bluuebunny/crossref_metadata_2025_split huggingface dataset:
Alcohol Intoxication Following Muscle Contraction in Mice Decreases Muscle Protein Synthesis But Not mTOR Signal Transduction
Authors: Steiner Jennifer L. , Lang Charles H. 
Published: January 2015

BackgroundAlcohol (ethanol [EtOH]) intoxication antagonizes stimulation of muscle protein synthesis and mammalian target of rapamycin (mTOR) signaling. However, whether the anabolic response can be reversed when alcohol is consumed after the stimulus is unknown.MethodsA single bout of electrically stimulated muscle contractions (10 sets of 6 contractions) was induced in fasted male C57BL/6 mice 2 hours prior to alcohol intoxication. EtOH was injected intraperitoneally (3 g/kg), and the gastrocnemius/plantaris muscle complex was collected 2 hours later from the stimulated and contralateral unstimulated control leg.ResultsMuscle contraction increased protein synthesis 28% in control mice, while EtOH abolished this stimulation‐induced increase. Further, EtOH suppressed the rate of synthesis ~75% compared to control muscle irrespective of stimulation. This decrease was associated with impaired protein elongation as EtOH increased the phosphorylation of eEF2 Thr56. In contrast, stimulation‐induced increases in mTOR protein complex‐1 (mTORC1) (S6K1 Thr421/Ser424, S6K1 Thr389, rpS6 Ser240/244, and 4E‐BP1 Thr37/46) and mitogen‐activated protein kinase (MAPK) (JNK Thr183/Tyr185, p38 Thr180/Tyr182, and rpS6S235/236) signaling were not reversed by acute EtOH.ConclusionsThese data suggest that EtOH‐induced decreases in protein synthesis in fasted mice may be independent of mTORC1 and MAPK signaling following muscle contraction and instead due to the antagonistic actions of EtOH on mRNA translation elongation. Therefore, EtOH suppresses the contraction‐induced increase in protein synthesis, and over time has the potential to prevent skeletal muscle hypertrophy induced by repeated muscle contraction.
Mediation of Cognitive Bias Modification for Alcohol Addiction via Stimulus‐Specific Alcohol Avoidance Association
Authors: Gladwin Thomas E. , Rinck Mike , Eberl Carolin , Becker Eni S. , Lindenmeyer Johannes , Wiers Reinout W. 
Published: January 2015

BackgroundCognitive bias modification (CBM) studies have provided evidence that cognitive biases play a causal role in alcohol use disorders. In this study, data from a CBM experiment in alcoholic patients were re‐analyzed. In the original study, no mediation by associations measured with an Implicit Association Test (IAT) was found. In this study, we explored the possibility that relevant alcohol‐related automatic processes may be cue‐specific.MethodsData from a previous clinical study in a sample of 214 alcohol‐addicted patients were re‐analyzed. Patients were assigned to a CBM intervention or control condition, performed an alcohol–approach IAT, and were followed up for relapse data a year after training. In this study, bias scores measured via the IAT were calculated and analyzed separately for different stimulus categories: Alcohol, Soft drink, Approach, and Avoid.ResultsTraining reversed the alcohol–approach bias for all categories. This reversal of bias also predicted reduced relapse, but involved a complex stimulus category‐dependent pattern in which an avoidance bias for Alcohol stimuli was most predictive of reduced relapse.ConclusionsThe results contribute to evidence that CBM indeed affects relapse probability via changes in automatic processes, although future study is needed to determine the precise nature of mediating processes. Automatic processes underlying alcohol‐related associations may be stimulus‐specific, which may be important for the methods of future studies involving implicit measures.
Ethanol Intake Under Social Circumstances or Alone inSprague–Dawley Rats: Impact of Age, Sex, Social Activity, and Social Anxiety‐Like Behavior
Authors: Varlinskaya Elena I. , Truxell Eric M. , Spear Linda P. 
Published: January 2015

BackgroundIn human adolescents, heavy drinking is often predicted by high sociability in males and high social anxiety in females. This study assessed the impact of baseline levels of social activity and social anxiety‐like behavior in group‐housed adolescent and adult male and femaleSprague–Dawley rats on ethanol (EtOH) intake when drinking alone or in a social group.MethodsSocial activity and anxiety‐like behavior initially were assessed in a modified social interaction test, followed by 6 drinking sessions that occurred every other day in animals given ad libitum food and water. Sessions consisted of 30‐minute access to 10%EtOHin a “supersac” (3% sucrose + 0.1% saccharin) solution given alone as well as in groups of 5 same‐sex littermates, with order of the alternating session types counterbalanced across animals.ResultsAdolescent males and adults of both sexes overall consumed moreEtOHunder social than alone circumstances, whereas adolescent females ingested moreEtOHwhen alone. Highly socially active adolescent males demonstrated elevated levels ofEtOHintake relative to their low and medium socially active counterparts when drinking in groups, but not when tested alone. Adolescent females with high levels of social anxiety‐like behavior demonstrated the highestEtOHintake under social, but not alone circumstances. Among adults, baseline levels of social anxiety‐like behavior did not contribute to individual differences inEtOHintake in either sex.ConclusionsThe results clearly demonstrate that in adolescent rats, but not their adult counterparts, responsiveness to a social peer predictsEtOHintake in a social setting—circumstances under which drinking typically occurs in human adolescents. High levels of social activity in males and high levels of social anxiety‐like behavior in females were associated with elevated social drinking, suggesting that males ingestEtOHfor its socially enhancing properties, whereas females ingestEtOHfor its socially anxiolytic effects.
Social Network Moderators of Naltrexone and Behavioral Treatment Effects on Heavy Drinking in the COMBINE Study
Authors: Worley Matthew J. , Witkiewitz Katie , Brown Sandra A. , Kivlahan Daniel R. , Longabaugh Richard 
Published: January 2015

BackgroundOral naltrexone is an efficacious medication for treatment of alcohol dependence, but small effect sizes and variability in outcomes suggest the presence of person‐level moderators of naltrexone response. Identification of contextual or psychosocial moderators may assist in guiding clinical recommendations. Given the established importance of social networks in drinking outcomes, as well as the potential effects of naltrexone in reducing cue reactivity which may be especially important among those with more heavy drinkers and more alcohol cues in their networks, we examined pretreatment social network variables as potential moderators of naltrexone treatment effects in the COMBINE study.MethodsThe sample included all COMBINE study participants in medication conditions with full data on the Important People Inventory (IPI) and covariates at intake (N = 1,197). The intake IPI assessed whether participants had any frequent drinkers in their network and the average frequency of contact with these drinkers. The effects of treatment condition, pretreatment network variables, and their interactions on percent heavy drinking days were tested in hierarchical linear models, controlling for demographics and baseline clinical covariates.ResultsIn treatment conditions involving medical management and combined behavioral intervention (CBI), the effects of active naltrexone on heavy drinking were significantly greater for individuals with frequent drinkers in their network (z = −2.66, p < 0.01) and greater frequency of contact with those drinkers (z = −3.19, p < 0.01). These network variables did not moderate the effects of active naltrexone without CBI.ConclusionsWhen delivered in conjunction with behavioral interventions, naltrexone can be more potent for alcohol‐dependent adults who have greater contact with frequent drinkers prior to treatment, which may indicate patterns of environmental exposure to alcohol. Contextual, social risk factors are a potential avenue to guide personalized treatment of alcohol dependence.
Apoptotic Cell Death and Temporal Expression of Apoptotic Proteins Bcl‐2 and Bax in the Hippocampus, Following Binge Ethanol in the Neonatal Rat Model
Authors: Smith Caine C. , Guévremont Diane , Williams Joanna M. , Napper Ruth M. A. 
Published: January 2015

BackgroundBinge‐like ethanol (EtOH) exposure during the early rat neonatal period results in acute cell loss in specific brain regions, but such acute cell death has not been well established in the hippocampus. Binge alcohol exposure can also result in protein expression changes in the cerebellum that could alter cell fate, but this has not been reported for the hippocampal subregions. This study investigates acute apoptotic cell death in hippocampal regions CA1, CA3, and dentate gyrus (DG) following a binge EtOH exposure on postnatal day (PN) 6, PN8, or PN6 + 8 and the alteration in pro‐ and anti‐apoptotic proteins following a single EtOH binge on PN6.MethodsApoptotic cell death was quantified 12 hours after EtOH binge exposure using the optical fractionator method. Western blot analysis determined expression of pro‐apoptotic Bax and anti‐apoptotic Bcl‐2, 12, 24, and 48 hours after binge EtOH exposure on PN6. The Bcl‐2:Bax ratio was used as a measure of vulnerability to apoptosis.ResultsAcute apoptosis increased significantly 12 hours following PN6 or 8 EtOH exposure in CA1, CA3, and DG, but the magnitude of apoptotic cell death was significantly greater in CA1 than in CA3 and DG, which did not differ. Significant cell death was not detected when a PN8 EtOH exposure was preceded by exposure on PN6. Binge EtOH exposure on PN6 resulted in a significant increase in expression of Bcl‐2 and the Bcl‐2:Bax ratio in the CA1/DG region at 24 hours after EtOH exposure on PN6. The Bcl‐2:Bax ratio in the CA3 region was not altered.ConclusionsThis study shows that repeated binge exposure does not have a cumulative effect on the magnitude of acute apoptotic cell death. This finding may be explained in part by changes in the Bcl‐2:Bax ratio after a single binge EtOH exposure.
β‐Endorphin Neuronal Transplantation Into the Hypothalamus Alters Anxiety‐Like Behaviors in Prenatal Alcohol‐Exposed Rats and Alcohol‐Non‐Preferring and Alcohol‐Preferring Rats
Authors: Logan Ryan W. , Wynne Olivia , Maglakelidze George , Zhang Changqing , O'Connell Stephanie , Boyadjieva Nadka I. , Sarkar Dipak K. 
Published: January 2015

BackgroundAlcohol exposure has adverse effects on stress physiology and behavioral reactivity. This is suggested to be due, in part, to the effect of alcohol on β‐endorphin (β‐EP)‐producing neurons in the hypothalamus. In response to stress, β‐EP normally provides negative feedback to the hypothalamic–pituitary–adrenal axis and interacts with other neurotransmitter systems in the amygdala to regulate behavior. We examined whether β‐EP neuronal function in the hypothalamus reduces the corticosterone response to acute stress, attenuates anxiety‐like behaviors, and modulates alcohol drinking in rats.MethodsTo determine whether β‐EP neuronal transplants modulate the stress response, anxiety behavior, and alcohol drinking, we implanted differentiated β‐EP neurons into the paraventricular nucleus (PVN) of the hypothalamus of normal, prenatal alcohol‐exposed, and alcohol‐preferring (P) and alcohol‐non‐preferring (NP) rats. We then assessed corticosterone levels in response to acute restraint stress and other markers of stress response in the brain and anxiety‐like behaviors in the elevated plus maze and open‐field assays.ResultsWe showed that β‐EP neuronal transplants into the PVN reduced the peripheral corticosterone response to acute stress and attenuated anxiety‐like behaviors. Similar transplants completely reduced the hypercorticosterone response and elevated anxiety behaviors in prenatal alcohol‐exposed adult rats. Moreover, we showed that β‐EP reduced anxiety behavior in P rats with minimal effects on alcohol drinking during and following restraint stress.ConclusionsThese data further establish a role of β‐EP neurons in the hypothalamus for regulating physiological stress response and anxiety behavior and resemble a potential novel therapy for treating stress‐related psychiatric disorders in prenatal alcohol‐exposed children and those genetically predisposed to increased alcohol consumption.
The cerebellum on cocaine: plasticity and metaplasticity
Authors: Vazquez‐Sanroman Dolores , Leto Ketty , Cerezo‐Garcia Miguel , Carbo‐Gas María , Sanchis‐Segura Carla , Carulli Daniela , Rossi Ferdinando , Miquel Marta 
Published: January 2015

AbstractDespite the fact that several data have supported the involvement of the cerebellum in the functional alterations observed after prolonged cocaine use, this brain structure has been traditionally ignored and excluded from the circuitry affected by addictive drugs. In the present study, we investigated the effects of a chronic cocaine treatment on molecular and structural plasticity in the cerebellum, including BDNF, D3 dopamine receptors, ΔFosB, the Glu2 AMPA receptor subunit, structural modifications in Purkinje neurons and, finally, the evaluation of perineuronal nets (PNNs) in the projection neurons of the medial nucleus, the output of the cerebellar vermis. In the current experimental conditions in which repeated cocaine treatment was followed by a 1‐week withdrawal period and a new cocaine challenge, our results showed that cocaine induced a large increase in cerebellar proBDNF levels and its expression in Purkinje neurons, with the mature BDNF expression remaining unchanged. Together with this, cocaine‐treated mice exhibited a substantial enhancement of D3 receptor levels. Both ΔFosB and AMPA receptor Glu2 subunit expressions were enhanced in cocaine‐treated animals. Significant pruning in Purkinje dendrite arborization and reduction in the size and density of Purkinje boutons contacting deep cerebellar projection neurons accompanied cocaine‐dependent increase in proBDNF. Cocaine‐associated effects point to the inhibitory Purkinje function impairment, as was evidenced by lower activity in these cells. Moreover, the probability of any remodelling in Purkinje synapses appears to be decreased due to an upregulation of extracellular matrix components in the PNNs surrounding the medial nuclear neurons.
The harmful dysfunction model of alcohol use disorder: revised criteria to improve the validity of diagnosis and prevalence estimates
Authors: Wakefield Jerome C. , Schmitz Mark F. 
Published: January 2015

AbstractAimsTo formulate harmful dysfunction (HD) diagnostic criteria for alcohol use disorder (AUD) and test whether they increase validity relative to standard DSM criteria, as evidenced by lowered prevalence, increased validator levels including service use, severity and family history and enhanced specificity.DesignDSM‐IV AUD, DSM‐IV dependence, DSM‐5 AUD and HD AUD definitions were compared on eight validity related tests using nationally representative community data.SettingUnited States.ParticipantsNational Epidemiologic Survey of Alcoholism and Related Conditions (NESARC) respondents, aged 18–54 years (wave 1, n = 29 673; wave 2, n = 24 244).MeasuresNESARC DSM‐IV and DSM‐5 criteria were taken from published studies. Whereas DSM‐5 diagnosis requires any two AUD symptoms, HD criteria were constructed from NESARC items to require symptoms of both impaired‐control dysfunction [withdrawal, drink to prevent/stop withdrawal, cannot stop/reduce drinking, or craving (wave 2 only)] and harm (sacrificed important activities, problems caring for home/family, job/school problems, health problems, psychological problems or problems with family/friends). Validators included service use, severity and family history, among others. Specificity was tested using a teen transient drinker criterion group.FindingsCompared with DSM‐5 AUD (DSM‐IV results were similar), HD criteria yielded lower prevalence (95% confidence intervals): HD life‐time 6.7% (6.2, 7.2%), 1‐year 2.3% (2.0, 2.5%); and DSM‐5 life‐time 38.2% (36.5, 39.9%), 1‐year 12.4% (11.7, 13.1%). HD AUD was higher than DSM‐5 on pathology validators, including: life‐time alcohol‐related service use: HD 41.0% (38.1, 43.9%), DSM‐5 11.5% (10.7, 12.3%); severity (number of life‐time alcohol symptoms): HD 20.8 (20.4, 21.2), DSM‐5 10.6 (10.4, 10.8); and family history of alcohol problems: HD 50.1% (47.3, 52.9), DSM‐5 32.8% (31.6, 34.0). HD criteria eliminated 83% of a DSM‐5 teen transient drinker false‐positives criterion group.ConclusionsPrevalence estimates of alcohol use disorder are lowered and diagnostic validity improved when using ‘harmful dysfunction’ diagnostic criteria compared with standard DSM criteria, partly by reducing misdiagnosis of teenage transient drinkers.
When Did the Swahili Become Maritime?
Authors: Fleisher Jeffrey , Lane Paul , LaViolette Adria , Horton Mark , Pollard Edward , Quintana Morales Eréndira , Vernet Thomas , Christie Annalisa , Wynne‐Jones Stephanie 
Published: January 2015

ABSTRACTIn this article, we examine an assumption about the historic Swahili of the eastern African coast: that they were a maritime society from their beginnings in the first millennium C.E. Based on historical and archaeological data, we suggest that, despite their proximity to and use of the sea, the level of maritimity of Swahili society increased greatly over time and was only fully realized in the early second millennium C.E. Drawing on recent theorizing from other areas of the world about maritimity as well as research on the Swahili, we discuss three arenas that distinguish first‐ and second‐millennium coastal society in terms of their maritime orientation. These are variability and discontinuity in settlement location and permanence; evidence of increased engagement with the sea through fishing and sailing technology; and specialized architectural developments involving port facilities, mosques, and houses. The implications of this study are that we must move beyond coastal location in determining maritimity; consider how the sea and its products were part of social life; and assess whether the marine environment actively influences and is influenced by broader patterns of sociocultural organization, practice, and belief within Swahili and other societies. [maritime, fishing and sailing, long‐distance trade, Swahili, eastern Africa]
Fifty years of chasing lizards: new insights advance optimal escape theory
Authors: Samia Diogo S. M. , Blumstein Daniel T. , Stankowich Theodore , Cooper William E. 
Published: January 2015

ABSTRACTSystematic reviews and meta‐analyses often examine data from diverse taxa to identify general patterns of effect sizes. Meta‐analyses that focus on identifying generalisations in a single taxon are also valuable because species in a taxon are more likely to share similar unique constraints. We conducted a comprehensive phylogenetic meta‐analysis of flight initiation distance in lizards. Flight initiation distance (FID) is a common metric used to quantify risk‐taking and has previously been shown to reflect adaptive decision‐making. The past decade has seen an explosion of studies focused on quantifying FID in lizards, and, because lizards occur in a wide range of habitats, are ecologically diverse, and are typically smaller and differ physiologically from the better studied mammals and birds, they are worthy of detailed examination. We found that variables that reflect the costs or benefits of flight (being engaged in social interactions, having food available) as well as certain predator effects (predator size and approach speed) had large effects on FID in the directions predicted by optimal escape theory. Variables that were associated with morphology (with the exception of crypsis) and physiology had relatively small effects, whereas habitat selection factors typically had moderate to large effect sizes. Lizards, like other taxa, are very sensitive to the costs of flight.
Methotrexate is effective for the treatment of neuromyelitis optica spectrum disorders in Asian patients
Authors: Ng Adeline S.L. , Tan Kevin 
Published: January 2015

AbstractBackgroundImmunosuppression is effective in the secondary prevention of neuromyelitis optica spectrum disorder (NMOSD) relapse. However, some of the newer immunosuppressive agents are costly or unavailable in resource‐poor countries; older immunosuppressive agents might be just as effective. We aimed to evaluate the efficacy and tolerability of methotrexate in treating NMOSD in an Asian cohort.MethodsWe retrospectively reviewed all patients with NMOSD treated with methotrexate at the National Neuroscience Institute, Singapore, between 1992 and September 2012. We compared the annualized relapse rates and disability as measured by the Expanded Disability Status Scale before and after methotrexate treatment.ResultsEight of 180 patients with central nervous system demyelinating diseases fulfilled the inclusion criteria. At median follow up of 53 months (range 42–70 months), the median post‐treatment annualized relapse rate was significantly lower than the pretreatment rate (0.00 [range 0.00–3.09] vs 0.97 [range 0.08–10.14] relapses). The median Expanded Disability Status Scale remained stable (pretreatment 6.5 [range 3.0–8.0] vs post‐treatment 6.0 [range 2.0–8.0], P = 0.238); 75% of our cohort remained relapse‐free on treatment. None of our patients were intolerant of methotrexate.ConclusionsMethotrexate is well‐tolerated in our NMOSD patients, and appears to be effective in decreasing relapse rates and preventing disability progression. It is widely available and less costly than newer immunomodulatory agents. As such, it can be recommended as a therapeutic option for NMOSD in patients who fail first‐line therapy.
Prenatal findings of holoprosencephaly
Authors: Hayashi Yuko , Suzumori Nobuhiro , Sugiura Tokio , Sugiura‐Ogasawara Mayumi 
Published: January 2015

AbstractHoloprosencephaly (HPE) is a rare brain abnormality characterized by an incomplete cleavage of the primitive prosencephalon of forebrain during early embryogenesis. To determine the clinical characteristics and outcome of fetuses with HPE, we retrospectively analyzed nine patients who were prenatally diagnosed as fetal HPE by ultrasounds. The mean diagnostic weeks were 20 weeks of gestation. Two cases died within one day after birth. The chromosomal examinations were performed in seven cases (trisomy 18: n = 2; trisomy 13: n = 2; 45,XX,der(18)t(18;21)(p10;p10)mat: n = 1; normal karyotype: n = 2). In our HPE cases, most cases had serious facial anomalies and poor prognosis. Our data suggested that the early prenatal diagnosis of HPE allowed time for parental counseling and delivery planning.