The Blood Alcohol Concentration Testing Emergency Room Investigation Analysis Study: A 1-Year  Review of Blood Alcohol Concentration Testing in an Emergency Department

Elgammal, Ayman; Eves, Doireann; Albaghli, Abbas; Kane, Daniel; Durcan, Robert; Storey, David; Gilligan, Peadar

doi:10.1155/2015/410827

Cited by 6 publications

(3 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In all groups treated with ethanol, a concentration of 100 mM (equivalent to 460 mg/dL or 0.46%) for 24 h was used. This high concentration is consistent with the high (>400 mg/dL) blood alcohol concentrations (BACs) achieved in alcoholics in emergency rooms [42], including awake and conscious patients with a BAC of greater than 500 mg/dL [43]. Binge models in rodents that achieve similarly high BACs have also been used to model heavy drinking [44].…”

Section: Methodsmentioning

confidence: 62%

Ethanol Induction of Innate Immune Signals Across BV2 Microglia and SH-SY5Y Neuroblastoma Involves Induction of IL-4 and IL-13

et al. 2019

View full text Add to dashboard Cite

Innate immune signaling molecules, such as Toll-like receptors (TLRs), cytokines and transcription factor NFκB, are increased in post-mortem human alcoholic brain and may play roles in alcohol dependence and neurodegeneration. Innate immune signaling involves microglia -neuronal signaling which while poorly understood, may impact learning and memory. To investigate mechanisms of ethanol induction of innate immune signaling within and between brain cells, we studied immortalized BV2 microglia and SH-SY5Y human neuroblastoma to model microglial and neuronal signaling. Cells were treated alone or in co-culture using a Transwell system, which allows transfer of soluble mediators. We determined immune signaling mRNA using real-time polymerase chain reaction. Ethanol induced innate immune genes in both BV2 and SH-SY5Y cultured alone, with co-culture altering gene expression at baseline and following ethanol exposure. Co-culture blunted ethanol-induced high mobility group box protein 1 (HMGB1)-TLR responses, corresponding with reduced ethanol induction of several proinflammatory NFκB target genes. In contrast, co-culture resulted in ethanol upregulation of cytokines IL-4 and IL-13 in BV2 and corresponding receptors, that is, IL-4 and IL-13 receptors, in SH-SY5Y, suggesting induction of a novel signaling pathway. Co-culture reduction in HMGB1-TLR levels occurs in parallel with reduced proinflammatory gene induction and increased IL-4 and IL-13 ligands and receptors. Findings from these immortalized and tumor-derived cell lines could provide insight into microglial-neuronal interactions via release of soluble mediators in vivo.

show abstract

Section: Methodsmentioning

confidence: 62%

Ethanol Induction of Innate Immune Signals Across BV2 Microglia and SH-SY5Y Neuroblastoma Involves Induction of IL-4 and IL-13

et al. 2019

View full text Add to dashboard Cite

show abstract

“…As a positive control for induction of steatosis, we exposed the chips to fatty acids, a reproducible experimental method for induction of the steatotic phenotype ( Breher-Esch et al, 2018 ). Ethanol concentrations ranging from 0.08% to 0.16% were chosen to mimic the BAC of human patients after alcohol consumption ( Elgammal et al, 2015 ). A BAC of 0.08% is the upper limit for legal driving in the United States and United Kingdom.…”

Section: Resultsmentioning

confidence: 99%

Modeling alcohol-associated liver disease in a human Liver-Chip

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Ethanol concentrations ranging from 0.08% to 0.16% (i.e., 80 mg/ml to 160 mg/ml, or 17.4mM to 34mM) were chosen to mimic the alcohol concentrations found in the blood (BAC) of human patients after alcohol consumption 32 . For comparison, a BAC of 0.08% is the upper limit to for legal driving in the United States and the UK.…”

Section: Ethanol-induced Steatosis In the Liver-chipmentioning

confidence: 99%

Modeling alcoholic liver disease in a human Liver-Chip

Nawroth

et al. 2020

Preprint

View full text Add to dashboard Cite

Fatty liver disease (FLD), is a major public health burden that affects up to 30% of people in Western countries and leads to progressive liver injury, comorbidities, and increased mortality. Key risk factors for developing FLD are obesity and alcohol consumption, both of which are growing in prevalence worldwide. There is an urgent need for human-relevant preclinical models to improve our understanding of FLD progression to steatohepatitis and for the development of sensitive noninvasive diagnostics and therapies. Alcohol-induced liver disease (ALD) represents an ideal case for modeling FDL as ethanol exposure is a comparatively simpler trigger for experimental induction of the pathology, as opposed to the complexity of modeling the diet- and life-style induced FLD. Further, despite their different root causes several common characteristics in disease progression and deterioration of liver function in the two disease entities, highlighting the potential of an ALD microphysiological model for broad application in translational research. Here, we leverage our recently reported human Liver-Chip for toxicity applications, to expand the capabilities of the platform for broad application in translational research. We report the first in vitro modeling of ALD that uses human relevant blood alcohol concentrations (BAC) and affords multimodal profiling of clinically relevant endpoints. Our ALD Liver-Chip recapitulates established FLD markers in response to ethanol in a concentration-dependent manner, including lipid accumulation and oxidative stress. Importantly, we show that the ALD Liver-Chip supports the study of secondary insults, as patients with advanced ALD often show high blood endotoxin levels due to alcohol-associated increased intestinal permeability and barrier dysfunction. Moreover, owing to new developments in the design, the ALD Liver-Chip enables the measurement of structural changes of the bile canaliculi (BC) network as a novel in vitro quantitative readout of alcoholic liver toxicity. In summary, we report the development of a human ALD Liver-Chip as a new platform for modeling the progression of alcohol-induced liver injury with direct translation to clinical research.

show abstract

The Blood Alcohol Concentration Testing Emergency Room Investigation Analysis Study: A 1-Year Review of Blood Alcohol Concentration Testing in an Emergency Department

Cited by 6 publications

References 18 publications

Ethanol Induction of Innate Immune Signals Across BV2 Microglia and SH-SY5Y Neuroblastoma Involves Induction of IL-4 and IL-13

Ethanol Induction of Innate Immune Signals Across BV2 Microglia and SH-SY5Y Neuroblastoma Involves Induction of IL-4 and IL-13

Modeling alcohol-associated liver disease in a human Liver-Chip

Modeling alcoholic liver disease in a human Liver-Chip

Contact Info

Product

Resources

About