bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of partial slip on axisymmetric flow of an electrically conducting viscoelastic fluid past a stretching sheet
Authors: Sahoo Bikash 
Published: July 2009

Abstract
The entrained flow of an electrically conducting non-Newtonian, viscoelastic second grade fluid due to an axisymmetric stretching surface with partial slip is considered. The partial slip is controlled by a dimensionless slip factor, which varies between zero (total adhesion) and infinity (full slip). Suitable similarity transformations are used to reduce the resulting highly nonlinear partial differential equation into an ordinary differential equation. The issue of paucity of boundary conditions is addressed, and an effective numerical scheme has been adopted to solve the obtained differential equation even without augmenting the boundary conditions. The important findings in this communication are the combined effects of the partial slip, magnetic interaction parameter and the second grade fluid parameter on the velocity and skin friction coefficient. It is observed that in presence of slip, the velocity decreases with an increase in the magnetic parameter. That is, the Lorentz force which opposes the flow leads to enhanced deceleration of the flow. Moreover, it is interesting to find that as slip increases in magnitude, permitting more fluid to slip past the sheet, the skin friction coefficient decreases in magnitude and approaches zero for higher values of the slip parameter, i.e., the fluid behaves as though it were inviscid.
Approximate analytical solution of continuous states for the l-wave Schrödinger equation with a diatomic molecule potential
Authors: Wei Gao-Feng , Qiang Wen-Chao , Chen Wen-Li 
Published: July 2009

Abstract
The continuous states of the l-wave Schrödinger equation for the diatomic molecule represented by the hyperbolical function potential are carried out by a proper approximation scheme to the centrifugal term. The normalized analytical radial wave functions of the l-wave Schrödinger equation for the hyperbolical function potential are presented and the corresponding calculation formula of phase shifts is derived. Also, we interestingly obtain the corresponding bound state energy levels by analyzing analytical properties of scattering amplitude.
Autoimmune thyroid disease in patients with anti-GAD positive type 1 diabetes mellitus
Authors: Gul Kamile , Ustun Ihsan , Aydin Yusuf , Berker Dilek , Erol Halil , Unal Mustafa , Barazi Ayse , Delibasi Tuncay , Guler Serdar 
Published: July 2009

Abstract
The aim of the study was to determine the frequency and titers of anti-thyroid peroxidase (Anti-TPO), anti-thyroglobulin (Anti-TG), and anti-glutamic acid decarboxylase (Anti-GAD) antibodies in Turkish patients with type 1 diabetes mellitus (DM), and to compare the frequency of anti-TPO and anti-TG titers in the presence or absence of anti-GAD. A total of 104 patients including 56 males and 48 females with type 1 DM and their age-, gender-, and body mass index-matched control group, including 31 males and 27 females, 58 cases in total with an age range of 15-50 years, were recruited into this study. In patients with type 1 DM, positive anti-GAD was detected in 30.8% (n=32). In patients with positive anti-GAD, rate of positive anti-TPO was 37.5%; however, in patients with negative anti-GAD, the rate of positive anti-TPO was 9.7% and the difference was statistically significant (p=0.001). In patients with positive anti-GAD, the rate of positive anti-TG was 18.8%. In patients with negative anti-GAD, the rate of positive anti-TG was 2.8%, and the difference between them was statistically significant (p=0.005). In patients with positive and negative anti-GAD, rates of both positive anti-TPO and anti-TG were 15.6% and 1.4%, respectively, with the difference showing statistical significance (p=0.004). Thyroid autoimmunity in type 1 DM patients with positive anti-GAD was apparently higher; therefore, these patients should be followed more frequently and carefully.
Manifestation peculiarities of idiopathic chronic eosinophilic pneumonia
Authors: Danila Edvardas , Norkūnienė Jolita , Nargėla Remigijus , Žurauskas Edvardas , Šatkauskas Bronislovas , Aleksonienė Regina 
Published: July 2009

Abstract
Chronic eosinophilic pneumonia is a rare interstitial lung disorder, which causes diagnostic difficulties. Often the disease is diagnosed correctly after several weeks or months following initial presentation. The aim of the study was to prospectively evaluate peculiarities of manifestation of idiopathic chronic eosinophilic pneumonia (ICEP), which may allow to improving early diagnosis. Twenty patients with ICEP were involved in this investigation. The cases of acute eosinophilic pneumonia and cases of chronic eosinophilic pneumonia of known origin were excluded. To define archetypal signs of the idiopathic chronic eosinophilic pneumonia, 3 comparable groups were selected. They were the group of 50 patients with community-acquired pneumonia (COP); the group of 21 asthmatic patients with COP, and the cluster of 10 patients with morphologically confirmed cryptogenic organizing pneumonia (OP). Clinical and radiological manifestation of ICEP was similar to COP and cryptogenic OP manifestation. We have found that chest pain; fine rales and pleurisy were unrepresentative for ICEP. However, blood eosinophilia was typical sign of ICEP and wheezing was a frequent observation. Usually ICEP patients had relative mild clinical symptoms and moderate increased C reactive protein (CRP) level even in cases of multiple pulmonary infiltrates. In conclusion, in cases of not typical pneumonia course, i.e. non-resolving or recurrent pulmonary infiltrates; relative mild clinical symptoms and moderate increased CRP level with multiple pulmonary infiltrates; blood eosinophilia and/or signs of airway obstruction eosinophilic pneumonia should be suspected and bronchoalveolar lavage and/or bronchoscopic lung biopsy performed.
Oxygenation by Hollow Plunging Water Jet
Authors: Deswal Surinder 
Published: July 2009

Oxygenation by a plunging water jet is a more attractive way to effect oxygen-transfer than conventional oxygenation systems. A lot of work has been reported on the oxygen-transfer by plunging water jets. However, few studies have been carried out on hollow plunging jet. In this paper, volumetric oxygen-transfer coefficient and oxygen-transfer efficiency has been studied experimentally for hollow plunging jet in a pool of water for different thicknesses of jets. This research suggests that the volumetric oxygen-transfer coefficient and oxygen-transfer efficiency of the hollow plunging jet for air-water system are competitive with other types of aeration systems. Further, relationships of volumetric oxygen-transfer coefficient with jet power per unit volume and jet parameters are also proposed. The suggested relationships predict the volumetric oxygen-transfer coefficient for hollow plunging water jet within a scatter of ±15%.Key words: hollow plunging jet, oxygenation, volumetric oxygen-transfer coefficient, oxygentransfer efficiency, jet power.Journal of the Institute of Engineering, Vol. 7, No. 1, 2009 July pp. 40-47doi: 10.3126/jie.v7i1.2061
Identification of DNA Methyltransferase 3a as a T Cell Receptor-Induced Regulator of Th1 and Th2 Differentiation
Authors: Gamper Christopher J. , Agoston Agoston T. , Nelson William G. , Powell Jonathan D. 
Published: July 2009

Abstract
Ag-specific T cell cytokine expression is dictated by the context in which TCR engagement occurs. Recently it has become clear that epigenetic changes play a role in this process. DNA methyltransferase 3a (DNMT3a) is a de novo methyltransferase important to the epigenetic control of cell fate. We have determined that DNMT3a expression is increased following TCR engagement and that costimulation mitigates DNMT3a protein expression. T cells lacking DNMT3a simultaneously express IFN-γ and IL-4 after expansion under nonbiasing conditions. While global methylation of DNA from wild-type and knockout T cells is similar, DNMT3a-null T cells demonstrate selective hypomethylation of both the Il4 and Ifng loci after activation. Such hypomethylated knockout Th2 cells retain a greater capacity to express IFN-γ protein when they are subsequently exposed to Th1-biasing conditions. Based on these findings we propose that DNMT3a is a key participant in regulating T cell polarization at the molecular level by promoting stable selection of a context-specific cell fate through methylation of selective targets in T cells.
Dendritic Cell Anergy Results from Endotoxemia in Severe Malnutrition
Authors: Hughes Stephen Miles , Amadi Beatrice , Mwiya Mwiya , Nkamba Hope , Tomkins Andrew , Goldblatt David 
Published: July 2009

Abstract
Malnutrition predicts an increased risk of morbidity and mortality from infection. Defects in cell-mediated immunity, such as thymic atrophy, impaired cutaneous tuberculin responses, and reduced T cell mitogenesis in vitro, are well characterized. There has been no convincing mechanism proposed for these T cell defects. However, as T cell responses rely on signals received from APCs, this study evaluates dendritic cell (DC) function in children with severe malnutrition. Repeated sampling of peripheral blood from 81 severely malnourished children at the University Teaching Hospital, Lusaka, Zambia, demonstrated for the first time a defect in DC numbers in children with malnutrition (28 per microliter) and a recovery in cell number (48 per microliter; p &lt; 0.01) with standard treatment. We describe normal DC maturation in the majority of malnourished children. However, in 17% of our study patients, in association with endotoxemia we describe the novel finding of DC maturation failure (down-regulation rather than up-regulation of HLA-DR). There was a strong correlation between the strength of HLA-DR up or down-regulation and the generation of IL-10 (r = −0.481; p = 0.003). These “anergic” DCs failed to support T cell proliferation. Defects in DC number and the immunosuppressive phenotype of DCs from severely malnourished children with endotoxemia provide a rational basis for the anergy found in severe malnutrition.
The Cathelicidin LL-37 Activates Human Mast Cells and Is Degraded by Mast Cell Tryptase: Counter-Regulation by CXCL4
Authors: Schiemann Florian , Brandt Ernst , Gross Roland , Lindner Buko , Mittelstädt Jessica , Sommerhoff Christian P. , Schulmistrat Jan , Petersen Frank 
Published: July 2009

AbstractThe cathelicidin LL-37 represents a potent antimicrobial and cell-stimulating agent, most abundantly expressed in peripheral organs such as lung and skin during inflammation. Because mast cells (MC) overtake prominent immunomodulatory roles in these organs, we wondered whether interactions exist between MC and LL-37. In this study, we show for the first time to our knowledge that physiological concentrations of LL-37 induce degranulation in purified human lung MC. Intriguingly, as a consequence LL-37 rapidly undergoes limited cleavage by a released protease. The enzyme was identified as β-tryptase by inhibitor studies and by comparison to the recombinant protease. Examining the resulting LL-37 fragments for their functional activity, we found that none of the typical capacities of intact LL-37, i.e., MC degranulation, bactericidal activity, and neutralization of LPS, were retained. Conversely, we found that another inflammatory protein, the platelet-derived chemokine CXCL4, protects LL-37 from cleavage by β-tryptase. Interestingly, CXCL4 did not act as a direct enzyme inhibitor, but destabilized active tetrameric β-tryptase by antagonizing the heparin component required for the integrity of the tetramer. Altogether our results suggest that interaction of LL-37 and MC initiates an effective feedback loop to limit cathelicidin activity during inflammation, whereas CXCL4 may represent a physiological counter-regulator of β-tryptase activity.
Thioredoxin-Interacting Protein Regulates Hematopoietic Stem Cell Quiescence and Mobilization under Stress Conditions
Authors: Jeong Mira , Piao Zheng-Hao , Kim Mi Sun , Lee Suk Hyung , Yun Sohyun , Sun Hu-nan , Yoon Suk Ran , Chung Jin Woong , Kim Tae-Don , Jeon Jun Ho , Lee Jiwon , Kim Hyun-Nam , Choi Je-Yong , Choi Inpyo 
Published: July 2009

Abstract
Hematopoietic stem cells (HSCs) are maintained in a quiescent state in bone marrow (BM) niches by intrinsic and extrinsic signals. The mechanisms regulating the quiescence and mobilization of HSCs, however, remain unclear. In this study, we report that the expression of thioredoxin-interacting protein (TXNIP) is decreased during HSC activation. In Txnip−/− mice, the long-term reconstituting HSC population is decreased and exhausted, and its capacity to repopulate is rapidly lost. These effects are associated with hyperactive Wnt signaling, an active cell cycle, and reduced p21 expression under conditions of stress. TXNIP deficiency reduced the CXCL12- and osteopontin-mediated interaction between HSCs and the bone marrow, and impaired homing and retention in the osteoblastic niche, resulting in mobilized HSCs. Therefore, we propose that TXNIP is essential for maintaining HSC quiescence and the interaction between HSCs and the BM niche.
TLR-Stimulated CD34 Stem Cell-Derived Human Skin-Like and Monocyte-Derived Dendritic Cells Fail to Induce Th17 Polarization of Naive T Cells but Do Stimulate Th1 and Th17 Memory Responses
Authors: Duraisingham Sai Suda , Hornig Julia , Gotch Frances , Patterson Steven 
Published: July 2009

Abstract
Dendritic cells (DCs) are important in linking innate and adaptive immune responses by priming and polarizing naive CD4+ Th cells, but little is known about the effect of different human DC subsets on Th cells, particularly Th17 cells. We have investigated the ability of TLR-stimulated human Langerhans cells (LC), dermal DCs (dDC), and monocyte-derived DCs (moDC) to affect naive and memory Th17 and Th1 responses. MoDCs stimulated greater memory T cell proliferation while LCs and dDCs more potently stimulated naive T cell proliferation, indicating functionally distinct subsets of DCs. TLR stimulation of all three DC types was unable to induce Th17 polarization from naive T cell precursors, despite inducing Th1 polarization. Dectin stimulation of DCs in IMDM was however able to produce Th17 cells. TLR-stimulated DCs were capable of inducing IL-17A and IFN-γ production from memory T cells, although the mechanism used by each DC subset differed. MoDCs partially mediated this effect on memory Th1 and Th17 cells by the production of soluble factors, which correlated with their ability to secrete IL-12p70 and IL-23. In contrast, LCs and dDCs were able to elicit a similar memory response to moDCs, but in a contact dependent manner. Additionally, the influence of microbial stimulation was demonstrated with TLR3 and TLR7/8 agonists inducing a Th1 response, whereas TLR2 or dectin stimulation of moDCs enhanced the IL-17 response. This study emphasizes the differences between human DC subsets and demonstrates that both the DC subset and the microbial stimulus influence the Th cell response.
IL-27 Is a Key Regulator of IL-10 and IL-17 Production by Human CD4+ T Cells
Authors: Murugaiyan Gopal , Mittal Akanksha , Lopez-Diego Rocio , Maier Lisa M. , Anderson David E. , Weiner Howard L. 
Published: July 2009

Abstract
Although the physiologic pathways that control regulatory T cells (Foxp3-expressing regulatory T cells, IL-10-secreting Tr1 cells) and Th17 cells in rodents have been defined, the factors that control these differentiation pathways in humans are not well understood. In this study, we show that IL-27 promotes the differentiation of IL-10-secreting Tr1 cells while inhibiting Th17 generation and molecules associated with Th17 function. Furthermore, IL-27 inhibits IL-17-polarizing cytokines on dendritic cells, which in turn decrease IL-17 secretion from T cells. Our results demonstrate that IL-27 plays a key role in human T cells by promoting IL-10-secreting Tr1 cells and inhibiting Th17 cells and thus provides a dual regulatory mechanism to control autoimmunity and tissue inflammation.
SUMOylation of Tissue Transglutaminase as Link between Oxidative Stress and Inflammation
Authors: Luciani Alessandro , Villella Valeria Rachela , Vasaturo Angela , Giardino Ida , Raia Valeria , Pettoello-Mantovani Massimo , D'Apolito Maria , Guido Stefano , Leal Teresinha , Quaratino Sonia , Maiuri Luigi 
Published: July 2009

Abstract
Cystic fibrosis (CF) is a monogenic disease caused by mutations in the CF transmembrane conductance regulator (CFTR) gene. CF is characterized by chronic bacterial lung infections and inflammation, and we have previously reported that tissue transglutaminase (TG2), a multifunctional enzyme critical to several diseases, is constitutively up-regulated in CF airways and drives chronic inflammation. Here, we demonstrate that the generation of an oxidative stress induced by CFTR-defective function leads to protein inhibitor of activated STAT (PIAS)y-mediated TG2 SUMOylation and inhibits TG2 ubiquitination and proteasome degradation, leading to sustained TG2 activation. This prevents peroxisome proliferator-activated receptor (PPAR)γ and IkBα SUMOylation, leading to NF-κB activation and to an uncontrolled inflammatory response. Cellular homeostasis can be restored by small ubiquitin-like modifier (SUMO)-1 or PIASy gene silencing, which induce TG2 ubiquitination and proteasome degradation, restore PPARγ SUMOylation, and prevent IkBα cross-linking and degradation, thus switching off inflammation. Manganese superoxide dismutase overexpression as well as the treatment with the synthetic superoxide dismutase mimetic EUK-134 control PIASy-TG2 interaction and TG2 SUMOylation. TG2 inhibition switches off inflammation in vitro as well as in vivo in a homozygous F508del-CFTR mouse model. Thus, TG2 may function as a link between oxidative stress and inflammation by driving the decision as to whether a protein should undergo SUMO-mediated regulation or degradation. Targeting TG2-SUMO interactions might represent a new option to control disease evolution in CF patients as well as in other chronic inflammatory diseases, neurodegenerative pathologies, and cancer.
HIV-1 Envelope Induces Memory B Cell Responses That Correlate with Plasma Antibody Levels after Envelope gp120 Protein Vaccination or HIV-1 Infection
Authors: Bonsignori Mattia , Moody M. Anthony , Parks Robert J. , Holl T. Matt , Kelsoe Garnett , Hicks Charles B. , Vandergrift Nathan , Tomaras Georgia D. , Haynes Barton F. 
Published: July 2009

Abstract
Successful vaccines (i.e., tetanus and diphtheria) can induce long-lived Ab levels that are maintained by bone marrow plasma cells and plasma Ab levels do not correlate with numbers of blood memory B cells. Destruction of CD4+ T cells early in HIV-1 acute infection may result in insufficient induction of neutralizing Ab responses; thus, an HIV-1 vaccine should elicit high levels of durable Abs by long-lived plasma cells to be protective. We asked if HIV-1 envelope-specific memory responses were sustained by memory B cells in the settings of HIV-1 gp120 envelope vaccination and chronic HIV-1 infection. Levels of anti-HIV-1 envelope plasma Abs and memory B cells were found to correlate in both settings. Moreover, whereas the expected half-life of plasma Ab levels to protein vaccines was &gt;10 years when maintained by long-lived plasma cells, anti-envelope Ab level half-lives were ∼33–81 wk in plasma from antiretroviral drug-treated HIV-1+ subjects. In contrast, anti-p55 Gag Ab level half-life was 648 wk, and Ab titers against influenza did not decay in-between yearly or biennial influenza vaccine boosts in the same patients. These data demonstrated that HIV-1 envelope induces predominantly short-lived memory B cell-dependent plasma Abs in the settings of envelope vaccination and HIV-1 infection. The inability to generate high titers of long-lived anti-envelope Abs is a major hurdle to overcome for the development of a successful HIV-1 vaccine.
Dicer-Dependent MicroRNA Pathway Controls Invariant NKT Cell Development
Authors: Fedeli Maya , Napolitano Anna , Wong Molly Pui Man , Marcais Antoine , de Lalla Claudia , Colucci Francesco , Merkenschlager Matthias , Dellabona Paolo , Casorati Giulia 
Published: July 2009

Abstract
Invariant NK T (iNKT) cells are a separate lineage of T lymphocytes with innate effector functions. They express an invariant TCR specific for lipids presented by CD1d and their development and effector differentiation rely on a unique gene expression program. We asked whether this program includes microRNAs, small noncoding RNAs that regulate gene expression posttranscriptionally and play a key role in the control of cellular differentiation programs. To this aim, we investigated iNKT cell development in mice in which Dicer, the RNase III enzyme that generates functional microRNAs, is deleted in cortical thymocytes. We find that Dicer deletion results in a substantial reduction of iNKT cells in thymus and their disappearance from the periphery, unlike mainstream T cells. Without Dicer, iNKT cells do not complete their innate effector differentiation and display a defective homeostasis due to increased cell death. Differentiation and homeostasis of iNKT cells require Dicer in a cell-autonomous fashion. Furthermore, we identify a miRNA profile specific for iNKT cells, which exhibits features of activated/effector T lymphocytes, consistent with the idea that iNKT cells undergo agonist thymic selection. Together, these results define a critical role of the Dicer-dependent miRNA pathway in the physiology of iNKT cells.
Requirement of JNK-Mediated Phosphorylation for Translocation of Group IVA Phospholipase A2 to Phagosomes in Human Macrophages
Authors: Casas Javier , Meana Clara , Esquinas Esperanza , Valdearcos Martín , Pindado José , Balsinde Jesús , Balboa María A. 
Published: July 2009

Abstract
Eicosanoids are a broad family of lipids that play a critical role in host defense against bacterial and fungal infections. The first enzyme in the metabolic pathway for the generation of eicosanoids is group IVA phospholipase A2, also known as cytosolic phospholipase A2α (cPLA2α). During phagocytosis, cPLA2α has been found to translocate to the phagosome, although the molecular mechanism involved in such a translocation has not been elucidated. By using enhanced GFP-tagged proteins we show in this work that a nonphosphorylatable cPLA2α mutant (S505A) does not translocate to the phagosomes, but a mutant that mimics phosphorylation on Ser505 (S505E) does it so readily. During phagocytosis, endogenous cPLA2α is phosphorylated at Ser505, and inhibitors of JNK, but not of other related kinases such as p38 or the extracellular-regulated kinases 1 and 2, completely block such a phosphorylation. Inhibition of JNK activity also inhibits the translocation of cPLA2α to phagosomal membranes, as well as arachidonic acid release to the extracellular medium. Moreover, the S505E mutant makes the enzyme refractory to JNK inhibition, translocating normally to phagosomal membranes. Collectively, these data support a key role for JNK-mediated cPLA2α phosphorylation at Ser505 in the sequence of events leading to translocation and activation of the enzyme to phagosomal membranes in human macrophages.