bluuebunny/crossref_metadata_2025_split huggingface dataset:
Men, Chronic Pain, and Prescription Pain Medication Use: The Role of Gender Role Beliefs in a Longitudinal Moderated Mediation Model
Authors: Daheim Jacob , Kim Shin Ye , Neduvelil Ashley , Nguyen Nguyen P 
Published: July 2019

AbstractObjectiveAlthough past research has established that men with chronic pain are more likely to misuse prescription pain medications in a myriad of ways compared with women, little is known about men’s medication use in the context of their gender role beliefs. The aim of the present study was to examine the role of men’s domestic gender role beliefs on their use of prescription pain medication for chronic pain.MethodsUsing a nationally representative data set with 304 men with chronic pain, this study examined a longitudinal moderated mediation model in which pain interference mediates the longitudinal relationship between somatic amplification and prescription pain medication use, with domestic gender role beliefs as a moderator of the aforementioned mediated relationship.ResultsResults indicated a significant moderated mediation model in which pain interference fully mediated the relationship between somatic amplification and prescription pain medication use, with men’s domestic gender role beliefs moderating this mediated relationship. Specifically, domestic gender role beliefs moderated the relationship between pain interference and prescription pain medication use. Men with higher levels of traditional domestic gender role beliefs strengthened the mediated relationship, contributing to increased prescription pain medication use.ConclusionsThese findings suggest that although men’s perceptions of somatic stimuli through its perceived interference contribute to their medication use, the extent to which they consume prescription pain medication depends on their beliefs in domestic gender roles during chronic pain.
A qualitative account of young people’s experiences of alcohol screening and brief interventions in schools: SIPS Jr-HIGH trial findings
Authors: Giles E L , McGeechan G J , Scott S J , McGovern R , Boniface S , Ramsay A , Hendrie N , McColl E , Sumnall H , Newbury-Birch D , Kaner E ,   the SIPS Jr-HIGH Study Team
Published: July 2019

Abstract

Background
The United Kingdom (UK) has seen a decrease in the number of young people drinking alcohol. However, the UK prevalence of underage drinking still ranks amongst the highest in Western Europe. Whilst there is a wealth of evidence reporting on the effectiveness of both primary, and secondary interventions, there are few reports of the experiences of young people who receive them.

Methods
The present study reports findings from interviews with 33 young people who were involved in an alcohol screening and brief intervention randomized controlled trial in schools in England. All interviews were analysed using inductive applied thematic analysis.

Results
Three major themes were identified following the analysis process: 1) drinking identities and awareness of risk; 2) access to support and advice in relation to alcohol use; and 3) appraisal of the intervention and potential impact on alcohol use.

Conclusions
There appeared to be a reluctance from participants to describe themselves as someone who drinks alcohol. Furthermore, those who did drink alcohol often did so with parental permission. There was variation amongst participants as to how comfortable they felt talking about alcohol issues with school staff. Overall participants felt the intervention was useful, but would be better suited to ‘heavier’ drinkers.
Overt acts of perceived discrimination reported by British working-age adults with and without disability
Authors: Emerson Eric , Milner Allison , Aitken Zoe , Krnjacki Lauren , Vaughan Cathy , Llewellyn Gwynnyth , Kavanagh Anne 
Published: July 2019

Abstract

Background
Exposure to discrimination can have a negative impact on health. There is little robust evidence on the prevalence of exposure of people with disabilities to discrimination, the sources and nature of discrimination they face, and the personal and contextual factors associated with increased risk of exposure.

Methods
Secondary analysis of de-identified cross-sectional data from the three waves of the UK’s ‘Life Opportunities Survey’.

Results
In the UK (i) adults with disabilities were over three times more likely than their peers to be exposed to discrimination, (ii) the two most common sources of discrimination were strangers in the street and health staff and (iii) discrimination was more likely to be reported by participants who were younger, more highly educated, who were unemployed or economically inactive, who reported financial stress or material hardship and who had impairments associated with hearing, memory/speaking, dexterity, behavioural/mental health, intellectual/learning difficulties and breathing.

Conclusions
Discrimination faced by people with disabilities is an under-recognised public health problem that is likely to contribute to disability-based health inequities. Public health policy, research and practice needs to concentrate efforts on developing programs that reduce discrimination experienced by people with disabilities.
The burden of mental disorders and access to mental health and psychosocial support services in Syria and among Syrian refugees in neighboring countries: a systematic review
Authors: Hendrickx M , Woodward A , Fuhr D C , Sondorp E , Roberts B 
Published: July 2019

AbstractBackgroundExposure to conflict, violence and forced displacement can increase poor mental health among affected populations. Our aim was to examine evidence on the burden of mental disorders and access to and effectiveness of mental health and psychosocial support (MHPSS) services in Syria and among Syrian refugees in neighboring countries.MethodsA systematic review was done following systematic review criteria. Twelve bibliographic databases and additional gray literature sources were searched for quantitative and qualitative studies. Descriptive analysis and quality assessment were conducted.ResultsTwenty-eight eligible studies were identified, of which two were with conflict-affected populations within Syria. Levels of post-traumatic stress disorder ranged from 16 to 84%, depression from 11 to 49%, and anxiety disorder from 49 to 55%. Common risk factors were exposures to trauma and having a personal or family history of mental disorder. Financial and socio-cultural barriers were identified as the main obstacles to accessing MHPSS care. Evaluations of MHPSS services, albeit from predominantly nonrandomised designs, reported positive treatment outcomes.ConclusionsThe MHPSS burden was high, but with considerable variation between studies. There are key evidence gaps on: MHPSS burden and interventions—particularly for those living within Syria; access and barriers to care; and implementation and evaluation of MHPSS interventions.
The outcomes of statin therapy in patients with acute ischemic stroke in Taiwan: a nationwide epidemiologic study
Authors: Lin H -C , Lin J -R , Tsai W -C , Lu C -H , Chang W -N , Huang C -C , Wang H -C , Kung C -T , Su C -M , Su Y -J , Lin W -C , Cheng B -C , Hsu C -W , Lai Y -R , Tsai N -W 
Published: July 2019

Summary

Background
Acute stroke is the third leading cause of death in Taiwan. Although statin therapy is widely recommended for stroke prevention, little is known about the epidemiology of statin therapy after acute ischemic stroke (AIS) in Taiwan. To investigate the effects of statin therapy on recurrent stroke, intracranial hemorrhage (ICH), coronary artery disease (CAD), cost of hospitalization and mortality, we conducted a nationwide population-based epidemiologic study.

Methods
Cases of AIS were identified from the annual hospitalization discharge diagnoses of the National Health Insurance Research Database with the corresponding International Classification of Diseases, ninth revision codes from January 2001 to December 2010. We divided the AIS patients into three groups: non-statin, pre-stroke statin and post-stroke statin.

Results
A total of 422 671 patients with AIS (including 365 419 cases in the non-statin group, 22 716 cases in the pre-stroke statin group and 34 536 cases in the post-stroke statin group) were identified. When compared to the non-statin group, both statin groups had a lower recurrent stroke risk [pre-stroke statin: odds ratio (OR) = 0.84; 95% confidence interval (CI) = 0.82–0.87; P < 0.0001; post-stroke statin: OR = 0.89; 95% CI = 0.86–0.91; P < 0.0001], lower ICH risk (pre-statin: OR = 0.75; 95% CI = 0.69–0.82; P < 0.0001; post-stroke statin: OR = 0.75; 95% CI = 0.71–0.81; P < 0.0001), and a lower mortality rate (pre-stroke statin: OR = 0.56; 95% CI = 0.53–0.59; P < 0.0001; post-stroke statin: OR = 0.51; 95% CI = 0.48–0.53; P < 0.0001). In terms of CAD, only the post-statin group had a lower risk (OR = 0.81; 95% CI = 0.79–0.84; P < 0.0001) than the non-statin group. The post-statin group had the lowest 1-year medical costs after index discharge among the three groups.

Conclusions
Statin therapy reduced the risks of recurrent stroke, CAD, ICH and the first year mortality in patients after AIS. Treatment with statin therapy after AIS is a cost-effective strategy in Taiwan.
Age, creatinine and ejection fraction (ACEF) score: a simple risk-stratified method for infective endocarditis
Authors: Wei X -B , Su Z -D , Liu Y -H , Wang Y , Huang J -L , Yu D -Q , Chen J -Y 
Published: July 2019

Summary

Background
Older age, renal dysfunction and low left ventricular ejection fraction are accepted predictors of poor outcome in patients with infective endocarditis (IE). This study aimed to investigate the prognostic significance of the age, creatinine and ejection fraction (ACEF) score in IE.

Methods
The study involved 1019 IE patients, who were classified into three groups according to the tertiles of ACEF score: low ACEF (<0.6, n = 379), medium ACEF (0.6–0.8, n = 259) and high ACEF (>0.8, n = 381). The ACEF score was calculated as follows: age (years)/ejection fraction (%)+1 (if serum creatinine value was >2 mg/dL). The relationship between ACEF score and adverse events was analyzed.

Results
In-hospital mortality was 8.2%, which increased with the increase of ACEF score (4.2% vs. 5.0% vs. 14.4% for the low-, medium- and high-ACEF groups, respectively; P < 0.001). ACEF score had a good discriminative ability for predicting in-hospital death [areas under the curve (AUC), 0.706, P < 0.001]. The predictive value of ACEF score in surgical treatment was significantly higher than in conservative treatment for predicting in-hospital death (AUC, 0.812 vs. 0.625; P = 0.001). Multivariable analysis revealed that ACEF score was independently associated with in-hospital mortality (adjusted odds ratio, 2.82; P < 0.001) and long-term mortality (adjusted hazard ratio, 2.51; P < 0.001).

Conclusion
ACEF was an independent predictor for in-hospital and long-term mortality in IE patients, and it could be considered as a useful tool for risk stratification. ACEF score was more suitable for surgical patients in terms of assessing the risk of in-hospital mortality.
British kindred with dominant FMF associated with high incidence of AA amyloidosis caused by novel MEFV variant, and a review of the literature
Authors: Rowczenio Dorota M , Youngstein Taryn , Trojer Hadija , Omoyinmi Ebun , Baginska Anna , Brogan Paul , Papadopoulou Charalampia , Rezk Tamer , Hawkins Philip N , Lachmann Helen J 
Published: July 2019

Abstract

Objectives
Hereditary systemic autoinflammatory diseases are rare genetic disorders, which if untreated, can be complicated by AA amyloidosis leading to renal failure and premature death. Our objective was to find a genetic cause in a British family with a dominantly inherited autoinflammatory disease complicated by AA amyloidosis.

Methods
The index patient and his sister underwent comprehensive clinical and laboratory assessment including the next-generation sequencing panel targeting autoinflammatory genes. Subsequently, other relatives underwent clinical evaluation and genetic testing. Screening of the SAA1 gene was performed in all symptomatic cases.

Results
The index case and his sister presented with proteinuria due to AA amyloidosis. They have been suffering from episodes of fever accompanied by severe abdominal and chest pain, arthritis and erythema since childhood. Their father died aged 52 years from complications following a cadaveric renal transplantation. The post-mortem examination demonstrated AA amyloidosis. The index case’s grandmother, two paternal cousins and two of their children described similar symptoms. All symptomatic individuals had excellent responses to colchicine. Next-generation sequencing analysis identified a single MEFV p.P373L variant in the index case, his sister and subsequently, in symptomatic family members. Sequencing of the SAA1 gene revealed all cases were heterozygous for the SAA1.1 allele.

Conclusion
Typically FMF is an autosomal recessive disorder; nonetheless rare cases of dominantly inherited disease have previously been described. Here we report a novel MEFV variant p.P373L, causing dominant FMF complicated by AA amyloidosis in four generations of a British family.
Reaching for Yield in the ABS Market: Evidence from German Bank Investments*
Authors: Efing Matthias 
Published: July 2019

Abstract
If regulation fails to differentiate between priced and idiosyncratic risk, it incentivizes investors to reach for yield. Studying securitization exposures on the balance sheets of German banks, I show evidence consistent with this prediction. Banks with tight regulatory constraints (low capital adequacy ratios) invest more in higher yielding ABSs conditionally on rating-implied regulatory risk weights. ABS investments of constrained banks tend to perform worse ex post in terms of collateral delinquency and lose value. Differences in bank sophistication, market power, or incentives to retain securitizations are unlikely to explain the riskier ABS investments of constrained banks.
Novel Mechanisms of Valproate Hepatotoxicity: Impaired Mrp2 Trafficking and Hepatocyte Depolarization
Authors: Fu Dong , Cardona Panli , Ho Henry , Watkins Paul B , Brouwer Kim L R 
Published: July 2019

AbstractDrug-induced liver injury (DILI) remains a major challenge in drug development. Although numerous mechanisms for DILI have been identified, few studies have focused on loss of hepatocyte polarization as a DILI mechanism. The current study investigated the effects of valproate (VPA), an antiepileptic drug with DILI risk, on the cellular mechanisms responsible for loss of hepatocyte polarization. Fully polarized collagen sandwich-cultured rat hepatocytes were treated with VPA (1–20 mM) for specified times (3–24 h). Hepatocyte viability was significantly decreased by 10 and 20 mM VPA. Valproate depolarized hepatocytes, even at noncytotoxic concentrations (≤5 mM). Depolarization was associated with significantly decreased canalicular levels of multidrug resistance-associated protein 2 (Mrp2) resulting in reduced canalicular excretion of the Mrp2 substrate carboxydichlorofluorescein. The decreased canalicular Mrp2 was associated with intracellular accumulation of Mrp2 in Rab11-positive recycling endosomes and early endosomes. Mechanistic studies suggested that VPA inhibited canalicular trafficking of Mrp2. This effect of VPA on Mrp2 appeared to be selective in that VPA had less impact on canalicular levels of the bile salt export pump (Bsep) and no detectable effect on P-glycoprotein (P-gp) canalicular levels. Treatment with VPA for 24 h also significantly downregulated levels of tight junction (TJ)-associated protein, zonula occludens 2 (ZO2), but appeared to have no effect on the levels of TJ proteins claudin 1, claudin 2, occludin, ZO1, and ZO3. These findings reveal that two novel mechanisms may contribute to VPA hepatotoxicity: impaired canalicular trafficking of Mrp2 and disruption of ZO2-associated hepatocyte polarization.
Nrf2-regulated miR-380-3p Blocks the Translation of Sp3 Protein and Its Mediation of Paraquat-Induced Toxicity in Mouse Neuroblastoma N2a Cells
Authors: Cai Zhipeng , Zheng Fuli , Ding Yan , Zhan Yanting , Gong Ruijie , Li Jing , Aschner Michael , Zhang Qunwei , Wu Siying , Li Huangyuan 
Published: July 2019

Abstract
Laboratorial and epidemiological research has established a relationship between paraquat (PQ) exposure and a risk for Parkinson’s disease. Previously, we have investigated the effects of nuclear factor erythroid 2 related factor 2 (Nrf2) and microRNAs in PQ-induced neurotoxicity, addressing the function of miR-380-3p, a microRNA dysregulated by PQ, as well as Nrf2 deficiency. Nrf2 is known to mediate the expression of a variety of genes, including noncoding genes. By chromatin immunoprecipitation, we identified the relationship between Nrf2 and miR-380-3p in transcriptional regulation. qRT-PCR, Western blots, and dual-luciferase reporter gene assay showed that miR-380-3p blocked the translation of the transcription factor specificity protein-3 (Sp3) in the absence of degradation of Sp3 mRNA. Results based on cell counting analysis, annexin v-fluorescein isothiocyanate/propidium iodide double-staining assay, and propidium iodide staining showed that overexpression of miR-380-3p inhibited cell proliferation, increased the apoptotic rate, induced cell cycle arrest, and intensified the toxicity of PQ in mouse neuroblastoma (N2a [Neuro2a]) cells. Knockdown of Sp3 inhibited cell proliferation and eclipsed the alterations induced by miR-380-3p in cell proliferation. Two mediators of apoptosis and cell cycle identified in previous studies as Sp3-regulated, namely cyclin-dependent kinase inhibitor 1 (p21) and calmodulin (CaM), were dysregulated by PQ, but not Sp3 deficiency. In conclusion, Nrf2-regulated miR-380-3p inhibited cell proliferation and enhanced the PQ-induced toxicity in N2a cells potentially by blocking the translation Sp3 mRNA. We conclude that CaM and p21 were involved in PQ-induced toxicity.
The Valosin-Containing Protein Protects the Heart Against Pathological Ca2+ Overload by Modulating Ca2+ Uptake Proteins
Authors: Stoll Shaunrick , Xi Jing , Ma Ben , Leimena Christiana , Behringer Erik J , Qin Gangjian , Qiu Hongyu 
Published: July 2019

AbstractStress-induced mitochondrial calcium (Ca2+) overload is a key cellular toxic effectors and a trigger of cardiomyocyte death during cardiac ischemic injury through the opening of mitochondrial permeability transition pore (mPTP). We previously found that the valosin-containing protein (VCP), an ATPase-associated protein, protects cardiomyocytes against stress-induced death and also inhibits mPTP opening in vitro. However, the underlying molecular mechanisms are not fully understood. Here, we tested our hypothesis that VCP acts as a novel regulator of mitochondrial Ca2+ uptake proteins and resists cardiac mitochondrial Ca2+ overload by modulating mitochondrial Ca2+ homeostasis. By using a cardiac-specific transgenic (TG) mouse model in which VCP is overexpressed by 3.5 folds in the heart compared to the wild type (WT) mouse, we found that, under the pathological extra-mitochondrial Ca2+ overload, Ca2+ entry into cardiac mitochondria was reduced in VCP TG mice compared to their little-matched WT mice, subsequently preventing mPTP opening and ATP depletion under the Ca2+ challenge. Mechanistically, overexpression of VCP in the heart resulted in post-translational protein degradation of the mitochondrial Ca2+ uptake protein 1, an activator of the mitochondria Ca2+ uniporter that is responsible for mitochondrial calcium uptake. Together, our results reveal a new regulatory role of VCP in cardiac mitochondrial Ca2+ homeostasis and unlock the potential mechanism by which VCP confers its cardioprotection.
Effects of Chlorpyrifos on Cholinesterase and Serine Lipase Activities and Lipid Metabolism in Brains of Rainbow Trout (Oncorhynchus mykiss)
Authors: Greer Justin B , Magnuson Jason T , Hester Kirstin , Giroux Marissa , Pope Carey , Anderson Timothy , Liu Jing , Dang Viet , Denslow Nancy D , Schlenk Daniel 
Published: July 2019

Abstract
Chlorpyrifos is an organophosphorus insecticide that elicits acute toxicity through inhibition of acetylcholinesterase (AChE), leading to acetylcholine accumulation and prolonged stimulation of cholinergic receptors throughout the central and peripheral nervous systems. Previous studies have indicated that neurodevelopment may also be impaired through alternative pathways, including reduction of cyclic adenosine monophosphate (cAMP)-catalyzed downstream events. The upstream initiating events that underlie noncholinergic neurological actions of chlorpyrifos and other organophosphorus compounds remain unclear. To investigate the potential role of fatty acid signaling disruption as a mechanism of toxicity, lipid metabolism and fatty acid profiles were examined to identify alterations that may play a critical role in upstream signaling in the central nervous system (CNS). Juvenile rainbow trout were treated for 7 days with nominal chlorpyrifos concentrations previously reported to diminish olfactory responses (10, 20, and 40 μg/l). Although lethality was noted higher in doses, measured chlorpyrifos concentrations of 1.38 μg/l (nominal concentration 10 μg/l) significantly reduced the activity of AChE and two serine lipases, monoacylglycerol lipase, and fatty acid amide hydrolase in the brain. Reductions in lysophosphatidylethanolamines (16:0, 18:0, 18:1, and 22:6) derived from the phosphatidylethanolamines and free fatty acids (palmitic acid 16:0, linolenic acid 18:3, eicosadienoic acid 20:2, arachidonic acid 20:4, and docosahexaenoic acid 22:6) were also noted, suggesting that chlorpyrifos inhibited the metabolism of select phospholipid signaling precursors at sublethal concentrations. These results indicate that in addition to AChE inhibition, environmentally relevant chlorpyrifos exposure alters serine lipase activity and lipid metabolites in the trout brain, which may compromise neuronal signaling and impact neurobehavioral responses in aquatic animals.
Beyond Poverty Escapes—Social Mobility in Developing Countries: A Review Article
Authors: Iversen Vegard , Krishna Anirudh , Sen Kunal 
Published: July 2019

AbstractWhile social mobility in advanced economies has received extensive scholarly attention, crucial knowledge gaps remain about the patterns and determinants of income, educational, and occupational mobility in developing countries. Focusing on intergenerational mobility, we find that estimates often differ greatly for the same country, depending on the concept and measure of mobility used, on variable constructions and on the data set utilized. There is also wide variation in mobility across regions and social groups. We discuss data and income and other variable measurement challenges when agriculture and the informal sector absorb most of the workforce, and illustrate why occupational classifications and widely used mobility measures may perform less well in such settings. Factors beyond those featuring in the literature on advanced economies are plausible determinants of social mobility, particularly of what we call moderate and large ascents (and descents), in developing country contexts. We highlight the lack of in-depth understanding of the multiple and often localized hurdles to such more pronounced progress. Similar knowledge gaps exist for large descents, which give rise to particularly profound concerns in low-income settings. We report and touch on the implications of suggestive findings of a disconnect between educational and occupational mobility. Innovative research requires critical engagement with theory and with methodology, identification, and data challenges that may overlap or deviate notably from those encountered in advanced economies.