Degrees of alcohol intoxication in 117 hospitalized cases.

Adachi, Junko; Mizoi, Y; Fukunaga, Tetsuo; Ogawa, Yumi; Ueno, Yoshio; Imamichi, Hiroyuki

doi:10.15288/jsa.1991.52.448

Cited by 104 publications

(79 citation statements)

References 8 publications

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“…Notably, these blood levels are within the range (0.5-5.6 mg/ml; 10-125 mM) typically seen in alcoholic patients (Adachi et al, 1991 Post hoc analysis showed EtOH treated animals had more weight loss during exposure (Po0.0001); males had modestly more weight loss during exposure than females (10 vs 14% respectively, P ¼ 0.009), consistent with their higher EtOH levels.…”

Section: Chronic Etoh Exposure and Withdrawalsupporting

confidence: 61%

Neurotoxic Consequences of Chronic Alcohol Withdrawal: Expression Profiling Reveals Importance of Gender Over Withdrawal Severity

Hashimoto

Wiren

2007

Neuropsychopharmacol

111

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While women are more vulnerable than men to many of the medical consequences of alcohol abuse, the role of sex in the response to ethanol is controversial. Neuroadaptive responses that result in the hyperexcitability associated with withdrawal from chronic ethanol likely reflect gene expression changes. We have examined both genders for the effects of withdrawal on brain gene expression using mice with divergent withdrawal severity that have been selectively bred from a genetically heterogeneous population. A total of 295 genes were identified as ethanol regulated from each gender of each selected line by microarray analyses. Hierarchical cluster analysis of the arrays revealed that the transcriptional response correlated with sex rather than with the selected withdrawal phenotype. Consistent with this, gene ontology category over-representation analysis identified cell death and DNA/RNA binding as targeted classes of genes in females, while in males, protein degradation, and calcium ion binding pathways were more altered by alcohol. Examination of ethanolregulated genes and these distinct signaling pathways suggested enhanced neurotoxicity in females. Histopathological analysis of brain damage following ethanol withdrawal confirmed elevated cell death in female but not male mice. The sexually dimorphic response was observed irrespective of withdrawal phenotype. Combined, these results indicate a fundamentally distinct neuroadaptive response in females compared to males during chronic ethanol withdrawal and are consistent with observations that female alcoholics may be more vulnerable than males to ethanol-induced brain damage associated with alcohol abuse.

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Section: Chronic Etoh Exposure and Withdrawalsupporting

confidence: 61%

Neurotoxic Consequences of Chronic Alcohol Withdrawal: Expression Profiling Reveals Importance of Gender Over Withdrawal Severity

Hashimoto

Wiren

2007

Neuropsychopharmacol

111

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“…Culture medium is changed every 2 d. Control and ethanol-treated flasks are capped tightly with phenolic caps, and sealed with parafilm to limit the loss of ethanol. These measured doses range in equivalence to consumption levels that can be attained by social drinkers (60 mg/dL) to those attained by chronic alcoholics (320-620 mg/dL, 70-135 mM (81,82)), to levels above those typically attainable in chronic alcoholics (920 mg/dL). Our analysis indicates that there is no significant change in ethanol content within culture dishes over the exposure time period (Fig.…”

Section: Ethanol Treatmentmentioning

confidence: 99%

Modeling the Impact of Alcohol on Cortical Development in a Dish: Strategies from Mapping Neural Stem Cell Fate

Miranda

Santillano

Camarillo

et al. 2008

Alcohol

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SummaryDuring the second trimester period, neuroepithelial stem cells give birth to millions of new neuroblasts, which migrate away from their germinal zones to populate the developing brain and terminally differentiate into neurons. During this period, large numbers of cells are also eliminated by programmed cell death. Therefore, the second trimester constitutes an important critical period for neuronal proliferation, migration, differentiation and apoptosis. Substantial evidence indicates that teratogens like ethanol can interfere with neuronal maturation. However, there is a paucity of good model systems to study early, second trimester events. In vivo models are inherently interpretatively complex because cell proliferation, migration, differentiation, and death mechanisms occur concurrently in regions like the cerebral cortex. This temporal overlap of multiple developmental critical periods makes it difficult to evaluate the relative vulnerability of any individual critical period. Our laboratory has elected to utilize fetal rodent cerebral corticalderived neurosphere cultures as an experimental model of the second-trimester ventricular neuroepithelium. This model has enabled us to use flow cytometric approaches to identify neuroepithelial stem cell and progenitor sub-populations and to show that ethanol accelerates the maturation of neural stem cells. We have also developed a simplified mitogen-withdrawal/matrixadhesion paradigm to model the exit of neuroepithelial cells from the ventricular zone towards the subventricular zone and cortical plate, and their maturation into multipolar neurons. We can treat neurosphere cultures with ethanol to mimic exposure during the period of neuroepithelial proliferation and by using the step-wise maturation model, ask questions about the impact of prior ethanol exposure on the subsequent maturation of neurons as they migrate and undergo terminal differentiation. The combination of neurosphere culture and stepwise maturation models will enable us to dissect out the contributions of specific developmental critical periods to the overall teratology of a drug of abuse like ethanol.

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“…Twenty-four hours after trypsinization, cells were rinsed and incubated in serum-free medium with N-2 Supplement (Invitrogen) for 18 h, and then microglial cells were treated with either ethanol (10, 50, 100, or 200 mM; Merck Sharp and Dohme), LPS (50 ng/ml; Sigma-Aldrich), or LTA (1 g/ml purified lipoteichoic acid from Staphylococcus aureus; InvivoGen) for different times. Most of the ethanol concentrations used in the present study were in the range of the blood alcohol levels found among alcoholics (50 -125 mM) (27,28). In some experiments, microglia were treated with 50 mM ethanol for 24 or 48 h. Then, the microglia-conditional medium, with or without 50 mM ethanol, was collected, frozen, and stored at Ϫ80°C until used.…”

Section: Culture Of Microglial Cellsmentioning

confidence: 99%

Critical Role of TLR4 Response in the Activation of Microglia Induced by Ethanol

Fernández‐Lizarbe

Pascual

Guerri

2009

The Journal of Immunology

325

324

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Microglial cells are the primary immune effector cells in the brain and play a pivotal role in the neuroinflammatory processes associated with a variety of neurological and pathological disorders. Alcohol consumption induces brain damage, although the neuropathological processes are poorly understood. We previously suggested that ethanol promotes inflammatory processes in the brain, up-regulating inflammatory mediators and signaling pathways associated with IL-1RI/TLR4 receptors. In the present study we investigate whether ethanol induces microglia activation by stimulating TLR4 response and whether this response causes neuronal death and contributes to ethanol-induced neuroinflammatory damage. We demonstrate that ethanol activates microglía and stimulates NF-κB, MAPKs, and MyD88-independent (IFN regulatory factor-3, IFN-β) pathways to trigger the production of inflammatory mediators, causing neuronal death. The inflammatory response induced by ethanol is completely abrogated in microglia of TLR4-deficient mice (TLR4−/−), thus supporting the role of these receptors in microglia activation and neuronal death. In accord with the in vitro findings, acute ethanol administration induces microglia activation (CD11b+ cells) in cerebral cortex of TLR4+/+ mice, but not in TLR4−/− mice. Taken together, our results not only provide the first evidence of the critical role of the TLR4 response in the ethanol-induced microglia activation, but also new insight into the basic mechanisms participating in ethanol-induced neuroinflammatory damage.

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Degrees of alcohol intoxication in 117 hospitalized cases.

Cited by 104 publications

References 8 publications

Neurotoxic Consequences of Chronic Alcohol Withdrawal: Expression Profiling Reveals Importance of Gender Over Withdrawal Severity

Neurotoxic Consequences of Chronic Alcohol Withdrawal: Expression Profiling Reveals Importance of Gender Over Withdrawal Severity

Modeling the Impact of Alcohol on Cortical Development in a Dish: Strategies from Mapping Neural Stem Cell Fate

Critical Role of TLR4 Response in the Activation of Microglia Induced by Ethanol

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