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Multiple Sclerosis (MS) is a neurological auto-immune disorder. Gadolinium agents, often used to identify inflammatory active lesions, have potential toxic effects. Our goal was to develop a lesion-level deep learning approach to predict lesion enhancement in non-enhanced MRI scans. A convolutional neural network was trained and tested on independent data sets. Statistical analysis of the results revealed that our approach is effective in predicting enhancing lesions from non-enhanced MRI images in MS patients on a lesion-level., Multiple Sklerose (MS) ist eine neurologische Autoimmunerkrankung. Gadolinium-Wirkstoffe, die häufig zur Erkennung aktiver Läsionen eingesetzt werden, haben möglicherweise Nebenwirkungen. Unser Ziel war die Entwicklung eines Deep Learning-Ansatzes als Alternative. Ein „convolutional neural network“ wurde anhand von unabhängigen Datensätzen trainiert und getestet. Die statistische Analyse der Ergebnisse zeigte, dass unser Ansatz bei der Vorhersage von anreichernden Läsionen auf nicht-anreichernden MRT-Bildern von MS-Patienten wirksam ist.

Shank is a post-synaptic scaffolding protein that has many binding partners. Shank mutations and copy number variations (CNVs) are linked to several psychiatric disorders, and to synaptic and behavioral defects in mice. It is not known which Shank binding partners are responsible for these defects. Here we show that the C. elegans SHN-1/Shank binds L-type calcium channels and that increased and decreased shn-1 gene dosage alter L-channel current and activity-induced expression of a CRH-1/CREB transcriptional target (gem-4 Copine), which parallels the effects of human Shank copy number variations (CNVs) on Autism spectrum disorders and schizophrenia. These results suggest that an important function of Shank proteins is to regulate L-channel current and activity induced gene expression.

Shank is a post-synaptic scaffolding protein that has many binding partners. Shank mutations and copy number variations (CNVs) are linked to several psychiatric disorders, and to synaptic and behavioral defects in mice. It is not known which Shank binding partners are responsible for these defects. Here we show that the C. elegans SHN-1/Shank binds L-type calcium channels and that increased and decreased shn-1 gene dosage alter L-channel current and activity-induced expression of a CRH-1/CREB transcriptional target (gem-4 Copine), which parallels the effects of human Shank copy number variations (CNVs) on Autism spectrum disorders and schizophrenia. These results suggest that an important function of Shank proteins is to regulate L-channel current and activity induced gene expression.

Shank is a post-synaptic scaffolding protein that has many binding partners. Shank mutations and copy number variations (CNVs) are linked to several psychiatric disorders, and to synaptic and behavioral defects in mice. It is not known which Shank binding partners are responsible for these defects. Here we show that the C. elegans SHN-1/Shank binds L-type calcium channels and that increased and decreased shn-1 gene dosage alter L-channel current and activity-induced expression of a CRH-1/CREB transcriptional target (gem-4 Copine), which parallels the effects of human Shank copy number variations (CNVs) on Autism spectrum disorders and schizophrenia. These results suggest that an important function of Shank proteins is to regulate L-channel current and activity induced gene expression.