bluuebunny/crossref_metadata_2025_split huggingface dataset:
Assessment of systemic inflammation by time‐trends of blood granulocyte count and plasma myeloperoxidase and elastase concentrations following colic surgery in horses
Authors: Salciccia Alexandra , Grulke Sigrid , de la Rebière de Pouyade Geoffroy , Franck Thierry , Detilleux Johann , Serteyn Didier , Sandersen Charlotte 
Published: May 2016

AbstractObjectiveTo determine changes in blood granulocyte counts and in plasma myeloperoxidase (MPO) and elastase (ELT) concentrations in surgical colic cases, and to determine the relationship between these changes and the surgical procedure performed, occurrence of postoperative ileus, and final outcome.DesignProspective clinical study conducted over a 12‐month period.SettingUniversity teaching hospital.AnimalsFifty‐three horses undergoing emergency laparotomy and surviving at least 12 hours postoperatively.InterventionsBlood samples were taken before surgery, during surgery, at the recovery from anesthesia, and then serially until the 150th hour after the first blood sampling. Granulocyte counts were performed by an automated cell hematology analyzer. Specific ELISAs were performed for the MPO and ELT measurements. Mixed models were used to compare the time‐trends of the 3 parameters.Measurements and Main ResultsTaking all horses together, the time‐trends of MPO and ELT were not significantly different from each other, but they were significantly different from the granulocyte time‐trend. The type of surgical procedure did not influence the time‐trends of the 3 parameters. Significant changes in the granulocyte time‐trends were associated with postoperative ileus and outcome. Significant changes in the MPO time‐trends were associated with outcome. The ELT time‐trends were not influenced by ileus or outcome.ConclusionsGranulocyte counts and MPO change over time and are related to the severity of the inflammatory reaction in surgical colic cases. These time‐trends may allow evaluation of treatment efficacy in an effort to modulate excessive granulocyte activation and degranulation.
Metabolic Pathway Involved in 6-Chloro-2-Benzoxazolinone Degradation by Pigmentiphaga sp. Strain DL-8 and Identification of the Novel Metal-Dependent Hydrolase CbaA
Authors: Dong Weiliang , Wang Fei , Huang Fei , Wang Yicheng , Zhou Jie , Ye Xianfeng , Li Zhoukun , Hou Ying , Huang Yan , Ma Jiangfeng , Jiang Min , Cui Zhongli 
Published: May 2016

ABSTRACT

6-Chloro-2-benzoxazolinone (CDHB) is a precursor of herbicide, insecticide, and fungicide synthesis and has a broad spectrum of biological activity.
Pigmentiphaga
sp. strain DL-8 can transform CDHB into 2-amino-5-chlorophenol (2A5CP), which it then utilizes as a carbon source for growth. The CDHB hydrolase (CbaA) was purified from strain DL-8, which can also hydrolyze 2-benzoxazolinone (BOA), 5-chloro-2-BOA, and benzamide. The specific activity of purified CbaA was 5,900 U · mg protein
−1
for CDHB, with

K
m

and
k
cat
values of 0.29 mM and 8,500 s
−1
, respectively. The optimal pH for purified CbaA was 9.0, the highest activity was observed at 55°C, and the inactive metal-free enzyme could be reactivated by Mg
2+
, Ni
2+
, Ca
2+
, or Zn
2+
. Based on the results obtained for the CbaA peptide mass fingerprinting and draft genome sequence of strain DL-8,
cbaA
(encoding 339 amino acids) was cloned and expressed in
Escherichia coli
BL21(DE3). CbaA shared 18 to 21% identity with some metal-dependent hydrolases of the PF01499 family and contained the signature metal-binding motif Q
127
XXXQ
131
XD
133
XXXH
137
. The conserved amino acid residues His288 and Glu301 served as the proton donor and acceptor.
E. coli
BL21(DE3-pET-
cbaA
) resting cells could transform 0.2 mM CDHB into 2A5CP. The mutant strain DL-8Δ
cbaA
lost the ability to degrade CDHB but retained the ability to degrade 2A5CP, consistent with strain DL-8. These results indicated that
cbaA
was the key gene responsible for CDHB degradation by strain DL-8.

IMPORTANCE
2-Benzoxazolinone (BOA) derivatives are widely used as synthetic intermediates and are also an important group of allelochemicals acting in response to tissue damage or pathogen attack in gramineous plants. However, the degradation mechanism of BOA derivatives by microorganisms is not clear. In the present study, we reported the identification of CbaA and metabolic pathway responsible for the degradation of CDHB in
Pigmentiphaga
sp. DL-8. This will provide microorganism and gene resources for the bioremediation of the environmental pollution caused by BOA derivatives.
Implications of Limited Thermophilicity of Nitrite Reduction for Control of Sulfide Production in Oil Reservoirs
Authors: Fida Tekle Tafese , Chen Chuan , Okpala Gloria , Voordouw Gerrit 
Published: May 2016

ABSTRACT

Nitrate reduction to nitrite in oil fields appears to be more thermophilic than the subsequent reduction of nitrite. Concentrated microbial consortia from oil fields reduced both nitrate and nitrite at 40 and 45°C but only nitrate at and above 50°C. The abundance of the
nirS
gene correlated with mesophilic nitrite reduction activity.
Thauera
and
Pseudomonas
were the dominant mesophilic nitrate-reducing bacteria (mNRB), whereas
Petrobacter
and
Geobacillus
were the dominant thermophilic NRB (tNRB) in these consortia. The mNRB
Thauera
sp. strain TK001, isolated in this study, reduced nitrate and nitrite at 40 and 45°C but not at 50°C, whereas the tNRB
Petrobacter
sp. strain TK002 and
Geobacillus
sp. strain TK003 reduced nitrate to nitrite but did not reduce nitrite further from 50 to 70°C. Testing of 12 deposited pure cultures of tNRB with 4 electron donors indicated reduction of nitrate in 40 of 48 and reduction of nitrite in only 9 of 48 incubations. Nitrate is injected into high-temperature oil fields to prevent sulfide formation (souring) by sulfate-reducing bacteria (SRB), which are strongly inhibited by nitrite. Injection of cold seawater to produce oil creates mesothermic zones. Our results suggest that preventing the temperature of these zones from dropping below 50°C will limit the reduction of nitrite, allowing more effective souring control.

IMPORTANCE
Nitrite can accumulate at temperatures of 50 to 70°C, because nitrate reduction extends to higher temperatures than the subsequent reduction of nitrite. This is important for understanding the fundamentals of thermophilicity and for the control of souring in oil fields catalyzed by SRB, which are strongly inhibited by nitrite.
Paralogous Regulators ArsR1 and ArsR2 of Pseudomonas putida KT2440 as a Basis for Arsenic Biosensor Development
Authors: Fernández Matilde , Morel Bertrand , Ramos Juan L. , Krell Tino 
Published: May 2016

ABSTRACT

The remarkable metal resistance of many microorganisms is related to the presence of multiple metal resistance operons.
Pseudomonas putida
KT2440 can be considered a model for these microorganisms since its arsenic resistance is due to the action of proteins encoded by the two paralogous arsenic resistance operons ARS1 and ARS2. Both operons contain the genes encoding the transcriptional regulators ArsR1 and ArsR2 that control operon expression. We show here that purified ArsR1 and ArsR2 bind the trivalent salt of arsenic (arsenite) with similar affinities (~30 μM), whereas no binding is observed for the pentavalent salt (arsenate). Furthermore, trivalent salts of bismuth and antimony showed binding to both paralogues. The positions of cysteines, found to bind arsenic in other homologues, indicate that ArsR1 and ArsR2 employ different modes of arsenite recognition. Both paralogues are dimeric and possess significant thermal stability. Both proteins were used to construct whole-cell,
lacZ
-based biosensors. Whereas responses to bismuth were negligible, significant responses were observed for arsenite, arsenate, and antimony. Biosensors based on the
P. putida
arsB1 arsB2
arsenic efflux pump double mutant were significantly more sensitive than biosensors based on the wild-type strain. This sensitivity enhancement by pump mutation may be a convenient strategy for the construction of other biosensors. A frequent limitation found for other arsenic biosensors was their elevated background signal and interference by inorganic phosphate. The constructed biosensors show no interference by inorganic phosphate, are characterized by a very low background signal, and were found to be suitable to analyze environmental samples.

IMPORTANCE
Arsenic is at the top of the priority list of hazardous compounds issued by the U.S. Agency for Toxic Substances and Disease. The reason for the stunning arsenic resistance of many microorganisms is the existence of paralogous arsenic resistance operons.
Pseudomonas putida
KT2440 is a model organism for such bacteria, and their duplicated
ars
operons and in particular their ArsR transcription regulators have been studied in depth by
in vivo
approaches. Here we present an analysis of both purified ArsR paralogues by different biophysical techniques, and data obtained provide valuable insight into their structure and function. Particularly insightful was the comparison of ArsR effector profiles determined by
in vitro
and
in vivo
experimentation. We also report the use of both paralogues to construct robust and highly sensitive arsenic biosensors. Our finding that the deletion of both arsenic efflux pumps significantly increases biosensor sensitivity is of general relevance in the biosensor field.
Detection of Zoonotic Enteropathogens in Children and Domestic Animals in a Semirural Community in Ecuador
Authors: Vasco Karla , Graham Jay P. , Trueba Gabriel 
Published: May 2016

ABSTRACT

Animals are important reservoirs of zoonotic enteropathogens, and transmission to humans occurs more frequently in low- and middle-income countries (LMICs), where small-scale livestock production is common. In this study, we investigated the presence of zoonotic enteropathogens in stool samples from 64 asymptomatic children and 203 domestic animals of 62 households in a semirural community in Ecuador between June and August 2014. Multilocus sequence typing (MLST) was used to assess zoonotic transmission of
Campylobacter jejuni
and atypical enteropathogenic
Escherichia coli
(aEPEC), which were the most prevalent bacterial pathogens in children and domestic animals (30.7% and 10.5%, respectively). Four sequence types (STs) of
C. jejuni
and four STs of aEPEC were identical between children and domestic animals. The apparent sources of human infection were chickens, dogs, guinea pigs, and rabbits for
C. jejuni
and pigs, dogs, and chickens for aEPEC. Other pathogens detected in children and domestic animals were
Giardia lamblia
(13.1%),
Cryptosporidium parvum
(1.1%), and Shiga toxin-producing
E. coli
(STEC) (2.6%).
Salmonella enterica
was detected in 5 dogs and
Yersinia enterocolitica
was identified in 1 pig. Even though we identified 7 enteric pathogens in children, we encountered evidence of active transmission between domestic animals and humans only for
C. jejuni
and aEPEC. We also found evidence that
C. jejuni
strains from chickens were more likely to be transmitted to humans than those coming from other domestic animals. Our findings demonstrate the complex nature of enteropathogen transmission between domestic animals and humans and stress the need for further studies.

IMPORTANCE
We found evidence that
Campylobacter jejuni
,
Giardia
, and aEPEC organisms were the most common zoonotic enteropathogens in children and domestic animals in a region close to Quito, the capital of Ecuador. Genetic analysis of the isolates suggests transmission of some genotypes of
C. jejuni
and aEPEC from domestic animals to humans in this region. We also found that the genotypes associated with
C. jejuni
from chickens were present more often in children than were those from other domestic animals. The potential environmental factors associated with transmission of these pathogens to humans then are discussed.
Cutting to the Core of the Issue: Emerging Strategies To Reduce Prostate Biopsy-Related Infections
Authors: Chamberland Robin R. 
Published: May 2016

ABSTRACT

Over 1 million men undergo biopsy in the United States each year to evaluate for prostate cancer (S. Loeb, H. B. Carter, S. I. Berndt, W. Ricker, and E. M. Schaeffer, J Urol 186:1830–1834, 2011,
http://dx.doi.org/10.1016/j.juro.2011.06.057
). In recent years, there has been a rise in infectious complications related to these procedures. This review aims to provide an overview of the guidelines that direct transrectal prostate biopsy, to describe associated infection, and to evaluate the published data driving the current trend toward prebiopsy screening for resistant organisms.
Malassezia arunalokei sp. nov., a Novel Yeast Species Isolated from Seborrheic Dermatitis Patients and Healthy Individuals from India
Authors: Honnavar Prasanna , Prasad Gandham S. , Ghosh Anup , Dogra Sunil , Handa Sanjeev , Rudramurthy Shivaprakash M. 
Published: May 2016

ABSTRACT

The majority of species within the genus
Malassezia
are lipophilic yeasts that colonize the skin of warm-blooded animals. Two species,
Malassezia globosa
and
Malassezia restricta
, are implicated in the causation of seborrheic dermatitis/dandruff (SD/D). During our survey of SD/D cases, we isolated several species of
Malassezia
and noticed vast variations within a few lipid-dependent species. Variations observed in the phenotypic characteristics (colony morphology, absence of catalase activity, growth at 37°C, and precipitation surrounding wells containing Tween 20 or Cremophor EL) suggested the possible presence of a novel species. Sequence divergence observed in the internal transcribed spacer (ITS) region, the D1/D2 domain, and the intergenic spacer 1 (IGS1) region of rDNA and the
TEF1
gene, PCR-restriction fragment length polymorphism (RFLP) analysis of the ITS2 region, and fluorescent amplified fragment length polymorphism analysis support the existence of a novel species. Based on phenotypic and molecular characterization of these strains, we propose a new species, namely,
M. arunalokei
sp. nov., and we designate NCCPF 127130 (= MTCC 12054 = CBS 13387) as the type strain.
The Emerging Duck Flavivirus Is Not Pathogenic for Primates and Is Highly Sensitive to Mammalian Interferon Antiviral Signaling
Authors: Wang Hong-Jiang , Li Xiao-Feng , Liu Long , Xu Yan-Peng , Ye Qing , Deng Yong-Qiang , Huang Xing-Yao , Zhao Hui , Qin E-De , Shi Pei-Yong , Gao George F. , Qin Cheng-Feng 
Published: May 2016

ABSTRACT

Flaviviruses pose a significant threat to both animals and humans. Recently, a novel flavivirus, duck Tembusu virus (DTMUV), was identified to be the causative agent of a serious duck viral disease in Asia. Its rapid spread, expanding host range, and uncertain transmission routes have raised substantial concerns regarding its potential threats to nonavian hosts, including humans. Here, we demonstrate that DTMUV is not pathogenic for nonhuman primates and is highly sensitive to mammal type I interferon (IFN) signaling.
In vitro
assays demonstrated that DTMUV infected and replicated efficiently in various mammalian cell lines. Further tests in mice demonstrated high neurovirulence and the age-dependent neuroinvasiveness of the virus. In particular, the inoculation of DTMUV into rhesus monkeys did not result in either viremia or apparent clinical symptoms, although DTMUV-specific humoral immune responses were detected. Furthermore, we revealed that although avian IFN failed to inhibit DTMUV in avian cells, DTMUV was more sensitive to the antiviral effects of type I interferon than other known human-pathogenic flaviviruses. Knockout of the type I IFN receptor in mice caused apparent viremia, viscerotropic disease, and mortality, indicating a vital role of IFN signaling in protection against DTMUV infection. Collectively, we provide direct experimental evidence that this novel avian-origin DTMUV possesses a limited capability to establish infection in immunocompetent primates due to its decreased antagonistic activity in the mammal IFN system. Furthermore, our findings highlight the potential risk of DTMUV infection in immunocompromised individuals and warrant studies on the cross-species transmission and pathogenesis of this novel flavivirus.

IMPORTANCE
Mosquito-borne flaviviruses comprise a large group of pathogenic and nonpathogenic members. The pathogenic flaviviruses include dengue, West Nile, and Japanese encephalitis viruses, and the nonpathogenic flaviviruses normally persist in a natural cycle and rarely cause disease in humans. A novel flavivirus, DTMUV (also known as duck egg drop syndrome flavivirus [DEDSV]) was identified in 2012 in ducks and then rapidly spread to several Asian countries. This new flavivirus was then shown to infect multiple avian species, resulting in neurological symptoms with unknown routes of transmission. There is public concern regarding its potential transmission from birds to humans and other nonavian hosts. Our present study shows that the mammalian IFN system can efficiently eliminate DTMUV infection and that the emergence of severe DTMUV-associated disease in mammals, especially humans, is unlikely. Currently, DTMUV infection mostly affects avian species.
Nipah Virus C and W Proteins Contribute to Respiratory Disease in Ferrets
Authors: Satterfield Benjamin A. , Cross Robert W. , Fenton Karla A. , Borisevich Viktoriya , Agans Krystle N. , Deer Daniel J. , Graber Jessica , Basler Christopher F. , Geisbert Thomas W. , Mire Chad E. 
Published: May 2016

ABSTRACT
Nipah virus (NiV) is a highly lethal paramyxovirus that recently emerged as a causative agent of febrile encephalitis and severe respiratory disease in humans. The ferret model has emerged as the preferred small-animal model with which to study NiV disease, but much is still unknown about the viral determinants of NiV pathogenesis, including the contribution of the C protein in ferrets. Additionally, studies have yet to examine the synergistic effects of the various P gene products on pathogenesis in animal models. Using recombinant NiVs (rNiVs), we examine the sole contribution of the NiV C protein and the combined contributions of the C and W proteins in the ferret model of NiV pathogenesis. We show that an rNiV void of C expression resulted in 100% mortality, though with limited respiratory disease, like our previously reported rNiV void of W expression; this finding is in stark contrast to the attenuated phenotype observed in previous hamster studies utilizing rNiVs void of C expression. We also observed that an rNiV void of both C and W expression resulted in limited respiratory disease; however, there was severe neurological disease leading to 60% mortality, and the surviving ferrets demonstrated sequelae similar to those for human survivors of NiV encephalitis.

IMPORTANCE
Nipah virus (NiV) is a human pathogen capable of causing lethal respiratory and neurological disease. Many human survivors have long-lasting neurological impairment. Using a ferret model, this study demonstrated the roles of the NiV C and W proteins in pathogenesis, where lack of either the C or the W protein independently decreased the severity of clinical respiratory disease but did not decrease lethality. Abolishing both C and W expression, however, dramatically decreased the severity of respiratory disease and the level of destruction of splenic germinal centers. These ferrets still suffered severe neurological disease: 60% succumbed to disease, and the survivors experienced long-term neurological impairment, such as that seen in human survivors. This new ferret NiV C and W knockout model may allow, for the first time, the examination of interventions to prevent or mitigate the neurological damage and sequelae experienced by human survivors.
Feline Calicivirus Infection Disrupts Assembly of Cytoplasmic Stress Granules and Induces G3BP1 Cleavage
Authors: Humoud Majid N. , Doyle Nicole , Royall Elizabeth , Willcocks Margaret M. , Sorgeloos Frederic , van Kuppeveld Frank , Roberts Lisa O. , Goodfellow Ian G. , Langereis Martijn A. , Locker Nicolas 
Published: May 2016

ABSTRACT

In response to stress such as virus infection, cells can stall translation by storing mRNAs away in cellular compartments called stress granules (SGs). This defense mechanism favors cell survival by limiting the use of energy and nutrients until the stress is resolved. In some cases it may also block viral propagation as viruses are dependent on the host cell resources to produce viral proteins. Human norovirus is a member of the
Caliciviridae
family responsible for gastroenteritis outbreaks worldwide. Previous studies on caliciviruses have identified mechanisms by which they can usurp the host translational machinery, using the viral protein genome-linked VPg, or regulate host protein synthesis through the mitogen-activated protein kinase (MAPK) pathway. Here, we examined the effect of feline calicivirus (FCV) infection on SG accumulation. We show that FCV infection impairs the assembly of SGs despite an increased phosphorylation of eukaryotic initiation factor eIF2α, a hallmark of stress pathway activation. Furthermore, SGs did not accumulate in FCV-infected cells that were stressed with arsenite or hydrogen peroxide. FCV infection resulted in the cleavage of the SG-nucleating protein Ras-GTPase activating SH3 domain-binding protein (G3BP1), which is mediated by the viral 3C-like proteinase NS6
Pro
. Using mutational analysis, we identified the FCV-induced cleavage site within G3BP1, which differs from the poliovirus 3C proteinase cleavage site previously identified. Finally, we showed that NS6
Pro
-mediated G3BP1 cleavage impairs SG assembly. In contrast, murine norovirus (MNV) infection did not impact arsenite-induced SG assembly or G3BP1 integrity, suggesting that related caliciviruses have distinct effects on the stress response pathway.

IMPORTANCE
Human noroviruses are a major cause of viral gastroenteritis, and it is important to understand how they interact with the infected host cell. Feline calicivirus (FCV) and murine norovirus (MNV) are used as models to understand norovirus biology. Recent studies have suggested that the assembly of stress granules is central in orchestrating stress and antiviral responses to restrict viral replication. Overall, our study provides the first insight on how caliciviruses impair stress granule assembly by targeting the nucleating factor G3BP1 via the viral proteinase NS6
Pro
. This work provides new insights into host-pathogen interactions that regulate stress pathways during FCV infection.