bluuebunny/crossref_metadata_2025_split huggingface dataset:
Electromechanical impedance instrumented circular piezoelectric-metal transducer for corrosion monitoring: modeling and validation
Authors: Li Weijie , Wang Jianjun , Liu Tiejun , Luo Mingzhang 
Published: January 2020

Abstract
Corrosion induced thickness loss of metallic structures is one of the most common issues across multiple industries. In our previous work, a new type of corrosion sensor based on lead zirconate titanate (PZT) using electromechanical impedance (EMI) technique was proposed. The sensor is fabricated by bonding a PZT patch onto a metal plate. The previous work has demonstrated that the peak frequencies in the conductance signatures decrease linearly with the increase of the corrosion induced thickness loss. However, a theoretical model that fully describe the coupled vibration between piezoelectric element and the metal plate, and the EMI characteristics has not been established. This paper presents the theoretical modeling of the EMI instrumented circular piezoelectric-metal transducer for corrosion monitoring purpose. Based on electro-elastic and Kirchhoff plate theory, the EMI responses of the transducer operated in transverse bending modes with free boundary conditions were modeled. Finite element modeling calculations and experimental measurement were conducted to validate the theoretical results with good agreement.
Epidermal ROCK2 induces AKT1/GSK3β/β-catenin, NFκB and dermal tenascin C; but enhanced differentiation and p53/p21 inhibit papilloma
Authors: Masre Siti F , Rath Nicola , Olson Michael F , Greenhalgh David A 
Published: January 2020

Abstract
ROCK2 roles in epidermal differentiation and carcinogenesis have been investigated in mice expressing an RU486-inducible, 4HT-activated ROCK2 transgene (K14.creP/lslROCKer). RU486/4HT-mediated ROCKer activation induced epidermal hyperplasia similar to cutaneous oncogenic rasHa (HK1.ras); however ROCKer did not elicit papillomas. Instead, anomalous basal-layer ROCKer expression corrupted normal ROCK2 roles underlying epidermal rigidity/stiffness and barrier maintanance, resulting in premature keratin K1, loricrin and filaggrin expression. Also, hyperproliferative/stress-associated keratin K6 was reduced; possibly reflecting altered ROCK2 roles in epidermal rigidity and keratinocyte flexibility/migration during wound healing. Consistent with increased proliferation, K14.creP/lslROCKer hyperplasia displayed supra-basal-to-basal increases in activated p-AKT1, inactivated p-GSK3β ser9 and membranous/nuclear β-catenin expression together with weak NFκB, which were absent in equivalent HK1.ras hyperplasia. Furthermore, ROCKer-mediated increases in epidermal rigidity via p-MypT1 inactivation/elevated MLC, coupled to anomalous β-catenin expression, induced tenascin C-positive dermal fibroblasts. Alongside an altered ECM, these latent tenascin C-positive dermal fibroblasts may become putative pre-cancer–associated fibroblasts (pre-CAFs) and establish a susceptibility that subsequently contributes to tumour progression. However, anomalous differentiation was also accompanied by an immediate increase in basal-layer p53/p21 expression; suggesting that while ROCK2/AKT1/β-catenin activation increased keratinocyte proliferation resulting in hyperplasia, compensatory p53/p21 and accelerated differentiation helped inhibit papillomatogenesis.
Family medicine physicians’ confidence and perceived effectiveness in delivering health behaviour change interventions
Authors: Sherman Michelle D , Hooker Stephanie A 
Published: January 2020

Abstract

Background
Approximately 40% of deaths in the USA are attributable to modifiable health behaviours. Despite clear recommendations and practice guidelines, primary care physicians (PCPs) generally do not dedicate much time to addressing health behaviours, thereby missing opportunities to improve patient well-being.

Objective(s)
To examine what health behaviour change techniques PCPs use with their patients, including frequency of use, confidence in and perceived effectiveness of those interventions.

Methods
Using a cross-sectional study design, family medicine resident and faculty physicians (n = 68) from three residency training programs completed an anonymous online survey. Questions explored their use of, confidence in and perceived effectiveness of health behaviour change interventions for six domains: physical activity, healthy eating, medication adherence, smoking cessation, sleep and alcohol reduction. Qualitative responses to open-ended questions were double coded by two independent raters. PCPs’ open-ended responses to questions regarding specific intervention techniques were coded using an evidence-based behaviour change taxonomy.

Results
Although PCPs indicated that they address health behaviour topics quite frequently with their patients, they reported only moderate confidence and low-to-moderate perceived effectiveness with their interventions. The most frequently cited technique was providing instruction (telling patients what to do). PCPs reported lowest frequency of addressing, lowest confidence and lowest effectiveness regarding helping patients decrease their use of alcohol. Insufficient time and perceived low patient motivation were commonly cited barriers.

Conclusion
These findings highlight the need for the development and evaluation of educational curricula to teach physicians brief, evidence-based approaches to helping patients make these changes in their health-related behaviours.
Sexuality as a Standard of Civilization: Historicizing (Homo)Colonial Intersections of Race, Gender, and Class
Authors: Delatolla Andrew 
Published: January 2020

AbstractIn recent years, acceptance and tolerance of homosexuality has become symbolic of Western liberal, social, and political progress. This has been noted in discussions on homonormativity, homonationalism, and homocolonialism. While some of these discussions have touched on the intersections between sexuality, race, gender, and class, this article argues that this relationship has been historically produced as a standard of civilization. It notes that the politics and governance of sexuality, and its intersections with race, gender, and class, have historical relevance in producing social and political exclusions. In building this argument, the article considers how the politics and governance of sexuality have maintained a “divided world,” from the nineteenth century to the twenty-first century, transforming from a hetero- to a homocolonial standard of civilization. It draws from a number of examples, from the nineteenth century to the contemporary period, using a diverse set of materials, including ethnographic research, fieldwork, and historical documents to explain temporal and geographic connections regarding the politics of sexuality.
Binding interface and impact on protease cleavage for an RNA aptamer to HIV-1 reverse transcriptase
Authors: Nguyen Phuong D M , Zheng Jie , Gremminger Thomas J , Qiu Liming , Zhang Dong , Tuske Steve , Lange Margaret J , Griffin Patrick R , Arnold Eddy , Chen Shi-Jie , Zou Xiaoqin , Heng Xiao , Burke Donald H 
Published: January 2020

AbstractRNA aptamers that bind HIV-1 reverse transcriptase (RT) inhibit RT in enzymatic and viral replication assays. Some aptamers inhibit RT from only a few viral clades, while others show broad-spectrum inhibition. Biophysical determinants of recognition specificity are poorly understood. We investigated the interface between HIV-1 RT and a broad–spectrum UCAA-family aptamer. SAR and hydroxyl radical probing identified aptamer structural elements critical for inhibition and established the role of signature UCAA bulge motif in RT-aptamer interaction. HDX footprinting on RT ± aptamer shows strong contacts with both subunits, especially near the C-terminus of p51. Alanine scanning revealed decreased inhibition by the aptamer for mutants P420A, L422A and K424A. 2D proton nuclear magnetic resonance and SAXS data provided constraints on the solution structure of the aptamer and enable computational modeling of the docked complex with RT. Surprisingly, the aptamer enhanced proteolytic cleavage of precursor p66/p66 by HIV-1 protease, suggesting that it stabilizes the productive conformation to allow maturation. These results illuminate features at the RT-aptamer interface that govern recognition specificity by a broad-spectrum antiviral aptamer, and they open new possibilities for accelerating RT maturation and interfering with viral replication.
Identifying Sources of Inefficiency in Healthcare*
Authors: Chandra Amitabh , Staiger Douglas O 
Published: January 2020

Abstract
In medicine, the reasons for variation in treatment rates across hospitals serving similar patients are not well understood. Some interpret this variation as unwarranted and push standardization of care as a way of reducing allocative inefficiency. An alternative interpretation is that hospitals with greater expertise in a treatment use it more because of their comparative advantage, suggesting that standardization is misguided. A simple economic model provides an empirical framework to separate these explanations. Estimating this model with data for heart attack patients, we find evidence of substantial variation across hospitals in allocative inefficiency and comparative advantage, with most hospitals overusing treatment in part because of incorrect beliefs about their comparative advantage. A stylized welfare calculation suggests that eliminating allocative inefficiency would increase the total benefits from the treatment that we study by 44%.
Histology of the Cochlear Outer Sulcus Cells in Normal Human Ears, Presbycusis, and Menière's Disease
Authors: Christov Florian , Nelson Erik G. , Xu Lucy J. , Lopez Ivan A. , Ishiyama Akira , Gluth Michael B. 
Published: January 2020

Hypothesis:
Outer sulcus cell features and distribution are hypothesized to differ throughout regions of the human cochlea and between diseased and normal specimens.

Background:
Outer sulcus cells play a role in inner ear fluid homeostasis. However, their anatomy and distribution in the human are not well described.

Methods:
Temporal bone specimens with normal hearing (n = 10), Menière's disease (n = 10), presbycusis with flat audiograms (n = 4), and presbycusis with sloping audiograms (n = 5) were examined by light microscopy. Outer sulcus cells were assessed quantitatively and qualitatively in each cochlear turn. One specimen was stained for tubulin immunofluorescence and imaged using confocal microscopy.

Results:
Outer sulcus cells interface with endolymph throughout the cochlea, with greatest contact in the apical turn. Mean outer sulcus cell counts in the upper apical turn (8.82) were generally smaller (all p < 0.05) than those of the upper basal (17.71), lower middle (18.99) upper middle (18.23), and lower apical (16.42) turns. Mean outer sulcus cell counts were higher (p < 0.05) in normal controls (20.1) than in diseased specimens (15.29). There was a significant correlation between mean cell counts and tonotopically expected hearing thresholds in the upper basal (r = −0.662, p = 0.0001), lower middle (r = −0.565, p = 0.0017), and upper middle (r = −0.507, p = 0.0136) regions. Other differences in cell morphology, distribution, or relationship with Claudius cells were not appreciated between normal and diseased specimens. Menière's specimens had no apparent unique features in the cochlear apex. Immunofluorescence staining demonstrated outer sulcus cells extending into the spiral ligament in bundles forming tapering processes which differed between the cochlear turns in morphology.

Conclusion:
Outer sulcus cells vary throughout the cochlear turns and correlate with hearing status, but not in a manner specific to the underlying diagnoses of Menière's disease or presbycusis.
CTCF orchestrates long-range cohesin-driven V(D)J recombinational scanning
Authors: Ba Zhaoqing , Lou Jiangman , Dring Edward W. , Ye Adam Yongxin , Lin Sherry G. , Jain Suvi , Kieffer-Kwon Kyong-Rim , Casellas Rafael , Alt Frederick W. 
Published: January 2020

AbstractRAG endonuclease initiates V(D)J recombination in progenitor (pro)-B cells1. Upon binding a recombination center (RC)-based JH, RAG scans upstream chromatin via loop extrusion, potentially mediated by cohesin2–10, to locate Ds and assemble a DJH-based RC11. CTCF looping factor-bound elements (CBEs) within IGCR1 upstream of Ds impede RAG-scanning12–15; but their inactivation allows scanning to proximal VHs where additional CBEs activate rearrangement and impede scanning any further upstream15, 16. Distal VHutilization is thought to involve diffusional RC access following large-scaleIghlocus contraction17–23. Here, we test the potential of linear RAG-scanning to mediate distal VHusage in G1-arrested,v-Abl-pro-B cell lines24, 25, which undergo robust D-to-JHbut little VH-to-DJHrearrangements, presumably due to lack of locus contraction11, 15. Through an auxin-inducible approach26, 27, we degrade the cohesin-component Rad214, 7, 27or CTCF7, 9in these G1-arrested lines, which maintain substantial viability throughout four-day experiments. Rad21 degradation eliminated all V(D)J recombination and RAG-scanning-associated interactions, except RC-located DQ52-to-JHjoining in which synapsis occurs by diffusion11. Remarkably, while CTCF degradation suppressed most CBE-based chromatin interactions, it promoted robust RC interactions with, and robust VH-to-DJHjoining of, distal VHs, with patterns similar to those of “locus-contracted” primary pro-B cells. Thus, down-modulation of CTCF-bound scanning-impediment activity promotes cohesin-driven RAG-scanning across the 2.7MbIghlocus.
Chemically Induced Chromosomal Interaction (CICI): A New Tool to Study Chromosome Dynamics and Its Biological Roles
Authors: Du Manyu , Zou Fan , Yan Yujie , Bai Lu 
Published: January 2020

AbstractNumerous intra- and inter-chromosomal contacts have been mapped in eukaryotic genomes, but it remains challenging to link these 3D structures to their regulatory functions. To establish the causal relationships between chromosome conformation and genome functions, we need a method that allows us to selectively perturb the conformation at targeted loci. Here, we developed a method in budding yeast, Chemically Induced Chromosomal Interaction (CICI), to engineer long-distance chromosomal interactions selectively and dynamically. We implemented CICI at multiple intra- and inter-chromosomal loci pairs and showed that CICI can form in >50% of cells, even between loci with very low Hi-C contact frequencies. CICI formation is slower at these low Hi-C sites, revealing the dynamic nature of the Hi-C signals. As a functional test, we forced the interaction between mating-type locus (MAT) andHMRand observed significant change in donor preference during mating-type switching, showing that chromosome conformation plays an important role in homology-directed DNA repair. Overall, these results demonstrate that CICI is a powerful tool to study chromosome dynamics and the 3D genome function.
Structural colours reflect individual quality: a meta-analysis
Authors: White Thomas E. 
Published: January 2020

AbstractOrnamental colouration often communicates salient information to mates, and theory predicts covariance between signal expression and individual quality. This has borne out among pigment-based signals, but the potential for ‘honesty’ in structural colouration is unresolved. Here I synthesised the available evidence to test this prediction via meta-analysis and found that, overall, the expression of structurally coloured sexual signals is positively associated with individual quality. The effects varied by measure of quality, however, with body condition and immune function reliably encoded across taxa, but not age nor parasite resistance. The relationship was apparent for both the colour and brightness of signals and was slightly stronger for iridescent ornaments. These results suggest diverse pathways to the encoding and exchange of information among structural colours, while highlighting outstanding questions as to the development, visual ecology, and evolution of this striking adornment.
KDM6A mediated expression of the long noncoding RNA DINO causes TP53 tumor suppressor stabilization in Human Papillomavirus type 16 E7 expressing cells
Authors: Sharma Surendra , Munger Karl 
Published: January 2020

ABSTRACTHPV16 E7 has long been noted to stabilize the TP53 tumor suppressor. However, the molecular mechanism of TP53 stabilization by HPV16 E7 has remained obscure and can occur independent of E2F regulated MDM2 inhibitor, p14ARF. Here, we report that the Damage Induced Noncoding (DINO) lncRNA (DINOL) is the missing link between HPV16 E7 and increased TP53 levels. DINO levels are decreased in cells where TP53 is inactivated, either by HPV16 E6, expression of a dominant negative TP53 minigene or by TP53 depletion. DINO levels are increased in HPV16 E7 expressing cells. HPV16 E7 causes increased DINO expression independent of RB1 degradation and E2F1 activation. Similar to the adjacent CDKN1A locus, DINO expression is regulated by the histone demethylase, KDM6A. DINO stabilizes TP53 in HPV16 E7 expressing cells and as a TP53 transcriptional target, DINO levels further increase. Similar to other oncogenes such as adenovirus E1A or MYC, HPV16 E7 expressing cells are sensitized to cell death under conditions of metabolic stress and in the case of E7, this has been linked to TP53 activation. Consistent with earlier studies, we show that HPV16 E7 expressing keratinocytes are highly sensitive to metabolic stress induced by the antidiabetic drug, metformin. Metformin sensitivity of HPV16 E7 expressing cells is rescued by DINO depletion. This work identifies DINO as a critical mediator TP53 stabilization and activation in HPV16 E7 expressing cells.IMPORTANCEViral oncoproteins, including HPV16 E6 and E7 have been instrumental in elucidating the activities of cellular signaling networks including those governed by the TP53 tumor suppressor. Our study demonstrates that the long noncoding RNA DINO is the long sought missing link between HPV16 E7 and elevated TP53 levels. Importantly, the TP53 stabilizing DINO plays a critical role in the predisposition of HPV16 E7 expressing cells to cell death under metabolic stress conditions from metformin treatment.
Colon-specific immune microenvironment regulates cancer progression versus rejection
Authors: Trimaglio Giulia , Tilkin-Mariamé Anne-Françoise , Feliu Virginie , Lauzeral-Vizcaino Françoise , Tosolini Marie , Valle Carine , Ayyoub Maha , Neyrolles Olivier , Vergnolle Nathalie , Rombouts Yoann , Devaud Christel 
Published: January 2020

AbstractBackgroundImmunotherapies have achieved clinical benefit in many types of cancer but remain limited to a subset of patients in colorectal cancer (CRC). Resistance to immunotherapy can be attributed in part to tissue-specific factors constraining antitumor immunity. Thus, a better understanding of how the colon microenvironment shapes the immune response to CRC is needed to identify mechanisms of resistance to immunotherapies and guide the development of novel therapeutics.MethodsIn an orthotopic mouse model of MC38-CRC, tumor progression was monitored by bioluminescence imaging and the immune signatures were assessed at a transcriptional level using NanoString and at a cellular level by flow cytometry.ResultsDespite initial tumor growth in all mice, only 25 to 35% of mice developed a progressive lethal CRC while the remaining animals spontaneously rejected their solid tumor. No tumor rejection was observed in the absence of adaptive immunity, nor when MC38 cells were injected in non-orthotopic locations, subcutaneously or into the liver. We observed that progressive CRC tumors exhibited a protumor immune response, characterized by a regulatory T-lymphocyte pattern, discernible shortly post-tumor implantation, as well as suppressive myeloid cells. In contrast, tumor-rejecting mice presented an early inflammatory response and an antitumor microenvironment enriched in CD8+T cells.ConclusionsTaken together, our data demonstrate the role of the colon microenvironment in regulating the balance between anti or protumor immune responses. While emphasizing the relevance of the CRC orthotopic model, they set the basis for exploring the impact of the identified signatures in colon cancer response to immunotherapy.
Chimera-competent eXtra-Embryonic eNdoderm (XEN) cells established from pig embryos
Authors: Park Chi , Jeoung Young , Uh Jun , Park Kieun , Bridge Jessica , Powell Anne , Li Jie , Pence Laramie , Liu Tianbin , Sun Hai-Xi , Gu Ying , Shen Yue , Wu Jun , Izpisua Belmonte Juan-Carlos , Telugu Bhanu P. 
Published: January 2020

AbstractIn this article, we report for the first time the derivation and characterization of extra-embryonic endoderm (XEN) cells from primitive endoderm (PrE) of porcine (p) embryos. The pXEN cells can be reliably and reproducibly generated from parthenote, in vitro and in vivo derived embryos. The pXEN cells retained all the hallmarks of PrE including expression of canonical PrE and XEN cell markers (GATA4, GATA6, SOX17, SALL4, FOXA2, andHNF4A). Transcriptome analysis further confirmed their XEN cell origin. The pXEN cells when introduced into blastocyst stage embryo contributed to wide-spread chimerism including visceral yolk sac, chorion, as well as embryonic gut and liver primordium in the fetus. The pXEN cells were shown to be an efficient nuclear donor for generating cloned offspring. Taken together, pXEN cells fulfil a longstanding need for a stable, chimera-competent, and nuclear transfer-compatible porcine embryonic cells with applications for agriculture and medicine.Significance StatementWe report for the first time, the derivation and characterization of extraembryonic endoderm (XEN) stem cells from porcine (p) embryos. The pXEN cells can be reliably and reproducibly derived from primitive endoderm precursors. When injected into blastocyst-stage embryos, the pXEN cells have contributed to wide-spread chimerism including visceral yolk sac, chorion of the extraembryonic membranes, as well as definitive endoderm of the fetus, primarily the embryonic gut and liver primordium. Additionally, these XEN cells have proven to be an efficient nuclear donor for generating cloned offspring. These newly discovered stem cells provide a novel model for studying lineage segregation, as well as a source for interspecies chimeras for generating endodermal organs, and for genome editing in livestock.
The transcriptional landscape of cultivated strawberry (Fragraia×ananassa) and its diploid ancestor (Fragraia×vesca) during fruit development
Authors: Li Yongping , Liu Tianjia , Luo Huifeng , Liu Shengcai 
Published: January 2020

AbstractCultivated strawberry (Fragaria ananassa) comes from four diploid ancestors:F.vesca, F.viridis, F. iinumae and F.nipponica. Among them, theF.vescais the most dominance subgenome for cultivated strawberry. It is not well understood how gene expression contributes to differences during fruit development between diploid and octoploid strawberry. Here, we used comprehensive transcriptomic analyses ofF.vescaandF. ×ananassato investigate gene expression at different stages of fruit development. In total, we obtained a total of 3,187 (turning stage) and 3,061 (red stage) differentially expressed genes with the pairwise comparisons between diploid and octoploid. Genes involved in flavonoids and phenlypropanoids biosynthesis, were almost up-regulated in the both turning and red stages of octoploid, and we also discovery a ripe-fruit specific module associated with several flavonoids biosynthesis genes, includingFveMYB10, FveMYB9/11, andFveRAPby using weighted gene coexpression network analysis (WGCNA). Furthermore, we identified the species-specific regulated network in the octoploid and diploid fruit. Notably, we found that the WAK and F-box genes were enriched in the octoploid and diploid fruits, respectively. As a whole, this study contributes to shed new light on the flavonoid biosynthetic and fruit size of strawberry, with important implications for future molecular breeding in the cultivated strawberry.