| 1. |
- Ablikim, M., et al.
(författare)
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Search for h(c) -> pi(+)pi(-) J/psi via psi(3686) -> pi(0)pi(+)pi(-) J/psi
- 2018
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Ingår i: Physical Review D. - : American Physical Society. - 2470-0010 .- 2470-0029. ; 97:5
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Tidskriftsartikel (refereegranskat)abstract
- Using a data sample of 448.1 x 10(6) psi(3686) events collected with the BESIII detector operating at the BEPCII, we perform search for the hadronic transition h(c)-> pi(+)pi(-) J/psi via psi (3686) -> pi(0)hc. No signals of the transition are observed, and the upper limit on the product branching fraction B(sigma(3686) -> pi(0)h(c))B(h(c) -> pi(+)pi(-) J/psi) at the 90% confidence level (C. L.) is determined to be 2.0 x 10(-6). This is the most stringent upper limit to date.
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| 2. |
- Du, Banghua, et al.
(författare)
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Energy management and performance analysis of an off-grid integrated hydrogen energy utilization system
- 2024
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Ingår i: Energy Conversion and Management. - 0196-8904. ; 299
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Tidskriftsartikel (refereegranskat)abstract
- In integrated hydrogen energy utilization systems, due to the low efficiency of hydrogen/electricity conversion, coordination of energy management and efficient waste heat recovery is required to optimize performance. To address this challenge, this paper presents a comprehensive and sophisticated modeling and energy management strategy to enhance the off-grid energy utilization rate while prolonging the main components' lifetime. The developed model incorporates multiphase flow and heat transport balance for electricity and heat production, enabling a highly accurate representation of real-world behaviors of the system. The proposed off-grid operation strategy is complemented by a designed heat recovery scheme, ensuring the use of energy resources and waste heat. In addition, the proposed energy management strategy monitors the real-time status of each subsystem, actively reducing the number of harmful start-stop cycles of the hydrogen production system, thereby mitigating short-term power impacts and delaying its aging. Specifically, the voltage degradation of the reduction cell is reduced from 4.67 mV to 4.48 mV, the energy utilization rate is increased from 47.6 % to 53.9 %, and the energy efficiency of fuel cells significantly increases from 53.6 % to 78.1 %.
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| 3. |
- Fu, Yifeng, 1984, et al.
(författare)
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Templated Growth of Covalently Bonded Three-Dimensional Carbon Nanotube Networks Originated from Graphene
- 2012
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Ingår i: Advanced Materials. - : Wiley. - 0935-9648 .- 1521-4095. ; 24:12, s. 1576-1581
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Tidskriftsartikel (refereegranskat)abstract
- A template-assisted method that enables the growth of covalently bonded three-dimensional carbon nanotubes (CNTs) originating from graphene at a large scale is demonstrated. Atomic force microscopy-based mechanical tests show that the covalently bonded CNT structure can effectively distribute external loading throughout the network to improve the mechanical strength of the material.
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| 4. |
- Hamidi, Anahita, et al.
(författare)
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TGF-β promotes PI3K-AKT signaling and prostate cancer cell migration through the TRAF6-mediated ubiquitylation of p85α
- 2017
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Ingår i: Science Signaling. - : American Association for the Advancement of Science. - 1945-0877 .- 1937-9145. ; 10:486
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- TGF-β signaling stimulates various intracellular pathways that can promote migration in tumor cells. These pathways are generally thought to be either dependent or independent of transcription factors called SMADs. One of the SMAD-independent pathways (PI3K-AKT) is mediated by a direct interaction between PI3K and the TGF-β type I receptor. However, Hamidi et al. found that the TGF-β–induced activation of PI3K depends on another ubiquitin ligase–mediated mechanism and a SMAD protein but is independent of the kinase function of TβRI. The binding of TGF-β to its receptor triggered the recruitment of PI3K and the ubiquitin ligase TRAF6, which polyubiquitylated the regulatory PI3K subunit p85α, thus enabling phosphorylation of the catalytic PI3K subunit p110, but only in the presence of SMAD7. The abundance of ubiquitylated p85α correlated with migration in cultured cells and prostate tumor grade in patient samples. TRAF6 mediates activation of the other “SMAD-independent” (JNK) pathway. These data suggest that, although distinct, the TGF-β signaling pathways are not as insulated from each other as was once thought.
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| 5. |
- Mu, Yabing, et al.
(författare)
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TGFβ-induced activation of PKCζ confers invasive prostate cancer growth
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- One of the hallmarks for aggressivecancer is the capability oftumor cells to become invasive and metastatic. Cancer cells and tumor stromal cells oftenproduce high levels of transforming growth factor b(TGFb) which initiates intracellular signaling pathways in cancer cells in a contextualdependentmanner. Atypical protein kinase C z(PKCz) is a multifunctional protein which maintains cell polarity of normal epithelial cells, while itsaberrantexpression and activation is linked to tumor progression. Tumor necrosisfactor receptor-associated factor6 (TRAF6) is amplified in lung cancer and caninitiate intracellular oncogenic signals. In prostate cancer cellsTRAF6 promotesligand-induced proteolytic cleavage of TGFbtype I receptor(TbRI), and nuclear translocation of its intracellular domain (ICD) to confer invasion of cancer cells. Here we report our novel findingsthat PKCzharboursa TRAF6 consensus binding site and that TRAF6 causes Lys63-linked polyubiquitination of PKCz. TGFb-induced phosphorylationof PKCzis dependent on TRAF6in prostate cancer cells and we have investigated the potential usefulness of twodifferent inhibitors of PKCzas potential novel anti-cancer drugs.
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| 6. |
- Song, Jie, 1984-
(författare)
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Non-canonical TGFb signaling pathways in prostate cancer
- 2016
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Prostate cancer is the second leading cause of cancer-related death in men in the Western world. Deregulation of transforming growth factor β (TGFβ) signaling pathway is frequently detected in prostate cancer and contributes to tumor growth, migration, and invasion. In normal tissue and the early stages of cancer, TGFβ acts as a tumor suppressor by regulating proliferation, differentiation, and apoptosis. In later stages of cancer, TGFβ acts as a tumor promoter by inducing angiogenesis, tumor invasion, and migration. Thus, it is important to investigate the molecular mechanisms behind the tumor-promoting effects of TGFβ, which is the topic of this thesis. The tumor necrosis factor receptor–associated factor 6 (TRAF6) controls non-canonical TGFβ signals due to its enzymatic activity, causing polyubiquitination of the cell membrane–bound, serine/threonine kinase TGFβ type I receptor (TβRI) and its subsequent cleavage in the extracellular domain by tumor necrosis factor a–converting enzyme (TACE) in a protein kinase C ζ (PKCζ)-dependent manner. TRAF6 also recruits the active g-secretase complex to the TβRI, resulting in a second cleavage in the transmembrane region and the liberation of the TβRI intracellular domain (TβRI-ICD), which enters the nucleus, where it associates with the transcriptional co-regulator p300. In Paper I, the aim was to elucidate by which mechanisms TβRI-ICD enters the nucleus. We found that the endocytic adaptor protein APPL1 interacts with TβRI and PKCζ. APPL proteins are required for TβRI translocation from endosomes to the nucleus via microtubules in a TRAF6-dependent manner. Moreover, APPL proteins are important for TGFβ-induced cell invasion, and high levels of APPL1 are detected by immunohistochemistry in prostate cancer. Finally, we demonstrated that the APPL1–TβRI complex visualized with the in situ proximity ligation assay (PLA) correlates with Gleason score, indicating that it might be a novel prognostic marker for aggressive prostate cancer. In Paper II, the aim was to explore by which mechanisms TGFβ causes activation of the AKT pathway, which regulates migration and therapy resistance of cancer cells. We found that the E3 ligase activity of TRAF6 induces Lys63-linked polyubiquitination of p85α upon TGFβ stimulation, resulting in plasma membrane recruitment, Lys63-linked polyubiquitination, and subsequent activation of AKT. Moreover, the TRAF6 and PI3K/AKT pathway were found to be crucial for the TGFβ-induced migration. Importantly, we demonstrated, by PLA, a correlation between Lys63-linked polyubiquitination of p85α and aggressive prostate cancer in tissue sections from patients with prostate cancer. In Paper III, the aim was to investigate the mechanisms for TGFβ-induced activation of PKCζ and the role of PKCζ in tumor regression. We found that TRAF6 caused Lys63-linked polyubiquitination of PKCζ. By using two novel chemical compounds that inhibit PKCζ, we demonstrated that PKCζ is crucial for prostate cancer cell survival and invasion. In Paper IV, the aim was to investigate further the target genes for the nuclear TβRI-ICD-APPL1 complex identified in Paper I. We provide evidence that APPL proteins and the TGFβ signaling pathway are important for cell proliferation. In summary, the results reported in this thesis suggest the potential usefulness of the identified signaling components of the tumor-promoting effects of TGFβ as drug targets and biomarkers for aggressive prostate cancer.
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| 7. |
- Song, Jie, 1984-, et al.
(författare)
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TGFb type I receptor and endosomal APPL regulate AURKB during mitosis and cytokinesis
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- The cytokine transforming growth factor b(TGFb) suppressescell proliferationand promotesapoptosis1. It signalsvia specific serine/threonine kinase receptors, i.e.TGFbtype I (TbRI) and type II (TbRII) receptors2,3,causing growth arrest of normal epithelial cells. However, TGFbis often overexpressed inadvanced cancers,and promotes proliferation of tumour cells and their invasion. The intracellular domain (ICD) of TbRI is cleaved offin cancer cells,and is translocated to the nucleus in an APPL1/2-dependent manner, drivingan invasiveness program4.The specific mechanism(s) whereby cancer cells escape pro-apoptotic signals induced by TGFbremainspoorly understood. Here, we report that TbRI and APPL1/2 proteins orchestrate this escape via the pro-survival protein survivin and Aurora kinase B (AURKB), a key regulatorof mitosis and chromosomal stability5. We show that TbRI and APPL1/2 control expression of AURKB and that TbRI-ICDand AURKB form a complex during the telophase in PC-3Uprostate cancerand KELLY neuroblastomacells. APPL1/2 and TbRI also form a complex with survivin, a pro-survival protein. The identified TbRI–AURKB-survivinpathwayrepresents a novel function for TbRI to promote survival and cell division of cancer cells.
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| 8. |
- Song, Jie, 1984-, et al.
(författare)
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The ubiquitin-ligase TRAF6 and TGFβ type I receptor form a complex with Aurora kinase B contributing to mitotic progression and cytokinesis in cancer cells
- 2022
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Ingår i: EBioMedicine. - : Elsevier. - 2352-3964. ; 82
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundTransforming growth factor β (TGFβ) is overexpressed in several advanced cancer types and promotes tumor progression. We have reported that the intracellular domain (ICD) of TGFβ receptor (TβR) I is cleaved by proteolytic enzymes in cancer cells, and then translocated to the nucleus in a manner dependent on the endosomal adaptor proteins APPL1/2, driving an invasiveness program. How cancer cells evade TGFβ-induced growth inhibition is unclear.MethodsWe performed microarray analysis to search for genes regulated by APPL1/2 proteins in castration-resistant prostate cancer (CRPC) cells. We investigated the role of TβRI and TRAF6 in mitosis in cancer cell lines cultured in 10% FBS in the absence of exogenous TGFβ. The molecular mechanism of the ubiquitination of AURKB by TRAF6 in mitosis and the formation of AURKB–TβRI complex in cancer cell lines and tissue microarrays was also studied.FindingsDuring mitosis and cytokinesis, AURKB–TβRI complexes formed in midbodies in CRPC and KELLY neuroblastoma cells. TRAF6 induced polyubiquitination of AURKB on K85 and K87, protruding on the surface of AURKB to facilitate its activation. AURKB–TβRI complexes in patient's tumor tissue sections correlated with the malignancy of prostate cancer.InterpretationThe AURKB–TβRI complex may become a prognostic biomarker for patients with risk of developing aggressive PC.
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| 9. |
- Thakur, Noopur, et al.
(författare)
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Smad7 Enhances TGF-β-Induced Transcription of c-Jun and HDAC6 Promoting Invasion of Prostate Cancer Cells
- 2020
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Ingår i: iScience. - : Cell Press. - 2589-0042. ; 23:9
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Tidskriftsartikel (refereegranskat)abstract
- Transforming growth factor β (TGF-β) enhances migration and invasion of cancer cells, causing life-threatening metastasis. Smad7 expression is induced by TGF-β to control TGF-β signaling in a negative feedback manner. Here we report an additional function of Smad7, i.e., to enhance TGF-β induction of c-Jun and HDAC6 via binding to their regulatory regions, promoting migration and invasion of prostate cancer cells. Lysine 102 in Smad7 is crucial for binding to specific consensus sites in c-Jun and HDAC6, even when endogenous Smad2, 3, and 4 were silenced by siRNA. A correlation between the mRNA expression of Smad7 and HDAC6, Smad7 and c-Jun, and c-Jun and HDAC6 was found in public databases from analyses of prostate cancer tissues. High expression of Smad7, HDAC6, and c-Jun correlated with poor prognosis for patients with prostate cancer. The knowledge that Smad7 can activate transcription of proinvasive genes leading to prostate cancer progression provides clinically relevant information.
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| 10. |
- Wan, Wenxin, et al.
(författare)
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Operating conditions combination analysis method of optimal water management state for PEM fuel cell
- 2023
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Ingår i: Green Energy and Intelligent Transportation. - 2773-1537 .- 2097-2512. ; 2:4
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Tidskriftsartikel (refereegranskat)abstract
- The water content of proton exchange membrane fuel cells (PEMFCs) affects the transport of reactants and the conductivity of the membrane. Effective water management measures can improve the performance and extend the lifespan of the fuel cell. The water management state of the stack is influenced by various external operating conditions, and optimizing the combination of these conditions can improve the water management state within the stack. Considering that the stack's internal resistance can reflect its water management state, this study first establishes an internal resistance-operating condition model that considers the coupling effect of temperature and humidity to determine the variation trend of total resistance and stack humidity with single-factor operating conditions. Subsequently, the water management state optimization method based on the ANN-HGPSO algorithm is proposed, which not only quantitatively evaluates the influence weights of different operating conditions on the stack's internal resistance but also efficiently and accurately obtains the optimal combination of five operating conditions: working temperature, anode gas pressure, cathode gas pressure, anode gas humidity, and cathode gas humidity to achieve the optimal water management state in the stack, within the entire range of current densities. Finally, the response surface experimental results of the stack also validate the effectiveness and accuracy of the ANN-HGPSO algorithm. The method mentioned in this article can provide effective strategies for efficient water management and output performance optimization control of PEMFC stacks.
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