bluuebunny/crossref_metadata_2025_split huggingface dataset:
Current Practice in Airway Management: A Descriptive Evaluation
Authors: Kjonegaard Rebecca , Fields Willa , King Major L. 
Published: April 2009

Background Ventilator-associated pneumonia, a common complication of mechanical ventilation, could be reduced if health care workers implemented evidence-based practices that decrease the risk for this complication.
Objectives To determine current practice and differences in practices between registered nurses and respiratory therapists in managing patients receiving mechanical ventilation.
Methods A descriptive comparative design was used. A convenience sample of 41 registered nurses and 25 respiratory therapists who manage critical care patients treated with mechanical ventilation at Sharp Grossmont Hospital, La Mesa, California, completed a survey on suctioning techniques and airway management practices. Descriptive and inferential statistics were used to analyze the data.
Results Significant differences existed between nurses and respiratory therapists for hyperoxygenation before suctioning (P =.03). In the 2 groups, nurses used the ventilator for hyper-oxygenation more often, and respiratory therapists used a bag-valve device more often (P =.03). Respiratory therapists instilled saline (P &lt;.001) and rinsed the closed system with saline after suctioning (P =.003) more often than nurses did. Nurses suctioned oral secretions (P &lt;.001) and the nose of orally intubated patients (P =.01), brushed patients’ teeth with a toothbrush (P&lt;.001), and used oral swabs to clean the mouth (P &lt;.001) more frequently than respiratory therapists did.
Conclusion Nurses and respiratory therapists differed significantly in the management of patients receiving mechanical ventilation. To reduce the risk of ventilator-associated pneumonia, both nurses and respiratory therapists must be consistent in using best practices when managing patients treated with mechanical ventilation.
IL-27 Blocks RORc Expression to Inhibit Lineage Commitment of Th17 Cells
Authors: Diveu Caroline , McGeachy Mandy J. , Boniface Katia , Stumhofer Jason S. , Sathe Manjiri , Joyce-Shaikh Barbara , Chen Yi , Tato Cristina M. , McClanahan Terrill K. , de Waal Malefyt René , Hunter Christopher A. , Cua Daniel J. , Kastelein Robert A. 
Published: April 2009

AbstractIL-27 is secreted by APCs in response to inflammatory stimuli and exerts a proinflammatory Th1-enhancing activity but also has significant anti-inflammatory functions. We examined the molecular mechanism by which IL-27 regulates TGFβ plus IL-6- or IL-23-dependent Th17 development in the mouse and human systems. IL-27 inhibited the production of IL-17A and IL-17F in naive T cells by suppressing, in a STAT1-dependent manner, the expression of the Th17-specific transcription factor RORγt. The in vivo significance of the role of IL-27 was addressed in delayed-type hypersensitivity response and experimental autoimmune encephalomyelitis (EAE). By generating mice deficient for the p28 subunit of IL-27, we showed that IL-27 regulated the severity of delayed-type hypersensitivity response and EAE through its effects on Th17 cells. Furthermore, up-regulation of IL-10 in the CNS, which usually occurs late after EAE onset and plays a role in the resolution of the disease, was notably absent in IL-27p28−/− mice. These results show that IL-27 acts as a negative regulator of the developing IL-17A response in vivo, suggesting a potential therapeutic role for IL-27 in autoimmune diseases.
Bone Marrow-Derived Mast Cells Accumulate in the Central Nervous System During Inflammation but Are Dispensable for Experimental Autoimmune Encephalomyelitis Pathogenesis
Authors: Bennett Jami L. , Blanchet Marie-Renée , Zhao Linlin , Zbytnuik Lori , Antignano Frann , Gold Matthew , Kubes Paul , McNagny Kelly M. 
Published: April 2009

AbstractReports showing that W/Wv mice are protected from experimental autoimmune encephalomyelitis (EAE, a murine model of multiple sclerosis), have implicated mast cells as an essential component in disease susceptibility, but the role of mast cell trafficking has not been addressed. In this study, we have used both mast cell transplantation and genetic mutations (Cd34−/−, W/Wv, Wsh/Wsh) to investigate the role of mast cell trafficking in EAE in detail. We show, for the first time, that bone marrow-derived mast cells are actively recruited to the CNS during EAE. Unexpectedly, however, we found that EAE develops unabated in two independent genetic backgrounds in the complete absence of mast cells or bone marrow-derived mast cell reconstitution. We conclude that although mast cells do accumulate in the brain and CNS during demyelinating disease via peripheral mast cell trafficking, they are completely dispensable for development of disease.
Galectin-2 Suppresses Contact Allergy by Inducing Apoptosis in Activated CD8+ T Cells
Authors: Loser Karin , Sturm Andreas , Voskort Maik , Kupas Verena , Balkow Sandra , Auriemma Matteo , Sternemann Carlo , Dignass Axel U. , Luger Thomas A. , Beissert Stefan 
Published: April 2009

Abstract
Galectins, a family of structurally related β-galactoside-binding proteins, are expressed by various cells of the immune systems and seem to be important for the regulation of immune responses and immune cell homeostasis. Since it has been demonstrated that galectin-2 regulates cell-mediated inflammatory bowel disease and colitis in mice, we intended to investigate the role of galectin-2 in inflammatory cutaneous T cell-mediated immune responses. To address this issue, groups of naive mice were sensitized to the contact allergen 2,4-dinitro-1-fluorobenzene and systemically treated with galectin-2 to analyze the effects of galectin-2 on contact allergy. Here we show that galectin-2 is expressed in murine skin and is up-regulated upon cutaneous inflammation. Interestingly, treatment of mice with galectin-2 significantly reduced the contact allergy response. This effect was long-lasting since rechallenge of galectin-2-treated mice after a 14-day interval still resulted in a decreased ear swelling. We were able to demonstrate that galectin-2 induced a reduction of MHC class I-restricted immune responses in the treated animals, which was mediated by the induction of apoptosis specifically in activated CD8+ T cells. Additionally, we report that the galectin-2-binding protein CD29 is up-regulated on the surface of activated CD8+ T cells compared with naive CD8+ T cells or CD4+ T cells, suggesting that increased galectin-2/CD29 signaling might be responsible for the proapoptotic effects of galectin-2 on activated CD8+ T cells. Taken together, these data indicate that galectin-2 may represent a novel therapeutic alternative for the treatment of CD8-mediated inflammatory disorders such as contact allergy.
IL-6 Modulates CD5 Expression in B Cells from Patients with Lupus by Regulating DNA Methylation
Authors: Garaud Soizic , Le Dantec Christelle , Jousse-Joulin Sandrine , Hanrotel-Saliou Catherine , Saraux Alain , Mageed Rizgar A. , Youinou Pierre , Renaudineau Yves 
Published: April 2009

Abstract
B lymphocytes from patients with systemic lupus erythematosus (SLE) are characterized by reduced expression levels of membrane CD5. Recent studies from our laboratory have revealed that the level of membrane CD5 is determined by the relative level of two alternative CD5 isoforms; CD5-E1A, which is expressed on the membrane, and CD5-E1B, which is retained in the cytoplasm. Using bisulfite sequencing and methylation-sensitive endonuclease assays we show that the promoter for the alternative CD5-E1B isoform is demethylated in B cells from patients with SLE but not in healthy controls. We go on to show that differential methylation is more pronounced following BCR engagement. As a result of this demethylation, CD5-E1B mRNA is transcribed at the expense of CD5-E1A mRNA transcription. We provide further evidence that production of high IL-6 levels by SLE B cells abrogates the ability of SLE B cells to induce DNA methyl transferase (DNMT1) and then to methylate DNA, an effect that is reversed in the presence of a blocking Ab to the IL-6 receptor. The pattern of demethylation of CpG islands in the CD5-E1B promoter in SLE B cells is similar to those in B cells from healthy controls stimulated in the presence of IL-6, or treated with the methylation inhibitor PD98059. The study reveals that engagement of the BCR with constitutive IL-6 down-regulates the level of membrane CD5, which negatively regulates BCR signaling, in SLE B cells. This altered signaling could, in turn, promote the activation and expansion of autoreactive B cells in SLE patients.
Regulation of NK Cell Function by Human Granulocyte Arginase
Authors: Oberlies Johanna , Watzl Carsten , Giese Thomas , Luckner Claudia , Kropf Pascale , Müller Ingrid , Ho Anthony D. , Munder Markus 
Published: April 2009

AbstractThe arginine-hydrolyzing enzyme arginase is constitutively expressed by human polymorphonuclear granulocytes (PMN). Upon PMN cell death arginase is liberated and depletes arginine in the microenvironment. This amino acid depletion suppresses T cell proliferation and cytokine secretion and emerges as a key mechanism of immunosuppression during chronic inflammation and tumor growth. Here we show that PMN arginase also severely impairs key functions of primary human NK cells as well as IL-2-activated NK cells. In the absence of arginine, NK cell proliferation and IL-12/IL-18-induced secretion of IFN-γ are severely diminished. In contrast, NK cell viability, granule exocytosis, and cytotoxicity are independent of extracellular arginine. The mechanism of NK cell suppression by arginine depletion is posttranscriptional since mRNA transcript frequency is unaffected upon NK cell activation in the absence of arginine. Finally, we demonstrate that human purulent exudate ex vivo inhibits NK cell functions exclusively due to liberated arginase. Arginase inhibitors are therefore promising pharmacological agents to treat unwanted suppression of the innate (NK cell) as well as the adaptive (T cell) immune system.
Experimental Autoimmune Encephalomyelitis in Lewis rats: IFN-β Acts As a Tolerogenic Adjuvant for Induction of Neuroantigen-Dependent Tolerance
Authors: Mannie Mark D. , Abbott Derek J. , Blanchfield J. Lori 
Published: April 2009

Abstract
Cytokine-Ag fusion proteins represent a novel approach for induction of Ag-specific tolerance and may constitute an efficient therapy for autoimmune disease. This study addressed whether a fusion protein containing rat IFN-β and the encephalitogenic 73–87 determinant of myelin basic protein (i.e., the neuroantigen, or NAg) could prevent or treat experimental autoimmune encephalomyelitis (EAE) in Lewis rats. The optimal structure of the fusion protein was comprised of the rat IFN-β cytokine as the N-terminal domain with an enterokinase (EK) linker to the NAg domain. Both cytokine and NAg domains had full biological activity. Subcutaneous administration of 1 nmol of IFNβ-NAg fusion protein in saline on days −21, −14, and −7 before encephalitogenic challenge on day 0 resulted in a substantial attenuation of EAE. In contrast, administration of IFN-β or NAg alone did not affect susceptibility to EAE. The covalent attachment of IFN-β and NAg was not necessary, because separate injections of IFN-β and NAg at adjacent sites were as effective as injection of IFNβ-NAg for prevention of disease. When treatment was initiated after disease onset, the rank order of inhibitory activity was as follows: the IFNβ-NAg fusion protein ≥ a mixture of IFN-β plus NAg &gt; IFN-β &gt; NAg. The novel finding that IFN-β acts as a tolerogenic adjuvant as well as a tolerogenic fusion partner may have significance for development of tolerogenic vaccines.
Gastrointestinal Nematode Infection Exacerbates Malaria-Induced Liver Pathology
Authors: Helmby Helena 
Published: April 2009

Abstract
Mixed parasite infections are common in many parts of the world, but little is known of the effects of concomitant parasite infections on the immune response or severity of clinical disease. We have used the nonlethal malaria infection model of Plasmodium chabaudi AS in combination with the gastrointestinal nematode Heligmosomoides bakeri polygyrus to investigate the impact of nematode infections on malarial morbidity and antimalarial immunity. The data demonstrate that wild-type C57BL/6 mice coinfected with both parasites simultaneously exhibit a striking increase in mortality, while mice deficient in IFN-γ or IL-23 survive coinfection. The increase in mortality in wild-type mice was associated with severe liver pathology characterized by extensive coagulative necrosis and an increase in hepatic IFN-γ, IL-17, and IL-22 mRNA expression. This is the first demonstration of increased malaria-associated pathology associated with a switch toward a proinflammatory environment, involving not only IFN-γ but also the IL-17/IL-23 axis, as a result of coinfection with a gastrointestinal helminth.
A Functional IL-13 Receptor Is Expressed on Polarized Murine CD4+ Th17 Cells and IL-13 Signaling Attenuates Th17 Cytokine Production
Authors: Newcomb Dawn C. , Zhou Weisong , Moore Martin L. , Goleniewska Kasia , Hershey Gurjit K. K. , Kolls Jay K. , Peebles R. Stokes 
Published: April 2009

Abstract
IL-17A is produced from Th17 cells, and is involved in many autoimmune and inflammatory diseases. IL-13R has not previously been reported to be functionally expressed on T cells; however, we found that purified BALB/c CD4+ cells polarized to Th17 with TGF-β, IL-6, and IL-23 have increased mRNA and protein expression of IL-13Rα1 and mRNA expression of IL-4Rα compared with Th0, Th1, or Th2 polarized cells. The addition of IL-13 at Th17 polarization negatively regulated IL-17A and IL-21 expression, and reduced the number of CD4+ T cells producing IL-17A. Further, adding IL-13 at the time of Th17 cell restimulation attenuated IL-17A expression. CD4+ Th17 polarized cells from IL-4 knockout (KO) mice also had IL-13-induced inhibition of IL-17A production, but this was not observed in IL-4R KO and STAT6 KO mice. Addition of IL-13 at polarization increased IL-13R expression in wild-type Th17 cells. Further, IL-13 administration during Th17 polarization down-regulated retinoic acid-related-γT, the transcription required for Th17 development; increased STAT6 phosphorylation, and up-regulated GATA3, the transcription factor activated during the development of Th2 cells. This IL-13-mediated effect was specific to Th17 cells as IL-13 neither decreased IFN-γ expression by Th1 cells nor affected Th2 cell production of IL-4. Collectively, we have shown that Th17 cells express a functional IL-13R and that IL-13 negatively regulates IL-17A and IL-21 production by decreasing retinoic acid-related-γT expression and while increasing phosphorylation of STAT6 and GATA3 expression. Therefore, therapeutic intervention inhibiting IL-13 production could have adverse consequences by up-regulating Th17 inflammation in certain disease states.
Rapid Up-Regulation and Granule-Independent Transport of Perforin to the Immunological Synapse Define a Novel Mechanism of Antigen-Specific CD8+ T Cell Cytotoxic Activity
Authors: Makedonas George , Banerjee Pinaki P. , Pandey Rahul , Hersperger Adam R. , Sanborn Keri B. , Hardy Gareth A. D. , Orange Jordan S. , Betts Michael R. 
Published: April 2009

Abstract
CTL are endowed with the ability to eliminate pathogens through perforin-mediated cytotoxic activity. The mechanism for perforin-mediated Ag-specific killing has been solely attributed to cytotoxic granule exocytosis from activated CD8+ T cells. In this study, we redefine this mechanism, demonstrating that virus-specific CD8+ T cells rapidly up-regulate perforin in response to stimulation temporally with IFN-γ and CD107a expression. Following Ag-specific activation, newly synthesized perforin rapidly appears at the immunological synapse, both in association with and independent of cytotoxic granules, where it functions to promote cytotoxicity. Our work suggests a novel mechanism of CTL cytotoxicity and identifies a novel correlate of CD8+ T cell-mediated immunity.
Pathogenic Natural Antibodies Recognizing Annexin IV Are Required to Develop Intestinal Ischemia-Reperfusion Injury
Authors: Kulik Liudmila , Fleming Sherry D. , Moratz Chantal , Reuter Jason W. , Novikov Aleksey , Chen Kuan , Andrews Kathy A. , Markaryan Adam , Quigg Richard J. , Silverman Gregg J. , Tsokos George C. , Holers V. Michael 
Published: April 2009

Abstract
Intestinal ischemia-reperfusion (IR) injury is initiated when natural IgM Abs recognize neo-epitopes that are revealed on ischemic cells. The target molecules and mechanisms whereby these neo-epitopes become accessible to recognition are not well understood. Proposing that isolated intestinal epithelial cells (IEC) may carry IR-related neo-epitopes, we used in vitro IEC binding assays to screen hybridomas created from B cells of unmanipulated wild-type C57BL/6 mice. We identified a novel IgM mAb (mAb B4) that reacted with the surface of IEC by flow cytometric analysis and was alone capable of causing complement activation, neutrophil recruitment and intestinal injury in otherwise IR-resistant Rag1−/− mice. mAb B4 was found to specifically recognize mouse annexin IV. Preinjection of recombinant annexin IV blocked IR injury in wild-type C57BL/6 mice, demonstrating the requirement for recognition of this protein to develop IR injury in the context of a complex natural Ab repertoire. Humans were also found to exhibit IgM natural Abs that recognize annexin IV. These data in toto identify annexin IV as a key ischemia-related target Ag that is recognized by natural Abs in a pathologic process required in vivo to develop intestinal IR injury.
An Atypical Protein Kinase C (PKCζ) Plays a Critical Role in Lipopolysaccharide-Activated NF-κB in Human Peripheral Blood Monocytes and Macrophages
Authors: Huang XueSong , Chen Ling-Yu , Doerner Astrid M. , Pan Warren W. , Smith Laura , Huang Shuang , Papadimos Thomas J. , Pan Zhixing K. 
Published: April 2009

Abstract
We have reported that the bacterial LPS induces the activation of NF-κB and inflammatory cytokine gene expression and that this requires the activity of small GTPase, RhoA. In this study, we show that an atypical protein kinase C isozyme, PKCζ, associates functionally with RhoA and that PKCζ acts as a signaling component downstream of RhoA. Stimulation of monocytes and macrophages with LPS resulted in PKCζ activation and that inhibition of PKCζ activity blocks both LPS-stimulated activation of NF-κB and IL-1β gene expression. Our results also indicate that transforming growth factor β-activated kinase 1 acts as a signaling component downstream of PKCζ in cytokine gene transcription stimulated by LPS in human peripheral blood monocytes and macrophages. The specificity of this response suggests an important role for the Rho GTPase/PKCζ/transforming growth factor β-activated kinase 1/NF-κB pathway in host defense and in proinflammatory cytokine synthesis induced by bacterial LPS.
Chronic Lymphocytic Leukemia and B and T Cells Differ in Their Response to Cyclic Nucleotide Phosphodiesterase Inhibitors
Authors: Meyers John A. , Su Derrick W. , Lerner Adam 
Published: April 2009

Abstract
Phosphodiesterase (PDE)4 inhibitors, which activate cAMP signaling by reducing cAMP catabolism, are known to induce apoptosis in B lineage chronic lymphocytic leukemia (CLL) cells but not normal human T cells. The explanation for such differential sensitivity remains unknown. In this study, we report studies contrasting the response to PDE4 inhibitor treatment in CLL cells and normal human T and B cells. Affymetrix gene chip analysis in the three cell populations following treatment with the PDE4 inhibitor rolipram identified a set of up-regulated transcripts with unusually high fold changes in the CLL samples, several of which are likely part of compensatory negative feedback loops. The high fold changes were due to low basal transcript levels in CLL cells, suggesting that cAMP-mediated signaling may be unusually tightly regulated in this cell type. Rolipram treatment augmented cAMP levels and induced ATF-1/CREB serine 63/133 phosphorylation in both B lineage cell types but not T cells. As treatment with the broad-spectrum PDE inhibitor 3-isobutyl-1-methylxanthine induced T cell CREB phosphorylation, we tested a series of family-specific PDE inhibitors for their ability to mimic 3-isobutyl-1-methylxanthine-induced ATF-1/CREB phosphorylation. Whereas PDE3 inhibitors alone had no effect, the combination of PDE3 and PDE4 inhibitors induced ATF-1/CREB serine 63/133 phosphorylation in T cells. Consistent with this observation, PDE3B transcript and protein levels were low in CLL cells but easily detectable in T cells. Combined PDE3/4 inhibition did not induce T cell apoptosis, suggesting that cAMP-mediated signal transduction that leads to robust ATF-1/CREB serine 63/133 phosphorylation is not sufficient to induce apoptosis in this lymphoid lineage.
Differential Regulation of Foxp3 and IL-17 Expression in CD4 T Helper Cells by IRAK-1
Authors: Maitra Urmila , Davis Sarah , Reilly Christopher M. , Li Liwu 
Published: April 2009

Abstract
Host immune responses are finely regulated by the opposing effects of Th17 and T regulatory (Treg) cells. Treg cells help to dampen inflammatory processes and Th17 cells facilitate various aspects of immune activation. The differentiation of Th cells depends on a unique combination of stimulants and subsequent activation of diverse transcription factors. In particular, cooperative activation of NFAT and Smad3 leads to the induction of Treg cells, and cooperation among STAT3 and Smad3 switches to the induction of Th17 cells. We have previously shown that the IL-1 receptor associated kinase 1 (IRAK-1) selectively activates STAT3 and inactivates NFAT. Physiological studies have shown that IRAK-1−/− mice are protected from developing various inflammatory diseases, including experimental autoimmune encephalomyelitis and atherosclerosis with unknown mechanism. In this study, we demonstrate that IRAK-1 plays a critical modulatory role in the differentiation of Th17 and Treg cells. Following stimulation with TCR agonists and TGFβ, IRAK-1−/− CD4 Th cells display elevated nuclear NFATc2 levels and increased interaction of NFATc2 and Smad3, resulting in increased expression of Foxp3, a key marker for Treg cells. IRAK-1−/− mice have constitutively higher populations of Treg cells. In contrast, when stimulated with TCR agonists together with IL-6 and TGF-β, IRAK-1−/− CD4 Th cells exhibit attenuated STAT3 Ser727 phosphorylation and reduced expression of IL-17 and RORγt compared with wild-type cells. Correspondingly, IRAK-1 deletion results in decreased IL-17 expression and dampened inflammatory responses in acute and chronic inflammatory mice models. Our data provides mechanistic explanation for the anti-inflammatory phenotypes of IRAK-1−/− mice.
Multimedia Video
Authors: Elmagarmid Ahmed K. , Jiang Haitao 
Published: April 2009

AbstractThe sections in this article areVideo CodecsJpeg and MjpegQuicktimeVideo DatabasesVideo Data ModelingVideo Cut Detection and SegmentationVideo IndexingVideo Query, Retrieval, and BrowsingVideo Authoring and EditingVideo ConferencingVideo‐on‐Demand
Inspection in Semiconductor Manufacturing
Authors: Sankaran Vijay , Weber Charles M. , Lakhani Fred , Tobin, Jr. Kenneth W. 
Published: April 2009

Abstract
The sections in this article are

Defect Reduction Cycle in Semiconductor Manufacturing

Inspection in the IC Manufacturing Process Life Cycle

Optical Imaging Technology

Laser‐Scattering Technology

Measurement of Optical Scatter from Contaminants on Wafers

Automatic Defect Classification

Future Challenges

Conclusions

Acknowledgments