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1.
J Dent ; 140: 104779, 2024 01.
Artigo em Inglês | MEDLINE | ID: mdl-38007173

RESUMO

INTRODUCTION: It is critical for dentists to identify and differentiate primary and permanent teeth, fillings, dental restorations and areas with pathological findings when reviewing dental radiographs to ensure that an accurate diagnosis is made and the optimal treatment can be planned. Unfortunately, dental radiographs are sometimes read incorrectly due to human error or low-quality images. While secondary or group review can help catch errors, many dentists work in practice alone and/or do not have time to review all of their patients' radiographs with another dentist. Artificial intelligence may facilitate the accurate interpretation of radiographs. To help support the review of panoramic radiographs, we developed a novel collaborative learning model that simultaneously identifies and differentiates primary and permanent teeth and detects fillings. METHODS: We used publicly accessible dental panoramic radiographic images and images obtained from the University of Missouri-Kansas City, School of Dentistry to develop and optimize two high-performance classifiers: (1) a system for tooth segmentation that can differentiate primary and permanent teeth and (2) a system to detect dental fillings. RESULTS: By utilizing these high-performance classifiers, we created models that can identify primary and permanent teeth (mean average precision [mAP] 95.32 % and performance [F-1] 92.50 %), as well as their associated dental fillings (mAP 91.53 % and F-1 91.00 %). We also designed a novel method for collaborative learning that utilizes these two classifiers to enhance recognition performance (mAP 94.09 % and F-1 93.41 %). CONCLUSIONS: Our model improves upon the existing machine learning models to simultaneously identify and differentiate primary and permanent teeth, and to identify any associated fillings. CLINICAL SIGNIFICANCE: Human error can lead to incorrect readings of panoramic radiographs. By developing artificial intelligence and machine learning methods to analyze panoramic radiographs, dentists can use this information to support their radiograph interpretations, help communicate the information to patients, and assist dental students learning to read radiographs.


Assuntos
Práticas Interdisciplinares , Dente , Humanos , Radiografia Panorâmica , Dentição Mista , Inteligência Artificial
2.
PLoS One ; 8(10): e76251, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-24204606

RESUMO

Genomic abnormalities leading to colorectal cancer (CRC) include somatic events causing copy number aberrations (CNAs) as well as copy neutral manifestations such as loss of heterozygosity (LOH) and uniparental disomy (UPD). We studied the causal effect of these events by analyzing high resolution cytogenetic microarray data of 15 tumor-normal paired samples. We detected 144 genes affected by CNAs. A subset of 91 genes are known to be CRC related yet high GISTIC scores indicate 24 genes on chromosomes 7, 8, 18 and 20 to be strongly relevant. Combining GISTIC ranking with functional analyses and degree of loss/gain we identify three genes in regions of significant loss (ATP8B1, NARS, and ATP5A1) and eight in regions of gain (CTCFL, SPO11, ZNF217, PLEKHA8, HOXA3, GPNMB, IGF2BP3 and PCAT1) as novel in their association with CRC. Pathway and target prediction analysis of CNA affected genes and microRNAs, respectively indicates TGF-ß signaling pathway to be involved in causing CRC. Finally, LOH and UPD collectively affected nine cancer related genes. Transcription factor binding sites on regions of >35% copy number loss/gain influenced 16 CRC genes. Our analysis shows patient specific CRC manifestations at the genomic level and that these different events affect individual CRC patients differently.


Assuntos
Neoplasias Colorretais/genética , Genômica/métodos , Oncogenes , Sítios de Ligação , Aberrações Cromossômicas , Neoplasias Colorretais/metabolismo , Análise Citogenética , Variações do Número de Cópias de DNA , Feminino , Humanos , Perda de Heterozigosidade , Masculino , Ligação Proteica , Fatores de Transcrição/metabolismo , Dissomia Uniparental
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