bluuebunny/crossref_metadata_2025_split huggingface dataset:
Self‐esteem trajectories across 25 years and midlife intimate relations
Authors: JOHNSON MATTHEW D. , GALAMBOS NANCY L. , KRAHN HARVEY J. 
Published: October 2015

AbstractGuided by a life‐span developmental systems approach, this study examined links between self‐esteem assessed over 25 years and adaptive interaction and relationship risk at midlife using data from 341 Canadian adults surveyed (or followed) from ages 18 to 43. Results showed higher self‐esteem at age 18 was associated with more adaptive interactions and lower perceived relationship risk at age 43. A more rapid increase in self‐esteem through the transition to adulthood into midlife (ages 18–43) was also associated with more frequent adaptive interactions and less relationship risk at age 43. These results held after accounting for potential confounding variables. This study is the first to demonstrate self‐esteem trajectories over a quarter century predict midlife intimate relationship functioning.
Sequential renal and bone marrow transplants in a child with Fanconi anemia
Authors: Vincent Carol L. , Primack William A. , Hipps John , Kasow Kimberly A. 
Published: October 2015

AbstractFA is an autosomal recessive disorder characterized by small stature and renal abnormalities. FA can lead to progressive bone marrow failure, myelodysplastic syndrome, or acute leukemia. Using a multidisciplinary team approach, we managed a 3‐yr‐old boy with FA who simultaneously developed renal and hematopoietic failure. Because renal function was insufficient to support the conditioning regimen for HCT, we performed a deceased donor renal transplant in December 2012 prior to HCT with the known risk of graft‐versus‐graft rejection of the donor kidney. Seven months later he underwent allogeneic HCT. He obtained myeloid engraftment on day +11 and peripheral blood chimerism demonstrated all donor by day +21. He developed asymptomatic CMV reactivation and despite antirejection medications, mild skin graft‐versus‐host disease. He has maintained excellent renal function and remains transfusion independent with full hematopoietic recovery. He has not experienced any renal rejection episodes nor developed donor‐specific antibodies toward his renal donor. Peripheral blood chimerism remains completely HCT donor. He is clinically well, now greater than two and a half yr after renal transplant and two yr after HCT. The continuing close collaboration between the Pediatric Nephrology and Bone Marrow Transplant teams is a major factor in this successful outcome.
Possible Common Aetiology behind Maternal Preeclampsia and Congenital Heart Defects in the Child: a Cardiovascular Diseases in Norway Project Study
Authors: Brodwall Kristoffer , Leirgul Elisabeth , Greve Gottfried , Vollset Stein Emil , Holmstrøm Henrik , Tell Grethe S. , Øyen Nina 
Published: October 2015

AbstractBackgroundThe aetiology of congenital heart defects (CHD) is mostly unknown, but maternal factors may modify the infant risk of CHD. We investigated the association between maternal preeclampsia and offspring risk of severe CHD in a nation‐wide cohort study.MethodsInformation on all births registered in the Medical Birth Registry of Norway, 1994–2009, was completed with information on CHD diagnoses from national health registries and the Cardiovascular Diseases in Norway Project (CVDNOR).ResultsAmong 914 703 singleton births without chromosomal abnormalities, 32 864 (3.6%) were born after a pregnancy with preeclampsia. The preeclampsia was diagnosed before the 34th week of pregnancy (early‐onset preeclampsia) in 2618 (8.0% of preeclamptic pregnancies). CHDs were diagnosed in 10 691 infants; of these, 2473 had severe CHD. The risk of severe CHD was compared between births with and without maternal preeclampsia and estimated with binomial log‐linear regression. When adjusting for year of birth, maternal age, parity, and pregestational diabetes, the risk ratio (RR) for severe CHD in offspring of mothers with any preeclampsia was 1.3 [95% confidence interval (CI) 1.1, 1.5], and in pregnancies with early‐onset preeclampsia, the RR was 2.8 (95% CI 1.8, 4.4). The association between early‐onset preeclampsia and specific types of severe CHD was stronger for atrioventricular septal defects (AVSD), with adjusted RR 13.5 (95% CI 6.8, 26.8).ConclusionsEarly‐onset preeclampsia was strongly associated with infant risk of severe CHD, specifically; the risk of AVSD was 15‐fold higher if the mother was diagnosed with early‐onset preeclampsia, suggesting common aetiological factors for early‐onset preeclampsia and erroneous fetal heart development.
Caveat Emptor: What Do We Know about Public Administration Evidence and How Do We Know It?
Authors: Isett Kimberley R. , Head Brian W. , VanLandingham Gary 
Published: October 2015

AbstractThis article provides an overview of a new feature in Public Administration Review called Evidence in Public Administration. This feature was created to provide a space in which scholars and practitioners of public administration can meet to engage in a dialogue about evidence in public decision making. In this feature, we will shine a light on the evidence needed to make effective decisions and examinations of the evidence that currently exists for contemporary public sector efforts. We explicitly want to create a resource for both practitioners and scholars to consult when trying to find evidence on a particular topic and to know the limitations and parameters of that evidence. This article lays out the purpose, scope, and rationale for the feature, as well as a call to engage in this endeavor.
Understanding the (Re)Definition of Nationhood in French Cities: A Case of Multiple States and Multiple Republics
Authors: Downing Joseph 
Published: October 2015

AbstractBoth theoretical and empirical accounts of the nation have neglected the city as an arena for the (re)definition of national belonging. This article analyses contemporary France to advance theoretical and empirical insights into this process. Rather than presenting France as characterized by a Republican, assimilationist position, this article argues France is better characterized by competing ‘multiple republics’ with numerous definitions of nationhood. This article identifies three mechanisms of the multiple Republic. In Marseille, the municipal administration acts to redefine the secular character of the nation by bringing religion directly into local politics. This use of religion to redefine nationhood is also present in Lyon, with the key difference that it occurs in symbiosis with European governance. Finally, the Nanterre suburb of Paris demonstrates that the local state also uses notions of ethnicity to redefine the French nation as compatible with ethnic difference.
Neutralization of Interleukin‐17 Attenuates Cholestatic Liver Fibrosis in Mice
Authors: Zhang S. , Huang D. , Weng J. , Huang Y. , Liu S. , Zhang Q. , Li N. , Wen M. , Zhu G. , Lin F. , Gu W. 
Published: October 2015

AbstractAnti‐inflammation strategy is one of the proposed therapeutic approaches to hepatic fibrosis. IL‐17 is critical in inflammation, but the role of IL‐17 in liver fibrosis has not yet been elucidated. In this study, we investigate the role of IL‐17 on bile duct ligation‐induced liver injury and fibrosis in C57BL/6 mice. Animals were sacrificed at designated times, and serum and liver tissues were collected for analysis of liver function and serum IL‐6, IL‐1β, tumour necrosis factor‐alpha (TNF‐α) and transforming growth factor‐β (TGF‐β) levels. IL‐17 blockade with anti‐IL‐17A mAb significantly improved liver function and decreased hepatocellular necrosis, pro‐inflammatory cytokines, neutrophils and macrophages influx. Furthermore, CD3 + and CD8 + lymphocytes, neutrophils and macrophages were found to express IL‐17, and neutrophils are the principal IL‐17‐producing cells after BDL‐induced liver injury. These data indicated that IL‐17 signal contributes to the pathogenesis of cholestatic liver injury and blocked of IL‐17 could potentially benefit patients with cholestatic liver disease.
Molecule Targeting Glucosyltransferase Inhibits Streptococcus mutans Biofilm Formation and Virulence
Authors: Ren Zhi , Cui Tao , Zeng Jumei , Chen Lulu , Zhang Wenling , Xu Xin , Cheng Lei , Li Mingyun , Li Jiyao , Zhou Xuedong , Li Yuqing 
Published: October 2015

ABSTRACTDental plaque biofilms are responsible for numerous chronic oral infections and cause a severe health burden. Many of these infections cannot be eliminated, as the bacteria in the biofilms are resistant to the host's immune defenses and antibiotics. There is a critical need to develop new strategies to control biofilm-based infections. Biofilm formation inStreptococcus mutansis promoted by major virulence factors known as glucosyltransferases (Gtfs), which synthesize adhesive extracellular polysaccharides (EPS). The current study was designed to identify novel molecules that target Gtfs, thereby inhibitingS. mutansbiofilm formation and having the potential to prevent dental caries. Structure-based virtual screening of approximately 150,000 commercially available compounds against the crystal structure of the glucosyltransferase domain of the GtfC protein fromS. mutansresulted in the identification of a quinoxaline derivative, 2-(4-methoxyphenyl)-N-(3-{[2-(4-methoxyphenyl)ethyl]imino}-1,4-dihydro-2-quinoxalinylidene)ethanamine, as a potential Gtf inhibitor.In vitroassays showed that the compound was capable of inhibiting EPS synthesis and biofilm formation inS. mutansby selectively antagonizing Gtfs instead of by killing the bacteria directly. Moreover, thein vivoanti-caries efficacy of the compound was evaluated in a rat model. We found that the compound significantly reduced the incidence and severity of smooth and sulcal-surface cariesin vivowith a concomitant reduction in the percentage ofS. mutansin the animals' dental plaque (P< 0.05). Taken together, these results represent the first description of a compound that targets Gtfs and that has the capacity to inhibit biofilm formation and the cariogenicity ofS. mutans.
Antimicrobial Susceptibilities of Aerobic and Facultative Gram-Negative Bacilli from Intra-abdominal Infections in Patients from Seven Regions in China in 2012 and 2013
Authors: Zhang Hui , Yang Qiwen , Liao Kang , Ni Yuxing , Yu Yunsong , Hu Bijie , Sun Ziyong , Huang Wenxiang , Wang Yong , Wu Anhua , Feng Xianju , Luo Yanping , Hu Zhidong , Chu Yunzhuo , Chen Shulan , Cao Bin , Su Jianrong , Gui Bingdong , Duan Qiong , Zhang Shufang , Shao Haifeng , Kong Haishen , Badal Robert E. , Xu Yingchun 
Published: October 2015

ABSTRACTTo evaluate the antimicrobial susceptibility of Gram-negative bacilli that caused hospital-acquired and community-acquired intra-abdominal infections (IAIs) in China between 2012 and 2013, we determined the susceptibilities to 12 antimicrobials and the extended-spectrum β-lactamase (ESBL) statuses of 3,540 IAI isolates from seven geographic areas in China in a central laboratory using CLSI broth microdilution and interpretive standards. Most infections were caused byEscherichia coli(46.3%) andKlebsiella pneumoniae(19.7%). Rates of ESBL-producingE. coli(P= 0.031),K. pneumoniae(P= 0.017), andProteus mirabilis(P= 0.004) were higher in hospital-acquired IAIs than in community-acquired IAIs. Susceptibilities of enterobacteriaceae to ertapenem, amikacin, piperacillin-tazobactam, and imipenem were 71.3% to 100%, 81.3% to 100%, 64.7% to 100%, and 83.1% to 100%, respectively, but imipenem was ineffective againstP. mirabilis(<20%). Although most ESBL-positive hospital-acquired isolates were resistant to third- and fourth-generation cephalosporins, the majority were susceptible to cefoxitin (47.9% to 83.9%). Susceptibilities of ESBL-positive isolates to ampicillin-sulbactam (<10%) were low, whereas susceptibilities to ciprofloxacin (0% to 54.6%) and levofloxacin (0% to 63.6%) varied substantially. The prevalences of cephalosporin-susceptibleE. coliandK. pneumoniaewere higher in the northeastern and southern regions than in the central and eastern regions, reflecting the ESBL-positive rates in these areas, and were lowest in the Jiangsu-Zhejiang (Jiang-Zhe) area where the rates of carbapenem resistance were also highest. Ertapenem, amikacin, piperacillin-tazobactam, and imipenem are the most efficacious antibiotics for treating IAIs in China, especially those caused byE. coliorK. pneumoniae. Resistance to cephalosporins and carbapenems is more common in the Jiang-Zhe area than in other regions in China.
Genomic Characteristics of NDM-Producing Enterobacteriaceae Isolates in Australia and Their
bla
NDM
Genetic Contexts
Authors: Wailan Alexander M. , Paterson David L. , Kennedy Karina , Ingram Paul R. , Bursle Evan , Sidjabat Hanna E. 
Published: October 2015

ABSTRACT

bla
NDM
has been reported in different
Enterobacteriaceae
species and on numerous plasmid replicon types (Inc). Plasmid replicon typing, in combination with genomic characteristics of the bacterial host (e.g., sequence typing), is used to infer the spread of antimicrobial resistance determinants between genetically unrelated bacterial hosts. The genetic context of
bla
NDM
is heterogeneous. In this study, we genomically characterized 12 NDM-producing
Enterobacteriaceae
isolated in Australia between 2012 and 2014:
Escherichia coli
(
n
= 6),
Klebsiella pneumoniae
(
n
= 3),
Enterobacter cloacae
(
n
= 2) and
Providencia rettgeri
(
n
= 1). We describe their
bla
NDM
genetic contexts within Tn
125
, providing insights into the acquisition of
bla
NDM
into
Enterobacteriaceae
. IncFII-type (
n
= 7) and IncX3 (
n
= 4) plasmids were the most common plasmid types found. The IncHI1B (
n
= 1) plasmid was also identified. Five different
bla
NDM
genetic contexts were identified, indicating four particular plasmids with specific
bla
NDM
genetic contexts (NGCs), three of which were IncFII plasmids (FII-A to -C). Of note, the
bla
NDM
genetic context of
P. rettgeri
was not conjugative. Epidemiological links between our NDM-producing
Enterobacteriaceae
were established by their acquisition of these five particular plasmid types. The combination of different molecular and genetic characterization methods allowed us to provide insight into the spread of plasmids transmitting
bla
NDM
.
Impact of a Cross-Kingdom Signaling Molecule of Candida albicans on Acinetobacter baumannii Physiology
Authors: Kostoulias Xenia , Murray Gerald L. , Cerqueira Gustavo M. , Kong Jason B. , Bantun Farkad , Mylonakis Eleftherios , Khoo Chen Ai , Peleg Anton Y. 
Published: October 2015

ABSTRACT

Multidrug-resistant (MDR)
Acinetobacter baumannii
is an opportunistic human pathogen that has become highly problematic in the clinical environment. Novel therapies are desperately required. To assist in identifying new therapeutic targets, the antagonistic interactions between
A. baumannii
and the most common human fungal pathogen,
Candida albicans
, were studied. We have observed that the
C. albicans
quorum-sensing molecule, farnesol, has cross-kingdom interactions, affecting the viability of
A. baumannii
. To gain an understanding of its mechanism, the transcriptional profile of
A. baumannii
exposed to farnesol was examined. Farnesol caused dysregulation of a large number of genes involved in cell membrane biogenesis, multidrug efflux pumps (AcrAB-like and AdeIJK-like), and
A. baumannii
virulence traits such as biofilm formation (
csuA
,
csuB
, and
ompA
) and motility (
pilZ
and
pilH
). We also observed a strong induction in genes involved in cell division (
minD
,
minE
,
ftsK
,
ftsB
, and
ftsL
). These transcriptional data were supported by functional assays showing that farnesol disrupts
A. baumannii
cell membrane integrity, alters cell morphology, and impairs virulence characteristics such as biofilm formation and twitching motility. Moreover, we showed that
A. baumannii
uses efflux pumps as a defense mechanism against this eukaryotic signaling molecule. Owing to its effects on membrane integrity, farnesol was tested to see if it potentiated the activity of the membrane-acting polymyxin antibiotic colistin. When coadministered, farnesol increased sensitivity to colistin for otherwise resistant strains. These data provide mechanistic understanding of the antagonistic interactions between diverse pathogens and may provide important insights into novel therapeutic strategies.
Antiretrovirals, Methamphetamine, and HIV-1 Envelope Protein gp120 Compromise Neuronal Energy Homeostasis in Association with Various Degrees of Synaptic and Neuritic Damage
Authors: Sanchez Ana B. , Varano Giuseppe P. , de Rozieres Cyrus M. , Maung Ricky , Catalan Irene C. , Dowling Cari C. , Sejbuk Natalia E. , Hoefer Melanie M. , Kaul Marcus 
Published: October 2015

ABSTRACT
HIV-1 infection frequently causes HIV-associated neurocognitive disorders (HAND) despite combination antiretroviral therapy (cART). Evidence is accumulating that components of cART can themselves be neurotoxic upon long-term exposure. In addition, abuse of psychostimulants, such as methamphetamine, seems to aggravate HAND and compromise antiretroviral therapy. However, the combined effect of virus and recreational and therapeutic drugs on the brain is poorly understood. Therefore, we exposed mixed neuronal-glial cerebrocortical cells to antiretrovirals (ARVs) (zidovudine [AZT], nevirapine [NVP], saquinavir [SQV], and 118-D-24) of four different pharmacological categories and to methamphetamine and, in some experiments, the HIV-1 gp120 protein for 24 h and 7 days. Subsequently, we assessed neuronal injury by fluorescence microscopy, using specific markers for neuronal dendrites and presynaptic terminals. We also analyzed the disturbance of neuronal ATP levels and assessed the involvement of autophagy by using immunofluorescence and Western blotting. ARVs caused alterations of neurites and presynaptic terminals primarily during the 7-day incubation and depending on the specific compounds and their combinations with and without methamphetamine. Similarly, the loss of neuronal ATP was context specific for each of the drugs or combinations thereof, with and without methamphetamine or viral gp120. Loss of ATP was associated with activation of AMP-activated protein kinase (AMPK) and autophagy, which, however, failed to restore normal levels of neuronal ATP. In contrast, boosting autophagy with rapamycin prevented the long-term drop of ATP during exposure to cART in combination with methamphetamine or gp120. Our findings indicate that the overall positive effect of cART on HIV infection is accompanied by detectable neurotoxicity, which in turn may be aggravated by methamphetamine.
RNA Helicase Important for Listeria monocytogenes Hemolytic Activity and Virulence Factor Expression
Authors: Netterling Sakura , Bäreclev Caroline , Vaitkevicius Karolis , Johansson Jörgen 
Published: October 2015

ABSTRACT

RNA helicases have been shown to be important for the function of RNA molecules at several levels, although their putative involvement in microbial pathogenesis has remained elusive. We have previously shown that
Listeria monocytogenes
DExD-box RNA helicases are important for bacterial growth, motility, ribosomal maturation, and rRNA processing. We assessed the importance of the RNA helicase Lmo0866 (here named CshA) for expression of virulence traits. We observed a reduction in hemolytic activity in a strain lacking CshA compared to the wild type. This phenomenon was less evident in strains lacking other RNA helicases. The reduced hemolysis was accompanied by lower expression of major listerial virulence factors in the Δ
cshA
strain, mainly listeriolysin O, but also to some degree the actin polymerizing factor ActA. Reduced expression of these virulence factors in the strain lacking CshA did not, however, correlate with a decreased level of the virulence regulator PrfA. When combining the Δ
cshA
knockout with a mutation creating a constitutively active PrfA protein (PrfA*), the effect of the Δ
cshA
knockout on LLO expression was negated. These data suggest a role for the RNA helicase CshA in posttranslational activation of PrfA. Surprisingly, although the expression of several virulence factors was reduced, the Δ
cshA
strain did not demonstrate any reduced ability to infect nonphagocytic cells compared to the wild-type strain.
The Trk Potassium Transporter Is Required for RsmB-Mediated Activation of Virulence in the Phytopathogen Pectobacterium wasabiae
Authors: Valente Rita S. , Xavier Karina B. 
Published: October 2015

ABSTRACT

Pectobacterium wasabiae
(previously known as
Erwinia carotovora
) is an important plant pathogen that regulates the production of plant cell wall-degrading enzymes through an
N
-acyl homoserine lactone-based quorum sensing system and through the GacS/GacA two-component system (also known as ExpS/ExpA). At high cell density, activation of GacS/GacA induces the expression of RsmB, a noncoding RNA that is essential for the activation of virulence in this bacterium. A genetic screen to identify regulators of RsmB revealed that mutants defective in components of a putative Trk potassium transporter (
trkH
and
trkA
) had decreased
rsmB
expression. Further analysis of these mutants showed that changes in potassium concentration influenced
rsmB
expression and consequent tissue damage in potato tubers and that this regulation required an intact Trk system. Regulation of
rsmB
expression by potassium via the Trk system occurred even in the absence of the GacS/GacA system, demonstrating that these systems act independently and are both required for full activation of RsmB and for the downstream induction of virulence in potato infection assays. Overall, our results identified potassium as an essential environmental factor regulating the Rsm system, and the consequent induction of virulence, in the plant pathogen
P. wasabiae
.

IMPORTANCE
Crop losses from bacterial diseases caused by pectolytic bacteria are a major problem in agriculture. By studying the regulatory pathways involved in controlling the expression of plant cell wall-degrading enzymes in
Pectobacterium wasabiae
, we showed that the Trk potassium transport system plays an important role in the regulation of these pathways. The data presented further identify potassium as an important environmental factor in the regulation of virulence in this plant pathogen. We showed that a reduction in virulence can be achieved by increasing the extracellular concentration of potassium. Therefore, this work highlights how elucidation of the mechanisms involved in regulating virulence can lead to the identification of environmental factors that can influence the outcome of infection.