Early goal enteral nutrition associated with decreased in-hospital death in mechanically ventilated critically ill adults: a retrospective cohort study.

Introduction: Early enteral nutrition (EN) in critically ill adult patients is thought to improve mortality and morbidity; expert guidelines recommend early initiation of EN in critically ill adults. However, the ideal schedule and dose of EN remain understudied.

Study Objective: Our objective was to evaluate the relationship between achieving 70% of recommended EN within 2 days of intubation ('early goal EN') and clinical outcomes in mechanically ventilated medically critically ill adults.

Tumor suppressor p53 regulates heat shock factor 1 protein degradation in Huntington's disease.

p53 and HSF1 are two major transcription factors involved in cell proliferation and apoptosis, whose dysregulation contributes to cancer and neurodegeneration. Contrary to most cancers, p53 is increased in Huntington's disease (HD) and other neurodegenerative diseases, while HSF1 is decreased. p53 and HSF1 reciprocal regulation has been shown in different contexts, but their connection in neurodegeneration remains understudied.

Heat Shock Factor 1 Directly Regulates Postsynaptic Scaffolding PSD-95 in Aging and Huntington's Disease and Influences Striatal Synaptic Density.

PSD-95 () is an ionotropic glutamate receptor scaffolding protein essential in synapse stability and neurotransmission. PSD-95 levels are reduced during aging and in neurodegenerative diseases like Huntington's disease (HD), and it is believed to contribute to synaptic dysfunction and behavioral deficits. However, the mechanism responsible for PSD-95 dysregulation under these conditions is unknown.

Mitochondrial Dysfunction in Huntington's Disease; Interplay Between HSF1, p53 and PGC-1α Transcription Factors.

Huntington's disease (HD) is a neurodegenerative disease caused by an expanded CAG repeat in the huntingtin () gene, causing the protein to misfold and aggregate. HD progression is characterized by motor impairment and cognitive decline associated with the preferential loss of striatal medium spiny neurons (MSNs). The mechanisms that determine increased susceptibility of MSNs to mutant HTT (mHTT) are not fully understood, although there is abundant evidence demonstrating the importance of mHTT mediated mitochondrial dysfunction in MSNs death.