<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Da Lozzo, Prisca</style></author><author><style face="normal" font="default" size="100%">Magnolato, Andrea</style></author><author><style face="normal" font="default" size="100%">Del Rizzo, Irene</style></author><author><style face="normal" font="default" size="100%">Sirchia, Fabio</style></author><author><style face="normal" font="default" size="100%">Bruno, Irene</style></author><author><style face="normal" font="default" size="100%">Barbi, Egidio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">When Long-Lasting Food Selectivity Leads to an Unusual Genetic Diagnosis: A Case Report.</style></title><secondary-title><style face="normal" font="default" size="100%">J Adolesc Health</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J Adolesc Health</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2019</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2019 Jan</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">64</style></volume><pages><style face="normal" font="default" size="100%">137-138</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Hereditary fructose intolerance is an autosomal recessive disorder of fructose metabolism caused by catalytic deficiency of aldolase B enzyme [1]. The disease is typically expressed when fructose- and sucrose-containing foods are first introduced in the diet; acute manifestations include nausea, vomiting, abdominal distress, and symptomatic hypoglycemia [1,2]. Chronic fructose ingestion eventually leads to poor feeding, growth retardation and gradual liver and/or renal failure [3,4]. Some patients may remain undiagnosed until adulthood because of a self-protective avoidance of sweet tasting food that prevents the development of acute toxicity from fructose containing food; however, these subjects may suffer intermittent symptoms throughout life, leading to potentially serious misdiagnosis [4]. We report the case of a patient with unrecognized hereditary fructose intolerance in which chronic gastrointestinal complaints, low body weight, and unexplained food avoidance were addressed as manifestations of an eating disorder during adolescence.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/30327278?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">L'Imperio, Vincenzo</style></author><author><style face="normal" font="default" size="100%">Bruno, Irene</style></author><author><style face="normal" font="default" size="100%">Rabach, Ingrid</style></author><author><style face="normal" font="default" size="100%">Smith, Andrew</style></author><author><style face="normal" font="default" size="100%">Chinello, Clizia</style></author><author><style face="normal" font="default" size="100%">Stella, Martina</style></author><author><style face="normal" font="default" size="100%">Magni, Fulvio</style></author><author><style face="normal" font="default" size="100%">Pagni, Fabio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Histoproteomic Characterization of Localized Cutaneous Amyloidosis in X-Linked Reticulate Pigmentary Disorder.</style></title><secondary-title><style face="normal" font="default" size="100%">Skin Pharmacol Physiol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Skin Pharmacol Physiol</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Amyloidosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Diseases, X-Linked</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Pigmentation Disorders</style></keyword><keyword><style  face="normal" font="default" size="100%">Proteomics</style></keyword><keyword><style  face="normal" font="default" size="100%">Skin Diseases</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">30</style></volume><pages><style face="normal" font="default" size="100%">90-93</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">2</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28376499?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Rabach, Ingrid</style></author><author><style face="normal" font="default" size="100%">Salis, Simona</style></author><author><style face="normal" font="default" size="100%">Bruno, Irene</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Macrocephaly and palmoplantar pitting.</style></title><secondary-title><style face="normal" font="default" size="100%">Arch Dis Child</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Arch. Dis. Child.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Jun 28</style></date></pub-dates></dates><language><style face="normal" font="default" size="100%">ENG</style></language><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27355975?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Gortani, Giulia</style></author><author><style face="normal" font="default" size="100%">Faletra, Flavio</style></author><author><style face="normal" font="default" size="100%">Bruno, Irene</style></author><author><style face="normal" font="default" size="100%">Berti, Irene</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">&quot;Blaschkoid dyspigmentation&quot; in a child: don't forget fibroblast chromosomal analysis.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Pediatr.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Abnormalities, Multiple</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Chromosomes</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Fibroblasts</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Phenotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Pigmentation Disorders</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Feb</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">166</style></volume><pages><style face="normal" font="default" size="100%">490-90.e1</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">2</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25433905?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Naviglio, Samuele</style></author><author><style face="normal" font="default" size="100%">Bruno, Irene</style></author><author><style face="normal" font="default" size="100%">Zanus, Caterina</style></author><author><style face="normal" font="default" size="100%">Faletra, Flavio</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A brain and heart connection: X-linked periventricular heterotopia.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Pediatr.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Brain</style></keyword><keyword><style  face="normal" font="default" size="100%">Diagnosis, Differential</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA Mutational Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Epilepsy</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Filamins</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Magnetic Resonance Imaging</style></keyword><keyword><style  face="normal" font="default" size="100%">Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Periventricular Nodular Heterotopia</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Mar</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">166</style></volume><pages><style face="normal" font="default" size="100%">776</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25557968?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Benelli, Elisa</style></author><author><style face="normal" font="default" size="100%">Bruno, Irene</style></author><author><style face="normal" font="default" size="100%">Belcaro, Chiara</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author><author><style face="normal" font="default" size="100%">Berti, Irene</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Legius syndrome: case report and review of literature.</style></title><secondary-title><style face="normal" font="default" size="100%">Ital J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Ital J Pediatr</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">41</style></volume><pages><style face="normal" font="default" size="100%">8</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;A 8-month-old child was referred to our Dermatologic Unit for suspected Neurofibromatosis type 1 (NF 1), because of the appearance, since few days after birth, of numerous café-au-lait spots (seven larger than 5 mm); no other sign evocative of NF 1 was found. Her family history was remarkable for the presence of multiple café-au-lait spots in the mother, the grandfather and two aunts. The family had been already examined for NF 1, but no sign evocative of the disease was found. We then suspected Legius syndrome, a dominant disease characterized by a mild neurofibromatosis 1 phenotype. The diagnosis was confirmed by the finding of a mutation in SPRED1 gene, a feedback regulator of RAS/MAPK signaling. Here, we discuss the differential diagnosis of cafè-au-lait spots and we briefly review the existing literature about Legius syndrome.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25883013?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Faletra, Flavio</style></author><author><style face="normal" font="default" size="100%">d'Adamo, Adamo P</style></author><author><style face="normal" font="default" size="100%">Bruno, Irene</style></author><author><style face="normal" font="default" size="100%">Athanasakis, Emmanouil</style></author><author><style face="normal" font="default" size="100%">Biskup, Saskia</style></author><author><style face="normal" font="default" size="100%">Esposito, Laura</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Autosomal recessive Stickler syndrome due to a loss of function mutation in the COL9A3 gene.</style></title><secondary-title><style face="normal" font="default" size="100%">Am J Med Genet A</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Am. J. Med. Genet. A</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Arthritis</style></keyword><keyword><style  face="normal" font="default" size="100%">Bone and Bones</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Collagen Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Collagen Type IX</style></keyword><keyword><style  face="normal" font="default" size="100%">Connective Tissue Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA Mutational Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Facies</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Genes, Recessive</style></keyword><keyword><style  face="normal" font="default" size="100%">Hearing Loss</style></keyword><keyword><style  face="normal" font="default" size="100%">Hearing Loss, Sensorineural</style></keyword><keyword><style  face="normal" font="default" size="100%">Homozygote</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Pedigree</style></keyword><keyword><style  face="normal" font="default" size="100%">Retinal Detachment</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014 Jan</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">164A</style></volume><pages><style face="normal" font="default" size="100%">42-7</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Stickler syndrome (STL) is a clinically variable and genetically heterogeneous syndrome characterized by ophthalmic, articular, orofacial, and auditory manifestations. STL has been described with both autosomal dominant and recessive inheritance. The dominant form is caused by mutations of COL2A1 (STL 1, OMIM 108300), COL11A1 (STL 2, OMIM 604841), and COL11A2 (STL 3, OMIM 184840) genes, while recessive forms have been associated with mutations of COL9A1 (OMIM 120210) and COL9A2 (OMIM 120260) genes. Type IX collagen is a heterotrimeric molecule formed by three genetically distinct chains: α1, α2, and α3 encoded by the COL9A1, COL9A2, and COL9A3 genes. Up to this time, only heterozygous mutations of COL9A3 gene have been reported in human and related to: (1) multiple epiphyseal dysplasia type 3, (2) susceptibility to an intervertebral disc disease, and (3) hearing loss. Here, we describe the first autosomal recessive Stickler family due to loss of function mutations (c.1176_1198del, p.Gln393Cysfs*25) of COL9A3 gene. These findings extend further the role of collagen genes family in the disease pathogenesis.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24273071?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Faletra, Flavio</style></author><author><style face="normal" font="default" size="100%">d'Adamo, Adamo Pio</style></author><author><style face="normal" font="default" size="100%">Pensiero, Stefano</style></author><author><style face="normal" font="default" size="100%">Athanasakis, Emmanouil</style></author><author><style face="normal" font="default" size="100%">Catalano, Dario</style></author><author><style face="normal" font="default" size="100%">Bruno, Irene</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A novel CRYBB2 missense mutation causing congenital autosomal dominant cataract in an Italian family.</style></title><secondary-title><style face="normal" font="default" size="100%">Ophthalmic Genet</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Ophthalmic Genet.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Amino Acid Sequence</style></keyword><keyword><style  face="normal" font="default" size="100%">beta-Crystallin B Chain</style></keyword><keyword><style  face="normal" font="default" size="100%">Cataract</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA Mutational Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Genes, Dominant</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Linkage</style></keyword><keyword><style  face="normal" font="default" size="100%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular Sequence Data</style></keyword><keyword><style  face="normal" font="default" size="100%">Mutation, Missense</style></keyword><keyword><style  face="normal" font="default" size="100%">Pedigree</style></keyword><keyword><style  face="normal" font="default" size="100%">Phenotype</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2013</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2013 Mar-Jun</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">34</style></volume><pages><style face="normal" font="default" size="100%">115-7</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Congenital cataract is a leading cause of visual impairment in children and brings approximately 10% of childhood blindness worldwide. Molecular analysis revealed ~60 loci to be associated with several phenotypes of childhood cataracts. Until now, more than 30 loci and 18 genes on different chromosomes have been associated with autosomal dominant congenital cataract (ADCC). Here, we present a three-generation Italian family with a non syndromic ADCC. A linkage analysis carried out using HumanCytoSNP-12 DNA Analysis BeadChip led us to identify ten genomic regions virtually involved in the disease. All the genes located in these regions were scored for possible relationship with ADCC and, according to a strict clinical and genetic selection, 4 genes have been analyzed. A novel sequence variant was found in the CRYBB2 gene (p.Ser143Phe). This variant affects a conserved aminoacid in the third Greek key motif of the protein, cosegregates with the disease phenotype in all affected individuals and is not present both in the unaffected family members and 100 healthy control subjects. Finally, we identified the first CRYBB2 mutation in an Italian family causing a clinical picture of ADCC.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1-2</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22846113?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Faletra, Flavio</style></author><author><style face="normal" font="default" size="100%">Bruno, Irene</style></author><author><style face="normal" font="default" size="100%">Berti, Irene</style></author><author><style face="normal" font="default" size="100%">Pastore, Serena</style></author><author><style face="normal" font="default" size="100%">Pirrone, Angela</style></author><author><style face="normal" font="default" size="100%">Tommasini, Alberto</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A red baby should not be taken too lightly.</style></title><secondary-title><style face="normal" font="default" size="100%">Acta Paediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Acta Paediatr.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Dermatitis</style></keyword><keyword><style  face="normal" font="default" size="100%">Ectodermal Dysplasia</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunologic Deficiency Syndromes</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Netherton Syndrome</style></keyword><keyword><style  face="normal" font="default" size="100%">Severe Combined Immunodeficiency</style></keyword><keyword><style  face="normal" font="default" size="100%">Skin</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Dec</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">101</style></volume><pages><style face="normal" font="default" size="100%">e573-7</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;AIM: &lt;/b&gt;To identify clinical and laboratory features that can drive the differential diagnosis of a primary immunodeficiency diseases in patients with ectodermal defects.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;Analysis of selected teaching cases.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;We identified four exemplary cases that allowed to point out specific clues.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;A careful evaluation of immune and ectodermal signs is the key to the diagnosis. Therefore, a multidisciplinary approach can lead to diagnosis and to an appropriate treatment in most of the cases.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">12</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22946961?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Londero, Margherita</style></author><author><style face="normal" font="default" size="100%">Pastore, Serena</style></author><author><style face="normal" font="default" size="100%">Zanazzo, Giulio A</style></author><author><style face="normal" font="default" size="100%">Bruno, Irene</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A child with pain after mild trauma.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Pediatr.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Antigens, CD</style></keyword><keyword><style  face="normal" font="default" size="100%">Antigens, CD31</style></keyword><keyword><style  face="normal" font="default" size="100%">Antigens, CD34</style></keyword><keyword><style  face="normal" font="default" size="100%">Antigens, Differentiation, Myelomonocytic</style></keyword><keyword><style  face="normal" font="default" size="100%">Biopsy</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Factor VIII</style></keyword><keyword><style  face="normal" font="default" size="100%">Fingers</style></keyword><keyword><style  face="normal" font="default" size="100%">Hand Injuries</style></keyword><keyword><style  face="normal" font="default" size="100%">Hemangioendothelioma</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunohistochemistry</style></keyword><keyword><style  face="normal" font="default" size="100%">Injury Severity Score</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Osteolysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Pain</style></keyword><keyword><style  face="normal" font="default" size="100%">Pain Measurement</style></keyword><keyword><style  face="normal" font="default" size="100%">S100 Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Vascular Neoplasms</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2010 Oct</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">157</style></volume><pages><style face="normal" font="default" size="100%">693</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">4</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/20553843?dopt=Abstract</style></custom1></record></records></xml>