bluuebunny/crossref_metadata_2025_split huggingface dataset:
L'extrême gauche française et l'écologie
Authors: Buton Philippe 
Published: January 2012

Résumé Lors de la décennie qui a suivi Mai 68, l’attitude des organisations de l’extrême gauche française envers l’écologie permet de distinguer trois groupes. En premier lieu, ceux qui s’ouvrent précocement à la préoccupation écologiste. Ces pionniers sont le parti socialiste unifié, la sensibilité maoïste dite spontanéiste (Vive la Révolution et la Gauche prolétarienne), et un petit groupe trotskyste (l’Alliance marxiste révolutionnaire). À ce premier groupe s’oppose le deuxième, celui des suivistes, essentiellement composé des principales organisations trotskystes (Ligue communiste, Lutte ouvrière) et anarchistes. Le troisième groupe, celui des réfractaires, rassemble la quasi-totalité des maoïstes et quelques organisations trotskystes (Organisation communiste internationaliste) ou anarchistes (Guerre de classes). Le croisement de trois paramètres permet de comprendre cette typologie : le rapport à la notion de modernité, la relation au marxisme et la notion d’optimisme révolutionnaire.
In Vitro Analysis of Nd:YAG Laser Damage to Hydrophilic Intraocular Lenses
Authors: Saffra Norman , Agarwal Swati , Enin Josh , Werner Liliana , Mamalis Nick 
Published: January 2012

BACKGROUND AND OBJECTIVE:
Damaged optics of an intraocular lens (IOL) can impair visual functioning. Damage can occur during the manufacturing process, during implantation, or during post-implantation Nd:YAG laser posterior capsulotomy. An in vitro experiment was performed to identify the potential IOL damage patterns associated with the use of the Nd:YAG laser for posterior capsulotomy.

PATIENTS AND METHODS:
A review of the literature regarding Nd:YAG laser damage to IOLs was performed. The objectives were to describe the damage patterns to a sample IOL by performing virtual posterior capsulotomies.

RESULTS:
Patterns of damage were demonstrated and described.

CONCLUSION:
Although optic damage can occur with use of the Nd:YAG laser, it is infrequent and usually the result of improper depth of focus.
A Novel C3 Mutation Causing Increased Formation of the C3 Convertase in Familial Atypical Hemolytic Uremic Syndrome
Authors: Sartz Lisa , Olin Anders I , Kristoffersson Ann-Charlotte , Ståhl Anne-lie , Johansson Martin E. , Westman Kerstin , Fremeaux-Bacchi Veronique , Nilsson-Ekdahl Kristina , Karpman Diana 
Published: January 2012

Abstract
Atypical hemolytic uremic syndrome has been associated with dysregulation of the alternative complement pathway. In this study, a novel heterozygous C3 mutation was identified in a factor B-binding region in exon 41, V1636A (4973 T &gt; C). The mutation was found in three family members affected with late-onset atypical hemolytic uremic syndrome and symptoms of glomerulonephritis. All three patients exhibited increased complement activation detected by decreased C3 levels and glomerular C3 deposits. Platelets from two of the patients had C3 and C9 deposits on the cell surface. Patient sera exhibited more C3 cleavage and higher levels of C3a. The C3 mutation resulted in increased C3 binding to factor B and increased net formation of the C3 convertase, even after decay induced by decay-accelerating factor and factor H, as assayed by surface plasmon resonance. Patient sera incubated with washed human platelets induced more C3 and C9 deposition on the cell surface in comparison with normal sera. More C3a was released into serum over time when washed platelets were exposed to patient sera. Results regarding C3 and C9 deposition on washed platelets were confirmed using purified patient C3 in C3-depleted serum. The results indicated enhanced convertase formation leading to increased complement activation on cell surfaces. Previously described C3 mutations showed loss of function with regard to C3 binding to complement regulators. To our knowledge, this study presents the first known C3 mutation inducing increased formation of the C3 convertase, thus explaining enhanced activation of the alternative pathway of complement.
CD69 Regulates Type I IFN-Induced Tolerogenic Signals to Mucosal CD4 T Cells That Attenuate Their Colitogenic Potential
Authors: Radulovic Katarina , Manta Calin , Rossini Valerio , Holzmann Karlheinz , Kestler Hans A. , Wegenka Ursula Maria , Nakayama Toshinori , Niess Jan Hendrik 
Published: January 2012

Abstract
CD69 is highly expressed by lymphocytes at mucosal surfaces. We aimed to investigate the role of CD69 in mucosal immune responses. The expression of CD69 by CD4 T cells isolated from the spleen, mesenteric lymph nodes, small intestinal lamina propria, and colonic lamina propria was determined in specific pathogen-free B6 and TCR transgenic animals, as well as in germ-free B6 mice. Transfer colitis was induced by transplanting RAG−/− mice with B6 or CD69−/−CD45RBhigh CD4 T cells. CD69 expression by CD4 T cells is induced by the intestinal microflora, oral delivery of specific Ag, and type I IFN (IFN-I) signals. CD4 T cells from CD69−/− animals produce higher amounts of the proinflammatory cytokines IFN-γ, TNF-α, and IL-21, whereas the production of TGF-β1 is decreased. CD69-deficient CD4 T cells showed reduced potential to differentiate into Foxp3+ regulatory T cells in vivo and in vitro. The transfer of CD69−/−CD45RBhigh CD4 T cells into RAG−/− hosts induced an accelerated colitis. Oral tolerance was impaired in CD69−/− and IFN-I receptor 1-deficient mice when compared with B6 and OT-II × RAG−/− animals. Polyinosinic-polycytidylic acid treatment of RAG−/− mice transplanted with B6 but not CD69−/− or IFN-I receptor 1-deficient CD45RBhigh CD4 T cells attenuated transfer colitis. CD69 deficiency led to the increased production of proinflammatory cytokines, reduced Foxp3+ regulatory T cell induction, impaired oral tolerance, and more severe colitis. Hence, the activation Ag CD69 plays an important role in regulating mucosal immune responses.
Membrane-Tethered MUC1 Mucin Is Phosphorylated by Epidermal Growth Factor Receptor in Airway Epithelial Cells and Associates with TLR5 To Inhibit Recruitment of MyD88
Authors: Kato Kosuke , Lillehoj Erik P. , Park Yong Sung , Umehara Tsuyoshi , Hoffman Nicholas E. , Madesh Muniswamy , Kim K. Chul 
Published: January 2012

Abstract
MUC1 is a membrane-tethered mucin glycoprotein expressed on the apical surface of mucosal epithelial cells. Previous in vivo and in vitro studies established that MUC1 counterregulates airway inflammation by suppressing TLR signaling. In this article, we elucidate the mechanism by which MUC1 inhibits TLR5 signaling. Overexpression of MUC1 in HEK293 cells dramatically reduced Pseudomonas aeruginosa-stimulated IL-8 expression and decreased the activation of NF-κB and MAPK compared with cells not expressing MUC1. However, overexpression of MUC1 in HEK293 cells did not affect NF-κB or MAPK activation in response to TNF-α. Overexpression of MyD88 abrogated the ability of MUC1 to inhibit NF-κB activation, and MUC1 overexpression inhibited flagellin-induced association of TLR5/MyD88 compared with controls. The MUC1 cytoplasmic tail associated with TLR5 in all cells tested, including HEK293T cells, human lung adenocarcinoma cell line A549 cells, and human and mouse primary airway epithelial cells. Activation of epidermal growth factor receptor tyrosine kinase with TGF-α induced phosphorylation of the MUC1 cytoplasmic tail at the Y46EKV sequence and increased association of MUC1/TLR5. Finally, in vivo experiments demonstrated increased immunofluorescence colocalization of Muc1/TLR5 and Muc1/phosphotyrosine staining patterns in mouse airway epithelium and increased Muc1 tyrosine phosphorylation in mouse lung homogenates following P. aeruginosa infection. In conclusion, epidermal growth factor receptor tyrosine phosphorylates MUC1, leading to an increase in its association with TLR5, thereby competitively and reversibly inhibiting recruitment of MyD88 to TLR5 and downstream signaling events. This unique ability of MUC1 to control TLR5 signaling suggests its potential role in the pathogenesis of chronic inflammatory lung diseases.
Activation of the NLRP3 Inflammasome by Group B Streptococci
Authors: Costa Alessandro , Gupta Rahul , Signorino Giacomo , Malara Antonio , Cardile Francesco , Biondo Carmelo , Midiri Angelina , Galbo Roberta , Trieu-Cuot Patrick , Papasergi Salvatore , Teti Giuseppe , Henneke Philipp , Mancuso Giuseppe , Golenbock Douglas T. , Beninati Concetta 
Published: January 2012

Abstract
Group B Streptococcus (GBS) is a frequent agent of life-threatening sepsis and meningitis in neonates and adults with predisposing conditions. We tested the hypothesis that activation of the inflammasome, an inflammatory signaling complex, is involved in host defenses against this pathogen. We show in this study that murine bone marrow-derived conventional dendritic cells responded to GBS by secreting IL-1β and IL-18. IL-1β release required both pro–IL-1β transcription and caspase-1–dependent proteolytic cleavage of intracellular pro–IL-1β. Dendritic cells lacking the TLR adaptor MyD88, but not those lacking TLR2, were unable to produce pro–IL-1β mRNA in response to GBS. Pro–IL-1β cleavage and secretion of the mature IL-1β form depended on the NOD-like receptor family, pyrin domain containing 3 (NLRP3) sensor and the apoptosis-associated speck-like protein containing a caspase activation and recruitment domain adaptor. Moreover, activation of the NLRP3 inflammasome required GBS expression of β-hemolysin, an important virulence factor. We further found that mice lacking NLRP3, apoptosis-associated speck-like protein, or caspase-1 were considerably more susceptible to infection than wild-type mice. Our data link the production of a major virulence factor by GBS with the activation of a highly effective anti-GBS response triggered by the NLRP3 inflammasome.
Cutting Edge: IL-21 Derived from Human Follicular Helper T Cells Acts as a Survival Factor for Secondary Lymphoid Organ, but Not for Bone Marrow, Plasma Cells
Authors: Rodríguez-Bayona Beatriz , Ramos-Amaya Ana , Bernal Jesús , Campos-Caro Antonio , Brieva José A. 
Published: January 2012

Abstract
IL-21 induces the differentiation of activated B lymphocytes into plasma cells (PC), but its direct effect on PC remains uncertain. This study analyzes the role of IL-21 on human in vivo-generated PC. IL-21R was clearly expressed on PC from the human tonsil, the lymph node, and the spleen (secondary lymphoid organs [SLO]) but barely on terminally mature bone marrow PC. IL-21 enhanced Ig secretion by isolated SLO PC but not bone marrow PC. Tonsillar T follicular helper (Tfh) lymphocytes are known to secrete IL-21. Purified Tfh cells induced a marked increase of Ig production by tonsillar PC, and this effect was impaired when endogenous IL-21 production was blocked. IL-21 provoked a rapid and transient phosphorylation of STAT3 in tonsillar PC. Tfh cells or exogenous IL-21 reduce tonsillar PC apoptosis and increases PC recovery but does not modify their nonproliferating status. These results suggest that IL-21 derived from Tfh cells acts as a survival factor for SLO PC in vivo.
PSGL-1 Regulates the Migration and Proliferation of CD8+ T Cells under Homeostatic Conditions
Authors: Veerman Krystle M. , Carlow Douglas A. , Shanina Iryna , Priatel John J. , Horwitz Marc S. , Ziltener Hermann J. 
Published: January 2012

Abstract
P-selectin glycoprotein ligand-1 (PSGL-1), a heavily glycosylated sialomucin expressed on most leukocytes, has dual function as a selectin ligand for leukocyte rolling on vascular selectins expressed in inflammation and as a facilitator of resting T cell homing into lymphoid organs. In this article, we document disturbances in T cell homeostasis present in PSGL-1null mice. Naive CD4+ and CD8+ T cell frequencies were profoundly reduced in blood, whereas T cell numbers in lymph nodes and spleen were at or near normal levels. Although PSGL-1null T cells were less efficient at entering lymph nodes, they also remained in lymph nodes longer than PSGL-1+/+ T cells, suggesting that PSGL-1 supports T cell egress. In addition, PSGL-1null CD8+ T cell proliferation was observed under steady-state conditions and PSGL-1null CD8+ T cells were found to be hyperresponsive to homeostatic cytokines IL-2, IL-4, and IL-15. Despite these disturbances in T cell homeostasis, PSGL-1null mice exhibited a normal acute response (day 8) to lymphocytic choriomeningitis virus infection but generated an increased frequency of memory T cells (day 40). Our observations demonstrate a novel pleiotropic influence of PSGL-1 deficiency on several aspects of T cell homeostasis that would not have been anticipated based on the mild phenotype of PSGL-1null mice. These potentially offsetting effects presumably account for the near-normal cellularity seen in lymph nodes of PSGL-1null mice.
Role of nitrosative and oxidative stress in neuropathy in patients with type 2 diabetes mellitus
Authors: Al-Nimer Marwan S , Al-Ani Fakhir S , Ali Fatima S 
Published: January 2012

ABSTRACT
Objectives : Evidences of oxidative and/or nitrosative stress in type 2 diabetes mellitus were demonstrated in experimental and human studies. This study is aimed to assess the serum peroxynitrite and oxidized lipoproteins in patients with type 2 diabetes mellitus presented with clinical and laboratory evidences of peripheral neuropathy. Materials and Methods : Eighty four patients with type 2 diabetes mellitus (51 of them had neuropathy) and 31 apparent healthy subjects were studied in the unit of neurophysiology at the University Hospital of Medical College, Al-Nahrin University in Baghdad, Iraq. Neuropathy total symptom score (NTSS), neuropathy impairment score in the lower leg (NIS-LL), and nerve conduction velocity of sensory (ulnar and sural) and motor (ulnar and common peroneal) nerves were used to assess the neuropathy. Fasting venous blood was obtained from each participant for the determination of serum glucose and oxidized lipoproteins. Results: The electrophysiology study revealed significant decrease in conduction velocity of ulnar (sensory and motor components), sural, and common peroneal nerves in diabetic neuropathy compared to diabetics without neuropathy and healthy subjects. Significant high level of serum peroxynitrite was found in diabetic patients with or without neuropathy compared with non-diabetics. The changes in serum-oxidized lipoproteins in patients with diabetics with or without neuropathy were non-significantly differed from healthy subjects. Neither nitrosative stress nor oxidative stress indices correlated with the variables that are related to the neuropathy. Conclusion: It concludes that evidence of nitrosative and to less extent the oxidative stress is associated with neuropathy in type 2 diabetes mellitus and their indices not correlated with variables related to neuropathy.
More Precise Diagnosis of Access Stenosis: Ultrasonography versus Angiography
Authors: Kudlicka Jaroslav , Kavan Jan , Tuka Vladimir , Malik Jan 
Published: January 2012

Purpose Patency of mature vascular access for hemodialysis is mostly limited by the growing stenoses leading to acute access thrombosis. The therapy of choice is usually percutaneous balloon angioplasty (PTA). However, PTA injures the vessel wall and subsequent re-stenosis develops faster than de novo stenosis. Therefore, the key is in appropriate timing of PTA procedures – as late as possible but before access thrombosis develops. Ultrasonography combines the morphologic and functional access assessment, but the former is less precise than angiography. The aim of this study was to compare ultrasonographic and angiographic measuring of residual diameter as the additional criterion of significant stenoses used in our center. Methods Residual diameter of significant stenoses was measured by B-mode ultrasonography three times in 20 patients. All the patients were indicated for angiography and the residual diameter of the stenoses was re-analyzed by this method. The repeatability of ultrasonographic residual diameter measurements and reproducibility in comparison to angiography were expressed by coefficients of variation (CV). Results The residual diameter was 1.69 ± 0.05 mm by ultrasound and 1.65 ± 0.59 mm measured by angiography. In the ultrasound repeatability study, CV was 3.17 ± 2.76% and in the reproducibility study CV was 18.0 ± 15.6%. All the stenoses found to be significant by ultrasound were above 65% by angiography and PTA was performed. Conclusions Ultrasonographic measurement of the residual diameter is stable in experienced hands and is well comparable to angiography results. These findings advocate residual diameter of 2.0 mm as the strong additional criterion of the significant stenoses, which can also be used in ultrasound surveillance of arteriovenous grafts.
The Importance of Bridging Points for Charge Transport in Webs of Conjugated Polymer Nanofibers
Authors: Bolsée Jean‐Christophe , Oosterbaan Wibren D. , Lutsen Laurence , Vanderzande Dirk , Manca Jean 
Published: January 2012

AbstractElectrical characterizations on webs of highly ordered semiconducting polymer nanofibers (NFs) are often performed with large electrodes devices (millimeter scale) for which the carrier transport is an average between transport within isolated NFs and transport at the intersection of two or more NFs. In order to assess the nanoscale electrical properties of the NFs, a field‐effect transistor based on conductive atomic force microscopy is introduced that allows the visualization of the current distribution at the nanometer scale within a web of poly(3‐butylthiophene) NFs. The contact resistance is evaluated to be ≈4 kΩ cm, which does not limit the charge transport process, and the mobility in one single NF is μNF = 0.07 ± 0.03 cm2 V−1 s−1. One NF can carry a current density of 20 kA cm−2 without being destroyed. Moreover, by observing the current maps in detail, it is found that the electrical resistance associated with the bridging of two or more individual NFs does not reduce the charge transport inside the web of NFs. Finally, different kinds of bridging geometries are shown and the role of tie molecules is discussed.
The role of immune tolerance induction in restoration of the efficacy of ERT in Pompe disease
Authors: Lacaná Emanuela , Yao Lynne P. , Pariser Anne R. , Rosenberg Amy S. 
Published: January 2012

AbstractPompe disease is a lysosomal storage disorder caused by deficiency in the enzyme acid α‐glucosidase (GAA). Pompe disease is characterized by the accumulation of glycogen, predominantly in muscle tissue, leading to progressive muscle weakness, loss of motor, respiratory, and, in the infantile‐onset form, cardiac function. Disease progression is highly variable depending on phenotype, but premature death due to respiratory complications occurs in most patients. Beginning in 2006, approved alglucosidase alfa enzyme replacement therapies [recombinant human (rh) GAA] have been available to treat Pompe patients. Treatment of classic infantile‐onset patients, who manifest the severest form of the disease, with alglucosidase alfa (Myozyme®) has led to extended survival and an evolving understanding of the pathophysiology and course of the disease. Moreover, such treatment has brought to light the role of the immune response in abrogating the efficacy of rhGAA in classic infantile‐onset patients with severe genetic mutations. Thus, optimization of treatment for such patients includes development and utilization of strategies to prevent or eliminate immune responses, including modulating the immune system (prophylactic and therapeutic immune tolerance induction regimens) and engineering the enzyme to be less immunogenic and more effective. Future research is also critical for evaluating and mitigating novel disease‐associated pathologies uncovered by prolonged survival of infantile‐onset patients including development of novel therapeutics, and for protein design strategies to increase delivery of enzyme replacement therapy to critical target tissues. Such efforts would be greatly bolstered by further development of predictive animal models and biomarkers to facilitate clinical trials and patient management. Published 2012. This article is a U.S. Government work and is in the public domain in the USA.
Cognitive and adaptive functioning of children with infantile Pompe disease treated with enzyme replacement therapy: Long‐term follow‐up
Authors: Spiridigliozzi Gail A. , Heller James H. , Kishnani Priya S. 
Published: January 2012

AbstractThis report documents the long‐term cognitive and adaptive outcome of children with infantile Pompe disease. Specifically, we describe the cognitive and adaptive functioning of seven children with classic infantile Pompe disease and two children with atypical infantile Pompe disease who have received enzyme replacement therapy (Myozyme®) for an average of 6 years, 8 months and 4 years, 1. 5 months, respectively. Multiple assessments of cognitive functioning were completed over time by means of individualized intelligence (IQ) testing. Adaptive functioning was measured by means of the Vineland Adaptive Behavior Scales‐Second Edition (VABS‐II). Consistent with our earlier findings regarding infants treated with ERT, children with classic infantile Pompe disease (ages 4 years, 11 months to 8 years, 11 months) were functioning at the lower end of the average range in comparison to their typical peers on their most recent IQ test. There was no evidence of a decline in their cognitive abilities over time. In contrast, the two children with atypical infantile Pompe disease (ages 5 years, 4 months and 5 years, 11 months) obtained above average IQ scores and demonstrated significant gains in IQ over time. For all children where adaptive functioning was assessed, their overall level of adaptive functioning on the VABS‐II was lower than their Full Scale IQ scores on cognitive testing. Motor function appears to be an important factor impacting on reduced adaptive behavior. The implication of these findings on our understanding of a possible relationship between CNS status in children with Pompe and their adaptive and cognitive function is discussed. © 2012 Wiley Periodicals, Inc.
Intranasal drug‐induced fungal rhinopharyngitis
Authors: Houlton Jeffrey J. , Donaldson Angela M. , Zimmer Lee , Seiden Allen 
Published: January 2012

AbstractBackground:Intranasal drug abuse has long been recognized as an etiology of sinonasal pathology. However, the intranasal use of prescription and nonprescription drugs has surpassed the use of illicit drugs, and the pattern of presentation and required therapeutic intervention appears to be different. We report on our experience with these patients, along with a successful treatment algorithm for this disease process.Methods:Retrospective chart review of 9 consecutive patients who presented with rhinopharyngitis and a history of intranasal opioid and/or acetaminophen abuse, from 2007 to 2010, at a tertiary referral center.Results:Nine patients were found to have abused intranasal hydrocodone/acetaminophen, oxycodone/aceta‐minophen, or acetaminophen and were diagnosed with rhinopharyngitis. Sinonasal pain and odynophagia were the most common chief complaints and 8 of 9 patients reported previous antibiotic failures. On endoscopy, all patients exhibited a thick, white, exudative process involving the nasal septum and lateral nasal mucosa. Five of 9 exhibited large septal perforations. Seven of 9 exhibited white, exudative pharyngitis. Seven of 9 patients had identifiable fungal organisms on culture, including 5 with species of Candida and 3 with Aspergillus. Two patients grew Staphylococcus aureus. Five patients were compliant with follow up. All 5 showed significant improvement in symptoms and examination, following treatment with oral and topical antifungal therapy and nasal irrigations.Conclusion:Intranasal opioid and acetaminophen abuse is often associated with the development of fungal rhinopharyngitis. Recognizing that this process is primarily fungal in origin is paramount to successful treatment, as most patients respond well to antifungal therapy when compliant with treatment. © 2012 ARS‐AAOA, LLC.