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[PMID]: 24866134
[Au] Autor:Lannoy M; Slove S; Louedec L; Choqueux C; Journé C; Michel JB; Jacob MP
[Ad] Address:From INSERM, U1148, Hôpital Bichat, Paris F-75018, France (M.L., S.S., L.L., C.C., C.J., J.-B.M., M.-P.J.); Univ Paris Diderot, Sorbonne Paris Cité, Paris F-75018, France (M.L., S.S., C.C., C.J., J.-B.M.); and Fédération de Recherche en Imagerie Multimodalité, Paris F-75018, France (C.J.). lannoy.mo...
[Ti] Title:Inhibition of ERK1/2 phosphorylation: a new strategy to stimulate elastogenesis in the aorta.
[So] Source:Hypertension;64(2):423-30, 2014 Aug.
[Is] ISSN:1524-4563
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Haploinsufficiency of elastin leads, in more than half of patients with Williams-Beuren syndrome, to development of supravalvular aortic stenosis and hypertension. Determining mechanisms implicated in elastin synthesis would be of interest to find new elastogenic molecules to treat such a pathology. Here, we analyzed the signaling pathway linking intracellular calcium concentration to elastin regulation to find new molecules able to increase elastin synthesis. Their elastogenic ability was then investigated, in vitro and in vivo, using inhibitors of the highlighted pathway. The Brown Norway rat strain was used here as an arterial elastin-deficient model. Our data indicated that A23187, a calcium ionophore, decreases elastin expression in cultured vascular smooth muscle cells, both transcriptionally and post-transcriptionally. Addition of A23187 induced transient activation of extracellular signal-regulated kinases 1/2, leading to an upregulation of activator protein-1 transcription factors, which correlated with the inhibition of elastin gene transcription. Pretreatment with U0126, an inhibitor of extracellular signal-regulated kinases 1/2 phosphorylation, abolished the inhibition of elastin gene transcription by A23187. In vitro, U0126 increased elastin synthesis and in vivo, 24 hours after an intravenous administration, elastin gene transcription and elastin mRNA levels were increased in the rat aorta. A chronic treatment, diffusing U0126 for 10 weeks, increased aortic elastin content without changing cell number and collagen content. In conclusion, calcium ionophore represses elastin gene transcription via activation of extracellular signal-regulated kinases 1/2 pathway and activator protein-1 transcription factors. Moreover, we provide strong evidence that inhibition of extracellular signal-regulated kinases 1/2 increases elastin synthesis and could thus be suitable for treating vascular pathologies characterized by diminished arterial elastin content.
[Mh] MeSH terms primary: Aorta/metabolism
Elastin/metabolism
Mitogen-Activated Protein Kinase 1/metabolism
Mitogen-Activated Protein Kinase 3/metabolism
Phosphorylation/drug effects
[Mh] MeSH terms secundary: Animals
Aorta/drug effects
Butadienes/pharmacology
Calcimycin/pharmacology
Calcium/metabolism
Calcium Ionophores/pharmacology
Enzyme Inhibitors/pharmacology
Mitogen-Activated Protein Kinase 1/antagonists & inhibitors
Mitogen-Activated Protein Kinase 3/antagonists & inhibitors
Muscle, Smooth, Vascular/drug effects
Muscle, Smooth, Vascular/metabolism
Nitriles/pharmacology
Rats
Williams Syndrome/metabolism
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Butadienes); 0 (Calcium Ionophores); 0 (Enzyme Inhibitors); 0 (Nitriles); 0 (U 0126); 37H9VM9WZL (Calcimycin); 9007-58-3 (Elastin); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); SY7Q814VUP (Calcium)
[Em] Entry month:1410
[Js] Journal subset:IM
[Da] Date of entry for processing:140710
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.114.03352

  2 / 5360 MEDLINE  
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[PMID]: 23494560
[Au] Autor:Cashon CH; Ha OR; DeNicola CA; Mervis CB
[Ad] Address:Department of Psychological and Brain Sciences, University of Louisville, Louisville, KY, 40292, USA, cara.cashon@louisville.edu.
[Ti] Title:Toddlers with Williams syndrome process upright but not inverted faces holistically.
[So] Source:J Autism Dev Disord;43(11):2549-57, 2013 Nov.
[Is] ISSN:1573-3432
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Holistic processing of upright, but not inverted, faces is a marker of perceptual expertise for faces. This pattern is shown by typically developing individuals beginning at age 7 months. Williams syndrome (WS) is a rare neurogenetic developmental disorder characterized by extreme interest in faces from a very young age. Research on the effects of inversion on holistic processing of faces by older children and adults with WS has produced mixed results. Younger children with WS were not included in these previous studies. Using the habituation switch paradigm, we demonstrated that 15-35-month-olds with WS process upright, but not inverted, faces holistically. This study provides evidence of perceptual expertise for faces in individuals with WS early in life.
[Mh] MeSH terms primary: Face
Orientation/physiology
Pattern Recognition, Visual/physiology
Williams Syndrome/physiopathology
[Mh] MeSH terms secundary: Child, Preschool
Female
Humans
Infant
Male
Photic Stimulation
Williams Syndrome/psychology
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Entry month:1410
[Js] Journal subset:IM
[Da] Date of entry for processing:131014
[St] Status:MEDLINE
[do] DOI:10.1007/s10803-013-1804-0

  3 / 5360 MEDLINE  
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[PMID]: 25222778
[Au] Autor:Kotecha UH; Movva S; Sharma D; Verma J; Puri RD; Verma IC
[Ti] Title:Molecular evaluation of a novel missense mutation & an insertional truncating mutation in SUMF1 gene.
[So] Source:Indian J Med Res;140(1):55-9, 2014 Jul.
[Is] ISSN:0971-5916
[Cp] Country of publication:India
[La] Language:eng
[Ab] Abstract:BACKGROUND & OBJECTIVES: Multiple suphphatase deficiency (MSD) is an autosomal recessive disorder affecting the post translational activation of all enzymes of the sulphatase family. To date, approximately 30 different mutations have been identified in the causative gene, sulfatase modifying factor 1 (SUMF1). We describe here the mutation analysis of a case of MSD. METHODS: The proband was a four year old boy with developmental delay followed by neuroregression. He had coarse facies, appendicular hypertonia, truncal ataxia and ichthyosis limited to both lower limbs. Radiographs showed dysostosis multiplex. Clinical suspicion of MSD was confirmed by enzyme analysis of four enzymes of the sulphatase group. RESULTS: The patient was compound heterozygote for a c.451A>G (p.K151E) substitution in exon 3 and a single base insertion mutation (c.690_691 InsT) in exon 5 in the SUMF1 gene. The bioinformatic analysis of the missense mutation revealed no apparent effect on the overall structure. However, the mutated 151-amino acid residue was found to be adjacent to the substrate binding and the active site residues, thereby affecting the substrate binding and/or catalytic activity, resulting in almost complete loss of enzyme function. CONCLUSIONS: The two mutations identified in the present case were novel. This is perhaps the first report of an insertion mutation in SUMF1 causing premature truncation of the protein.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1409
[Js] Journal subset:IM
[St] Status:In-Data-Review

  4 / 5360 MEDLINE  
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[PMID]: 25296029
[Au] Autor:Schratzberger M; Larcombe P
[Ad] Address:Centre for Environment, Fisheries and Aquaculture Science, Lowestoft Laboratory, Lowestoft, Suffolk, United Kingdom.
[Ti] Title:The role of the sedimentary regime in shaping the distribution of subtidal sandbank environments and the associated meiofaunal nematode communities: an example from the southern north sea.
[So] Source:PLoS One;9(10):e109445, 2014.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:We combined sediment and faunal data to explore the role of the sedimentary regime in shaping the distribution of subtidal sandbank environments and the associated meiofaunal nematode communities at Broken Bank and Swarte Bank, in the southern North Sea. A variety of sediment transport processes occur in the area, differing in the frequency and magnitude of sediment mobility, and the continuum between erosion, translation and sediment accumulation. The seabed contained a variety of bedforms, including longitudinal furrows, and small to very large sandwaves. The bed sediments were dominated by fine and medium sands, with admixtures of silt and gravel. Based on sedimentary bedforms and grain size analysis, a total of 11 sedimentary facies were delineated, of which 8 were analysed in detail for their relationships with the meiofauna. The sedimentary facies fell clearly into groups of facies, respectively representing high, high-moderate and moderate, and episodic sediment mobility. For those sedimentary facies where daily movement of sediments and bedforms occurred ('high' sediment mobility), the resulting spatially homogeneous environments were dominated by an impoverished nematode community comprising small deposit feeders and large predators. Resistance to sediment movement and the ability to exploit alternative food sources were prominent functional features of the successful colonisers. Those facies characterised by relatively infrequent sediment mobility ('episodic' and 'high-moderate and moderate' sediment mobility) comprised a heterogeneous suite of benthic habitats, containing taxonomically and functionally diverse assemblages of nematodes of various sizes, feeding types and reproductive potential. Faunal distribution patterns here indicated trade-offs between the resistance to sediment movement, environmental tolerance and competitive abilities. Our focus on diverse assemblages of organisms with high turnover times, inhabiting highly dynamic sedimentary environments, has revealed new animal-sediment relationships of relevance to pure and applied science.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0109445

  5 / 5360 MEDLINE  
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[PMID]: 24698626
[Au] Autor:Kadaba P; Arepalli S; Shields JA; Shields CL
[Ad] Address:Ocular Oncology Service, Wills Eye Hospital, Thomas Jefferson University, Philadelphia, Pennsylvania....
[Ti] Title:Combined hamartoma of the retina and retinal pigment epithelium in branchio-otic syndrome.
[So] Source:J AAPOS;18(2):201-3, 2014 Apr.
[Is] ISSN:1528-3933
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:A 15-month-old boy with established branchio-otic syndrome was evaluated for decreased red reflex in the left eye. Fundus examination of left eye revealed a gray epiretinal membrane with retinal traction and ill-defined macular thickening, found on ultrasonography as a dense flat region 1.7 mm in thickness. Enhanced depth imaging optical coherence tomography revealed an epiretinal membrane with macular thickening, retinal folding, and full-thickness retinal disorganization, consistent with combined hamartoma of the retina and retinal pigment epithelium. Over 5 years of follow-up, the branchio-otic syndrome was unchanged and the combined hamartoma remained stable.
[Mh] MeSH terms primary: Branchio-Oto-Renal Syndrome/complications
Hamartoma/etiology
Retinal Diseases/etiology
Retinal Pigment Epithelium/pathology
[Mh] MeSH terms secundary: Branchio-Oto-Renal Syndrome/diagnosis
Epiretinal Membrane/diagnosis
Fluorescein Angiography
Hamartoma/diagnosis
Hearing Loss/diagnosis
Humans
Infant
Male
Retinal Diseases/diagnosis
Tomography, Optical Coherence
Visual Acuity/physiology
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1410
[Js] Journal subset:IM
[Da] Date of entry for processing:140404
[St] Status:MEDLINE

  6 / 5360 MEDLINE  
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[PMID]: 25004850
[Au] Autor:Farid A; Khalid P; Jadoon KZ; Jouini MS
[Ad] Address:Institute of Geology, University of Punjab, P.O. Box 54590, Lahore, Pakistan, asam.farid@gmail.com.
[Ti] Title:The depositional setting of the Late Quaternary sedimentary fill in southern Bannu basin, Northwest Himalayan fold and thrust belt, Pakistan.
[So] Source:Environ Monit Assess;186(10):6587-604, 2014 Oct.
[Is] ISSN:1573-2959
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Geostatistical variogram and inversion techniques combined with modern visualization tools have made it possible to re-model one-dimensional electrical resistivity data into two-dimensional (2D) models of the near subsurface. The resultant models are capable of extending the original interpretation of the data to depict alluvium layers as individual lithological units within the 2D space. By tuning the variogram parameters used in this approach, it is then possible to visualize individual lithofacies and geomorphological features for these lithologic units. The study re-examines an electrical resistivity dataset collected as part of a groundwater study in an area of the Bannu basin in Pakistan. Additional lithological logs from boreholes throughout the area have been combined with the existing resistivity data for calibration. Tectonic activity during the Himalayan orogeny uplifted and generated significant faulting in the rocks resulting in the formation of a depression which subsequently has been filled with clay-silt and dirty sand facies typical of lacustrine and flood plain environments. Streams arising from adjacent mountains have reworked these facies which have been eroded and replaced by gravel-sand facies along channels. It is concluded that the sediments have been deposited as prograding fan shaped bodies, flood plain, and lacustrine deposits. Clay-silt facies mark the locations of paleo depressions or lake environments, which have changed position over time due to local tectonic activity and sedimentation. The Lakki plain alluvial system has thus formed as a result of local tectonic activity with fluvial erosion and deposition characterized by coarse sediments with high electrical resistivities near the mountain ranges and fine sediments with medium to low electrical resistivities towards the basin center.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1409
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1007/s10661-014-3876-5

  7 / 5360 MEDLINE  
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[PMID]: 23832138
[Au] Autor:Woolf AS; Stuart HM; Roberts NA; McKenzie EA; Hilton EN; Newman WG
[Ad] Address:Institute of Human Development, Faculty of Medical and Human Sciences, Manchester Academic Health Science Centre, University of Manchester, Michael Smith Building, Oxford Road, Manchester, M13 9PT, UK, adrian.woolf@manchester.ac.uk.
[Ti] Title:Urofacial syndrome: a genetic and congenital disease of aberrant urinary bladder innervation.
[So] Source:Pediatr Nephrol;29(4):513-8, 2014 Apr.
[Is] ISSN:1432-198X
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:The urofacial, or Ochoa, syndrome is characterised by congenital urinary bladder dysfunction together with an abnormal grimace upon smiling, laughing and crying. It can present as fetal megacystis. Postnatal features include urinary incontinence and incomplete bladder emptying due to simultaneous detrusor muscle and bladder outlet contractions. Vesicoureteric reflux is often present, and the condition can be complicated by urosepsis and end-stage renal disease. The syndrome has long been postulated to have neural basis, and it can be familial when it is inherited in an autosomal recessive manner. Most individuals with urofacial syndrome genetically studied to date carry biallelic, postulated functionally null mutations of HPSE2 or, less commonly, of LRIG2. Little is known about the biology of the respective encoded proteins, heparanase 2 and leucine-rich repeats and immunoglobulin-like domains 2. Nevertheless, the observations that heparanase 2 can bind heparan sulphate proteolgycans and inhibit heparanase 1 enzymatic activity and that LRIG2 can modulate receptor tyrosine kinase growth factor signalling each point to biological roles relevant to tissue differentiation. Moreover, both heparanase 2 and LRIG2 proteins are detected in autonomic nerves growing into fetal bladders. The collective evidence is consistent with the hypothesis that urofacial syndrome genes code for proteins which work in a common pathway to facilitate neural growth into, and/or function within, the bladder. This molecular pathway may also have relevance to our understanding of the pathogenesis of other lower tract diseases, including Hinman-Allen syndrome, or non-neurogenic neurogenic bladder, and of the subset of individuals who have primary vesicoureteric reflux accompanied by bladder dysfunction.
[Mh] MeSH terms primary: Facies
Urinary Bladder/abnormalities
Urologic Diseases
[Mh] MeSH terms secundary: Humans
Urinary Bladder/innervation
Urologic Diseases/congenital
Urologic Diseases/genetics
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Em] Entry month:1410
[Js] Journal subset:IM
[Da] Date of entry for processing:140219
[St] Status:MEDLINE
[do] DOI:10.1007/s00467-013-2552-2

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[PMID]: 24374682
[Au] Autor:Maclellan RA; Luks VL; Vivero MP; Mulliken JB; Zurakowski D; Padwa BL; Warman ML; Greene AK; Kurek KC
[Ad] Address:Boston, Mass. From the Departments of Plastic and Oral Surgery, Orthopaedic Surgery, and Pathology and Howard Hughes Medical Institute, Boston Children's Hospital; and the Department of Genetics, Harvard Medical School.
[Ti] Title:PIK3CA activating mutations in facial infiltrating lipomatosis.
[So] Source:Plast Reconstr Surg;133(1):12e-9e, 2014 Jan.
[Is] ISSN:1529-4242
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Facial infiltrating lipomatosis is a nonheritable disorder characterized by hemifacial soft-tissue and skeletal overgrowth, precocious dental development, macrodontia, hemimacroglossia, and mucosal neuromas. The authors tested the hypothesis that this condition is caused by a somatic mutation in the phosphatidylinositide-3 kinase (PI3K) signaling pathway, which has been indicted in other anomalies with overgrowth. METHODS: The authors extracted DNA from abnormal tissue in six individuals, generated sequencing libraries, enriched the libraries for 26 genes involved in the PI3K pathway, and designed and applied a sequential filtering strategy to analyze the sequence data for mosaic mutations. RESULTS: Unfiltered sequence data contained variant reads affecting ~12 percent of basepairs in the targeted genes. Filtering reduced the fraction of targeted basepairs containing variant reads to ~0.008 percent, allowing the authors to identify causal missense mutations in PIK3CA (p.E453K, p.E542K, p.H1047R, or p.H1047L) in each affected tissue sample. CONCLUSIONS: Affected tissue from individuals with facial infiltrating lipomatosis contains PIK3CA mutations that have previously been reported in cancers and in affected tissue from other nonheritable, overgrowth disorders, including congenital lipomatous overgrowth, vascular, epidermal, and skeletal anomalies syndrome, Klippel-Trenaunay syndrome, hemimegalencephaly, fibroadipose overgrowth, and macrodactyly. Because PIK3CA encodes a catalytic subunit of PI3K, and in vitro studies have shown that the overgrowth-associated mutations increase this enzyme's activity, PI3K inhibitors currently in clinical trials for patients with cancer may have a therapeutic role in patients with facial infiltrating lipomatosis. The strategy used to identify somatic mutations in patients with facial infiltrating lipomatosis is applicable to other somatic mosaic disorders that have allelic heterogeneity.
[Mh] MeSH terms primary: Lipomatosis/genetics
Lipomatosis/pathology
Mutation, Missense
Phosphatidylinositol 3-Kinases/genetics
[Mh] MeSH terms secundary: Child, Preschool
Face/pathology
Facies
Gene Library
Genetic Heterogeneity
Humans
Lipomatosis/metabolism
Magnetic Resonance Imaging
Male
Mosaicism
Phosphatidylinositol 3-Kinases/metabolism
Signal Transduction/genetics
Subcutaneous Tissue/pathology
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.1.137 (PIK3CA protein, human)
[Em] Entry month:1403
[Cu] Class update date: 141013
[Lr] Last revision date:141013
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:131230
[St] Status:MEDLINE
[do] DOI:10.1097/01.prs.0000436822.26709.7c

  9 / 5360 MEDLINE  
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[PMID]: 23340515
[Au] Autor:Stasia MJ; Mollin M; Martel C; Satre V; Coutton C; Amblard F; Vieville G; van Montfrans JM; Boelens JJ; Veenstra-Knol HE; van Leeuwen K; de Boer M; Brion JP; Roos D
[Ad] Address:1] Chronic Granulomatous Disease Diagnosis and Research Centre, Therex-TIMC/Imag, UMR CNRS 5525, UJF-Grenoble 1, Grenoble, France [2] Pôle Biologie, CHU de Grenoble, Grenoble, France.
[Ti] Title:Functional and genetic characterization of two extremely rare cases of Williams-Beuren syndrome associated with chronic granulomatous disease.
[So] Source:Eur J Hum Genet;21(10):1079-84, 2013 Oct.
[Is] ISSN:1476-5438
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Williams-Beuren syndrome (WBS) is a neurodevelopmental disorder with multi-systemic manifestations, caused by a heterozygous segmental deletion of 1.55-1.83 Mb at chromosomal band 7q11.23. The deletion can include the NCF1 gene that encodes the p47(phox) protein, a component of the leukocyte NADPH oxidase enzyme, which is essential for the defense against microbial pathogens. It has been postulated that WBS patients with two functional NCF1 genes are more susceptible to occurrence of hypertension than WBS patients with only one functional NCF1 gene. We now describe two extremely rare WBS patients without any functional NCF1 gene, because of a mutation in NCF1 on the allele not carrying the NCF1-removing WBS deletion. These two patients suffer from chronic granulomatous disease with increased microbial infections in addition to WBS. Interestingly, one of these patients did suffer from hypertension, indicating that other factors than NADPH oxidase in vascular tissue may be involved in causing hypertension.
[Mh] MeSH terms primary: Granulomatous Disease, Chronic/genetics
NADPH Oxidase/deficiency
Williams Syndrome/genetics
[Mh] MeSH terms secundary: Adolescent
Alleles
Child, Preschool
Gene Deletion
Granulomatous Disease, Chronic/complications
Granulomatous Disease, Chronic/diagnosis
Granulomatous Disease, Chronic/metabolism
Humans
Male
NADPH Oxidase/genetics
NADPH Oxidase/metabolism
Neutrophils/metabolism
Williams Syndrome/complications
Williams Syndrome/diagnosis
Williams Syndrome/metabolism
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:EC 1.6.3.1 (NADPH Oxidase); EC 1.6.3.1 (neutrophil cytosolic factor 1)
[Em] Entry month:1405
[Cu] Class update date: 141012
[Lr] Last revision date:141012
[Js] Journal subset:IM
[Da] Date of entry for processing:130919
[St] Status:MEDLINE
[do] DOI:10.1038/ejhg.2012.310

  10 / 5360 MEDLINE  
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[PMID]: 25172001
[Au] Autor:Koch A; Eisig S
[Ad] Address:Hospital Dentistry, Oral and Maxillofacial Surgery, Columbia University College of Dental Medicine, New York, NY, USA; Hospital Dental Service, New York-Presbyterian/Columbia University Medical Center, 180 Fort Washington Avenue, New York, NY 10032, USA. Electronic address: ak2045@columbia.edu.
[Ti] Title:Syndromes with unusual facies.
[So] Source:Atlas Oral Maxillofac Surg Clin North Am;22(2):205-10, 2014 Sep.
[Is] ISSN:1558-4275
[Cp] Country of publication:United States
[La] Language:eng
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:D
[St] Status:In-Process


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