Publications by authors named "Liam L Chen"

Article Synopsis
  • In 2008, guidelines were established for researching autophagy, which has since gained significant interest and new technologies, necessitating regular updates to monitoring methods across various organisms.
  • The new guidelines emphasize selecting appropriate techniques to evaluate autophagy while noting that no single method suits all situations; thus, a combination of methods is encouraged.
  • The document highlights that key proteins involved in autophagy also impact other cellular processes, suggesting genetic studies should focus on multiple autophagy-related genes to fully understand these pathways.
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Necrotizing enterocolitis (NEC) causes acute intestinal necrosis in premature infants and is associated with severe neurological impairment. In NEC, Toll-like receptor 4 is activated in the intestinal epithelium, and NEC-associated brain injury is characterized by microglial activation and white matter loss through mechanisms that remain unclear. We now show that the brains of mice and humans with NEC contained CD4 T lymphocytes that were required for the development of brain injury.

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Current studies underestimate the prevalence of brain injury in patients with left ventricular assist devices (LVADs), as CT scans are not sensitive in detecting cerebral ischemia. Using postmortem neuropathological evaluation, we sought to characterize the types and risk factors of brain injury in LVAD patients. We reviewed 24 LVAD patients who underwent brain autopsy with gross and microscopic examinations from 1993 through 2019 at a single tertiary center.

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Objectives: Characterization of the types and timing of acute brain injury in infant autopsy patients after extracorporeal membrane oxygenation.

Design: Retrospective cohort study.

Setting: Single tertiary-care center.

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Objectives: Current studies lack information on characteristics of acute brain injury in patients with extracorporeal membrane oxygenation. We sought to characterize the types, timing, and risk factors of acute brain injury in extracorporeal membrane oxygenation.

Design: Retrospective analysis.

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We sought to describe the relation between neuropathology and clinical information including neurological examination and electroencephalogram findings in extracorporeal membrane oxygenation. We reviewed the patients who had undergone brain autopsy from November 2017 through December 2018. Four patients with neuromonitoring had post mortem examination with brain autopsy.

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Necrotizing enterocolitis (NEC) is a severe gastrointestinal disease of the premature infant. One of the most important long-term complications observed in children who survive NEC early in life is the development of profound neurological impairments. However, the pathways leading to NEC-associated neurological impairments remain unknown, thus limiting the development of prevention strategies.

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Introduction: The recent approval of Spinraza (nusinersen), an antisense oligonucleotide, by U.S. Food and Drug Administration to treat patients with spinal muscular atrophy, has reignited interests of researchers in designing and testing new gene therapy approaches to treat neurological disorders, in particular, to curb neurodegenerative diseases of the central nervous system which represent an ever-increasing public health burden to today's society.

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Chronic Traumatic Encephalopathy (CTE) is an established neurodegenerative disease that is closely associated with exposure to repetitive mild Traumatic Brain Injury (mTBI). The mechanisms responsible for its complex pathological changes remain largely elusive, despite a recent consensus to define the neuropathological criteria. Here, we describe a novel method to develop a model of CTE in Drosophila melanogaster (Drosophila ) in an attempt to identify the key genes and pathways that lead to the characteristic hyperphosphorylated tau accumulation and neuronal death in the brain.

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Abnormal accumulation of TDP-43 into cytoplasmic or nuclear inclusions with accompanying nuclear clearance, a common pathology initially identified in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), has also been found in Alzheimer' disease (AD). TDP-43 serves as a splicing repressor of nonconserved cryptic exons and that such function is compromised in brains of ALS and FTD patients, suggesting that nuclear clearance of TDP-43 underlies its inability to repress cryptic exons. However, whether TDP-43 cytoplasmic aggregates are a prerequisite for the incorporation of cryptic exons is not known.

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