bluuebunny/crossref_metadata_2025_split huggingface dataset:
Development of an Algorithm for Assessing the Risk to Food Safety Posed by a New Animal Disease
Authors: Parker E. M. , Jenson I. , Jordan D. , Ward M. P. 
Published: September 2011

SummaryAn algorithm was developed as a tool to rapidly assess the potential for a new or emerging disease of livestock to adversely affect humans via consumption or handling of meat product, so that the risks and uncertainties can be understood and appropriate risk management and communication implemented. An algorithm describing the sequence of events from occurrence of the disease in livestock, release of the causative agent from an infected animal, contamination of fresh meat and then possible adverse effects in humans following meat handling and consumption was created. A list of questions complements the algorithm to help the assessors address the issues of concern at each step of the decision pathway. The algorithm was refined and validated through consultation with a panel of experts and a review group of animal health and food safety policy advisors via five case studies of potential emerging diseases of cattle. Tasks for model validation included describing the path taken in the algorithm and stating an outcome. Twenty‐nine per cent of the 62 experts commented on the model, and one‐third of those responding also completed the tasks required for model validation. The feedback from the panel of experts and the review group was used to further develop the tool and remove redundancies and ambiguities. There was agreement in the pathways and assessments for diseases in which the causative agent was well understood (for example, bovine pneumonia due to Mycoplasma bovis). The stated pathways and assessments of other diseases (for example, bovine Johne’s disease) were not as consistent. The framework helps to promote objectivity by requiring questions to be answered sequentially and providing the opportunity to record consensus or differences of opinion. Areas for discussion and future investigation are highlighted by the points of diversion on the pathway taken by different assessors.
Development rate of chronic kidney disease in hepatitis C virus patients with advanced fibrosis after interferon therapy
Authors: Arase Yasuji , Suzuki Fumitaka , Kawamura Yusuke , Suzuki Yoshiyuki , Kobayashi Masahiro , Matsumoto Naoki , Akuta Norio , Sezaki Hitomi , Hosaka Tetsuya , Ogawa Kyoko , Imai Norihiro , Seko Yuya , Saito Satoshi , Ikeda Kenji , Kobayashi Mariko , Kumada Hiromitsu 
Published: September 2011

Aim:  The aim of this retrospective cohort study is to assess the development incidence and predictive factors for chronic kidney disease (CKD) after the termination of interferon therapy in hepatitis C virus (HCV) positive Japanese patients with liver cirrhosis.Methods:  A total of 650 HCV positive, liver cirrhotic patients who were treated with interferon and showed an estimated glomerular filtration rate (eGFR) of ≥60 mL/min per 1.73 m2 after the termination of interferon therapy were enrolled. CKD was defined as an eGFR of <60 mL/min per 1.73 m2. End‐stage‐CKD was defined as an eGFR of <15 mL/min/1.73 m2. The primary goal is the new development of CKD and end‐stage‐CKD.Results:  Eighty‐five patients developed CKD, and six patients progressed to end‐stage‐CKD. The development rate of CKD was 5.2% at the 5th year, 14.5% at the 10th year and 30.6% at the 15th year. Multivariate Cox proportional hazards analysis showed that CKD occurred when patients had age increments of 10 years (hazard ratio: 2.32; 95% confidence interval [CI] 1.61–3.35; P < 0.001), eGFR decrements of 10 mL/min per 1.73 m2 (hazard ratio: 1.66; 95% CI 1.27–2.16; P < 0.001), hypertension (hazard ratio: 2.00; 95% CI 1.13–3.53; P = 0.017), diabetes (hazard ratio: 1.79; 95% CI 1.02–3.14; P = 0.042), and non‐clearance of HCV (hazard ratio: 2.67; 95% CI 1.34–5.32; P = 0.005). The development rate of end‐stage‐CKD was 0.4% at the 5th year, 1.6% at the 10th year and 2.8% at the 15th year.Conclusions:  The annual incidence for CKD among cirrhotic patients with HCV was determined to be about 1.0–1.5%. In addition, the annual incidence for end‐stage‐CKD is one order of magnitude lower than that of CKD.
Easy‐to‐use phylogenetic analysis system for hepatitis B virus infection
Authors: Sugiyama Masaya , Inui Ayano , Shin‐I Tadasu , Komatsu Haruki , Mukaide Motokazu , Masaki Naohiko , Murata Kazumoto , Ito Kiyoaki , Nakanishi Makoto , Fujisawa Tomoo , Mizokami Masashi 
Published: September 2011

Aim:  The molecular phylogenetic analysis has been broadly applied to clinical and virological study. However, the appropriate settings and application of calculation parameters are difficult for non‐specialists of molecular genetics. In the present study, the phylogenetic analysis tool was developed for the easy determination of genotypes and transmission route.Methods:  A total of 23 patients of 10 families infected with hepatitis B virus (HBV) were enrolled and expected to undergo intrafamilial transmission. The extracted HBV DNA were amplified and sequenced in a region of the S gene.Results:  The software to automatically classify query sequence was constructed and installed on the Hepatitis Virus Database (HVDB). Reference sequences were retrieved from HVDB, which contained major genotypes from A to H. Multiple‐alignments using CLUSTAL W were performed before the genetic distance matrix was calculated with the six‐parameter method. The phylogenetic tree was output by the neighbor‐joining method. User interface using WWW‐browser was also developed for intuitive control. This system was named as the easy‐to‐use phylogenetic analysis system (E‐PAS). Twenty‐three sera of 10 families were analyzed to evaluate E‐PAS. The queries obtained from nine families were genotype C and were located in one cluster per family. However, one patient of a family was classified into the cluster different from her family, suggesting that E‐PAS detected the sample distinct from that of her family on the transmission route.Conclusions:  The E‐PAS to output phylogenetic tree was developed since requisite material was sequence data only. E‐PAS could expand to determine HBV genotypes as well as transmission routes.
DNA repair gene XRCC7 polymorphisms (rs#7003908 and rs#10109984) and hepatocellular carcinoma related to AFB1 exposure among Guangxi population, China
Authors: Long Xi‐Dai , Yao Jin‐Guang , Huang Yong‐Zhi , Huang Xiao‐Ying , Ban Fu‐Zhi , Yao Li‐Ming , Fan Lu‐Dan 
Published: September 2011

Aim:  The X‐ray repair cross‐complementing group 7 (XRCC7) plays an important role in the repair of DNA double‐strand breaks by nonhomologous end‐joining repair (NEJR) pathway. However, the role of XRCC7 polymorphisms (rs#7003908 and rs#10109984) possibly influencing NEJR capacity in hepatocellular carcinoma (HCC) induced by aflatoxin B1 (AFB1) has not been well elaborated.Methods:  This hospital‐based case‐control study, including 348 patients with newly diagnosed HCC and 597 controls without any evidence of liver diseases, was conducted to elucidate the association between these two polymorphisms and the risk of HCC related to AFB1 exposure among a Guangxi population from a high AFB1‐exposure area by means of TaqMAN‐polymerase chain reaction technique.Results:  We observed that HCC patients featured higher AFB1 exposure than control group (odds ratios [OR] = 6.49 and 6.75 for exposure years and exposure levels, respectively). Furthermore, these individuals with the genotypes of XRCC7 rs#7003908 G alleles (namely XRCC7‐TG or ‐GG), compared the homozygote of XRCC7 rs#7003908 T alleles (XRCC7‐TT), faced increasing risk of HCC (OR, 3.45 and 5.04; 95% confidence intervals [CIs], 2.40–4.94 and 3.28–7.76, respectively). We also found some evidence that this polymorphism interacted with AFB1‐expousure years or levels in the process of HCC carcinogenesis. Additionally, XRCC7 rs#7003908 polymorphism was correlated with the levels of AFB1‐DNA adducts (r = 0.142, P < 0.001). XRCC7 rs#10109984 polymorphism, however, did not modify the risk of HCC related to AFB1 exposure (P > 0.05).Conclusion:  These data suggest that XRCC7 rs#7003908 polymorphism may be one of the genetic modifiers for AFB1‐related HCC among Guangxi population.
Leaf extract of Rhus verniciflua Stokes protects dopaminergic neuronal cells in a rotenone model of Parkinson's disease
Authors: Kim Seung , Park Se-Eun , Sapkota Kumar , Kim Myung-Kon , Kim Sung-Jun 
Published: September 2011

Abstract

Objectives
The present study investigated the neuroprotective effects of Rhus verniciflua Stokes (RVS) leaf extract on rotenone-induced apoptosis in human dopaminergic cells, SH-SY5Y.

Methods
Cells were pretreated with RVS extract for 1 h then treated with vehicle or rotenone for 24 h. Cell viability, cell cytotoxicity, cell morphology and nuclear morphology were examined by MTT assay, lactate dehydrogenase release assay, phase contrast microscopy and staining with Hoechast 33342, respectively. Reactive oxygen species were measured by 2′7′-dichlorofluorescein diacetate and fragmented DNA was observed by TUNEL assay. Mitochondrial membrane potential was determined by Rhodamine 123. Pro-apoptotic and anti-apoptotic proteins and tyrosine hydroxylase were analysed by Western blotting.

Key findings
Results showed that RVS suppressed rotenone-induced reactive oxygen species generation, cellular injury and apoptotic cell death. RVS also prevented rotenone-mediated changes in Bax/Bcl-2 levels, mitochondrial membrane potential dissipation and Caspase 3 activation. Moreover, RVS pretreatment increased the tyrosine hydroxylase levels in SH-SY5Y cells.

Conclusions
These findings demonstrate that RVS protects SH-SY5Y cells against rotenone-induced injury and suggest that RVS may have potential therapeutic value for neurodegenerative disease associated with oxidative stress.
Dexamethasone-Induced Cytokine Changes Associated with Diminished Disease Severity in Horses Infected with Anaplasma phagocytophilum
Authors: Davies R. S. , Madigan J. E. , Hodzic E. , Borjesson D. L , Dumler J. S. 
Published: September 2011

ABSTRACT

Anaplasma phagocytophilum
is the zoonotic cause of granulocytic anaplasmosis. We hypothesized that immune response, specifically gamma interferon (IFN-γ), plays a role in disease severity. To test this, horses were infected and
IFNG
expression was pharmacologically downregulated using corticosteroids. Eight horses were infected with
A. phagocytophilum
; 4 received dexamethasone on days 4 to 8 of infection. Clinical signs, hematologic parameters, and transcription of cytokine/chemokine genes were compared among treated and untreated horses. Infection was quantitated by
msp2
real-time PCR and microscopy. As anticipated, there was significantly greater leukopenia, thrombocytopenia, and anemia in infected versus uninfected horses. The
A. phagocytophilum
load was higher for dexamethasone-treated horses. Dexamethasone reduced
IFNG
transcription by day 12 and
IL-8
and
IL-18
by days 7 to 9 and increased
IL-4
on day 7. The ratio of
IL-10
to
IFNG
was increased by dexamethasone on day 9. There were no hematologic differences between the infected horses. Dexamethasone suppression of proinflammatory response resulted in delayed infection-induced limb edema and decreased icterus, anorexia, and reluctance to move between days 6 and 9 and lower fever on day 7. These results underscore the utility of the equine model of granulocytic anaplasmosis and suggest that Th1 proinflammatory response plays a role in worsening disease severity and that disease severity can be decreased by modulating proinflammatory response. A role for Th1 response and macrophage activation in hematologic derangements elicited by
A. phagocytophilum
is not supported by these data and remains unproven.
Intranasal Administration of an Inactivated Yersinia pestis Vaccine with Interleukin-12 Generates Protective Immunity against Pneumonic Plague
Authors: Kumar Devender , Kirimanjeswara Girish , Metzger Dennis W. 
Published: September 2011

ABSTRACT

Inhalation of
Yersinia pestis
causes pneumonic plague, which rapidly progresses to death. A previously licensed killed whole-cell vaccine is presently unavailable due to its reactogenicity and inconclusive evidence of efficacy. The present study now shows that vaccination intranasally (i.n.) with inactivated
Y. pestis
CO92 (iYp) adjuvanted with interleukin-12 (IL-12) followed by an i.n. challenge with a lethal dose of
Y. pestis
CO92 prevented bacterial colonization and protected 100% of mice from pneumonic plague. Survival of the vaccinated mice correlated with levels of systemic and lung antibodies, reduced pulmonary pathology and proinflammatory cytokines, and the presence of lung lymphoid cell aggregates. Protection against pneumonic plague was partially dependent upon Fc receptors and could be transferred to naïve mice with immune mouse serum. On the other hand, protection was not dependent upon complement, and following vaccination, depletion of CD4 and/or CD8 T cells before challenge did not affect survival. In summary, the results demonstrate the safety, immunogenicity, and protective efficacy of i.n. administered iYp plus IL-12 in a mouse model of pneumonic plague.
Age-Specific Seroprevalence of Merkel Cell Polyomavirus, BK Virus, and JC Virus
Authors: Viscidi Raphael P. , Rollison Dana E. , Sondak Vernon K. , Silver Barbara , Messina Jane L. , Giuliano Anna R. , Fulp William , Ajidahun Abidemi , Rivanera Daniela 
Published: September 2011

ABSTRACTWe produced capsids of Merkel cell polyomavirus (MCPyV) in a baculovirus expression system and developed a virus-like particle (VLP) enzyme-linked immunosorbent assay (ELISA). To determine age-specific seroprevalence, serum samples were collected from 947 individuals attending hospital outpatient clinics and ranging in age from 1 to 93 years. To evaluate the association between exposure to MCPyV and Merkel cell cancer (MCC), plasma samples were obtained from 33 MCC patients and 37 controls. MCPyV seroprevalence was 45% in children under 10 years of age, increased to 60% in the next decade of life, and peaked at 81% among those 60 to 69 years of age. Levels of MCPyV capsid antibodies were positively correlated with age (P= 0.007). Virus specificity of MCPyV seroreactivity was supported by competitive inhibition of reactivity by MCPyV VLPs and not by BK polyomavirus (BKPyV) VLPs. MCPyV seroprevalence was greater among MCC patients (91%) than controls (68%; age-adjustedPvalue, 0.32); the mean level of MCPyV antibodies was also greater (P= 0.04). The age-specific seroprevalence of MCPyV shares with previously known polyomaviruses, BKPyV and JC polyomavirus (JCPyV), evidence of widespread exposure in human populations beginning early in life. MCPyV age-specific seroprevalence also has unique features. Seroprevalence among children is higher than that of JCPyV but lower than that of BKPyV. Among older adults, MCPyV seroprevalence remains high, while that of BKPyV declines and that of JCPyV continues to rise. In agreement with results from other studies, we found an association between MCPyV seropositivity and MCC, and higher levels of serum MCPyV capsid antibodies in MCC patients than in controls.
Multilocus Sequence Typing of Streptococcus pneumoniae by Use of Mass Spectrometry
Authors: Dunne Eileen M. , Ong Eng Kok , Moser Ralf J. , Siba Peter M. , Phuanukoonnon Suparat , Greenhill Andrew R. , Robins-Browne Roy M. , Mulholland E. Kim , Satzke Catherine 
Published: September 2011

ABSTRACT

Multilocus sequence typing (MLST) is an important tool for the global surveillance of bacterial pathogens that is performed by comparing the sequences of designated housekeeping genes. We developed and tested a novel mass spectrometry-based method for MLST of
Streptococcus pneumoniae
. PCR amplicons were subjected to
in vitro
transcription and base-specific cleavage, followed by analysis of the resultant fragments by using matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS). Comparison of the cleavage fragment peak patterns to a reference sequence set permitted automated identification of alleles. Validation experiments using 29 isolates of
S. pneumoniae
revealed that the results of MALDI-TOF MS MLST matched those obtained by traditional sequence-based MLST for 99% of alleles and that the MALDI-TOF MS method accurately identified two single-nucleotide variations. The MADLI-TOF MS method was then used for MLST analysis of 43
S. pneumoniae
isolates from Papua New Guinean children. The majority of the isolates present in this population were not clonal and contained seven new alleles and 30 previously unreported sequence types.
Genetic Response to Bacteriophage Infection in Lactococcus lactis Reveals a Four-Strand Approach Involving Induction of Membrane Stress Proteins,
d
-Alanylation of the Cell Wall, Maintenance of Proton Motive Force, and Energy Conservation
Authors: Fallico Vincenzo , Ross R. Paul , Fitzgerald Gerald F. , McAuliffe Olivia 
Published: September 2011

ABSTRACT

In this study, whole-genome microarrays were used to gain insights into the global molecular response of
Lactococcus lactis
subsp.
lactis
IL1403 at an early stage of infection with the lytic phage c2. The bacterium differentially regulated the expression of 61 genes belonging to 14 functional categories, including cell envelope processes (12 genes), regulatory functions (11 genes), and carbohydrate metabolism (7 genes). The nature of these genes suggests a complex response involving four main mechanisms: (i) induction of membrane stress proteins, (ii)
d
-alanylation of cell wall lipoteichoic acids (LTAs), (iii) maintenance of the proton motive force (PMF), and (iv) energy conservation. The phage presence is sensed as a membrane stress in
L. lactis
subsp.
lactis
IL1403, which activated a cell wall-targeted response probably orchestrated by the concerted action of membrane phage shock protein C-like homologues, the global regulator SpxB, and the two-component system CesSR. The bacterium upregulated genes (
ddl
and
dltABCD
) responsible for incorporation of
d
-alanine esters into LTAs, an event associated with increased resistance to phage attack in Gram-positive bacteria. The expression of genes (
yshC
,
citE
,
citF
) affecting both PMF components was also regulated to restore the physiological PMF, which was disrupted following phage infection. While mobilizing the response to the phage-mediated stress, the bacterium activated an energy-saving program by repressing growth-related functions and switching to anaerobic respiration, probably to sustain the PMF and the overall cell response to phage. To our knowledge, this represents the first detailed description in
L. lactis
of the molecular mechanisms involved in the host response to the membrane perturbations mediated by phage infection.
Mechanism of Glycyrrhizic Acid Inhibition of Kaposi's Sarcoma-Associated Herpesvirus: Disruption of CTCF-Cohesin-Mediated RNA Polymerase II Pausing and Sister Chromatid Cohesion
Authors: Kang Hyojeung , Lieberman Paul M. 
Published: September 2011

ABSTRACT

Glycyrrhizic acid (GA), a derivative of licorice, selectively inhibits the growth of lymphocytes latently infected with Kaposi's sarcoma-associated herpesvirus. The mechanism involves the deregulation of the multicistronic latency transcript, including the failure to generate the mature forms of viral mRNA encoding LANA. We show here that GA disrupts an RNA polymerase II (RNAPII) complex that accumulates at the CTCF-cohesin binding site within the first intron of the latency transcript. GA altered the enrichment of the RNAPII pausing complex, along with pausing factors SPT5 and NELF-A, at the intragenic CTCF-cohesin binding sites. GA blocked the interaction of cohesin subunit SMC3 with another cohesin subunit, RAD21, and reduced SPT5 interaction with RNAPII. Covalent coupling of GA to a solid support revealed that GA interacts with several cellular proteins, including SMC3 and SPT5, but not their respective interaction partners RAD21 and RNAPII. GA treatment also inhibited the transcription of some cellular genes, like c-
myc
, which contain a similar CTCF-cohesin binding site within the first intron. We also found that GA leads to a more general loss of sister chromatid cohesion for cellular chromosomes. These findings suggest that RNAPII pauses at intragenic CTCF-cohesin binding sites and that abrogation of this pausing by GA leads to loss of proper mRNA production and defects in sister chromatid cohesion, a process important for both viral and cellular chromosome stability.
Identification of Autographa californica Nucleopolyhedrovirus ac93 as a Core Gene and Its Requirement for Intranuclear Microvesicle Formation and Nuclear Egress of Nucleocapsids
Authors: Yuan Meijin , Huang Zhenqiu , Wei Denghui , Hu Zhaoyang , Yang Kai , Pang Yi 
Published: September 2011

ABSTRACT

Autographa californica
nucleopolyhedrovirus (AcMNPV)
orf93
(
ac93
) is a highly conserved uncharacterized gene that is found in all of the sequenced baculovirus genomes except for
Culex nigripalpus
NPV. In this report, using bioinformatics analyses,
ac93
and
odv-e25
(
ac94
) were identified as baculovirus core genes and thus
p33-ac93-odv-e25
represent a cluster of core genes. To investigate the role of
ac93
in the baculovirus life cycle, an
ac93
knockout AcMNPV bacmid was constructed via homologous recombination in
Escherichia coli
. Fluorescence and light microscopy showed that the AcMNPV
ac93
knockout did not spread by infection, and titration assays confirmed a defect in budded virus (BV) production. However, deletion of
ac93
did not affect viral DNA replication. Electron microscopy indicated that
ac93
was required for the egress of nucleocapsids from the nucleus and the formation of intranuclear microvesicles, which are precursor structures of occlusion-derived virus (ODV) envelopes. Immunofluorescence analyses showed that Ac93 was concentrated toward the cytoplasmic membrane in the cytoplasm and in the nuclear ring zone in the nucleus. Western blot analyses showed that Ac93 was associated with both nucleocapsid and envelope fractions of BV, but only the nucleocapsid fraction of ODV. Our results suggest that
ac93
, although not previously recognized as a core gene, is one that plays an essential role in the formation of the ODV envelope and the egress of nucleocapsids from the nucleus.
Identification of Human Endogenous Retrovirus-Specific T Cell Responses in Vertically HIV-1-Infected Subjects
Authors: Tandon Ravi , SenGupta Devi , Ndhlovu Lishomwa C. , Vieira Raphaella G. S. , Jones R. Brad , York Vanessa A. , Vieira Vinicius A. , Sharp Elizabeth R. , Wiznia Andrew A. , Ostrowski Mario A. , Rosenberg Michael G. , Nixon Douglas F. 
Published: September 2011

ABSTRACT

Human endogenous retrovirus (HERV)-specific T cell responses in HIV-1-infected adults have been reported. Whether HERV-specific immunity exists in vertically HIV-1-infected children is unknown. We performed a cross-sectional analysis of HERV-specific T cell responses in 42 vertically HIV-1-infected children. HERV (-H, -K, and -L family)-specific T cell responses were identified in 26 of 42 subjects, with the greatest magnitude observed for the responses to HERV-L. These HERV-specific T cell responses were inversely correlated with the HIV-1 plasma viral load and positively correlated with CD4
+
T cell counts. These data indicate that HERV-specific T cells may participate in controlling HIV-1 replication and that certain highly conserved HERV-derived proteins may serve as promising therapeutic vaccine targets in HIV-1-infected children.