loading of a Sn2Fe nanoalloy on sea-sponge-like carbon spheres (SCSs), followed by a graphene oxide (GO) wrapping process. In such a designed composite, the SCS skeleton ensures electronic conductivity and shorts Na+ and Li+ diffusion pathways, while the Sn2Fe nanoalloy delivers a high capacity and prevents excessive pulverization. The GO shell around SCS/Sn2Fe greatly enhances the cyclability. Used as an anode, the SCS/Sn2Fe@GO nanocomposite enables a high capacity up to 660 mAh g–1 at 50 mA g–1, which is maintained without decay up to 800 cycles in SIBs, and up to 850 mAh g–1 at 500 mA g–...

Esophageal squamous cell carcinoma (ESCC) is one of the most common and deadly diseases. In our previous comprehensive genomics study, we found that family with sequence similarity 135 member B (FAM135B) was a novel cancer-related gene, yet its biological functions and molecular mechanisms remain unclear. In this study, we demonstrate that the protein levels of FAM135B are significantly higher in ESCC tissues than in precancerous tissues, and high expression of FAM135B correlates with poorer clinical prognosis. Ectopic expression of FAM135B promoted ESCC cell proliferation in vitro and in vivo, likely through its direct interaction with growth factor GRN, thus forming a feedforward loop with AKT/mTOR signaling. Patients with ESCC with overexpression of both FAM135B and GRN had worse prognosis; multivariate Cox model analysis indicated that high expression of both FAM135B and GRN was an independent prognostic factor for patients with ESCC. FAM135B transgenic mice bore heavier tumor burden than wild-type mice and survived a relatively shorter lifespan after 4-nitroquinoline 1-oxide treatment. In addition, serum level of GRN in transgenic mice was higher than in wild-type mice, suggesting that serum GRN levels might provide diagnostic discrimination for patients with ESCC. These findings suggest that the interaction between FAM135B and GRN plays critical roles in the regulation of ESCC progression and both FAM135B and GRN might be potential therapeutic targets and prognostic factors in ESCC.Significance:These findings investigate the mechanisms of FAM135B in promoting ESCC progression and suggest new potential prognostic biomarkers and therapeutic targets in patients with ESCC.

To meet the demands of long cycle life under high rate for lithium-ion batteries, the advancement of anode materials with stable structural properties is necessarily demanded. Such promotion needs to design reasonable structure to facilitate the transportation of electron and lithium ions (Li+). Herein, a novel C/Fe3O4 sea-sponge-like structure was synthesized by ultrasonic spray pyrolysis following thermal decomposition process. On the basis of sea-sponge carbon (SSC) excellences in electronic conductivity and short Li+ diffusion pathway, nano-Fe3O4 anchored on stable SSC skeleton can deliver high electrochemical performance with long cycle life under high rate. During electrochemical cycling, well-dispersed nano-Fe3O4 in ∼6 nm not only averts excessive pulverization and is enveloped by solid electrolyte interphase film, but also increases Li+ diffusion efficiency. The much improved electrochemical properties showed a capacity of around 460 mAh g–1 at a high rate of 1.5C with a retention rate of 93%, whi...

Glioma is the most common type of primary brain tumors in the central nervous system (CNS). Migfilin occurs in human glioma and enhances cellular motility via the epidermal growth factor receptor (EGFR) pathway. However, the underlying molecular mechanism is not fully understood. In this study, we found that Migfilin promoted matrix metalloproteinase-2 (MMP-2) activity, and restrained the expression of tissue inhibitor of metalloproteinase 2 (TIMP2), which is an MMP-2 inhibitor. Functional and structural studies showed that the LIM1 domain of Migfilin was required for Migfilin-mediated TIMP2 expression inhibition and MMP-2 activity, and was also necessary in promoting cell motility. Furthermore, Migfilin-induced EGFR phosphorylation was greatly reduced by MMP-2 inhibitor (GM6001) or siRNA, while Migfilin-induced MMP-2 activation was also blocked by the EGFR inhibitor (AG1478) or siRNA. MMP-2 and EGFR inhibitors and their siRNAs can block Migfilin-induced migration and invasion, respectively. These results demonstrated that EGFR and MMP-2 signalings may form a positive feedback loop to enhance Migfilin-induced migration and invasion. Finally, we detected that the expression of Migfilin, EGFR phosphorylation (Tyr1173) and MMP-2 activity had a positive correlation in the clinical glioma sample. Taken together, these results suggest that Migfilin is a critical regulator in cellular motility by driving the EGFR-MMP-2 feedback loop, and may be considered as a potential therapeutic target in glioma.

Development of highly stabile battery-type electrode materials with superior capacity has been a critical challenge for hybrid supercapacitors. We report a high-performance electrode material, tubular sandwich-structured CNT@Ni@Ni2(CO3)(OH)2, synthesized via a scalable, dynamic, controlled in situ reduction–chemical deposition process. Applied as a battery-type electrode material, this novel nanostructure exhibits excellent electrochemical stability, majorly attributed to the Ni midshell serving a dual role as “capacity supplement” and “electron highway”, which, to our knowledge, was incorporated into the nanocomposite electrodes for the first time. Also benefiting from the high conductivity of carbon nanotubes (CNTs) and the high capacity of the amorphous NiOOH ultrathin film [converted from the Ni2(CO3)(OH)2 outer shell], the resulting CNT@Ni@Ni2(CO3)(OH)2 material as a battery-type electrode achieves a superior capacity of 221 mAh·g–1 at 5 A·g–1 with 76% capacity retention at 50 A·g–1 and maintains 81%...

A well-structured anode nanomaterial, which can ensure electron and ion transport and avoid excessive pulverization, is of crucial importance to achieve high capacity with superior cycling stability for both sodium- and lithium-ion batteries (SIBs and LIBs). For the purpose of a superior rate performance, this work here has designed and successfully synthesized a new Na

// Yunwei Ou 1, 2, 3, 4, 7 , Zitong Zhao 2 , Weimin Zhang 2 , Qingnan Wu 2 , Chuanyue Wu 5, 6 , Xuefeng Liu 2 , Ming Fu 2 , Nan Ji 1 , Dan Wang 1 , Jiaji Qiu 1 , Liwei Zhang 1 , Chunjiang Yu 4 , Yongmei Song 2 , Qimin Zhan 2 1 Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China 2 State Key Laboratory of Molecular Oncology, Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China 3 Beijing Neurosurgical Institute, Capital Medical University, Beijing 100050, China 4 Department of Neurosurgery, Beijing Sanbo Brain Hospital, Capital Medical University, Beijing 100093, China 5 Department of Pathology, University of Pittsburgh, Pittsburgh, PA 15261, USA 6 Department of Biology and Shenzhen Key Laboratory of Cell Microenvironment, South University of Science and Technology of China, Shenzhen, 518055, China 7 China National Clinical Research Center for Neurological Diseases, Beijing 100050, China Correspondence to: Chunjiang Yu, email: cjyu1955@sina.com Yongmei Song, email: symlh2006@163.com Qimin Zhan, email: zhanqimin@pumc.edu.cn Keywords: EGFR, glioma, Kindlin-2, transcription Received: April 20, 2016 Accepted: August 11, 2016 Published: October 04, 2016 ABSTRACT Kindlin-2 promotes carcinogenesis through regulation of cell-cell and cell-extracellular matrix adhesion. However, the role of Kindlin-2 in glioma has not been elucidated. We investigated Kindlin-2 expression in 188 human glioma tissue samples. High Kindlin-2 expression was correlated with high pathological grade and a worse prognosis. Kindlin-2 promoted glioma cell motility and proliferation both in vitro and in vivo . Importantly, Kindlin-2 activated the EGFR pathway and increased EGFR mRNA levels. In addition to up-regulating Y-box binding protein-1 (YB-1) and β-catenin expression, Kindlin-2 formed a transcriptional complex with YB-1 and β-catenin that bound to the EGFR promoter and enhanced transcription. The β-catenin/YB-1/EGFR pathway was required for Kindlin-2-mediated functions. Our data provide a better understanding of the mechanisms underlying glioma progression, and suggest that Kindlin-2 may be a biomarker and therapeutic target in glioma.

Metabolic activities are often accompanied by cell-cycle progression, yet known connections between these two processes remain limited. Here, we identified the isocitrate dehydrogenase 3β (IDH3β) as a novel substrate of anaphase-promoting complex/cyclosome (APC/C)-CDH1 and an important regulator of the cell cycle. In esophageal squamous cell carcinoma (ESCC), IDH3β was posttranslationally upregulated in late G1 phase, and overexpression of IDH3β accelerated G1–S transition, contributing to the promotion of cell proliferation in vitro and in vivo. α-Ketoglutarate (α-KG), a crucial metabolite in tricarboxylic acid (TCA) cycle, was dependent on IDH3β level and partially accounted for IDH3β-mediated cell growth. IDH3β expression increased PFKFB3 protein levels and enhanced glucose uptake, and high expression of IDH3β correlated with poor survival in patients with ESCC, suggesting a potential application of IDH3β in prognosis. Overall, our results highlight a new molecular connection between cell-cycle regulation and the TCA cycle in ESCC. Significance: These findings show that IDH3β is an APC/C-CDH1 substrate and is expressed in a cell-cycle–dependent manner, highlighting novel molecular cross-talk between the TCA cycle and cell cycle in cancer cells.

To meet the demands of long cycle life under high rate for lithium-ion batteries, the advancement of anode materials with stable structural properties is necessarily demanded. Such promotion needs to design reasonable structure to facilitate the transportation of electron and lithium ions (Li

Ni(OH) 2 /CNTs/Ni(OH) 2 lamellar-crossing-nanostructure with a single lamellar spacing of ∼5 nm was effectively constructed through two-phase-interface reaction process followed by the CNTs crossed among the lamellar-nanostructured Ni(OH) 2 . The resultant nanocomposite can offer large active surface areas and short diffusion paths for electrons and ions, and is investigated as a potential pseudocapacitor electrode material for electrochemical energy storage applications. Electrochemical data demonstrate that the as-prepared nanocomposite exhibits a high specific capacitance of ∼1600 F g −1 at the scan rate of 1 mV s −1 in 6 M KOH solution at normal pressure and temperature, which is great higher than Ni(OH) 2 (∼1200 F g −1 ). Furthermore, Ni(OH) 2 /CNTs/Ni(OH) 2 nanocomposite shows a higher energy density (∼125 Wh kg −1 , 2 A g −1 ) and has a slightly decrease of 5% in specific capacitance after 1000 continuous charge/discharge cycles.

Supplementary Methods and Figures. (DOCX 3297 kb)

Magnetic Ru-capped/FeCo nanoflowers are solvothermally synthesised through a self-catalytic growth and assembly process. The synthesised Ru-capped/FeCo nanoflowers (∼3.63 μm) consist of Ru-capped FeCo nanorods with an average diameter of ∼13 nm and a length ranging from 1.33 to 2.1 μm. A vibration sample magnetometer measurement reveals that the ferromagnetic behaviours depend on nanomaterial composition. Particularly, an appropriate quantity of Fe in the composition improved catalytic activity. The Fe 22 Co 73 /Ru 5 nanoflowers exhibits the highest catalytic activity towards NaBH 4 hydrolytic dehydrogenation at ambient pressure and room temperature (the dehydrogenation rate is 4293.75 mL min −1 g −1 ; the activation energy is 42.95 kJ mol −1 ).

New NiCo–Pt nanopolyhedron inlay-structures with an average diameter of ∼450 nm have been synthesized through replacement deposition Co or Ni by reductive replacement with a Pt submonolayer (galvanic replacement) on NiCo hexagonal nanoplates and nanoicosahedrons. The resultant products are investigated as hydrolytic dehydrogenation catalyst for potential hydrogen energy applications. The NiCo–Pt nanopolyhedrons exhibit higher catalytic activity than NiCo nanopolyhedrons for the hydrolysis of borane in aqueous ammonia borane at ambient atmosphere and room temperature. In particular, the NiCo–Pt hexagonal nanoplates exhibit efficient catalytic activity with a lower activation energy of 45.72 kJ mol −1 than that (49.4 kJ mol −1 ) for NiCo.

Novel, urchinlike FeNi–Ru(tips) hierarchical-structured nanospheres (≈9.17 µm) were constructed through a controllable assembly process. Offering large surface areas and macropores as well as more active sites, this special structured catalyst can greatly facilitate reactant diffusion and transport to promote reactivity. By combining the advantages of Ru and FeNi nanomaterials, the resultant urchinlike FeNi–Ru(tips) nanospheres exhibit excellent catalytic activity with the dehydrogenation rate of 2245.87 mL min−1 g−1 toward the hydrolytic dehydrogenation of aqueous NaBH4 under ambient atmosphere at room temperature, in which Fe19Ni76–Ru5 shows the best dehydrogenation reactivity with low activation energy (41.57 kJ mol−1). Additionally, these new structured nanoalloys present controllable ferromagnetic behavior by means of adjusting the molar content of Fe, Ni, and Ru.

A new magnetic Pt-loaded NiCo nanochain, with the diameter from 80 nm to 120 nm, has been prepared through microwave-induced assembly process followed by the galvanic displacement performance. Pt nanoparticles are distributed on the surface of NiCo nanochains. The products are investigated as hydrolytic dehydrogenation catalyst for potential hydrogen energy applications. Compared with NiCo nanochains, the Pt-loaded NiCo nanochains present exceedingly high catalytic activity toward the hydrolytic dehydrogenation of ammonia borane aqueous under ambient atmosphere at room temperature, where the Ni16Co80/Pt4 nanochains exhibit high catalytic activity with a lower activation energy of 45.72 kJ mol(-1) and a superior dehydrogenation rate of 1.17 × 10(4) mL min(-1) g(-1), suggesting the potential application in hydrogen fuel and chemical industry.