bluuebunny/crossref_metadata_2025_split huggingface dataset:
The confining color field in SU(3) gauge theory
Authors: Baker M. , Cea P. , Chelnokov V. , Cosmai L. , Cuteri F. , Papa A. 
Published: June 2020

AbstractWe extend a previous numerical study of SU(3) Yang–Mills theory in which we measured the spatial distribution of all components of the color fields surrounding a static quark–antiquark pair and provided evidence that the simulated gauge invariant chromoelectric field can be separated into a Coulomb-like ‘perturbative’ field and a ‘non-perturbative’ confining field. In this paper we hypothesize that the fluctuating color fields not measured in our simulations do not contribute to the string tension. Under this assumption the string tension is determined by the color fields we measure, which form a field strength tensor pointing in a single direction in color space. We call this the ‘Maxwell picture of confinement’. We provide an additional procedure to isolate the confining field. We then extract the string tension from a stress energy-momentum tensor having the Maxwell form, constructed from the simulated non-perturbative part of the field strength tensor. To test our hypothesis we calculate the string tension for values of the quark–antiquark separation ranging from 0.37 fm to 1.2 fm. We also calculate the spatial distributions of the energy-momentum tensor surrounding static quarks for this range of separations, and we compare with the distributions obtained from direct simulations of the energy-momentum tensor.
Strong Logic Obfuscation with Low Overhead against IC Reverse Engineering Attacks
Authors: Alasad Qutaiba , Yuan Jiann-Shuin , Subramanyan Pramod 
Published: June 2020

Untrusted foundries pose threats of integrated circuit (IC) piracy and counterfeiting, and this has motivated research into logic locking. Strong logic locking approaches potentially prevent piracy and counterfeiting by preventing unauthorized replication and use of ICs. Unfortunately, recent work has shown that most state-of-the-art logic locking techniques are vulnerable to attacks that utilize Boolean Satisfiability (SAT) solvers.
In this article, we extend our prior work on using silicon nanowire (SiNW) field-effect transistors (FETs) to produce obfuscated ICs that are resistant to reverse engineering attacks, such as the sensitization attack, SAT and approximate SAT attacks, as well as tracked signal attacks. Our method is based on exchanging some logic gates in the original design with a set of polymorphic gates (PLGs), designed using SiNW FETs, and augmenting the circuit with a small block, whose output is untraceable, namely, URSAT. The URSAT may not offer very strong resilience against the combined AppSAT-removal attack. Strong URSAT is achieved using only CMOS-logic gates, namely, S-URSAT. The proposed technique, S-URSAT + PLG-based traditional encryption, designed using SiNW FETs, increases the security level of the design to robustly thwart all existing attacks, including combined AppSAT-removal attack, with small penalties. Then, we evaluate the effectiveness of our proposed methods and subject it to a thorough security analysis. We also evaluate the performance penalty of the technique and find that it results in very small overheads in comparison to other works. The average area, power, and delay overheads of implementing 64 baseline key-bits of S-URSAT for small benchmarks are 5.03%, 2.60%, and −2.26%, respectively, while for large benchmarks they are 2.37%, 1.18%, and −1.93%.
Metastasis-Specific Gene Expression in Autochthonous and Allograft Mouse Mammary Tumor Models: Stratification and Identification of Targetable Signatures
Authors: Ross Christina , Szczepanek Karol , Lee Maxwell , Yang Howard , Peer Cody J. , Kindrick Jessica , Shankarappa Priya , Lin Zhi-Wei , Sanford Jack D. , Figg William D. , Hunter Kent W. 
Published: June 2020

Abstract

Breast cancer metastasis is a leading cause of cancer-related death of women in the United States. A hurdle in advancing metastasis-targeted intervention is the phenotypic heterogeneity between primary and secondary lesions. To identify metastasis-specific gene expression profiles we performed RNA-sequencing of breast cancer mouse models; analyzing metastases from models of various drivers and routes. We contrasted the models and identified common, targetable signatures. Allograft models exhibited more mesenchymal-like gene expression than genetically engineered mouse models (GEMM), and primary culturing of GEMM-derived metastatic tissue induced mesenchymal-like gene expression. In addition, metastasis-specific transcriptomes differed between tail vein and orthotopic injection of the same cell line. Gene expression common to models of spontaneous metastasis included sildenafil response and nicotine degradation pathways. Strikingly, in vivo sildenafil treatment significantly reduced metastasis by 54%, while nicotine significantly increased metastasis by 46%. These data suggest that (i) actionable metastasis-specific pathways can be readily identified, (ii) already available drugs may have great potential to alleviate metastatic incidence, and (iii) metastasis may be influenced greatly by lifestyle choices such as the choice to consume nicotine products. In summary, while mouse models of breast cancer metastasis vary in ways that must not be ignored, there are shared features that can be identified and potentially targeted therapeutically.

Implications:
The data we present here exposes critical variances between preclinical models of metastatic breast cancer and identifies targetable pathways integral to metastatic spread.

Visual Overview:
http://mcr.aacrjournals.org/content/molcanres/18/9/1278/F1.large.jpg.
Single-Cell Transcriptomics Analysis Identifies Nuclear Protein 1 as a Regulator of Docetaxel Resistance in Prostate Cancer Cells
Authors: Schnepp Patricia M. , Shelley Greg , Dai Jinlu , Wakim Nicole , Jiang Hui , Mizokami Atsushi , Keller Evan T. 
Published: June 2020

Abstract

The majority of patients with prostate cancer treated with docetaxel develop resistance to it. To better understand the mechanism behind the acquisition of resistance, we conducted single-cell RNA-sequencing (scRNA-seq) of docetaxel-sensitive and -resistant variants of DU145 and PC3 prostate cancer cell lines. Overall, sensitive and resistant cells clustered separately. Differential gene expression analysis between resistant and sensitive cells revealed 182 differentially expressed genes common to both prostate cancer cell lines. A subset of these genes gave a gene expression profile in the resistant transcriptome-like–sensitive cells similar to the resistant cells. Exploration for functional gene pathways identified 218 common pathways between the two cell lines. Protein ubiquitination was the most differentially regulated pathway and was enriched in the resistant cells. Transcriptional regulator analysis identified 321 potential regulators across both cell lines. One of the top regulators identified was nuclear protein 1 (NUPR1). In contrast to the single-cell analysis, bulk analysis of the cells did not reveal NUPR1 as a promising candidate. Knockdown and overexpression of NUPR1 in the prostate cancer cells demonstrated that NUPR1 confers docetaxel resistance in both cell lines. Collectively, these data demonstrate the utility of scRNA-seq to identify regulators of drug resistance. Furthermore, NUPR1 was identified as a mediator of prostate cancer drug resistance, which provides the rationale to explore NUPR1 and its target genes for reversal of docetaxel resistance.

Implications:
Using single-cell sequencing of prostate cancer, we show that NUPR1 plays a role in docetaxel resistance.
Bacterial SOS Genes mucAB/umuDC Promote Mouse Tumors by Activating Oncogenes Nedd9/Aurkb via a miR-145 Sponge
Authors: Tanooka Hiroshi , Inoue Ayako , Takahashi Ryou-u , Tatsumi Kouichi , Fujikawa Kazuo , Nagao Tetsuji , Ishiai Masamichi , Chiwaki Fumiko , Aoyagi Kazuhiko , Sasaki Hiroki , Ochiya Takahiro 
Published: June 2020

Abstract

The mechanism of cancer induction involves an aberrant expression of oncogenes whose functions can be controlled by RNAi with miRNA. Even foreign bacterial RNA may interfere with the expression of oncogenes. Here we show that bacterial plasmid mucAB and its Escherichia coli genomic homolog umuDC, carrying homologies that match the mouse anti-miR-145, sequestered the miR-145 function in mouse BALB 3T3 cells in a tetracycline (Tet)-inducible manner, activated oncogene Nedd9 and its downstream Aurkb, and further enhanced microcolony formation and cellular transformation as well as the short fragments of the bacterial gene containing the anti-miR-145 sequence. Furthermore, mucAB transgenic mice showed a 1.7-fold elevated tumor incidence compared with wild-type mice after treatments with 3-methylcolanthrene. However, the mutation frequency in intestinal stem cells of the mucAB transgenic mice was unchanged after treatment with X-rays or ethyl-nitrosourea, indicating that the target of mucAB/umuDC is the promotion stage in carcinogenesis.

Implications:
Foreign bacterial genes can exert oncogenic activity via RNAi, if endogenously expressed.

Visual Overview:
http://mcr.aacrjournals.org/content/molcanres/18/9/1271/F1.large.jpg.
Role of Rare and Low-Frequency Variants in Gene-Alcohol Interactions on Plasma Lipid Levels
Authors: Wang Zhe , Chen Han , Bartz Traci M. , Bielak Lawrence F. , Chasman Daniel I. , Feitosa Mary F. , Franceschini Nora , Guo Xiuqing , Lim Elise , Noordam Raymond , Richard Melissa A. , Wang Heming , Cade Brian , Cupples L. Adrienne , de Vries Paul S. , Giulanini Franco , Lee Jiwon , Lemaitre Rozenn N. , Martin Lisa W. , Reiner Alex P. , Rich Stephen S. , Schreiner Pamela J. , Sidney Stephen , Sitlani Colleen M. , Smith Jennifer A. , Willems van Dijk Ko , Yao Jie , Zhao Wei , Fornage Myriam , Kardia Sharon L.R. , Kooperberg Charles , Liu Ching-Ti , Mook-Kanamori Dennis O. , Province Michael A. , Psaty Bruce M. , Redline Susan , Ridker Paul M. , Rotter Jerome I. , Boerwinkle Eric , Morrison Alanna C. ,   on behalf of the CHARGE Gene-Lifestyle Interactions Working Group
Published: June 2020

Background:
Alcohol intake influences plasma lipid levels, and such effects may be moderated by genetic variants. We aimed to characterize the role of aggregated rare and low-frequency protein-coding variants in gene by alcohol consumption interactions associated with fasting plasma lipid levels.

Methods:
In the Cohorts for Heart and Aging Research in Genomic Epidemiology consortium, fasting plasma triglycerides and high- and low-density lipoprotein cholesterol were measured in 34 153 individuals with European ancestry from 5 discovery studies and 32 277 individuals from 6 replication studies. Rare and low-frequency functional protein-coding variants (minor allele frequency, ≤5%) measured by an exome array were aggregated by genes and evaluated by a gene-environment interaction test and a joint test of genetic main and gene-environment interaction effects. Two dichotomous self-reported alcohol consumption variables, current drinker, defined as any recurrent drinking behavior, and regular drinker, defined as the subset of current drinkers who consume at least 2 drinks per week, were considered.

Results:

We discovered and replicated 21 gene-lipid associations at 13 known lipid loci through the joint test. Eight loci (
PCSK9
,
LPA
,
LPL
,
LIPG
,
ANGPTL4
,
APOB
,
APOC3
, and
CD300LG
) remained significant after conditioning on the common index single-nucleotide polymorphism identified by previous genome-wide association studies, suggesting an independent role for rare and low-frequency variants at these loci. One significant gene-alcohol interaction on triglycerides in a novel locus was significantly discovered (
P
=6.65×10
−6
for the interaction test) and replicated at nominal significance level (
P
=0.013) in
SMC5
.

Conclusions:
In conclusion, this study applied new gene-based statistical approaches and suggested that rare and low-frequency genetic variants interacted with alcohol consumption on lipid levels.
Inflammation and Circulating Natriuretic Peptide Levels
Authors: Fish-Trotter Hannah , Ferguson Jane F. , Patel Nirav , Arora Pankaj , Allen Norrina B. , Bachmann Katherine N. , Daniels Lori B. , Reilly Muredach P. , Lima Joao A.C. , Wang Thomas J. , Gupta Deepak K. 
Published: June 2020

Background:
NPs (natriuretic peptides) are cardiac-derived hormones that promote natriuresis, diuresis, and vasodilation. Preclinical evidence suggests that nonhemodynamic triggers for NP release exist, with a few studies implicating inflammatory stimuli. We examined the association between inflammation and NP levels in humans.

Methods:
The associations between inflammation and NP levels were examined in 3 independent studies. First, in 5481 MESA (Multi-Ethnic Study of Atherosclerosis) participants, the cross-sectional (exam 1) and longitudinal (exams 1 to 3) associations between circulating IL6 (interleukin-6) and NT-proBNP (N terminal pro B-type natriuretic peptide) levels were examined in multivariable-adjusted models. Second, in a prospective study of 115 healthy individuals, changes in NP levels were quantified following exposure to lipopolysaccharide as an inflammatory stimulus. Third, in 13 435 hospitalized patients, the association between acute inflammatory conditions and circulating NP levels was assessed using multivariable-adjusted models.

Results:

At the baseline MESA exam, each 1-unit higher natural log IL6 was associated with 16% higher NT-proBNP level ([95% CI, 10%–22%];
P
=0.002). Each 1-unit higher baseline natural log IL6 level also associated with 6% higher NT-proBNP level ([95% CI, 1%–11%];
P
=0.02) at 4-year follow-up. In the lipopolysaccharide study, median NT-proBNP levels rose from 21 pg/mL pre-lipopolysaccharide to 54 pg/mL post-lipopolysaccharide,
P
<0.001. In the hospitalized patient study, acute inflammatory conditions were associated with 36% higher NP levels ([95% CI, 17%–60%];
P
<0.001).

Conclusions:
Inflammation appears to be associated with NP release. Interpretation of NP levels should therefore take into account inflammatory conditions.
O‐GlcNAcylation Mediates Glucose‐Induced Alterations in Endothelial Cell Phenotype in Human Diabetes Mellitus
Authors: Masaki Nobuyuki , Feng Bihua , Bretón‐Romero Rosa , Inagaki Elica , Weisbrod Robert M. , Fetterman Jessica L. , Hamburg Naomi M. 
Published: June 2020

Background

Posttranslational protein modification with O‐linked
N
‐acetylglucosamine (O‐Glc
NA
c) is linked to high glucose levels in type 2 diabetes mellitus (T2
DM
) and may alter cellular function. We sought to elucidate the involvement of O‐Glc
NA
c modification in endothelial dysfunction in patients with T2
DM
.

Methods and Results

Freshly isolated endothelial cells obtained by J‐wire biopsy from a forearm vein of patients with T2
DM
(n=18) was compared with controls (n=10). Endothelial O‐Glc
NA
c levels were 1.8‐ford higher in T2
DM
patients than in nondiabetic controls (
P
=0.003). Higher endothelial O‐Glc
NA
c levels correlated with serum fasting blood glucose level (
r
=0.433,
P
=0.024) and hemoglobin A
1c
(
r
=0.418,
P
=0.042). In endothelial cells from patients with T2
DM
, normal glucose conditions (24 hours at 5 mmol/L) lowered O‐Glc
NA
c levels and restored insulin‐mediated activation of endothelial nitric oxide synthase, whereas high glucose conditions (30 mmol/L) maintained both O‐Glc
NA
c levels and impaired insulin action. Treatment of endothelial cells with Thiamet G, an O‐Glc
NA
case inhibitor, increased O‐Glc
NA
c levels and blunted the improvement of insulin‐mediated endothelial nitric oxide synthase phosphorylation by glucose normalization.

Conclusions

Taken together, our findings indicate a role for O‐Glc
NA
c modification in the dynamic, glucose‐induced impairment of endothelial nitric oxide synthase activation in endothelial cells from patients with T2
DM
. O‐Glc
NA
c protein modification may be a treatment target for vascular dysfunction in T2
DM
.
You Can Lead a Horse to Water, But You Can’t Make It Drink
Authors: Levy Gabriel 
Published: June 2020

Abstract
As I understand it, the central aim of the field of CSR is to reconcile (in the sense of “consilience”) methods and theories from the natural sciences with research on religion, which though defined in various ways, is usually understood as a universal human phenomenon. This does not necessarily mean religion is innate, but like all universal human phenomena, there will be an evolutionary story to tell about how it, or its constituent elements, came about. The stories are usually about the phenomena of religion writ-large, variously defined, rarely reaching the granularity to make claims about specific historical and cultural circumstances where religion is most relevant to agents. I challenge all scholars of religion to make their metaphysics explicit.
A Consensus Approach for Estimating Tropical Cyclone Intensity from Meteorological Satellites: SATCON
Authors: Velden Christopher S. , Herndon Derrick 
Published: June 2020

ABSTRACTA consensus-based algorithm for estimating the current intensity of global tropical cyclones (TCs) from meteorological satellites is described. The method objectively combines intensity estimates from infrared and microwave-based techniques to produce a consensus TC intensity estimate, which is more skillful than the individual members. The method, called Satellite Consensus (SATCON), can be run in near–real time and employs information sharing between member algorithms and a weighting strategy that relies on the situational precision of each member. An evaluation of the consensus algorithm’s performance in comparison with its individual members and other available operational estimates of TC intensity is presented. It is shown that SATCON can provide valuable objective intensity estimates for poststorm assessments, especially in the absence of other data such as provided by reconnaissance aircraft. It can also serve as a near-real-time estimator of TC intensity for forecasters, with the ability to quickly reconcile differences in objective intensity methods and thus decrease the uncertainty and amount of time spent on the intensity analysis. Near-real-time SATCON estimates are being provided to global operational TC forecast centers.
Cardiothoracic Patients with Unilateral Vocal Fold Paralysis: Pneumonia Rates Following Injection Laryngoplasty
Authors: Barnes Jason H. , Orbelo Diana M. , Armstrong Michael F. , Bayan Semirra L. , Lohse Christine M. , Ekbom Dale C. 
Published: June 2020

Objective: Recurrent laryngeal nerve injury is a potential complication of cardiothoracic surgery and cause of unilateral vocal fold paralysis (UVFP). Injection laryngoplasty (IL) is an intervention offered to patients with UVFP to alleviate symptoms including dysphagia, dysphonia and weak cough. There is no definitive evidence that IL prevents pneumonia. In this study, we compare rates of pneumonia in patients with UVFP secondary to cardiothoracic surgery who did or did not undergo IL. Methods: A retrospective chart review identified patients diagnosed with UVFP by an otolaryngologist using flexible laryngoscopy following cardiothoracic surgery from January 1, 2008 to December 31, 2017. Each subject was grouped by IL status and assessed for subsequent pneumonia within 6 months of their diagnosis of UVFP. The association of IL with pneumonia was evaluated using Cox proportional hazards regression. Results: Of 92 patients who met inclusion criteria, 35 (38%) underwent IL and 57 (62%) did not. Twenty patients developed pneumonia, four who had undergone IL and 16 who had not; 12 patients developed aspiration pneumonia including two having undergone IL and 10 who had not. Those who had IL were less likely to develop total pneumonia compared to those who had not (HR = 0.33, P = .045). The protective effect of IL was not as clearly sustained when measuring for aspiration pneumonia, specifically (HR = 0.34; P = .10). Discussion: Injection laryngoplasty may reduce the risk of pneumonia in patients with UVFP secondary to cardiothoracic surgery; however, further research is needed to quantify the potential protective nature of IL in this patient population. Level of evidence: 3 (A retrospective cohort study).
Social Network Analysis of Patient Movement Across Health Care Entities in Orange County, Florida
Authors: Rankin Danielle A. , Matthews Sarah D. 
Published: June 2020

Objective Multidrug-resistant organisms (MDROs) are continually emerging and threatening health care systems. Little attention has been paid to the effect of patient transfers on MDRO dissemination among health care entities in health care systems. In this study, the Florida Department of Health in Orange County (DOH-Orange) developed a baseline social network analysis of patient movement across health care entities in Orange County, Florida, and regionally, within 6 surrounding counties in Central Florida. Materials and Methods DOH-Orange constructed 2 directed network sociograms—graphic visualizations that show the direction of relationships (ie, county and regional)—by using 2016 health insurance data from the Centers for Medicare & Medicaid Services, which include metrics that could be useful for local public health interventions, such as MDRO outbreaks. Results We found that both our county and regional networks were sparse and centralized. The county-level network showed that acute-care hospitals had the highest influence on controlling the flow of patients between health care entities that would otherwise not be connected. The regional-level network showed that post–acute-care hospitals and other facilities (behavioral hospitals and mental health/substance abuse facilities) served as the primary controls for flow of patients between health care entities. The most prominent health care entities in both networks were the same 2 acute-care hospitals. Practice Implications Social network analysis can help local public health officials respond to MDRO outbreak investigations by determining which health care facilities are the main contributors of dissemination of MDROs or are at high risk of receiving patients with MDROs. This information can help epidemiologists prioritize prevention efforts and develop county- or regional-specific interventions to control and halt MDRO transmission across a health care network.
Understanding Determinants for STEM Major Choice Among Students Beginning Community College
Authors: Evans Colleen A. , Chen Rong , Hudes Ryan P. 
Published: June 2020

Objective: This study explored how high school and postsecondary academic parameters may relate to the choice of science, technology, engineering, and mathematics (STEM) major for students beginning their postsecondary education at community colleges. Our study incorporated these two clusters of factors into a statistical model to examine STEM major choice in community colleges. In particular, our study was one of the first to examine the direction and magnitude of the relationship between earned college credits in science laboratories and advanced mathematics and STEM college major selection. Method: We analyzed national data from the Education Longitudinal Study (2002) for students who were in 10th grade in 2002, entered community college as their first postsecondary institution, and declared a college major by 2006. A comprehensive integrated model was analyzed through binary logistic regression with the outcome variable of choice of STEM major or not. Results: We found math self-efficacy in high school, postsecondary introductory science laboratory courses, and postsecondary advanced mathematics courses were each positively associated with the choice of STEM major among community college students. Gender continues to be influential, with women less likely to pursue STEM than men. Contributions: Our study highlights the opportunities the science laboratory holds for engaging beginning community college students interested in STEM fields. The linchpin role of mathematics and science for students aspiring to study STEM is underscored by the findings of this study.