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Curr Diab Rep ; 21(1): 1, 2021 Jan 02.
Artigo em Inglês | MEDLINE | ID: mdl-33387073


PURPOSE OF REVIEW: Type 1 diabetes (T1D) develops as a consequence of a combination of genetic predisposition and environmental factors. Combined, these events trigger an autoimmune disease that results in progressive loss of pancreatic ß cells, leading to insulin deficiency. This article reviews the current knowledge on the genetics of T1D with a specific focus on genetic variation in pancreatic islet regulatory networks and its implication to T1D risk and disease development. RECENT FINDINGS: Accumulating evidence suggest an active role of ß cells in T1D pathogenesis. Based on such observation several studies aimed in mapping T1D risk variants acting at the ß cell level. Such studies unravel T1D risk loci shared with type 2 diabetes (T2D) and T1D risk variants potentially interfering with ß-cell responses to external stimuli. The characterization of regulatory genomics maps of disease-relevant states and cell types can be used to elucidate the mechanistic role of ß cells in the pathogenesis of T1D.

Phys Rev Lett ; 123(12): 126401, 2019 Sep 20.
Artigo em Inglês | MEDLINE | ID: mdl-31633970


We propose a driving protocol which allows us to use quantum dot arrays as quantum simulators for 1D topological phases. We show that by driving the system out of equilibrium, one can imprint bond order in the lattice (producing structures such as dimers, trimers, etc.) and selectively modify the hopping amplitudes at will. Our driving protocol also allows for the simultaneous suppression of all the undesired hopping processes and the enhancement of the necessary ones, enforcing certain key symmetries which provide topological protection. In addition, we have discussed its implementation in a 12-QD array with two interacting electrons and found correlation effects in their dynamics, when configurations with different number of edge states are considered.

Endocr Relat Cancer ; 26(7): R415-R439, 2019 07.
Artigo em Inglês | MEDLINE | ID: mdl-31035251


In recent years, cancer genomics has provided new insights into genetic alterations and signaling pathways involved in thyroid cancer. However, the picture of the molecular landscape is not yet complete. DNA methylation, the most widely studied epigenetic mechanism, is altered in thyroid cancer. Recent technological advances have allowed the identification of novel differentially methylated regions, methylation signatures and potential biomarkers. However, despite recent progress in cataloging methylation alterations in thyroid cancer, many questions remain unanswered. The aim of this review is to comprehensively examine the current knowledge on DNA methylation in thyroid cancer and discuss its potential clinical applications. After providing a general overview of DNA methylation and its dysregulation in cancer, we carefully describe the aberrant methylation changes in thyroid cancer and relate them to methylation patterns, global hypomethylation and gene-specific alterations. We hope this review helps to accelerate the use of the diagnostic, prognostic and therapeutic potential of DNA methylation for the benefit of thyroid cancer patients.

Metilação de DNA , Neoplasias da Glândula Tireoide/genética , Antineoplásicos/uso terapêutico , Biomarcadores Tumorais/genética , Biomarcadores Tumorais/metabolismo , Metilação de DNA/efeitos dos fármacos , Metilação de DNA/genética , Desmetilação , Epigenoma , Regulação Neoplásica da Expressão Gênica , Humanos , Prognóstico , Transdução de Sinais/genética , Neoplasias da Glândula Tireoide/tratamento farmacológico , Neoplasias da Glândula Tireoide/patologia