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[PMID]: 25049390
[Au] Autor:Chen PC; Yin J; Yu HW; Yuan T; Fernandez M; Yung CK; Trinh QM; Peltekova VD; Reid JG; Tworog-Dube E; Morgan MB; Muzny DM; Stein L; McPherson JD; Roberts AE; Gibbs RA; Neel BG; Kucherlapati R
[Ad] Address:Department of Genetics, Harvard Medical School, Boston, MA 02115;Department of Medicine, Division of Genetics, Brigham and Women's Hospital, Boston, MA 02115;Institute of Clinical Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan 70457, Ta...
[Ti] Title:Next-generation sequencing identifies rare variants associated with Noonan syndrome.
[So] Source:Proc Natl Acad Sci U S A;111(31):11473-8, 2014 Aug 5.
[Is] ISSN:1091-6490
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Noonan syndrome (NS) is a relatively common genetic disorder, characterized by typical facies, short stature, developmental delay, and cardiac abnormalities. Known causative genes account for 70-80% of clinically diagnosed NS patients, but the genetic basis for the remaining 20-30% of cases is unknown. We performed next-generation sequencing on germ-line DNA from 27 NS patients lacking a mutation in the known NS genes. We identified gain-of-function alleles in Ras-like without CAAX 1 (RIT1) and mitogen-activated protein kinase kinase 1 (MAP2K1) and previously unseen loss-of-function variants in RAS p21 protein activator 2 (RASA2) that are likely to cause NS in these patients. Expression of the mutant RASA2, MAP2K1, or RIT1 alleles in heterologous cells increased RAS-ERK pathway activation, supporting a causative role in NS pathogenesis. Two patients had more than one disease-associated variant. Moreover, the diagnosis of an individual initially thought to have NS was revised to neurofibromatosis type 1 based on an NF1 nonsense mutation detected in this patient. Another patient harbored a missense mutation in NF1 that resulted in decreased protein stability and impaired ability to suppress RAS-ERK activation; however, this patient continues to exhibit a NS-like phenotype. In addition, a nonsense mutation in RPS6KA3 was found in one patient initially diagnosed with NS whose diagnosis was later revised to Coffin-Lowry syndrome. Finally, we identified other potential candidates for new NS genes, as well as potential carrier alleles for unrelated syndromes. Taken together, our data suggest that next-generation sequencing can provide a useful adjunct to RASopathy diagnosis and emphasize that the standard clinical categories for RASopathies might not be adequate to describe all patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1073/pnas.1324128111

  2 / 5297 MEDLINE  
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[PMID]: 24219698
[Au] Autor:Mills DL; Dai L; Fishman I; Yam A; Appelbaum LG; St George M; Galaburda A; Bellugi U; Korenberg JR
[Ad] Address:a School of Psychology, Bangor University , Bangor , United Kingdom.
[Ti] Title:Genetic mapping of brain plasticity across development in Williams syndrome: ERP markers of face and language processing.
[So] Source:Dev Neuropsychol;38(8):613-42, 2013.
[Is] ISSN:1532-6942
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:In Williams Syndrome (WS), a known genetic deletion results in atypical brain function with strengths in face and language processing. We examined how genetic influences on brain activity change with development. In three studies, event-related potentials (ERPs) from large samples of children, adolescents, and adults with the full genetic deletion for WS were compared to typically developing controls, and two adults with partial deletions for WS. Studies 1 and 2 identified ERP markers of brain plasticity in WS across development. Study 3 suggested that, in adults with partial deletions for WS, specific genes may be differentially implicated in face and language processing.
[Mh] MeSH terms primary: Evoked Potentials/physiology
Face
Language
Recognition (Psychology)
Williams Syndrome/physiopathology
[Mh] MeSH terms secundary: Adolescent
Adult
Brain/physiopathology
Child
Electroencephalography
Face/physiopathology
Female
Humans
Male
Mental Processes
Reaction Time
Speech Perception/physiology
Williams Syndrome/complications
Williams Syndrome/genetics
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Entry month:1404
[Cu] Class update date: 140815
[Lr] Last revision date:140815
[Js] Journal subset:IM
[Da] Date of entry for processing:131113
[St] Status:MEDLINE
[do] DOI:10.1080/87565641.2013.825617

  3 / 5297 MEDLINE  
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[PMID]: 23578821
[Au] Autor:Li H; Sheridan R; Williams T
[Ad] Address:Department of Craniofacial Biology and Cell and Developmental Biology, University of Colorado Denver, Aurora, CO 80045, USA.
[Ti] Title:Analysis of TFAP2A mutations in Branchio-Oculo-Facial Syndrome indicates functional complexity within the AP-2α DNA-binding domain.
[So] Source:Hum Mol Genet;22(16):3195-206, 2013 Aug 15.
[Is] ISSN:1460-2083
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Multiple lines of evidence indicate that the AP-2 transcription factor family has an important regulatory function in human craniofacial development. Notably, mutations in TFAP2A, the gene encoding AP-2α, have been identified in patients with Branchio-Oculo-Facial Syndrome (BOFS). BOFS is an autosomal-dominant trait that commonly presents with facial clefting, eye defects and branchial skin anomalies. Examination of multiple cases has suggested either simple haploinsufficiency or more complex genetic causes for BOFS, especially as the clinical manifestations are variable, with no clear genotype-phenotype correlation. Mutations occur throughout TFAP2A, but mostly within conserved sequences within the DNA contact domain of AP-2α. However, the consequences of the various mutations for AP-2α protein function have not been evaluated. Therefore, it remains unclear if all BOFS mutations result in similar changes to the AP-2α protein or if they each produce specific alterations that underlie the spectrum of phenotypes. Here, we have investigated the molecular consequences of the mutations that localize to the DNA-binding region. We show that although individual mutations have different effects on DNA binding, they all demonstrate significantly reduced transcriptional activities. Moreover, all mutant derivatives have an altered nuclear:cytoplasmic distribution compared with the predominantly nuclear localization of wild-type AP-2α and several can exert a dominant-negative activity on the wild-type AP-2α protein. Overall, our data suggest that the individual TFAP2A BOFS mutations can generate null, hypomorphic or antimorphic alleles and that these differences in activity, combined with a role for AP-2α in epigenetic events, may influence the resultant pathology and the phenotypic variability.
[Mh] MeSH terms primary: Branchio-Oto-Renal Syndrome/genetics
Transcription Factor AP-2/genetics
Transcription Factor AP-2/metabolism
[Mh] MeSH terms secundary: Branchio-Oto-Renal Syndrome/diagnosis
Branchio-Oto-Renal Syndrome/pathology
DNA/genetics
DNA/metabolism
DNA-Binding Proteins/chemistry
DNA-Binding Proteins/genetics
DNA-Binding Proteins/metabolism
Epigenesis, Genetic
Eye/pathology
Gene Expression Regulation
Humans
Mutagenesis
Mutation, Missense
Phenotype
Transcription Factor AP-2/chemistry
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Name of substance:0 (DNA-Binding Proteins); 0 (TFAP2A protein, human); 0 (Transcription Factor AP-2); 9007-49-2 (DNA)
[Em] Entry month:1402
[Cu] Class update date: 140815
[Lr] Last revision date:140815
[Js] Journal subset:IM
[Da] Date of entry for processing:130726
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddt173

  4 / 5297 MEDLINE  
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[PMID]: 25121495
[Au] Autor:Duarte Lda S; Bergamin RS; Marcilio-Silva V; Seger GD; Marques MC
[Ad] Address:Departamento de Ecologia, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil....
[Ti] Title:Phylobetadiversity among Forest Types in the Brazilian Atlantic Forest Complex.
[So] Source:PLoS One;9(8):e105043, 2014.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Phylobetadiversity is defined as the phylogenetic resemblance between communities or biomes. Analyzing phylobetadiversity patterns among different vegetation physiognomies within a single biome is crucial to understand the historical affinities between them. Based on the widely accepted idea that different forest physiognomies within the Southern Brazilian Atlantic Forest constitute different facies of a single biome, we hypothesize that more recent phylogenetic nodes should drive phylobetadiversity gradients between the different forest types within the Atlantic Forest, as the phylogenetic divergence among those forest types is biogeographically recent. We compiled information from 206 checklists describing the occurrence of shrub/tree species across three different forest physiognomies within the Southern Brazilian Atlantic Forest (Dense, Mixed and Seasonal forests). We analyzed intra-site phylogenetic structure (phylogenetic diversity, net relatedness index and nearest taxon index) and phylobetadiversity between plots located at different forest types, using five different methods differing in sensitivity to either basal or terminal nodes (phylogenetic fuzzy weighting, COMDIST, COMDISTNT, UniFrac and Rao's H). Mixed forests showed higher phylogenetic diversity and overdispersion than the other forest types. Furthermore, all forest types differed from each other in relation phylobetadiversity patterns, particularly when phylobetadiversity methods more sensitive to terminal nodes were employed. Mixed forests tended to show higher phylogenetic differentiation to Dense and Seasonal forests than these latter from each other. The higher phylogenetic diversity and phylobetadiversity levels found in Mixed forests when compared to the others likely result from the biogeographical origin of several taxa occurring in these forests. On one hand, Mixed forests shelter several temperate taxa, like the conifers Araucaria and Podocarpus. On the other hand, tropical groups, like Myrtaceae, are also very representative of this forest type. We point out to the need of more attention to Mixed forests as a conservation target within the Brazilian Atlantic Forest given their high phylogenetic uniqueness.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0105043

  5 / 5297 MEDLINE  
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[PMID]: 24924585
[Au] Autor:Lindy AS; Bupp CP; McGee SJ; Steed E; Stevenson RE; Basehore MJ; Friez MJ
[Ad] Address:Greenwood Genetic Center, Greenwood, South Carolina.
[Ti] Title:Truncating mutations in LRP4 lead to a prenatal lethal form of Cenani-Lenz syndrome.
[So] Source:Am J Med Genet A;164(9):2391-7, 2014 Sep.
[Is] ISSN:1552-4833
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Cenani-Lenz syndrome (CLS) is an autosomal recessive skeletal dysplasia that results in malformations of the distal limb, renal anomalies, and characteristic facies. In 2010, this condition was found to be caused by mutations in LRP4, a member of the low-density lipoprotein family of receptors. LRP4 has been shown to antagonize LRP5/LRP6 activation of WNT and -catenin signaling. Loss of LRP4 function leads to excessive Wnt and -catenin signaling in the limb bud, which causes abnormal limb development. The large majority of patients with CLS reported in the literature have splicing and missense mutations, which result in syndactyly, oligodactyly, and minor renal malformations. More recently, a patient with CLS has been identified with a homozygous nonsense mutation and a more severe presentation of findings typically associated with this condition. Here we present two sibling fetuses with a prenatal lethal presentation of mesomelic limb reductions, oligosyndactyly, genitourinary malformation and compound heterozygosity for two novel truncating mutations in LRP4. These findings lend further support to the CLS genotype-phenotype correlation presented in recent publications. 2014 Wiley Periodicals, Inc.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1002/ajmg.a.36647

  6 / 5297 MEDLINE  
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[PMID]: 24924433
[Au] Autor:Lazier J; Chernos J; Lowry RB
[Ad] Address:Department of Medical Genetics, Alberta Children's Hospital, University of Calgary, Calgary, Alberta.
[Ti] Title:A 2q24.3q31.1 microdeletion found in a patient with Filippi-like syndrome phenotype: A case report.
[So] Source:Am J Med Genet A;164(9):2385-7, 2014 Sep.
[Is] ISSN:1552-4833
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Filippi syndrome is characterized by developmental delay, growth failure, cryptorchidism, bilateral hand and foot syndactyly, and facial dysmorphism. The 2q24q31 contiguous deletion syndrome has similarly been associated with hand and foot anomalies, growth retardation, microcephaly, characteristic facies with a broad prominent nasal root and thin alae nasi, and intellectual disability. We present a patient with this deletion who has a Filippi-like phenotype, which may be the first causative cytogenetic result in this syndrome. This suggests the importance of array comparative genomic hybridization in evaluation of patients with Filippi syndrome, and suggests that the inheritance may not always be autosomal recessive. 2014 Wiley Periodicals, Inc.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1002/ajmg.a.36636

  7 / 5297 MEDLINE  
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[PMID]: 22891008
[Au] Autor:Chavan A; Shastri AR; Ross-Russell RI
[Ad] Address:Paediatrics Department, Addenbrookes Hospital, Cambridge, UK. arjunsc@gmail.com
[Ti] Title:Branchio-oto-renal syndrome with obstructive sleep apnoea.
[So] Source:BMJ Case Rep;2012, 2012.
[Is] ISSN:1757-790X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Branchio-oto-renal (BOR) syndrome is a rare autosomal dominant disorder characterised by branchial arch anomalies, otological and renal abnormalities. To the best of our knowledge, upper airway obstruction has not been hitherto reported in BOR. The authors report a 19-month-old girl with BOR syndrome with features of severe airway obstruction needing tracheostomy.
[Mh] MeSH terms primary: Branchio-Oto-Renal Syndrome/complications
Sleep Apnea, Obstructive/complications
[Mh] MeSH terms secundary: Branchio-Oto-Renal Syndrome/surgery
Branchio-Oto-Renal Syndrome/ultrasonography
Female
Humans
Infant
Pregnancy
Sleep Apnea, Obstructive/diagnosis
Sleep Apnea, Obstructive/surgery
Tracheostomy
Ultrasonography, Prenatal
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Em] Entry month:1402
[Cu] Class update date: 140814
[Lr] Last revision date:140814
[Js] Journal subset:IM
[Da] Date of entry for processing:120814
[St] Status:MEDLINE

  8 / 5297 MEDLINE  
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[PMID]: 24757038
[Au] Autor:Jones W; Chastain CA; Wright PW
[Ad] Address:Department of Pharmaceutical Services, Vanderbilt University Medical Center, Nashville, Tennessee; Vanderbilt University Medical Center, Nashville, Tennessee.
[Ti] Title:Iatrogenic cushing syndrome secondary to a probable interaction between voriconazole and budesonide.
[So] Source:Pharmacotherapy;34(7):e116-9, 2014 Jul.
[Is] ISSN:1875-9114
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Oral budesonide is commonly used for the management of Crohn's disease given its high affinity for glucocorticoid receptors and low systemic activity due to extensive first-pass metabolism through hepatic cytochrome P450 (CYP) 3A4. Voriconazole, a second-generation triazole antifungal agent, is both a substrate and potent inhibitor of CYP isoenzymes, specifically CYP2C19, CYP2C9, and CYP3A4; thus, the potential for drug-drug interactions with voriconazole is high. To our knowledge, drug-drug interactions between voriconazole and corticosteroids have not been specifically reported in the literature. We describe a 48-year-old woman who was receiving oral budesonide 9mg/day for the management of Crohn's disease and was diagnosed with fluconazole-resistant Candida albicans esophagitis; oral voriconazole 200mg every 12hours for 3weeks was prescribed for treatment. Because the patient experienced recurrent symptoms of dysphagia, a second 3-week course of voriconazole therapy was taken. Seven weeks after originally being prescribed voriconazole, she came to her primary care clinic with elevated blood pressure, lower extremity edema, and weight gain; she was prescribed a diuretic and evaluated for renal dysfunction. At a follow-up visit 6weeks later with her specialty clinic, the patient's blood pressure was elevated, and her physical examination was notable for moon facies, posterior cervical fat pad prominence, and lower extremity pitting edema. Iatrogenic Cushing syndrome due to a drug-drug interaction between voriconazole and budesonide was suspected, and voriconazole was discontinued. Budesonide was continued as previously prescribed for her Crohn's disease. On reevaluation 2months later, the patient's Cushingoid features had markedly regressed. To our knowledge, this is the first published case report of iatrogenic Cushing syndrome due to a probable interaction between voriconazole and oral budesonide. In patients presenting with Cushingoid features who have received these drugs concomitantly, clinicians should consider the potential drug interaction between these agents, and the risks and benefits of continued therapy must be considered.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1407
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1002/phar.1432

  9 / 5297 MEDLINE  
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[PMID]: 24093546
[Au] Autor:Gourier D; Delpoux O; Binet L; Vezin H
[Ad] Address:1 TGE Rseau National de RPE interdisciplinaire (RENARD, FR-CNRS 3443).
[Ti] Title:Nuclear magnetic biosignatures in the carbonaceous matter of ancient cherts: comparison with carbonaceous meteorites.
[So] Source:Astrobiology;13(10):932-47, 2013 Oct.
[Is] ISSN:1557-8070
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The search for organic biosignatures is motivated by the hope of understanding the conditions of emergence of life on Earth and the perspective of finding traces of extinct life in martian sediments. Paramagnetic radicals, which exist naturally in amorphous carbonaceous matter fossilized in Precambrian cherts, were used as local structural probes and studied by electron paramagnetic resonance (EPR) spectroscopy. The nuclear magnetic resonance transitions of elements inside and around these radicals were detected by monitoring the nuclear modulations of electron spin echo in pulsed EPR. We found that the carbonaceous matter of fossilized microorganisms with age up to 3.5 billion years gives specific nuclear magnetic signatures of hydrogen (H), carbon (C), and phosphorus (P) nuclei. We observed that these potential biosignatures of extinct life are found neither in the carbonaceous matter of carbonaceous meteorites (4.56 billion years), the most ancient objects of the Solar System, nor in any carbonaceous matter resulting from carbonization of organic and bioorganic precursors. These results indicate that these nuclear signatures are sensitive to thermal episodes and can be used for Archean cherts with metamorphism not higher than the greenschist facies.
[Mh] MeSH terms primary: Carbon/chemistry
Exobiology/methods
Geologic Sediments/chemistry
Magnetic Resonance Spectroscopy
Meteoroids
[Mh] MeSH terms secundary: Electron Spin Resonance Spectroscopy
Temperature
[Pt] Publication type:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:7440-44-0 (Carbon)
[Em] Entry month:1408
[Js] Journal subset:IM
[Da] Date of entry for processing:131022
[St] Status:MEDLINE
[do] DOI:10.1089/ast.2013.0971

  10 / 5297 MEDLINE  
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[PMID]: 24738919
[Au] Autor:Zollino M; Orteschi D; Ruiter M; Pfundt R; Steindl K; Cafiero C; Ricciardi S; Contaldo I; Chieffo D; Ranalli D; Acquafondata C; Murdolo M; Marangi G; Asaro A; Battaglia D
[Ad] Address:Institute of Medical Genetics, Catholic University, University Hospital A. Gemelli, Roma, Italy.
[Ti] Title:Unusual 4p16.3 deletions suggest an additional chromosome region for the Wolf-Hirschhorn syndrome-associated seizures disorder.
[So] Source:Epilepsia;55(6):849-57, 2014 Jun.
[Is] ISSN:1528-1167
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Seizure disorder is one of the most relevant clinical manifestations in Wolf-Hirschhorn syndrome (WHS) and it acts as independent prognostic factor for the severity of intellectual disability (ID). LETM1, encoding a mitochondrial protein playing a role in K(+) /H(+) exchange and in Ca(2+) homeostasis, is currently considered the major candidate gene. However, whether haploinsufficiency limited to LETM1 is enough to cause epilepsy is still unclear. The main purpose of the present research is to define the 4p chromosome regions where genes for seizures reside. METHODS: Comparison of our three unusual 4p16.3 deletions with 13 literature reports. Array-comparative genomic hybridization (a-CGH). Real-time polymerase chain reaction (RT-PCR) on messanger RNA (mRNA) of LETM1 and CPLX1. Direct sequencing of LETM1. RESULTS: Three unusual 4p16.3 deletions were detected by array-CGH in absence of a obvious clinical diagnosis of WHS. Two of these, encompassing LETM1, were found in subjects who never had seizures. The deletions were interstitial, spanning 1.1 Mb with preservation of the terminal 1.77 Mb region in one case and 0.84 Mb with preservation of the terminal 1.07 Mb region in the other. The other deletion was terminal, affecting a 0.564 Mb segment, with preservation of LETM1, and it was associated with seizures and learning difficulties. Upon evaluating our patients along with literature reports, we noted that six of eight subjects with terminal 4p deletions preserving LETM1 had seizures, whereas seven of seven with interstitial deletions including LETM1 and preserving the terminal 1 Mb region on 4p did not. An additional chromosome region for seizures is suggested, falling within the terminal 1.5 Mb on 4p, not including LETM1. SIGNIFICANCE: We consider that haploinsufficiency not limited to LETM1 but including other genes acts as a risk factor for the WHS-associated seizure disorder, according to a comorbidity model of pathogenesis. Additional candidate genes reside in the terminal 1.5 Mb region on 4p, most likely distal to LETM1. A PowerPoint slide summarizing this article is available for download in the Supporting Information section here.
[Mh] MeSH terms primary: Chromosomes, Human, Pair 4/genetics
Gene Deletion
Seizures/genetics
Wolf-Hirschhorn Syndrome/genetics
[Mh] MeSH terms secundary: Adolescent
Calcium-Binding Proteins/genetics
Child
Child, Preschool
Comparative Genomic Hybridization
Female
Humans
Male
Membrane Proteins/genetics
Oligonucleotide Array Sequence Analysis
Real-Time Polymerase Chain Reaction
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Calcium-Binding Proteins); 0 (LETM1 protein, human); 0 (Membrane Proteins)
[Em] Entry month:1408
[Js] Journal subset:IM
[Da] Date of entry for processing:140613
[St] Status:MEDLINE
[do] DOI:10.1111/epi.12617


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