bluuebunny/crossref_metadata_2025_split huggingface dataset:
Assessment of Tryptophol Genotoxicity in Four Cell Lines In Vitro: A Pilot Study with Alkaline Comet Assay
Authors: Kosalec Ivan , Ramić Snježana , Jelić Dubravko , Antolović Roberto , Pepeljnjak Stjepan , Kopjar Nevenka 
Published: March 2011

Assessment of Tryptophol Genotoxicity in Four Cell LinesIn Vitro: A Pilot Study with Alkaline Comet AssayTryptophol is an aromatic alcohol and secondary metabolite of the opportunistic fungusCandida albicans. Although its toxicity profile at cell level has been poorly investigated, recent data point to cytotoxic, cytostatic, and genotoxic effects in lymphocytes and the induction of apoptosis in leukaemic blood monocytes. In this pilot study we evaluated the genotoxicity of tryptopholin vitroon four permanent cell lines of animal and human origin: ovary cells, alveolar epithelium, liver cells, and blood monocytes using the alkaline comet assay. We selected cells that might be principal targets of tryptophol and other low-molecular geno(toxins) secreted byCandida albicansduring host invasion. Our results suggest that tryptophol appliedin vitroat 2 mmol L-1for 24 h damages DNA in HepG2, A549 and THP-1 cells, obviously due to bioactivation and/or decomposition of the parent compound, which results in the formation of more genotoxic compound(s) and production of reactive species that additionally damage DNA. On the other hand, notably lower levels of primary DNA damage were recorded in CHO cells, which lack metabolic activity. Future studies with tryptophol should look further into mechanisms involved in its toxic action and should focus on other cell types prone to infection withCandidaspp. such as vaginal epithelial cells or keratinocytes of human origin.
Transnational Bio/Necropolitics: Hindutva and its Avatars (Australia/India)
Authors: Osuri Goldie 
Published: March 2011

In the US diasporic context, Kamat and Matthews (2003) have traced how Hindu nationalists draw on multiculturalist discourse for their presence while simultaneously funding cultural and political projects in India that incite hate and conduct violence against Muslim and Christian communities.In the Australian context, Hindu nationalist organisations have legitimised and consolidate themselves through the rhetoric of liberal multiculturalism. Such strategies which draw on state rhetoric of multiculturalism while simultaneously engaging in hate campaigns against Muslim and Christian others demonstrates Hindutva's ability to operate through a transnational necropolitics. This paper explores how a state biopolitics of multiculturalism enables the violence of Hindutva's necropolitics in the transnational routes between Australia and India.
Sismondi et la question du progrès
Authors: Gillard Lucien 
Published: March 2011

Résumé Contre les engouements nés de la révolution industrielle, Sismondi propose de raison garder. Il préconise d’analyser les effets produits par un choc technologique sur le fonctionnement d’un modèle de croissance équilibrée. Puis, d’analyser aussi comment se répartissent par classes sociales les bénéfices et inconvénients de l’industrialisation. Par-delà l’opposition traditionnelle entre richesse et bonheur, l’œuvre économique de Sismondi ouvre la voie à des recherches techniques sur les questions de « neutralité du progrès » et de « préférences collectives ».
Endogenous Opioid-Mediated Analgesia Is Dependent on Adaptive T Cell Response in Mice
Authors: Boué Jérôme , Blanpied Catherine , Brousset Pierre , Vergnolle Nathalie , Dietrich Gilles 
Published: March 2011

Abstract
Pain is an inherent component of inflammation often accompanying immune response. A large spectrum of molecules released within the inflamed tissue induces pain by stimulating primary afferent neurons in situ. Activity of primary sensitive fibers can be counteracted by local opioid release by leukocytes. In this study, we investigated the endogenous regulation of CFA-induced inflammatory pain in the context of adaptive T cell immune response. The nociceptive response to mechanical stimuli was studied using von Frey filaments in mice immunized with OVA in CFA. The nociceptive response of nude versus wild-type mice was dramatically increased, demonstrating T cell deficiency associated with increased pain sensitivity. Based on adoptive transfer experiments of OVA-specific CD4+ T lymphocytes into nude mice, we show that Ag-specific activated, but not resting T lymphocytes are responsible for the spontaneous relief of inflammation-induced pain following Ag challenge. The analgesia was dependent on opioid release by Ag-primed CD4+ T lymphocytes at the inflammatory site. Indeed, T cell-mediated analgesia was inhibited by local injection of an opioid receptor antagonist, unable to cross the blood-brain barrier. Notably, we found opioid precursor mRNA to be &gt;7-fold increased in Ag-specific activated CD4+ T lymphocytes, as compared with resting T lymphocytes in vivo. Taken together, our results show that CD4+ T lymphocytes acquire antinociceptive effector properties when specifically primed by Ag and point out analgesia as a property linked to the effector phase of adaptive T cell response.
Control of TNF-Induced Dendritic Cell Maturation by Hybrid-Type N-Glycans
Authors: Schlickeiser Stephan , Stanojlovic Svetlana , Appelt Christine , Vogt Katrin , Vogel Simone , Haase Stefanie , Ritter Thomas , Volk Hans-Dieter , Pleyer Uwe , Sawitzki Birgit 
Published: March 2011

Abstract
The activity of α-1,2-mannosidase I is required for the conversion of high-mannose to hybrid-type (ConA reactive) and complex-type N-glycans (Phaseolus vulgaris-leukoagglutinin [PHA-L] reactive) during posttranslational protein N-glycosylation. We recently demonstrated that α-1,2-mannosidase I mRNA decreases in graft-infiltrating CD11c+ dendritic cells (DCs) prior to allograft rejection. Although highly expressed in immature DCs, little is known about its role in DC functions. In this study, analysis of surface complex-type N-glycan expression by lectin staining revealed the existence of PHA-Llow and PHA-Lhigh subpopulations in murine splenic conventional DCs, as well as in bone marrow-derived DC (BMDCs), whereas plasmacytoid DCs are nearly exclusively PHA-Lhigh. Interestingly, all PHA-Lhigh DCs displayed a strongly reduced responsiveness to TNF-α–induced p38-MAPK activation compared with PHA-Llow DCs, indicating differences in PHA-L–binding capacities between DCs with different inflammatory properties. However, p38 phosphorylation levels were increased in BMDCs overexpressing α-1,2-mannosidase I mRNA. Moreover, hybrid-type, but not complex-type, N-glycans are required for TNF-α–induced p38-MAPK activation and subsequent phenotypic maturation of BMDCs (MHC-II, CD86, CCR7 upregulation). α-1,2-mannosidase I inhibitor-treated DCs displayed diminished transendothelial migration in response to CCL19, homing to regional lymph nodes, and priming of IFN-γ–producing T cells in vivo. In contrast, the activity of α-1,2-mannosidase I is dispensable for LPS-induced signaling, as well as the DCs’ general capability for phenotypic and functional maturation. Systemic application of an α-1,2-mannosidase I inhibitor was able to significantly prolong allograft survival in a murine high-responder corneal transplantation model, further highlighting the importance of N-glycan processing by α-1,2-mannosidase I for alloantigen presentation and T cell priming.
IL-6 Production Is Positively Regulated by Two Distinct Src Homology Domain 2-Containing Tyrosine Phosphatase-1 (SHP-1)–Dependent CCAAT/Enhancer-Binding Protein β and NF-κB Pathways and an SHP-1–Independent NF-κB Pathway in Lipopolysaccharide-Stimulated Bone Marrow-Derived Macrophages
Authors: Rego Dorothy , Kumar Ashok , Nilchi Ladan , Wright Kathryn , Huang Stephen , Kozlowski Maya 
Published: March 2011

Abstract
Comparison of the inflammatory cytokine profile in bone marrow-derived macrophages (BMDMs) from normal and Src homology domain 2-containing tyrosine phosphatase-1 (SHP-1)–deficient Motheaten (me/me) mice revealed a dramatic suppression of IL-6 transcript and protein in me/me BMDMs after LPS stimulation. Interfering with SHP-1 expression using antisense SHP-1 oligonucleotides led to a significant downregulation of IL-6 in normal BMDMs. Conversely, reconstitution of me/me BMDMs with the SHP-1 gene using adenoviral vectors restored IL-6 production. Expression of only SHP-1 Src homology region 2 domains in normal BMDMs inhibited IL-6 production, confirming that IL-6 regulation depends on SHP-1 phosphatase activity. We further demonstrated that loss of SHP-1 function affects proper phosphorylation of Erk1/2 MAPKs and, to a lesser degree, of NF-κB downstream of TLR4 in BMDMs. Inefficient phosphorylation of Erk1/2 MAPKs abrogated the activation of C/EBPβ transcription factor, which was reversed on restoration of SHP-1 function and led to a concomitant enhancement of IL-6 production. We demonstrate that IL-6 production is regulated by a complex network of signaling pathways that include SHP-1–dependent activation of Erk1/2–C/EBPβ and NF-κB, in addition to SHP-1–independent IκB pathway through the activation of protein tyrosine kinases downstream of TLR4. Taken together, these results revealed for the first time, to our knowledge, a positive and critical role of SHP-1 in IL-6 regulation and dependence of Erk1/2–C/EBPβ pathway in addition to that of IκB on SHP-1 activity required for IL-6 induction after LPS stimulation.
Use of Ultrasound Biomicroscopy to Predict Long-Term Outcome of Sub-Tenon Needle Revision of Failed Trabeculectomy Blebs: A Pilot Study
Authors: Kaushik Sushmita , Tiwari Anamika , Singh Pandav Surinder , Ichhpujani Parul , Gupta Amod 
Published: March 2011

Purpose. To evaluate the role of ultrasound biomicroscopy (UBM) in predicting the long-term outcome of sub-Tenon needling revision of failed trabeculectomy blebs. Methods. Adult patients with a failed trabeculectomy bleb and unsatisfactory intraocular pressure (IOP) control were recruited. The aqueous flow under the partial thickness scleral flap was looked for and the blebs classified on UBM as scleral route patent (SRP) or scleral route occluded (SRO). All blebs underwent needling revision with injection of 5 mg/0.1 mL 5-fluorouracil. Survival of the revision procedure at the end of 2 years follow-up with regards to the baseline UBM characterization of the bleb was noted. Successful outcome was defined as IOP <22.0 mmHg and/or 30% reduction of baseline IOP with or without medication. Results. A total of 13 eyes had SRP and 5 eyes had SRO blebs on UBM. Only SRP blebs survived the needling procedure by the end of 2 years. Of the 13 SRP blebs, 10 blebs survived (76.9%). Needling had failed in all 5 SRO blebs. The overall success rate was 55.6 % at 2 years. There was no difference in age, IOP, and time from initial trabeculectomy between the failed and successful group. The outcome correlated significantly to the patency of the scleral route assessed by UBM (p=0.07). Conclusions. Ultrasound biomicroscopy characterization of failed blebs appears to help in predicting the outcome of needle revision. In SRO blebs, it may be better to plan a full bleb revision rather than needling alone. Ultrasound biomicroscopy may help in avoiding an unnecessary needling procedure in SRO blebs where it is likely to fail.
Prothrombotic Changes in Platelet, Endothelial and Coagulation Function following Hemodialysis
Authors: Milburn James A. , Cassar Kevin , Ford Isobel , Fluck Nicholas , Brittenden Julie 
Published: March 2011

Purpose Patients on hemodialysis (HD) have an increased risk of thrombotic events, including myocardial infarction and vascular access thrombosis. The study hypothesis is that a single session of dialysis leads to platelet, endothelial & coagulation activation. Our aim is to determine the effect of a single HD session on prothrombotic vascular biomarkers before and after a single session of hemodialysis. Methods Blood samples were taken from the vascular access of 55 patients immediately before and after a hemodialysis session. Platelet function was assessed by (1) flow cytometric measurement of P-selectin expression and fibrinogen binding ± ADP stimulation, (2) Ultegra rapid platelet function assay (RPFA) using the agonists thrombin receptor activating peptide (TRAP) and arachidonic acid (AA), (3) soluble P-selectin, and (4) soluble CD40L. Coagulation (thrombin-antithrombin III [TAT] and D-dimer), endothelial von Willebrand factor (vWF) and high sensitivity C-Reactive protein (hsCRP) were assessed by ELISA. Results Unfractionated heparin was given to all patients during dialysis and 30 patients (55%) were on antiplatelet agents. Post-hemodialysis there were significant increases in unstimulated platelet P-selectin (p=.037), stimulated P-selectin (p<.001), soluble P-selectin (p<.001) and soluble CD40L (p=.036). Stimulated platelet fibrinogen binding was increased post-hemodialysis (p<.001) but unstimulated fibrinogen binding was unchanged. TRAP- (p<.001) and AA-(p=.009) stimulated aggregation were reduced post-hemodialysis. There were increases post-hemodialysis in TAT (p<.001), D-dimer (p<.001), vWF (p<.001) and hsCRP (p=.011). Conclusion This study has shown that despite heparin therapy, a single session of HD induced increases in platelet, endothelial, and coagulation activation. More effective medical strategies to reduce the prothrombotic state of patients on hemodialysis should be investigated.
Effect of Coupled Plasma Filtration Adsorption on Endothelial Cell Function in Patients with Multiple Organ Dysfunction Syndrome
Authors: Mao Huijuan , Yu Shu , Yu Xiangbao , Zhang Bo , Zhang Li , Hu Jianming , Xu Xianrong , Zhu Yamei , Wang Xiaoyun , Xing Changying 
Published: March 2011

Objective The purpose of our study was to investigate the effect of coupled plasma filtration adsorption (CPFA) on endothelial cell (EC) function in patients with multiple organ dysfunction syndrome (MODS). Methods Besides routine therapy, the 24 MODS patients underwent both CPFA and high volume hemofiltration (HVHF), scheduled randomly at intervals of 12 hours. Patient serum from 0, 5, and 10 hours of therapy was collected to measure soluble E-selectin (sE-selectin) and soluble thrombomodulin (sTM) by the ELISA method. Human umbilical vein endothelial cells (HUVEC) were incubated for 24 hours with the patient serum and the supernatant liquid was gathered to detect sTM and sE-selectin. The proliferation function of the ECs was detected by methyl thiazolyl tetrazolium (MTT) method. Results 1. The serum levels of sE-selectin and sTM were significantly higher in MODS patients than in controls; serum sE-selectin and sTM decreased remarkably after a single circulation in CPFA (p<0. 05) but not in HVHF (p>0. 05); the level of sE-selectin and sTM in systemic circulation had no change during CPFA or HVHF (p>0.05); 2. sTM in supernatant liquid incubated with serum from 5 hours of CPFA and 10 hours of HVHF decreased remarkably (p<0.05), while sE-selectin decreased significantly (p<0. 05) from 10 hours of CPFA, but there was no change from 5 hours and 10 hours of HVHF (p>0. 05); 3. when incubated with serum taken from the device pre- or post-CPFA, the optical density (OD) value of the latter was higher. The OD value increased gradually when incubated with serum from 0, 5, and 10 hours of CPFA (p<0.05), but changed little from HVHF. Conclusions CPFA can eliminate sE-selectin and sTM and improve the secretion function of ECs. CPFA was somewhat better and earlier than HVHF, while to a certain degree it can weaken the inhibitory effect of serum on the proliferation function of ECs.
Nf1 mutant mice with p19ARF gene loss develop accelerated hematopoietic disease resembling acute leukemia with a variable phenotype
Authors: Wiesner Stephen M. , Geurts Jennifer L. , Diers Miechaleen D. , Bergerson Rachel J. , Hasz Diane E. , Morgan Kelly J. , Largaespada David A. 
Published: March 2011

AbstractJuvenile Myelomonocytic Leukemia (JMML) is a relentlessly progressive myeloproliferative/myelodysplastic (MPD/MDS) hematopoietic disorder more common in patients with any one of at least three distinct genetic lesions, specifically NF1 gene loss and PTPN11 and NRAS mutations. NF1 and PTPN11 are molecular lesions associated with Neurofibromatosis Syndrome Type I (NF1 Syndrome) and Noonan's Syndrome, respectively. The occurrence of JMML is rare; even among those predisposed with these syndromes to development of disease, and secondary genetic events likely contribute to the development and progression of disease. In NF1 syndrome, loss of p53 function is a common event in solid tumors, but uncommon in JMML, suggesting that the p53 pathway may be modified by other events in this hematopoietic disorder. The work presented here investigates the possible role of the p19Arf (p19) tumor suppressor in development of MPD associated with Nf1 gene loss in mice. We find that Nf1 mutant hematopoietic cells with loss of p19 develop accelerated hematopoietic disease similar to acute leukemia with a variable phenotype. This suggests that p19 may play a role in development of JMML and evaluation of the human p19 homolog (p14ARF) in JMML may be informative. Am. J. Hematol. 86:579–585, 2011. © 2011 Wiley‐Liss, Inc.
Mechanisms of fingolimod's efficacy and adverse effects in multiple sclerosis
Authors: Cohen Jeffrey A. , Chun Jerold 
Published: March 2011

AbstractUntil recently, all approved multiple sclerosis (MS) disease treatments were administered parenterally. Oral fingolimod was approved in September 2010 by the US Food and Drug Administration to reduce relapses and disability progression in relapsing forms of MS. In the clinical trials that led to approval, fingolimod reduced not only acute relapses and magnetic resonance imaging lesion activity but also disability progression and brain volume loss, suggesting preservation of tissue. Fingolimod's mechanism of action in MS is not known with certainty. Its active form, fingolimod‐phosphate (fingolimod‐P), is a sphingosine 1‐phosphate receptor (S1PR) modulator that inhibits egress of lymphocytes from lymph nodes and their recirculation, potentially reducing trafficking of pathogenic cells into the central nervous system (CNS). Fingolimod also readily penetrates the CNS, and fingolimod‐P formed in situ may have direct effects on neural cells. Fingolimod potently inhibits the MS animal model, experimental autoimmune encephalomyelitis, but is ineffective in mice with selective deficiency of the S1P1 S1PR subtype on astrocytes despite normal expression in the immune compartment. These findings suggest that S1PR modulation by fingolimod in both the immune system and CNS, producing a combination of beneficial anti‐inflammatory and possibly neuroprotective/reparative effects, may contribute to its efficacy in MS. In clinical trials, fingolimod was generally safe and well tolerated. Its interaction with S1PRs in a variety of tissues largely accounts for the reported adverse effects, which were seen more frequently with doses 2.5 to 10× the approved 0.5mg dose. Fingolimod's unique mechanism of action distinguishes it from all other currently approved MS therapies. Ann Neurol 2011;69:759–777
Synthesis and recognition of molecularly imprinted polymers for gastrodin based on surface‐modified silica nanoparticles
Authors: He Minqiang , Song Chengcheng , Yan Yongsheng , Chen Yongqiang , Wan Jincheng 
Published: March 2011

AbstractA molecular imprinting material with high performance for recognizing Gastrodin (GAS) was prepared by adopting the novel surface molecular imprinting technique. Silica nanoparticles were first modified with 3‐methacryloxypropyltrimethoxysilane (KH‐570) as a carrier material. Then, GAS surface molecule‐imprinted polymer (GAS‐SMIP) were prepared by polymerization with methacrylic acid as the functional monomer, ethylene glycol dimethacrylate as the crosslinker. The equilibrium adsorptive experiments indicated that GAS‐SMIP had significantly higher adsorption capacity for GAS than its nonimprinted polymers. Scatchard analysis revealed that two classes of binding sites were formed in GAS‐SMIP with dissociation constants of 1.019 and 7.278 μmol/mL, and the affinity binding sites of 17.82 and 83.11 μmol/g, respectively. The selectivity coefficient of GAS‐SMIP for GAS in respect to competition species obtained was 3.455, which revealed GAS‐SMIP had excellent selectivity and site accessibility for GAS. Kinetic binding study showed GAS‐SMIP adsorbed quickly in the first 40 min, and reached saturation adsorption at 1 h. © 2011 Wiley Periodicals, Inc. J Appl Polym Sci, 2011
Processing, tensile, and fracture properties of injection molded Hdpe‐Al2O3‐HAp hybrid composites
Authors: Basu Bikramjit , Jain Divya , Kumar Nitish , Choudhury Pritha , Bose Animesh , Bose Shree , Bose Pinaki 
Published: March 2011

AbstractThe aim of this study is to characterize the physical and mechanical properties of HDPE‐alumina‐HAp composites prepared by injection molding techniques and to demonstrate their superiority over unreinforced HDPE. Composites with up to 30 vol. % of filler, composed of equal volumes of HAp and alumina, were successfully processed by injection molding. On the basis of the analysis of processing results, i.e., melt viscosity, volume flow rate, shear rate, mixing torque, the critical ceramic loading was determined. Tensile tests done at varying crosshead speeds confirm that an increase in ceramic loading results in an increase in strength, as well as a simultaneous decrease in the total elongation at failure. A maximum strength of 20 MPa and a maximum tensile modulus of around 1 GPa was achieved with 30 vol % ceramic loading in semicrystalline HDPE matrix. SEVNB test results demonstrate an improvement in toughness at 20 vol %. The fracture properties are discussed in terms of interfacial bonding between ceramic fillers and the semicrystalline HDPE matrix. © 2011 Wiley Periodicals, Inc. J Appl Polym Sci, 2011
Making new out of old: Recycling and modification of an ancient protein translocation system during eukaryotic evolution
Authors: Bolte Kathrin , Gruenheit Nicole , Felsner Gregor , Sommer Maik S. , Maier Uwe‐G. , Hempel Franziska 
Published: March 2011

AbstractAt first glance the three eukaryotic protein translocation machineries – the ER‐associated degradation (ERAD) transport apparatus of the endoplasmic reticulum, the peroxisomal importomer and SELMA, the pre‐protein translocator of complex plastids – appear quite different. However, mechanistic comparisons and phylogenetic analyses presented here suggest that all three translocation machineries share a common ancestral origin, which highlights the recycling of pre‐existing components as an effective evolutionary driving force.Editor's suggested further reading in BioEssays ERAD ubiquitin ligases Abstract