bluuebunny/crossref_metadata_2025_split huggingface dataset:
Xenophobia
Authors: Bastian Brock 
Published: November 2011

Abstract

Xenophobia is a concept that has not received a great deal of attention in the psychological literature. According to the
Oxford English Dictionary
, the word consists of two parts:
xeno
(referring to “guest, stranger, person that looks different, foreigner”) and
phobia
(“fear, horror or aversion”). Although there has been little research or writing focusing directly on xenophobia, as a concept it raises three important issues that are relevant for research on prejudice and which have received a good deal of attention in the literature. First, prejudice does not necessarily involve negative attitudes towards others (e.g., they are dirty or untrustworthy). Simply perceiving a person as foreign, alien, or strange is sufficient to produce aversion or a preference for reduced contact. Second, xenophobia highlights the fact that prejudice against others involves both cognitive and emotional elements: It involves not only viewing other groups as different along some socially important dimension, but also having an aversive emotional reaction towards that difference. Third, prejudice is often studied within the context of intergroup relations or as attitudes held towards specific social groups; however, prejudice can also involve an aversion to difference
per se
. Xenophobia highlights the fact that sometimes people show dislike for others simply when they appear different to one's own “kind.” This form of prejudice is anchored in a love of or preference for people who are similar to one's self and an aversion to anyone who differs from one's self. In what follows I will review research and theory that elucidates each of these three central components of xenophobia, therefore providing some grounding for a term that has itself received little empirical investigation.
The Intrinsic Ability of Silk Fibroin to Direct the Formation of Diverse Aragonite Aggregates
Authors: Wang Ting , Porter David , Shao Zhengzhong 
Published: November 2011

AbstractAs an analogue of the main protein contained in naturally formed nacre, reconstituted silk fibroin (SF) from theBombyx morisilkworm silk shows a strong preference for the formation of the aragonite form of CaCO3crystals and allows fine control over their size and morphology. The aragonite phase could be generated via two different routes: direct growth or dissolution and recrystallization, depending on the concentration of Ca2+and SF. Generally, lower concentrations of Ca2+and SF favor the formation of aragonite needles and their aggregates, of which the lattice structure of the precursor is similar to that of the organic matrix in natural shell. Higher concentrations lead to the formation of aragonite aggregates via a dissolution and recrystallization process through intermediates of lens‐like vaterite. Molecular modeling shows that theβ‐strand conformers of silk fibroin molecules has an excellent match with the ionic spacing in the aragonite (010) plane, which can promote growth along the (001) long axis of aragonite crystals. This synergy between silk fibroin and the aragonite phase may help our understanding of the function of organic matrices involved in the biomineralization process, and facilitate the fabrication of synthetic materials with the potential for high performance mechanical properties.
Geochemical and Process Engineering Challenges for Geothermal Power Generation
Authors: Frick Stephanie , Regenspurg Simona , Kranz Stefan , Milsch Harald , Saadat Ali , Francke Henning , Brandt Wulf , Huenges Ernst 
Published: November 2011

AbstractHandling of the geothermal fluid, which is typically a complex mixture of salt solution and dissolved gases, is one of the main challenges for designing and operating reliable and efficient geothermal power plants. In the geothermal fluid loop, undesired mineral precipitation and fluid‐material interactions must be prevented and the design and dimensioning of all components must be adapted according to the characteristics of the geothermal fluid. This paper outlines geochemical and process engineering aspects as well as research activities in these fields and introduces the Groß Schönebeck site, which is a central site for geothermal research.
Androgen deprivation and thromboembolic events in men with prostate cancer
Authors: Ehdaie Behfar , Atoria Coral L. , Gupta Amit , Feifer Andrew , Lowrance William T. , Morris Michael J. , Scardino Peter T. , Eastham James A. , Elkin Elena B. 
Published: November 2011

AbstractBACKGROUND:Androgen deprivation therapy (ADT) improves prostate cancer outcomes in specific clinical settings, but is associated with adverse effects, including cardiac complications and possibly thromboembolic complications. The objective of this study was to estimate the impact of ADT on thromboembolic events (TEs) in a population‐based cohort.METHODS:In the linked Surveillance, Epidemiology and End Results–Medicare database, we identified men older than 65 who were diagnosed with nonmetastatic prostate cancer between 1999 and 2005. Medical or surgical ADT was identified by Medicare claims for gonadotropin‐releasing hormone agonists or bilateral orchiectomy at any time following diagnosis. TEs included deep venous thrombosis, pulmonary embolism, and arterial embolism. The impact of ADT on the risk of any TE and on total number of events was estimated, controlling for patient and tumor characteristics.RESULTS:Of 154,611 patients with prostate cancer, 58,466 (38%) received ADT. During a median follow‐up of 52 months, 15,950 men had at least 1 TE, including 8829 (55%) who had ADT and 7121 (45%) with no ADT. ADT was associated with increased risk of a TE (adjusted hazard ratio = 1.56; 95% confidence interval, 1.50‐1.61; P < .0001), and duration of ADT was associated with the total number of events (P < .0001).CONCLUSIONS:In this population‐based cohort, ADT was associated with increased risk of a TE, and longer durations of ADT were associated with more TEs. Men with intermediate‐ and low‐risk prostate cancer should be assessed for TE risk factors before starting ADT and counseled regarding the risks and benefits of this therapy. Cancer 2011. © 2011 American Cancer Society.
Matrix metalloproteinase‐2 polymorphisms and clinical outcome of Chinese patients with nonsmall cell lung cancer treated with first‐line, platinum‐based chemotherapy
Authors: Zhao Xueying , Wang Xun , Wu Wenting , Gao Zhiqiang , Wu Junjie , Garfield David H. , Wang Haijian , Wang Jiucun , Qian Ji , Li Huan , Jin Li , Li Qiang , Han Baohui , Lu Daru , Bai Chunxue 
Published: November 2011

AbstractBACKGROUND:Matrix metalloproteinase‐2 (MMP‐2) is well known for its critical role in cell survival and cancer development. It also plays an important role in hematopoietic recovery after chemotherapy‐induced myelosuppression. In this study, the authors investigated the association of MMP‐2 polymorphisms with treatment efficacy and the occurrence of severe toxicity in patients with nonsmall cell lung cancer (NSCLC) who were receiving first‐line, platinum‐based chemotherapy.METHODS:A pharmacogenetic association study was performed in 663 Chinese patients who had inoperable stage III/IV NSCLC and were receiving first‐line, platinum‐based regimens. Information about objective response, progression‐free survival, overall survival, grade 3 or 4 gastrointestinal toxicity (nausea/vomiting), and hematologic toxicity (neutropenia, anemia, thrombocytopenia) was available. Sixteen tag single nucleotide polymorphisms (SNPs) of MMP‐2 were assessed.RESULTS:In 7 polymorphisms, significant associations were observed with the incidence of grade 3 or 4 neutropenia. The variant homozygotes of reference SNP rs12934241 exhibited the most significant effect on the risk of neutropenia, leading to an incidence rate that increased from 12.3% (for the C/C genotype) to 50% (for the T/T genotype; odds ratio, 8.33; P = 8.8 × 10−5). Stratified analyses indicated that rs12934241 exhibited a much stronger influence in the cisplatin‐gemcitabine regimen subgroup than subgroups that received other regimens (Pinteraction = .003). Further haplotype analyses produced results that were consistent with results from single‐SNP analyses. However, no significant association was observed between MMP‐2 polymorphisms and treatment efficacy, including response rate, clinical benefit, progression‐free survival, and overall survival.CONCLUSIONS:To the authors' knowledge, this study provides the first evidence for a predictive role of MMP‐2 polymorphisms in the variability of severe chemotherapy‐related neutropenia among Chinese patients with platinum‐treated, advanced NSCLC. Cancer 2012;3587–3598. © 2011 American Cancer Society.
Scripting distributed scientific workflows using Weaver
Authors: Bui Peter , Yu Li , Thrasher Andrew , Carmichael Rory , Lanc Irena , Donnelly Patrick , Thain Douglas 
Published: November 2011

SUMMARYWeaver is a high‐level distributed computing framework that enables researchers to construct scalable scientific data‐processing workflows. Instead of developing a new workflow language, we introduce a domain‐specific language built on top of Python called Weaver, which takes advantage of users' familiarity with the programming language, minimizes barriers to adoption, and allows for integration with a rich ecosystem of existing software. In this paper, we provide an overview of Weaver's programming model, which allows users to organize and specify scientific workflows by using a collection of datasets, functions, and abstractions. We also explain how these workflow specifications are compiled into a directed acyclic graph that is used by the Makeflow workflow manager to dispatch work to a variety of distributed execution platforms. To demonstrate the power and benefits of using the framework in constructing scientific research applications, the paper examines four distinct real‐world applications scripted using Weaver and analyzes the performance, scalability, and impact of the distributed generated scientific workflows. Copyright © 2011 John Wiley & Sons, Ltd.
Mothers' responses to children's negative emotions and child emotion regulation: The moderating role of vagal suppression
Authors: Perry Nicole B. , Calkins Susan D. , Nelson Jackie A. , Leerkes Esther M. , Marcovitch Stuart 
Published: November 2011

AbstractThe current study examined the moderating effect of children's cardiac vagal suppression on the association between maternal socialization of negative emotions (supportive and nonsupportive responses) and children's emotion regulation behaviors. One hundred and ninety‐seven 4‐year‐olds and their mothers participated. Mothers reported on their reactions to children's negative emotions and children's regulatory behaviors. Observed distraction, an adaptive self‐regulatory strategy, and vagal suppression were assessed during a laboratory task designed to elicit frustration. Results indicated that children's vagal suppression moderated the association between mothers' nonsupportive emotion socialization and children's emotion regulation behaviors such that nonsupportive reactions to negative emotions predicted lower observed distraction and lower reported emotion regulation behaviors when children displayed lower levels of vagal suppression. No interaction was found between supportive maternal emotion socialization and vagal suppression for children's emotion regulation behaviors. Results suggest physiological regulation may serve as a buffer against nonsupportive emotion socialization. © 2011 Wiley Periodicals,Inc. Dev Psychobiol 54: 503–513, 2012.
Long‐term effects of differential early rearing in rhesus macaques: Behavioral reactivity in adulthood
Authors: Corcoran Christopher A. , Pierre Peter J. , Haddad Tyler , Bice Christina , Suomi Stephen J. , Grant Kathleen A. , Friedman David P. , Bennett Allyson J. 
Published: November 2011

AbstractAdverse early experiences are associated with a range of deleterious health outcomes in humans, including higher risk for affective disorders. Studies using a long‐standing model of nonhuman primate model of early adversity have demonstrated that nursery‐reared (NR) monkeys exhibit alterations in multiple aspects of biobehavioral development; however, few studies have evaluated the persistence of socioaffective behavioral changes through adulthood. We evaluated the effects of early rearing experience on adult animals' response to a well‐validated assessment of anxiety‐like behavior, the human intruder paradigm (HIP). We tested 22 rhesus monkeys who were either nursery‐reared (NR) or reared with their mothers (mother‐reared; MR). NR monkeys were inhibited in their behavior compared to MR monkeys, with reduced locomotion and exploratory behaviors. NR animals showed a marginal increase in freezing. Together these findings demonstrate that the consequences of differential infant rearing experience on socioaffective behavior persist into adulthood, with evidence of greater inhibition in NR monkeys. © 2011 Wiley Periodicals,Inc. Dev Psychobiol 54: 546–555, 2012.
Role of TLR2 in the pathogenesis of autoimmune diabetes and its therapeutic implication
Authors: Lee Myung‐Shik , Kim Do‐Hoon , Lee June‐Chul , Kim Sunshin , Kim Hun Sik 
Published: November 2011

AbstractRecently, a couple of articles suggested the possibility that apoptosis of pancreatic β‐cells induces inflammatory/immune responses to β‐cells. Such a theory is based on the assumption that apoptotic cells can, under certain circumstances, induce immune responses, inflammatory and autoimmune disorders, which is in contrast to the dogma that apoptotic cells result in immunosuppression and necrotic cells provoke inflammation/immunity. We observed that late apoptotic β‐cells with secondary necrosis elicited inflammatory responses in macrophages through the toll‐like receptor 2 (TLR2)/MyD88/nuclear factor‐κB signalling pathway. Late apoptotic cells also induced TLR2‐dependent maturation of dendritic cells and then activation of autoreactive T‐cells. TLR2 knockout mice showed defective priming of diabetogenic T‐cells by apoptotic β‐cells in the pancreatic lymph nodes. Furthermore, TLR2 deficiency conferred a significant protection against type 1 diabetes (T1D) and insulitis in T1D animal models. These findings present evidence suggesting that apoptosis of pancreatic β‐cells could be one of the initial events in T1D and provide a novel strategy for therapeutic or preventive intervention in T1D. Copyright © 2011 John Wiley & Sons, Ltd.
Interleukin‐6 treatment induces beta‐cell apoptosis via STAT‐3‐mediated nitric oxide production
Authors: Oh Yoon Sin , Lee Youn‐Jung , Park Eun Young , Jun Hee‐Sook 
Published: November 2011

AbstractBackgroundType 2 diabetes is characterized by progressive beta‐cell failure and apoptosis is probably the main form of beta‐cell death in this disease. It was reported that circulating levels of interleukin‐6 are elevated in type 2 diabetic patients, but whether this is involved in the pathogenesis of type 2 diabetes is still debated. In this study, we examined whether interleukin‐6 can induce beta‐cell damage in vitro and elucidated its mechanisms.MethodsTo examine the effect of interleukin‐6 on beta cells, glucose‐stimulated insulin secretion (GSIS) by enzyme immunoassay (EIA) method and cell apoptosis by propidium iodide and annexin‐V staining were measured in a rat beta‐cell line (INS‐1 or INS‐832/13) after treatment with interleukin‐6. The expression of apoptosis‐related molecules was measured using western blotting and nitric oxide (NO) production was measured using Griess assay. AG490 and N‐monomethyl‐L‐arginine were used to inhibit Janus kinase‐mediated signal transducers and activators of transcription signalling and NO production, respectively.ResultsExposure (48 h) of INS‐1 cells to 20 ng/mL interleukin‐6 significantly decreased GSIS as well as cell viability. We found that sub‐G1/G0 population was increased as compared with untreated cells and expression of cleaved caspase‐3, cleaved poly(ADP‐ribose) polymerase, phosphorylated p38 mitogen‐activated protein kinase and phosphorylated nuclear factor‐κB was increased in interleukin‐6‐treated INS‐1 cells. Interleukin‐6 increased the amount of early apoptotic cells; this increase was blocked by AG490 or N‐monomethyl‐L‐arginine treatment. Moreover, NO production, which is known to induce apoptosis, was increased by interleukin‐6 treatment but abrogated in AG490‐treated cells.ConclusionOur results show that exposure to interleukin‐6 for 48 h can induce beta‐cell death, in part via signal transducers and activators of transcription‐3‐mediated NO production. Copyright © 2011 John Wiley & Sons, Ltd.
The combination of metallothionein and superoxide dismutase protects pancreatic β cells from oxidative damage
Authors: Park Leejin , Min Dongsoo , Kim Hyunok , Park Jinseu , Choi Sooyoung , Park Yongsoo 
Published: November 2011

AbstractBackgroundReactive oxygen species are considered an important cause of the death of pancreatic β cells, thereby triggering the development of type 2 diabetes as well as failure of islet transplantation. The biological properties of metallothionein (MT) and superoxide dismutase (SOD) are likely to be related to their antioxidant and free‐radical scavenging abilities, but their access across biological membranes is limited.MethodsWe investigated whether Tat‐MT and Tat‐SOD fusion protein could be introduced into islets by a novel protein transduction technology and protect them from oxidative damage. We used 3‐[4,5‐dimethylthiazol‐2‐yl]‐2,5‐diphenyl tetrazolium bromide (MTT) and Annexin V/propidium iodide assays to analyse cell viability, and assessed expression of apoptosis marker proteins by Western blotting. We examined the protective effect of Tat‐MT and Tat‐SOD on the development of diabetes and on graft failure after syngeneic islet transplantation into Otsuka Long Evans Tokushima Fatty (OLETF) rats and Imprinting Control Region (ICR) mice, respectively.ResultsTat‐MT and Tat‐SOD were successfully delivered into the rat islets, and reactive oxygen species, nitric oxide, glucolipotoxicity‐induced cell death, cytokine injury, and DNA fragmentation due to ischaemia‐reperfusion in pancreatic β cells were significantly reduced. In addition Tat‐MT and Tat‐SOD treatment protected OLETF rats from developing diabetes, and enhanced the survival of antioxidant‐treated islets transplanted into the renal capsules of diabetic mice.ConclusionsTransduction of Tat‐MT and Tat‐SOD proteins offers a new strategy for protecting against the development of diabetes by relieving oxidative stress. Copyright © 2011 John Wiley & Sons, Ltd.
Increased expression of microRNA miR‐326 in type 1 diabetic patients with ongoing islet autoimmunity
Authors: Sebastiani Guido , Grieco Fabio Arturo , Spagnuolo Isabella , Galleri Letizia , Cataldo Dorica , Dotta Francesco 
Published: November 2011

AbstractBackgroundThe current paradigm that microRNAs represent a new layer of gene regulation has generated much interest in this field. MicroRNAs have emerged as important regulatory factors involved in the developmental processes and in the regulation of insulin secretion and signalling. Furthermore, recent studies revealed an altered microRNA profiling in lymphocytes of patients with autoimmune diseases like multiple sclerosis, in which a hyperexpression of miR‐326 was reported. Here, we analysed the expression levels of miR‐326 in peripheral blood lymphocytes from type 1 diabetic (T1D) patients in relationship with ongoing islet autoimmunity.MethodsPeripheral blood lymphocytes were obtained from 19 T1D patients; 4/19 patients were positive for both glutamic acid decarboxylase (GAD) and islet cell antigen 512 autoantibodies; 10/19 were single GAD or IA‐2 Ab positive and 5/19 were GAD antibodies and IA‐2 antibodies (IA‐2A) negative. Quantitative analysis of miR‐326 was performed using specific stem–loop primers followed by real‐time polymerase chain reaction. All values were normalized to endogenous control U6.ResultsmiR‐326 resulted increased in Ab‐positive versus Ab‐negative T1D subjects. Its expression levels were 2.05 ± 0.38‐fold increased in peripheral blood lymphocytes from patients expressing both GADA and IA‐2A and 2.93 ± 0.46‐fold increased in single Ab‐positive versus Ab‐negative individuals (p < 0.05).ConclusionIn conclusion, we have shown that miR‐326 is expressed at higher levels in T1D subjects with ongoing islet autoimmunity, similar to what has been observed in multiple sclerosis, in which levels of this microRNA were highly correlated with disease severity. Interestingly, an online search of miR‐326 predicted targets revealed vitamin D receptor and Erythroblastosis virus E26 oncogene homologue 1, two molecules highly involved in immune regulation. Copyright © 2011 John Wiley & Sons, Ltd.
Killer cell immunoglobulin‐like receptor along with HLA‐C ligand genes are associated with type 1 diabetes in Chinese Han population
Authors: Zhi Dijing , Sun Chengjun , Sedimbi Saikiran K. , Luo Feihong , Shen Shuixian , Sanjeevi Carani B. 
Published: November 2011

AbstractObjectiveKiller cell immunoglobulin‐like receptor (KIR) genes and their putative ligands human leukocyte antigen (HLA)‐C genes have been associated with type 1 diabetes (T1D). We hypothesize that KIR genes and their ligands HLA‐C genes are important in T1D aetiology.Research design and methodsKIR and HLA‐C ligand genotyping was performed in 259 T1D patients and 262 healthy children.ResultsNo significant difference was observed in the distribution of KIR genes between T1D patients and healthy controls. However, frequency of HLA‐C1 gene and HLA‐C2 gene (marginal association) was higher in patient group. The combinations 2DL2 − /HLA‐C1+; 2DL3 + /HLA‐C1+; 2DS2 − /HLAC1+ were positively associated with T1D. The combinations 2DL1 + /HLA‐C2−; 2DL2 − /HLA‐C1−; 2DL3 + /HLA‐C1−; 2DS2 − /HLAC1− were found to be negatively associated with T1D. Among the genes we tested, a combination of HLA‐C1 and ‐C2 conferred the strongest association with T1D and the strength of this association was higher than that of HLA‐C1 alone. The frequencies of KIR 2DL1, 2DL2 and 2DL3 and HLA‐C1 were higher in T1D patients positive for GAD65 autoantibody; frequency of KIR 2DS4 is higher in T1D patients positive for IA‐2 autoantibody. The association between KIR/HLA‐C gene and autoantibody status was not statistically significant after applying Bonferroni correction.ConclusionIn our study of a Han population (East China), we found no direct association of KIR genes with T1D. However, a combination of HLA‐C1 and ‐C2 showed a positive association with T1D. Different combinations of HLA‐C and KIR showed positive and negative association with T1D. Copyright © 2011 John Wiley & Sons, Ltd.