20 research outputs found
Concert recording 2014-01-18
[Track 01]. Preludium and allegro / Kreisler -- [Track 02]. Meditation from Thais / Massenet -- [Track 03]. Violin concerto in A minor / Accolay -- [Track 04]. Czardas / Monti -- [Track 05]. Violin concerto in G. Allegro / Mozart
Concert recording 2017-04-15a
[Track 1]. Invierno porteno (Winter) / Astor Piazzolla -- [Track 2]. G minor sonata. I. Adagio [Track 3]. II. Fuga [Track 4]. III. Siciliana [Track 5]. IV. Presto / J.S. Bach -- [Track 6]. Sonata No. 5 (Spring). I. Allegro [Track 7]. II. Adagio [Track 8]. III. Scherzo IV. Rondo / Beethoven -- [Track 9]. Valse triste / Ferenc de Vecsey
Concert recording 2016-04-28
[Track 01]. Four seasons of Buenos Aires. Winter / Piazzolla -- [Track 02]. Sonata for violin solo in G minor. Adagio ; [Track 03]. Fuga (Allegro) / J.S. Bach -- [Track 04]. Violin concerto no. 22 in A minor. Moderato ; [Track 05]. Adagio / Viotti -- [Track 06]. Introduction et rondo capriccioso, op. 28 violin concerto / Saint Saens -- [Track 07]. Valse triste / Franz von Vecsey
Concert recording 2017-09-13
[Tracks 1-4]. String quartet in D major, op. 18, no. 3 [Tracks 5-8]. String quartet in C minor, op. 18, no. 4 / Ludwig van Beethoven
Concert recording 2018-04-28
[Track 1] Nightmares and Daydreams -- [Track 2] Theme and Variations on a Mendelssohn Theme -- [Track 3] Bare-Bones Quartet. I. March ; II. Ethereal Serenade ; III. Finale -- [Track 4] Caged
Concert recording 2016-04-03
[Track 01]. Fanfare pour précéder \u27La Péri\u27 / Paul Dukas -- [Track 02]. French dances revisted. I ; [Track 03]. II ; [Track 04]. III ; [Track 05]. IV ; [Track 06]. V ; [Track 07]. VI / Adam Gorb -- [Track 08]. Danses sacrée et profane / Claude Debussy -- [Track 09]. Dance mix / Rob Smith
Multiancestry analysis of the HLA locus in Alzheimer’s and Parkinson’s diseases uncovers a shared adaptive immune response mediated by HLA-DRB1*04 subtypes
Across multiancestry groups, we analyzed Human Leukocyte Antigen (HLA) associations in over 176,000 individuals with Parkinson’s disease (PD) and Alzheimer’s disease (AD) versus controls. We demonstrate that the two diseases share the same protective association at the HLA locus. HLA-specific fine-mapping showed that hierarchical protective effects of HLA-DRB1*04 subtypes best accounted for the association, strongest with HLA-DRB1*04:04 and HLA-DRB1*04:07, and intermediary with HLA-DRB1*04:01 and HLA-DRB1*04:03. The same signal was associated with decreased neurofibrillary tangles in postmortem brains and was associated with reduced tau levels in cerebrospinal fluid and to a lower extent with increased Aβ42. Protective HLA-DRB1*04 subtypes strongly bound the aggregation-prone tau PHF6 sequence, however only when acetylated at a lysine (K311), a common posttranslational modification central to tau aggregation. An HLA-DRB1*04-mediated adaptive immune response decreases PD and AD risks, potentially by acting against tau, offering the possibility of therapeutic avenues
Concert recording 2014-03-31
[Track 01]. No title / Kreisler -- [Track 02]. Movement 1 ; [Track 03]. Movement 2 ; [Track 04]. Movement 3 / Mozart
Cigar Man
A café in Paris, Francehttps://scholarworks.uark.edu/gsiestdabphoto/1048/thumbnail.jp
Effects of tumor necrosis factor antagonist treatment on hepatitis C-related immunological abnormalities.
International audienceBACKGROUND: Chronic hepatitis C infection is frequently associated with a mixed cryoglobulinaemia and circulating auto-antibodies, especially anti-smooth muscle cells (SMA) and anti-liver/kidney/microsome type 1 (LKM-1) anti-tissue antibodies. Treatments with TNF antagonists favour the emergence of auto-antibodies, and particularly anti-dsDNA antibodies. OBJECTIVE: To determine the impact of TNF antagonists on hepatitis C-related immune abnormalities. METHODS: We prospectively monitored for 14 weeks, six patients with actively replicating chronic hepatitis C, initiating an anti-TNF treatment for an associated rheumatoid arthritis. RESULTS: Anti-nuclear and anti-dsDNA antibodies were induced in two and three patients, respectively. Treatment had no impact on the production of antibodies against extractable nuclear antigens, and it did not induce anti-tissues antibodies in any patient. Cryoglobulinaemia appeared in 2/6 patients, and it persisted in 2 others. No patient developed any news signs of autoimmunity. HCV viraemia remained unchanged. CONCLUSIONS: Induction of auto-antibodies by TNF antagonist treatments does not involve anti-tissues antibodies, even in patients with actively replicating chronic hepatitis C prone to produce anti-SMA and anti-LKM-1 antibodies. In contrast, TNF antagonists may favour emergence of cryoglobulinaemia in such patients