bluuebunny/crossref_metadata_2025_split huggingface dataset:
Analysis of interpeak latencies of brainstem auditory evoked potential waveforms during microvascular decompression of cranial nerve VII for hemifacial spasm
Authors: Thirumala Parthasarathy D. , Ilangovan Preethi , Habeych Miguel , Crammond Donald J. , Balzer Jeffrey 
Published: March 2013

Object
Microvascular decompression (MVD) of the facial nerve is an effective treatment for patients with hemifacial spasm. Intraoperative monitoring of brainstem auditory evoked potentials (BAEPs) during MVD can reduce the incidence of hearing loss. In this study the authors' goal was to evaluate changes in interpeak latencies (IPLs) of Waves I–V, Waves III–V, and Waves I–III of BAEP Waveforms I, III, and V during MVD and correlate them with postoperative hearing loss. To date, no such study has been performed. Hearing loss is defined as nonuseful hearing (Class C/D), which is a pure tone average of more than 50 dB and/or speech discrimination score of less than 50%.

Methods
The authors performed a retrospective analysis of IPLs of BAEPs in 93 patients who underwent intraoperative BAEP monitoring during MVD. Patients who did not have hearing loss were in Class A/B and those who had hearing loss were in Class C/D.

Results
Binary logistic regression analysis of independent IPL variables was performed. A maximum change in IPLs of Waves I–III and Waves I–V and on-skin change in IPLs of Waves I–V increases the odds of hearing loss. However, on adjusting the same variables for loss of response, change in IPLs did not increase the odds of hearing loss.

Conclusions
Changes in IPL measurements did not increase the odds of postoperative hearing loss. This information might be helpful in evaluating the value of IPLs as alarm criteria during MVD to prevent hearing loss.
Cost Analysis of Hemodialysis and Peritoneal Dialysis Access in Incident Dialysis Patients
Authors: Coentrão Luis A. , Araújo Carla S. , Ribeiro Carlos A. , Dias Claúdia C. , Pestana Manuel J. 
Published: March 2013

Background Although several studies have demonstrated the economic advantages of peritoneal dialysis (PD) over hemodialysis (HD), few reports in the literature have compared the costs of HD and PD access. The aim of the present study was to compare the resources required to establish and maintain the dialysis access in patients who initiated HD with a tunneled cuffed catheter (TCC) or an arteriovenous fistula (AVF) and in patients who initiated PD. Methods We retrospectively analyzed the 152 chronic kidney disease patients who consecutively initiated dialysis treatment at our institution in 2008 (HD-AVF, n = 65; HD-CVC, n = 45; PD, n = 42). Detailed clinical and demographic information and data on access type were collected for all patients. A comprehensive measure of total dialysis access costs, including surgery, radiology, hospitalization for access complications, physician costs, and transportation costs was obtained at year 1 using an intention-to-treat approach. All resources used were valued using 2010 prices, and costs are reported in 2010 euros. Results Compared with the HD-AVF and HD-TCC modalities, PD was associated with a significantly lower risk of access-related interventions (adjusted rate ratios: 1.572 and 1.433 respectively; 95% confidence intervals: 1.253 to 1.891 and 1.069 to 1.797). The mean dialysis access–related costs per patient–year at risk were €1171.6 [median: €608.8; interquartile range (IQR): €563.1 – €936.7] for PD, €1555.2 (median: €783.9; IQR: €371.4 – €1571.7) for HD-AVF, and €4208.2 (median: €1252.4; IQR: €947.9 – €2983.5) for HD-TCC ( p < 0.001). In multivariate analysis, total dialysis access costs were significantly higher for the HD-TCC modality than for either PD or HD-AVF (β = –0.53; 95% CI: –1.03 to –0.02; and β = –0.50; 95% CI: –0.96 to –0.04). Conclusions Compared with patients initiating HD, those initiating PD required fewer resources to establish and maintain a dialysis access during the first year of treatment.
Periarticular Bone Gain at Proximal Interphalangeal Joints and Changes in Bone Turnover Markers in Response to Tumor Necrosis Factor Inhibitors in Rheumatoid and Psoriatic Arthritis
Authors: Szentpetery Agnes , McKenna Malachi J. , Murray Barbara F. , Ng Chin Teck , Brady Jennifer J. , Morrin Michelle , Radovits Bea , Veale Douglas J. , FitzGerald Oliver 
Published: March 2013

Objective.Rheumatoid arthritis (RA) and psoriatic arthritis (PsA) are characterized by periarticular bone erosion; periarticular bone formation is a feature in PsA. The effect of anti-tumor necrosis factor-α (TNF-α) on periarticular bone remodeling is unclear in both diseases. Our aim was to assess the response of bone turnover markers (BTM) and hand bone mineral density (BMD) to anti-TNF over 3 years in RA and PsA.Methods.We measured serum bone-specific alkaline phosphatase (bone ALP), procollagen type-I N-propeptide (PINP), intact osteocalcin, C-terminal cross-linking telopeptides (CTX-I), urinary N-terminal cross-linking telopeptide of type-I collagen (NTX-I), and free deoxypyridinoline crosslinks (fDPD) at baseline, 1, 12, and 36 months. BMD measurements (hands/spine/hip) were obtained at 3 timepoints.Results.We recruited 62 patients (RA 35; PsA 27). BTM correlated significantly with hand BMD but not with central BMD. Low hand BMD was associated with RA and increased BTM. Following anti-TNF therapy, hip BMD declined while spine and hand BMD were unchanged. Periarticular BMD at proximal interphalangeal (PIP) joints increased while it decreased at metacarpophalangeal joints. Bone ALP increased steadily and was always higher in PsA. PINP and intact osteocalcin increased to a lesser extent, but resorption markers did not change.Conclusion.At baseline, hand BMD was inversely associated with BTM. Bone formation rather than resorption markers better showed the bone response to anti-TNF. Despite a lack of effect on central BMD, the modest effect of anti-TNF on PIP BMD may provide evidence that BTM reflect specifically bone remodeling activity at periarticular sites of inflammation in RA and PsA.
Evaluation of Serum Biomarkers Associated with Radiographic Progression in Methotrexate-naive Rheumatoid Arthritis Patients Treated with Methotrexate or Golimumab
Authors: Wagner Carrie , Chen Dion , Fan Hongtao , Hsia Elizabeth C. , Mack Michael , Emery Paul , Fleischmann Roy M. 
Published: March 2013

Objective.To evaluate associations between biomarkers and radiographic progression in methotrexate (MTX)-naive patients with rheumatoid arthritis (RA) treated with MTX or golimumab, a tumor necrosis factor inhibitor (with or without MTX).Methods.Serum samples from 152 MTX-naive adults with active RA who received placebo + MTX (n = 37) or golimumab (combined 50 mg + MTX or 100 mg ± MTX; n = 115) were analyzed for selected markers of inflammation and bone/cartilage turnover. One hundred patients were randomly selected for additional protein profiling using multianalyte profiles (HumanMap v1.6, Rules Based Medicine). Radiographs at baseline, Week 28, and Week 52 were scored using van der Heijde-Sharp (vdH-S) methodology. Correlations were assessed between biomarker levels (baseline and change at Week 4) and joint space narrowing, erosion, and total vdH-S scores (changes at Weeks 28 and 52). Statistical significance was defined as a correlation coefficient with an absolute value ≥ 0.3 and p < 0.05.Results.Biomarker correlations with changes in vdH-S scores at Week 28 and/or 52 were observed predominantly in the placebo + MTX group and rarely in the combined golimumab treatment group. Changes in epidermal growth factor (EGF) and CD40 ligand (CD40L) at Week 4 were positively correlated with changes in total vdH-S scores at Weeks 28 and 52 in the placebo + MTX group.Conclusion.These preliminary findings indicate that EGF and CD40L may have utility in monitoring MTX-treated patients with RA who are more likely to have radiographic progression as measured by increases in vdH-S scores.
Progression of Nailfold Microvascular Damage and Antinuclear Antibody Pattern in Systemic Sclerosis
Authors: Sulli Alberto , Ruaro Barbara , Smith Vanessa , Pizzorni Carmen , Zampogna Giuseppe , Gallo Maurizio , Cutolo Maurizio 
Published: March 2013

Objective.This study evaluates possible correlations between the pattern of antinuclear antibodies (ANA) on indirect immunofluorescence (IIF) testing and nailfold microangiopathy stage (early, active, and late stage) in systemic sclerosis (SSc). Patients with SSc were followed prospectively to monitor progression of microvascular damage.Methods.The ANA pattern on IIF was searched in 42 patients with SSc showing an early pattern of nailfold microangiopathy at baseline, and was followed using nailfold videocapillaroscopy (NVC) for a median time of 91 months.Results.Among patients whose microangiopathy showed a rapid progression from early to late pattern on NVC, the IIF pattern was fine-speckled + nucleolar (Scl-70+) in 44%, centromeric in 33%, nucleolar in 11%, and homogeneous in 11% of patients with SSc. Antitopoisomerase I antibodies were significantly more frequent (57%) in patients with late pattern of microangiopathy on NVC. The median time of progression from early to active disease was significantly lower in patients with both fine-speckled + nucleolar and nucleolar ANA positivity. The severity of microangiopathy was higher in patients with the nucleolar pattern on IIF. Patients already showing a slight reduction of capillary number at baseline were likely to have either the nucleolar or the fine-speckled + nucleolar pattern on IIF. Of note, 37% of patients still showing the early microangiopathy pattern on NVC at the end of the followup were ANA-negative.Conclusion.ANA-negative patients with SSc display a slower progression of nailfold microangiopathy characterized by the early pattern on NVC. Progression to the late NVC pattern (more advanced stage of microvascular damage) seems to be associated with a different autoantibody pattern on IIF (fine-speckled + nucleolar pattern being the most prevalent).
Efficacy and Tolerability of Probenecid as Urate-lowering Therapy in Gout; Clinical Experience in High-prevalence Population
Authors: Pui Karen , Gow Peter J. , Dalbeth Nicola 
Published: March 2013

Objective.Probenecid is recommended as urate-lowering therapy (ULT) in patients with gout where xanthine oxidase inhibitors are ineffective, not tolerated, or contraindicated. The aim of our study was to determine the efficacy of probenecid to achieve serum urate (SU) targets (< 0.36 mmol/l) in clinical practice.Methods.We identified 57 patients prescribed with probenecid from a database of 521 rheumatology clinic attenders with gout. Demographic characteristics, indications for probenecid, probenecid doses, side effects, and laboratory data including estimated glomerular filtration rate (eGFR) and SU were recorded.Results.There were 30/57 (53%) patients treated with probenecid as monotherapy and 27/57 (47%) patients treated with probenecid in combination with allopurinol. Target SU concentrations (< 0.36 mmol/l) were achieved in 10/30 (33%) of the probenecid monotherapy group and 10/27 (37%) of the combination treatment group. Baseline SU concentrations, but not eGFR or probenecid dose, independently predicted achievement of target SU. Target SU was achieved in 5/15 (33%) patients with eGFR < 50 ml/min/1.73 m2. There was no difference in the percentage of patients achieving SU target in those with eGFR < 50 ml/min/1.73 m2 compared with those with eGFR ≥ 50 ml/min/1.73 m2. Adverse events attributed to probenecid were observed in 8/42 (19%) patients with eGFR ≥ 50 ml/min/1.73 m2 and in 2/15 (13%) patients with eGFR < 50 ml/min/1.73 m2.Conclusion.Probenecid has moderate efficacy as ULT in clinical management of patients with complex gout who have a lack of efficacy or intolerance to allopurinol. Patients with chronic kidney disease may respond to probenecid with similar rates of adverse events.
Étude comparative de quelques marqueurs de reformulation paraphrastique dans les articles de recherche et les articles de vulgarisation
Authors: Pic Elsa , Furmaniak Grégory , Hugou Vincent 
Published: March 2013

Cette étude est menée dans le cadre d’un projet visant à mettre au jour les spécificités grammaticales des articles de recherche et des articles de vulgarisation. Il s’agit de montrer que si, comme l’ont exposé de nombreux auteurs, vulgarisation et reformulation en tant qu’activités discursives sont effectivement étroitement associées, cette corrélation fonctionnelle n’implique pas pour autant une surutilisation des marqueurs explicites de reformulation dans les textes vulgarisés. Trois marqueurs (en particulier « that is, i.e. » et « namely ») sont clairement propres aux articles de recherche. Pour rendre compte de ce résultat, nous dégageons deux paramètres, l’un formel, l’autre fonctionnel, dont les valeurs se combinent pour générer quatre grands types de reformulation : hétérogène clarifiante, hétérogène précisante, homogène clarifiante et homogène précisante. Ainsi, il apparaît que chacun des deux discours étudiés privilégie, en raison de sa visée socio-pragmatique, certaines combinaisons, tandis que chacun des marqueurs de reformulation est employé prioritairement dans un ou deux types de reformulation, ce qui explique leur fréquence dans les articles de recherche et leur relative rareté en discours vulgarisé.
L’imaginaire écologique
Authors: Manceron Vanessa , Roué Marie 
Published: March 2013

Ce numéro de Terrain rassemble les contributions d’auteurs qui s’intéressent à la manière dont les mouvements et les groupes qui se réclament ou s’inspirent de l’écologisme œuvrent aujourd’hui comme force de contestation et de proposition politique et sociale. Les rêves libertaires de contre-société se sont éloignés et l’écologisation de nos sociétés est en marche. Peut-on pour autant parler de la fin des grandes espérances ? C’est l’une des questions que pose ce numéro, en s’attachant à décrire comment les rapports aux lieux, aux milieux et au vivant sont mobilisés çà et là, et ouvrent toujours des horizons d’action et de transformation. L’écologisme apparaît à présent comme un monde échevelé et diversifié, particulièrement conflictuel, mais qui permet aussi de multiples formes d’arrangements avec le réel et qui de fait le transforme, en accommodant des mondes que l’on pensait irréconciliables.
Isac Chiva, ethnologie et politique patrimoniale
Authors: Barbe Noël 
Published: March 2013

La Mission du patrimoine ethnologique du ministère de la Culture naît, au début des années 1980, d’une opportunité partagée entre une politique et une discipline. La discipline, l’ethnologie de la France, manque à ce moment-là de lieux propres, dans les établissements d’enseignement supérieur comme dans ceux de recherche. Son objet, le « proche », fait par ailleurs discuter sa légitimité scientifique. La politique, installée à la direction du Patrimoine du ministère, entend quant à elle réguler des activités patrimoniales amateures, qui foisonnent alors. C’est à ce point de rencontre entre science et politique que se constitue le patrimoine ethnologique théorisé par Isac Chiva (1925- 2012), qui s’attache à le construire comme une notion. Chiva pratiqua pour ce faire une série d’opérations intellectuelles : rupture, dans son esprit sans doute épistémologique, avec les usages idéologiques du mot « patrimoine » ; insertion dans l’histoire de la discipline ; emprunts à d’autres disciplines telle la génétique des populations ; définition positive de la notion qu’il lie étroitement à la recherche. Du côté de la politique, ce projet disciplinaire servira de point d’appui contre une ethnologie dite « sauvage ».
Independent and Interdependent Immunoregulatory Effects of IL-27, IFN-β, and IL-10 in the Suppression of Human Th17 Cells and Murine Experimental Autoimmune Encephalomyelitis
Authors: Fitzgerald Denise C. , Fonseca-Kelly Zoë , Cullimore Melissa L. , Safabakhsh Pegah , Saris Christiaan J. M. , Zhang Guang-Xian , Rostami Abdolmohamad 
Published: March 2013

Abstract
IFN-β, IL-27, and IL-10 have been shown to exert a range of similar immunoregulatory effects in murine and human experimental systems, particularly in Th1- and Th17-mediated models of autoimmune inflammatory disease. In this study we sought to translate some of our previous findings in murine systems to human in vitro models and delineate the interdependence of these different cytokines in their immunoregulatory effects. We demonstrate that human IL-27 upregulates IL-10 in T cell–activated PBMC cultures and that IFN-β drives IL-27 production in activated monocytes. IFN-β–driven IL-27 is responsible for the upregulation of IL-10, but not IL-17 suppression, by IFN-β in human PBMCs. Surprisingly, IL-10 is not required for the suppression of IL-17 by either IL-27 or IFN-β in this model or in de novo differentiating Th17 cells, nor is IL-27 signaling required for the suppression of experimental autoimmune encephalomyelitis (EAE) by IFN-β in vivo. Furthermore, and even more surprisingly, IL-10 is not required for the suppression of Th17-biased EAE by IL-27, in sharp contrast to Th1-biased EAE. In conclusion, IFN-β and IL-27 both induce human IL-10, both suppress human Th17 responses, and both suppress murine EAE. However, IL-27 signaling is not required for the therapeutic effect of IFN-β in EAE. Suppression of Th17-biased EAE by IL-27 is IL-10–independent, in contrast to its mechanism of action in Th1-biased EAE. Taken together, these findings delineate a complex set of interdependent and independent immunoregulatory mechanisms of IFN-β, IL-27, and IL-10 in human experimental models and in murine Th1- and Th17-driven autoimmunity.
Regulation of Foxp3+ Inducible Regulatory T Cell Stability by SOCS2
Authors: Knosp Camille A. , Schiering Chris , Spence Shaun , Carroll Helen P. , Nel Hendrick J. , Osbourn Megan , Jackson Ruaidhri , Lyubomska Oksana , Malissen Bernard , Ingram Rebecca , Fitzgerald Denise C. , Powrie Fiona , Fallon Padraic G. , Johnston James A. , Kissenpfennig Adrien 
Published: March 2013

Abstract
Suppressor of cytokine signaling (SOCS) proteins are key regulators of CD4+ T cell differentiation, and in particular, we have recently shown that SOCS2 inhibits the development of Th2 cells and allergic immune responses. Interestingly, transcriptome analyses have identified SOCS2 as being preferentially expressed in both natural regulatory T cells (Tregs) and inducible Tregs (iTregs); however, the role of SOCS2 in Foxp3+ Treg function or development has not been fully elucidated. In this study, we show that despite having no effect on natural Treg development or function, SOCS2 is highly expressed in iTregs and required for the stable expression of Foxp3 in iTregs in vitro and in vivo. Indeed, SOCS2-deficient CD4+ T cells upregulated Foxp3 following in vitro TGF-β stimulation, but failed to maintain stable expression of Foxp3. Moreover, in vivo generation of iTregs following OVA feeding was impaired in the absence of SOCS2 and could be rescued in the presence of IL-4 neutralizing Ab. Following IL-4 stimulation, SOCS2-deficient Foxp3+ iTregs secreted elevated IFN-γ and IL-13 levels and displayed enhanced STAT6 phosphorylation. Therefore, we propose that SOCS2 regulates iTreg stability by downregulating IL-4 signaling. Moreover, SOCS2 is essential to maintain the anti-inflammatory phenotype of iTregs by preventing the secretion of proinflammatory cytokines. Collectively, these results suggest that SOCS2 may prevent IL-4–induced Foxp3+ iTreg instability. Foxp3+ iTregs are key regulators of immune responses at mucosal surfaces; therefore, this dual role of SOCS2 in both Th2 and Foxp3+ iTregs reinforces SOCS2 as a potential therapeutic target for Th2-biased diseases.
Galectin-3 Negatively Regulates Dendritic Cell Production of IL-23/IL-17–Axis Cytokines in Infection by Histoplasma capsulatum
Authors: Wu Sheng-Yang , Yu Jhang-Sian , Liu Fu-Tong , Miaw Shi-Chuen , Wu-Hsieh Betty A. 
Published: March 2013

Abstract
Galectin-3 (gal3) is known for its immunoregulatory functions in infectious, autoimmune, and inflammatory diseases. However, little is known about its regulatory role in the host's IL-17A response to infection. Using a mouse model of histoplasmosis in which both Th1 and Th17 responses contribute to fungal clearance, we investigated how gal3 regulates IL-17A responses. Our study showed that Histoplasma infection induced gal3−/− dendritic cells to produce significantly higher levels of IL-23, TGF-β1, and IL-1β than did gal3+/+ cells. Infected by the same inoculum of Histoplasma, gal3−/− mice had lower fungal burden and produced higher levels of IL-23/IL-17–axis cytokines and lower levels of IL-12 and IFN-γ. Additionally, there was an increase in Th17 cells and a reduction in Th1 cells in infected gal3−/− mice. In vitro Th1/Th17-skewing experiments excluded the intrinsic effect of gal3 on Th cell differentiation. Although neutrophils from both gal3+/+ and gal3−/− mice produced IL-17A upon IL-23 stimulation, their contribution to IL-17A production was greater in gal3−/− mice than in gal3+/+ mice. Compared with gal3+/+ dendritic cells, adoptive transfer of gal3−/− dendritic cells resulted in production of significantly higher levels of IL-17–axis cytokines and reduced fungal burden. It appears that reduced fungal burden and preferential IL-17A response in gal3−/− mice by both Th17 cells and neutrophils were the result of preferential production of IL-23/IL-17–axis cytokines by dendritic cells. Our study showed that gal3 negatively regulates IL-17A responses through inhibition of IL-23/IL-17–axis cytokine production by dendritic cells.
A Critical Role for TLR4 Induction of Autophagy in the Regulation of Enterocyte Migration and the Pathogenesis of Necrotizing Enterocolitis
Authors: Neal Matthew D. , Sodhi Chhinder P. , Dyer Mitchell , Craig Brian T. , Good Misty , Jia Hongpeng , Yazji Ibrahim , Afrazi Amin , Richardson Ward M. , Beer-Stolz Donna , Ma Congrong , Prindle Thomas , Grant Zachary , Branca Maria F. , Ozolek John , Hackam David J. 
Published: March 2013

Abstract
Necrotizing enterocolitis (NEC) develops in response to elevated TLR4 signaling in the newborn intestinal epithelium and is characterized by TLR4-mediated inhibition of enterocyte migration and reduced mucosal healing. The downstream processes by which TLR4 impairs mucosal healing remain incompletely understood. In other systems, TLR4 induces autophagy, an adaptive response to cellular stress. We now hypothesize that TLR4 induces autophagy in enterocytes and that TLR4-induced autophagy plays a critical role in NEC development. Using mice selectively lacking TLR4 in enterocytes (TLR4ΔIEC) and in TLR4-deficient cultured enterocytes, we now show that TLR4 activation induces autophagy in enterocytes. Immature mouse and human intestine showed increased expression of autophagy genes compared with full-term controls, and NEC development in both mouse and human was associated with increased enterocyte autophagy. Importantly, using mice in which we selectively deleted the autophagy gene ATG7 from the intestinal epithelium (ATG7ΔIEC), the induction of autophagy was determined to be required for and not merely a consequence of NEC, because ATG7ΔIEC mice were protected from NEC development. In defining the mechanisms involved, TLR4-induced autophagy led to impaired enterocyte migration both in vitro and in vivo, which in cultured enterocytes required the induction of RhoA-mediated stress fibers. These findings depart from current dogma in the field by identifying a unique effect of TLR4-induced autophagy within the intestinal epithelium in the pathogenesis of NEC and identify that the negative consequences of autophagy on enterocyte migration play an essential role in its development.