bluuebunny/crossref_metadata_2025_split huggingface dataset:
Do Political Similarities Facilitate Interlocal Collaboration?
Authors: Song Minsun , Park Hyung Jun , Jung Kyujin 
Published: December 2017

AbstractThis research examines the extent to which political similarities—that is, homophily between political actors at the local level—affect patterns of interorganizational collaboration in an emergency response situation. While the field of emergency management has focused on implementation‐oriented arrangements among key stakeholders, few studies have systemically investigated the creation and development of interorganizational collaborations led by political actors, especially following catastrophic events. The analysis reveals that a dyadic tie with political homophily boosts local responders’ ties with other agencies during emergencies. Findings indicate that political solidarity, formulated by chief elected officials of municipalities and council members, can broaden the scope of interorganizational collaboration by mitigating institutional collective action problems at the local level. This research presents a critical recommendation for emergency managers that interlocal collaboration for timely response to a disaster is attributable to political similarities that facilitate frequent interlocal interactions through formal and/or informal agreements.
Playground or Church? Implications for Public Administration fromTrinity Lutheran v. Comer
Authors: Candreva Philip J. 
Published: December 2017

AbstractThe roots of public administration are in the fields of management, political science, and the law. The law is underrepresented in the literature and is not as well understood by nonlawyer practitioners, yet it increasingly enables, constrains, and prescribes government action. In 2017, the U.S. Supreme Court ruled on a case involving whether a government grant awarded on secular criteria must be provided to a qualified church. This article contributes to the field's understanding of the interplay of law and administration by examining the constitutional issues in the case and their implications for public administration. By considering how this dispute was framed and the ways in which the court approached its resolution, public officials can better understand the issues in similar cases; anticipate potential disputes; and (re)design policies that will serve their communities, remain within constitutional limits, and reduce the likelihood of litigation.
Estimation of the Leukemia Risk in Human Populations Exposed to Benzene from Tobacco Smoke Using Epidemiological Data
Authors: Fiebelkorn Stacy , Meredith Clive 
Published: December 2017

AbstractSeveral epidemiological studies have demonstrated an association between occupational benzene exposure and increased leukemia risk, in particular acute myeloid leukemia (AML). However, there is still uncertainty as to the risk to the general population from exposure to lower environmental levels of benzene. To estimate the excess risk of leukemia from low‐dose benzene exposure, various methods for incorporating epidemiological data in quantitative risk assessment were utilized. Tobacco smoke was identified as one of the main potential sources of benzene exposure and was the focus of this exposure assessment, allowing further investigation of the role of benzene in smoking‐induced leukemia. Potency estimates for benzene were generated from individual occupational studies and meta‐analysis data, and an exposure assessment for two smoking subgroups (light and heavy smokers) carried out. Subsequently, various techniques, including life‐table analysis, were then used to evaluate both the excess lifetime risk and the contribution of benzene to smoking‐induced leukemia and AML. The excess lifetime risk for smokers was estimated at between two and six additional leukemia deaths in 10,000 and one to three additional AML deaths in 10,000. The contribution of benzene to smoking‐induced leukemia was estimated at between 9% and 24% (UpperCL 14–31%). For AML this contribution was estimated as 11–30% (UpperCL 22–60%). From the assessments carried out here, it appears there is an increased risk of leukemia from low‐level exposure to benzene and that benzene may contribute up to a third of smoking‐induced leukemia. Comparable results from using methods with varying degrees of complexity were generated.
The formation of convolute lamination in mud‐rich turbidites
Authors: Gladstone Charlotte , McClelland Harry L. O. , Woodcock Nigel H. , Pritchard David , Hunt James E. 
Published: December 2017

AbstractConvolute lamination is a common fold structure within turbidite beds, attributed to the deformation of sediment during or soon after deposition of the host bed. Despite the prevalence of this feature, the formational processes are still not well understood. Possible mechanisms are investigated here through redescription and analysis of convolute lamination from the Aberystwyth Grits Group (Silurian, west Wales, UK), in which ‘convolute bedding’ was first defined. Internal bed structures have been studied in clean coastal exposures and on high‐resolution optical scans of cut surfaces. Convolute lamination occurs in intervals 2 to 10 cm thick, spanning the top of the very fine sand Bouma C division through the D division of interlaminated silt and clay. Observed growth geometries confirm that the structure formed during sedimentation of the host graded bed. Folds show a down‐flow asymmetry and doubly‐vergent diapiric geometries (‘mushroom’‐shaped structures). Grain size measurements from a modern turbidite (Icod bed, ca 165 ka, Moroccan Turbidite System) suggest that there is an optimal ‘window’ of average grain size and mud content parameter space, within which convolute lamination develops. It is proposed that this window coincides with a bed density inversion created during deposition of a graded bed as clean sand (with pore spaces infilled by water) fines upward into mud‐rich sand (with pores infilled by an increasing proportion of mud). Porosity decreases and bulk bed density correspondingly increases. The resulting unstable density gradient may lead to vertical buoyancy‐driven overturn, manifest as growing folds. Subsequent amplification of the folds due to density differences and modification due to horizontal shear imposed by the depositing turbidity current may then occur. The bed density gradient stabilizes with deposition of low permeability mud, suppressing further fold development. Quantitatively, both Rayleigh–Taylor instability and Kelvin–Helmholtz instability are theoretically possible in forming folds in this context.
Asymmetrical changes of gene expression, small RNAs and chromatin in two resynthesized wheat allotetraploids
Authors: Jiao Wu , Yuan Jingya , Jiang Shan , Liu Yanfeng , Wang Lili , Liu Mingming , Zheng Dewei , Ye Wenxue , Wang Xiue , Chen Z. Jeffrey 
Published: December 2017

SummaryPolyploidy occurs in some animals and all flowering plants, including important crops such as wheat. The consequences of polyploidy in crops remain elusive, partly because their progenitors are unknown. Using two resynthesized wheat allotetraploids SlSlAA and AADD with known diploid progenitors, we analyzed mRNA and small RNA transcriptomes in the endosperm, compared transcriptomes between endosperm and root in AADD, and examined chromatin changes in the allotetraploids. In the endosperm, there were more non‐additively expressed genes in SlSlAA than in AADD. In AADD, non‐additively expressed genes were developmentally regulated, and the majority (62–70%) were repressed. The repressed genes in AADD included a group of histone methyltransferase gene homologs, which correlated with reduced histone H3K9me2 levels and activation of various transposable elements in AADD. In SlSlAA, there was a tendency for expression dominance of Sl over A homoeologs, but the histone methyltransferase gene homologs were additively expressed, correlating with insignificant changes in histone H3K9me2 levels. Moreover, more 24‐nucleotide small inferring RNAs (siRNAs) in the A subgenome were disrupted in AADD than in SlSlAA, which were associated with expression changes of siRNA‐associated genes. Our results indicate that asymmetrical changes in siRNAs, chromatin modifications, transposons and gene expression coincide with unstable AADD genomes and stable SlSlAA genomes, which could help explain the evolutionary trajectories of wheat allotetraploids formed by different progenitors.
Largely unlinked gene sets targeted by selection for domestication syndrome phenotypes in maize and sorghum
Authors: Lai Xianjun , Yan Lang , Lu Yanli , Schnable James C. 
Published: December 2017

SummaryThe domestication of diverse grain crops from wild grasses was a result of artificial selection for a suite of overlapping traits producing changes referred to in aggregate as ‘domestication syndrome’. Parallel phenotypic change can be accomplished by either selection on orthologous genes or selection on non‐orthologous genes with parallel phenotypic effects. To determine how often artificial selection for domestication traits in the grasses targeted orthologous genes, we employed resequencing data from wild and domesticated accessions of Zea (maize) and Sorghum (sorghum). Many ‘classic’ domestication genes identified through quantitative trait locus mapping in populations resulting from wild/domesticated crosses indeed show signatures of parallel selection in both maize and sorghum. However, the overall number of genes showing signatures of parallel selection in both species is not significantly different from that expected by chance. This suggests that while a small number of genes will extremely large phenotypic effects have been targeted repeatedly by artificial selection during domestication, the optimization part of domestication targeted small and largely non‐overlapping subsets of all possible genes which could produce equivalent phenotypic alterations.
Reversal of Azole Resistance in Candida albicans by Sulfa Antibacterial Drugs
Authors: Eldesouky Hassan E. , Mayhoub Abdelrahman , Hazbun Tony R. , Seleem Mohamed N. 
Published: December 2017

ABSTRACT

Invasive candidiasis presents an emerging global public health challenge due to the emergence of resistance to the frontline treatment options, such as fluconazole. Hence, the identification of other compounds capable of pairing with fluconazole and averting azole resistance would potentially prolong the clinical utility of this important group. In an effort to repurpose drugs in the field of antifungal drug discovery, we explored sulfa antibacterial drugs for the purpose of reversing azole resistance in
Candida
. In this study, we assembled and investigated a library of 21 sulfa antibacterial drugs for their ability to restore fluconazole sensitivity in
Candida albicans
. Surprisingly, the majority of assayed sulfa drugs (15 of 21) were found to exhibit synergistic relationships with fluconazole by checkerboard assay with fractional inhibitory concentration index (ΣFIC) values ranging from <0.0312 to 0.25. Remarkably, five sulfa drugs were able to reverse azole resistance in a clinically achievable range. The structure-activity relationships (SARs) of the amino benzene sulfonamide scaffold as antifungal agents were studied. We also identified the possible mechanism of the synergistic interaction of sulfa antibacterial drugs with azole antifungal drugs. Furthermore, the ability of sulfa antibacterial drugs to inhibit
Candida
biofilm by 40%
in vitro
was confirmed. In addition, the effects of sulfa-fluconazole combinations on
Candida
growth kinetics and efflux machinery were explored. Finally, using a
Caenorhabditis elegans
infection model, we demonstrated that the sulfa-fluconazole combination does possess potent antifungal activity
in vivo
, reducing
Candida
in infected worms by ∼50% compared to the control.
Identification of Bacterial Species That Can Utilize Fructose-Asparagine
Authors: Sabag-Daigle Anice , Wu Jikang , Borton Mikayla A. , Sengupta Anindita , Gopalan Venkat , Wrighton Kelly C. , Wysocki Vicki H. , Ahmer Brian M. M. 
Published: December 2017

ABSTRACT

Salmonella enterica
serovar Typhimurium is the only organism demonstrated to utilize fructose-asparagine (F-Asn) as a source of carbon and nitrogen. In this report, we first used a bioinformatics approach to identify other microorganisms that encode homologs of the
Salmonella
F-Asn utilization enzymes FraB (deglycase), FraD (kinase), and FraE (asparaginase). These candidate organisms were then tested with up to four different methods to confirm their ability to utilize F-Asn. The easiest and most broadly applicable method utilized a biological toxicity assay, which is based on the observation that F-Asn is toxic to a
Salmonella fraB
mutant. Candidate organisms were grown in a rich medium containing F-Asn, and depletion of F-Asn from the medium was inferred by the growth of a
Salmonella fraB
mutant in that same medium. For select organisms, the toxicity assay was cross-validated by direct mass spectrometry-aided measurement of F-Asn in the spent-culture media and through demonstration of FraB and FraD enzyme activity in cellular extracts. For prototrophs, F-Asn utilization was additionally confirmed by growth in a minimal medium containing F-Asn as the sole carbon source. Collectively, these studies established that
Clostridium
bolteae
,
Clostridium acetobutylicum
, and
Clostridium clostridioforme
can utilize F-Asn, but
Clostridium difficile
cannot;
Klebsiella oxytoca
and some
Klebsiella pneumoniae
subspecies can utilize F-Asn; and some
Citrobacter rodentium
and
Citrobacter freundii
strains can also utilize F-Asn. Within
Salmonella enterica
, the host-adapted serovars Typhi and Paratyphi A have lost the ability to utilize F-Asn.

IMPORTANCE
Fructose-asparagine (F-Asn) is a precursor to acrylamide that is found in human foods, and it is also a nutrient source for
Salmonella enterica
, a foodborne pathogen. Here, we determined that among the normal intestinal microbiota, there are species of
Clostridium
that encode the enzymes required for F-Asn utilization. Using complementary experimental approaches, we have confirmed that three members of
Clostridium
, two members of
Klebsiella
, and two members of
Citrobacter
can indeed utilize F-Asn. The
Clostridium
spp. likely compete with
Salmonella
for F-Asn in the gut and contribute to competitive exclusion. FraB, one of the enzymes in the F-Asn utilization pathway, is a potential drug target because inhibition of this enzyme leads to the accumulation of a toxic metabolite that inhibits the growth of
Salmonella
species. This study identifies the potential off-target organisms that need to be considered when developing therapeutics directed at FraB.
Development of Envelope Protein Antigens To Serologically Differentiate Zika Virus Infection from Dengue Virus Infection
Authors: Premkumar Lakshmanane , Collins Matthew , Graham Stephen , Liou Guei-Jiun Alice , Lopez Cesar A. , Jadi Ramesh , Balmaseda Angel , Brackbill James A. , Dietze Reynaldo , Camacho Erwin , De Silva Aruna D. , Giuberti Camila , dos Reis Helena Lucia , Singh Tulika , Heimsath Holly , Weiskopf Daniela , Sette Alessandro , Osorio Jorge E. , Permar Sallie R. , Miley Michel J. , Lazear Helen M. , Harris Eva , de Silva Aravinda M. 
Published: December 2017

ABSTRACT
Zika virus (ZIKV) is an emerging flavivirus that can cause birth defects and neurologic complications. Molecular tests are effective for diagnosing acute ZIKV infection, although the majority of infections produce no symptoms at all or present after the narrow window in which molecular diagnostics are dependable. Serology is a reliable method for detecting infections after the viremic period; however, most serological assays have limited specificity due to cross-reactive antibodies elicited by flavivirus infections. Since ZIKV and dengue virus (DENV) widely cocirculate, distinguishing ZIKV infection from DENV infection is particularly important for diagnosing individual cases or for surveillance to coordinate public health responses. Flaviviruses also elicit type-specific antibodies directed to non-cross-reactive epitopes of the infecting virus; such epitopes are attractive targets for the design of antigens for development of serological tests with greater specificity. Guided by comparative epitope modeling of the ZIKV envelope protein, we designed two recombinant antigens displaying unique antigenic regions on domain I (Z-EDI) and domain III (Z-EDIII) of the ZIKV envelope protein. Both the Z-EDI and Z-EDIII antigens consistently detected ZIKV-specific IgG in ZIKV-immune sera but not cross-reactive IgG in DENV-immune sera in late convalescence (>12 weeks postinfection). In contrast, during early convalescence (2 to 12 weeks postinfection), secondary DENV-immune sera and some primary DENV-immune sera cross-reacted with the Z-EDI and Z-EDIII antigens. Analysis of sequential samples from DENV-immune individuals demonstrated that Z-EDIII cross-reactivity peaked in early convalescence and declined steeply over time. The Z-EDIII antigen has much potential as a diagnostic antigen for population-level surveillance and for detecting past infections in patients.
Naturally Occurring Frameshift Mutations in the
tvb
Receptor Gene Are Responsible for Decreased Susceptibility of Chicken to Infection with Avian Leukosis Virus Subgroups B, D, and E
Authors: Li Xinjian , Chen Weiguo , Zhang Huanmin , Li Aijun , Shu Dingming , Li Hongxing , Dai Zhenkai , Yan Yiming , Zhang Xinheng , Lin Wencheng , Ma Jingyun , Xie Qingmei 
Published: December 2017

ABSTRACT

The group of highly related avian leukosis viruses (ALVs) in chickens are thought to have evolved from a common retroviral ancestor into six subgroups, A to E and J. These ALV subgroups use diverse cellular proteins encoded by four genetic loci in chickens as receptors to gain entry into host cells. Hosts exposed to ALVs might be under selective pressure to develop resistance to ALV infection. Indeed, resistance alleles have previously been identified in all four receptor loci in chickens. The
tvb
gene encodes a receptor, which determines the susceptibility of host cells to ALV subgroup B (ALV-B), ALV-D, and ALV-E. Here we describe the identification of two novel alleles of the
tvb
receptor gene, which possess independent insertions each within exon 4. The insertions resulted in frameshift mutations that reveal a premature stop codon that causes nonsense-mediated decay of the mutant mRNA and the production of truncated Tvb protein. As a result, we observed that the frameshift mutations in the
tvb
gene significantly lower the binding affinity of the truncated Tvb receptors for the ALV-B, ALV-D, and ALV-E envelope glycoproteins and significantly reduce susceptibility to infection by ALV-B, ALV-D and ALV-E
in vitro
and
in vivo
. Taken together, these findings suggest that frameshift mutation can be a molecular mechanism of reducing susceptibility to ALV and enhance our understanding of virus-host coevolution.

IMPORTANCE
Avian leukosis virus (ALV) once caused devastating economic loss to the U.S. poultry industry prior the current eradication schemes in place, and it continues to cause severe calamity to the poultry industry in China and Southeast Asia, where deployment of a complete eradication scheme remains a challenge. The
tvb
gene encodes the cellular receptor necessary for subgroup B, D, and E ALV infection. Two
tvb
allelic variants that resulted from frameshift mutations have been identified in this study, which have been shown to have significantly reduced functionality in mediating subgroup B, D, and E ALV infection. Unlike the control of herpesvirus-induced diseases by vaccination, the control of avian leukosis in chickens has relied totally on virus eradication measures and host genetic resistance. This finding enriches the allelic pool of the
tvb
gene and expands the potential for genetic improvement of ALV resistance in varied chicken populations by selection.
Actin-Dependent Nonlytic Rotavirus Exit and Infectious Virus Morphogenetic Pathway in Nonpolarized Cells
Authors: Trejo-Cerro Óscar , Eichwald Catherine , Schraner Elisabeth M. , Silva-Ayala Daniela , López Susana , Arias Carlos F. 
Published: December 2017

ABSTRACT
During the late stages of rotavirus morphogenesis, the surface proteins VP4 and VP7 are assembled onto the previously structured double-layered virus particles to yield a triple-layered, mature infectious virus. The current model for the assembly of the outer capsid is that it occurs within the lumen of the endoplasmic reticulum. However, it has been shown that VP4 and infectious virus associate with lipid rafts, suggesting that the final assembly of the rotavirus spike protein VP4 involves a post-endoplasmic reticulum event. In this work, we found that the actin inhibitor jasplakinolide blocks the cell egress of rotavirus from nonpolarized MA104 cells at early times of infection, when there is still no evidence of cell lysis. These findings contrast with the traditional assumption that rotavirus is released from nonpolarized cells by a nonspecific mechanism when the cell integrity is lost. Inspection of the virus present in the extracellular medium by use of density flotation gradients revealed that a fraction of the released virus is associated with low-density membranous structures. Furthermore, the intracellular localization of VP4, its interaction with lipid rafts, and its targeting to the cell surface were shown to be prevented by jasplakinolide, implying a role for actin in these processes. Finally, the VP4 present at the plasma membrane was shown to be incorporated into the extracellular infectious virus, suggesting the existence of a novel pathway for the assembly of the rotavirus spike protein.

IMPORTANCE
Rotavirus is a major etiological agent of infantile acute severe diarrhea. It is a nonenveloped virus formed by three concentric layers of protein. The early stages of rotavirus replication, including cell attachment and entry, synthesis and translation of viral mRNAs, replication of the genomic double-stranded RNA (dsRNA), and the assembly of double-layered viral particles, have been studied widely. However, the mechanisms involved in the later stages of infection, i.e., viral particle maturation and cell exit, are less well characterized. It has been assumed historically that rotavirus exits nonpolarized cells following cell lysis. In this work, we show that the virus exits cells by a nonlytic, actin-dependent mechanism, and most importantly, we describe that VP4, the spike protein of the virus, is present on the cell surface and is incorporated into mature, infectious virus, indicating a novel pathway for the assembly of this protein.