bluuebunny/crossref_metadata_2025_split huggingface dataset:
Variability in student perceptions of mistreatment
Authors: Ellis Samantha , Purkiss Joel , Abdoler Emily , Opaskar Amanda , Mangrulkar Rajesh S , Kolars Joseph C , Santen Sally A 
Published: May 2018

SummaryBackgroundAs medical schools strive to improve the learning environment, it is important to understand medical students’ perceptions of mistreatment. The purpose of this study was to explore student interpretations of previously reported mistreatment incidents to better understand how they conceptualise the interactions.MethodsMedical students were presented with case scenarios of previously reported instances of mistreatment and asked to indicate their agreement as to whether the scenarios demonstrated mistreatment, using a five‐point Likert scale (1, strongly disagree; 5, strongly agree).It is important to understand medical student’s perceptions of mistreatmentResultsOne hundred and twenty‐seven third‐year medical students gave feedback on 21 mistreatment cases. There was variability in the categorisation of the scenarios as mistreatment. The highest degree of consensus (96% agreement) was for a scenario in which a resident claimed a student made statements about a patient’s status that the student did not make. There was also relative consensus on three additional scenarios: (1) a patient making disparaging remarks about a student’s role in health care in relation to the student’s ethnicity (88% agreement); (2) a resident asking a student to run personal errands (86% agreement); and (3) a nurse calling a student an expletive in front of others (77% agreement). For the majority of the cases, there was no consensus amongst students as to whether mistreatment had occurred. Students self‐identifying as minorities and students who had previously reported mistreatment were more likely to perceive mistreatment in the scenarios.ConclusionsThere is remarkable variability, and in many cases a lack of agreement, in medical student perceptions of mistreatment. This inconsistency needs to be considered in order to effectively address and mitigate the issue.
Social Transmission of False Memory in Small Groups and Large Networks
Authors: Maswood Raeya , Rajaram Suparna 
Published: May 2018

AbstractSharing information and memories is a key feature of social interactions, making social contexts important for developing and transmitting accurate memories and also false memories. False memory transmission can have wide‐ranging effects, including shaping personal memories of individuals as well as collective memories of a network of people. This paper reviews a collection of key findings and explanations in cognitive research on the transmission of false memories in small groups. It also reviews the emerging experimental work on larger networks and collective false memories. Given the reconstructive nature of memory, the abundance of misinformation in everyday life, and the variety of social structures in which people interact, an understanding of transmission of false memories has both scientific and societal implications.
Topical polyhydroxy acid treatment for autosomal recessive congenital ichthyosis in the golden retriever: a prospective pilot study
Authors: Puigdemont Anna , Furiani Nicla , De Lucia Michela , Carrasco Isaac , Ordeix Laura , Fondevila Dolors , Ramió‐Lluch Laura , Brazis Pilar 
Published: May 2018

BackgroundAutosomal recessive congenital ichthyosis (ARCI) in golden retrievers is due to a PNPLA1 gene mutation, which plays a role in epidermal lipid organization and metabolism. Topical therapies are used to reduce scaling; however, there are few published efficacy studies.ObjectivesTo examine the efficacy of topical treatment based on gluconolactone, a polyhydroxy acid with known beneficial effects on stratum corneum structure.AnimalsSixteen golden retriever dogs with clinical signs of ARCI and PCR‐confirmed PNPLA1 gene mutation.MethodsThis was a prospective, multicentre, noncontrolled study. Dogs were treated with a shampoo and lotion containing gluconolactone and other hydroxyl acids. Treatments were administered initially twice weekly for two weeks, then once weekly for two weeks and finally once monthly. Examinations were performed prior to and at 14 and 30 days of treatment to assess scaling, presence of other skin lesions and pruritus. In two dogs, pre‐ and 30 day post‐treatment, skin biopsies were obtained.ResultsThe extent and size of the scales were reduced by 60% and 75% after 14 and 30 days of treatment, respectively (P < 0.001). In 20% of the dogs, scaling was no longer observed after the first 30 days of treatment. No other skin lesions or pruritus were observed in any dog. Post‐treatment biopsies showed normalization of the stratum corneum morphology and reduced hyperpigmentation.Conclusion and clinical importanceThe frequent use of a shampoo and lotion containing gluconolactone may be an effective measure to improve skin scaling in golden retrievers with ARCI.
Expression of ZO‐1 and claudin‐1 in a 3D epidermal equivalent using canine progenitor epidermal keratinocytes
Authors: Teramoto Keiji , Asahina Ryota , Nishida Hidetaka , Kamishina Hiroaki , Maeda Sadatoshi 
Published: May 2018

BackgroundPrevious studies indicate that tight junctions are involved in the pathogenesis of canine atopic dermatitis (cAD). An in vitro skin model is needed to elucidate the specific role of tight junctions in cAD. A 3D epidermal equivalent model using canine progenitor epidermal keratinocytes (CPEK) has been established; the expression of tight junctions within this model is uncharacterized.Hypothesis/ObjectivesTo investigate the expression of tight junctions in the 3D epidermal equivalent.AnimalsTwo normal laboratory beagle dogs served as donors of full‐thickness skin biopsy samples for comparison to the in vitro model.MethodsImmunohistochemical techniques were employed to investigate the expression of tight junctions including zonula occludens (ZO)‐1 and claudin‐1 in normal canine skin, and in the CPEK 3D epidermal equivalent.ResultsResults demonstrated the expression of ZO‐1 and claudin‐1 in the CPEK 3D epidermal equivalent, with staining patterns that were similar to those in normal canine skin.Conclusions and clinical importanceThe CPEK 3D epidermal equivalent has the potential to be a suitable in vitro research tool for clarifying the specific role of tight junctions in cAD.
Characterization of efficacy and safety of pathogen inactivated and quarantine plasma in routine use for treatment of acquired immune thrombotic thrombocytopenic purpura
Authors: Herbrecht R. , Ojeda‐Uribe M. , Kientz D. , Fohrer C. , Bohbot A. , Hinschberger O. , Liu K.‐L. , Remy E. , Ernst C. , Lin J.‐S. , Corash L. , Cazenave J. P. 
Published: May 2018

BackgroundAuto‐immune thrombotic thrombocytopenic purpura (TTP) is a morbid multi‐organ disorder. Cardiac involvement not recognized in initial disease descriptions is a major cause of morbidity. Therapeutic plasma exchange (TPE) requires exposure to multiple plasma donors with risk of transfusion‐transmitted infection (TTI). Pathogen inactivation (PI) with amotosalen‐UVA, the INTERCEPT Blood System for Plasma (IBSP) is licensed to reduce TTI risk.MethodsAn open‐label, retrospective study evaluated the efficacy of quarantine plasma (QP) and IBSP in TTP and defined treatment emergent cardiac abnormalities. Medical record review of sequential patient cohorts treated with QP and IBSP characterized efficacy by remission at 30 and 60 days (d) of treatment, time to remission, and volume (L/kg) of plasma required. Safety outcomes focused on cardiac adverse events (AE), relapse rates, and mortality.ResultsThirty‐one patients (18 IBSP and 13 QP) met study criteria for auto‐immune TTP. The proportions (%) of patients in remission at 30 d (IBSP = 61·1, QP = 46·2, P = 0·570) and 60 d (IBSP = 77·8, QP = 76·9, P = 1·00) were not different. Median days to remission were less for IBSP (15·0 vs. 24·0, P = 0·003). Relapse rates (%) 60 d after remission were not different between cohorts (IBSP = 7·1, QP = 40·0, P = 0·150). ECG abnormalities before and during TPE were frequent; however, cardiac AE and mortality were not different between treatment cohorts.ConclusionsCardiac and a spectrum of ECG findings are common in TTP. In this study, IBSP and QP had similar therapeutic profiles for TPE.
Evidence of Australian bat lyssavirus infection in diverse Australian bat taxa
Authors: Field Hume Ernest 
Published: May 2018

AbstractHistorically, Australia was considered free of rabies and rabieslike viruses. Thus, the identification of Australian bat lyssavirus (ABLV) in 1996 in a debilitated bat found by a member of the public precipitated both public health consternation and a revision of lyssavirus taxonomy. Subsequent observational studies sought to elaborate the occurrence and frequency of ABLV infection in Australian bats. This paper describes the taxonomic diversity of bat species showing evidence of ABLV infection to better inform public health considerations. Blood and/or brain samples were collected from two cohorts of bats (wild‐caught and diagnostic submissions) from four Australian states or territories between April 1996 and October 2002. Fresh brain impression smears were tested for ABLV antigen using fluorescein‐labelled anti‐rabies monoclonal globulin (CENTOCOR) in a direct fluorescent antibody test; sera were tested for the presence of neutralising antibodies using a rapid fluorescent focus inhibition test. A total of 3,217 samples from 2,633 bats were collected and screened: brain samples from 1,461 wild‐caught bats and 1,086 submitted bats from at least 16 genera and seven families, and blood samples from 656 wild‐caught bats and 14 submitted bats from 14 genera and seven families. Evidence of ABLV infection was found in five of the six families of bats occurring in Australia, and in three of the four Australian states/territories surveyed, supporting the historic presence of the virus in Australia. While the infection prevalence in the wild‐caught cohort is evidently low, the significantly higher infection prevalence in rescued bats in urban settings represents a clear and present public health significance because of the higher risk of human exposure.
Genetic Variation of the SusC/SusD Homologs from a Polysaccharide Utilization Locus Underlies Divergent Fructan Specificities and Functional Adaptation in
Bacteroides thetaiotaomicron
Strains
Authors: Joglekar Payal , Sonnenburg Erica D. , Higginbottom Steven K. , Earle Kristen A. , Morland Carl , Shapiro-Ward Sarah , Bolam David N. , Sonnenburg Justin L. 
Published: May 2018

Dietary polysaccharides play a dominant role in shaping the composition and functionality of our gut microbiota. Dietary interventions using these
m
icrobiota-
a
ccessible
c
arbohydrates (MACs) serve as a promising tool for manipulating the gut microbial community. However, our current gap in knowledge regarding microbial metabolic pathways that are involved in the degradation of these MACs has made the design of rational interventions difficult. The issue is further complicated by the diversity of pathways observed for the utilization of similar MACs, even in closely related microbial strains. Our current work focuses on divergent fructan utilization pathways in two closely related
B. thetaiotaomicron
strains and provides an integrated approach to characterize the molecular basis for strain-level functional differences.
Maternal polycystic ovarian syndrome and offspring growth: the Upstate KIDS Study
Authors: Bell Griffith A , Sundaram Rajeshwari , Mumford Sunni L , Park Hyojun , Broadney Miranda , Mills James L , Bell Erin M , Yeung Edwina H 
Published: May 2018

BackgroundPolycystic ovarian syndrome (PCOS) is the most common cause of female infertility and is associated with higher levels of circulating androgens. Exposure to higher levels of androgens in utero may be a risk factor for obesity among children of women with PCOS.MethodsWe examined whether maternal PCOS was associated with differences in offspring growth and obesity in the Upstate KIDS study, a prospective cohort study of infants born in New York State (excluding New York City) oversampled for fertility treatments and multiple births. Measurements of offspring length/height and weight were recorded at doctor’s visits through 3 years of age. PCOS diagnosis was self-reported by mothers at baseline. We used linear mixed models with robust SEs to estimate differences in growth by maternal PCOS exposure. We used logistic regression to examine whether infants experienced rapid weight gain at 4, 9 and 12 months. Growth measures were reported by 4098 mothers for 4949 children (1745 twins). Of these, 435 mothers (10.6%) had a diagnosis of PCOS.ResultsCompared with children born to mothers without PCOS, children of mothers with PCOS did not have significant differences in weight (4.81 g, 95% CI −95.1 to 104.7), length/height (0.18 cm, 95% CI −0.16 to 0.52) and body mass index (−0.14 kg/m2, 95% CI −0.30 to 0.01) through 3 years of age. We also observed no association between maternal PCOS and offspring rapid weight gain.ConclusionsOverall, we found little evidence to suggest that maternal PCOS influences early childhood growth in this large, prospective cohort study.
Detection of Urothelial Bladder Carcinoma via Microfluidic Immunoassay and Single-Cell DNA Copy-Number Alteration Analysis of Captured Urinary-Exfoliated Tumor Cells
Authors: Chen Anqi , Fu Guanghou , Xu Zhijie , Sun Yukun , Chen Xiaoyi , Cheng Kok Suen , Neoh Kuang Hong , Tang Zhewen , Chen Shifu , Liu Ming , Huang Tanxiao , Dai Yun , Wang Qibo , Jin Jing , Jin Baiye , Han Ray P.S. 
Published: May 2018

Abstract
The increasing incidence of bladder cancer and its high rate of recurrence over a 5-year period necessitate the need for diagnosis and surveillance amelioration. Cystoscopy and urinary cytology are the current tools, and molecular techniques such as BTA stat, NMP22, survivin mRNA, and urovysion FISH have attracted attention; however, they suffer from insufficient sensitivity or specificity. We developed a novel microfluidic approach for harvesting intact urinary-exfoliated tumor cells (UETC), either individually or in clusters, in a clean and segregated environment, which is crucial to minimize cross-contamination and misreads. To reliably and accurately identify UETC, our quantitative immunoassay involved concurrent use of two oncoproteins CK20 and CD44v6 antigen. CK20 is an intermediate filament protein overexpressed in urothelial tumors, and CD44v6 is a membrane adhesion molecule closely associated with cell invasion, tumor progression, and metastatic spread. Single-cell whole-genome sequencing on 12 captured UETCs and copy number alteration analysis showed that 11/12 (91.7%) of the immunofluorescence-identified UETCs possessed genomic instability. A total of 79 patients with bladder cancer and 43 age-matched normal controls (NC) were enrolled in the study. We detected considerably higher UETC counts in patients with bladder cancer versus the NC group [53.3 (10.7–1001.9) vs. 0.0 (0–3.0) UETCs/10 mL; P &lt; 0.0001]. For bladder cancer detection, a stratified 10-fold cross-validation of training data reveals an overall predictive accuracy of 0.84 [95% confidence interval (CI), 0.76–0.93] with an 89.8% (95% CI, 71.5%–86.4%) for sensitivity and 71.5% (95% CI, 59.7%–83.3%) for specificity. Overall, the microfluidic immunoassay demonstrates increased sensitivity and specificity compared with other techniques for the detection of bladder cancer.
Significance: A unique and promising diagnostic assay for bladder cancer is proposed with potential clinical utility as a complement for cytology. Cancer Res; 78(14); 4073–85. ©2018 AACR.
Macrophage-Derived Granulin Drives Resistance to Immune Checkpoint Inhibition in Metastatic Pancreatic Cancer
Authors: Quaranta Valeria , Rainer Carolyn , Nielsen Sebastian R. , Raymant Meirion L. , Ahmed Muhammad S. , Engle Dannielle D. , Taylor Arthur , Murray Trish , Campbell Fiona , Palmer Daniel H. , Tuveson David A. , Mielgo Ainhoa , Schmid Michael C. 
Published: May 2018

Abstract
The ability of disseminated cancer cells to evade the immune response is a critical step for efficient metastatic progression. Protection against an immune attack is often provided by the tumor microenvironment that suppresses and excludes cytotoxic CD8+ T cells. Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive metastatic disease with unmet needs, yet the immunoprotective role of the metastatic tumor microenvironment in pancreatic cancer is not completely understood. In this study, we find that macrophage-derived granulin contributes to cytotoxic CD8+ T-cell exclusion in metastatic livers. Granulin expression by macrophages was induced in response to colony-stimulating factor 1. Genetic depletion of granulin reduced the formation of a fibrotic stroma, thereby allowing T-cell entry at the metastatic site. Although metastatic PDAC tumors are largely resistant to anti–PD-1 therapy, blockade of PD-1 in granulin-depleted tumors restored the antitumor immune defense and dramatically decreased metastatic tumor burden. These findings suggest that targeting granulin may serve as a potential therapeutic strategy to restore CD8+ T-cell infiltration in metastatic PDAC, thereby converting PDAC metastatic tumors, which are refractory to immune checkpoint inhibitors, into tumors that respond to immune checkpoint inhibition therapies.
Significance: These findings uncover a mechanism by which metastatic PDAC tumors evade the immune response and provide the rationale for targeting granulin in combination with immune checkpoint inhibitors for the treatment of metastatic PDAC.
Graphical Abstract: http://cancerres.aacrjournals.org/content/canres/78/15/4253/F1.large.jpg. Cancer Res; 78(15); 4253–69. ©2018 AACR.
Pericytes in the Premetastatic Niche
Authors: Paiva Ana E. , Lousado Luiza , Guerra Daniel A.P. , Azevedo Patrick O. , Sena Isadora F.G. , Andreotti Julia P. , Santos Gabryella S.P. , Gonçalves Ricardo , Mintz Akiva , Birbrair Alexander 
Published: May 2018

Abstract
The premetastatic niche formed by primary tumor–derived molecules contributes to fixation of cancer metastasis. The design of efficient therapies is limited by the current lack of knowledge about the details of cellular and molecular mechanisms involved in the premetastatic niche formation. Recently, the role of pericytes in the premetastatic niche formation and lung metastatic tropism was explored by using state-of-the-art techniques, including in vivo lineage-tracing and mice with pericyte-specific KLF4 deletion. Strikingly, genetic inactivation of KLF4 in pericytes inhibits pulmonary pericyte expansion and decreases metastasis in the lung. Here, we summarize and evaluate recent advances in the understanding of pericyte contribution to premetastatic niche formation. Cancer Res; 78(11); 2779–86. ©2018 AACR.
Genomic-Epidemiologic Evidence That Estrogens Promote Breast Cancer Development
Authors: Parl Fritz F. , Crooke Philip S. , Plummer W. Dale , Dupont William D. 
Published: May 2018

Abstract
Background: Estrogens are a prime risk factor for breast cancer, yet their causal relation to tumor formation remains uncertain. A recent study of 560 breast cancers identified 82 genes with 916 point mutations as drivers in the genesis of this malignancy. Because estrogens play a major role in breast cancer development and are also known to regulate the expression of numerous genes, we hypothesize that the 82 driver genes are likely to be influenced by estrogens, such as 17ß-estradiol (E2), and the estrogen receptor ESR1 (ERα). Because different types of tumors are characterized by unique sets of cancer driver genes, we also argue that the fraction of driver genes regulated by E2-ESR1 is lower in malignancies not associated with estrogens, e.g., acute myeloid leukemia (AML).
Methods: We performed a literature search of each driver gene to determine its E2-ESR1 regulation.
Results: Fifty-three of the 82 driver genes (64.6%) identified in breast cancers showed evidence of E2-ESR1 regulation. In contrast, only 19 of 54 mutated driver genes (35.2%) identified in AML were linked to E2-ESR1. Among the 916 driver mutations found in breast cancers, 813 (88.8%) were linked to E2-ESR1 compared with 2,046 of 3,833 in AML (53.4%).
Conclusions: Risk assessment revealed that mutations in estrogen-regulated genes are much more likely to be associated with elevated breast cancer risk, while mutations in unregulated genes are more likely to be associated with AML.
Impact: These results increase the plausibility that estrogens promote breast cancer development. Cancer Epidemiol Biomarkers Prev; 27(8); 899–907. ©2018 AACR.
PGC-1α as a Biomarker of Physical Activity-Protective Effect on Colorectal Cancer
Authors: de Souza-Teixeira Fernanda , Alonso-Molero Jéssica , Ayán Carlos , Vilorio-Marques Laura , Molina Antonio Jose , González-Donquiles Carmen , Dávila-Batista Veronica , Fernández-Villa Tania , de Paz Jose Antonio , Martín Vicente 
Published: May 2018

Abstract
Colorectal cancer is a significant public health concern. As a multistage and multifactorial disease, environmental and genetic factors interact at each stage of the process, and an individual's lifestyle also plays a relevant role. We set out to review the scientific evidence to study the need to investigate the role of the peroxisome proliferator–activated receptor gamma coactivator 1 alpha (PGC-1α) gene as a biomarker of the physical activity's (PA) effect on colorectal cancer. PA is a protective factor against colorectal cancer and usually increases the expression of PGC-1α. This gene has pleiotropic roles and is the main regulator of mitochondrial functions. The development of colorectal cancer has been associated with mitochondrial dysfunction; in addition, alterations in this organelle are associated with colorectal cancer risk factors, such as obesity, decreased muscle mass, and the aging process. These are affected by PA acting, among other aspects, on insulin sensitivity and oxygen reactive species/redox balance. Therefore, this gene demands special attention in the understanding of its operation in the consensual protective effect of PA in colorectal cancer. A significant amount of indirect evidence points to PGC-1α as a potential biomarker in the PA-protective effect on colorectal cancer. The article focuses on the possible involvement of PGC-1α in the protective role that physical activity has on colorectal cancer. This is an important topic both in relation to advances in prevention of the development of this widespread disease and in its therapeutic treatment. We hope to generate an initial hypothesis for future studies associated with physical activity–related mechanisms that may be involved in the development or prevention of colorectal cancer. PGC-1α is highlighted because it is the main regulator of mitochondrial functions. This organelle, on one hand, is positively stimulated by physical activity; on the other hand, its dysfunction or reduction increases the probability of developing colorectal cancer. Therefore, we consider the compilation of existing information about the possible ways to understand the mechanisms of this gene to be highly relevant. This study is based on evidence of PGC-1α and physical activity, on PGC-1α and colorectal cancer, on colorectal cancer and physical activity/inactivity, and the absence of studies that have sought to relate all of these variables. Cancer Prev Res; 11(9); 523–34. ©2018 AACR.