bluuebunny/crossref_metadata_2025_split huggingface dataset:
Accuracy and Validity of Commercially Available Kayak Ergometers
Authors: Borges Thiago Oliveira , Bullock Nicola , Aitken David , Coutts Aaron J. 
Published: February 2017

Methods:This study compared 3 commercially available ergometers for within- and between-brands difference to a first-principle calibration rig.
Results:All ergometers underestimated true mean power, with errors of 27.6% ± 3.7%, 4.5% ± 3.5%, and 22.5% ± 1.9% for the KayakPro, WEBA, and Dansprint, respectively. Within-brand ergometer power differences ranged from 17 ± 9 to 22 ± 11 W for the KayakPro, 3 ± 4 to 4 ± 4 W for the WEBA, and 5 ± 3 to 5 ± 4 W for the Dansprint. The linear-regression analysis showed that most kayak ergometers have a stable coefficient of variation (0.9–1.7%) with a moderate effect size.
Conclusion:Taken collectively, these findings show that different ergometers present inconsistent outcomes. Therefore, we suggest that athlete testing be conducted on the same ergometer brand, preferably the same ergometer. Optimally, that ergometer should be calibrated using a first-principle device before any athlete testing block.
Monitoring Hitting Load in Tennis Using Inertial Sensors and Machine Learning
Authors: Whiteside David , Cant Olivia , Connolly Molly , Reid Machar 
Published: February 2017

Context:Quantifying external workload is fundamental to training prescription in sport. In tennis, global positioning data are imprecise and fail to capture hitting loads. The current gold standard (manual notation) is time intensive and often not possible given players’ heavy travel schedules.
Purpose:To develop an automated stroke-classification system to help quantify hitting load in tennis.
Methods:Nineteen athletes wore an inertial measurement unit (IMU) on their wrist during 66 video-recorded training sessions. Video footage was manually notated such that known shot type (serve, rally forehand, slice forehand, forehand volley, rally backhand, slice backhand, backhand volley, smash, or false positive) was associated with the corresponding IMU data for 28,582 shots. Six types of machine-learning models were then constructed to classify true shot type from the IMU signals.
Results:Across 10-fold cross-validation, a cubic-kernel support vector machine classified binned shots (overhead, forehand, or backhand) with an accuracy of 97.4%. A second cubic-kernel support vector machine achieved 93.2% accuracy when classifying all 9 shot types.
Conclusions:With a view to monitoring external load, the combination of miniature inertial sensors and machine learning offers a practical and automated method of quantifying shot counts and discriminating shot types in elite tennis players.
Is State Anxiety, Trait Anxiety, or Anxiety Sensitivity a Clinical Predictor of Symptoms in Those Presenting With Mild Traumatic Brain Injury or Concussion?
Authors: Hixson Krista M. , Allen Alex N. , Williams Andrew S. , McLeod Tamara C. Valovich 
Published: February 2017

Clinical Scenario:Mild traumatic brain injury, or concussion, has been associated with physical, cognitive, and emotional sequelae. Little is understood in regard to many characteristics, such as anxiety, and their effect on post-concussion symptoms.Clinical Question:Is state anxiety, trait anxiety, or anxiety sensitivity a clinical predictor of symptoms in those presenting with mild traumatic brain injury or concussion?Summary of Key Findings:A literature search returned 3 possible studies; 3 studies met inclusion criteria and included. One study reported in athletes that greater social support was associated with decreased state-anxiety, lower state anxiety post-concussion was associated with increased social support, and that those with greater social support may experience reduced anxiety, regardless of injury type sustained. One study reported baseline trait anxiety in athletes was not significantly associated with post-concussion state anxiety, but that symptoms of depression at baseline was the strongest predictor for post-concussion state anxiety. Three studies reported that state and trait anxiety are not related to increased post-concussion symptom scores. One study reported that greater anxiety sensitivity is related to higher reported post-concussion symptom scores, which may manifest as somatic symptoms following concussion, and revealed that anxiety sensitivity may be a risk factor symptom development.Clinical Bottom Line:There is low-level to moderate evidence to support that anxiety sensitivity is linked to post-concussion symptoms. State and trait anxiety do not appear to be related to post-concussion symptoms alone. Post-concussion state anxiety may occur if post-concussion symptoms of depression are present or if baseline symptoms of depression are present. Better social support may improve state anxiety post-concussion.Strength of Recommendation:There is grade B evidence to support that state and trait anxiety are not risk factors for post-concussion symptom development. There is grade C evidence to support anxiety sensitivity as a risk factor for developing post-concussion symptoms.
Evaluation of Plasmodium vivax Cell-Traversal Protein for Ookinetes and Sporozoites as a Preerythrocytic P. vivax Vaccine
Authors: Alves Eduardo , Salman Ahmed M. , Leoratti Fabiana , Lopez-Camacho Cesar , Viveros-Sandoval Martha Eva , Lall Amar , El-Turabi Aadil , Bachmann Martin F. , Hill Adrian V. S. , Janse Chris J. , Khan Shahid M. , Reyes-Sandoval Arturo 
Published: February 2017

ABSTRACT

Four different vaccine platforms, each targeting the human malaria parasite
Plasmodium vivax
cell-traversal protein for ookinetes and sporozoites (
Pv
CelTOS), were generated and assessed for protective efficacy. These platforms consisted of a recombinant chimpanzee adenoviral vector 63 (ChAd63) expressing
Pv
CelTOS (Ad), a recombinant modified vaccinia virus Ankara expressing
Pv
CelTOS (MVA),
Pv
CelTOS conjugated to bacteriophage Qβ virus-like particles (VLPs), and a recombinant
Pv
CelTOS protein expressed in eukaryotic HEK293T cells (protein). Inbred BALB/c mice and outbred CD-1 mice were immunized using the following prime-boost regimens: Ad-MVA, Ad-VLPs, and Ad-protein. Protective efficacy against sporozoite challenge was assessed after immunization using a novel chimeric rodent
Plasmodium berghei
parasite (
Pb-Pv
CelTOS). This chimeric parasite expresses
P. vivax
CelTOS in place of the endogenous
P. berghei
CelTOS and produces fully infectious sporozoites. A single Ad immunization in BALB/c and CD-1 mice induced anti-
Pv
CelTOS antibodies which were boosted efficiently using MVA, VLP, or protein immunization.
Pv
CelTOS-specific gamma interferon- and tumor necrosis factor alpha-producing CD8
+
T cells were induced at high frequencies by all prime-boost regimens in BALB/c mice but not in CD-1 mice; in CD-1 mice, they were only marginally increased after boosting with MVA. Despite the induction of anti-
Pv
CelTOS antibodies and
Pv
CelTOS-specific CD8
+
T-cell responses, only low levels of protective efficacy against challenge with
Pb-Pv
CelTOS sporozoites were obtained using any immunization strategy. In BALB/c mice, no immunization regimens provided significant protection against a
Pb-Pv
CelTOS chimeric sporozoite challenge. In CD-1 mice, modest protective efficacy against challenge with chimeric
P. berghei
sporozoites expressing either
Pv
CelTOS or
P. falciparum
CelTOS was observed using the Ad-protein vaccination regimen.
Calprotectin as a Biomarker for Melioidosis Disease Progression and Management
Authors: Natesan Mohan , Corea Enoka , Krishnananthasivam Shivankari , Sathkumara Harindra Darshana , Dankmeyer Jennifer L. , Dyas Beverly K. , Amemiya Kei , De Silva Aruna Dharshan , Ulrich Robert G. 
Published: February 2017

ABSTRACT

Melioidosis is a neglected tropical disease that is caused by the bacterium
Burkholderia pseudomallei
and is underreported in many countries where the disease is endemic. A long and costly administration of antibiotics is needed to clear infections, and there is an unmet need for biomarkers to guide antibiotic treatment and increase the number of patients that complete therapy. We identified calprotectin as a lead biomarker of
B. pseudomallei
infections and examined correlations between this serum protein and the antibiotic treatment outcomes of patients with melioidosis. Serum levels of calprotectin and C-reactive protein were significantly higher in patients with melioidosis and nonmelioidosis sepsis than in healthy controls. Median calprotectin levels were higher in patients with melioidosis than in those with nonmelioidosis sepsis, whereas C-reactive protein levels were similar in both groups. Notably, intensive intravenous antibiotic treatment of patients with melioidosis resulted in lower levels of calprotectin and C-reactive protein (
P
< 0.0001), coinciding with recovery. The median percent reduction of calprotectin and C-reactive protein was 71% for both biomarkers after antibacterial therapy. In contrast, we found no significant differences in calreticulin levels between the two melioidosis treatment phases. Thus, reductions in serum calprotectin levels were linked to therapeutic responses to antibiotics. Our results suggest that calprotectin may be a sensitive indicator of melioidosis disease activity and illustrate the potential utility of this biomarker in guiding the duration of antibiotic therapy.
Japanese Encephalitis Virus NS5 Inhibits Type I Interferon (IFN) Production by Blocking the Nuclear Translocation of IFN Regulatory Factor 3 and NF-κB
Authors: Ye Jing , Chen Zheng , Li Yunchuan , Zhao Zikai , He Wen , Zohaib Ali , Song Yunfeng , Deng Chenglin , Zhang Bo , Chen Huanchun , Cao Shengbo 
Published: February 2017

ABSTRACT
The type I interferon (IFN) response is part of the first-line defense against viral infection. To initiate replication, viruses have developed powerful evasion strategies to counteract host IFN responses. In the present study, we found that the Japanese encephalitis virus (JEV) NS5 protein could inhibit double-stranded RNA (dsRNA)-induced IFN-β expression in a dose-dependent manner. Our data further demonstrated that JEV NS5 suppressed the activation of the IFN transcriptional factors IFN regulatory factor 3 (IRF3) and NF-κB. However, there was no defect in the phosphorylation of IRF3 and degradation of IκB, an upstream inhibitor of NF-κB, upon NS5 expression, indicating a direct inhibition of the nuclear localization of IRF3 and NF-κB by NS5. Mechanistically, NS5 was shown to interact with the nuclear transport proteins KPNA2, KPNA3, and KPNA4, which competitively blocked the interaction of KPNA3 and KPNA4 with their cargo molecules, IRF3 and p65, a subunit of NF-κB, and thus inhibited the nuclear translocation of IRF3 and NF-κB. Furthermore, overexpression of KPNA3 and KPNA4 restored the activity of IRF3 and NF-κB and increased the production of IFN-β in NS5-expressing or JEV-infected cells. Additionally, an upregulated replication level of JEV was shown upon KPNA3 or KPNA4 overexpression. These results suggest that JEV NS5 inhibits the induction of type I IFN by targeting KPNA3 and KPNA4.

IMPORTANCE
JEV is the major cause of viral encephalitis in South and Southeast Asia, with high mortality. However, the molecular mechanisms contributing to the severe pathogenesis are poorly understood. The ability of JEV to counteract the host innate immune response is potentially one of the mechanisms responsible for JEV virulence. Here we demonstrate the ability of JEV NS5 to interfere with the dsRNA-induced nuclear translocation of IRF3 and NF-κB by competitively inhibiting the interaction of IRF3 and NF-κB with nuclear transport proteins. Via this mechanism, JEV NS5 suppresses the induction of type I IFN and the antiviral response in host cells. These findings reveal a novel strategy for JEV to escape the host innate immune response and provide new insights into the pathogenesis of JEV.
A Point Mutation in the RNA-Binding Domain of Human Parainfluenza Virus Type 2 Nucleoprotein Elicits Abnormally Enhanced Polymerase Activity
Authors: Matsumoto Yusuke , Ohta Keisuke , Kolakofsky Daniel , Nishio Machiko 
Published: February 2017

ABSTRACT
The genome RNA of human parainfluenza virus type 2 (hPIV2) that acts as the template for the polymerase complex is entirely encapsidated by the nucleoprotein (NP). Recently, the crystal structure of NP of PIV5, a virus closely related to hPIV2, was resolved in association with RNA. Ten amino acids that contact the bound RNA were identified and are strictly conserved between PIV5 and hPIV2 NP. Mutation of hPIV2 NP Q202 (which contacts a base rather than the RNA backbone) to various amino acids resulted in an over 30-fold increase of polymerase activity as evidenced by a minireplicon assay, even though the RNA-binding affinity was unaltered. Using various modified minireplicons, we found that the enhanced reporter gene expression could be accounted for by increased minigenome replication, whereas mRNA synthesis itself was not affected by Q202 mutation. Moreover, the enhanced activities were still observed in minigenomes partially lacking the leader sequence and which were not of hexamer genome length. Unexpectedly, recombinant hPIV2 possessing the NP Q202A mutation could not be recovered from cDNA.

IMPORTANCE
We examined the importance of amino acids in the putative RNA-binding domain of hPIV2 NP for polymerase activity using minireplicons. Abnormally enhanced genome replication was observed upon substitution mutation of the NP Q202 position to various amino acids. Surprisingly, this mutation enabled polymerase to use minigenomes that were partially lacking the leader sequence and not of hexamer genome length. This mutation does not affect fundamental properties of NP, e.g., recognition of gene junctional and editing signals. However, the strongly enhanced polymerase activity may not be viable for the infectious life cycle. This report highlights the potential of the polymerase complex with point mutations in NP and helps our detailed understanding of the molecular basis of gene expression.
Differentiation-Dependent LMP1 Expression Is Required for Efficient Lytic Epstein-Barr Virus Reactivation in Epithelial Cells
Authors: Nawandar Dhananjay M. , Ohashi Makoto , Djavadian Reza , Barlow Elizabeth , Makielski Kathleen , Ali Ahmed , Lee Denis , Lambert Paul F. , Johannsen Eric , Kenney Shannon C. 
Published: February 2017

ABSTRACT

Epstein-Barr virus (EBV)-associated diseases of epithelial cells, including tumors that have latent infection, such as nasopharyngeal carcinoma (NPC), and oral hairy leukoplakia (OHL) lesions that have lytic infection, frequently express the viral latent membrane protein 1 (LMP1). In lytically infected cells, LMP1 expression is activated by the BRLF1 (R) immediate early (IE) protein. However, the mechanisms by which LMP1 expression is normally regulated in epithelial cells remain poorly understood, and its potential roles in regulating lytic reactivation in epithelial cells are as yet unexplored. We previously showed that the differentiation-dependent cellular transcription factors KLF4 and BLIMP1 induce lytic EBV reactivation in epithelial cells by synergistically activating the two EBV immediate early promoters (Zp and Rp). Here we show that epithelial cell differentiation also induces LMP1 expression. We demonstrate that KLF4 and BLIMP1 cooperatively induce the expression of LMP1, even in the absence of the EBV IE proteins BZLF1 (Z) and R, via activation of the two LMP1 promoters. Furthermore, we found that differentiation of NOKs-Akata cells by either methylcellulose suspension or organotypic culture induces LMP1 expression prior to Z and R expression. We show that LMP1 enhances the lytic infection-inducing effects of epithelial cell differentiation, as well as 12-
O
-tetradecanoylphorbol-13-acetate (TPA) and sodium butyrate treatment, in EBV-infected epithelial cells by increasing expression of the Z and R proteins. Our results suggest that differentiation of epithelial cells activates a feed-forward loop in which KLF4 and BLIMP1 first activate LMP1 expression and then cooperate with LMP1 to activate Z and R expression.

IMPORTANCE
The EBV protein LMP1 is expressed in EBV-associated epithelial cell diseases, regardless of whether these diseases are due to lytic infection (such as oral hairy leukoplakia) or latent infection (such as nasopharyngeal carcinoma). However, surprisingly little is known about how LMP1 expression is regulated in epithelial cells, and there are conflicting reports about whether it plays any role in regulating viral lytic reactivation. In this study, we show that epithelial cell differentiation induces LMP1 expression by increasing expression of two cellular transcription factors (KLF4 and BLIMP1) which cooperatively activate the two LMP1 promoters. We also demonstrate that LMP1 promotes efficient lytic reactivation in EBV-infected epithelial cells by enhancing expression of the Z and R proteins. Thus, in EBV-infected epithelial cells, LMP1 expression is promoted by differentiation and positively regulates lytic viral reactivation.
A Murine Herpesvirus Closely Related to Ubiquitous Human Herpesviruses Causes T-Cell Depletion
Authors: Patel Swapneel J. , Zhao Guoyan , Penna Vinay R. , Park Eugene , Lauron Elvin J. , Harvey Ian B. , Beatty Wandy L. , Plougastel-Douglas Beatrice , Poursine-Laurent Jennifer , Fremont Daved H. , Wang David , Yokoyama Wayne M. 
Published: February 2017

ABSTRACTThe human roseoloviruses human herpesvirus 6A (HHV-6A), HHV-6B, and HHV-7 comprise theRoseolovirusgenus of the humanBetaherpesvirinaesubfamily. Infections with these viruses have been implicated in many diseases; however, it has been challenging to establish infections with roseoloviruses as direct drivers of pathology, because they are nearly ubiquitous and display species-specific tropism. Furthermore, controlled study of infection has been hampered by the lack of experimental models, and until now, a mouse roseolovirus has not been identified. Herein we describe a virus that causes severe thymic necrosis in neonatal mice, characterized by a loss of CD4+T cells. These phenotypes resemble those caused by the previously described mouse thymic virus (MTV), a putative herpesvirus that has not been molecularly characterized. By next-generation sequencing of infected tissue homogenates, we assembled a contiguous 174-kb genome sequence containing 128 unique predicted open reading frames (ORFs), many of which were most closely related to herpesvirus genes. Moreover, the structure of the virus genome and phylogenetic analysis of multiple genes strongly suggested that this virus is a betaherpesvirus more closely related to the roseoloviruses, HHV-6A, HHV-6B, and HHV-7, than to another murine betaherpesvirus, mouse cytomegalovirus (MCMV). As such, we have named this virus murine roseolovirus (MRV) because these data strongly suggest that MRV is a mouse homolog of HHV-6A, HHV-6B, and HHV-7.IMPORTANCEHerein we describe the complete genome sequence of a novel murine herpesvirus. By sequence and phylogenetic analyses, we show that it is a betaherpesvirus most closely related to the roseoloviruses, human herpesviruses 6A, 6B, and 7. These data combined with physiological similarities with human roseoloviruses collectively suggest that this virus is a murine roseolovirus (MRV), the first definitively described rodent roseolovirus, to our knowledge. Many biological and clinical ramifications of roseolovirus infection in humans have been hypothesized, but studies showing definitive causative relationships between infection and disease susceptibility are lacking. Here we show that MRV infects the thymus and causes T-cell depletion, suggesting that other roseoloviruses may have similar properties.
Density-Dependent Recycling Promotes the Long-Term Survival of Bacterial Populations during Periods of Starvation
Authors: Takano Sotaro , Pawlowska Bogna J. , Gudelj Ivana , Yomo Tetsuya , Tsuru Saburo 
Published: February 2017

ABSTRACT
The amount of natural resources in the Earth’s environment is in flux, which can trigger catastrophic collapses of ecosystems. How populations survive under nutrient-poor conditions is a central question in ecology. Curiously, some bacteria persist for a long time in nutrient-poor environments. Although this survival may be accomplished through cell death and the recycling of dead cells, the importance of these processes and the mechanisms underlying the survival of the populations have not been quantitated. Here, we use microbial laboratory experiments and mathematical models to demonstrate that death and recycling are essential activities for the maintenance of cell survival. We also show that the behavior of the survivors is governed by population density feedback, wherein growth is limited not only by the available resources but also by the population density. The numerical simulations suggest that population density-dependent recycling could be an advantageous behavior under starvation conditions.

IMPORTANCE
How organisms survive after exhaustion of resources is a central question in ecology. Starving
Escherichia coli
constitute a model system to understand survival mechanisms during long-term starvation. Although death and the recycling of dead cells might play a key role in the maintenance of long-term survival, their mechanisms and importance have not been quantitated. Here, we verified the significance of social recycling of dead cells for long-term survival. We also show that the survivors restrained their recycling and did not use all available nutrients released from dead cells, which may be advantageous under starvation conditions. These results indicate that not only the utilization of dead cells but also restrained recycling coordinate the effective utilization of limited resources for long-term survival under starvation.
The Antigenic Structure of Zika Virus and Its Relation to Other Flaviviruses: Implications for Infection and Immunoprophylaxis
Authors: Heinz Franz X. , Stiasny Karin 
Published: February 2017

SUMMARY
Zika virus was discovered ∼70 years ago in Uganda and maintained a low profile as a human disease agent in Africa and Asia. Only recently has it caused explosive outbreaks in previously unaffected regions, first in Oceania and then in the Americas since 2015. Of special concern is the newly identified link between congenital malformations (especially microcephaly) and Zika virus infections during pregnancy. At present, it is unclear whether Zika virus changed its pathogenicity or whether the huge number of infections allowed the recognition of a previously cryptic pathogenic property. The purpose of this review is to discuss recent data on the molecular antigenic structure of Zika virus in the context of antibody-mediated neutralization and antibody-dependent enhancement (ADE) of infection, a phenomenon that has been implicated in the development of severe disease caused by the related dengue viruses. Emphasis is given to epitopes of antibodies that potently neutralize Zika virus and also to epitopes that provide antigenic links to other important human-pathogenic flaviviruses such as dengue, yellow fever, West Nile, Japanese encephalitis, and tick-borne encephalitis viruses. The antigenic cross talk between Zika and dengue viruses appears to be of special importance, since they cocirculate in many regions of endemicity and sequential infections are likely to occur frequently. New insights into the molecular antigenic structure of Zika virus and flaviviruses in general have provided the foundation for great progress made in developing Zika virus vaccines and antibodies for passive immunization.