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[PMID]:27749004
[Au] Autor:Gilpin NW; Weiner JL
[Ad] Endereço:Department of Physiology, Louisiana State University Health Sciences Center, New Orleans, LA.
[Ti] Título:Neurobiology of comorbid post-traumatic stress disorder and alcohol-use disorder.
[So] Source:Genes Brain Behav;16(1):15-43, 2017 Jan.
[Is] ISSN:1601-183X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Post-traumatic stress disorder (PTSD) and alcohol-use disorder (AUD) are highly comorbid in humans. Although we have some understanding of the structural and functional brain changes that define each of these disorders, and how those changes contribute to the behavioral symptoms that define them, little is known about the neurobiology of comorbid PTSD and AUD, which may be due in part to a scarcity of adequate animal models for examining this research question. The goal of this review is to summarize the current state-of-the-science on comorbid PTSD and AUD. We summarize epidemiological data documenting the prevalence of this comorbidity, review what is known about the potential neurobiological basis for the frequent co-occurrence of PTSD and AUD and discuss successes and failures of past and current treatment strategies. We also review animal models that aim to examine comorbid PTSD and AUD, highlighting where the models parallel the human condition, and we discuss the strengths and weaknesses of each model. We conclude by discussing key gaps in our knowledge and strategies for addressing them: in particular, we (1) highlight the need for better animal models of the comorbid condition and better clinical trial design, (2) emphasize the need for examination of subpopulation effects and individual differences and (3) urge cross-talk between basic and clinical researchers that is reflected in collaborative work with forward and reverse translational impact.
[Mh] Termos MeSH primário: Transtornos do Sistema Nervoso Induzidos por Álcool/fisiopatologia
Transtornos de Estresse Pós-Traumáticos/fisiopatologia
[Mh] Termos MeSH secundário: Transtornos do Sistema Nervoso Induzidos por Álcool/complicações
Transtornos do Sistema Nervoso Induzidos por Álcool/terapia
Animais
Seres Humanos
Transtornos de Estresse Pós-Traumáticos/complicações
Transtornos de Estresse Pós-Traumáticos/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161018
[St] Status:MEDLINE
[do] DOI:10.1111/gbb.12349


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[PMID]:28068280
[Au] Autor:Oyinbo CA; Igbigbi PS; Avwioro GO
[Ad] Endereço:Department of Human Anatomy, Faculty of Basic Medical Sciences, College of Health Sciences, Niger Delta University, Wilberforce Island, Bayelsa State, Nigeria
[Ti] Título:Landolphia owariensis Attenuates Alcohol-induced Cerebellar Neurodegeneration: Significance of Neurofilament Protein Alteration in the Purkinje Cells.
[So] Source:Folia Med (Plovdiv);58(4):241-249, 2016 12 01.
[Is] ISSN:0204-8043
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Alcohol-induced cerebellar neurodegeneration is a neuroadaptation that is associated with chronic alcohol abuse. Conventional drugs have been largely unsatisfactory in preventing neurodegeneration. Yet, multimodal neuro-protective therapeutic agents have been hypothesised to have high therapeutic potential for the treatment of CNS conditions; there is yet a dilemma of how this would be achieved. Contrarily, medicinal botanicals are naturally multimodal in their mechanism of action. AIM: The effect of L. owariensis was therefore assessed in alcohol-induced neurodegeneration of the cerebellar cortex in rats. MATERIALS AND METHODS: Two groups of rats were oro-gastrically fed thrice daily with 5 g/kg ethanol (25% w/v), and 5 g/kg ethanol (25% w/v) plus L. owariensis (100 mg/kg body weight) respectively in diluted nutritionally complete diet (50% v/v). A control group was correspondingly fed a nutritionally complete diet (50% v/v) made isocaloric with glucose. Cytoarchitectural study of the cerebellar cortex was examined with H&E. Immunocytochemical analysis was carried out with the use of monoclonal antibody anti-NF in order to detect alterations in the neuronal cytoskeleton. RESULTS: After 4 days of binge alcohol treatment, we observed that L. owariensis supplementation significantly lowered the levels of histologic and biochemical indices of neurodegeneration. The level of neurodegeneration and cytoarchitecture distortion of the cerebellar cortex of rats exposed to ethanol was reduced by L. owariensis. Neurofilament-immunoreactivity (NF-IR) was evoked in the Purkinje cells of rats that received L. owariensis supplement. CONCLUSIONS: L. owariensis attenuates alcohol-induced cerebellar degeneration in the rat by alleviating oxidative stress and alteration of NF protein expression in the Purkinje cells.
[Mh] Termos MeSH primário: Apocynaceae
Depressores do Sistema Nervoso Central/toxicidade
Cerebelo/efeitos dos fármacos
Etanol/toxicidade
Proteínas de Neurofilamentos/efeitos dos fármacos
Preparações de Plantas/farmacologia
Células de Purkinje/efeitos dos fármacos
[Mh] Termos MeSH secundário: Transtornos do Sistema Nervoso Induzidos por Álcool
Animais
Doenças Cerebelares
Cerebelo/metabolismo
Modelos Animais de Doenças
Imuno-Histoquímica
Masculino
Doenças Neurodegenerativas
Proteínas de Neurofilamentos/metabolismo
Células de Purkinje/metabolismo
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Central Nervous System Depressants); 0 (Neurofilament Proteins); 0 (Plant Preparations); 3K9958V90M (Ethanol)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170110
[St] Status:MEDLINE


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[PMID]:27460131
[Au] Autor:Perry CJ
[Ad] Endereço:Behavioural Neuroscience Division, Florey Institute for Neuroscience and Mental Health, Kenneth Myer Building, 30 Royal Pde, Parkville, VIC, 3010, Australia. Christina.perry@florey.edu.au.
[Ti] Título:Cognitive Decline and Recovery in Alcohol Abuse.
[So] Source:J Mol Neurosci;60(3):383-389, 2016 Nov.
[Is] ISSN:1559-1166
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alcohol consumption triggers a neuroinflammatory response which, if prolonged, can lead to substantial volume loss in both gray and white matter. This brain injury is associated with characteristic cognitive deficits, and, in extreme cases, with dementia. Even mild cognitive impairment creates a significant hurdle for alcohol rehabilitation, because the domains that are affected tend to be those important for sustaining abstinence. Thus, cognitive decline induced by alcohol contributes to the persistence of alcoholism. Here, I present converging data from animal and clinical studies that show how alcohol affects the brain and behavior. Although there is currently no targeted treatment for overcoming alcohol-induced cognitive decline, emerging evidence suggests that physical activity is both protective and restorative. This is a potential avenue for future programs targeted at treating alcohol abuse.
[Mh] Termos MeSH primário: Transtornos do Sistema Nervoso Induzidos por Álcool/fisiopatologia
Cognição
Demência/fisiopatologia
Terapia por Exercício
[Mh] Termos MeSH secundário: Transtornos do Sistema Nervoso Induzidos por Álcool/patologia
Transtornos do Sistema Nervoso Induzidos por Álcool/reabilitação
Animais
Demência/patologia
Demência/reabilitação
Seres Humanos
Recuperação de Função Fisiológica
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160728
[St] Status:MEDLINE


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[PMID]:27391464
[Au] Autor:Drake-Pérez M; Marco de Lucas E; Lyo J; Fernández-Torre JL
[Ad] Endereço:Department of Radiology, Marqués de Valdecilla University Hospital, Santander, Cantabria, Spain; Biomedical Research Institute (IDIVAL), Santander, Spain. Electronic address: drake.marta@gmail.com.
[Ti] Título:Neuroimaging features in subacute encephalopathy with seizures in alcoholics (SESA syndrome).
[So] Source:Seizure;40:102-7, 2016 Aug.
[Is] ISSN:1532-2688
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To describe the neuroimaging findings in subacute encephalopathy with seizures in alcoholics (SESA syndrome). METHODS: We reviewed all cases reported previously, as well as 4 patients diagnosed in our center. We included a total of 8 patients. All subjects had clinical and EEG findings compatible with SESA syndrome and at least one MRI study that did not show other underlying condition that could be responsible for the clinical presentation. RESULTS: Initial MRI studies revealed the following features: cortical-subcortical areas of increased T2/FLAIR signal and restricted diffusion (6 patients), hyperperfusion (3 patients), atrophy (5 patients), chronic microvascular ischemic changes (4 patients). Follow-up MRI was performed in half of the patients, all showing a resolution of the hyperintense lesions, but developing focal atrophic changes in 75%. CONCLUSIONS: SESA syndrome should be included among the alcohol-related encephalopathies. Its radiological features include transient cortical-subcortical T2-hyperintense areas with restricted diffusion (overlapping the typical findings in status epilepticus) observed in a patient with atrophy and chronic multifocal vascular lesions.
[Mh] Termos MeSH primário: Transtornos do Sistema Nervoso Induzidos por Álcool/diagnóstico por imagem
Convulsões/diagnóstico por imagem
[Mh] Termos MeSH secundário: Transtornos do Sistema Nervoso Induzidos por Álcool/complicações
Seres Humanos
Convulsões/etiologia
Síndrome
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170827
[Lr] Data última revisão:
170827
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160709
[St] Status:MEDLINE


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[PMID]:27030756
[Au] Autor:Schindler AG; Soden ME; Zweifel LS; Clark JJ
[Ad] Endereço:Departments of Psychiatry and Behavioral Sciences and.
[Ti] Título:Reversal of Alcohol-Induced Dysregulation in Dopamine Network Dynamics May Rescue Maladaptive Decision-making.
[So] Source:J Neurosci;36(13):3698-708, 2016 Mar 30.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Alcohol is the most commonly abused substance among adolescents, promoting the development of substance use disorders and compromised decision-making in adulthood. We have previously demonstrated, with a preclinical model in rodents, that adolescent alcohol use results in adult risk-taking behavior that positively correlates with phasic dopamine transmission in response to risky options, but the underlying mechanisms remain unknown. Here, we show that adolescent alcohol use may produce maladaptive decision-making through a disruption in dopamine network dynamics via increased GABAergic transmission within the ventral tegmental area (VTA). Indeed, we find that increased phasic dopamine signaling after adolescent alcohol use is attributable to a midbrain circuit, including the input from the pedunculopontine tegmentum to the VTA. Moreover, we demonstrate that VTA dopamine neurons from adult rats exhibit enhanced IPSCs after adolescent alcohol exposure corresponding to decreased basal dopamine levels in adulthood that negatively correlate with risk-taking. Building on these findings, we develop a model where increased inhibitory tone on dopamine neurons leads to a persistent decrease in tonic dopamine levels and results in a potentiation of stimulus-evoked phasic dopamine release that may drive risky choice behavior. Based on this model, we take a pharmacological approach to the reversal of risk-taking behavior through normalization of this pattern in dopamine transmission. These results isolate the underlying circuitry involved in alcohol-induced maladaptive decision-making and identify a novel therapeutic target. SIGNIFICANCE STATEMENT: One of the primary problems resulting from chronic alcohol use is persistent, maladaptive decision-making that is associated with ongoing addiction vulnerability and relapse. Indeed, studies with the Iowa Gambling Task, a standard measure of risk-based decision-making, have reliably shown that alcohol-dependent individuals make riskier, more maladaptive choices than nondependent individuals, even after periods of prolonged abstinence. Using a preclinical model, in the current work, we identify a selective disruption in dopamine network dynamics that may promote maladaptive decision-making after chronic adolescent alcohol use and demonstrate its pharmacological reversal in adulthood. Together, these results highlight a novel neural mechanism underlying heightened risk-taking behavior in alcohol-dependent individuals and provide a potential therapeutic target for further investigation.
[Mh] Termos MeSH primário: Transtornos do Sistema Nervoso Induzidos por Álcool/complicações
Depressores do Sistema Nervoso Central/toxicidade
Tomada de Decisões/efeitos dos fármacos
Dopamina/metabolismo
Neurônios Dopaminérgicos/efeitos dos fármacos
Etanol/toxicidade
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Modelos Animais de Doenças
Estimulação Elétrica
Técnicas In Vitro
Potenciais Pós-Sinápticos Inibidores/efeitos dos fármacos
Masculino
Microdiálise
Vias Neurais/efeitos dos fármacos
Técnicas de Patch-Clamp
Ratos
Ratos Sprague-Dawley
Assunção de Riscos
Área Tegmentar Ventral/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Central Nervous System Depressants); 3K9958V90M (Ethanol); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160401
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.4394-15.2016


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[PMID]:26893017
[Au] Autor:Brotherton AL; Hamilton EP; Kloss HG; Hammond DA
[Ad] Endereço:University of Arkansas for Medical Sciences Medical Center, Little Rock, Arkansas.
[Ti] Título:Propofol for Treatment of Refractory Alcohol Withdrawal Syndrome: A Review of the Literature.
[So] Source:Pharmacotherapy;36(4):433-42, 2016 Apr.
[Is] ISSN:1875-9114
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The authors evaluated all available evidence on the use of propofol as an adjuvant for the treatment of resistant alcohol withdrawal syndrome (AWS) in comparison to other therapies. A comprehensive PubMed search (1966-December 2015) was conducted using the search terms propofol, alcohol withdrawal, and drug therapy. Articles were cross-referenced for other citations. Clinical studies, case series, and case reports published in the English language assessing the use of propofol in adult patients for treatment of AWS were reviewed for inclusion. Propofol is a sedative-hypnotic that exerts its actions through agonism of GABAA receptors at a different binding site than benzodiazepines and reduces glutamatergic activity through N-methyl-d-aspartase (NMDA) receptor blockade. Dosages from 5 to 100 µg/kg/minute reduced AWS symptoms with frequent development of hypotension and requirement for mechanical ventilation. Patients on propofol often experienced longer durations of mechanical ventilation and length of stay, which may be attributed to more-resistant cases of AWS. When propofol was compared with dexmedetomidine as adjuncts in AWS, both agents showed similar benzodiazepine- and haloperidol-sparing effects. Dexmedetomidine was associated with more numerical rates of bradycardia, while propofol was associated with more numerical instances of hypotension. Dexmedetomidine was used more frequently in nonintubated patients. The available data assessing the utility of propofol for AWS exhibited significant heterogeneity. Propofol may be useful in a specific population of patients with AWS, limited to those who are not clinically responding to first-line therapy with benzodiazepines. Specifically, propofol should be considered in patients who are refractory to or not candidates for other adjuvant therapies, patients already requiring mechanical ventilation, or those with seizure activity or refractory delirium tremens. In severe, refractory AWS, adjuvant therapy with propofol may be considered but requires further research to recommend its use either preferentially or as monotherapy.
[Mh] Termos MeSH primário: Transtornos do Sistema Nervoso Induzidos por Álcool/tratamento farmacológico
Resistência a Medicamentos
Medicina Baseada em Evidências
Agonistas de Receptores de GABA-A/uso terapêutico
Hipnóticos e Sedativos/uso terapêutico
Medicina de Precisão
Propofol/uso terapêutico
[Mh] Termos MeSH secundário: Agonistas de Receptores Adrenérgicos alfa 2/administração & dosagem
Agonistas de Receptores Adrenérgicos alfa 2/efeitos adversos
Agonistas de Receptores Adrenérgicos alfa 2/uso terapêutico
Adulto
Transtornos do Sistema Nervoso Induzidos por Álcool/fisiopatologia
Transtornos do Sistema Nervoso Induzidos por Álcool/terapia
Bradicardia/induzido quimicamente
Bradicardia/fisiopatologia
Quimioterapia Adjuvante/efeitos adversos
Dexmedetomidina/administração & dosagem
Dexmedetomidina/efeitos adversos
Dexmedetomidina/uso terapêutico
Relação Dose-Resposta a Droga
Agonistas de Receptores de GABA-A/administração & dosagem
Agonistas de Receptores de GABA-A/efeitos adversos
Seres Humanos
Hipnóticos e Sedativos/administração & dosagem
Hipnóticos e Sedativos/efeitos adversos
Hipotensão/induzido quimicamente
Hipotensão/fisiopatologia
Hipotensão/terapia
Tempo de Internação
Guias de Prática Clínica como Assunto
Propofol/administração & dosagem
Propofol/efeitos adversos
Respiração Artificial
Índice de Gravidade de Doença
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adrenergic alpha-2 Receptor Agonists); 0 (GABA-A Receptor Agonists); 0 (Hypnotics and Sedatives); 67VB76HONO (Dexmedetomidine); YI7VU623SF (Propofol)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170105
[Lr] Data última revisão:
170105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160220
[St] Status:MEDLINE
[do] DOI:10.1002/phar.1726


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[PMID]:26786850
[Au] Autor:Riar AK; Narasimhan M; Rathinam ML; Henderson GI; Mahimainathan L
[Ad] Endereço:Department of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, 3601 4th Street, Lubbock, TX, 79430, USA.
[Ti] Título:Ethanol induces cytostasis of cortical basal progenitors.
[So] Source:J Biomed Sci;23:6, 2016 Jan 19.
[Is] ISSN:1423-0127
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Developing brain is a major target for alcohol's actions and neurological/functional abnormalities include microencephaly, reduced frontal cortex, mental retardation and attention-deficits. Previous studies have shown that ethanol altered the lateral ventricular neuroepithelial cell proliferation. However, the effect of ethanol on subventricular basal progenitors which generate majority of the cortical layers is not known. METHODS: We utilized spontaneously immortalized rat brain neuroblasts obtained from cultures of 18-day-old fetal rat cerebral cortices using in vitro ethanol exposures and an in utero binge model. In the in vitro acute model, cells were exposed to 86 mM ethanol for 8, 12 and 24 h. The second in vitro model comprised of chronic intermittent ethanol (CIE) exposure which consisted of 14 h of ethanol treatment followed by 10 h of withdrawal with three repetitions. RESULTS: E18 neuroblasts expressing Tbr2 representing immature basal progenitors displayed significant reduction of proliferation in response to ethanol in both the models. The decreased proliferation was accompanied by absence of apoptosis or autophagy as illustrated by FACS analysis and expression of apoptotic and autophagic markers. The BrdU incorporation assay indicated that ethanol enhanced the accumulation of cells at G1 with reduced cell number in S phase. In addition, the ethanol-inhibited basal neuroblasts proliferation was connected to decrease in cyclin D1 and Rb phosphorylation indicating cell cycle arrest. Further, in utero ethanol exposure in pregnant rats during E15-E18 significantly decreased Tbr2 and cyclin D1 positive cell number in cerebral cortex of embryos as assessed by cell sorting analysis by flow cytometry. CONCLUSIONS: Altogether, the current findings demonstrate that ethanol impacts the expansion of basal progenitors by inducing cytostasis that might explain the anomalies of cortico-cerebral development associated with fetal alcohol syndrome.
[Mh] Termos MeSH primário: Transtornos do Sistema Nervoso Induzidos por Álcool/metabolismo
Etanol/toxicidade
Transtornos do Espectro Alcoólico Fetal/metabolismo
Lobo Frontal/metabolismo
Fase G1/efeitos dos fármacos
Células-Tronco Neurais/metabolismo
Fase S/efeitos dos fármacos
[Mh] Termos MeSH secundário: Transtornos do Sistema Nervoso Induzidos por Álcool/patologia
Animais
Ciclina D1/metabolismo
Feminino
Transtornos do Espectro Alcoólico Fetal/patologia
Lobo Frontal/patologia
Células-Tronco Neurais/patologia
Gravidez
Ratos
Proteínas com Domínio T-Box/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Ccnd1 protein, rat); 0 (T-Box Domain Proteins); 136601-57-5 (Cyclin D1); 3K9958V90M (Ethanol)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160121
[St] Status:MEDLINE
[do] DOI:10.1186/s12929-016-0225-8


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[PMID]:26848494
[Au] Autor:Lee JH; Heo SH; Chang DI
[Ti] Título:Early-stage Alcoholic Cerebellar Degeneration: Diagnostic Imaging Clues.
[So] Source:J Korean Med Sci;30(11):1539, 2015 Nov.
[Is] ISSN:1598-6357
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Mh] Termos MeSH primário: Transtornos do Sistema Nervoso Induzidos por Álcool/patologia
Alcoolismo/patologia
Cerebelo/patologia
Imagem por Ressonância Magnética/métodos
Degenerações Espinocerebelares/etiologia
Degenerações Espinocerebelares/patologia
[Mh] Termos MeSH secundário: Idoso
Transtornos do Sistema Nervoso Induzidos por Álcool/etiologia
Alcoolismo/complicações
Diagnóstico Diferencial
Diagnóstico Precoce
Seres Humanos
Masculino
Reprodutibilidade dos Testes
Sensibilidade e Especificidade
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1608
[Cu] Atualização por classe:160207
[Lr] Data última revisão:
160207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160206
[St] Status:MEDLINE


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[PMID]:26737712
[Au] Autor:Aarabi P; Norouzi N; Dear T; Carver S; Bromberg S; Gray S; Kahan M; Borgundvaag B
[Ti] Título:A quantitative evaluation of alcohol withdrawal tremors.
[So] Source:Conf Proc IEEE Eng Med Biol Soc;2015:6215-8, 2015.
[Is] ISSN:1557-170X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This paper evaluates the relation between Alcohol Withdrawal Syndrome tremors in the left and right hands of patients. By analyzing 122 recordings from 61 patients in emergency departments, we found a weak relationship between the left and right hand tremor frequencies (correlation coefficient of 0.63). We found a much stronger relationship between the expert physician tremor ratings (on CIWA-Ar 0-7 scale) of the two hands, with a correlation coefficient of 0.923. Next, using a smartphone to collect the tremor data and using a previously developed model for obtaining estimated tremor ratings, we also found a strong correlation (correlation coefficient of 0.852) between the estimates of each hand. Finally, we evaluated different methods of combining the data from the two hands for obtaining a single tremor rating estimate, and found that simply averaging the tremor ratings of the two hands results in the lowest tremor estimate error (an RMSE of 0.977). Looking at the frequency dependence of this error, we found that higher frequency tremors had a much lower estimation error (an RMSE of 1.102 for tremors with frequencies in the 3-6Hz range as compared to 0.625 for tremors with frequencies in the 7-10Hz range).
[Mh] Termos MeSH primário: Transtornos do Sistema Nervoso Induzidos por Álcool/diagnóstico
Mãos/fisiopatologia
Síndrome de Abstinência a Substâncias/diagnóstico
Tremor/diagnóstico
[Mh] Termos MeSH secundário: Acelerometria
Transtornos do Sistema Nervoso Induzidos por Álcool/fisiopatologia
Serviço Hospitalar de Emergência
Seres Humanos
Atividade Motora
Análise de Regressão
Reprodutibilidade dos Testes
Smartphone
Síndrome de Abstinência a Substâncias/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1609
[Cu] Atualização por classe:160107
[Lr] Data última revisão:
160107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160107
[St] Status:MEDLINE
[do] DOI:10.1109/EMBC.2015.7319812


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[PMID]:26610589
[Au] Autor:Natarajan SK; Pachunka JM; Mott JL
[Ad] Endereço:Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, 985870 Nebraska Medical Center, Omaha, NE 68198, USA. s.natarajan@unmc.edu.
[Ti] Título:Role of microRNAs in Alcohol-Induced Multi-Organ Injury.
[So] Source:Biomolecules;5(4):3309-38, 2015 Nov 20.
[Is] ISSN:2218-273X
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Alcohol consumption and its abuse is a major health problem resulting in significant healthcare cost in the United States. Chronic alcoholism results in damage to most of the vital organs in the human body. Among the alcohol-induced injuries, alcoholic liver disease is one of the most prevalent in the United States. Remarkably, ethanol alters expression of a wide variety of microRNAs that can regulate alcohol-induced complications or dysfunctions. In this review, we will discuss the role of microRNAs in alcoholic pancreatitis, alcohol-induced liver damage, intestinal epithelial barrier dysfunction, and brain damage including altered hippocampus structure and function, and neuronal loss, alcoholic cardiomyopathy, and muscle damage. Further, we have reviewed the role of altered microRNAs in the circulation, teratogenic effects of alcohol, and during maternal or paternal alcohol consumption.
[Mh] Termos MeSH primário: Transtornos do Sistema Nervoso Induzidos por Álcool/genética
Cardiomiopatia Alcoólica/genética
Hepatopatias Alcoólicas/genética
MicroRNAs/genética
Pancreatite Alcoólica/genética
[Mh] Termos MeSH secundário: Transtornos do Sistema Nervoso Induzidos por Álcool/metabolismo
Animais
Cardiomiopatia Alcoólica/metabolismo
Seres Humanos
Hepatopatias Alcoólicas/metabolismo
Pancreatite Alcoólica/metabolismo
RNA Longo não Codificante/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (MicroRNAs); 0 (RNA, Long Noncoding)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151128
[St] Status:MEDLINE
[do] DOI:10.3390/biom5043309



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