bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hypercoagulability in Cats with Cardiomyopathy
Authors: Stokol T. , Brooks M. , Rush J.E. , Rishniw M. , Erb H. , Rozanski E. , Kraus M.S. , Gelzer A.L. 
Published: December 2008

Background: Arterial thromboembolism (ATE) is a common complication of feline cardiomyopathy; however, the pathogenesis of ATE is unknown.Hypothesis: Systemic activation of the coagulation cascade (hypercoagulability) and endothelial injury promote ATE in cardiomyopathic cats.Animals: Healthy cats (n = 30) and 3 groups of cardiomyopathic cats: Group (1) left atrial enlargement only (LAE [n = 11]), ie, left atrial to aortic ratio >1.4; Group (2) LAE with spontaneous echocardiographic contrast, atrial thrombi or both (SEC‐T [n = 16]); and Group (3) acute ATE with LAE (n = 16).Methods: Hypercoagulability was defined by 2 or more laboratory abnormalities reflecting coagulation factor excess (high fibrinogen concentration or Factor VIII coagulant activity), inhibitor deficiency (low antithrombin activity), or thrombin generation (high thrombin‐antithrombin complex [TAT] and d‐dimer concentrations). High von Willebrand factor antigen concentration (vWF : Ag) was considered a marker of endothelial injury. Data were analyzed using nonparametric statistics.Results: The 3 groups of cats with cardiac disease had higher median fibrinogen concentrations than did the healthy cats. Criteria of hypercoagulability were found exclusively in cats with SEC‐T (50%) and ATE (56%). Hypercoagulability was not associated with left atrial size or congestive heart failure (CHF). ATE cats had significantly higher median vWF : Ag concentration than did the other groups.Conclusinos and Clinical Importance: Systemic hypercoagulability is evident in many cardiomyopathic cats, often without concurrent CHF or overt ATE. Hypercoagulabilty may represent a risk factor for ATE. High vWF : Ag in ATE cats was attributed to downstream endothelial injury from the occlusive thrombus.
Estimation of Left Ventricular Filling Pressure by Doppler Echocardiography in Dogs with Pacing‐Induced Heart Failure
Authors: Schober K.E. , Stern J.A. , DaCunha D.N.Q.T. , Pedraza‐Toscano A.M. , Shemanski D. , Hamlin R.L. 
Published: December 2008

Background: Congestive heart failure (CHF) is a common clinical syndrome characterized by elevated filling pressure.Hypothesis: Doppler echocardiographic (DE) variables of left ventricular (LV) filling can predict a decline of LV end‐diastolic pressure (LVEDP) induced by acute preload reduction in dogs with compensated CHF.Animals: Five male hound dogs.Methods: Dogs previously instrumented with a transvenous cardiac pacemaker and a LV pressure gauge were paced at 160–180 bpm to induce mild CHF characterized by LVEDP > 20 mmHg. LVEDP and 9 DE variables of LV filling derived from diastolic time intervals, transmitral and pulmonary venous flow, and tissue Doppler imaging were measured simultaneously at baseline and 30, 60, 120, and 240 minutes after furosemide (4 mg/kg, IV) or placebo (0.9% saline, IV). Repeated measures analysis of variance and correlation analysis were used to determine the association between the decline of LVEDP after furosemide and DE measures of LV filling pressure (LVFP).Results: Furosemide but not placebo decreased LVEDP (P < .001). The ratio of early transmitral flow velocity to LV isovolumic relaxation time (E : IVRT) predicted LVEDP best (R2= .50; P < .001). Correlations were also found between LVEDP and IVRT, E, ratio between E and late diastolic transmitral flow velocity (E : A), and early diastolic velocity of the mitral annulus (Ea). The ratio of E to Ea (E : Ea) was not useful in the prediction of LVEDP in this model.Conclusion and Clinical Importance: E : IVRT can be used to predict LVFP in dogs with mild left‐sided CHF induced by rapid pacing.
Idiopathic Chronic Eosinophilic Pneumonia in 7 Horses
Authors: Bell S.A. , Drew C.P. , Wilson W.D. , Pusterla N. 
Published: December 2008

Background: Idiopathic chronic eosinophilic pneumonia of horses is incompletely described.Objectives: To describe the physical examination, clinicopathologic, histopathologic, and radiographic features and response to corticosteroid treatment of idiopathic chronic eosinophilic pneumonia of horses.Animals: Seven horses with eosinophilic pneumonia.Methods: Retrospective, descriptive study.Results: Anamnesis, clinical signs, and clinicopathologic and radiologic findings in 7 adult horses with histologically confirmed eosinophilic pneumonia were reviewed. The horses were examined for signs of chronic respiratory disease. The horses ranged in age from 8 to 20 years. Significant findings on physical examination included tachypnea and abnormal respiratory sounds. Thoracic radiography revealed severe diffuse interstitial patterns of increased pulmonary density in all horses. There was a predominance of eosinophils in bronchoalveolar lavage fluid (BALF), and 6 of 7 horses had peripheral blood eosinophilia. Lung biopsies revealed eosinophilic infiltrates in all horses. Dexamethasone was administered to 3 horses and resulted in short‐term clinical improvement in all three.Conclusions and Clinical Importance: A diagnosis of idiopathic eosinophilic pneumonia should be considered in horses with a history of chronic pulmonary disease, diffuse interstitial pattern of increased pulmonary density on thoracic radiographs, and a predominance of eosinophils in BALF. Horses with this condition may show a temporary response to treatment with dexamethasone.
Molecular Characterization and Antimicrobial Susceptibility of
Salmonella
Isolates from Infections in Humans in Henan Province, China
Authors: Xia Shengli , Hendriksen Rene S. , Xie Zhiqiang , Huang Lili , Zhang Jin , Guo Wanshen , Xu Bianli , Ran Lu , Aarestrup Frank M. 
Published: December 2008

ABSTRACT

We characterized 208 human
Salmonella
isolates from 2006 to 2007 and 27 human
Salmonella enterica
serovar Typhimurium isolates from 1987 to 1993 from Henan Province, China, by serotyping, by antimicrobial susceptibility testing, and, for the most common serovars, by pulsed-field gel electrophoresis (PFGE). The most common serovars among the 2006-2007 isolates were
S. enterica
serovar Typhimurium (27%),
S. enterica
serovar Enteritidis (17%),
S. enterica
serovar Derby (10%),
S. enterica
serovar Indiana (6%), and
S. enterica
serovar Litchfield (6%). A high percentage of the isolates were multiple-drug resistant, and 54% were resistant to both nalidixic acid and ciprofloxacin. Of these, 42% were resistant to a high level of ciprofloxacin (MIC > 4 μg/ml), whereas for the remaining isolates, the MICs ranged from 0.125 to 2 μg/ml. Five isolates (2%) were ceftiofur resistant and harbored
bla
CTX-M14
or
bla
CTX-M15
. With the possible exception of the quinolones and cephalosporins, the 1987-1993
S. enterica
serovar Typhimurium isolates were almost as resistant as the recent isolates. PFGE typing of
S. enterica
serovar Typhimurium showed that the most common cluster predominated over time. Two other clusters have emerged, and another cluster has disappeared.
Diagnosis of Human Immunodeficiency Virus Type 1 Infection in Infants by Use of Dried Blood Spots and an Ultrasensitive p24 Antigen Assay
Authors: Cachafeiro Ada , Sherman Gayle G. , Sohn Annette H. , Beck-Sague Consuelo , Fiscus Susan A. 
Published: December 2008

ABSTRACT

We tested 617 dried blood spots (DBS) from human immunodeficiency virus-exposed infants from five countries using an ultrasensitive p24 antigen assay (Up24). The sensitivity was 94.4% (67/71) and the specificity was 100% (431/431) for infants with DBS specimens ≤20 months old; DBS older than 30 months demonstrated only 72.2% sensitivity (39/54) (
P
< 0.001) but displayed 100% specificity (61/61).
Development of a Rapid High-Throughput Method for High-Resolution Melting Analysis for Routine Detection and Genotyping of Noroviruses
Authors: Tajiri-Utagawa Etsuko , Hara Masayuki , Takahashi Kuniaki , Watanabe Mayumi , Wakita Takaji 
Published: December 2008

ABSTRACT
We developed a simple, rapid, high-throughput detection and genotyping method for noroviruses using real-time reverse transcription-PCR (RT-PCR) and high-resolution melting (HRM) analysis to create a difference plot. The capsid gene was amplified by real-time RT-PCR in the presence of ResoLight HRM dye, a saturating DNA dye. Following optimization of the HRM assay conditions, the major norovirus genotypes were selected. Because we had only small quantities of the patient stool samples used in this study, we constructed plasmids for each genotype and used these to optimize the HRM assay. We selected six stool samples, each positive for one of the six dominant subtypes of noroviruses that have been circulating in Japan, namely, genotypes 4, 8, and 9 from genogroup 1 and genotypes 3, 4, and 10 from genogroup 2. The specific high-resolution derivate plot of the HRM assay for each plasmid was constructed by subtracting the melting-curve shape of the plasmid from the reference or base curve. The RNAs extracted from 14 clinical samples positive for small round structured viruses were then directly analyzed using the HRM assay. The HRM data from the clinical RNA samples corresponded with the genotype results obtained by RT-PCR and sequencing of the clinical samples. In addition, the HRM data from the clinical RNA samples corresponded with the HRM data from the six reference plasmid DNAs, indicating that this assay is useful for the direct detection and genotyping of noroviruses in clinical samples. This assay requires no multiplexing or hybridization probes and provides a new approach to the genetic screening of noroviruses in clinical virology laboratories.
Comparison of a Commercial Real-Time PCR Assay for
tcdB
Detection to a Cell Culture Cytotoxicity Assay and Toxigenic Culture for Direct Detection of Toxin-Producing
Clostridium difficile
in Clinical Samples
Authors: Stamper Paul D. , Alcabasa Romina , Aird Deborah , Babiker Wisal , Wehrlin Jennifer , Ikpeama Ijeoma , Carroll Karen C. 
Published: December 2008

ABSTRACT

Rapid detection of toxin-producing strains of
Clostridium difficile
is essential for optimal management of patients with
C. difficile
infection. The BD GeneOhm (San Diego, CA) Cdiff assay, a real-time PCR assay that amplifies
tcdB
, was compared to a cell culture neutralization assay (Wampole
C. difficile
Toxin B [TOX-B] test; TechLab, Blacksburg, VA) and to toxigenic culture. Using liquid (
n
= 273) and soft (
n
= 131) stool specimens from 377 symptomatic patients, all testing was performed on the same day by independent laboratory staff according to the manufacturers' protocols. Toxigenic bacterial culture was performed as follows. A 0.5-ml aliquot of stool was heated to 80°C for 10 min, followed by inoculation onto modified cycloserine cefoxitin fructose agar with and without horse blood (Remel, Lenexa, KS) and into prereduced chopped-meat broth. Of the 404 stool specimens tested, 340 were negative and 40 were positive (10.0% prevalence) both by PCR for
tcdB
and by cytotoxin production. The overall agreement between the BD GeneOhm Cdiff assay and the TOX-B test was 94.8% (380/401). When the TOX-B test was used as the reference method, the initial sensitivity, specificity, and positive and negative predictive values of the BD GeneOhm Cdiff assay were 90.9% (40/44), 95.2% (340/357), 70.2% (40/57), and 98.8% (340/344), respectively. When toxigenic culture was used as the “gold standard,” the sensitivity, specificity, and positive and negative predictive values of the BD GeneOhm Cdiff assay were 83.6%, 98.2%, 89.5%, and 97.1%, respectively, and those of the TOX-B test were 67.2%, 99.1%, 93.2%, and 94.4%, respectively. PCRs for three samples were inhibited upon initial testing; one sample was resolved upon retesting. One sample produced nonspecific cytotoxin results. The BD GeneOhm Cdiff assay performed well compared to a standard cell culture neutralization assay and to toxigenic culture for the detection of toxigenic
C. difficile
directly from fecal specimens.
Multiplex Assay for Simultaneously Typing and Subtyping Influenza Viruses by Use of an Electronic Microarray
Authors: Huang Ying , Tang Huong , Duffy Stuart , Hong Yuwen , Norman Sylvia , Ghosh Madhu , He Jie , Bose Michael , Henrickson Kelly J. , Fan Jiang , Kraft Andrea J. , Weisburg William G. , Mather Elizabeth L. 
Published: December 2008

ABSTRACT

We report on the use of an electronic microarray to simultaneously type influenza A and B viruses and to distinguish influenza A virus subtypes H1N1 and H3N2 from the potentially pandemic avian virus subtype H5N1. The assay targets seven genes: the H1, H3, H5, N1, and N2 genes of influenza A virus; the matrix protein M1 gene of influenza A virus; and the nonstructural protein (NS) gene of influenza B virus. By combining a two-step reverse transcription-multiplex PCR with typing and subtyping on the electronic microarray, the assay achieved an analytical sensitivity of 10
2
to 10
3
copies of transcripts per reaction for each of the genes. The assay correctly typed and subtyped 15 different influenza virus isolates, including two influenza B virus, five A/H1N1, six A/H3N2, and two A/H5N1 isolates. In addition, the assay correctly identified 8 out of 10 diluted, archived avian influenza virus specimens with complete typing and subtyping information and 2 specimens with partial subtyping information. In a study of 146 human clinical specimens that had previously been shown to be positive for influenza virus or another respiratory virus, the assay showed a clinical sensitivity of 96% and a clinical specificity of 100%. The assay is a rapid, accurate, user-friendly method for simultaneously typing and subtyping influenza viruses.
Vaccinia Virus-Mediated Inhibition of Type I Interferon Responses Is a Multifactorial Process Involving the Soluble Type I Interferon Receptor B18 and Intracellular Components
Authors: Waibler Zoe , Anzaghe Martina , Frenz Theresa , Schwantes Astrid , Pöhlmann Christopher , Ludwig Holger , Palomo-Otero Marcos , Alcamí Antonio , Sutter Gerd , Kalinke Ulrich 
Published: December 2008

ABSTRACTPoxviruses such as virulent vaccinia virus (VACV) strain Western Reserve encode a broad range of immune modulators that interfere with host responses to infection. Upon more than 570 in vitro passages in chicken embryo fibroblasts (CEF), chorioallantois VACV Ankara (CVA) accumulated mutations that resulted in highly attenuated modified vaccinia virus Ankara (MVA). MVA infection of mice and of dendritic cells (DC) induced significant type I interferon (IFN) responses, whereas infection with VACV alone or in combination with MVA did not. These results implied that VACV expressed an IFN inhibitor(s) that was functionally deleted in MVA. To further characterize the IFN inhibitor(s), infection experiments were carried out with CVA strains isolated after 152 (CVA152) and 386 CEF passages (CVA386). Interestingly, neither CVA152 nor CVA386 induced IFN-α, whereas the latter variant did induce IFN-β. This pattern suggested a consecutive loss of inhibitors during MVA attenuation. Similar to supernatants of VACV- and CVA152-infected DC cultures, recombinantly expressed soluble IFN decoy receptor B18, which is encoded in the VACV genome, inhibited MVA-induced IFN-α but not IFN-β. In the same direction, a B18R-deficient VACV variant triggered only IFN-α, confirming B18 as the soluble IFN-α inhibitor. Interestingly, VACV infection inhibited IFN responses induced by a multitude of different stimuli, including oligodeoxynucleotides containing CpG motifs, poly(I:C), and vesicular stomatitis virus. Collectively, the data presented show that VACV-mediated IFN inhibition is a multistep process involving secreted factors such as B18 plus intracellular components that cooperate to efficiently shut off systemic IFN-α and IFN-β responses.
Construction and Characterization of a Single-Cycle Chimeric Flavivirus Vaccine Candidate That Protects Mice against Lethal Challenge with Dengue Virus Type 2
Authors: Suzuki Ryosuke , Winkelmann Evandro R. , Mason Peter W. 
Published: December 2008

ABSTRACT
We have previously described a novel flavivirus vaccine technology based on a single-cycle, capsid (C) gene-deleted flavivirus called RepliVAX. RepliVAX can be propagated in cells that express high levels of C but undergoes only a single cycle of infection in vaccinated hosts. Here we report that we have adapted our RepliVAX technology to produce a dengue vaccine by replacing the prM/E genes of RepliVAX WN (a West Nile virus [WNV] RepliVAX) with the same genes of dengue virus type 2 (DENV2). Our first RepliVAX construct for dengue virus (RepliVAX D2) replicated poorly in WNV C-expressing cells. However, addition of mutations in prM and E that were selected during blind passage of a RepliVAX D2 derivative was used to produce a second-generation RepliVAX D2 (designated D2.2) that displayed acceptable growth in WNV C-expressing cells. RepliVAX D2.2 grew better in DENV2 C-expressing cells than WNV C-expressing cells, but after several passages in DENV2 C-expressing cells it acquired further mutations that permitted efficient growth in WNV C-expressing cells. We tested the potency and efficacy of RepliVAX D2.2 in a well-described immunodeficient mouse model for dengue (strain AG129; lacking the receptors for both type I and type II interferons). These mice produced dose-dependent DENV2-neutralizing antibody responses when vaccinated with RepliVAX D2.2. When challenged with 240 50% lethal doses of DENV2, mice given a single inoculation of RepliVAX D2.2 survived significantly longer than sham-vaccinated animals, although some of these severely immunocompromised mice eventually died from the challenge. Taken together these studies indicate that the RepliVAX technology shows promise for use in the development of vaccines that can be used to prevent dengue.
Assembly Properties of Human Immunodeficiency Virus Type 1 Gag-Leucine Zipper Chimeras: Implications for Retrovirus Assembly
Authors: Crist Rachael M. , Datta Siddhartha A. K. , Stephen Andrew G. , Soheilian Ferri , Mirro Jane , Fisher Robert J. , Nagashima Kunio , Rein Alan 
Published: December 2008

ABSTRACT
Expression of the retroviral Gag protein leads to formation of virus-like particles in mammalian cells. In vitro and in vivo experiments show that nucleic acid is also required for particle assembly. However, several studies have demonstrated that chimeric proteins in which the nucleocapsid domain of Gag is replaced by a leucine zipper motif can also assemble efficiently in mammalian cells. We have now analyzed assembly by chimeric proteins in which nucleocapsid of human immunodeficiency virus type 1 (HIV-1) Gag is replaced by either a dimerizing or a trimerizing zipper. Both proteins assemble well in human 293T cells; the released particles lack detectable RNA. The proteins can coassemble into particles together with full-length, wild-type Gag. We purified these proteins from bacterial lysates. These recombinant “Gag-Zipper” proteins are oligomeric in solution and do not assemble unless cofactors are added; either nucleic acid or inositol phosphates (IPs) can promote particle assembly. When mixed with one equivalent of IPs (which do not support assembly of wild-type Gag), the “dimerizing” Gag-Zipper protein misassembles into very small particles, while the “trimerizing” protein assembles correctly. However, addition of both IPs and nucleic acid leads to correct assembly of all three proteins; the “dimerizing” Gag-Zipper protein also assembles correctly if inositol hexakisphosphate is supplemented with other polyanions. We suggest that correct assembly requires both oligomeric association at the C terminus of Gag and neutralization of positive charges near its N terminus.
Origin and Biology of Simian Immunodeficiency Virus in Wild-Living Western Gorillas
Authors: Takehisa Jun , Kraus Matthias H. , Ayouba Ahidjo , Bailes Elizabeth , Van Heuverswyn Fran , Decker Julie M. , Li Yingying , Rudicell Rebecca S. , Learn Gerald H. , Neel Cecile , Ngole Eitel Mpoudi , Shaw George M. , Peeters Martine , Sharp Paul M. , Hahn Beatrice H. 
Published: December 2008

ABSTRACT

Western lowland gorillas (
Gorilla gorilla gorilla
) are infected with a simian immunodeficiency virus (SIVgor) that is closely related to chimpanzee and human immunodeficiency viruses (SIVcpz and HIV-1, respectively) in west central Africa. Although existing data suggest a chimpanzee origin for SIVgor, a paucity of available sequences has precluded definitive conclusions. Here, we report the molecular characterization of one partial (BQ664) and three full-length (CP684, CP2135, and CP2139) SIVgor genomes amplified from fecal RNAs of wild-living gorillas at two field sites in Cameroon. Phylogenetic analyses showed that all SIVgor strains clustered together, forming a monophyletic lineage throughout their genomes. Interestingly, the closest relatives of SIVgor were not SIVcpz
Ptt
strains from west central African chimpanzees (
Pan troglodytes troglodytes
) but human viruses belonging to HIV-1 group O. In trees derived from most genomic regions, SIVgor and HIV-1 group O formed a sister clade to the SIVcpz
Ptt
lineage. However, in a tree derived from 5′
pol
sequences (∼900 bp), SIVgor and HIV-1 group O fell within the SIVcpz
Ptt
radiation. The latter was due to two SIVcpz
Ptt
strains that contained mosaic
pol
sequences, pointing to the existence of a divergent SIVcpz
Ptt
lineage that gave rise to SIVgor and HIV-1 group O. Gorillas appear to have acquired this lineage at least 100 to 200 years ago. To examine the biological properties of SIVgor, we synthesized a full-length provirus from fecal consensus sequences. Transfection of the resulting clone (CP2139.287) into 293T cells yielded infectious virus that replicated efficiently in both human and chimpanzee CD4
+
T cells and used CCR5 as the coreceptor for viral entry. Together, these results provide strong evidence that
P. t. troglodytes
apes were the source of SIVgor. These same apes may also have spawned the group O epidemic; however, the possibility that gorillas served as an intermediary host cannot be excluded.
Body mass index and injury risk among US children 9–15 years old in motor vehicle crashes
Authors: Pollack K M , Xie D , Arbogast K B , Durbin D R 
Published: December 2008

Objective:To determine the relationship between body mass index (BMI) and injury risk among US children in motor vehicle crashes.Design:Cross-sectional study using data from the Partners for Child Passenger Safety study, a child-focused crash surveillance system.Participants:A probability sample of children, 9–15 years of age, involved in crashes in parent-operated vehicles between 1 December 2000 and 31 December 2006.Main outcome measure:The odds ratio of Abbreviated Injury Severity (AIS) 2+ injuries (overall and body region specific) by BMI category: underweight, normal, overweight, and obese.Results:The study sample included 3232 children in 2873 vehicles, representing a population estimate of 54 616 children in 49 037 vehicles. Approximately 15% (n = 502) sustained an AIS 2+ injury to any body region; 34% of the children were overweight or obese. There was no overall increase in injury risk by BMI; however, body region differences were found. In multivariate logistic regression, compared with normal weight children, the odds of sustaining an AIS 2+ injury to the extremities for overweight and obese children was 2.64 (95% CI 1.64 to 4.77) and 2.54 (95% CI 1.15 to 5.59), respectively.Conclusions:Although overweight and obese children are not at increased overall risk of injury, they are at increased risk of injury to the lower and upper extremities. This increased risk may be due to a combination of physiology, biomechanical forces, and vehicle design.