bluuebunny/crossref_metadata_2025_split huggingface dataset:
Who becomes a sperm donor: personality characteristics in a national sample of identifiable donors
Authors: Sydsjö G , Lampic C , Brändström S , Gudmundsson J , Karlström P‐O , Solensten NG , Thurin‐Kjellberg A , Skoog Svanberg A 
Published: October 2011

Please cite this paper as:Sydsjö G, Lampic C, Brändström S, Gudmundsson J, Karlström P, Solensten N, Thurin‐Kjellberg A, Skoog Svanberg A. Who becomes a sperm donor: personality characteristics in a national sample of identifiable donors. BJOG 2012;119:33–39.Objective To study the personality characteristics of identifiable sperm donors in a national sample in comparison with the same characteristics of a control group.Design Descriptive study.Setting All clinics (n = 7) performing gamete donation in Sweden.Population All Swedish sperm donors recruited during 2005–08. An age‐matched group of Swedish men served as controls.Methods Standardised questionnaires were used to measure personality.Main outcome measures Demographics and the Temperament and Character Inventory (TCI).Results The mean age of the donors was 33.8 ± 7.8 years (18–56 years). About one‐third (36.5%) of the donors had biological children of their own. With regard to personality, significant differences were present on harm avoidance, with lower means for sperm donors (P = 0.002, 95% CI −3.74 to −0.85), and on self‐directedness and cooperativeness, with higher means for donors (P = 0.002, 95% CI 0.97–4.19;P = 0.001; 95% CI 0.75–2.95, respectively), compared with controls. This indicates that the donors in general feel less worried and suffer less from uncertainty, shyness and fatigability than controls. They also perceive themselves as being autonomous, with a capacity to take responsibility, to behave in a goal‐directed manner, to be resourceful and self‐acceptant, and to behave in a manner guided by meaningful values and goals. Furthermore, they describe themselves as being well integrated in humanity or society, and having a good capacity for identification with and acceptance of other people.Conclusions The screening process at the clinics seems to generate a group of stable, mature and well‐integrated donors, and this is a promising result for the future.
gp130 cytokines stimulate proteasomal degradation of tyrosine hydroxylase via extracellular signal regulated kinases 1 and 2
Authors: Shi Xiao , Habecker Beth A. 
Published: October 2011

J. Neurochem. (2012) 120, 239–247.AbstractInjury‐induced cytokines act through gp130 in sympathetic neurons to suppress expression of tyrosine hydroxylase (TH) and other genes associated with noradrenergic transmission. These cytokines also trigger the local loss of TH in peri‐infarct sympathetic axons after myocardial infarction, but altered gene expression cannot explain the selective loss of TH enzyme in one region of the heart. We hypothesized that inflammatory cytokines, which are highest near the infarct, stimulated local degradation of TH protein. We used cultured sympathetic neurons and neuroblastoma cells to test this hypothesis. The cytokines ciliary neurotrophic factor (CNTF) and leukemia inhibitory factor (LIF) suppressed TH content in both neurons and neuroblastoma cells. CNTF suppressed TH in a gp130‐dependent manner, and decreased the half‐life of TH protein by approximately 50%. CNTF stimulated the ubiquitination of TH in both neurons and neuroblastoma cells, and the proteasome inhibitors MG‐132 and lactacystin prevented the CNTF‐induced loss of TH protein. Inhibiting activation of extracellular signal regulated kinases 1&2 (ERK1/2) with U0126 prevented the CNTF‐induced ubiquitination of TH and the associated decrease in protein half‐life. Likewise, inhibiting ERK1/2 activation blunted the cytokine‐stimulated loss of TH protein in sympathetic neurons, despite enhancing the loss of TH mRNA. These data suggest that gp130 cytokines stimulate proteasomal degradation of TH through an ERK1/2 dependent pathway, and may have important implications for local regulation of neurotransmission at sites of inflammation.
Prion protein polymerisation triggered by manganese‐generated prion protein seeds
Authors: Hesketh Shirley , Thompsett Andrew R. , Brown David R. 
Published: October 2011

J. Neurochem. (2012) 120, 177–189.AbstractPrion diseases are neurodegenerative diseases that can be transmitted between individuals. The exact cause of these diseases remains unknown. However, one of the key events associates with the disease is the aggregation of a cellular protein, the prion protein. The mechanism of this is still unclear. However, it is likely that the aggregation is trigged by a seeding mechanism in which an oligomer of the prion protein is able to catalyse polymerisation of further prion protein into larger aggregates. We have developed a model of this process using an oligomeric species generated from recombinant protein by exposure to manganese. On fractionation of the seeding species, we estimated that the smallest size the oligomer would be is an octomer. We analysed the catalytic mechanism of the seeding oligomer and its interaction with substrate. Different domains of the protein are necessary for the seeding ability of the prion protein as opposed to those required for it to form a substrate for the polymerisation reaction. Prion seeds formed from different sheep alleles are able to reproduce the characteristics of scrapie in terms of resistance to disease. However, we were also able to generate prion seed from chicken PrP a species where no prion disease is known. Our findings provide an insight into the aggregation process of the prion protein and its potential relation to disease progress.
Costs of Addressing Heroin Addiction inMalaysia and 32 Comparable Countries Worldwide
Authors: Ruger Jennifer Prah , Chawarski Marek , Mazlan Mahmud , Luekens Craig , Ng Nora , Schottenfeld Richard 
Published: October 2011

ObjectiveDevelop and apply new costing methodologies to estimate costs of opioid dependence treatment in countries worldwide.Data Sources/Study SettingMicro‐costing methodology developed and data collected during randomized controlled trial (RCT) involving 126 patients (July 2003–May 2005) inMalaysia. Gross‐costing methodology developed to estimate costs of treatment replication in 32 countries with data collected from publicly available sources.Study DesignFixed, variable, and societal cost components ofMalaysianRCTmicro‐costed and analytical framework created and employed for gross‐costing in 32 countries selected by three criteria relative toMalaysia: major heroin problem, geographic proximity, and comparable gross domestic product (GDP) per capita.Principal FindingsMedication, and urine and blood testing accounted for the greatest percentage of total costs for both naltrexone (29–53 percent) and buprenorphine (33–72 percent) interventions. In 13 countries, buprenorphine treatment could be provided for under $2,000 per patient. For all countries exceptUnitedKingdom andSingapore, incremental costs per person were below $1,000 when comparing buprenorphine to naltrexone. An estimated 100 percent of opiate users inCambodia andLaoPeople'sDemocraticRepublic could be treated for $8 and $30 million, respectively.ConclusionsBuprenorphine treatment can be provided at low cost in countries across the world. This study's new costing methodologies provide tools for health systems worldwide to determine the feasibility and cost of similar interventions.
Costs and Health Resources Utilization Following Switching to Pregabalin in Individuals with Gabapentin‐Refractory Neuropathic Pain: A post hoc Analysis
Authors: Navarro Ana , Saldaña María T. , Pérez Concepción , Masramón Xavier , Rejas Javier 
Published: October 2011

AbstractPurpose:  To analyze the changes in pain severity and associated costs resulting from resource utilization and reduced productivity in patients with gabapentin‐refractory peripheral neuropathic pain who switched to pregabalin therapy in primary care settings in Spain.Patients and Methods:  This is a post hoc analysis of a 12‐week, multicentre, noninterventional cost‐of‐illness study. Patients were included in the study if they were over 18 years of age and had a diagnosis of chronic, treatment‐refractory peripheral neuropathic pain. The analysis included all pregabalin‐naïve patients who had previously shown an inadequate response to gabapentin and switched to pregabalin. Severity of pain before and after treatment with pregabalin, alone or as an add‐on therapy, was assessed using the Short‐Form McGill Pain Questionnaire (SF‐MPQ) and its related visual analogue scale (VA). Healthcare resource utilization, productivity (including lost‐workday equivalents [LWDE]), and related costs were assessed at baseline and after pregabalin treatment.Results:  A total of 174 patients switched to pregabalin had significant and clinically relevant reductions in pain severity (mean [SD] change on SF‐MPQ VA scale, −31.9 [22.1]; P < 0.05 vs. baseline; effect size, 1.87). Reduction in pain was similar with both pregabalin monotherapy and add‐on therapy. Significant reductions in healthcare resource utilization (concomitant drug use [in pregabalin add‐on group], ancillary tests, and unscheduled medical visits) were observed at the end of trial. Additionally, there were substantial improvements in productivity, including a reduction in the number of LWDE following pregabalin treatment (−18.9 [26.0]; P < 0.0001). These changes correlated with substantial reductions in both direct (−652.9 ± 1622.4 €; P < 0.0001) and indirect healthcare costs (−851.6 [1259.6] €; P < 0.0001).Conclusions:  The cost of care in patients with gabapentin‐refractory peripheral neuropathic pain appeared to be significantly reduced after switching to pregabalin treatment, alone or in combination with other analgesic drugs, in a real‐life setting.
Rejecting Darwin and Support for Science Funding
Authors: Freeman Patricia K. , Houston David J. 
Published: October 2011

ObjectiveExamine variables relating to support for science in the United States to determine whether a rejection of Darwinian evolution is related to support for government funding of science.MethodsOrdinal logistic regression using questions from the 2006 General Social Survey.ResultsA rejection of human evolution is significantly related to support for science even after controlling for a variety of variables.ConclusionBeliefs regarding human evolution have a unique effect on attitudes regarding government support for scientific research that do not merely channel religion and/or politics. Debate today over evolutionary theory revolves around what constitutes good science. Those who reject Darwinian evolution may do so because of the messages critical of scientists and the scientific method. A possible consequence of this controversy is lower support for science.
Gender Differences in the Paths Leading to a STEM Baccalaureate
Authors: Ma Yingyi 
Published: October 2011

ObjectivesMany have wondered why U.S. women continue to shun certain STEM fields, including science, technology, engineering, and mathematics. This study investigates this question and examines the pathways that women and men follow in attaining their STEM bachelor's degrees.MethodsUsing NELS 88‐00 and the postsecondary transcript data, the descriptive analysis examines gender differences in the three stages of the STEM pipeline: expected college major, first major, and bachelor degree major. The multivariate analysis examines the outcomes of STEM degree attainment, the subfields attainment and the pathways in a series of logical steps.ResultsDrawing from the pipeline model and its associated cumulative disadvantage theory, and the alternative framework of revolving door theory, analyses from this study indicate that men are more likely than women to follow the complete persistence pathway to attain STEM degrees, but women are as persistent as men once they expect a major in STEM as high school seniors. High school achievement, attitudes, and course taking are related to the subfields attainment, as well as the pathways of the STEM degree attainment.ConclusionsTaken together, the results are more aligned with revolving door theory and support the contextual variability in the salience of gender to understand gender differences in attaining STEM fields.
Genetics, Personality, and Group Identity
Authors: Weber Christopher , Johnson Martin , Arceneaux Kevin 
Published: October 2011

ObjectiveGroup identity is a central concept in many social science disciplines. We investigate why people identify with groups and show favoritism to in‐group members. We anticipate group identifications are substantially influenced by genes and social environments, likely working through stable personality traits.MethodsUsing twin study data from the National Survey of Midlife Development in the United States (MIDUS I), we investigate the heritability of in‐group identification and favoritism, as well as the extent to which the genetic bases of these orientations are shared with genetic underpinnings of personality traits, primarily focusing on the “Big Five”: openness to experience, conscientiousness, extraversion, agreeableness, and emotional stability/neuroticism.ResultsGroup identification is largely attributable to genetic factors. However, environments also affect group identification. The heritability of personality traits accounts for a modest portion of the genetic variation of group identification.ConclusionOur findings have implications for the study of collective action, identity politics, and the growing research program investigating social and political behavior genetics.
Framing Nicotine Addiction as a “Disease of the Brain”: Social and Ethical Consequences
Authors: Dingel Molly J. , Karkazis Katrina , Koenig Barbara A. 
Published: October 2011

ObjectivesIn this article, we seek to better understand how a genomic vision of addiction may influence drug prevention and treatment. Thoughsocialinfluences on substance use and abuse (e.g., peer and family influence, socioeconomic status) are well documented, biomedical intervention is becoming increasingly technoscientific in nature. We wish to elucidate how emphasizing biological influences on substance use may lead to a vision of addiction as a phenomenon isolated within our bodies and neurochemistry, not lived daily within a complex social web of relationships and a particular political economy, including the tobacco industry, which aggressively markets products known to cause harm.MethodsWe explore the emerging view of addiction as a “disease of the brain” in open‐ended interviews with 86 stakeholders from the fields of nicotine research and tobacco control. Interview data were analyzed using standard qualitative techniques.ResultsMost stakeholders hold a medicalized view of addiction. Though environmental variables are understood to be a primary cause of smoking initiation, the speed and strength with which addiction occurs is understood to be a largely biological process. Though stakeholders believe that an increased focus on addiction as a disease of the brain is not likely to lead to widespread unrealistic expectations for cessation therapies, they remain concerned that it may reinforce teenagers’ expectations that quitting is not difficult. Finally, stakeholder responses indicate that genetic and neuroscientific research is unlikely to increase or decrease stigmatization, but will be used by interest groups to buttress their existing views of the stigma associated with smoking.ConclusionWe argue that the main potential harms of focusing on biological etiology stem from a concept of addiction that is disassociated from social context. Focusing on genetic testing and brain scans may lead one to overemphasize pharmaceutical “magic bullet cures” and underemphasize, and underfund, more traditional therapies and public health prevention strategies that have proven to be effective. Genetic research on addiction may fundamentally change our conception of deviance and our identities, and may thus transform our susceptibility to substance use into something isolated in our biology, not embedded in a biosocial context.
Heat shock protein 27 as a prognostic and predictive biomarker in pancreatic ductal adenocarcinoma
Authors: Schäfer Claus , Seeliger Hendrik , Bader Dominik C. , Assmann Gerald , Buchner Denise , Guo Yang , Ziesch Andreas , Palagyi Andreas , Ochs Stephanie , Laubender Rüdiger P. , Jung Andreas , De Toni Enrico N. , Kirchner Thomas , Göke Burkhard , Bruns Christiane , Gallmeier Eike 
Published: October 2011

AbstractA role of heat shock protein 27 (HSP27) as a potential biomarker has been reported in various tumour entities, but comprehensive studies in pancreatic cancer are lacking. Applying tissue microarray (TMA) analysis, we correlated HSP27 protein expression status with clinicopathologic parameters in pancreatic ductal adenocarcinoma specimens from 86 patients. Complementary, we established HSP27 overexpression and RNA‐interference models to assess the impact of HSP27 on chemo‐ and radiosensitivity directly in pancreatic cancer cells. In the TMA study, HSP27 expression was found in 49% of tumour samples. Applying univariate analyses, a significant correlation was found between HSP27 expression and survival. In the multivariate Cox‐regression model, HSP27 expression emerged as an independent prognostic factor. HSP27 expression also correlated inversely with nuclear p53 accumulation, indicating either protein interactions between HSP27 and p53 or TP53 mutation‐dependent HSP27‐regulation in pancreatic cancer. In the sensitivity studies, HSP27 overexpression rendered HSP27 low‐expressing PL5 pancreatic cancer cells more susceptible towards treatment with gemcitabine. Vice versa, HSP27 protein depletion in HSP27 high‐expressing AsPC‐1 cells caused increased gemcitabine resistance. Importantly, HSP27 expression was inducible in pancreatic cancer cell lines as well as primary cells. Taken together, our study suggests a role for HSP27 as a prognostic and predictive marker in pancreatic cancer. Assessment of HSP27 expression could thus facilitate the identification of specific patient subpopulations that might benefit from individualized treatment options. Additional studies need to clarify whether modulation of HSP27 expression could represent an attractive concept to support the incorporation of hyperthermia in clinical treatment protocols for pancreatic cancer.
Neural correlates of self‐reflection in post‐traumatic stress disorder
Authors: Bluhm R. L. , Frewen P. A. , Coupland N. C. , Densmore M. , Schore A. N. , Lanius R. A. 
Published: October 2011

Bluhm RL, Frewen PA, Coupland NC, Densmore M, Schore AN, Lanius RA. Neural correlates of self‐reflection in post‐traumatic stress disorder.Objective:  Disturbances in self‐referential processing (SRP) are increasingly recognized in post‐traumatic stress disorder (PTSD). In healthy adults, SRP tasks engage the medial prefrontal cortex (MPFC) and posterior cingulate cortex (PCC) brain regions that have shown altered function in PTSD. We hypothesized that individuals with PTSD would differ from controls in functional activation of the MPFC and PCC during SRP.Method:  We compared neural activation in healthy controls (n = 15) and participants with PTSD (n = 20) during a SRP task, using fMRI at 4.0T.Results:  Controls made faster responses to the self‐relevance of personal characteristics than to the accuracy of general facts, whereas response times did not differ between these conditions in PTSD. Controls also demonstrated greater MPFC (dorsal and ventral) and PCC response when considering the self‐relevance of personal characteristics in comparison with the accuracy of general facts. Individuals with PTSD demonstrated less MPFC response than did healthy controls for the contrast of self‐relevance of personal characteristics relative to general facts.Conclusions:  These results implicate MPFC in SRP disturbances associated with PTSD. These findings are relevant to current proposals for including symptoms of negative self‐referential cognition and identity‐existential disturbance as diagnostically relevant to PTSD.
Altered microRNA expression profile with miR‐27b down‐regulation correlated with disease activity of oral lichen planus
Authors: Zhang W‐Y , Liu W , Zhou Y‐M , Shen X‐M , Wang Y‐F , Tang G‐Y 
Published: October 2011

Oral Diseases (2012) 18, 265–270Background:  Increasing evidence indicates that microRNAs (miRNAs) play a vital role in the pathogenesis of inflammatory and autoimmune diseases. The objective of this study was to investigate the altered miRNA expression profile in patients with oral lichen planus (OLP) and determine the miR‐27b expression.Methods:  We compared miRNA expression patterns in oral biopsy specimens from patients with OLP (n = 3) with those from normal controls (n = 3) using microarray technology. We further assessed the miR‐27b expression in specimens from patients with OLP (n = 53) against controls (n = 34) using real‐time quantitative PCR (RT‐QPCR), and miR‐27b expression in specimens from patients with OLP (n = 15) against controls (n = 12) using in situ hybridization (ISH).Results:  Using microarray analysis, a total of 46 differentially expressed miRNAs with more than 2‐fold change were identified, including 8 up‐regulated and 38 down‐regulated miRNAs. Both RT‐QPCR and ISH analyses revealed that miR‐27b was significantly down‐regulated in OLP tissue, and miR‐27b expression was even more suppressed in atrophic‐erosive OLP than in reticular OLP. In addition, miR‐27b was found to be expressed in the epithelial keratinocyte layer of both normal and OLP tissues.Conclusion:  These data indicate that miRNAs may be the novel candidate biomarkers for the implication of miRNAs in the pathogenesis of OLP.
Periostin‐like‐factor‐induced bone formation within orthopedic maxillary expansion
Authors: Zhong W‐J , Zhang W‐B , Ma J‐Q , Wang H , Pan Y‐C , Wang L 
Published: October 2011

To cite this article:
Zhong W‐J, Zhang W‐B, Ma J‐Q, Wang H, Pan Y‐C, Wang L:  Periostin‐like‐factor‐induced bone formation within orthopedic maxillary expansion  Orthod Craniofac Res 2011;14: 198–205Structured AbstractAuthors –  Zhong W‐J, Zhang W‐B, Ma J‐Q, Wang H, Pan Y‐C, Wang LObjective –  To examine whether periostin‐like factor (PLF) stimulation of the expanded palatal suture would accelerate mineral formation of bone.Materials and Methods –  Expanded palates of 6‐week‐old male C57BL/6 mice were maintained in an organ culture system, and tissue was either unstimulated or stimulated with PLF or BMP‐7 for 8 days. Bone mineral formation was assessed by Raman microspectroscopy analysis and histological examination.Results –  Raman microspectroscopy analysis demonstrated that unstimulated palates maintained their bone mineral concentration within the palatal suture over 8 days (%increase = 11.29 ± 2.34). In comparison, palates exposed to either PLF (%increase = 29.33 ± 1.61, p = 0.012) or BMP‐7 (% increase = 25.49 ± 1.09, p = 0.016) formed significantly more bone at the osteogenic fronts of the palatal suture compared with unstimulated samples at day 8. Alkaline phosphatase activity along the bone edges was markedly greater in the PLF and BMP‐7 groups compared with that in unstimulated groups at day 0 and day 8. The levels of osteocalcin proteins in the palatal suture tissues of the PLF and BMP‐7 groups were significantly higher than those in the unstimulated group.Conclusion –  PLF can increase bone mineral formation within the expanded palatal suture.