gebhart/patrepeval huggingface dataset:
Employment and Domestic Work: A Comparison of Samples of British and French Women (1992)

Increasing attention has recently been paid to the comparative analysis of women’s labour force participation (Jenson, 1988; Mincer, 1985; Paukert, 1984; Rubery, 1988). Whilst labour economists have highlighted a converging trend, linked with hypotheses on the role of human capital (Mincer, 1985), sociologists have focussed upon significant differences associated with variation in the social institutional context in which the labour market operates.2 Here the comparison of Britain and France becomes clearly relevant (Beechey, 1989; Benoit Guilbot, 1987; Dex and Walters, 1989; Walters and Dex in this volume). Both are developed industrialised societies with roughly similar rates of overall female labour force participation.3 Yet two differences stand out, the propensity to continuity of women’s employment over their working lives and the proportion of women who work part-time.
Supplementary Table 5 from MYC Phosphorylation at Novel Regulatory Regions Suppresses Transforming Activity (2023)

&lt;p&gt;XLSX file, 14K, Gene expression changes common to wild type MYC and all phosphorylation mutants (112 genes).&lt;/p&gt;
Deletion of the p16INK4a tumor suppressor and expression of the androgen receptor induce sarcomatoid carcinomas with signet ring cells in the mouse prostate (2019)

The tumor suppressor p16Ink4a, encoded by the INK4a gene, is an inhibitor of cyclin D-dependent kinases 4 and 6, CDK4 and CDK6. This inhibition prevents the phosphorylation of the retinoblastoma protein (pRb), resulting in cellular senescence through inhibition of E2F-mediated transcription of S phase genes required for cell proliferation. The p16Ink4a plays an important role in tumor suppression, whereby its deletion, mutation, or epigenetic silencing is a frequently observed genetic alteration in prostate cancer. To assess its roles and related molecular mechanisms in prostate cancer initiation and progression, we generated a mouse model with conditional deletion of p16Ink4a in prostatic luminal epithelium. The mice underwent oncogenic transformation and developed prostatic intraepithelial neoplasia (PIN) from eight months of age, but failed to develop prostatic tumors. Given the prevalence of aberrant androgen signaling pathways in prostate cancer initiation and progression, we then generated R26hARL/wt:p16L/L: PB-Cre4 compound mice, in which conditional expression of the human AR transgene and deletion of p16Ink4a co-occur in prostatic luminal epithelial cells. While R26hARL/wt:PB-Cre4 mice showed no visible pathological changes, R26hARL/wt:p16L/L: PB-Cre4 compound mice displayed an early onset of high-grade PIN (HGPIN), prostatic carcinoma, and metastatic lesions. Strikingly, we observed tumors resembling human sarcomatoid carcinoma with intermixed focal regions of signet ring cell carcinoma (SRCC) in the prostates of the compound mice. Further characterization of these tumors showed they were of luminal epithelial cell origin, and featured characteristics of epithelial to mesenchymal transition (EMT) with enhanced proliferative and invasive capabilities. Our results not only implicate a biological role for AR expression and p16Ink4a deletion in the pathogenesis of prostatic SRCC, but also provide a new and unique genetically engineered mouse (GEM) model for investigating the molecular mechanisms for SRCC development.
Functional Stability of Unliganded Envelope Glycoprotein Spikes among Isolates of Human Immunodeficiency Virus Type 1 (HIV-1) (2011)

The HIV-1 envelope glycoprotein (Env) spike is challenging to study at the molecular level, due in part to its genetic variability, structural heterogeneity and lability. However, the extent of lability in Env function, particularly for primary isolates across clades, has not been explored. Here, we probe stability of function for variant Envs of a range of isolates from chronic and acute infection, and from clades A, B and C, all on a constant virus backbone. Stability is elucidated in terms of the sensitivity of isolate infectivity to destabilizing conditions. A heat-gradient assay was used to determine T(90) values, the temperature at which HIV-1 infectivity is decreased by 90% in 1 h, which ranged between ∼40 to 49°C (n = 34). For select Envs (n = 10), the half-lives of infectivity decay at 37°C were also determined and these correlated significantly with the T(90) (p = 0.029), though two 'outliers' were identified. Specificity in functional Env stability was also evident. For example, Env variant HIV-1(ADA) was found to be labile to heat, 37°C decay, and guanidinium hydrochloride but not to urea or extremes of pH, when compared to its thermostable counterpart, HIV-1(JR-CSF). Blue native PAGE analyses revealed that Env-dependent viral inactivation preceded complete dissociation of Env trimers. The viral membrane and membrane-proximal external region (MPER) of gp41 were also shown to be important for maintaining trimer stability at physiological temperature. Overall, our results indicate that primary HIV-1 Envs can have diverse sensitivities to functional inactivation in vitro, including at physiological temperature, and suggest that parameters of functional Env stability may be helpful in the study and optimization of native Env mimetics and vaccines.
Abstract 1892: Identification of differentially methylated genes associated with cetuximab and erlotinib resistance (2012)

Abstract Anti-EGFR therapy is among the most promising molecular targeted therapies against cancer developed in the past decade. Two classes of EGFR-directed therapeutic inhibitors are currently in clinical use: anti-EGFR monoclonal antibodies, such as cetuximab, and small-molecule tyrosine kinase inhibitors (TKIs) of EGFR, such as erlotinib. Although both classes of drugs are capable of inducing an initial therapeutic response, primary as well as acquired drug resistance is frequently observed. Emerging evidence has linked epigenetic changes, such as DNA methylation at CpG islands, to the development of cytotoxic chemotherapeutic drug resistance. To identify genes that are specifically methylated during the evolution of resistance to anti-EGFR therapeutic agents, we employed two parental NSCLC and HNSCC cell lines and their resistant derivatives to either erlotinib or cetuximab. DNA from each pair was used for methylation-specific array containing a panel of 64 genes that are commonly known to be regulated through promoter methylation. We found that death-associated protein kinase 1 (DAPK1) was hypermethylated in drug resistant cells generated from both parental cell lines. Restoration of DAPK1 into the resistant cells by stable transfection re-sensitized the cells to both erlotinib and cetuximab. Conversely, siRNA-mediated knockdown of DAPK1 induced resistance in the parental sensitive cells. These results demonstrate that DAPK1 plays an important role in both cetuximab and erlotinib resistance in NSCLC and HNSCC cancer cells, and that promoter methylation of its gene frequently occurs during the chronic treatment of anti-EGFR agents. In conclusion, DAPK1 could be a novel target for the improvement of therapeutic benefit of anti-EGFR therapy. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1892. doi:1538-7445.AM2012-1892
Design of a micro-pattern structure for a three dimensionally macroporous Sn–Ni alloy anode with high areal capacity (2011)

A highly patterned porous Sn-Ni anode with various patterns was investigated as an anode for a lithium battery and showed much higher areal capacity than a conventional graphite electrode. This result proves the importance of a structured electrode for development of an electrode with higher performance.
Feasibility of quantifying the mechanical properties of lung parenchyma in a small‐animal model using 1H magnetic resonance elastography (MRE) (2009)

It is feasible to perform lung MRE in small animals using conventional MR imaging technologies.
Amide-to-ester substitution as a stable alternative to N-methylation for increasing membrane permeability in cyclic peptides (2023)

Naturally occurring peptides with high membrane permeability often have ester bonds on their backbones. However, the impact of amide-to-ester substitutions on the membrane permeability of peptides has not been directly evaluated. Here we report the effect of amide-to-ester substitutions on the membrane permeability and conformational ensemble of cyclic peptides related to membrane permeation. Amide-to-ester substitutions are shown to improve the membrane permeability of dipeptides and a model cyclic hexapeptide. NMR-based conformational analysis and enhanced sampling molecular dynamics simulations suggest that the conformational transition of the cyclic hexapeptide upon membrane permeation is differently influenced by an amide-to-ester substitution and an amide N-methylation. The effect of amide-to-ester substitution on membrane permeability of other cyclic hexapeptides, cyclic octapeptides, and a cyclic nonapeptide is also investigated to examine the scope of the substitution. Appropriate utilization of amide-to-ester substitution based on our results will facilitate the development of membrane-permeable peptides.
Peptidylarginine Deiminase of Porphyromonas gingivalis Modulates the Interactions between Candida albicans Biofilm and Human Plasminogen and High-Molecular-Mass Kininogen (2020)

Microorganisms that create mixed-species biofilms in the human oral cavity include, among others, the opportunistic fungus <i>Candida albicans</i> and the key bacterial pathogen in periodontitis, <i>Porphyromonas gingivalis</i>. Both species use arsenals of virulence factors to invade the host organism and evade its immune system including peptidylarginine deiminase that citrullinates microbial and host proteins, altering their function. We assessed the effects of this modification on the interactions between the <i>C. albicans</i> cell surface and human plasminogen and kininogen, key components of plasma proteolytic cascades related to the maintenance of hemostasis and innate immunity. Mass spectrometry was used to identify protein citrullination, and microplate tests to quantify the binding of modified plasminogen and kininogen to <i>C. albicans</i> cells. Competitive radioreceptor assays tested the affinity of citrullinated kinins to their specific cellular receptors. The citrullination of surface-exposed fungal proteins reduced the level of unmodified plasminogen binding but did not affect unmodified kininogen binding. However, the modification of human proteins did not disrupt their adsorption to the unmodified fungal cells. In contrast, the citrullination of kinins exerted a significant impact on their interactions with cellular receptors reducing their affinity and thus affecting the role of kinin peptides in the development of inflammation.
Front Matter: Volume 7090 (2008)

This PDF file contains the front matter associated with SPIE Proceedings Volume 7090, including the Title Page, Copyright information, Table of Contents, Introduction (if any), and the Conference Committee listing.
The Selective α7 Agonist GTS-21 Attenuates Cytokine Production in Human Whole Blood and Human Monocytes Activated by Ligands for TLR2, TLR3, TLR4, TLR9, and RAGE (2009)

The cholinergic antiinflammatory pathway modulates inflammatory cytokine production through a mechanism dependent on the vagus nerve and the alpha7 subunit of the nicotinic acetylcholine receptor. GTS-21 [3-(2,4-dimethoxybenzylidene) anabaseine], a selective alpha7 agonist, inhibits inflammatory cytokine production in murine and human macrophages and in several models of inflammatory disease in vivo, but to date its antiinflammatory efficacy in human monocytes has not been characterized. We report here our findings that GTS-21 attenuates tumor necrosis factor (TNF) and interleukin 1beta levels in human whole blood activated by exposure to endotoxin. GTS-21 inhibited TNF production in endotoxin-stimulated primary human monocytes in vitro at the transcriptional level. The suppressive effect of GTS-21 was more potent than nicotine in whole blood and monocytes. Furthermore, GTS-21 attenuated TNF production in monocytes stimulated with peptidoglycan, polyinosinic-polycytidylic acid, CpG, HMGB1 (high-mobility group box 1 protein), and advanced glycation end product-modified albumin. GTS-21 decreased TNF levels in endotoxin-stimulated whole blood obtained from patients with severe sepsis. These findings establish the immunoregulatory effect of GTS-21 on human monocytes, and indicate the potential benefits of further exploration of GTS-21's therapeutic uses in human inflammatory disease.
Asynchronous Evolution of Deep Neural Network Architectures (2023)

Many evolutionary algorithms (EAs) take advantage of parallel evaluation of candidates. However, if evaluation times vary significantly, many worker nodes (i.e.,\ compute clients) are idle much of the time, waiting for the next generation to be created. Evolutionary neural architecture search (ENAS), a class of EAs that optimizes the architecture and hyperparameters of deep neural networks, is particularly vulnerable to this issue. This paper proposes a generic asynchronous evaluation strategy (AES) that is then adapted to work with ENAS. AES increases throughput by maintaining a queue of up to $K$ individuals ready to be sent to the workers for evaluation and proceeding to the next generation as soon as $M&lt;
SU‐D‐202‐01: Functional Lung Avoidance and Response‐Adaptive Escalation (FLARE) RT: Feasibility of a Precision Radiation Oncology Strategy (2016)

Purpose: NSCLC patient RT is planned without consideration of spatial heterogeneity in lung function or tumor response, which may have contributed to failed uniform dose escalation in a randomized trial. The feasibility of functional lung avoidance and response‐adaptive escalation (FLARE) RT to reduce dose to [ 9 9m Tc]MAA‐SPECT/CT perfused lung while redistributing 74Gy within [ 1 8 F]FDG‐PET/CT biological target volumes was assessed. Methods: Eight Stage IIB–IIIB NSCLC patients underwent FDG‐PET/CT and MAA‐SPECT/CT treatment planning scans. Perfused lung objectives were derived from scatter/collimator/attenuation‐corrected MAA‐SPECT uptake relative to ITV‐subtracted lung to maintain &lt;20Gy mean lung dose (MLD). Prescriptions included 60Gy to PTV and concomitant boost of 74Gy mean to biological target volumes (BTV=GTV+PET margin) scaled to each BTV voxel by relative FDG‐PET SUV. Dose‐painting‐by‐numbers prescriptions were integrated into commercial TPS via previously reported ROI discretization. Dose constraints for lung, heart, cord, and esophagus were defined. FLARE RT plans were optimized with VMAT, proton pencil beam scanning (PBS) with 3%‐3mm robust optimization, and combination PBS (avoidance) plus VMAT (escalation). Dosimetric differences were evaluated by Friedman non‐parametric paired test with multiple sampling correction. Results: PTV and normal tissue objectives were not violated in 24 FLARE RT plans. Population median of mean BTV dose was 73.7Gy (68.5–75.5Gy), mean FDG‐PET peak dose was 89.7Gy (73.5–103Gy), MLD was 12.3Gy (7.5–19.6Gy), and perfused MLD was 4.8Gy (0.9–12.1Gy). VMAT achieved higher dose to the FDG‐PET peak subvolume (p=0.01), while PBS delivered lower dose to lung (p&lt;0.001). Voxelwise linear correlation between BTV dose and FDG‐PET uptake was higher for VMAT (R=0.93) and PBS+VMAT (R=0.94) compared to PBS alone (R=0.89). Conclusion: FLARE RT is feasible with VMAT and PBS. A combination of PBS for functional lung avoidance and VMAT for FDG‐PET dose escalation balances target/normal tissue objective tradeoffs. These results support future testing of FLARE RT safety and efficacy within a precision radiation oncology trial. This work was supported by a Research Scholar grant from the Radiological Society of North American Research &amp; Education Foundation.
Correction to Synthesis and Characterization of Thermosetting Furan-Based Epoxy Systems (2016)

ADVERTISEMENT RETURN TO ISSUEPREVAddition/CorrectionNEXTORIGINAL ARTICLEThis notice is a correctionCorrection to Synthesis and Characterization of Thermosetting Furan-Based Epoxy SystemsFengshuo Hu, John J. La Scala, Joshua M. Sadler, and Giuseppe R. Palmese*Cite this: Macromolecules 2016, 49, 6, 2408Publication Date (Web):March 7, 2016Publication History Published online7 March 2016Published inissue 22 March 2016https://pubs.acs.org/doi/10.1021/acs.macromol.5b02801https://doi.org/10.1021/acs.macromol.5b02801correctionACS PublicationsCopyright © 2016 American Chemical Society. This publication is available under these Terms of Use. Request reuse permissions This publication is free to access through this site. Learn MoreArticle Views1369Altmetric-Citations5LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail PDF (120 KB) Get e-AlertscloseSupporting Info (1)»Supporting Information Supporting Information Get e-Alerts
Ca‐Doping and Thermoelectric Properties of Ca x CoO 2 Epitaxial Films (2009)

This chapter contains sections titled: Introduction Experimental Methods Results and Discussions Conclusions
TWO- AND THREE-DIMENSIONAL ALGORITHMS FOR MICROWAVE IMAGING AND INVERSE SCATTERING (2003)

Abstract In this paper the Contrast Source Inversion method using a multiplicative weighted L2-norm Total Variation regularizer is applied to two- and three-dimensional image reconstruction from electromagnetic microwave tomography data. This iterative method avoids solving a full forward problem in each iteration which makes the method suitable to handle a large scale computational problem. Numerical results both from simulation and experimental data with high contrast biological objects in two- and three-dimensional are presented and discussed. Keywords:
Small Cell Clustering for Efficient Distributed Fog Computing: A Multi-User Case (2015)

Ultra-dense deployment of radio access points is a key enabler for future 5G networks. It allows the network to cope with the ever increasing mobile data traffic. In addition, these radio access points can serve as an infrastructure for a local mobile cloud computing platform referred to as fog computing. The fog is a capillary edge cloud that enables joint optimization of communication and computational resources for maintaining an efficient and scalable network design. In this paper, we address the problem of radio access points clustering for fog computing applications. We focus on the case where multiple users require fog computing services. We formulate the distributed clustering problem as a joint optimization of the computation and communication resources. We transform the non-convex original problem into an equivalent convex one. Our simulation results show that the clustering solution derived from this problem yields high users' satisfaction ratio while keeping low the communication power consumption of the computation cluster.
Gq/11-Mediated Signaling and Hypertrophy in Mice with Cardiac-Specific Transgenic Expression of Regulator of G-Protein Signaling 2 (2012)

Cardiac hypertrophy is a well-established risk factor for cardiovascular morbidity and mortality. Activation of G(q/11)-mediated signaling is required for pressure overload-induced cardiomyocyte (CM) hypertrophy to develop. We previously showed that among Regulators of G protein Signaling, RGS2 selectively inhibits G(q/11) signaling and its hypertrophic effects in isolated CM. In this study, we generated transgenic mice with CM-specific, conditional RGS2 expression (dTG) to investigate whether RGS2 overexpression can be used to attenuate G(q/11)-mediated signaling and hypertrophy in vivo. Transverse aortic constriction (TAC) induced a comparable rise in ventricular mass and ANF expression and corresponding hemodynamic changes in dTG compared to wild types (WT), regardless of the TAC duration (1-8 wks) and timing of RGS2 expression (from birth or adulthood). Inhibition of endothelin-1-induced G(q/11)-mediated phospholipase C β activity in ventricles and atrial appendages indicated functionality of transgenic RGS2. However, the inhibitory effect of transgenic RGS2 on G(q/11)-mediated PLCβ activation differed between ventricles and atria: (i) in sham-operated dTG mice the magnitude of the inhibitory effect was less pronounced in ventricles than in atria, and (ii) after TAC, negative regulation of G(q/11) signaling was absent in ventricles but fully preserved in atria. Neither difference could be explained by differences in expression levels, including marked RGS2 downregulation after TAC in left ventricle and atrium. Counter-regulatory changes in other G(q/11)-regulating RGS proteins (RGS4, RGS5, RGS6) and random insertion were also excluded as potential causes. Taken together, despite ample evidence for a role of RGS2 in negatively regulating G(q/11) signaling and hypertrophy in CM, CM-specific RGS2 overexpression in transgenic mice in vivo did not lead to attenuate ventricular G(q/11)-mediated signaling and hypertrophy in response to pressure overload. Furthermore, our study suggests chamber-specific differences in the regulation of RGS2 functionality and potential future utility of the new transgenic model in mitigating G(q/11) signaling in the atria in vivo.
Synthesis, Molecular and Crystal Structure of 3′-N-Alkylamino-3′-deoxythymidines and Some Biochemical Properties of Their Phosphorous Esters (1995)

Abstract Two approaches for the synthesis of 3′-N-alkylated 3′-amino-3′-deoxythymidines were developed, including both the reaction of 3′-amino-3′-deoxythymidine with aldehydes followed by the sodium borohydride reduction and preparation of the triphenylphosphinimine derivative and subsequent reaction with alkyl iodide. 5′-Triphosphates of the synthesized compounds were shown to be terminating substrates for human immunodeficiency virus and avian myeloblastosis virus reverse transcriptases as well as for DNA polymerase β from rat liver. At the same time these compounds did not demonstrate the properties of a terminating substrate in DNA synthesis catalyzed by human DNA polymerases α, ∊, and I from E. coli.
Figure S6 from Cathepsin B Is Dispensable for Cellular Processing of Cathepsin B-Cleavable Antibody–Drug Conjugates (2023)

&lt;p&gt;Supplementary Figure 6: Predicted catabolic pathway for mAb-VC-MMAE ADCs.&lt;/p&gt;