bluuebunny/crossref_metadata_2025_split huggingface dataset:
Use of Fused Deposition Modeling of Polyphenylsulfone for Centrifugal
Casting of Polyurethane: Material, Surface, and Process
Considerations
Authors: Martens Thomas , Mears Laine , Dotson Mike , Graham Monty , Sanger Phillip 
Published: September 2011

Abstract
For the development of a rotational symmetrical polyurethane part with a steel reinforcement, a requirement/constraint driven approach to process design has been taken. In this approach a scale model of the casting mold was built using fused deposition modeling rapid prototyping technique, then used to validate design, material and process parameters. After selection and testing on the scaled prototype, results were used to define a full-sized spin casting mold built using polyphenylsulfone material. This material was selected based on the process temperature and stress requirements. However, surface roughness in the as-built condition is unacceptable for demolding; this paper describes secondary processing to mitigate this effect. The result is a feasible process for manufacturing of centrifugal casting molds for polyurethane.
Comparison of the INNO-LiPA and PapType Assays for Detection of Human Papillomavirus in Archival Vulva Dysplasia and/or Neoplasia Tissue Biopsy Specimens
Authors: Tan Sarah E. , Garland Suzanne M. , Rumbold Alice R. , Tabrizi Sepehr N. 
Published: September 2011

ABSTRACT
INNO-LiPA and PapType human papillomavirus (HPV) genotyping assays were compared for detection of HPV genotypes on archival vulvar tissue. The INNO-LiPA assay detected 49 HPV-16 infections, compared with 47 detected by the PapType assay. The INNO-LiPA assay detected amplifiable DNA in 59 (91%) biopsy specimens, compared with 57 (88%) specimens for which amplifiable DNA was detected by the PapType assay. The two genotyping assays were highly comparable.
Characterization of Microevolution Events in Mycobacterium tuberculosis Strains Involved in Recent Transmission Clusters
Authors: Pérez-Lago Laura , Herranz Marta , Martínez Lirola Miguel , Bouza Emilio , García de Viedma Darío 
Published: September 2011

ABSTRACT

Under certain circumstances, it is possible to identify clonal variants of
Mycobacterium tuberculosis
infecting a single patient, probably as a result of subtle genetic rearrangements in part of the bacillary population. We systematically searched for these microevolution events in a different context, namely, recent transmission chains. We studied the clustered cases identified using a population-based universal molecular epidemiology strategy over a 5-year period. Clonal variants of the reference strain defining the cluster were found in 9 (12%) of the 74 clusters identified after the genotyping of 612
M. tuberculosis
isolates by IS
6110
restriction fragment length polymorphism analysis and mycobacterial interspersed repetitive units–variable-number tandem repeat typing. Clusters with microevolution events were epidemiologically supported and involved 4 to 9 cases diagnosed over a 1- to 5-year period. The IS
6110
insertion sites from 16 representative isolates of reference and microevolved variants were mapped by ligation-mediated PCR in order to characterize the genetic background involved in microevolution. Both intragenic and intergenic IS
6110
locations resulted from these microevolution events. Among those cases of IS
6110
locations in intergenic regions which could have an effect on the regulation of adjacent genes, we identified the overexpression of cytochrome P450 in one microevolved variant using quantitative real-time reverse transcription-PCR. Our results help to define the frequency with which microevolution can be expected in
M. tuberculosis
transmission chains. They provide a snapshot of the genetic background of these subtle rearrangements and identify an event in which IS
6110
-mediated microevolution in an isogenic background has functional consequences.
Molecular Testing for Trichomonas vaginalis in Women: Results from a Prospective U.S. Clinical Trial
Authors: Schwebke Jane R. , Hobbs Marcia M. , Taylor Stephanie N. , Sena Arlene C. , Catania Michael G. , Weinbaum Barbara S. , Johnson Ann D. , Getman Damon K. , Gaydos Charlotte A. 
Published: September 2011

ABSTRACT

Trichomoniasis is a common sexually transmitted disease associated with preterm birth, low birth weight, and increased susceptibility to infection with other pathogenic sexually transmitted microorganisms. Nucleic acid amplification tests for
Trichomonas vaginalis
have improved sensitivity for detecting infected individuals compared to existing culture-based methods. This prospective, multicenter U.S. clinical trial evaluated the performance of the automated Aptima
T. vaginalis
assay for detecting
T. vaginalis
in 1,025 asymptomatic and symptomatic women. Vaginal swab, endocervical swab, ThinPrep PreservCyt, and urine specimens were collected. Subject infection status was determined by wet-mount microscopy and culture. Aptima
T. vaginalis
assay performance was determined for each specimen type by comparison to subject infection status. Of 933 subjects analyzed, 59.9% were symptomatic. Aptima
T. vaginalis
clinical sensitivity and specificity were, respectively, 100% and 99.0% for vaginal swabs, 100% and 99.4% for endocervical swabs, 100% and 99.6% in ThinPrep samples, and 95.2% and 98.9% in urine specimens. Aptima
T. vaginalis
performance levels were similar in asymptomatic and symptomatic subjects. This study validates the clinical performance of the Aptima
T. vaginalis
assay for screening asymptomatic and symptomatic women for
T. vaginalis
infection.
DNA Microarray Genotyping and Virulence and Antimicrobial Resistance Gene Profiling of Methicillin-Resistant Staphylococcus aureus Bloodstream Isolates from Renal Patients
Authors: McNicholas Sinead , Shore Anna C. , Coleman David C. , Humphreys Hilary , Hughes Deirdre Fitzgerald 
Published: September 2011

ABSTRACT

Thirty-six methicillin-resistant
Staphylococcus aureus
(MRSA) bloodstream isolates from renal patients were genetically characterized by DNA microarray analysis and
spa
typing. The isolates were highly clonal, belonging mainly to ST22-MRSA-IV. The immune evasion and enterotoxin gene clusters were found in 29/36 (80%) and 33/36 (92%) isolates, respectively.
Prevalence of Shiga Toxin-Producing Escherichia coli as Detected by Enzyme-Linked Immunoassays and Real-Time PCR during the Summer Months in Northern Alberta, Canada
Authors: Chui Linda , Lee Mao-Cheng , Malejczyk Kathy , Lim Lillian , Fok Daniel , Kwong Pauline 
Published: September 2011

ABSTRACT

Shiga toxin-producing
Escherichia coli
(STEC) in northern Alberta was detected using two enzyme immunoassays and an in-house real-time PCR. Of 2,328 stool samples, 8 were positive for O157:H7 STEC and 13 were positive for non-O157 STEC. No significant gender (
P
= 0.17) or age (
P
= 0.81) differences between groups were seen. Most positive diarrheal stool samples were nonbloody.
Molecular Epidemiology of Clostridium difficile Strains in Children Compared with That of Strains Circulating in Adults with Clostridium difficile-Associated Infection
Authors: Stoesser Nicole , Crook Derrick W. , Fung Rowena , Griffiths David , Harding Rosalind M. , Kachrimanidou Melina , Keshav Satish , Peto Tim E. , Vaughan Alison , Walker A. Sarah , Dingle Kate E. 
Published: September 2011

ABSTRACT

Molecular analysis of
Clostridium difficile
(28 isolates) from children (
n
= 128) in Oxfordshire, United Kingdom, identified eight toxigenic genotypes. Six of these were isolated from 27% of concurrent adult
C. difficile
-associated infections studied (
n
= 83). No children carried hypervirulent PCR ribotype 027. Children could participate in the transmission of some adult disease-causing genotypes.
Generic Microtiter Plate Assay for Triaging Clinical Specimens Prior to Genotyping of Human Papillomavirus DNA via Consensus PCR
Authors: Legault Véronique , Burchell Ann , Goggin Patricia , Nicolau Belinda , Brassard Paul , Guenoun Julie , Forest Pierre , Mayrand Marie-Hélène , Franco Eduardo Luis , Coutlée Francois 
Published: September 2011

ABSTRACT
A generic human papillomavirus (HPV) probe assay was compared to the Linear Array to detect HPV DNA in 1,013 clinical specimens. The sensitivity, specificity, and negative predictive value of the assay were 99.5% (95% confidence interval [CI], 98.4% to 99.9%), 58.6% (95% CI, 53.9% to 63.1%), and 98.9% (95% CI, 96.5% to 99.8%), respectively. This assay conveniently identifies HPV-positive specimens.
Avian-Type Receptor-Binding Ability Can Increase Influenza Virus Pathogenicity in Macaques
Authors: Watanabe Tokiko , Shinya Kyoko , Watanabe Shinji , Imai Masaki , Hatta Masato , Li Chengjun , Wolter Ben F. , Neumann Gabriele , Hanson Anthony , Ozawa Makoto , Yamada Shinya , Imai Hirotaka , Sakabe Saori , Takano Ryo , Iwatsuki-Horimoto Kiyoko , Kiso Maki , Ito Mutsumi , Fukuyama Satoshi , Kawakami Eiryo , Gorai Takeo , Simmons Heather A. , Schenkman Daniel , Brunner Kevin , Capuano Saverio V. , Weinfurter Jason T. , Nishio Wataru , Maniwa Yoshimasa , Igarashi Tatsuhiko , Makino Akiko , Travanty Emily A. , Wang Jieru , Kilander Anette , Dudman Susanne G. , Suresh M. , Mason Robert J. , Hungnes Olav , Friedrich Thomas C. , Kawaoka Yoshihiro 
Published: September 2011

ABSTRACTThe first influenza pandemic of the 21st century was caused by novel H1N1 viruses that emerged in early 2009. An Asp-to-Gly change at position 222 of the receptor-binding protein hemagglutinin (HA) correlates with more-severe infections in humans. The amino acid at position 222 of HA contributes to receptor-binding specificity with Asp (typically found in human influenza viruses) and Gly (typically found in avian and classic H1N1 swine influenza viruses), conferring binding to human- and avian-type receptors, respectively. Here, we asked whether binding to avian-type receptors enhances influenza virus pathogenicity. We tested two 2009 pandemic H1N1 viruses possessing HA-222G (isolated from severe cases) and two viruses that possessed HA-222D. In glycan arrays, viruses possessing HA-222D preferentially bound to human-type receptors, while those encoding HA-222G bound to both avian- and human-type receptors. This difference in receptor binding correlated with efficient infection of viruses possessing HA-222G, compared to those possessing HA-222D, in human lung tissue, including alveolar type II pneumocytes, which express avian-type receptors. In a nonhuman primate model, infection with one of the viruses possessing HA-222G caused lung damage more severe than did infection with a virus encoding HA-222D, although these pathological differences were not observed for the other virus pair with either HA-222G or HA-222D. These data demonstrate that the acquisition of avian-type receptor-binding specificity may result in more-efficient infection of human alveolar type II pneumocytes and thus more-severe lung damage. Collectively, these findings suggest a new mechanism by which influenza viruses may become more pathogenic in mammals, including humans.
Human Cytomegalovirus Induces Multiple Means To Combat Reactive Oxygen Species
Authors: Tilton Carisa , Clippinger Amy J. , Maguire Tobi , Alwine James C. 
Published: September 2011

ABSTRACT

Reactive oxygen species (ROS) are generated as by-products of many cellular processes and can modulate cellular signaling pathways. However, high ROS levels are toxic; thus, intracellular ROS need to be tightly controlled. Therefore, cells use a group of antioxidant molecules and detoxifying enzymes that remove or detoxify reactive species. We found that the level of the antioxidant glutathione is greatly increased in human cytomegalovirus (HCMV)-infected cells due to activation of glutathione synthetic enzymes. In addition, our data suggest that virus-specific mechanisms are used to induce the expression of target antioxidant and detoxifying enzymes critical for the success of the infection. As a result of this virus-induced anti-ROS environment, key signaling kinases, such as the mammalian target of rapamycin (mTOR) kinase in mTOR complex 1 (mTORC1), are protected from inhibition by exogenous hydrogen peroxide (H
2
O
2
). In this regard, we found that phosphorylation of mTOR kinase at serine 2448 (suggested to be activating) was maintained during infection even under ROS stress conditions that inhibited it in uninfected cells. We also show that AMP-dependent kinase (AMPK)-mediated phosphorylation of serine 792 of raptor, the specificity subunit of mTORC1, increases in infected cells after H
2
O
2
treatment. This phosphorylation is normally inhibitory for mTORC1. However, in infected cells this did not result in inhibition of mTORC1 activity, suggesting that inhibitory effects of raptor phosphorylation are circumvented. Overall, our data suggest that HCMV utilizes virus-specific mechanisms to activate a variety of means to protect the cell and mTORC1 from the effects of ROS.
Inhibition of Inflammatory Interleukin-6 Activity via Extracellular Signal-Regulated Kinase–Mitogen-Activated Protein Kinase Signaling Antagonizes Human Cytomegalovirus Reactivation from Dendritic Cells
Authors: Reeves Matthew B. , Compton Teresa 
Published: September 2011

ABSTRACT

Human cytomegalovirus (HCMV) remains a major cause of viral disease in immunosuppressed transplant patients. The ability of HCMV to establish lifelong infection in humans and reactivate with devastating clinical consequences underscores the importance of understanding the triggers of HCMV reactivation in mature myeloid cells. Dendritic cell (DC) differentiation is concomitant with the activation of cellular signaling pathways and inflammatory gene expression and also HCMV reactivation. Here, we show a major role for interleukin-6 (IL-6) through extracellular signal-regulated kinase–mitogen-activated protein kinase (ERK-MAPK) signaling upon DC differentiation to promote HCMV reactivation. IL-6 drives reactivation by transcriptional upregulation of the major immediate-early (IE) genes, resulting in efficient progression of the virus life cycle and, ultimately, higher titers of infectious virus. Furthermore, the interception of IL-6 signaling with biological inhibitors significantly abrogated HCMV reactivation from experimental latency. Crucially, using cells derived from healthy seropositive donors, we observed a key role for IL-6 during reactivation from natural latency
ex vivo
in interstitial DCs. Clinically, HCMV reactivation occurs in highly inflammatory environments (i.e., transplantation); thus, the implications of this study could potentially provide novel approaches for therapeutic intervention.
Human Breast Tumor Cells Induce Self-Tolerance Mechanisms to Avoid NKG2D-Mediated and DNAM-Mediated NK Cell Recognition
Authors: Mamessier Emilie , Sylvain Aude , Bertucci François , Castellano Rémy , Finetti Pascal , Houvenaeghel Gilles , Charaffe-Jaufret Emmanuelle , Birnbaum Daniel , Moretta Alessandro , Olive Daniel 
Published: September 2011

Abstract
Breast cancer is the leading cause of death for women between the ages of 35 to 65. This is mostly due to intertumor heterogeneity and the lack of specific therapies for all subtypes. However, some breast cancers with an unexpected good prognosis are associated with enhanced antitumor immunity in situ. We studied whether breast cancer subtypes might have different susceptibilities to natural killer (NK) cells' antitumor immunity. We collected a large public set of microarray data for primary breast tumors and determined NK cell ligand expression. We found that despite heterogeneous levels of inhibitory HLA members, NKG2D ligands and DNAM ligands are expressed in virtually all breast tumor subtypes. Functional experiments in breast cancer subtypes expressing various levels of NK cell ligands showed that NK-mediated cytotoxicity is mainly HLA, NKG2D, and DNAM dependent. In parallel, we showed that cell lines and primary breast tumor cells secrete soluble inhibitory factors that alter NK cell functions. Finally, we showed that these mechanisms of escape occur in vivo in the MMTV-Neu model of spontaneous murine breast cancer. Our study shows that breast cancer cells, independent of the subtype, have developed different mechanisms to escape from NK cells' antitumor immunity. These results emphasize the role of NK cells in breast tumor clearance and underlie the importance of devising future therapy aiming at enhancing NK cell–mediated recognition in parallel with the prevention of the tumor-editing process. Cancer Res; 71(21); 6621–32. ©2011 AACR.
Binding of the JmjC Demethylase JARID1B to LSD1/NuRD Suppresses Angiogenesis and Metastasis in Breast Cancer Cells by Repressing Chemokine CCL14
Authors: Li Qian , Shi Lei , Gui Bin , Yu Wenhua , Wang Jiamu , Zhang Di , Han Xiao , Yao Zhi , Shang Yongfeng 
Published: September 2011

Abstract
JARID1B is a member of the JmjC/ARID family of demethylases that specifically demethylates tri- and di-methylated forms of histone H3 lysine 4 (H3K4) that are associated with active genes. JARID1B expression is dysregulated in several cancers in which it has been implicated, but how it might affect tumor progression is unclear. In this study, we report that JARID1B is a physical component of the LSD1/NuRD complex that functions in transcriptional repression. JARID1B and LSD1 acted in a sequential and coordinated manner to demethylate H3K4. A genome-wide transcriptional analysis revealed that among the cellular signaling pathways targeted by the JARID1B/LSD1/NuRD complex is the CCL14 chemokine pathway of cell migration and angiogenesis. JARID1B repressed the expression of CCL14, an epithelial derived chemokine, suppressing the angiogenic and metastatic potential of breast cancer cells in vivo. Our findings indicate that CCL14 is a critical mediator of the JARID1B/LSD1/NuRD complex in regulation of angiogenesis and metastasis in breast cancer, identifying a novel potential therapeutic target for breast cancer intervention. Cancer Res; 71(21); 6899–908. ©2011 AACR.
Interactions between residues 2228–2240 within factor VIIIa C2 domain and factor IXa Gla domain contribute to propagation of clot formation
Authors: Soeda Tetsuhiro , Ogiwara Kenichi , Shima Midori , Nogami Keiji 
Published: September 2011

SummaryFactor (F)VIII functions as a cofactor in the tenase complex responsible for phospholipid (PL)-dependent FXa generation by FIXa. We have recently reported that the FVIIIa C2 domain (residues 2228–2240) interacts with the FIXa Gla domain in this complex. We examined the role of this interaction in the generation of tenase activity during the process of clot formation, using a synthetic peptide corresponding to residues 2228–2240. The peptide 2228–2240 inhibited FVIIIa/FIXa-mediated FX activation dose-dependently in the presence of PL by >95% (IC50; ~10 μM). This effect was significantly greater than that obtained by peptide 1804–1818 (IC50; ~180 μM) which corresponds to another FIXa-interactive site in the light chain that provides the majority of binding energy for FIXa interaction. Peptide 2228–2240 had little effect on the prothrombin time and did not inhibit FIX activation in the coagulation process mediated by FVIIa/tissue factor or FXIa, suggesting specific inhibition of the intrinsic tenase complex. Clot waveform analysis, a plasma based-assay used to evaluate the process of intrinsic coagulation, demonstrated that peptide 2228–2240 significantly depressed both maximum coagulation velocity (|min1|) and acceleration (|min2|), reflecting the propagation of clot formation, although the clotting time was only marginally prolonged. Thromboelastography, an alternative whole blood based-assay, demonstrated that the peptide inhibited clot formation time, α-angle and maximal clot firmness, but had little effect on the clotting time. Interactions of the FVIIIa C2 domain (residues 2228–2240) with the FIXa Gla domain in the tenase complex appeared to contribute essentially to the propagation of clot formation.
Natural killer T cells in lipoprotein metabolism and atherosclerosis
Authors: Getz Godfrey , VanderLaan Paul , Reardon Catherine 
Published: September 2011

SummaryCells of both the innate and adaptive immune system participate in the development of atherosclerosis, a chronic inflammatory disorder of medium and large arteries. Natural killer T (NKT) cells express surface markers characteristic of natural killer cells and conventional T cells and bridge the innate and adaptive immune systems. The development and activation of NKT cells is dependent upon CD1d, a MHC-class I-type molecule that presents lipids, especially glycolipids to the T cell receptors on NKT cells. There are two classes of NKT cells; invariant NKT cells that express a semi-invariant T cell receptor and variant NKT cells. This review summarises studies in murine models in which the effect of the activation, overexpression or deletion of NKT cells or only invariant NKT cells on atherosclerosis has been examined.
Distinct classes of c-Kit–activating mutations differ in their ability to promote RUNX1-ETO–associated acute myeloid leukemia
Authors: Nick Heidi J. , Kim Hyung-Gyoon , Chang Chia-Wei , Harris Kevin W. , Reddy Vishnu , Klug Christopher A. 
Published: September 2011

Abstract
The t(8;21) RUNX1-ETO translocation is one of the most frequent cytogenetic abnormalities in acute myeloid leukemia (AML). In RUNX1-ETO+ patient samples, differing classes of activating c-KIT receptor tyrosine kinase mutations have been observed. The most common (12%-48%) involves mutations, such as D816V, which occur in the tyrosine kinase domain, whereas another involves mutations within exon 8 in a region mediating receptor dimerization (2%-13% of cases). To test whether distinct subtypes of activating c-KIT mutations differ in their leukemogenic potential in association with RUNX1-ETO, we used a retroviral transduction/transplantation model to coexpress RUNX1-ETO with either c-KitD814V or c-KitT417IΔ418-419 in murine hematopoietic stem/progenitor cells used to reconstitute lethally irradiated mice. Analysis of reconstituted animals showed that RUNX1-ETO;c-KitD814V coexpression resulted in 3 nonoverlapping phenotypes. In 45% of animals, a transplantable AML of relatively short latency and frequent granulocytic sarcoma was noted. Other mice exhibited a rapidly fatal myeloproliferative phenotype (35%) or a lethal, short-latency pre-B-cell leukemia (20%). In contrast, RUNX1-ETO;c-KitT417IΔ418-419 coexpression promoted exclusively AML in a fraction (51%) of reconstituted mice. These observations indicate that c-KitD814V promotes a more varied and aggressive leukemic phenotype than c-KitT417IΔ418-419, which may be the result of differing potencies of the activating c-Kit alleles.