bluuebunny/crossref_metadata_2025_split huggingface dataset:
Soil nematode community changes associated with windfall and wildfire in forest soil at the High Tatras National Park, Slovak Republic
Authors: Čerevková A. , Renčo M. 
Published: June 2009

Abstract
The paper presents research findings on the influence of windfall and wildfire on nematode communities in Lariceto-Piceetum forest in the High Tatras in Slovakia. Comparison was made of an intact (REF), affected and extracted (EXT), non-extracted (NEX) and burnt (FIR) forest stand. A total of 55 species belonging to 36 genera were found. The EXT locality harboured the majority of the identified species, but the highest abundance of nematodes was observed in the FIR locality. Bacterial feeders were the dominant trophic group in all investigated plots. In the REF bacterial feeders were followed by root-fungal feeders, fungal feeders and omnivores, in the EXT by omnivores and plant parasites, in the FIR by omnivores and root-fungal feeders and in the NEX by fungal feeders and omnivores. The MI and SI were higher in the REF and the EXT compared to those in the FIR and the NEX, the highest B/F ratio was observed in the FIR and the highest EI was found in the REF. We can conclude that disturbance of forest vegetation and soil has had a clear and demonstrable impact on nematode communities.
Introductory: Perspectives on Reality and "The World" in the Realism Debate
Authors: Ginev Dimitri 
Published: June 2009

Introductory: Perspectives on Reality and "The World" in the Realism Debate
One of the "characteristic parameters" dividing up analytical and Continental philosophizing is the interpretation of the concepts of "reality" and "the world". The paper offers an analysis of this characteristic parameter with regard to the relations between epistemologically centred and hermeneutically oriented doctrines of realism.
A chemical method of the production of "heavy" sodium tripolyphosphate with the high content of Form I or Form II
Authors: Banach Marcin , Kowalski Zygmunt , Wzorek Zbigniew , Gorazda Katarzyna 
Published: June 2009

A chemical method of the production of "heavy" sodium tripolyphosphate with the high content of Form I or Form II
Sodium tripolyphosphate STPP is used in laundry detergent as a detergent "builder". The paper presents the chemical method of obtaining "heavy", i.e. with higher bulk density granulated sodium tripolyphosphate. The bulk density of sodium tripolyphosphate was increased by preparing a mixture of the dried sodium phosphates, the recycled subgrain of STPP and water in specific proportions and calcining this mixture for 1 hour at 400°C and 550°C (to obtain a proper STPP form) in the chamber kiln. This method allows producing the granular sodium tripolyphosphate with high bulk density (1.04-1.07 kg/dm3) and a high content of Form I or Form II, respectively.
Application of pervaporation and osmotic membrane distillation to the regeneration of spent solutions from the osmotic food dehydration
Authors: Kujawski Wojciech , Gierszewska-Drużyńska Magdalena , Warczok Justyna , Güell Carme 
Published: June 2009

Application of pervaporation and osmotic membrane distillation to the regeneration of spent solutions from the osmotic food dehydration
Results of pervaporation (PV) of sucrose and calcium chloride spent solutions were presented. Additionally, osmotic membrane distillation (OMD) of sucrose solutions was investigated. It was found that the regeneration of spent sucrose solution for the reuse is possible by using PV or OMD processes. However, OMD process produces another spent stream i.e. CaCl2. Pervaporation membranes showed fluxes in the range of 0.5 - 0.9 kg m-2 h-1 in contact with 40° Brix sucrose solution, whereas OMD water permeate fluxes were in the range of 4 - 5 kg m-2 h-1 for the same feed concentration.
Two different hybrid processes were suggested: i) pretreatment followed by OMD reconcentration of spent sucrose solution and independently PV for CaCl2 regeneration; ii) membrane pretreatment (MP) followed by PV of sucrose solution. Based on the experimental results, the membrane areas for both systems were calculated and compared. MP-PV system seems to be a better solution for the spent mixtures management.
The natural history of untreated sporadic vestibular schwannomas: a comprehensive review of hearing outcomes
Authors: Sughrue Michael E. , Yang Isaac , Aranda Derick , Lobo Khadja , Pitts Lawrence H. , Cheung Steven W. , Parsa Andrew T. 
Published: June 2009

Object
Observation is an important consideration when discussing management options for patients with vestibular schwannoma (VS). Most data regarding clinical outcomes after conservative management come from modestsized series performed at individual centers. The authors performed an analysis of the published literature on the natural history of VSs with respect to hearing outcome. Their objective was to provide a comprehensive and unbiased description of outcomes in patients whose disease was managed conservatively.

Methods
The authors identified a total of 34 published studies containing hearing outcome data in patients with VSs < 25 mm in largest diameter who underwent observation management. The effects of initial tumor size and tumor growth rate on hearing function at latest follow-up were analyzed. Data from individual and aggregated cases were extracted from each study. Patients with poorer hearing (American Association of Otolaryngology–Head and Neck Surgery Classes C or D, or Gardner-Robertson Classes III, IV, or V) at the time of presentation were excluded.

Results
A total of 982 patients met the inclusion criteria for this analysis, with a mean initial tumor size of 11.3 ± 0.68 mm. The mean growth rate was 2.9 ± 1.2 mm/year. The length of follow-up for these studies ranged from 26 to 52 months. Patients with preserved hearing at latest follow-up had a statistically larger initial tumor size than those whose hearing declined during the observation period (11.5 ± 2.3 mm vs 9.3 ± 2.7 mm, p < 0.0001), but the 2-mm difference of means was at the limit of imaging resolution and observer reliability. In contrast, patients with lower rates of tumor growth (≤ 2.5 mm/year) had markedly higher rates of hearing preservation (75 vs 32%, p < 0.0001) compared with patients with higher tumor growth rates. Interestingly, the authors' analysis found no difference in the rate of reported intervention for patients in either group (16 vs 18%, p = not significant).

Conclusions
These data suggest that a growth rate of > 2.5 mm/year is a better predictor of hearing loss than the initial tumor size for patients undergoing observation management of VSs < 25 mm in largest diameter.
The Effects of Cytokines on Suppression of Lymphocyte Proliferation by Dexamethasone
Authors: Creed Tom J. , Lee Richard W. , Newcomb Paul V. , di Mambro Alexandra J. , Raju Madhuri , Dayan Colin M. 
Published: June 2009

Abstract
Treatment failure occurs in up to 30% of patients treated with steroids for inflammatory diseases. The aim of this study was to explore the potential role of 21 cytokines in steroid-resistant inflammatory disease and to develop methods to restore steroid sensitivity through cytokine manipulation. The dexamethasone inhibition of lymphocyte proliferation assay correlates with the outcome of steroid therapy in ulcerative colitis (UC) and other inflammatory diseases. Using this assay, PBMC production of 21 cytokines, assayed by cytokine bead array, was correlated with percentage of suppression of proliferation by 10−6 M dexamethasone (Imax) in 26 healthy volunteers. Effects of the addition of exogenous cytokines to induce steroid resistance in PBMCs from healthy volunteers and cytokine blockade to improve steroid sensitivity in PBMCs from patients with steroid-resistant UC were then explored. Production of IL-1α, IL-10, IL-17, IFN-γ, G-CSF, GM-CSF, TNF-α, and IFN-inducible protein 10 (IP-10) correlated significantly with in vitro steroid sensitivity; however, only IL-2 and TNF-α reduced steroid sensitivity when added exogenously. Addition of IL-10 enhanced steroid suppression. Immunoneutralization or receptor blockade of IL-2, but not TNF-α, IFN-γ, IL-4, IL-17, or IP-10 increased steroid sensitivity in cells from steroid-resistant UC patients. Neutralization of IL-10 reduced steroid sensitivity. Of the large panel of cytokines studied, IL-2 appears to have the greatest antagonistic effect on the antiproliferative effect of steroids. These data suggest that IL-2 inhibition in vivo may improve the response to steroids in steroid-resistant individuals.
In Vivo Lipopolysaccharide Exposure of Human Blood Leukocytes Induces Cross-Tolerance to Multiple TLR Ligands
Authors: de Vos Alex F. , Pater Jennie M. , van den Pangaart Petra S. , de Kruif Martijn D. , van 't Veer Cornelis , van der Poll Tom 
Published: June 2009

Abstract
In vitro and in vivo experiments in mice have shown that exposure of cells to the TLR4 ligand LPS induces tolerance toward a second exposure to LPS and induces cross-tolerance to certain other TLR ligands. Recently, we found that LPS tolerance in experimental human endotoxemia and Gram-negative sepsis is associated with elevated levels of IL-1R-associated kinase M, an intracellular negative regulator of MyD88-dependent TLR signaling. In the present study, we investigated whether in vivo exposure of humans to LPS induces tolerance in circulating leukocytes to other TLR agonists that rely either on MyD88- dependent or on MyD88-independent signaling. Analysis of TNF, IL-1β, IL-6, and IL-10 levels in whole blood demonstrated that leukocytes were hyporesponsive to ex vivo LPS restimulation 3–8 h after i.v. LPS injection (4 ng/kg). Reduced cytokine release during the same interval was also observed in whole blood further stimulated with MyD88-dependent ligands for TLR2, TLR5, and TLR7 or with whole bacteria. Strikingly, blood leukocytes were also tolerant to a ligand for TLR3, which signals solely through a MyD88-independent (Toll IL-1R domain-containing adaptor-inducing IFN-β (TRIF)-dependent) pathway. The hyporesponsiveness of leukocytes to TLR3 ligation was associated with reduced rather than increased levels of the recently identified TRIF inhibitor SARM. Taken together, these data indicate that systemic LPS challenge of human volunteers induces cross-tolerance to multiple TLR ligands that signal in a MyD88-dependent or MyD88-independent manner and suggest that LPS exposure of human blood leukocytes may hamper the inflammatory response to various microbial components.
Pulmonary Eosinophils and Their Role in Immunopathologic Responses to Formalin-Inactivated Pneumonia Virus of Mice
Authors: Percopo Caroline M. , Qiu Zhijun , Phipps Simon , Foster Paul S. , Domachowske Joseph B. , Rosenberg Helene F. 
Published: June 2009

Abstract
Enhanced disease is the term used to describe the aberrant Th2-skewed responses to naturally acquired human respiratory syncytial virus (hRSV) infection observed in individuals vaccinated with formalin-inactivated viral Ags. Here we explore this paradigm with pneumonia virus of mice (PVM), a pathogen that faithfully reproduces features of severe hRSV infection in a rodent host. We demonstrate that PVM infection in mice vaccinated with formalin-inactivated Ags from PVM-infected cells (PVM Ags) yields Th2-skewed hypersensitivity, analogous to that observed in response to hRSV. Specifically, we detect elevated levels of IL-4, IL-5, IL-13, and eosinophils in bronchoalveolar lavage fluid of PVM-infected mice that were vaccinated with PVM Ags, but not among mice vaccinated with formalin-inactivated Ags from uninfected cells (control Ags). Interestingly, infection in PVM Ag-vaccinated mice was associated with a ∼10-fold reduction in lung virus titer and protection against weight loss when compared with infected mice vaccinated with control Ags, despite the absence of serum-neutralizing Abs. Given recent findings documenting a role for eosinophils in promoting clearance of hRSV in vivo, we explored the role of eosinophils in altering the pathogenesis of disease with eosinophil-deficient mice. We found that eosinophil deficiency had no impact on virus titer in PVM Ag-vaccinated mice, nor on weight loss or levels of CCL11 (eotaxin-1), IFN-γ, IL-5, or IL-13 in bronchoalveolar lavage fluid. However, levels of both IL-4 and CCL3 (macrophage inflammatory protein-1α) in bronchoalveolar lavage fluid were markedly diminished in PVM Ag-vaccinated, PVM-infected eosinophil-deficient mice when compared with wild-type controls.
Role of CD44 in the Differentiation of Th1 and Th2 Cells: CD44-Deficiency Enhances the Development of Th2 Effectors in Response to Sheep RBC and Chicken Ovalbumin
Authors: Guan Hongbing , Nagarkatti Prakash S. , Nagarkatti Mitzi 
Published: June 2009

Abstract
CD4 T cells can be primarily polarized to differentiate into Th1 or Th2 cells. CD44 is a marker of T cell activation and a property of long-lived memory cells and implicated in cell migration, activation, and differentiation. To date, whether CD44 has a role in regulating Th1-Th2 differentiation has not been determined. In this study, we compared Th1 and Th2 responses in wild-type and CD44-deficient mice in response to sheep RBC and chicken OVA, as well as examined Th1-Th2 differentiation in vivo and in vitro from CD44-sufficient and CD44-deficient naive CD4 T cells. We observed that deficiency of CD44 tended to inhibit Th1 while promoting Th2 differentiation. Furthermore, chimeric studies suggested that CD44 expression by CD4 T cells was essential for such Th2 bias. The regulation by CD44 occurred at the transcription level leading to up-regulated GATA3 and down-regulated T-bet expression in activated CD4 T cells. We also noted that CD44-deficiency could modify the state of dendritic cell subsets to induce a Th2-biased development. Results presented in this study demonstrate for the first time that CD44 participates in the regulation of Th1-Th2 differentiation.
Blocking CD27-CD70 Costimulatory Pathway Suppresses Experimental Colitis
Authors: Manocha Monika , Svend Rietdijk , Laouar Amale , Liao Gongxian , Bhan Atul , Borst Jannine , Terhorst Cox , Manjunath N. 
Published: June 2009

Abstract
The pathogenesis of human inflammatory bowel disease (IBD) and most experimental models of IBD is dependent on the activation and expansion of CD4+ T cells via interaction with mucosal APCs. The costimulatory receptor CD70 is transiently expressed on the surface of conventional dendritic cells, but is constitutively expressed by a unique APC population in the intestinal lamina propria. We used two experimental IBD models to evaluate whether interfering the interaction between CD70 and its T cell ligand CD27 would affect the development of colitis. Adoptive transfer of naive CD27-deficient CD45RBhigh CD4+ T cells into Rag-1−/− mice resulted in significantly less disease than when wild-type CD45RBhighCD4+ T cells were used. Moreover, a monoclonal anti-CD70 Ab prevented the disease caused by the transfer of wild-type CD45RBhigh CD4+ T cells into Rag-1−/− mice and the same Ab also ameliorated an established disease. The colitis associated proinflammatory cytokines IL-6, TNF-α and IFN-γ were significantly reduced after anti-CD70 Ab treatment, suggesting an overall reduction in inflammation due to blockade of pathogenic T cell expansion. Anti-CD70 Ab treatment also suppressed trinitrobenzene sulfonic acid-induced colitis in SJL/J mice. Because anti-CD70 Ab treatment suppressed multiple proinflammatory cytokines, this may be a more potent therapeutic approach for IBD than blockade of individual cytokines.
Cholinergic Neural Signals to the Spleen Down-Regulate Leukocyte Trafficking via CD11b
Authors: Huston Jared M. , Rosas-Ballina Mauricio , Xue Xiangying , Dowling Oonagh , Ochani Kanta , Ochani Mahendar , Yeboah Michael M. , Chatterjee Prodyot K. , Tracey Kevin J. , Metz Christine N. 
Published: June 2009

Abstract
The cholinergic anti-inflammatory pathway is a physiological mechanism that inhibits cytokine production and diminishes tissue injury during inflammation. Recent studies demonstrate that cholinergic signaling reduces adhesion molecule expression and chemokine production by endothelial cells and suppresses leukocyte migration during inflammation. It is unclear how vagus nerve stimulation regulates leukocyte trafficking because the vagus nerve does not innervate endothelial cells. Using mouse models of leukocyte trafficking, we show that the spleen, which is a major point of control for cholinergic modulation of cytokine production, is essential for vagus nerve-mediated regulation of neutrophil activation and migration. Administration of nicotine, a pharmacologic agonist of the cholinergic anti-inflammatory pathway, significantly reduces levels of CD11b, a β2-integrin involved in cell adhesion and leukocyte chemotaxis, on the surface of neutrophils in a dose-dependent manner and this function requires the spleen. Similarly, vagus nerve stimulation significantly attenuates neutrophil surface CD11b levels only in the presence of an intact and innervated spleen. Further mechanistic studies reveal that nicotine suppresses F-actin polymerization, the rate-limiting step for CD11b surface expression. These studies demonstrate that modulation of leukocyte trafficking via cholinergic signaling to the spleen is a specific, centralized neural pathway positioned to suppress the excessive accumulation of neutrophils at inflammatory sites. Activating this mechanism may have important therapeutic potential for preventing tissue injury during inflammation.
Increased Intracellular, Cell Surface, and Secreted Inducible Heat Shock Protein 70 Responses Are Triggered during the Monocyte to Dendritic Cell (DC) Transition by Cytokines Independently of Heat Stress and Infection and May Positively Regulate DC Growth
Authors: Martin Carla A. , Kurkowski Danielle L. , Valentino Alisa M. , Santiago-Schwarz Frances 
Published: June 2009

Abstract
Physiologic triggers and functional consequences of endogenous heat shock protein (HSP) responses in dendritic cells (DC) are poorly defined. In this study, we show that even in the absence of heat stress and infection, a specific cohort of DC/proinflammatory cytokines (IL-4-IL-13/IL-6/GM-CSF) institutes an enhanced inducible (i)HSP70 intracellular and extracellular response in human monocyte-derived DC, especially during the monocyte to DC transition. Interestingly, whereas heat stress alone initiated an intracellular iHSP70 response in monocyte DC precursors, it did not promote cell surface or secreted iHSP70 responses, both of which were induced by cytokines independently of heat. The cytokine-induced iHSP70 response, which did not occur in lymphocytes, or monocytes-macrophages generated with M-CSF, was instituted within 48 h of cytokine exposure, and peaked upon commitment to DC growth at 72 h. Although a return to baseline levels was noted after this period, a distinct rise in iHSP70 occurred again during terminal DC maturation. Chemical inhibition of the iHSP70 response with either triptolide or KNK-437 was coupled with inhibition of DC differentiation and yielded cells displaying features of monocytes-macrophages. Exogenously supplied riHSP70 amplified events associated with cytokine-advanced DC differentiation/maturation, most notably the up-regulation of antiapoptotic proteins (Bcl-xL). Engaging the HSP receptor CD40 with CD40L produced identical results as extracellular riHSP70, and, moreover, an enhanced iHSP70 response. Thus, distinct iHSP70 and HSP receptor-mediated responses are triggered by cytokines irrespective of heat stress and infection in monocyte-derived DC and may function to positively regulate monocyte-derived DC, especially during critical periods of their growth.
IFN-γ Attenuates Antigen-Induced Overall Immune Response in the Airway As a Th1-Type Immune Regulatory Cytokine
Authors: Nakagome Kazuyuki , Okunishi Katsuhide , Imamura Mitsuru , Harada Hiroaki , Matsumoto Taku , Tanaka Ryoichi , Miyazaki Jun-ichi , Yamamoto Kazuhiko , Dohi Makoto 
Published: June 2009

AbstractAllergic inflammation in the airway is generally considered a Th2-type immune response. However, recent studies demonstrated that Th1- and Th17-type immune responses also play important roles in this process. IFN-γ is a Th1-type cytokine that generally counteracts the Th2 response. Although previous studies suggest that exogenous IFN-γ suppresses allergic airway inflammation, the mechanism of suppression has not been fully clarified. In this study, we elucidated whether IFN-γ suppresses Ag-induced immune responses including the production of Th1- and Th17-type cytokines in the lung, and examined its mechanism of action. BALB/c mice were sensitized and challenged with OVA-Ag to induce airway inflammation. An IFN-γ-producing plasmid vector was delivered before systemic Ag sensitization. IFN-γ suppressed indicators of Th2-type immune responses such as airway eosinophilia, IL-5 and IL-13 production in the lung, and bronchial mucus production. Moreover, IFN-γ also suppressed the production of IL-17 and IFN-γ itself. The suppression was not mediated by inducing regulatory T cells or by inducing apoptosis in immunocytes. Instead, IFN-γ suppressed the Ag-presenting capacity and cytokine production of splenic dendritic cells and thus subsequently suppressed OVA-induced activation of CD4+ T cells. Furthermore, IFN-γ also attenuated allergic airway inflammation when delivered during the OVA challenge. Various functions of lung CD11c+ APCs and their migration to regional lymph nodes were also suppressed. These results suggest that the Th1 cytokine IFN-γ has broad immune regulatory potential through suppressing APC functions. They also suggest that delivery of IFN-γ could be an effective strategy for regulating Ag-induced immune responses in the lung.
Notch Ligands Expressed by Follicular Dendritic Cells Protect Germinal Center B Cells from Apoptosis
Authors: Yoon Sun-Ok , Zhang Xin , Berner Paul , Blom Bianca , Choi Yong Sung 
Published: June 2009

Abstract
The Notch signaling pathway is one of the most conserved mechanisms to regulate cell fate in many tissues during development and postnatal life. In the immune system, Notch signaling regulates T and B cell development and modulates the differentiation of T and B cells. In this study, we investigated the functional roles of Notch signaling in human B cell differentiation within the germinal center (GC). Notch ligands, Delta-like 1 (Dll1) and Jagged 1 (Jg1), are expressed by follicular dendritic cells (FDC) but not by B cells in the GC, while GC-B cells express the Notch receptors, Notch1 and Notch2. The blockade of Notch signaling pathways using a γ-secretase inhibitor, DAPT (N-[N-(3,5-difluorophenacetyl-l-alanyl)]-S-phenylglycine t-butyl ester), reduces the survival of GC-B cells in the presence of FDC/HK cells. Jg1 has a dominant effect on GC-B cell survival mediated by Notch signaling. Furthermore, Notch cooperates with another anti-apoptotic factor, BAFF/Blys produced by FDC to support GC-B cell growth. Taken together, our data shows the important role of Notch signaling provided by FDC in the survival of GC-B cells in vitro.