This product is isolated and purified from the herbs of Hippophae rhamnoides Linn.
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
999.4±65.0 °C at 760 mmHg
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provides coniferyl ferulate(CAS#:18016-58-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Antisynthetase syndrome (ASSD) is a rare clinical condition that is characterized by the occurrence of a classic clinical triad, encompassing myositis, arthritis, and interstitial lung disease (ILD), along with specific autoantibodies that are addressed to different aminoacyl tRNA synthetases (ARS). Until now, it has been unknown whether the presence of a different ARS might affect the clinical presentation, evolution, and outcome of ASSD. In this study, we retrospectively recorded the time of onset, characteristics, clustering of triad findings, and survival of 828 ASSD patients (593 anti-Jo1, 95 anti-PL7, 84 anti-PL12, 38 anti-EJ, and 18 anti-OJ), referring to AENEAS (American and European NEtwork of Antisynthetase Syndrome) collaborative group’s cohort. Comparisons were performed first between all ARS cases and then, in the case of significance, while using anti-Jo1 positive patients as the reference group. The characteristics of triad findings were similar and the onset mainly began with a single triad finding in all groups despite some differences in overall prevalence. The “ex-novo” occurrence of triad findings was only reduced in the anti-PL12-positive cohort, however, it occurred in a clinically relevant percentage of patients (30%). Moreover, survival was not influenced by the underlying anti-aminoacyl tRNA synthetase antibodies’ positivity, which confirmed that antisynthetase syndrome is a heterogeneous condition and that antibody specificity only partially influences the clinical presentation and evolution of this condition.
antisynthetase syndrome, antisynthetase antibodies, arthritis, myositis, interstitial lung disease
Influence of Antisynthetase Antibodies Specificities on Antisynthetase Syndrome Clinical Spectrum Time Course
Lorenzo Cavagna,1,* Ernesto Trallero-Araguas,2 Federica Meloni,3 Ilaria Cavazzana,4 Jorge Rojas-Serrano,5 Eugen Feist,6 Giovanni Zanframundo,1 Valentina Morandi,1 Alain Meyer,7,8 Jose Antonio Pereira da Silva,9 Carlo Jorge Matos Costa,9 Oyvind Molberg,10 Helena Andersson,10 Veronica Codullo,11 Marta Mosca,12 Simone Barsotti,12 Rossella Neri,12 Carlo Scire,13 Marcello Govoni,13 Federica Furini,13 Francisco Javier Lopez-Longo,14 Julia Martinez-Barrio,14 Udo Schneider,6 Hanns-Martin Lorenz,15 Andrea Doria,16 Anna Ghirardello,16 Norberto Ortego-Centeno,17 Marco Confalonieri,18 Paola Tomietto,19 Nicolò Pipitone,20 Ana Belen Rodriguez Cambron,21 Maria angeles Blazquez CaNamero,21 Reinhard Edmund Voll,22 Sarah Wendel,22 Salvatore Scarpato,23 Francois Maurier,24 Massimiliano Limonta,25 Paolo Colombelli,26 Margherita Giannini,8 Bernard Geny,8 Eugenio Arrigoni,27 Elena Bravi,27 Paola Migliorini,28 Alessandro Mathieu,29 Matteo Piga,29 Ulrich Drott,30 Christiane Delbrueck,30 Jutta Bauhammer,31 Giovanni Cagnotto,32 Carlo Vancheri,33 Gianluca Sambataro,33 Ellen De Langhe,34 Pier Paolo Sainaghi,35 Cristina Monti,36 Francesca Gigli Berzolari,36 Mariaeva Romano,37 Francesco Bonella,38 Christof Specker,39 Andreas Schwarting,40 Ignacio Villa Blanco,41 Carlo Selmi,42 Angela Ceribelli,42 Laura Nuno,43 Antonio Mera-Varela,44 Nair Perez Gomez,44 Enrico Fusaro,45 Simone Parisi,45 Luigi Sinigaglia,46 Nicoletta Del Papa,46 Maurizio Benucci,47 Marco Amedeo Cimmino,48 Valeria Riccieri,49 Fabrizio Conti,49 Gian Domenico Sebastiani,50 Annamaria Iuliano,50 Giacomo Emmi,51 Daniele Cammelli,52 Marco Sebastiani,53 Andreina Manfredi,53 Javier Bachiller-Corral,54 Walter Alberto Sifuentes Giraldo,54 Giuseppe Paolazzi,55 Lesley Ann Saketkoo,56 Roberto Giorgi,57 Fausto Salaffi,58 Jose Cifrian,59 Roberto Caporali,60 Francesco Locatelli,1 Enrico Marchioni,61 Alberto Pesci,62 Giulia Dei,62 Maria Rosa Pozzi,62 Lomater Claudia,63 Jorg Distler,64 Johannes Knitza,64 George Schett,64 Florenzo Iannone,65 Marco Fornaro,65 Franco Franceschini,4 Luca Quartuccio,66 Roberto Gerli,67 Elena Bartoloni,67 Silvia Bellando Randone,68 Giuseppe Zampogna,69 Montserrat I. Gonzalez Perez,5 Mayra Mejia,5 Esther Vicente,70 Konstantinos Triantafyllias,71 Raquel Lopez-Mejias,72 Marco Matucci-Cerinic,68 Albert Selva-O’Callaghan,2 Santos CastaNeda,70,73 Carlomaurizio Montecucco,1 and Miguel Angel Gonzalez-Gay72
The heterogeneity of tinnitus is likely accounting for the lack of effective treatment approaches. Headaches have been related to tinnitus, yet little is known on how headaches impact tinnitus. We use cross-sectional data from the Swedish Tinnitus Outreach Project to i) evaluate the association between headaches and tinnitus (n = 1,984 cases and 1,661 controls) and ii) investigate the phenotypic characteristics of tinnitus subjects with tinnitus (n = 660) or without (n = 1,879) headaches. In a multivariable logistic regression model, headache was significantly associated with any tinnitus (odds ratio, OR = 2.61) and more so with tinnitus as a big problem (as measured by the tinnitus functional index, TFI ≥ 48; OR = 5.63) or severe tinnitus (using the tinnitus handicap inventory, THI ≥ 58; OR = 4.99). When focusing on subjects with tinnitus, the prevalence of headaches was 26% and reached 40% in subjects with severe tinnitus. A large number of socioeconomic, phenotypic and psychological characteristics differed between headache and non-headache subjects with any tinnitus. With increasing tinnitus severity, fewer differences were found, the major ones being vertigo, neck pain and other pain syndromes, as well as stress and anxiety. Our study suggests that headaches could contribute to tinnitus distress and potentially its severity.
Subject terms: Headache, Risk factors, Auditory system
Relationship between headaches and tinnitus in a Swedish study
Alessandra Lugo,#1 Niklas K. Edvall,#2 Andra Lazar,3 Golbarg Mehraei,4 Jose-Antonio Lopez-Escamez,5,6 Jan Bulla,7,8 Inger Uhlen,3 Barbara Canlon,2 Silvano Gallus,1 and Christopher R. Cederrothcorresponding author2
Systemic juvenile idiopathic arthritis (sJIA) is an often severe, potentially life-threatening childhood inflammatory disease, the pathophysiology of which is poorly understood. To determine whether genetic variation within the MHC locus on chromosome 6 influences sJIA susceptibility, we performed an association study of 982 children with sJIA and 8,010 healthy control subjects from nine countries. Using meta-analysis of directly observed and imputed SNP genotypes and imputed classic HLA types, we identified the MHC locus as a bona fide susceptibility locus with effects on sJIA risk that transcended geographically defined strata. The strongest sJIA-associated SNP, rs151043342 [P = 2.8 × 10−17, odds ratio (OR) 2.6 (2.1, 3.3)], was part of a cluster of 482 sJIA-associated SNPs that spanned a 400-kb region and included the class II HLA region. Conditional analysis controlling for the effect of rs151043342 found that rs12722051 independently influenced sJIA risk [P = 1.0 × 10−5, OR 0.7 (0.6, 0.8)]. Meta-analysis of imputed classic HLA-type associations in six study populations of Western European ancestry revealed that HLA-DRB1*11 and its defining amino acid residue, glutamate 58, were strongly associated with sJIA [P = 2.7 × 10−16, OR 2.3 (1.9, 2.8)], as was the HLA-DRB1*11—HLA-DQA1*05—HLA-DQB1*03 haplotype [6.4 × 10−17, OR 2.3 (1.9, 2.9)]. By examining the MHC locus in the largest collection of sJIA patients assembled to date, this study solidifies the relationship between the class II HLA region and sJIA, implicating adaptive immune molecules in the pathogenesis of sJIA.
systemic juvenile idiopathic arthritis, Still’s disease, human leukocyte antigen, autoinflammation
HLA-DRB1*11 and variants of the MHC class II locus are strong risk factors for systemic juvenile idiopathic arthritis
Michael J. Ombrello,a,1 Elaine F. Remmers,b Ioanna Tachmazidou,c Alexei Grom,d,e Dirk Foell,f Johannes-Peter Haas,g Alberto Martini,h,i Marco Gattorno,i Seza ozen,j Sampath Prahalad,k,l Andrew S. Zeft,m John F. Bohnsack,n Elizabeth D. Mellins,o Norman T. Ilowite,p Ricardo Russo,q Claudio Len,r Maria Odete E. Hilario,r Sheila Oliveira,s Rae S. M. Yeung,t,u,v Alan Rosenberg,w Lucy R. Wedderburn,x,y Jordi Anton,z Tobias Schwarz,aa Anne Hinks,bb Yelda Bilginer,j Jane Park,o Joanna Cobb,bb,cc Colleen L. Satorius,b Buhm Han,dd,ee,ff Elizabeth Baskin,a Sara Signa,h Richard H. Duerr,gg,hh J. P. Achkar,ii,jj M. Ilyas Kamboh,gg Kenneth M. Kaufman,d,e Leah C. Kottyan,d,e Dalila Pinto,kk Stephen W. Scherer,ll Marta E. Alarcon-Riquelme,mm,nn Elisa Docampo,oo,pp Xavier Estivill,pp Ahmet Gul,qq British Society of Pediatric and Adolescent Rheumatology (BSPAR) Study Group,2 Childhood Arthritis Prospective Study (CAPS) Group,2 Randomized Placebo Phase Study of Rilonacept in sJIA (RAPPORT) Investigators,2 Sparks-Childhood Arthritis Response to Medication Study (CHARMS) Group,2 Biologically Based Outcome Predictors in JIA (BBOP) Group,2 Paul I. W. de Bakker,rr,ss,tt Soumya Raychaudhuri,bb,dd,ee Carl D. Langefeld,uu Susan Thompson,d,e Eleftheria Zeggini,c Wendy Thomson,bb,cc Daniel L. Kastner,b,1 Patricia Woo,y and the International Childhood Arthritis Genetics (INCHARGE) Consortium2
2015 Dec 29