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1.
Zhong Nan Da Xue Xue Bao Yi Xue Ban ; 46(4): 432-437, 2021 Apr 28.
Artigo em Inglês, Chinês | MEDLINE | ID: mdl-33967092

RESUMO

Cardio-facio-cutaneous (CFC) syndrome is an extremely rare autosomal dominant genetic disease due to BRAF and other gene mutations. The main characteristics of the patients are craniofacial deformities, cardiac malformations, skin abnormalities, delay of language and motor development, gastrointestinal dysfunction, intellectual disability, and epilepsy. In this case, the child has a typical CFC syndrome face and developmental delay. The gene results of the second-generation sequencing technology showed that there was a mutation site c.1741A>G (p. Asn581Asp) (heterozygous) in exon 14 of the BRAF (NM_004333.5) gene. The mutation was not observed in the child's parents. The above-mentioned mutation may be a de novo mutation. There is no effective therapy for this disease so far.


Assuntos
Anormalidades Múltiplas , Displasia Ectodérmica , Cardiopatias Congênitas , Criança , Displasia Ectodérmica/genética , Facies , Insuficiência de Crescimento , Cardiopatias Congênitas/genética , Humanos , Mutação , Proteínas Proto-Oncogênicas B-raf/genética
2.
Zhonghua Yi Xue Yi Chuan Xue Za Zhi ; 38(5): 469-471, 2021 May 10.
Artigo em Chinês | MEDLINE | ID: mdl-33974258

RESUMO

OBJECTIVE: To explore the clinical and genetic characteristics of a child with X-linked hypohidrotic ectodermal dysplasia (XLHED). METHODS: Clinical data of the child was collected. Peripheral blood samples were taken from the child and his parents with informed consent and subjected to copy number variation (CNV) analysis and whole exome sequencing (WES). RESULTS: The male infant manifested sparse hair, anhidrosis, anuresis due to polycystic kidney dysplasia, external genital malformation and anal atresia. WES has revealed a 406 bp hemizygous deletion at Xq13 (68 836 147-68 836 553) in the proband, which encompassed exon 1 of the EDA gene. A heterozygous deletion at the same site was detected in the mother, while no deletion or duplication of the site was detected in the father. CONCLUSION: The hemizygous deletion of EDA gene exon 1 probably underlay the ectodermal dysplasia in the proband. Above result has provided a basis for genetic counseling and prenatal diagnosis for the family.


Assuntos
Displasia Ectodérmica Anidrótica Tipo 1 , Displasia Ectodérmica , Criança , Variações do Número de Cópias de DNA , Displasia Ectodérmica/genética , Displasia Ectodérmica Anidrótica Tipo 1/genética , Ectodisplasinas/genética , Testes Genéticos , Humanos , Lactente , Masculino , Linhagem
3.
West Afr J Med ; 38(4): 391-394, 2021 Apr 23.
Artigo em Inglês | MEDLINE | ID: mdl-33904163

RESUMO

Aplasia cutis congenita (ACC) is a rare developmental disorder that is not fully understood. It often occurs in isolation but can also be syndromic. Usually, there is an absence of the epidermis and dermis. It may be limited to the skin alone but may involve deeper structures. Research has identified a heterogeneous predisposition including genetic factors. Among patients with ACC, scalp involvement is common, however large scalp defects with the involvement of the skull is not common. We present a preterm neonate with a large scalp ACC with a wide skull defect.


Assuntos
Displasia Ectodérmica , Crânio , Displasia Ectodérmica/diagnóstico , Displasia Ectodérmica/genética , Humanos , Recém-Nascido , Couro Cabeludo , Pele , Crânio/diagnóstico por imagem
4.
Nat Commun ; 12(1): 2028, 2021 04 01.
Artigo em Inglês | MEDLINE | ID: mdl-33795686

RESUMO

Germline mutations in BRAF and other components of the MAPK pathway are associated with the congenital syndromes collectively known as RASopathies. Here, we report the association of Septo-Optic Dysplasia (SOD) including hypopituitarism and Cardio-Facio-Cutaneous (CFC) syndrome in patients harbouring mutations in BRAF. Phosphoproteomic analyses demonstrate that these genetic variants are gain-of-function mutations leading to activation of the MAPK pathway. Activation of the MAPK pathway by conditional expression of the BrafV600E/+ allele, or the knock-in BrafQ241R/+ allele (corresponding to the most frequent human CFC-causing mutation, BRAF p.Q257R), leads to abnormal cell lineage determination and terminal differentiation of hormone-producing cells, causing hypopituitarism. Expression of the BrafV600E/+ allele in embryonic pituitary progenitors leads to an increased expression of cell cycle inhibitors, cell growth arrest and apoptosis, but not tumour formation. Our findings show a critical role of BRAF in hypothalamo-pituitary-axis development both in mouse and human and implicate mutations found in RASopathies as a cause of endocrine deficiencies in humans.


Assuntos
Mutação com Ganho de Função , Hipopituitarismo/genética , Hipotálamo/metabolismo , Hipófise/metabolismo , Proteínas Proto-Oncogênicas B-raf/genética , Animais , Proteínas de Ciclo Celular/genética , Proteínas de Ciclo Celular/metabolismo , Células Cultivadas , Criança , Pré-Escolar , Corticotrofos/citologia , Corticotrofos/metabolismo , Displasia Ectodérmica/genética , Facies , Insuficiência de Crescimento/genética , Células HEK293 , Cardiopatias Congênitas/genética , Humanos , Lactente , Sistema de Sinalização das MAP Quinases/genética , Melanotrofos/citologia , Melanotrofos/metabolismo , Camundongos Knockout , Camundongos Transgênicos , Proteínas Proto-Oncogênicas B-raf/metabolismo , Sequenciamento Completo do Exoma/métodos
5.
Medicine (Baltimore) ; 100(9): e24633, 2021 Mar 05.
Artigo em Inglês | MEDLINE | ID: mdl-33655927

RESUMO

RATIONALE: Familial exudative vitreoretinopathy (FEVR) is an inherited disorder, which is mostly reported to be associated with the mutation of genes involved in the Wnt signaling pathway related to ß-catenin. To the best of our knowledge, the involvement of Adams-Oliver syndrome (AOS) genes in FEVR patients have not been reported before. PATIENT CONCERNS: Two patients with FEVR presented with microcephaly. One of them showed slight scarring of the scalp vertex which is a typical manifestation of AOS. The whole exon sequencing confirmed the diagnosis of AOS with 2 AOS-gene mutations at DOCK6 and ARHGAP31. Further clinical examination revealed that their parents with the same mutations showed FEVR-like vascular anomalies. DIAGNOSIS: Both patients were diagnosed with AOS through whole exon sequencing, and they presented with some FEVR-like retinopathy including retinal detachment. INTERVENTIONS: Both patients received vitrectomy for tractional retinal detachment with proliferative vitreoretinopathy. During the follow-up, 1 patient received additional laser photocoagulation for tractional retinal detachment. OUTCOMES: The 2 patients remained stable in the latest follow up after the treatment. LESSONS: Microcephaly could be associated with some form of retinopathy. We proposed that mutation of DOCK6 and ARHGAP31 genes could be the possible cause of FEVR associated with microcephaly. Our study suggested that these genes may be candidate genes of FEVR.


Assuntos
Displasia Ectodérmica/genética , Vitreorretinopatias Exsudativas Familiares/genética , Proteínas Ativadoras de GTPase/genética , Fatores de Troca do Nucleotídeo Guanina/genética , Deformidades Congênitas dos Membros/genética , Microcefalia/genética , Fosfoproteínas/genética , Dermatoses do Couro Cabeludo/congênito , Oftalmopatias Hereditárias/genética , Feminino , Humanos , Lactente , Masculino , Mutação/genética , Descolamento Retiniano/genética , Dermatoses do Couro Cabeludo/genética
6.
Zhonghua Yi Xue Yi Chuan Xue Za Zhi ; 38(3): 219-223, 2021 Mar 10.
Artigo em Chinês | MEDLINE | ID: mdl-33751528

RESUMO

OBJECTIVE: To investigate the clinical phenotype and genetic characteristics of a patient with hypohidrotic ectodermal dysplasia (HED) due to partial deletion of EDA gene. METHODS: The child has presented with HED complicated with epilepsy. Family trio whole exome sequencing (Trio-WES), copy number variation sequencing (CNV-seq), and karyotype analysis were carried out to explore the underlying genetic etiology. RESULTS: The proband, a 7-year-and-8-month-old boy, presented with thin curly hair, thin and sparse eyebrow, xerosis cutis, susceptibility to hyperthermia from childhood, hypohidrosis, sharp/sparse/absent teeth, saddle nose, prominent forehead, auricle adulation and seizure. He was found to have a normal chromosomal karyotype, and no abnormality was found by Trio-WES. Genome-wide CNV-seq revealed a 341.90 kb deletion at Xq13.1q13.1 (chrX: 68 796 566-69 138 468). As verified by PCR-electrophoresis, the deletion has removed part of the EDA gene. The deletion was derived from his mother with normal hair, mild xerosis cutis, and sparse, decidulated and nail-like teeth. The mother was detected with a heterozygous 242.10 kb deletion at Xq13.1q13.1 (chrX: 68 836 154-69 078 250). CONCLUSION: Both the proband and his mother have carried a Xq13.1 microdeletion involving part of the EDA gene. The clinical phenotypes of the mother and the proband were consistent with the clinical characteristics of X-linked recessive HED, for which partial deletion of the EDA gene is probably accountable.


Assuntos
Variações do Número de Cópias de DNA , Displasia Ectodérmica Anidrótica Tipo 1 , Displasia Ectodérmica , Criança , Displasia Ectodérmica Anidrótica Tipo 1/genética , Ectodisplasinas/genética , Humanos , Masculino , Fenótipo
7.
Artigo em Inglês | MEDLINE | ID: mdl-33669496

RESUMO

Background: Setleis syndrome (SS) is a focal facial dermal dysplasia presenting with bilateral temporal skin lesions, eyelash abnormalities and absent meibomian glands. SS is a rare autosomal recessive disorder caused by mutations in the TWIST2 gene, which codes for a transcription factor of the bHLH family known to be involved in skin and facial development. Methods: We obtained gene expression profiles by microarray analyses from control and SS patient primary skin fibroblast and lymphoblastoid cell lines. Results: Out of 983 differentially regulated genes in fibroblasts (fold change ≥ 2.0), 479 were down-regulated and 509 were up-regulated, while in lymphoblasts, 1248 genes were down-regulated and 73 up-regulated. RT-PCR reactions confirmed altered expression of selected genes. Conclusions: TWIST2 is described as a repressor, but expression profiling suggests an important role in gene activation as well, as evidenced by the number of genes that are down-regulated, with a much higher proportion of down-regulated genes found in lymphoblastoid cells from an SS patient. As expected, both types of cell types showed dysregulation of cytokine genes. These results identify potential TWIST2 target genes in two important cell types relevant to rare disorders caused by mutations in this bHLH gene.


Assuntos
Proteínas Repressoras , Proteína 1 Relacionada a Twist , Displasia Ectodérmica , Fibroblastos , Perfilação da Expressão Gênica , Humanos , Proteínas Repressoras/genética , Proteína 1 Relacionada a Twist/genética
8.
J Med Case Rep ; 15(1): 110, 2021 Mar 04.
Artigo em Inglês | MEDLINE | ID: mdl-33658072

RESUMO

BACKGROUND: Aplasia cutis congenita is regarded as congenital focal absence of skin in the newborn, and occurrence of more than three similar skin defects is rare. The etiology is thought to be multifactorial, and precise etiopathogenesis is unknown. CASE PRESENTATION: A 13-day-old newborn Sri Lankan Tamil girl was referred to the dermatologic clinic with multiple skin defects at birth. There were six lesions on the body, and two of them had healed during intrauterine period, leaving scars. This was a second twin of her pregnancy. Her first twin fetus had demised before 19 weeks of pregnancy and was confirmed to be fetus papyraceous based on ultrasound-guided fetal assessment. The said child was thoroughly investigated and found to have no other congenital abnormalities. Chromosomal studies yielded normal findings. She was treated with tropical antibacterial ointment, and all lesions resolved spontaneously within 4 weeks, leaving scars. Physiotherapy was commenced to prevent contracture formation, and follow-up was arranged in collaboration with the plastic surgical team. CONCLUSIONS: Aplasia cutis congenita is a rare condition of uncertain etiology, but consanguinity may play a role. This report described a newborn with type V cutis aplasia congenita in whom the diagnosis was confirmed based on clinical features and revision of antenatal history. The management depends on the pattern, extent, location, severity, underlying causes, and associated anomalies.


Assuntos
Displasia Ectodérmica , Criança , Displasia Ectodérmica/diagnóstico , Displasia Ectodérmica/genética , Displasia Ectodérmica/terapia , Feminino , Feto , Humanos , Índia , Recém-Nascido , Gravidez , Pele , Gêmeos
11.
Pediatr Dermatol ; 38(2): 533-535, 2021 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-33464633

RESUMO

Xia Gibbs syndrome is a genetic disorder first defined in 2014 characterized by hypotonia, intellectual disability, global developmental delay, and dysmorphic facial features. While many additional features may be present, there are few reports of dermatologic findings. We report a case of atypical aplasia cutis in a female infant who was found to have Xia Gibbs syndrome. This case highlights consideration of cutaneous manifestations of Xia Gibbs syndrome which may aid in diagnosis.


Assuntos
Anormalidades Múltiplas , Displasia Ectodérmica , Deficiência Intelectual , Anormalidades Musculoesqueléticas , Anormalidades Múltiplas/diagnóstico , Displasia Ectodérmica/complicações , Displasia Ectodérmica/diagnóstico , Feminino , Humanos , Lactente , Deficiência Intelectual/diagnóstico
12.
Pediatr Dermatol ; 38(2): 472-476, 2021 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-33481290

RESUMO

Aplasia cutis congenita (ACC) is characterized by the complete or partial absence of skin at birth, with 85% of cases of ACC involving the scalp vertex. The etiology of ACC is unclear and appears to be multifactorial. We present the case of a 3-month-old boy who presented with a diagnosis of non-scalp ACC affecting approximately 80% of his total body surface area at birth. This case adds to the literature due to the patient's survival beyond the first day of life and his unique and severe distribution of defects, which led to respiratory compromise and required multidisciplinary management.


Assuntos
Displasia Ectodérmica , Displasia Ectodérmica/diagnóstico , Displasia Ectodérmica/terapia , Humanos , Lactente , Recém-Nascido , Masculino , Couro Cabeludo , Pele
13.
Pediatr Dermatol ; 38(2): 530-532, 2021 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-33486784

RESUMO

Basan syndrome is a rare autosomal dominant genodermatosis, characterized by rapidly healing congenital acral bullae, congenital milia and adermatoglyphia (lack of finger and toeprints). This type of ectodermal dysplasia has been infrequently reported in the literature. A pathogenic mutation in the SMARCAD1 gene has been demonstrated to cause this rare disorder.


Assuntos
Displasia Ectodérmica , Unhas Malformadas , Dermatopatias Genéticas , DNA Helicases/genética , Displasia Ectodérmica/diagnóstico , Displasia Ectodérmica/genética , Humanos , Mutação , Unhas Malformadas/diagnóstico , Unhas Malformadas/genética
14.
Arch. Soc. Esp. Oftalmol ; 96(1): 45-47, ene. 2021. ilus
Artigo em Espanhol | IBECS | ID: ibc-200184

RESUMO

El síndrome de Haberland o lipomatosis encefalocraneocutánea es un síndrome muy infrecuente caracterizado por la tríada clásica de afectación cutánea, ocular y del sistema nervioso central. Fue descrito por primera vez en 1970 por Haberland y Perou, habiéndose descrito unos 60 casos desde entonces. Presentamos un caso de un varón de 14 semanas diagnosticado de síndrome de Haberland con afectación ocular bilateral en forma de coloboma palpebral y coristomas


Haberland syndrome or encephalocutaneous lipomatosis is a very uncommon syndrome that is characterised by changes in the skin, eye, and central nervous system. It was first described in 1970 by Haberland and Perou, with about 60 cases having been reported since then. A case is reported of a 14-week-old male diagnosed with Haberland syndrome with bilateral ocular involvement in the form of palpebral coloboma and choristomas


Assuntos
Humanos , Masculino , Recém-Nascido , Anormalidades do Olho/genética , Fenda Labial/genética , Anormalidades Congênitas/genética , Displasia Ectodérmica Hipo-Hidrótica Autossômica Recessiva/genética , Anormalidades do Olho/diagnóstico , Fenda Labial/diagnóstico , Transtornos Cromossômicos/diagnóstico , Transtornos Cromossômicos/genética , Diagnóstico Diferencial , Displasia Ectodérmica/diagnóstico , Displasia Ectodérmica/genética
15.
Am J Hum Genet ; 108(1): 134-147, 2021 01 07.
Artigo em Inglês | MEDLINE | ID: mdl-33340455

RESUMO

The ubiquitin-proteasome system facilitates the degradation of unstable or damaged proteins. UBR1-7, which are members of hundreds of E3 ubiquitin ligases, recognize and regulate the half-life of specific proteins on the basis of their N-terminal sequences ("N-end rule"). In seven individuals with intellectual disability, epilepsy, ptosis, hypothyroidism, and genital anomalies, we uncovered bi-allelic variants in UBR7. Their phenotype differs significantly from that of Johanson-Blizzard syndrome (JBS), which is caused by bi-allelic variants in UBR1, notably by the presence of epilepsy and the absence of exocrine pancreatic insufficiency and hypoplasia of nasal alae. While the mechanistic etiology of JBS remains uncertain, mutation of both Ubr1 and Ubr2 in the mouse or of the C. elegans UBR5 ortholog results in Notch signaling defects. Consistent with a potential role in Notch signaling, C. elegans ubr-7 expression partially overlaps with that of ubr-5, including in neurons, as well as the distal tip cell that plays a crucial role in signaling to germline stem cells via the Notch signaling pathway. Analysis of ubr-5 and ubr-7 single mutants and double mutants revealed genetic interactions with the Notch receptor gene glp-1 that influenced development and embryo formation. Collectively, our findings further implicate the UBR protein family and the Notch signaling pathway in a neurodevelopmental syndrome with epilepsy, ptosis, and hypothyroidism that differs from JBS. Further studies exploring a potential role in histone regulation are warranted given clinical overlap with KAT6B disorders and the interaction of UBR7 and UBR5 with histones.


Assuntos
Epilepsia/genética , Hipotireoidismo/genética , Transtornos do Neurodesenvolvimento/genética , Receptores Notch/genética , Transdução de Sinais/genética , Ubiquitina-Proteína Ligases/genética , Animais , Anus Imperfurado/genética , Caenorhabditis elegans/genética , Linhagem Celular , Displasia Ectodérmica/genética , Transtornos do Crescimento/genética , Células HEK293 , Perda Auditiva Neurossensorial/genética , Histonas/genética , Humanos , Deficiência Intelectual/genética , Camundongos , Mutação/genética , Nariz/anormalidades , Pancreatopatias/genética , Complexo de Endopeptidases do Proteassoma/genética
17.
Methods Mol Biol ; 2248: 167-183, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33185875

RESUMO

Genetic deficiency of ectodysplasin A (EDA) causes X-linked hypohidrotic ectodermal dysplasia, a congenital condition characterized by the absence or abnormal formation of sweat glands, teeth, and several skin appendages. Stimulation of the EDA receptor (EDAR) with agonists in the form of recombinant EDA or anti-EDAR antibodies can compensate for the absence of Eda in a mouse model of Eda deficiency, provided that agonists are administered in a timely manner during fetal development. Here we provide detailed protocols for the administration of EDAR agonists or antagonists, or other proteins, by the intravenous, intraperitoneal, and intra-amniotic routes as well as protocols to collect blood, to visualize sweat gland function, and to prepare skulls in mice.


Assuntos
Receptor Edar/metabolismo , Transdução de Sinais/efeitos dos fármacos , Animais , Animais Recém-Nascidos , Modelos Animais de Doenças , Vias de Administração de Medicamentos , Displasia Ectodérmica/tratamento farmacológico , Displasia Ectodérmica/genética , Displasia Ectodérmica/metabolismo , Receptor Edar/genética , Camundongos , Fenótipo , Proteínas Recombinantes/administração & dosagem , Resultado do Tratamento
18.
Artigo em Inglês | MEDLINE | ID: mdl-33379169

RESUMO

Ectodermal dysplasia (ED) refers to a heterogeneous group of genetic diseases of the skin, skin appendages, and teeth. People with ED experience a poorer oral health-related quality of life (OHRQoL) compared to the general population. The aim of this study was to examine the OHRQoL of people with ED and to measure their objective physical oral health to confirm or disprove evidence of poorer oral health in this population. To determine OHRQoL, the German version of the 14-item Oral Health Impact Profile (OHIP-14G) was used. All the participants in the study were clinically examined, and the measured parameters were recorded using the Physical Oral Health Index (PhOX). In total, 10 male and 11 female participants, with an average age of 22.0 ± 9.0 years, were included in this study. The OHIP-14G summary score was 23.9 (±15.2) points (range: 0-56 points). The PhOX summary score was 61.2 (±5.1) points (range: 22-80 points). The findings indicated that both the OHRQoL and physical oral health of the participants were highly impaired and that their objective and subjective oral health were worse than those of the general population in Germany.


Assuntos
Displasia Ectodérmica/fisiopatologia , Saúde Bucal , Qualidade de Vida , Adolescente , Adulto , Feminino , Alemanha , Humanos , Masculino , Inquéritos e Questionários , Adulto Jovem
19.
Reumatol. clín. (Barc.) ; 16(6): 499-501, nov.-dic. 2020. ilus, graf
Artigo em Espanhol | IBECS | ID: ibc-201056

RESUMO

El síndrome tricorinofalángico I (TPRSI) tiene una herencia autosómica dominante, la proporción de casos «de novo» es desconocida1. Se caracteriza por rasgos faciales únicos, nariz de extremo bulboso, surco nasolabial plano y alargado, cabello escaso y de crecimiento lento. Anomalías esqueléticas que incluyen falanges y metacarpianos cortos -braquidactilia-, epífisis en forma de cono, displasia de cadera y estatura baja1-3. Presentamos los casos de una familia con 7 miembros afectos de TRPSI


Trichorhinophalangeal syndrome I (TPRSI) has an autosomal dominant inheritance; the proportion of «de novo» cases is unknown1. It is characterized by unique facial features, bulbous nose, flat and elongated nasolabial furrow, thin hair and slow growth. Skeletal abnormalities that include short phalanges and metacarpals -brachydactyly-, cone-shaped epiphyses, hip dysplasia and short stature1-3


Assuntos
Humanos , Síndrome de Langer-Giedion/diagnóstico , Facies , Anormalidades Musculoesqueléticas/diagnóstico por imagem , Displasia Ectodérmica/diagnóstico , Doenças Genéticas Inatas/diagnóstico , Osso e Ossos/anormalidades
20.
Zhonghua Yi Xue Yi Chuan Xue Za Zhi ; 37(11): 1265-1268, 2020 Nov 10.
Artigo em Chinês | MEDLINE | ID: mdl-33179236

RESUMO

OBJECTIVE: To explore the genetic cause of a patient suspected for congenital ectodermal dysplasia with repeated hyperthermia and to assess the reproductive risk for his family. METHODS: Medical whole-exome sequencing (WES) were used to detect single-nucleotide variations and low-coverage massively parallel copy number variation sequencing (CNV-seq) were employed to verify suspected CNVs. PCR and real-time quantitative PCR were applied to confirm the deletion of EDA gene. RESULTS: The results of WES suggested that the patient carried a hemizygous deletion for chrX:69 243 016-69 395 730. CNV-seq indicated that the patient carried a deletion of approximately 0.12 Mb on Xq13.1, which encompassed the EDA gene. The PCR results confirmed that there was a hemizygous deletion of exons 3 to 8 of the EDA gene. The same deletion was not found in his mother. CONCLUSION: The congenital ectodermal dysplasia of the patient may be attributed to deletion of exons 3 to 8 of the EDA gene, which could be de novo or derive from germline mosaicism of his mother. The WES and CNV-seq are of great value for the diagnosis of rare diseases.


Assuntos
Variações do Número de Cópias de DNA , Displasia Ectodérmica , Sequenciamento Completo do Exoma , Displasia Ectodérmica/genética , Ectodisplasinas/genética , Éxons , Testes Genéticos , Sequenciamento de Nucleotídeos em Larga Escala , Humanos , Mosaicismo , Deleção de Sequência
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