Publications by authors named "Jiuling Chen"

15 Publications

  • Page 1 of 1

Cytosporone B (Csn-B), an NR4A1 agonist, attenuates acute cardiac allograft rejection by inducing differential apoptosis of CD4+T cells.

Int Immunopharmacol 2022 Jan 10;104:108521. Epub 2022 Jan 10.

Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Electronic address:

CD4+T cell-mediated acute rejection remains a major factor that affects the early survival of transplanted organs post-transplantation. Here, we reveal that nuclear receptor subfamily 4 Group A member 1 (Nr4A1) was upregulated during cardiac allograft rejection and that the increased Nr4A1 was primarily localized in intragraft-infiltrating CD4+T cells. Nr4A1 acts as a transcription factor with an important role in CD4+T cell apoptosis, differentiation and T cell dysfunction, which indicates that Nr4A1 may play a critical role in transplant rejection. Cytosporone B (Csn-B) is a naturally occurring agonist of Nr4A1, and the role of Csn-B in the physiological process of cardiac rejection is poorly defined. This study constructed an acute rejection model of abdominal heterotopic cardiac transplantation in mice and investigated whether Csn-B could attenuate acute transplant rejection by modulating the CD4+T lymphocyte response. The results showed that Csn-B prolonged murine cardiac allograft survival and reduced inflammation in allografts. Subsequently, it was confirmed that Csn-B functions by inducing non-Treg apoptosis and promoting Treg cell differentiation. Finally, we also confirmed that Csn-B attenuates acute rejection by directly targeting Nr4A1 in CD4+T cells. Our data suggest that Csn-B is a promising novel therapeutic approach for acute cardiac allograft rejection.
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http://dx.doi.org/10.1016/j.intimp.2022.108521DOI Listing
January 2022

Inhibition of S-adenosyl-L-homocysteine hydrolase alleviates alloimmune response by down-regulating CD4 T-cell activation in a mouse heart transplantation model.

Ann Transl Med 2020 Dec;8(23):1582

Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Background: Transmethylation reactions play an important role on lymphocyte activation and function. S-adenosyl-L-homocysteine hydrolase (SAHH) inhibitors prevent the feedback of transmethylation reactions by S-adenosyl-L-homocysteine (SAH) accumulation, a competitive antagonist of S-adenosylmethionine (SAM)-dependent methyltransferases. However, the role of SAH in solid organ transplantation is currently unclear.

Methods: A murine model of cardiac transplantation (BALB/C to C57B/6) was established to assess allograft survival, histology, and T cell infiltration. The reversible SAHH inhibitor, DZ2002, and irreversible SAHH inhibitor, adenosine dialdehyde (AdOx), were used to assess their immunosuppressive effects in murine cardiac transplantation, compared with mice with DMSO.

Results: Both SAHH inhibitors prolonged the survival of cardiac allografts and alleviated alloimmune response. Notably, AdOx and DZ2002 both eliminated frequencies of Th1 and Th17 in CD4 T cells in cardiac transplantation, and reduced the frequency of active CD4 T cell (CD44 CD62L). The irreversible SAHH inhibitor facilitated the differentiation of regulatory T cells (Tregs) and increased Bim expression. Furthermore, both SAHH inhibitors alleviated infiltration of CD4 T cells in cardiac allografts.

Conclusions: The SAHH inhibitors (AdOx and DZ2002) alleviates allograft rejection in cardiac transplantation by inhibition of CD4 T alloimmune response. SAHH inhibitors, especially DZ2002, is a promising complementary therapeutic agent in organ transplantation.
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http://dx.doi.org/10.21037/atm-20-2899DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7791210PMC
December 2020

Ribavirin therapy for severe COVID-19: a retrospective cohort study.

Int J Antimicrob Agents 2020 Sep 23;56(3):106114. Epub 2020 Jul 23.

Department of Respiratory and Critical Care Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, China. Electronic address:

The aim of this study was to compare ribavirin therapy versus supportive therapy only for patients with severe coronavirus disease 2019 (COVID-19). A total of 115 patients with laboratory-confirmed COVID-19 were retrospectively analysed. All patients received supportive care as well as regular laboratory and clinical monitoring. The 115 patients comprised 44 patients who received intravenous ribavirin (treatment group) and 71 who did not (control group). Baseline laboratory and clinical characteristics were similar between the two groups. The negative conversion time for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RT-PCR in the ribavirin group was 12.8 ± 4.1 days compared with 14.1 ± 3.5 days in the control group (P = 0.314). Moreover, 7/41 patients (17.1%) in the ribavirin group died compared with 17/69 (24.6%) in the control group (P = 0.475). Adverse effects were similar between the two groups. In conclusion, in patients with severe COVID-19, ribavirin therapy is not associated with improved negative conversion time for SARS-CoV-2 test and is not associated with an improved mortality rate. Further assessment in designed randomised controlled trials is recommended.
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http://dx.doi.org/10.1016/j.ijantimicag.2020.106114DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7377772PMC
September 2020

Nanostructured NiMoS₂/Carbon Catalysts for Syngas Conversion to Higher Alcohols.

J Nanosci Nanotechnol 2020 08;20(8):5260-5266

Australian Institute of Bioengineering and Nanotechnology, The University of Queensland St. Lucia, QLD, 4072, Australia.

Syngas conversion to higher alcohols remains a very attractive alternative due to the abundance of syngas feedstock, such as renewable carbon and waste-carbon resources. Catalysts suitable for syngas conversion still show low selectivity to alcohols. In this article, we present nanostructured NiMoS₂ and CoMoS₂ catalysts supported on activated carbon pellets and design strategies to improve its selectivity towards higher alcohols. Activated carbon pellets were treated with concentrated HNO₃ to enlarge porous channels and enable better dispersion of NiMoS₂ and CoMoS₂. These treatment steps lead to a formation of nanostructured NiMoS₂ and CoMoS₂ catalysts and promoted higher selectivity to ethanol, propanol and butanol. BET surface area of 532 m² g was obtained for NiMoS₂/Carbon catalysts from the nitrogen physisorption analysis. In catalytic tests, the highest CO conversion (39.1%) was achieved by the NiMoS₂/Carbon, whereas the CoMoS₂/Carbon showed the highest alcohol selectivity (74.4%). CoMoS₂ catalysts supported on activated carbon pellets proved to be highly active towards undesired by-product "filamentous carbon."
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http://dx.doi.org/10.1166/jnn.2020.18525DOI Listing
August 2020

PDGFR-β Signaling Regulates Cardiomyocyte Proliferation and Myocardial Regeneration.

Cell Rep 2019 07;28(4):966-978.e4

State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China. Electronic address:

Platelet-derived growth factor receptor (PDGFR) signaling is involved in proliferation and survival in a wide array of cell types. The role of PDGFR signaling in heart regeneration is still unknown. We find that PDGFR-β signaling decreases in myocardium with age and that conditional activation PDGFR-β in cardiomyocytes promotes heart regeneration. Employing RNA sequencing, we show that the enhancer of zeste homolog 2 (Ezh2) can be upregulated by PDGFR-β signaling in primary cardiomyocytes. Conditional knockout of Ezh2 blocks cardiomyocyte proliferation and H3K27me3 modification during neonatal heart regeneration with Ink4a/Arf upregulation, even in mice with myocyte-specific conditional activation of PDGFR-β. We also show that PDGFR-β controls EZH2 expression via the phosphatidylinositol 3-kinase (PI3K)/p-Akt pathway in cardiomyocytes. Gene therapy with adeno-associated virus serotype 9 (AAV9) encoding activated PDGFR-β enhances adult heart regeneration and systolic function. Our data demonstrate that the PDGFR-β/EZH2 pathway is critical for promoting cardiomyocyte proliferation and heart regeneration, providing a potential target for cardiac repair.
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http://dx.doi.org/10.1016/j.celrep.2019.06.065DOI Listing
July 2019

Nucleotide-Binding Oligomerization Domain-Like Receptor Protein 3 Deficiency in Vascular Smooth Muscle Cells Prevents Arteriovenous Fistula Failure Despite Chronic Kidney Disease.

J Am Heart Assoc 2019 01;8(1):e011211

1 Department of Cardiovascular Surgery Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China.

Background The arteriovenous fistula ( AVF ) is the preferred hemodialysis access for patients with chronic kidney disease. Chronic kidney disease can increase neointima formation, which greatly contributes to AVF failure by an unknown mechanism. Our study aimed to determine the role of nucleotide-binding oligomerization domain-like receptor protein 3 ( NLRP 3) in neointima formation induced by experimental AVF s in the presence of chronic kidney disease. Methods and Results From our findings, NLRP 3 was upregulated in the intimal lesions of AVF s in both uremic mice and patients. Smooth muscle-specific knockout NLRP 3 mice exhibited markedly decreased neointima formation in the outflow vein of AVF s. Compared with primary vascular smooth muscle cells isolated from control mice, those isolated from smooth muscle-specific knockout NLRP 3 mice showed compromised proliferation, migration, phenotypic switching, and a weakened ability to activate mononuclear macrophages. To identify how NLRP 3 functions, several small-molecule inhibitors were used. The results showed that NLRP 3 regulates smooth muscle cell proliferation and migration through Smad2/3 phosphorylation rather than through caspase-1/interleukin-1 signaling. Unexpectedly, the selective NLRP 3-inflammasome inhibitor MCC 950 also repressed Smad2/3 phosphorylation and relieved chronic kidney disease-promoted AVF failure independent of macrophages. Conclusions Our findings suggest that NLRP 3 in vascular smooth muscle cells may play a crucial role in uremia-associated AVF failure and may be a promising therapeutic target for the treatment of AVF failure.
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http://dx.doi.org/10.1161/JAHA.118.011211DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6405733PMC
January 2019

A long noncoding RNA NR_045363 controls cardiomyocyte proliferation and cardiac repair.

J Mol Cell Cardiol 2019 02 13;127:105-114. Epub 2018 Dec 13.

State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China. Electronic address:

Long noncoding RNAs (lncRNAs) play important roles in the regulation of genes involved in cell proliferation. We have previously sought to more globally understand the differences of lncRNA expression between human fetal heart and adult heart to identify some functional lncRNAs which involve in the process of heart repair. We found that a highly conserved long noncoding RNA NR_045363 was mainly expressed in cardiomyocytes and rarely in non-cardiomyocytes. NR_045363 overexpression in 7-day-old mice heart could improve cardiac function and stimulate cardiomyocyte proliferation after myocardial infarction. Furthermore, NR_045363 knockdown inhibited proliferation of primary embryonic cardiomyocytes, while NR_045363 overexpression enhanced DNA synthesis and cytokinesis in neonatal cardiomyocytes in vitro. Mechanistic analysis revealed that NR_045363 promoted cardiomyocyte proliferation through interaction with miR-216a, which regulated the JAK2-STAT3 pathway. Our results showed that NR_045363 is a potent lncRNA modulator essential for cardiomyocyte proliferation.
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http://dx.doi.org/10.1016/j.yjmcc.2018.12.005DOI Listing
February 2019

ADAM23 in Cardiomyocyte Inhibits Cardiac Hypertrophy by Targeting FAK - AKT Signaling.

J Am Heart Assoc 2018 09;7(18):e008604

4 Department of Cardiovascular Surgery Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China.

Background Cardiac hypertrophy has been recognized as an important independent risk factor for the development of heart failure and increases the risk of cardiac morbidity and mortality. A disintegrin and metalloprotease 23 (ADAM23), a member of ADAM family, is involved in cancer and neuronal differentiation. Although ADAM23 is expressed in the heart, the role of ADAM23 in the heart and in cardiac diseases remains unknown. Methods and Results We observed that ADAM23 expression is decreased in both failing human hearts and hypertrophic mice hearts. Cardiac-specific conditional ADAM23-knockout mice significantly exhibited exacerbated cardiac hypertrophy, fibrosis, and dysfunction, whereas transgenic mice overexpressing ADAM23 in the heart exhibited reduced cardiac hypertrophy in response to pressure overload. Consistent results were also observed in angiotensin II -induced neonatal rat cardiomyocyte hypertrophy. Mechanistically, ADAM23 exerts anti-hypertrophic effects by specifically targeting the focal adhesion kinase-protein kinase B (FAK-AKT) signaling cascade. Focal adhesion kinase inactivation by inhibitor ( PF -562271) greatly reversed the detrimental effects in ADAM23-knockout mice subjected to aortic banding. Conclusion Altogether, we identified ADAM23 as a negative regulator of cardiac hypertrophy through inhibiting focal adhesion kinase-protein kinase B signaling pathway, which could be a promising therapeutic target for this malady.
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http://dx.doi.org/10.1161/JAHA.118.008604DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6222933PMC
September 2018

MicroRNA-21 Knockout Exacerbates Angiotensin II-Induced Thoracic Aortic Aneurysm and Dissection in Mice With Abnormal Transforming Growth Factor-β-SMAD3 Signaling.

Arterioscler Thromb Vasc Biol 2018 05 8;38(5):1086-1101. Epub 2018 Mar 8.

From the Department of Cardiovascular Surgery, Union Hospital (X.H., Z.Y., J.C., J.W., P.D., K.W., C.W., X.D., J.X.)

Objective: Thoracic aortic aneurysm and dissection (TAAD) are severe vascular conditions. Dysfunctional transforming growth factor-β (TGF-β) signaling in vascular smooth muscle cells and elevated angiotensin II (AngII) levels are implicated in the development of TAAD. In this study, we investigated whether these 2 factors lead to TAAD in a mouse model and explored the possibility of using microRNA-21 () for the treatment of TAAD.

Approach And Results: TAAD was developed in (mothers against decapentaplegic homolog 3) heterozygous (S3) mice infused with AngII. We found that p-ERK (phosphorylated extracellular regulated protein kinases)- and p-JNK (phosphorylated c-Jun N-terminal kinase)-associated was higher in TAAD lesions. We hypothesize that downregulation of mitigate TAAD formation. However, (S321) mice exhibited conspicuous TAAD formation after AngII infusion. The vascular wall was dilated, and aortic rupture occurred within 23 days during AngII infusion. We then examined canonical and noncanonical TGF-β signaling and found that knockout in S3 mice increased SMAD7 and suppressed canonical TGF-β signaling. Vascular smooth muscle cells lacking TGF-β signals tended to switch from a contractile to a synthetic phenotype. The silencing of with lentivirus prevented AngII-induced TAAD formation in S321 mice.

Conclusions: Our study demonstrated that knockout exacerbated AngII-induced TAAD formation in mice, which was associated with TGF-β signaling dysfunction. Therapeutic strategies targeting TAAD should consider unexpected side effects associated with alterations in TGF-β signaling.
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http://dx.doi.org/10.1161/ATVBAHA.117.310694DOI Listing
May 2018

Inhibition of intimal hyperplasia in murine aortic allografts by administration of a small-molecule TLR4 inhibitor TAK-242.

Sci Rep 2017 Nov 17;7(1):15799. Epub 2017 Nov 17.

Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Graft arteriosclerosis (GA) is the leading cause of late cardiac allograft dysfunction. The innate immune system plays a major role in GA, paprticularly Toll-like receptor 4 (TLR4) signaling. Here we characterized the role of TLR4 and its antagonist TAK-242 in a mouse model of GA. BALB/c (H-2d) donor aortas were transplanted into C57BL/6 (H-2b) recipients, and the mice received intraperitoneal injection of 3 or 10 mg/kg of TAK-242 or vehicle every other day for 1, 2, 4, 6, 8 and 12 weeks. With TAK-242 administration, intimal hyperplasia initially appeared at 2 weeks after transplantation, and TAK-242 postponed the progression of neointimal formation in allogeneic aortic grafts. TAK-242 treatment reduced CD68+ macrophage accumulation in the allografts, reduced the levels of ly-6C monocytes in peripheral blood, bone marrow and spleen, and downregulated proinflammatory cytokine and chemokine levels. Ex vivo we observed that TAK-242 could improve the graft microenvironment by interfering the Tck/Mφ IL12p70 and IFNγ axis, reducing CCL2-mediated migration of vascular smooth cells.
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http://dx.doi.org/10.1038/s41598-017-16160-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5693917PMC
November 2017

Knockout of microRNA-155 ameliorates the Th1/Th17 immune response and tissue injury in chronic rejection.

J Heart Lung Transplant 2017 Feb 6;36(2):175-184. Epub 2016 May 6.

Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Department of Cardiovascular Medicine, Central Hospital of Wuhan, Wuhan, China; Department of Cardiovascular Surgery, Central Hospital of Wuhan, Wuhan, China. Electronic address:

Background: MicroRNAs (miRNAs) are integral for maintaining immune homeostasis and self-tolerance. The influence of miRNAs on T-cell differentiation and plasticity are critical in the development of chronic rejection of transplanted hearts. In this study, we sought to determine whether the knockout of miR-155 affects the development of cardiac allograft vasculopathy (CAV) in a murine model.

Methods: miRNA microarray and quantitative polymerase chain reaction (qPCR) analyses were performed for allograft neointimal lesion samples in chronic rejection. A model of heterotopic murine heart transplantation (bm12 to miR-155 or miR-155 mice) was then used to analyze allograft survival, histology, mRNA expression and T-cell sub-populations in spleens. The accelerated experiments were performed by intraperitoneal injection of either recombinant interleukin-17A or phosphate-buffered saline (PBS) after heart transplantation. For the competitive transfer experiments, CD4 splenocytes from wild-type (WT) or miR-155 mice were mixed and injected into Rag1 mice, and cardiac transplantation was performed after 24 hours. The differentiation of T-helper subsets (Th1/Th17/iTreg) was investigated in vitro.

Results: miR-155 mice showed resistance to cardiac rejection along with weakened T-cell-mediated inflammation, especially for Th17 cells. Recombinant IL-17A could restore this relieved injury. The competitive experiments implied that miR-155 plays a vital role in the stability of the Th17 phenotype. In vitro, we also demonstrated that miR-155 mice exhibit a defect in Th17 differentiation.

Conclusions: miR-155 regulates Th1/Th17-related inflammation in chronic cardiac rejection and may be a potential therapeutic target to attenuate cardiac allograft rejection. Despite advancements in immunosuppressive therapy, the immunologic mechanisms responsible for allograft rejection remain an important issue for both clinicians and researchers. Allograft rejection is a T-cell-dependent phenomenon and is critically dependent on inflammation mediated by CD4 Th subsets, including Th1, Th2, Th17, Th9 and regulatory T (Treg) cells.
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http://dx.doi.org/10.1016/j.healun.2016.04.018DOI Listing
February 2017

MicroRNA-155 Promotes the Directional Migration of Resident Smooth Muscle Progenitor Cells by Regulating Monocyte Chemoattractant Protein 1 in Transplant Arteriosclerosis.

Arterioscler Thromb Vasc Biol 2016 06 14;36(6):1230-9. Epub 2016 Apr 14.

From the Department of Vascular Surgery, The Clinical Medical College of Yangzhou University, Yangzhou, China (Y.S., Z.C.); Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China (Y.S., K.W., J.W., L.R., A.Z., X.H., P.D., C.W., Z.Y., X.D., J.C., J.X.); and Departments of Cardiovascular Medicine (P.Y., L.R., J.X.) and Cardiovascular Surgery (P.Y., L.R., J.X.), Central Hospital of Wuhan, Wuhan, China.

Objective: Smooth muscle-like cells are major cell components of transplant arteriosclerosis lesions. This study investigated the origin of the smooth muscle-like cells, the mechanisms responsible for their accumulation in the neointima, and the factors that drive these processes.

Approach And Results: A murine aortic transplantation model was established by transplanting miR-155(-/-) bone marrow cells into miR-155(+/+) mice. MicroRNA-155 was found to play a functional role in the transplant arteriosclerosis. Moreover, we found that the nonbone marrow-derived progenitor cells with markers of both early differentiated smooth muscles and stem cells in the allograft adventitia were smooth muscle progenitor cells. Purified smooth muscle progenitor cells expressed a mature smooth muscle cell marker when induced by platelet-derived growth factor-BB in vitro. In vivo, these cells could migrate into the intima from the adventitia and could contribute to the neointimal hyperplasia. The loss of microRNA-155 in bone marrow-derived cells decreased the concentration gradient of monocyte chemoattractant protein 1 between the intima and the adventitia of the allografts, which reduced the migration of smooth muscle progenitor cells from the adventitia into the neointima.

Conclusions: This study demonstrated that microRNA-155 promoted the directional migration of smooth muscle progenitor cells from the adventitia by regulating the monocyte chemoattractant protein 1 concentration gradient, which aggravated transplant arteriosclerosis.
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http://dx.doi.org/10.1161/ATVBAHA.115.306691DOI Listing
June 2016

Study on the controllable scale-up growth of vertically-aligned carbon nanotube arrays.

J Nanosci Nanotechnol 2012 Mar;12(3):2722-32

School of Chemical Engineering, University of Queensland, QL 4072, Australia.

Vertically aligned carbon nanotubes (VA-CNTs) with high purity have been grown on quartz substrate via the gas phase catalytic chemical vapour deposition (CVD) by using ferrocene as the catalyst source and camphor as the carbon source. The effects of catalyst concentration, flow rate and water assistance on the morphology and structure of VA-CNTs are investigated by SEM, TEM, Raman and XPS characterizations. Under the optimized CVD conditions with modest ferrocene concentration and flow rate, dense and well VA-CNT arrays have been obtained. The water concentration should be controlled to improve CNTs alignment and impurity without damaging the walls of CNTs.
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http://dx.doi.org/10.1166/jnn.2012.5726DOI Listing
March 2012

Heterostructured electrode with concentration gradient shell for highly efficient oxygen reduction at low temperature.

Sci Rep 2011 14;1:155. Epub 2011 Nov 14.

Division of Chemical Engineering, The University of Queensland, Brisbane, Queensland 4072, Australia.

Heterostructures of oxides have been widely investigated in optical, catalytic and electrochemical applications, because the heterostructured interfaces exhibit pronouncedly different transport, charge, and reactivity characteristics compared to the bulk of the oxides. Here we fabricated a three-dimensional (3D) heterostructured electrode with a concentration gradient shell. The concentration gradient shell with the composition of Ba(0.5-x)Sr(0.5-y)Co(0.8)Fe(0.2)O(3-δ) (BSCF-D) was prepared by simply treating porous Ba(0.5)Sr(0.5)Co(0.8)Fe(0.2)O(3-δ) (BSCF) backbone with microwave-plasma. Electrochemical impedance spectroscopy reveals that the oxygen surface exchange rate of the BSCF-D is enhanced by ~250% that of the pristine BSCF due to the appearance of the shell. The heterostructured electrode shows an interfacial resistance as low as 0.148 Ω cm(2) at 550°C and an unchanged electrochemical performance after heating treatment for 200 h. This method offers potential to prepare heterostructured oxides not only for electrochemical devices but also for many other applications that use ceramic materials.
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http://dx.doi.org/10.1038/srep00155DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240982PMC
September 2013

Influence of surface functionalization via chemical oxidation on the properties of carbon nanotubes.

J Colloid Interface Sci 2012 Mar 8;370(1):32-8. Epub 2012 Jan 8.

Department of Catalysis Science & Technology, School of Chemical Engineering, Tianjin University, Tianjin 300072,

The surface of carbon nanotubes (CNTs) was functionalized in different chemical oxidants, hydrogen peroxide, mixed concentrated HNO(3)/H(2)SO(4) and acidic KMnO(4) solution. The influences on the properties of CNTs were systematically investigated, such as the structure, the kinds and the contents of the formed surface oxygen-containing functional groups, the pH(PZC) values and the surface hydrophilicity using XRD, HREM, FTIR and chemical titration. The results show that the kinds and the contents of the surface oxygen-containing groups are dependent on the functionalization methods. The formation of the oxygen-containing groups can decrease pH(PZC) values and improve surface hydrophilicity of CNTs. The dispersion of the supported Pd-Pt particles on the functionalized CNTs and their catalytic activity in the profile reaction of naphthalene hydrogenation to tetralin are both promoted due to the presence of these oxygen-containing groups.
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http://dx.doi.org/10.1016/j.jcis.2011.12.073DOI Listing
March 2012
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