MBNL deficiency in motor neurons disrupts neuromuscular junction maintenance and gait coordination.

Muscleblind-like proteins (MBNLs) are a family of RNA-binding proteins that play essential roles in the regulation of RNA metabolism. Beyond their canonical role in RNA regulation, MBNL proteins have emerged as key players in the pathogenesis of Myotonic Dystrophy type 1 (DM1). In DM1, sequestration of MBNL proteins by expansion of the CUG repeat RNA leads to functional depletion of MBNL, resulting in deregulated alternative splicing and aberrant RNA processing, which underlie the clinical features of the disease.

A Novel Traffic Prediction Method Using Machine Learning for Energy Efficiency in Service Provider Networks.

This paper presents a systematic approach for solving complex prediction problems with a focus on energy efficiency. The approach involves using neural networks, specifically recurrent and sequential networks, as the main tool for prediction. In order to test the methodology, a case study was conducted in the telecommunications industry to address the problem of energy efficiency in data centers.

Exposures to psycholeptics, psychoanaleptics, and cardiovascular drugs reported to the PIC erfurt during heat waves from 2003 to 2018.

Psycholeptics, psychoanaleptics, and cardiovascular drugs alter individual tolerance to extreme heat. To explore the influence of heat waves on their toxicity in acute overdose, we retrospectively analyzed all human exposures to psycholeptics and psychoanaleptics (PLAexp) as well as cardiovascular drugs (CVDexp) registered by the Poisons Information Center (PIC) Erfurt between June to September of the years 2003 to 2018 for frequency, age groups, sex, circumstances of exposure, and symptom severity. The results of the non-heat years (NHY) 2004-2005 and 2007-2014 (average air temperature June-September 16.

Reversal of RNA toxicity in myotonic dystrophy via a decoy RNA-binding protein with high affinity for expanded CUG repeats.

Myotonic dystrophy type 1 (DM1) is an RNA-dominant disease whose pathogenesis stems from the functional loss of muscleblind-like RNA-binding proteins (RBPs), which causes the formation of alternative-splicing defects. The loss of functional muscleblind-like protein 1 (MBNL1) results from its nuclear sequestration by mutant transcripts containing pathogenic expanded CUG repeats (CUGexp). Here we show that an RBP engineered to act as a decoy for CUGexp reverses the toxicity of the mutant transcripts.