Database : MEDLINE
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[PMID]: 29524834
[Au] Autor:Gil-Ranedo J; Hernando E; Valle N; Riolobos L; Maroto B; Almendral JM
[Ad] Address:Centro de Biología Molecular "Severo Ochoa" (Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid), Cantoblanco, 28049 Madrid, Spain.
[Ti] Title:Differential phosphorylation and n-terminal configuration of capsid subunits in parvovirus assembly and viral trafficking.
[So] Source:Virology;518:184-194, 2018 Mar 07.
[Is] ISSN:1096-0341
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The T1 parvovirus Minute Virus of Mice (MVM) was used to study the roles that phosphorylation and N-terminal domains (Nt) configuration of capsid subunits may play in icosahedral nuclear viruses assembly. In synchronous MVM infection, capsid subunits newly assembled as two types of cytoplasmic trimeric intermediates (3VP2, and 1VP1:2VP2) harbored a VP1 phosphorylation level fivefold higher than that of VP2, and hidden Nt. Upon nuclear translocation at S phase, VP1-Nt became exposed in the heterotrimer and subsequent subviral assembly intermediates. Empty capsid subunits showed a phosphorylation level restored to VP1:VP2 stoichiometry, and the Nt concealed in their interior. However ssDNA-filled virus maturing at S/G2 lacked VP1 phosphorylation and one major VP2 phosphopeptide, and exposed VP2-Nt. Endosomal VP2-Nt cleavage resulted in VP3 subunits devoid of any phospholabel, implying that incoming viral particles specifically harbor a low phosphorylation status. Phosphorylation provides a mechanistic coupling of parvovirus nuclear assembly to the cell cycle.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 286638 MEDLINE  
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[PMID]: 29524829
[Au] Autor:Aupperlee MD; Kariagina A; Zaremba N; Basson MD; Schwartz RC; Haslam SZ
[Ad] Address:Breast Cancer and the Environment Research Program, Michigan State University, East Lansing, MI; Department of Physiology, Michigan State University, East Lansing, MI. Electronic address: aupperl4@msu.edu.
[Ti] Title:The Proliferative Response to p27 Down-Regulation in Estrogen Plus Progestin Hormonal Therapy is Lost in Breast Tumors.
[So] Source:Transl Oncol;11(2):518-527, 2018 Mar 07.
[Is] ISSN:1936-5233
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Increased proliferation and breast cancer risk has been observed in postmenopausal women receiving estrogen (E) + progestin hormone replacement therapy (HRT). Progestin action is mediated through two progesterone receptor (PR) isoforms, PRA and PRB, with unique transcriptional activity and function. The current study examines hormonal regulation of PR isoforms in the normal postmenopausal human breast and the mechanism by which progestins increase proliferation and breast cancer risk. Archival benign breast biopsies from postmenopausal and premenopausal women, and luminal breast tumor biopsies from postmenopausal women, were analyzed for regulation of PRA and PRB expression by E and E+medroxyprogesterone acetate (MPA). In the postmenopausal breast without HRT, PRA and PRB expression was decreased compared to the premenopausal breast. Both E (n = 12) and E+MPA (n = 13) HRT in the postmenopausal breast were associated with increased PRA and PRB expression, increased nuclear cyclin E expression, and decreased nuclear p27 expression compared to no HRT (n = 16). With E+MPA HRT, there was a further decrease in nuclear p27 and increased Receptor Activator of NF-kappa B Ligand (RANKL) expression compared to E-alone HRT. In luminal breast cancers, E+MPA HRT (n = 6) was also associated with decreased nuclear expression of the cell cycle inhibitor p27 compared to E HRT (n = 6), but was not associated with increased proliferation. These results suggest that p27 mediates progestin-induced proliferation in the normal human breast and that regulation of this proliferative response by E+MPA is lost in breast tumors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 286638 MEDLINE  
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[PMID]: 29524808
[Au] Autor:Zhao C; Liu Q; Xu S; Xiao Y; Wang W; Yang J; Yang Y; Wang Y; Song Z; Li J
[Ad] Address:Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao, 266071, China; University of Chinese Academy of Sciences, Beijing 100049, China; Laboratory for Marine Biology and Biotechnology, Qingdao National Laboratory for Marine Science and Technolog
[Ti] Title:Identification of type A spermatogonia in turbot (Scophthalmus maximus) using a new cell-surface marker of Lymphocyte antigen 75 (ly75/CD205).
[So] Source:Theriogenology;113:137-145, 2017 Dec 16.
[Is] ISSN:1879-3231
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Turbot (Schophthalmus maximus) is one of the most important economic marine flatfish species. However, due to rapid development of the industry, genetic resource recession has brought down the efficiency of aquaculture. Therefore, conservation of the genetic resource is increasingly demanded. Recent research proved that type A spermatogonia possesses the properties of spermatogonia stem cell, and it might provide an ideal solution. Therefore, it is necessary to develop an appropriate molecular marker on type A spermatogonia to further isolate and purify of type A spermatogonia in turbot. In this study, turbot lymphocyte antigen 75 (smly75) gene was identified and its localizations of expressions and the temporal transcription patterns were evaluated qualitatively and semiquantitatively. Investigation in testes of development of spermatogonia showed that smly75 mRNA, contrast with vasa and dnd mRNA, was exclusively localized in type A spermatogonia and not detected in type B spermatogonia, spermatocytes or gonadal somatic cells by in situ hybridization. Thus, the smly75 could be a new and convincing molecular marker on identification of type A spermatogonia. In addition, specifically to development pattern of type A spermatogonia, from 7- to 14- month testes, spermatogonia were dominated and the number of type A spermatogonia was increased, corresponding that smly75 expression was up-regulated gradually, while, in 16 month testes, accompanied by that several spermatogonia differentiated into primary spermatocytes, the smly75 expression down-regulated. Finally, broaden in the whole reproductive cycle, the smly75 transcription significantly variated with the differentiation of germ cells and in accordance with the number of type A spermatogonia. It is suggested that testes from 8 to 14 month old males could be used for further isolation and purification of type A-SG. These results will not only help to better understand type A spermatogonia, but also further facilitate type A spematogonia-mediated germ cell manipulation in turbot.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524728
[Au] Autor:Han T; Tian K; Pan H; Liu Y; Xu F; Li Z; Uchita T; Gao M; Hua H; Li D
[Ad] Address:Key Laboratory of Structure-Based Drug Design & Discovery, Ministry of Education, and School of Traditional Chinese Materia Medica, Shenyang Pharmaceutical University, 103 Wenhua Road, Shenyang 110016, PR China.
[Ti] Title:Novel hybrids of brefeldin A and nitrogen mustards with improved antiproliferative selectivity: Design, synthesis and antitumor biological evaluation.
[So] Source:Eur J Med Chem;150:53-63, 2018 Mar 01.
[Is] ISSN:1768-3254
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:A series of novel conjugates of brefeldin A (11a-c, 12a-c and 13a-c) were obtained by introducing a variety of nitrogen mustards at 4-OH or 7-OH position to explore more efficacious and less toxic antitumor agents. The antiproliferative activities were tested against three cancer cell lines (HL-60, PC-3 and Bel-7402) and one multidrug resistant cell line Bel-7402/5-FU. Among them, compound 11a was the strongest derivative with IC values of 4.48, 9.37, 0.2 and 0.84 µM, respectively, and more potent than nitrogen mustards. Though the antiproliferative potency was weaker than the lead compound brefeldin A, 11a displayed lower toxicity than brefeldin A (IC < 0.001 µM) with an IC of 9.74 µM against normal human liver L-O2 cells, showing good selectivity between normal and malignant liver cells. The mechanism studies confirmed that 11a could induce apoptosis, arrest cell cycle at the G1 phase and lead to mitochondrial dysfunction in Bel-7402 cells at submicromolar concentrations. Furthermore, 11a induced the intrinsic apoptotic mitochondrial pathway in Bel-7402 cells, evidenced by the enhanced expression of the pro-apoptotic protein Bax, cyto-c and p53, and the reduced expression of the anti-apoptotic protein Bcl-2. The caspase-9 and -3 levels were also up-regulated.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524659
[Au] Autor:Wang S; Shi L; Hu Y; Liu R; Ren A; Zhu J; Zhao M
[Ad] Address:Key Laboratory of Agricultural Environmental Microbiology, Ministry of Agriculture, Microbiology Department, College of Life Sciences, Nanjing; Agricultural University, Nanjing 210095, Jiangsu, P.R. China.
[Ti] Title:Roles of the Skn7 response regulator in stress resistance, cell wall integrity and GA biosynthesis in Ganoderma lucidum.
[So] Source:Fungal Genet Biol;, 2018 Mar 07.
[Is] ISSN:1096-0937
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The transcription factor Skn7 is a highly conserved fungal protein that participates in a variety of processes, including oxidative stress adaptation, fungicide sensitivity, cell wall biosynthesis, cell cycle, and sporulation. In this study, a homologous gene of Saccharomyces cerevisiae Skn7 was cloned from Ganoderma lucidum. RNA interference (RNAi) was used to study the functions of Skn7, and the two knockdown strains Skn7i-5 and Skn7i-7 were obtained in G. lucidum. The knockdown of GlSkn7 resulted in hypersensitivity to oxidative and cell wall stresses. The concentrations of chitin and ß-1,3-glucan distinctly decreased in the GlSkn7 knockdown strains compared with those of the wild type (WT). In addition, the expression of cell wall biosynthesis related genes was also significantly down-regulated and the thickness of the cell wall also significantly reduced in the GlSkn7 knockdown strains. The intracellular reactive oxygen species (ROS) content and ganoderic acids biosynthesis increased significantly in the GlSkn7 knockdown strains. Interestingly, the level of intracellular ROS and the content of ganoderic acids decreased after N-acetyl-L-cysteine (NAC), an ROS scavenger, was added, indicating that GlSkn7 might regulate ganoderic acids biosynthesis via the intracellular ROS level. The transcript level of GlSkn7 were up-regulated in osmotic stress, heat stress and fungicide condition. At the same time, the content of ganoderic acids in the GlSkn7 knockdown strains also changed distinctly in these conditions. Overall, GlSkn7 is involved in stress resistance, cell wall integrity and ganoderic acid biosynthesis in G. lucidum.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 286638 MEDLINE  
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[PMID]: 29524605
[Au] Autor:Weyand CM; Shen Y; Goronzy J
[Ad] Address:Department of Medicine, Division of Immunology and Rheumatology, Stanford University, Stanford, CA 94305; Department of Medicine, Veterans Affairs Palo Alto Health Care System Palo Alto, CA 94306. Electronic address: cweyand@stanford.edu.
[Ti] Title:Redox-Sensitive Signaling in Inflammatory T cells and in Autoimmune Disease.
[So] Source:Free Radic Biol Med;, 2018 Mar 07.
[Is] ISSN:1873-4596
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Reactive oxygen species (ROS) are byproducts of oxygen metabolism best known for their damaging potential, but recent evidence has exposed their role as secondary messengers, which regulate cell function through redox-activatable signaling systems. In immune cells, specifically in T cells, redox-sensitive signaling pathways have been implicated in controlling several functional domains; including cell cycle progression, T effector cell differentiation, tissue invasion and inflammatory behavior. T cells from patients with the autoimmune disease rheumatoid arthritis (RA) have emerged as a valuable model system to examine the functional impact of ROS on T cell function. Notably, RA T cells are distinguished from healthy T cells based on reduced ROS production and undergo "reductive stress". Upstream defects leading to the ROS status of RA T cells are connected to metabolic reorganization. RA T cells shunt glucose away from pyruvate and ATP production towards the pentose phosphate pathway, where they generate NADPH and consume cellular ROS. Downstream consequences of the ROS conditions in RA T cells include insufficient activation of the DNA repair kinase ATM, bypassing of the G2/M cell cycle checkpoint and biased differentiation of T cells into IFN-γ and IL-17-producing inflammatory cells. Also, ROS T cells rapidly invade into peripheral tissue due to dysregulated lipogenesis, excessive membrane ruffling, and overexpression of a motility module dominated by the scaffolding protein Tks5. These data place ROS into a pinnacle position in connecting cellular metabolism and protective versus auto-aggressive T cell immunity. Therapeutic interventions for targeted ROS enhancement instead of ROS depletion should be developed as a novel strategy to treat autoimmune tissue inflammation.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 286638 MEDLINE  
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[PMID]: 29524520
[Au] Autor:Malojirao VH; Vigneshwaran V; Thirusangu P; Mahmood R; Prabhakar BT
[Ad] Address:Molecular Biomedicine Laboratory, Postgraduate Department of Studies and Research in Biotechnology, Sahyadri Science College (Autonomous), Kuvempu University, Shivamogga 577203, Karnataka, India.
[Ti] Title:The tumor antagonistic steroidal alkaloid Solanidine prompts the intrinsic suicidal signal mediated DFF-40 nuclear import and nucleosomal disruption.
[So] Source:Life Sci;, 2018 Mar 07.
[Is] ISSN:1879-0631
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Aim Deformity in the cellular homeostatic event associated with cell survival and apoptosis are committing factors for carcinogenesis. Interventions of these events by pharmacologically active agent gain predominance in cancer treatment. In current investigation Solanidine, a steroidal alkaloid was evaluated on tumorigenesis by targeting death signal using multiple tumor cells and model systems. MAIN METHODS: Anti-proliferative effect was evaluated using cytotoxic studies. Prolonged cytotoxic effect of Solanidine was examined by colony formation assay. Exhibition of apoptotic hallmark induced by Solanidine was examined using FACS analysis, Annexin-V staining, Acridine orange staining, TUNEL assay. Altered gene expression was evaluated using Immunoblot, Immunofluorescence and Immunohistochemistry technique. In-vitro results were revalidated in EAC solid tumor and CAM xenograft model. KEY FINDINGS: Solanidine exerts its potential effect in a target specific manner. The cytotoxic/anticlonogenic activity was due to induction of typical cellular apoptotic hallmarks and cell cycle blockage at S-G2/M phase. The molecular events underlying this effect is through activation of intrinsic pathway via Bax, Bad and Cytochrome c activation by neutralizing Bcl-2 expression, along with downregulated PI3K/Akt survival signal. As a consequence, downstream pro apoptogenic gene, active Caspase-3 was over expressed by Solanidine to cleave its substrate PARP and promotes nuclear import of DFF-40. Anti-carcinogenic aptitude was further confirmed by murine solid tumors and in-vivo CAM xenograft studies. SIGNIFICANCE: Solanidine emerged as active molecule against tomorigenesis by activating nuclear import of DFF-40 mediated nucleosomal disruption and cell demise. It can be developed as a potential apoptogenic small molecule for cancer therapy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524413
[Au] Autor:Park SJ; Lee SK; Lim CR; Park HW; Liu F; Kim SJ; Kim BC
[Ad] Address:Department of Biochemistry, College of Natural Sciences, Kangwon National University, Chuncheon, 24341, Republic of Korea.
[Ti] Title:Heme oxygenase-1/carbon monoxide axis suppresses transforming growth factor-ß1-induced growth inhibition by increasing ERK1/2-mediated phosphorylation of Smad3 at Thr-179 in human hepatocellular carcinoma cell lines.
[So] Source:Biochem Biophys Res Commun;, 2018 Mar 07.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Heme oxygenase-1 (HO-1) has been implicated in tumor progression, but the underlying molecular mechanisms remain largely unknown. Transforming growth factor-ß1 (TGF-ß1) exhibits cytostatic and apoptotic effects in hepatocytes and several types of hepatocellular carcinoma (HCC) cell lines, and deregulation of its signaling pathway is linked to hepatic tumorigenesis. In the present study, we observed that HO-1 is expressed at higher levels in HCC tissues than in paired normal tissues. Moreover, TGF-ß1-induced cell cycle arrest and up-regulation of cyclin-dependent kinase inhibitors in HCC cell lines were significantly attenuated by overexpression of HO-1 or treatment with tricarbonyldichlororuthenium(II) dimer ([Ru(CO) Cl ] , suggesting an inhibitory role of the HO-1/CO axis in TGF-ß signaling to growth inhibition in HCC cell lines. Interestingly, we observed that [Ru(CO) Cl ] inhibits TGF-ß1-induced Smad3-dependent reporter activity without affecting its C-terminus phosphorylation, complex formation with Smad4, and nuclear translocation. Additional experiments revealed that HO-1/CO axis selectively induces phosphorylation of Smad3 at Thr-179 residue in the linker region through activation of extracellular signal-activated kinase (ERK) 1/2. Transfection with a phospho-deficient Smad3 (T179A) mutant or treatment with FR180204, a specific inhibitor for ERK1/2, significantly reversed the inhibitory effects of HO-1 and [Ru(CO) Cl ] on cell cycle arrest induced by TGF-ß1. These findings for the first time demonstrate that HO-1/CO axis confer resistance of HCC cells to TGF-ß growth inhibitory signal by increasing Smad3 phosphorylation at Thr-179 via ERK1/2 pathway.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  9 / 286638 MEDLINE  
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[PMID]: 29515107
[Au] Autor:Lei Z; Duan H; Zhao T; Zhang Y; Li G; Meng J; Zhang S; Yan W
[Ad] Address:Department of orthopedics Research Institute, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, Zhejiang, China.
[Ti] Title:PARK2 inhibits osteosarcoma cell growth through the JAK2/STAT3/VEGF signaling pathway.
[So] Source:Cell Death Dis;9(3):375, 2018 Mar 07.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Osteosarcoma (OS) is the most common primary malignant bone tumor mainly occurring in children and adolescents. In past decades, studies revealed that PARK2 was a vital tumor suppressor gene in many malignant solid tumors. However, the role of PARK2 in OS remains largely unclear. Therefore, we assessed PARK2 expression in OS tissue and adjacent non-tumor tissues by immunohistochemical (IHC) analysis, and evaluated PARK2 mRNA expression in OS cell lines by real-time PCR analysis. The HOS and U2OS cell lines were employed to establish a PARK2 overexpression model. Using this model, we investigated the potential role of PARK2 in OS and explored the underlying molecular mechanisms. Our study showed PARK2 was downregulated in OS tissue and cell lines, which was significantly associated with higher tumor stage (P < 0.05). Overexpression of PARK2 arrested the cell cycle, inhibited cell proliferation, migration, and invasion, induced cell apoptosis, and reduced tube formation in vitro. Moreover, overexpression of PARK2 significantly suppressed tumor growth and angiogenesis in vivo. Additionally, PARK2 negatively regulated OS development through the JAK2/STAT3/VEGF pathway. Our findings demonstrate that PARK2 is a tumor suppressor gene that may negatively affect OS growth and angiogenesis via partly inhibiting the JAK2/STAT3/VEGF signaling pathway.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1038/s41419-018-0401-8

  10 / 286638 MEDLINE  
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[PMID]: 29515100
[Au] Autor:Kuo CJ; Wang ST; Lin CM; Chiu HC; Huang CR; Lee DY; Chang GD; Chou TC; Chen JW; Chen CS
[Ad] Address:Department of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
[Ti] Title:A multi-omic analysis reveals the role of fumarate in regulating the virulence of enterohemorrhagic Escherichia coli.
[So] Source:Cell Death Dis;9(3):381, 2018 Mar 07.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The enteric pathogen enterohemorrhagic Escherichia coli (EHEC) is responsible for outbreaks of bloody diarrhea and hemolytic uremic syndrome (HUS) worldwide. Several molecular mechanisms have been described for the pathogenicity of EHEC; however, the role of bacterial metabolism in the virulence of EHEC during infection in vivo remains unclear. Here we show that aerobic metabolism plays an important role in the regulation of EHEC virulence in Caenorhabditis elegans. Our functional genomic analyses showed that disruption of the genes encoding the succinate dehydrogenase complex (Sdh) of EHEC, including the sdhA gene, attenuated its toxicity toward C. elegans animals. Sdh converts succinate to fumarate and links the tricarboxylic acid (TCA) cycle and the electron transport chain (ETC) simultaneously. Succinate accumulation and fumarate depletion in the EHEC sdhA mutant cells were also demonstrated to be concomitant by metabolomic analyses. Moreover, fumarate replenishment to the sdhA mutant significantly increased its virulence toward C. elegans. These results suggest that the TCA cycle, ETC, and alteration in metabolome all account for the attenuated toxicity of the sdhA mutant, and Sdh catabolite fumarate in particular plays a critical role in the regulation of EHEC virulence. In addition, we identified the tryptophanase (TnaA) as a downstream virulence determinant of SdhA using a label-free proteomic method. We demonstrated that expression of tnaA is regulated by fumarate in EHEC. Taken together, our multi-omic analyses demonstrate that sdhA is required for the virulence of EHEC, and aerobic metabolism plays important roles in the pathogenicity of EHEC infection in C. elegans. Moreover, our study highlights the potential targeting of SdhA, if druggable, as alternative preventive or therapeutic strategies by which to combat EHEC infection.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1038/s41419-018-0423-2


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