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Background: Spatial working memory is crucial for processing visual and spatial information, serving as a foundation for complex cognitive tasks. However, the effects of prolonged sleep deprivation on its dynamics and underlying neural mechanisms remain unclear. This study aims to investigate the specific trends and neural mechanisms underlying spatial working memory alterations during 36 h of acute sleep deprivation.

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Objective: This study aimed to explore longitudinal relationships between neurophysiological biomarkers and upper limb motor function recovery in stroke patients, focusing on electroencephalography (EEG) and transcranial magnetic stimulation (TMS) metrics.

Methods: This longitudinal cohort study analyzed neurophysiological, clinical, and demographic data from 102 stroke patients enrolled in the DEFINE cohort. We investigated the associations between baseline and post-intervention changes in the EEG theta/alpha ratio (TAR) and TMS metrics with upper limb motor functionality, assessed using the outcomes of five tests: the Fugl-Meyer Assessment (FMA), Handgrip Strength Test (HST), Pinch Strength Test (PST), Finger Tapping Test (FTT), and Nine-Hole Peg Test (9HPT).

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Glypican-3 (GPC3) is overexpressed in hepatocellular carcinomas and hepatoblastomas and represents an important therapeutic target but the biologic importance of GPC3 in liver cancer is unclear. To date, there are limited data characterizing the biological implications of GPC3 knockout (KO) in liver cancers that intrinsically express this target. Here, we report on the development and characterization of GPC3-KO liver cancer cell lines and compare to them to parental lines.

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Deficiency in the membrane cytoskeletal protein dystrophin is the underlying cause of the progressive muscle wasting disease named Duchenne muscular dystrophy. In order to detect novel disease marker candidates and confirm the complexity of the pathobiochemical signature of dystrophinopathy, mass spectrometric screening approaches represent ideal tools for comprehensive biomarker discovery studies. In this report, we describe the comparative proteomic analysis of young versus aged diaphragm muscles from wild type versus the dystrophic mouse model of X-linked muscular dystrophy.

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Biology of myocardial recovery in advanced heart failure with long-term mechanical support.

J Heart Lung Transplant

October 2022

Division of Cardiovascular Medicine, University of Utah Health, Salt Lake City, UT; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah Health, Salt Lake City, UT. Electronic address:

Cardiac remodeling is an adaptive, compensatory biological process following an initial insult to the myocardium that gradually becomes maladaptive and causes clinical deterioration and chronic heart failure (HF). This biological process involves several pathophysiological adaptations at the genetic, molecular, cellular, and tissue levels. A growing body of clinical and translational investigations demonstrated that cardiac remodeling and chronic HF does not invariably result in a static, end-stage phenotype but can be at least partially reversed.

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