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Melanoma neuronal learning

Titus J Brinker, Achim Hekler, Alexander H Enk, Joachim Klode, Axel Hauschild, Carola Berking, Bastian Schilling, Sebastian Haferkamp, Dirk Schadendorf, Stefan Fröhling, Jochen S Utikal, Christof von Kalle
BACKGROUND: Recent studies have demonstrated the use of convolutional neural networks (CNNs) to classify images of melanoma with accuracies comparable to those achieved by board-certified dermatologists. However, the performance of a CNN exclusively trained with dermoscopic images in a clinical image classification task in direct competition with a large number of dermatologists has not been measured to date. This study compares the performance of a convolutional neuronal network trained with dermoscopic images exclusively for identifying melanoma in clinical photographs with the manual grading of the same images by dermatologists...
March 7, 2019: European Journal of Cancer
JianJun Yang, BeiBei Lai, AiLi Xu, Yu Liu, XiaoMin Li, YongNa Zhao, WeiFeng Li, MuHuo Ji, Gang Hu, Xiang Gao, Jun Gao
Maged1 is a member of the type II melanoma antigen (MAGE) family of proteins, which is highly conserved in the brain between mouse and human. Recently, Maged1 has been reported to be involved in depression and impaired sexual behavior. However, the role of Maged1 in learning and memory remains unknown. The aim of the present study was therefore to investigate whether Maged1 deficiency can impair learning and memory formation. By behavioral tests and electrophysiological recording, we observed that 5-6-month-old Maged1 knockout mice displayed the reduced basal synaptic transmission, pronounced hippocampal dysfunction, impaired spatial learning, and a deficit in long-term potentiation induction...
February 2015: Molecular Neurobiology
Isabelle Rapin
Deficient repair of ubiquitous errors in the genome risks faulty transcription or replication. Its direct and indirect phenotypic consequences are rare, complex, dementing, lethal disorders of children with inadequately understood overlapping genotypes and variable severity. Mutations of CSA or CSB responsible for impaired transcription-coupled repair cause Cockayne syndrome (CS). Its characteristics are (1) profound growth deficiency affecting all tissues, including the brain, (2) premature aging marked by cachexia, vascular disease, exocrine deficiency, and osteopenia, but not cancer, and (3) a selective degenerative disorder of central and peripheral myelin and by neuronal loss in the retina and inner ear, and in the cerebellum and basal ganglia where it is associated with calcification...
2013: Handbook of Clinical Neurology
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