bluuebunny/crossref_metadata_2025_split huggingface dataset:
Translation, Validity, and Reliability of the Chinese Version of the Breast Cancer Survivor Self-efficacy Scale in China
Authors: Yuan Xiaoling , Wu Fulei , Howell Doris , Yuan Changrong 
Published: August 2019

Background
Self-efficacy is a crucial variable that is related to quality of life. Patients who have high self-efficacy will exert sufficient effort and have better health outcomes and improved quality of life. Appropriate and precise measurement of self-efficacy can help promote better care. The Breast Cancer Survivor Self-efficacy Scale (BCSES) is designed to measure the perceived confidence of breast cancer patients in managing the tasks for self-management. Originally developed in America, it has not been used in China.

Objectives
The aims of this study were to translate BCSES into Chinese and assess its psychometric properties among Chinese patients.

Methods
In phase 1, the translation of BCSES closely followed the Principles of Good Practices. In phase 2, data on reliability and validity were evaluated in terms of internal consistency, item-total correlations, test-retest reliability, criterion validity, and construct validity. A total sample of 630 native Chinese-speaking patients from 5 hospitals in China participated, including a pilot sample of 182 and a validation sample of 448.

Results
Minor modifications in 5 items were recommended after translation. Both exploratory and confirmatory factor analyses suggested a 2-factor structure was more ideal than the original 1-factor model. Cronbach's α coefficient for the Chinese version of BCSES was .82, intraclass correlation coefficient was 0.97, and item-total correlations were from 0.61 to 0.76.

Conclusions
The Chinese version of BCSES appears to be culturally appropriate, reliable, and valid for assessing self-efficacy among patients with breast cancer in China.

Implication for Practice
The Chinese version of BCSES could help measure the breast cancer patients' self-efficacy and provide evidence to develop culturally sensitive interventions for Chinese patients.
Health literacy, cognitive ability and self-reported diabetes in the English Longitudinal Study of Ageing
Authors: Fawns-Ritchie Chloe , Price Jackie , Deary Ian J 
Published: August 2019

AbstractObjectiveTo examine the association of health literacy and cognitive ability with risk of diabetes.Research Design and Methods: Participants were 8,669 English Longitudinal Study of Ageing participants (mean age 66.7 years, SD 9.7) who completed health literacy and cognitive ability tests at wave 2 (2004-2005), and who answered a self-reported question on whether a doctor had ever diagnosed them with diabetes. Logistic regression was used to examine the cross-sectional associations of health literacy and cognitive ability with diabetes status. In those without diabetes at wave 2, Cox regression was used to test the associations of health literacy and cognitive ability with risk of diabetes over a median of 9.5 years follow-up (n=6,961).ResultsAdequate (compared to limited) health literacy (OR 0.72, 95% CI 0.61-0.84) and higher cognitive ability (OR per 1 SD 0.73, CI 0.67-0.80) were both associated with lower odds of self-reported diabetes. Adequate health literacy (HR 0.64; CI 0.53-0.77) and higher cognitive ability (HR 0.77, CI 0.69-0.85) were also associated with lower risk of self-reporting diabetes during follow-up. When both health literacy and cognitive ability were added to the same model, these associations were slightly attenuated. Additional adjustment for health behaviours, education and social class attenuated associations further, and neither health literacy nor cognitive ability were significantly associated with diabetes.ConclusionsAdequate health literacy and better cognitive ability were associated with reduced risk of diabetes. These associations were independent of each other, but not of other health- and socioeconomic-related variables.
Research on Artificial Intelligence and Primary Care: A Scoping Review
Authors: Kueper Jacqueline K. , Terry Amanda L. , Zwarenstein Merrick , Lizotte Daniel J. 
Published: August 2019

ABSTRACTObjectiveThe purpose of this study was to assess the nature and extent of the body of research on artificial intelligence (AI) and primary care.MethodsWe performed a scoping review, searching 11 published and grey literature databases with subject headings and key words pertaining to the concepts of 1) AI and 2) primary care: MEDLINE, EMBASE, Cinahl, Cochrane Library, Web of Science, Scopus, IEEE Xplore, ACM Digital Library, MathSciNet, AAAI, arXiv. Screening included title and abstract and then full text stages. Final inclusion criteria: 1) research study of any design, 2) developed or used AI, 3) used primary care data and/or study conducted in a primary care setting and/or explicit mention of study applicability to primary care; exclusion criteria: 1) narrative, editorial, or textbook chapter, 2) not applicable to primary care population or settings, 3) full text inaccessible in the English Language. We extracted and summarized seven key characteristics of included studies: overall study purpose(s), author appointments, primary care functions, author intended target end user(s), target health condition(s), location of data source(s) (if any), subfield(s) of AI.ResultsOf 5,515 non-duplicate documents, 405 met our eligibility criteria. The body of literature is primarily focused on creating novel AI methods or modifying existing AI methods to support physician diagnostic or treatment recommendations, for chronic conditions, using data from higher income countries. Meaningfully more studies had at least one author with a technology, engineering, or math appointment than with a primary care appointment (57 (14%) compared to 217 (54%)). Predominant AI subfields were supervised machine learning and expert systems.DiscussionOverall, AI research associated with primary care is at an early stage of maturity with respect to widespread implementation in practice settings. For the field to progress, more interdisciplinary research teams with end-user engagement and evaluation studies are needed.SUMMARY BOXESSection 1: What is already known on this topicAdvancements in technology and the availability of health data have increased opportunities for artificial intelligence to be used for primary care purposes.No comprehensive review of research on artificial intelligence associated with primary care has been performed.Section 2: What this study addsThe body of research on artificial intelligence and primary care is driven by authors without appointments in primary care departments and is focused on developing artificial intelligence methods to support diagnostic and treatment decisions.There is a need for more interdisciplinary research teams and evaluation of artificial intelligence projects in ‘real world’ practice settings.
Candidate molecular predictors of outcome after aneurysmal subarachnoid haemorrhage: a systematic review of haemoglobin metabolism, inflammation and oxidative injury pathways
Authors: Gaastra Ben , Galea Ian 
Published: August 2019

AbstractAneurysmal subarachnoid haemorrhage (aSAH) is a devastating form of stroke associated with significant morbidity and mortality. Very little is known about the predictors of poor outcome and the pathophysiological mechanisms underlying neurological injury following aSAH. Three molecular pathways have been shown to be important: haemoglobin metabolism, inflammation and oxidative injury. The aim of this review is to use a systematic approach to identify a panel of key genes within these three pathways in order to focus future studies investigating predictors of poor outcome and the mechanisms of neurological injury following aSAH. Manual searching and bioinformatic mining tools were used. Studies of experimental or human SAH were included, and outcome was broadly defined to include all encountered readouts such as mortality, neurological scores, and neuropathological markers of tissue damage. If two or more molecules belonged to the same biochemical pathway, this pathway was examined in detail to identify all its components, which were then searched individually for any evidence of association with outcome using the same broad definition as before. This resulted in the identification of 58 candidate genes within the three pathways of interest (haemoglobin metabolism, inflammation and oxidative injury) potentially linked to outcome after aSAH.
Evolution of a novel and adaptive floral scent in wild tobacco
Authors: Guo Han , Lackus Nathalie D. , Köllner Tobias G. , Li Ran , Bing Julia , Wang Yangzi , Baldwin Ian T. , Xu Shuqing 
Published: August 2019

AbstractMany plants emit diverse floral scents that mediate plant-environment interactions and attain reproductive success. However, how plants evolve novel adaptive floral volatiles remains unclear. Here, we show that in the wild tobacco, Nicotiana attenuata, a dominant species-specific floral volatile (benzyl acetone, BA) that attracts pollinators and deters florivore is synthesized by phenylalanine ammonia-lyase 4 (NaPAL4), isoflavone reductase 3 (NaIFR3), and chalcone synthase 3 (NaCHAL3). Transient expression of NaFIR3 alone in N. attenuata leaves is sufficient and necessary for ectopic foliar BA emissions, and the BA emission level is increased by co-expressing NaIFR3 with NaPAL4 and NaCHAL3. Independent changes in transcription in all three genes contributed to intraspecific variations of floral BA emission. However, among species, the gain-of-expression in NaIFR3 resulted in the biosynthesis of BA that was only found in N. attenuata. This study suggests that novel metabolic pathways associated with adaptation can arise via re-configurations of gene expression.
Machine-driven parameter optimisation of biochemical reactions
Authors: Poulain Stéphane , Arnaud Ophélie , Kato Sachi , Chen Iris , Ishida Hiro , Carninci Piero , Plessy Charles 
Published: August 2019

AbstractThe development of complex, multi-step methods in molecular biology is a laborious, costly, iterative and often intuition-bound process where an optimum is sought in a multidimensional parameter space through step-by-step optimisations. The difficulty of miniaturising reactions under the microliter volumes usually handled in multiwell plates by robots, plus the cost of the experiments, limit the number of parameters and the dynamic ranges that can be explored. Nevertheless, because of non-linearities of the response of biochemical systems to their reagent concentrations, broad dynamic ranges are necessary. Here we use a high-performance nanoliter handling platform and computer generation of liquid transfer programs to explore in quadruplicates more than 600 combinations of 4 parameters of a biochemical reaction, the reverse-transcription, which lead us to uncover non-linear responses, parameter interactions and novel mechanistic insights. With the increased availability of computer-driven laboratory platforms for biotechnology, our results demonstrate the feasibility and advantage of methods development based on reproducible, computer-aided exhaustive characterisation of biochemical systems.
Regulation of circular RNA circNFATc3 in cancer cells alters proliferation, migration and oxidative phosphorylation
Authors: Karedath Thasni , Al-Dasim Fatima M. , Ahmed Ikhlak , Al-Qurashi Albandary , Raza Afsheen , Andrews Simeon S. , Ahmed Ayeda Abdulsalam , Mohamoud Yasmin Ali , Dermime Said , Malek Joel A. 
Published: August 2019

AbstractCircular RNAs were once considered artifacts of transcriptome sequencing but have recently been identified as functionally relevant in multiple cancers. Although there is still no clear main function of circRNAs, several studies have revealed that circRNAs are expressed in a variety of eukaryotic organisms, demonstrate conservation across species, and are expressed in a regulated manner often independent of their parental linear isoforms. circNFATC3, an abundant and uncharacterized circular isoform of NFATC3 gene (which is formed form backsplicing of exon 2 and 3) in solid tumors was identified from transcriptomic data. Here we show that circNFATC3 gain of and loss of function experiments using RNAi mediated circRNA silencing and circular mini vector-mediated overexpression of circularized constructs in breast and ovarian cancer cell lines affects molecular phenotypes. Knockdown of circNFATC3 induces a reduction in cell proliferation, invasion, migration, and oxidative phosphorylation. Gain of function of circNFATc3 in MDA-MB -231 cells and SKOV3 cells shows a significant increase in cell proliferation, migration, and respiration. The above results suggest that circNFATC3 is a functionally relevant circular RNA in cancer
Brunner Syndrome associated MAOA dysfunction in human induced dopaminergic neurons results in dysregulated NMDAR expression and increased network activity
Authors: Shi Y. , van Rhijn J.R. , Bormann M. , Mossink B. , Frega M. , Hakobjan M. , Kittel-Schneider S. , Schubert D. , Brunner H. , Franke B. , Kasri N. Nadif 
Published: August 2019

AbstractMonoamine oxidase A (MAOA) is an enzyme that catalyzes the degradation of dopamine, noradrenaline, and serotonin. Regulation of monoamine neurotransmitter abundance through MAOA activity strongly affects motor control, emotion, and cognitive function. Mutations in MAOA cause Brunner Syndrome, which is characterized by impulsive aggressive behavior and mild intellectual disability (ID). The impaired MAOA activity in Brunner Syndrome patients results in bioamine aberration, but it is currently unknown how this affects neuronal function. MAOA is highly expressed in serotonergic and dopaminergic neurons, and dysfunction of both neurotransmission systems is associated with aggressive behavior in mice and humans. Research has so far mainly focused on the serotonergic system. Here, we generated human induced pluripotent stem cell-derived induced dopaminergic neurons (iDANs) from individuals with known MAOA mutations, to investigate MAOA-dependent effects on dopamine neuronal function in the context of Brunner Syndrome. We assessed iDAN lines from three patients and combined data from morphological analysis, gene expression, single-cell electrophysiology, and network analysis using micro-electrode arrays (MEAs). We observed mutation-dependent functional effects as well as overlapping changes in iDAN morphology. The most striking effect was a clear increase in N-methyl-D-aspartate (NMDA) receptor mRNA expression in all patient lines. A marked increase was also seen in coordinated network activity (network bursts) on the MEA in all patient lines, while single-cell intrinsic properties and spontaneous excitatory postsynaptic currents activity appeared normal. Together, our data indicate that dysfunction of MAOA leads to increased coordinated network activity in iDANs, possibly caused by increased synaptic NMDA receptor expression.
AttenuatedSalmonellatyphimurium cancer therapy has direct effects on the tumor epithelium in colorectal cancer
Authors: Maslowski Kendle M. , Takahashi Masumi , Nakanishi Yumiko , Mackie Gillian M. , Everard Isabel , Copland Alastair , Oda Hirotsugu , Kanaya Takashi , Ohno Hiroshi 
Published: August 2019

AbstractBacterial cancer therapy (BCT) shows great promise for treatment of solid tumors, yet basic mechanisms of bacterial-induced tumor suppression remain undefined. The intestinal epithelium is the natural route of infection forSalmonellaand thus harbors innate immune defenses which protect against infection. Attenuated strains ofSalmonella entericaserovar Typhimurium (STm) have commonly been used in mouse models of BCT, largely with the use of xenograft and orthotopic transplant cancer models. We aimed to better understand the tumor epithelium-targeted mechanisms of BCT by using mouse models of intestinal tumorigenesis and tumor organoid cultures to assess the effectiveness and mechanisms of treatment with aromatase A-deficientSTm (STmΔaroA).STmΔaroAdelivered by oral gavage could significantly reduce tumor burden and tumor load in both a colitis-associated colon cancer model (CAC) and in a spontaneous intestinal cancer model,Apcmin/+mice.STmΔaroAcolonization of tumors caused alterations in transcription of mRNAs associated with epithelial–mesenchymal transition as well as metabolic and cell cycle-related transcripts. Metabolomic analysis of tumors demonstrated alteration in the metabolic environment ofSTmΔaroA-treated tumors, suggestingSTmΔaroAimposes metabolic competition on the tumor. Use of tumor organoid culturesin vitrodemonstrated thatSTmΔaroAcan directly affect the tumor epithelium with alterations in transcripts and metabolites similar toin vivo-treated tumors. Thereby, we demonstrate that bacterial cancer therapy is efficacious in autochthonous intestinal cancer models, that BCT imposes metabolic competition, and that BCT has direct effects on the tumor epithelium, which have not previously been appreciated.One Sentence SummaryAttenuatedSalmonella entericaserovar Typhimurium can home to gastrointestinal tumors and directly affect the tumor epithelium, inducing transcriptional and metabolic changes that lead to reduced tumor burden in mice.
The evolution of parental effects when selection acts on fecundity versus viability
Authors: Kuijper Bram , Johnstone Rufus A. 
Published: August 2019

AbstractMost predictions on the evolution of adaptive parental effects and phenotypic memory exclusively focus on the role of the abiotic environment. How parental effects are affected by population demography and life history is less well understood. To overcome this, we use an analytical model to assess whether selection acting on fecundity versus viability affects the evolution of parental effects in a viscous population experiencing a spatiotemporally varying environment. We find that parental effects commonly evolve in regimes of viability selection, but are less likely to evolve in regimes of fecundity selection. In regimes of viability selection, an individual’s phenotype becomes correlated with its local environment during its lifetime, as those individuals with a locally adapted phenotype are more likely to survive until parenthood. Hence, a parental phenotype rapidly becomes an informative cue about its local environment, favoring the evolution of parental effects. By contrast, in regimes of fecundity selection, locally maladapted and adapted parents survive at equal rates, so that the parental phenotype, by itself, is not informative about the local environment. Correlations between phenotype and environment still arise, but only when more fecund, locally adapted individuals leave more successfully established offspring to the local patch. Hence, correlations take at least two generations to develop, making them more sensitive to distortion by environmental change or competition with immigrant offspring. Hence, we conclude that viability selection is most conducive to the evolution of adaptive parental effects in spatially structured populations.
Molecular profiling of driver events and tumor-infiltrating lymphocytes in metastatic uveal melanoma
Authors: Karlsson Joakim , Nilsson Lisa M. , Forsberg Elin MV , Mitra Suman , Alsén Samuel , Shelke Ganesh , Sah Vasu R , Stierner Ulrika , All-Eriksson Charlotta , Einarsdottir Berglind , Jespersen Henrik , Ny Lars , Lindnér Per , Larsson Erik , Bagge Roger Olofsson , Nilsson Jonas A. 
Published: August 2019

AbstractUveal melanoma (UM) is a rare form of melanoma with a genetics and immunology that is different from skin melanoma. Previous studies have identified genetic driver events of early stage disease when the tumor is confined to the eye. However due to lack of a clinical rationale to biopsy metastatic disease, access to tumor material to perform molecular profiling of metastases has been limited. In this study, we have characterized genomic events in UM metastases using whole-genome sequencing of fresh frozen biopsies from thirty-two patients and profiled the transcriptomes of individual tumor infiltrating lymphocytes in eight patients by single-cell sequencing. We find that 91% of the patients have metastases carrying inactivating events in the tumor suppressor BAP1 and this coincided with somatic alterations in GNAQ, GNA11, CYSLTR2, PLCB4, SF3B1 and/or CDKN2A. Mutational signature analysis revealed a rare subset of tumors with prominent signs of UV damage, associated with outlier mutational burden. We study copy number variations (CNV) and find overrepresented events, some of which were not altered in matched primary eye tumors. A focused siRNA screen identified functionally significant genes of some of the segments recurrently gained. We reintroduced a functional copy of BAP1 into a patient-derived BAP1 deficient tumor cell line and found broad transcriptomic changes of genes associated with subtype distinction and prognosis in primary UM. Lastly, our analysis of the immune microenvironments of metastases revealed a presence of tumor-reactive T cells. However, a majority expressed the immune checkpoint receptors TIM-3, LAG3 and TIGIT, and to a lesser extent PD-1. These results provide an updated view of genomic events represented in metastatic UM and immune interactions in advanced lesions.
Nutrient regulation of the islet epigenome controls adaptive insulin secretion
Authors: Wortham Matthew , Liu Fenfen , Fleischman Johanna Y. , Wallace Martina , Mulas Francesca , Vinckier Nicholas K. , Harrington Austin R. , Cross Benjamin R. , Chiou Joshua , Patel Nisha A. , Sui Yinghui , Jhala Ulupi S. , Shirihai Orian S. , Huising Mark O. , Gaulton Kyle J. , Metallo Christian M. , Sander Maike 
Published: August 2019

AbstractAdaptation of the islet β-cell insulin secretory response to changing insulin demand is critical for blood glucose homeostasis, yet the mechanisms underlying this adaptation are unknown. Here, we show that nutrient-stimulated histone acetylation plays a key role in adapting insulin secretion through regulation of genes involved in β-cell nutrient sensing and metabolism. Nutrient regulation of the epigenome occurs at sites occupied by the chromatin-modifying enzyme Lsd1 in islets. We demonstrate that β-cell-specific deletion ofLsd1leads to insulin hypersecretion, aberrant expression of nutrient response genes, and histone hyperacetylation. Islets from mice adapted to chronically increased insulin demand exhibited similar epigenetic and transcriptional changes. Moreover, genetic variants associated with fasting glucose and type 2 diabetes are enriched at LSD1-bound sites in human islets, suggesting that interpretation of nutrient signals is genetically determined. Our findings reveal that adaptive insulin secretion involves Lsd1-mediated coupling of nutrient state to regulation of the islet epigenome.
Controlling the Mitochondrial Protonmotive Force with Light to Impact Cellular Stress Resistance
Authors: Berry Brandon J. , Trewin Adam J. , Milliken Alexander S. , Baldzizhar Aksana , Amitrano Andrea M. , Kim Minsoo , Wojtovich Andrew P. 
Published: August 2019

ABSTRACTMitochondrial respiration generates an electrochemical proton gradient across the mitochondrial inner membrane called the protonmotive force (PMF) to drive diverse functions and make ATP. Current techniques to manipulate the PMF are limited to its dissipation; there is no precise, reversible method to increase the PMF. To address this issue, we used an optogenetic approach and engineered a mitochondria-targeted light-activated proton pumping protein we called mitochondria-ON (mtON) to selectively increase the PMF. Here, mtON increased the PMF light dose-dependently, supported ATP synthesis, increased resistance to mitochondrial toxins, and modulated energy-sensing behavior in Caenorhabditis elegans. Moreover, transient mtON activation during hypoxia prevented the well-characterized adaptive response of hypoxic preconditioning. Our novel optogenetic approach demonstrated that a decreased PMF is both necessary and sufficient for hypoxia-stimulated stress resistance. Our results show that optogenetic manipulation of the PMF is a powerful tool to modulate metabolic and cell signaling outcomes.