bluuebunny/crossref_metadata_2025_split huggingface dataset:
Biomechanical characterisation of equine laryngeal cartilage
Authors: PASSMAN S. N. , CHEETHAM J. , BONASSAR L. J. , DUCHARME N. G. , RAWLINSON J. J. 
Published: May 2011

SummaryReasons for performing the study:Upper airway obstruction is a common problem in the performance horse as the soft tissues of the larynx collapse into the airway, yet there is a paucity of information on biomechanical properties for the structural cartilage components.Objective:To measure the geometry and compressive mechanical properties of the hyaline cartilage to improve understanding of laryngeal function and morphology.Methods:A total of 11 larynges were harvested from Thoroughbred and Standardbred racehorses. During gross dissection, linear dimensions of the cricoid were obtained. From both the cricoid and arytenoid, specimens were cored to obtain 6 mm disc samples from 3 sites within the dorsal cricoid (caudal, middle and rostral) and 2 central sites in the arytenoids (inner, outer). The specimens were mechanically tested using radial confined compression to calculate the aggregate modulus and permeability of the tissue. The biomechanical data were analysed using a nested mixed effects model.Results:Geometrically, the cricoid has relatively straight walls compared to the morphology of human, ovine and canine larynges. There were significant observations of higher modulus with increasing age (0.13 MPa per year; P = 0.007) and stiffer cricoid cartilage (2.29 MPa) than the arytenoid cartilage (0.42 MPa; P<0.001), but no difference was observed between the left and right sides. Linear contrasts showed that the rostral aspect (2.51 MPa) of the cricoid was 20% stiffer than the caudal aspect (2.09 MPa; P = 0.025), with no difference between the arytenoid sites.Conclusions:The equine larynx is a well supported structure due to both the geometry and material properties of the cricoid cartilage. The hyaline structure is an order of magnitude higher in compressive modulus compared to the arytenoids and other hyaline‐composed tissues.Potential relevance:These characterisations are important to understand the biomechanics of laryngeal function and the mechanisms involved with surgical interventions.
Intranasal Immunization of Ferrets with Commercial Trivalent Influenza Vaccines Formulated in a Nanoemulsion-Based Adjuvant
Authors: Hamouda Tarek , Sutcliffe Joyce A. , Ciotti Susan , Baker James R. 
Published: May 2011

ABSTRACT

NB-1008 is a surfactant-stabilized soybean oil-in-water nanoemulsion (NE) adjuvant with influenza virus antigen incorporated into the NE by simple mixing. Intranasal administration of the antigen with NE adjuvant efficiently produces both mucosal and serum antibody responses as well as a robust cellular Th1 immune response. To demonstrate the adjuvant effect of the W
80
5EC NE, a killed commercial influenza vaccine for intramuscular administration (Fluzone or Fluvirin) was mixed with the W
80
5EC NE adjuvant and administered intranasally to naïve ferrets. After a single intranasal immunization, the adjuvanted influenza vaccine elicited elevated serum hemagglutination inhibition (HAI) geometric mean titers (GMTs) ranging from 196 to 905 for the three hemagglutinin (HA) antigens present in the vaccine, which are approximately 19- to 90-fold higher titers at 1/50 the standard intramuscular commercial nonadjuvanted influenza vaccine dose. Seroconversion rates of 67% to 100% were achieved against each of the three viral strains present. The adjuvanted nasal influenza vaccine also produced significant cross immunity to five other H3N2 influenza virus strains not present in the vaccine and produced sterile immunity after challenge with homologous live virus. No safety issues were observed in 249 ferrets receiving the adjuvanted influenza vaccine. These findings demonstrate the ability of W
80
5EC NE to adjuvant nasally administered influenza vaccine and provide a basis for studying the intranasal W
80
5EC-adjuvanted influenza vaccine in humans.
Induction of B Cell Responses upon Experimental Infection of Neonatal Calves with Mycobacterium avium subsp. paratuberculosis
Authors: Stabel J. R. , Bannantine J. P. , Eda Shigetoshi , Robbe-Austerman S. 
Published: May 2011

ABSTRACTThe objective of this study was to determine if experimental infection of neonatal calves withMycobacterium aviumsubsp.paratuberculosiswould invoke changes in the percentages of total B cells in the peripheral blood mononuclear cell population and of subpopulations of B cells as determined by CD5, CD25, and CD45RO markers during a 12-month period. Experimental infection groups included control (noninfected), oral (infected withM. aviumsubsp.paratuberculosisstrain K-10), oral/DXM (pretreatment with dexamethasone before oral inoculation), i.p. (intraperitoneal inoculation), and oral/M (oral inoculation with mucosal scrapings from a cow with clinical disease) groups. Over the course of the study, the percentages of total B cells in nonstimulated and antigen-stimulated cell cultures increased for oral and i.p. group calves, with the highest percentages noted at 3 and 6 months. Oral/M group calves had increased percentages of activated B cells, as determined by CD5dimand CD5brightmarkers, at 9 and 12 months. Experimental infection by all methods resulted in increased expression of CD25+and CD45RO+B cells early in the study, but the most significant results were observed at 12 months for oral/DXM and oral/M group calves. Immunoblot analyses with a whole-cell sonicate ofM. aviumsubsp.paratuberculosisdemonstrated the most reactivity with sera from i.p. group calves and the least reactivity with sera from oral group calves. Further evidence ofM. aviumsubsp.paratuberculosis-specific antibody responses in the i.p. group calves was demonstrated using the ethanol vortex enzyme-linked immunosorbent assay (EvELISA) method. In summary, an induction of B cell responses was noted after experimental infection withM. aviumsubsp.paratuberculosis, with differences in responses noted according to the method of experimental inoculation.
Echinocandin Susceptibility Testing of Candida Isolates Collected during a 1-Year Period in Sweden
Authors: Axner-Elings Marlene , Botero-Kleiven Silvia , Jensen Rasmus Hare , Arendrup Maiken Cavling 
Published: May 2011

ABSTRACT

The susceptibilities of
Candida
isolates to the echinocandins anidulafungin, caspofungin, and micafungin were determined by using the recently revised CLSI breakpoints and Etest on 238 clinical bloodstream
Candida
isolates collected between September 2005 and August 2006. The isolates represent approximately 95% of all non
-albicans Candida
bloodstream infections and one-third of
Candida albicans
bloodstream infections during this 1-year period in Sweden. The collection included 81
C. albicans
, 81
C. glabrata
, 36
C. parapsilosis
, 14
C. dubliniensis
, 8
C. tropicalis
, 8
C. lusitaniae
, 5
C. krusei
, 2
C. guilliermondii
and 2
C. inconspicua
isolates as well as 1
C. pelliculosa
isolate. The MICs were largely consistent with the global epidemiology of bloodstream
Candida
isolates. All
C. albicans
and
C. glabrata
isolates were susceptible to all 3 echinocandins (MIC ≤ 0.016 μg/ml in all instances). Resistance (MIC ≥ 8 μg/ml) to anidulafungin alone was observed for 4 (11.1%)
C. parapsilosis
isolates and for 1/2
C. guilliermondii
isolates. Intermediate susceptibility to caspofungin alone was observed for 2/5
C. krusei
isolates. One of the eight
C. tropicalis
isolates was classified as being intermediately susceptible to micafungin (MIC, 0.5 μg/ml) and as being resistant to anidulafungin and caspofungin (MIC ≥ 1 μg/ml). This isolate harbored a heterozygous
FKS1
hot spot mutation (S80P) known to confer echinocandin resistance. This first study to apply the revised CLSI breakpoints for Etest endpoints showed that the breakpoints worked successfully in detecting an isolate with a hot spot mutation. Acquired echinocandin resistance is rare in Sweden. Echinocandin MICs against
C. parapsilosis
and
C. guilliermondii
were lowest for micafungin.
Sensitive and Specific Phenotypic Assay for Metallo-β-Lactamase Detection in Enterobacteria by Use of a Moxalactam Disk Supplemented with EDTA
Authors: Pluquet Emilie , Arlet Guillaume , Bingen Edouard , Drieux Laurence , Mammeri Hedi 
Published: May 2011

ABSTRACT
Moxalactam is highly hydrolyzed by plasmid-mediated metallo-β-lactamases (MBLs), whereas it is poorly inactivated by serine-active carbapenemases. This study demonstrated that moxalactam resistance constituted an effective screen for MBL expression in enterobacteria, which could be confirmed, even in low-MBL-producing isolates, by a disk potentiation test using moxalactam and EDTA.
RNA versus DNA (NucliSENS EasyQ HIV-1 v1.2 versus Amplicor HIV-1 DNA Test v1.5) for Early Diagnosis of HIV-1 Infection in Infants in Senegal
Authors: Kébé K. , Ndiaye O. , Ndiaye H. Diop , Mengue P. Mbakob , Guindo P. M. M. , Diallo S. , Léye N. , Gueye S. B. , Diallo A. Gaye , Kane C. Touré , Mboup S. 
Published: May 2011

ABSTRACTThe objective of this study was to compare the performance of the NucliSENS EasyQ HIV-1 v1.2 platform (bioMérieux, France) to the Amplicor HIV-1 DNA test v1.5 (Roche Molecular Systems, Switzerland) in detecting HIV-1 infection in infants using venipuncture-derived whole blood in tubes and dried blood spots. A total of 149 dried blood spots and 43 EDTA-anticoagulated peripheral blood samples were collected throughout Dakar and other areas in Senegal from infants and children aged 3 weeks to 24 months who were born to HIV-1-infected mothers. Samples were tested using the NucliSENS and Amplicor technologies. The NucliSENS and Amplicor results were 100% concordant using either EDTA-anticoagulated peripheral blood or dried blood spots. Compared to Amplicor, the sensitivity and specificity of the NucliSENS test were 100%. The NucliSENS EasyQ HIV-1 RNA assay performed as well as the Amplicor HIV-1 DNA test in detecting HIV-1 infection in infants. In addition, this platform can give an indication of the viral load baseline. The NucliSENS EasyQ platform is a good alternative for early infant diagnosis of HIV-1 infection.
Host-Based Ribavirin Resistance Influences Hepatitis C Virus Replication and Treatment Response
Authors: Ibarra Kristie D. , Jain Mamta K. , Pfeiffer Julie K. 
Published: May 2011

ABSTRACTMany individuals infected with hepatitis C virus (HCV) develop a chronic infection, and of those who are treated with pegylated interferon and ribavirin (RBV), many do not respond. While the nucleoside analog RBV improves treatment outcome, and will likely be an important component of therapy with next-generation viral inhibitors, RBV's mechanism is controversial. Most of RBV's proposed mechanisms require RBV import into cells. Therefore, we explored whether host-based RBV resistance develops through reduced cellular uptake, akin to chemotherapy resistance in some cancers. We examined the effect of host-based RBV resistance on HCV replication in cultured hepatoma Huh7.5 liver cells and whether RBV resistance develops in HCV patients. When Huh7.5 cells were exposed to RBV, resistance developed through reduced RBV uptake via the ENT1 nucleoside transporter and antiviral efficacy was reduced. The uptake defect in RBV-resistant cells was specific to RBV, since transport of another ENT1 substrate, cytidine, was unaffected. Importantly, RBV uptake significantly declined in HCV patient peripheral blood mononuclear cells (PBMCs) following 4 weeks of therapy. Furthermore, maintenance of RBV uptake correlated with rapid treatment response. Our results uncovered a novel form of antiviral drug resistance and suggest that host-based RBV resistance develops in HCV patients undergoing therapy and that maintenance of RBV uptake may contribute to rapid viral clearance.
Different Regions of HIV-1 Subtype CenvAre Associated with Placental Localization andIn UteroMother-to-Child Transmission
Authors: Kumar Surender B. , Handelman Samuel K. , Voronkin Igor , Mwapasa Victor , Janies Daniel , Rogerson Stephen J. , Meshnick Steven R. , Kwiek Jesse J. 
Published: May 2011

ABSTRACTHIV infections are initiated by a limited number of variants that diverge into a diverse quasispecies swarm. Duringin uteromother-to-child transmission (IU MTCT), transmitted viral variants must pass through multiple unique environments, and our previously published data suggest a nonstochastic model of transmission. As an alternative to a stochastic model of viral transmission, we hypothesize that viral selection in the placental environment influences the character of the viral quasispecies when HIV-1 is transmittedin utero. To test this hypothesis, we used single-template amplification to isolate HIV-1 envelope gene (env) sequences from both peripheral plasma and the placentas of eight nontransmitting (NT) and nine IU-transmitting participants. Statistically significant compartmentalization between peripheral and placental HIV-1envwas detected in one of the eight NT cases and six of the nine IU MTCT cases. In addition, viral sequences isolated from IU MTCT placental tissue showed variation inenvV1 loop lengths compared to matched maternal sequences, while NT placentalenvsequences did not. Finally, comparison ofenvsequences from NT and IU MTCT participants indicated statistically significant differences in Kyte-Doolittle hydropathy in the signal peptide, C2, V3, and C3 regions. Our working hypothesis is that the hydropathy differences in Env associated with IU MTCT alter viral cellular tropism or affinity, allowing HIV-1 to efficiently infect placentally localized cells.
Mechanism of Inhibition of Retrovirus Release from Cells by Interferon-Induced Gene ISG15
Authors: Kuang Zhizhou , Seo Eun Joo , Leis Jonathan 
Published: May 2011

ABSTRACT

Budding of retroviruses from cell membranes requires ubiquitination of Gag and recruitment of cellular proteins involved in endosome sorting, including
e
ndosome
s
orting
c
omplex
r
equired for
t
ransport III (ESCRT-III) protein complex and
v
acuolar
p
rotein
s
orting 4 (VPS4) and its ATPase. In response to infection, a cellular mechanism has evolved that blocks virus replication early and late in the budding process through expression of interferon-stimulated gene 15 (ISG15), a dimer homologue of ubiquitin. Interferon treatment of DF-1 cells blocks avian sarcoma/leukosis virus release, demonstrating that this mechanism is functional under physiological conditions. The late block to release is caused in part by a loss in interaction between VPS4 and its coactivator protein LIP5, which is required to promote the formation of the ESCRT III-VPS4 double-hexamer complex to activate its ATPase. ISG15 is conjugated to two different LIP5-ESCRT-III-binding
ch
arged
m
ultivesicular body proteins, CHMP2A and CHMP5. Upon ISGylation of each, interaction with LIP5 is no longer detected. Two other ESCRT-III proteins, CHMP4B and CHMP6, are also conjugated to ISG15. ISGylation of CHMP2A, CHMP4B, and CHMP6 weakens their binding directly to VPS4, thereby facilitating the release of this protein from the membrane into the cytosol. The remaining budding complex fails to release particles from the cell membrane. Introducing a mutant of ISG15 into cells that cannot be conjugated to proteins prevents the ISG15-dependent mechanism from blocking virus release. CHMP5 is the primary switch to initiate the antiviral mechanism, because removal of CHMP5 from cells prevents ISGylation of CHMP2A and CHMP6.
Predicting the long-term performance of a geogrid-reinforced embankment on soft soil using two-dimensional finite element analysis
Authors: Karim M.R. , Manivannan G. , Gnanendran C.T. , Lo S-C.R. 
Published: May 2011

The consolidation of the soft foundation soil of a geogrid-reinforced embankment, improved with prefabricated vertical drains (PVDs), is modelled in this paper using two-dimensional (2D) plane strain coupled finite element (FE) analysis to predict long-term multiple behaviour characteristics (e.g., settlement, lateral displacement, excess pore-water pressure response, geosynthetic strain) of the embankment. Two sets of analyses were carried out with the foundation soil being modelled using relatively simple elastic–viscoplastic (EVP) models. A nonlinear creep function was used in association with them. The input material parameters were determined from extensive laboratory testing or were taken from reliable sources except for the horizontal permeability, which was systematically back-estimated using oedometer test data and the first year of field settlement data. The results from both analyses were compared with the long-term (up to 6 years) field-monitoring data and were found to be in good agreement with the field measurements.
Body Mass Index and Obesity- and Diabetes-Associated Genotypes and Risk for Pancreatic Cancer
Authors: Tang Hongwei , Dong Xiaoqun , Hassan Manal , Abbruzzese James L. , Li Donghui 
Published: May 2011

Abstract
Background: The genetic factors predisposing individuals with obesity or diabetes to pancreatic cancer have not been identified.
Aims: To investigate the hypothesis that obesity- and diabetes-related genes modify the risk of pancreatic cancer.
Methods: We genotyped 15 single nucleotide polymorphisms of fat mass and obesity-associated (FTO), peroxisome proliferators-activated receptor gamma (PPARγ), nuclear receptor family 5 member 2 (NR5A2), AMPK, and ADIPOQ genes in 1,070 patients with pancreatic cancer and 1,175 cancer-free controls. Information on risk factors was collected by personal interview. Adjusted ORs (AOR) and 95% CIs were calculated using unconditional logistic regression.
Results: The PPARγ P12A GG genotype was inversely associated with risk of pancreatic cancer (AOR, 0.21; 95% CI, 0.07–0.62). Three NR5A2 variants that were previously identified in a genome-wide association study were significantly associated with reduced risk of pancreatic cancer, AORs ranging from 0.57 to 0.79. Two FTO gene variants and one ADIPOQ variant were differentially associated with pancreatic cancer according to levels of body mass index (BMI; Pinteraction = 0.0001, 0.0015, and 0.03). For example, the AOR (95% CI) for FTO IVS1-2777AC/AA genotype was 0.72 (0.55–0.96) and 1.54 (1.14–2.09) in participants with a BMI of less than 25 or 25 kg/m2 or more, respectively. We observed no significant association between AMPK genotype and pancreatic cancer and no genotype interactions with diabetes or smoking.
Conclusion: Our findings suggest the PPARγ P12A GG genotype and NR5A2 variants may reduce the risk for pancreatic cancer. A positive association of FTO and ADIPOQ gene variants with pancreatic cancer may be limited to persons who are overweight.
Impact: The discovery of genetic factors modifying the risk of pancreatic cancer may help to identify high-risk individuals for prevention efforts. Cancer Epidemiol Biomarkers Prev; 20(5); 779–92. ©2011 AACR.
Common Genetic Variation at BARD1 Is Not Associated with Breast Cancer Risk in BRCA1 or BRCA2 Mutation Carriers
Authors: Spurdle Amanda B. , Marquart Louise , McGuffog Lesley , Healey Sue , Sinilnikova Olga , Wan Fei , Chen Xiaoqing , Beesley Jonathan , Singer Christian F. , Dressler Anne-Catharine , Gschwantler-Kaulich Daphne , Blum Joanne L. , Tung Nadine , Weitzel Jeff , Lynch Henry , Garber Judy , Easton Douglas F. , Peock Susan , Cook Margaret , Oliver Clare T. , Frost Debra , Conroy Don , Evans D. Gareth , Lalloo Fiona , Eeles Ros , Izatt Louise , Davidson Rosemarie , Chu Carol , Eccles Diana , Selkirk Christina G. , Daly Mary , Isaacs Claudine , Stoppa-Lyonnet Dominique , Sinilnikova Olga M. , Buecher Bruno , Belotti Muriel , Mazoyer Sylvie , Barjhoux Laure , Verny-Pierre Carole , Lasset Christine , Dreyfus Hélène , Pujol Pascal , Collonge-Rame Marie-Agnès ,   for the GEMO Study Collaborators, Rookus Matti A. , Verhoef Senno , Kriege Mieke , Hoogerbrugge Nicoline , Ausems Margreet G. E. M. , van Os Theo A. , Wijnen Juul , Devilee Peter , Meijers-Heijboer Hanne E. J. , Blok Marinus J. , Heikkinen Tuomas , Nevanlinna Heli , Jakubowska Anna , Lubiński Jan , Huzarski Tomasz , Byrski Tomasz , Durocher Francine , Couch Fergus J. , Lindor Noralane M. , Wang Xianshu , Thomassen Mads , Domchek Susan , Nathanson Kate , Caligo MA , Jernström Helena , Liljegren Annelie , Ehrencrona Hans , Karlsson Per ,   for SWE-BRCA, Ganz Patricia A. , Olopade Olufunmilayo I. , Tomlinson Gail , Neuhausen Susan , Antoniou Antonis C. , Chenevix-Trench Georgia , Rebbeck Timothy R. 
Published: May 2011

Abstract
Background: Inherited BRCA1 and BRCA2 (BRCA1/2) mutations confer elevated breast cancer risk. Knowledge of factors that can improve breast cancer risk assessment in BRCA1/2 mutation carriers may improve personalized cancer prevention strategies.
Methods: A cohort of 5,546 BRCA1 and 2,865 BRCA2 mutation carriers was used to evaluate risk of breast cancer associated with BARD1 Cys557Ser. In a second nonindependent cohort of 1,537 of BRCA1 and 839 BRCA2 mutation carriers, BARD1 haplotypes were also evaluated.
Results: The BARD1 Cys557Ser variant was not significantly associated with risk of breast cancer from single SNP analysis, with a pooled effect estimate of 0.90 (95% CI: 0.71–1.15) in BRCA1 carriers and 0.87 (95% CI: 0.59–1.29) in BRCA2 carriers. Further analysis of haplotypes at BARD1 also revealed no evidence that additional common genetic variation not captured by Cys557Ser was associated with breast cancer risk.
Conclusion: Evidence to date does not support a role for BARD1 variation, including the Cy557Ser variant, as a modifier of risk in BRCA1/2 mutation carriers.
Impact: Interactors of BRCA1/2 have been implicated as modifiers of BRCA1/2-associated cancer risk. Our finding that BARD1 does not contribute to this risk modification may focus research on other genes that do modify BRCA1/2-associated cancer risk. Cancer Epidemiol Biomarkers Prev; 20(5); 1032–8. ©2011 AACR.
Human Papillomavirus (HPV) 6, 11, 16, and 18 Seroprevalence Is Associated with Sexual Practice and Age: Results from the Multinational HPV Infection in Men Study (HIM Study)
Authors: Lu Beibei , Viscidi Raphael P. , Lee Ji-Hyun , Wu Yougui , Villa Luisa L. , Lazcano-Ponce Eduardo , Carvalho da Silva Roberto J. , Baggio Maria Luiza , Quiterio Manuel , Salmerón Jorge , Smith Danelle C. , Abrahamsen Martha , Papenfuss Mary , Stockwell Heather G. , Giuliano Anna R. 
Published: May 2011

Abstract
Background: Few human papillomavirus (HPV) serology studies have evaluated type-specific seroprevalence of vaccine HPV types in men. This study investigates seroprevalence of HPV 6, 11, 16, and 18, and associated risk factors in men residing in three countries (United States, Mexico, and Brazil).
Methods: Data from 1,477 men aged 18 to 70 enrolled in the HPV Infection in Men Study (HIM Study) were analyzed. Serum antibody testing was performed with virus-like particle-based ELISA. Potential risk factors were assessed for individual HPV types by the use of logistic regression.
Results: Overall, HPV-6, 11, 16, and 18 seroprevalence was 14.8%, 17.3%, 11.2%, and 5.8%, respectively. Thirty-four percent of men were seropositive to one or more HPV types. When examined by sexual practice, 31.2% of men who had sex with women, 65.6% of men who had sex with men (MSM), and 59.4% of men who had sex with both men and women (MSMW) were seropositive to one or more HPV types. Seroprevalence increased with age among young-to-middle-aged men with significant upward age trends observed for HPV 11, 16, and 18. Men with multiple lifetime male anal sex partners were 2 to 4 times more likely to be HPV 6 or 11 seropositive and 3 to 11 times more likely to be HPV 16 or 18 seropositive.
Conclusion: Our data indicate that exposures to vaccine HPV types were common in men and highly prevalent among MSM and MSMW.
Impact: Our study provides strong evidence that the practice of same-sex anal intercourse is an independent risk factor for seroprevalence of individual vaccine HPV types. Examination of antibody responses to HPV infections at various anatomic sites in future studies is needed to elaborate on the mechanism. Cancer Epidemiol Biomarkers Prev; 20(5); 990–1002. ©2011 AACR.