bluuebunny/crossref_metadata_2025_split huggingface dataset:
Orbitofrontal gray matter deficits as marker of Internet gaming disorder: converging evidence from a cross‐sectional and prospective longitudinal design
Authors: Zhou Feng , Montag Christian , Sariyska Rayna , Lachmann Bernd , Reuter Martin , Weber Bernd , Trautner Peter , Kendrick Keith M. , Markett Sebastian , Becker Benjamin 
Published: October 2017

AbstractInternet gaming disorder represents a growing health issue. Core symptoms include unsuccessful attempts to control the addictive patterns of behavior and continued use despite negative consequences indicating a loss of regulatory control. Previous studies revealed brain structural deficits in prefrontal regions subserving regulatory control in individuals with excessive Internet use. However, because of the cross‐sectional nature of these studies, it remains unknown whether the observed brain structural deficits preceded the onset of excessive Internet use. Against this background, the present study combined a cross‐sectional and longitudinal design to determine the consequences of excessive online video gaming. Forty‐one subjects with a history of excessive Internet gaming and 78 gaming‐naive subjects were enrolled in the present study. To determine effects of Internet gaming on brain structure, gaming‐naive subjects were randomly assigned to 6 weeks of daily Internet gaming (training group) or a non‐gaming condition (training control group). At study inclusion, excessive Internet gamers demonstrated lower right orbitofrontal gray matter volume compared with Internet gaming‐naive subjects. Within the Internet gamers, a lower gray matter volume in this region was associated with higher online video gaming addiction severity. Longitudinal analysis revealed initial evidence that left orbitofrontal gray matter volume decreased during the training period in the training group as well as in the group of excessive gamers. Together, the present findings suggest an important role of the orbitofrontal cortex in the development of Internet addiction with a direct association between excessive engagement in online gaming and structural deficits in this brain region.
Association of the alcohol dehydrogenase gene polymorphism rs1789891 with gray matter brain volume, alcohol consumption, alcohol craving and relapse risk
Authors: Bach Patrick , Zois Evangelos , Vollstädt‐Klein Sabine , Kirsch Martina , Hoffmann Sabine , Jorde Anne , Frank Josef , Charlet Katrin , Treutlein Jens , Beck Anne , Heinz Andreas , Walter Henrik , Rietschel Marcella , Kiefer Falk 
Published: October 2017

AbstractAlcohol metabolizing enzymes, such as the alcohol dehydrogenases and the aldehyde dehydrogenases, regulate the levels of acetaldehyde in the blood and play an important role in the development and maintenance of alcohol addiction. Recent genome‐wide systematic searches found associations between a single nucleotide polymorphism (rs1789891, risk allele: A, protective allele: C) in the alcohol dehydrogenase gene cluster and the risk of alcohol dependence. The current study investigated the effect of this single nucleotide polymorphism on alcohol consumption, craving for alcohol, relapse risk and brain gray matter volume. Alcohol‐dependent patients (n = 74) and controls (n = 43) were screened, genotyped and underwent magnetic resonance imaging scanning, and relapse data were collected during 3 months following the experiment. Alcohol‐dependent A allele carriers reported increased alcohol craving and higher alcohol consumption compared with the group of alcohol‐dependent individuals homozygous for the C allele, which displayed craving values similar to the control group. Further, follow‐up data indicated that A allele carriers relapsed earlier to heavy drinking compared with individuals with two C alleles. Analyses of gray matter volume indicated a significant genotype difference in the patient group: individuals with two C alleles had reduced gray matter volume in the left and right superior, middle and inferior temporal gyri.Findings of the current study further support the relevance of genetic variants in alcohol metabolizing enzymes to addictive behavior, brain tissue volume and relapse risk. Genotype‐dependent differences in acetaldehyde formation, implicated by earlier studies, might be the biological substrate of the genotype differences.
Genome‐wide association study of alcohol use disorder identification test (AUDIT) scores in 20 328 research participants of European ancestry
Authors: Sanchez‐Roige Sandra , Fontanillas Pierre , Elson Sarah L. ,   The 23andMe Research Team, Gray Joshua C. , de Wit Harriet , Davis Lea K. , MacKillop James , Palmer Abraham A. 
Published: October 2017

AbstractGenetic factors contribute to the risk for developing alcohol use disorder (AUD). In collaboration with the genetics company 23andMe, Inc., we performed a genome‐wide association study of the alcohol use disorder identification test (AUDIT), an instrument designed to screen for alcohol misuse over the past year. Our final sample consisted of 20 328 research participants of European ancestry (55.3% females; mean age = 53.8, SD = 16.1) who reported ever using alcohol. Our results showed that the ‘chip‐heritability’ of AUDIT score, when treated as a continuous phenotype, was 12%. No loci reached genome‐wide significance. The geneADH1C, which has been previously implicated in AUD, was among our most significant associations (4.4 × 10−7; rs141973904). We also detected a suggestive association on chromosome 1 (2.1 × 10−7; rs182344113) near the geneKCNJ9, which has been implicated in mouse models of high ethanol drinking. Using linkage disequilibrium score regression, we identified positive genetic correlations between AUDIT score, high alcohol consumption and cigarette smoking. We also observed an unexpected positive genetic correlation between AUDIT and educational attainment and additional unexpected negative correlations with body mass index/obesity and attention‐deficit/hyperactivity disorder. We conclude that conducting a genetic study using responses to an online questionnaire in a population not ascertained for AUD may represent a cost‐effective strategy for elucidating aspects of the etiology of AUD.
The genetic and environmental architecture of substance use development from early adolescence into young adulthood: a longitudinal twin study of comorbidity of alcohol, tobacco and illicit drug use
Authors: Waaktaar Trine , Kan Kees‐Jan , Torgersen Svenn 
Published: October 2017

AbstractAimsTo investigate how use of alcohol, illicit drugs and tobacco come from substance‐specific pathways and from pathways general to all three substances through adolescent development.DesignAnalysis of population‐based survey. Adolescent twins reported alcohol use (AU), tobacco use (TU) and illicit drug use (IDU) in three waves (2006, 2008, 2010). Restructuring data by age allowed for variance decomposition into age‐ and substance‐specific and common genetic and environmental variance components.SettingNorway.ParticipantsSeven national twin birth cohorts from 1988 to 1994, totalling 1483 pairs (558 monozygotic; 925 dizygotic, same and opposite sex).MeasurementsSix‐point Likert scores of AU, TU and IDU on items from the Monitoring the Future Study.FindingsSubstance use was found to be highly heritable; a2 = 0.73 [95% confidence interval (CI) = 0.61–0.94] for AU, a2 = 0.36 (CI = 0.18–0.52); d2 = 0.49 (95% CI = 0.29–0.62) for IDU and a2 = 0.46 (95% CI = 0.23–0.54); d2 = 0.05 (95% CI = 0.00–0.07) for TU during the whole adolescence period. General substance use (GSU) was also highly heritable at each age and averaged a2 = 0.57 (95% CI = 0.48–0.66). There was a high genetic carry‐over from earlier age to later age. Genetic effects on GSU at ages 12–14 years were still detectable 4 years later. New substance (general and specific)‐genetic effects also appeared. IDU demonstrated significant non‐additive genetic effects (ages 12–14 years). Shared environment had a small impact on AU only. There was almost no non‐shared environmental carry‐over from age to age, the effect probably due partly to reliability deficiency. Common genetic effects among substance and substance‐specific genetic effects were observed at each age‐period.ConclusionsAmong Norwegian adolescents, there appear to be strong genetic effects on both substance‐specific and comorbid use of alcohol, illicit drugs and tobacco; individual differences in alcohol use can be explained partially by family background.
Efficacy and toxicity of pegylated liposomal doxorubicin‐based chemotherapy in early‐stage breast cancer: a multicenter retrospective case–control study
Authors: Yang Fu Ou , Hsu Nicholas C. , Moi Sin‐Hua , Lu Yin‐Che , Hsieh Chia‐Ming , Chang King‐Jen , Chen Dar‐Ren , Tu Chi‐Wen , Wang Hwei‐Chung , Hou Ming‐Feng 
Published: October 2017

AbstractAimPEGylated liposomal doxorubicin (PLD) has comparable efficacy and differing toxicity from conventional anthracyclines used to treat advanced breast cancer. This study compared disease‐free survival and toxicity between PLD‐based and conventional anthracycline‐based regimens as adjuvant treatments for early‐stage breast cancer.MethodsWe analyzed disease‐free survival (DFS) rates, and adverse events in 102 women with early‐stage (I−IIIa) breast cancer who received adjuvant PLD‐based chemotherapy from 2002 to 2008. Each patient was matched for age, stage at diagnosis, HER‐2 expression and hormone therapy use to a patient treated with an epirubicin‐based regimen. Fisher's exact and Pearson's chi‐square tests were used for categorical data analysis. Kaplan−Meier analysis and Cox regression models were used to analyze DFS.ResultsDFS at 5 years was 81.3% for PLD‐based regimen and 82.3% for epirubicin‐based regimen. This difference was not significant (p = 0.939). Stage IIIa disease was associated with a shorter DFS in univariate analysis (p = 0.048). In multivariate analysis that controlled for adjuvant treatment, age at diagnosis, stage, HER‐2 expression, type of surgery and hormone and radiation therapy, stage IIIa disease (P = 0.023) and lack of hormone therapy (P = 0.024) were each independently associated with shorter DFS. Adverse events were evaluated, and with the exception of hand‐foot syndrome, more grade 3 and 4 toxicities occurred in patients who received epirubicin‐based regimens than in those given PLD‐based regimens.ConclusionFor patients with early‐stage breast cancer who received PLD‐based adjuvant chemotherapy, 5‐year DFS was comparable and toxicity was acceptable, yet different from those of patients who received epirubicin‐based regimens.
Learning about Voter Rationality
Authors: Ashworth Scott , Bueno de Mesquita Ethan , Friedenberg Amanda 
Published: October 2017

AbstractAn important empirical literature evaluates whether voters are rational by examining how electoral outcomes respond to events outside the control of politicians, such as natural disasters or economic shocks. The argument is that rational voters should not base electoral decisions on such events, so evidence that these events affect electoral outcomes is evidence of voter irrationality. We show that such events can affect electoral outcomes, even if voters are rational and have instrumental preferences. The reason is that these events change voters' opportunities to learn new information about incumbents. Thus, identifying voter (ir)rationality requires more than just identifying the impact of exogenous shocks on electoral fortunes. Our analysis highlights systematic ways in which electoral fortunes are expected to change in response to events outside incumbents' control. Such results can inform empirical work attempting to identify voter (ir)rationality.
Ethnic disparities in rates of publicly funded bariatric surgery in New Zealand (2009–2014)
Authors: Rahiri Jamie‐Lee , Lauti Mel , Harwood Matire , MacCormick Andrew D. , Hill Andrew G. 
Published: October 2017

BackgroundPublicly funded bariatric surgery in New Zealand (NZ) is steadily on the rise to meet the obesity epidemic. Ethnic disparities in obesity rates exist in NZ with Māori and Pacific people having three to five times higher rates than all other ethnic groups within NZ. Ethnic disparities in rates of bariatric surgery have been reported internationally. This research sought to describe rates of publically funded bariatric surgery by self‐identified ethnicity in NZ.MethodsUsing reported census and hospitalization discharge data from Statistics NZ and the NZ Ministry of Health, we calculated estimate rates of publicly funded bariatric surgery in the morbidly obese population from June 2009 to July 2014.ResultsThe average number of publicly funded bariatric procedures performed per 1000 morbidly obese patients from June 2009 to July 2014 was 3.0 for European, 1.4 for Māori and 0.7 for Pacific ethnicities.ConclusionWhile these data should be interpreted cautiously due to data limitations, the estimated rates may indicate that bariatric services are currently being provided inequitably across the major ethnic groups within NZ. We suggest that further studies should be performed to explore potential patient, healthcare provider and system‐level factors that may contribute to ethnic disparities in the rates of publicly funded bariatric surgery in NZ.
Short‐ and long‐term complications of in utero exposure to lamotrigine
Authors: Cohen‐Israel Merav , Berger Itai , Martonovich Einat Y. , Klinger Gil , Stahl Bracha , Linder Nehama 
Published: October 2017

AimsThe present study evaluates the effect of antenatal lamotrigine exposure, on short‐ and long‐term paediatric outcome.MethodsThe study included the children of 83 epileptic women treated with lamotrigine during pregnancy, at a tertiary medical centre between 2004–2014. All newborns were monitored for vital signs, congenital malformations and Finnegan score. In addition, the parents completed a questionnaire regarding their child's development and health up to the age of 12 years.ResultsNo major malformations were found in the newborns. None of the newborns had significant withdrawal symptoms by Finnegan score. The children were followed‐up to the age of 12 years (56.6% were 6–12 years at the time of evaluation). There were no significant findings in the incidence of neurodevelopmental disorders.ConclusionsAccording to our experience, lamotrigine is generally safe for pregnancy use, associated with minimal short‐term complications with no long‐term effects on the outcome.
A relative weights comparison of trauma‐related shame and guilt as predictors ofDSM‐5 posttraumatic stress disorder symptom severity amongUSveterans and military members
Authors: Cunningham Katherine C. , Davis Joanne L. , Wilson Sarah M. , Resick Patricia A. 
Published: October 2017

ObjectivesVeterans and military service members have increased risk for post‐traumatic stress disorder (PTSD) and consequent problems with health, psychosocial functioning, and quality of life. In this population and others, shame and guilt have emerged as contributors toPTSD, but there is a considerable need for research that precisely demonstrates how shame and guilt are associated withPTSD. This study examined whether a) trauma‐related shame predictsPTSDseverity beyond the effects of trauma‐related guilt and b) shame accounts for a greater proportion of variance inPTSDsymptoms than guilt.DesignWe collected cross‐sectional self‐report data on measures ofPTSDsymptom severity based onDiagnostic and Statistical Manual of Mental Disorders, Fifth Edition(DSM‐5) criteria, trauma‐related shame, and trauma‐related guilt via online survey.MethodParticipants included 61USveterans and active duty service members. Hierarchical multiple regression and relative weights analysis were used to test hypotheses.ResultsIn step 1 of regression analysis, guilt was significantly associated withPTSD. However, when shame was added to the model, the effect of guilt became non‐significant, and only shame significant predictedPTSD. Results from relative weights analysis indicated that both shame and guilt predictedPTSD, jointly accounting for 46% of the variance inPTSD. Compared to guilt, trauma‐related shame accounted for significantly more explained variance inPTSD.ConclusionsThis study provided evidence that amongUSveterans and service members, trauma‐related shame and guilt differ in their association withPTSDand that trauma‐related shame, in particular, is associated with the severity ofPTSD.Practitioner pointsTrauma‐related shame and guilt explained almost half of the observed variance inPTSDsymptom severity among this sample ofUSmilitary veterans and service members.Trauma‐related shame and guilt each made a unique contribution toPTSDseverity after accounting for the similarity between these two emotions; however, shame was particularly associated with increasedPTSDseverity.These results highlight the importance of assessing and addressing trauma‐related shame and guilt inPTSDtreatment among military populations. We suggest that emotion‐ and compassion‐focused techniques may be particularly relevant for addressing trauma‐related shame and guilt.Limitations of the studyCross‐sectional data does not allow for determination of causal relationships.Although sufficiently powered, the sample size is small.The present sample self‐selected to participate in a study about stress and emotions.
Analysis of the regulatory function of natural killer cells from patients with systemic lupus erythematosus
Authors: Cruz-González D de J , Gómez-Martin D , Layseca-Espinosa E , Baranda L , Abud-Mendoza C , Alcocer-Varela J , González-Amaro R , Monsiváis-Urenda A E 
Published: October 2017

SummaryNatural killer (NK) cells participate in the regulation of the immune response. However, the immunomodulatory function of NK cells in systemic lupus erythematosus (SLE) is not well understood. The aim of this study was to evaluate the regulatory function of NK cells in SLE patients and to identify the NK cells involved in the pathogenesis of this complex disease. We analysed the expression of NK receptors and co-stimulatory molecules in peripheral NK cells (CD3−CD56+) from SLE patients, as well as the numbers of human leucocyte antigen D-related (HLA-DR)/CD11c+ NK cells. In addition, NK cell regulatory function was assessed by the detection of NK cell-mediated dendritic cell (DC) lysis. We found that SLE patients showed increased numbers of immunoglobulin-like transcript 2 (ILT2)+, CD86+ and CD134+ NK cells. Furthermore, NK cells from SLE patients induced higher levels of DC lysis. We were able to identify a new subset of NK cells co-expressing CD11c and HLA-DR. These atypical NK cells were increased in SLE patients when compared with controls. We have identified an expanded new subset of NK cells in SLE patients. This is the first study, to our knowledge, which demonstrates that NK cells in SLE patients have an altered phenotype with a high expression of receptors characteristic of dendritic cells. Our results suggest that the impairment in the regulatory function of NK cells, together with the increased number of DC-like NK cells, could play an important role in the development of SLE and highlight the importance of NK cells as a future therapeutic target.
Genetic immunization with mouse thyrotrophin hormone receptor plasmid breaks self-tolerance for a murine model of autoimmune thyroid disease and Graves' orbitopathy
Authors: Schlüter A , Horstmann M , Diaz-Cano S , Plöhn S , Stähr K , Mattheis S , Oeverhaus M , Lang S , Flögel U , Berchner-Pfannschmidt U , Eckstein A , Banga J P 
Published: October 2017

SummaryExperimental models of Graves' hyperthyroid disease accompanied by Graves' orbitopathy (GO) can be induced efficiently in susceptible inbred strains of mice by immunization by electroporation of heterologous human TSH receptor (TSHR) A-subunit plasmid. In this study, we report on the development of a bona fide murine model of autoimmune Graves' disease induced with homologous mouse TSHR A-subunit plasmid. Autoimmune thyroid disease in the self-antigen model was accompanied by GO and characterized by histopathology of hyperplastic glands with large thyroid follicular cells. Examination of orbital tissues showed significant inflammation in extra-ocular muscle with accumulation of T cells and macrophages together with substantial deposition of adipose tissue. Notably, increased levels of brown adipose tissue were present in the orbital tissue of animals undergoing experimental GO. Further analysis of inflammatory loci by 19F-magnetic resonance imaging showed inflammation to be confined to orbital muscle and optic nerve, but orbital fat showed no difference in inflammatory signs in comparison to control β-Gal-immunized animals. Pathogenic antibodies induced to mouse TSHR were specific for the self-antigen, with minimal cross-reactivity to human TSHR. Moreover, compared to other self-antigen models of murine Graves' disease induced in TSHR knock-out mice, the repertoire of autoantibodies to mouse TSHR generated following the breakdown of thymic self-tolerance is different to those that arise when tolerance is not breached immunologically, as in the knock-out models. Overall, we show that mouse TSHR A-subunit plasmid immunization by electroporation overcomes tolerance to self-antigen to provide a faithful model of Graves' disease and GO.
AFAP1‐AS1: A novel oncogenic long non‐coding RNA in human cancers
Authors: Zhang Fuyou , Li Jianfa , Xiao Huizhong , Zou Yifan , Liu Yuchen , Huang Weiren 
Published: October 2017

AbstractLong non‐coding RNAs (lncRNAs), a group of non‐protein‐coding RNAs with more than 200 nucleotides in length, are involved in multiple biological processes, such as the proliferation, apoptosis, migration and invasion. Moreover, numerous studies have shown that lncRNAs play important roles as oncogenes or tumour suppressor genes in human cancers. In this paper, we concentrate on actin filament‐associated protein 1‐antisense RNA 1 (AFAP1‐AS1), a well‐known long non‐coding RNA that is overexpressed in various tumour tissues and cell lines, including oesophageal cancer, pancreatic ductal adenocarcinoma, nasopharyngeal carcinoma, lung cancer, hepatocellular carcinoma, ovarian cancer, colorectal cancer, biliary tract cancer and gastric cancer. Moreover, high expression of AFAP1‐AS1 was associated with the clinicopathological features and cancer progression. In this review, we sum up the current studies on the characteristics of AFAP1‐AS1 in the biological function and mechanism of human cancers.