N=1 supersymmetric Yang-Mills theory on the lattice

Numerical simulations of supersymmetric theories on the lattice are intricate and challenging with respect to their theoretical foundations and algorithmic realisation. Nevertheless, the simulations of a four-dimensional supersymmetric gauge theory have made considerable improvements over the recent years. In this contribution we summarise the results of our collaboration concerning the mass spectrum of this theory. The investigation of systematic errors allows now a more precise estimate concerning the expected formation of supersymmetric multiplets of the lightest particles. These multiplets contain flavour singlet mesons, glueballs, and an additional fermionic state.Comment: presented at the 31st International Symposium on Lattice Field Theory (Lattice 2013), 29 July - 3 August 2013, Mainz, German

Numerische Bestimmung von Quarkpotential, Glueball-Massen und Phasenstruktur in der N = 1 supersymmetrischen Yang-Mills-Theorie

Eines der vielversprechendsten Modelle für Physik jenseits des Standardmodells ist die Supersymmetrie. Diese Arbeit entstand im Rahmen der DESY-Münster-Kollaboration, die sich insbesondere mit der N=1 supersymmetrischen Yang-Mills-Theorie (SYM) beschäftigt. Der Schwerpunkt dieser Arbeit liegt auf der numerischen Bestimmung von Quarkpotential, Glueball-Massen und der Phasenstruktur in der N=1 supersymmetrischen Yang-Mills-Theorie mit Hilfe von Monte-Carlo-Simulationen auf dem Gitter. Es werden verschiedene Methoden untersucht, um die Unsicherheiten bei der Massenbestimmung der Gluebälle zu verringern. Der Fokus liegt dabei auf den Smearing-Methoden und ihrem Einsatz beim variational smearing sowie der Verwendung verschiedener Glueball-Operatoren. Parallel zu den Simulationen bei Temperatur Null wurden Simulationen bei endlicher Temperatur durchgeführt, um das Verhalten der Polyakov-Schleifen und des Gluino-Kondensats im Phasendiagramm genauer zu analysieren

Molecular mechanism underlying the impact of vitamin D on disease activity of MS

Objective: Some previous studies suggest modest to strong effects of 25-hydroxyvitamin D (25(OH)D) on multiple sclerosis (MS) activity. The objective of this study was to explore the mechanistic rationale that may explain potential clinical effects of 25(OH)D. Methods: This study measured serum 25(OH)D levels and global gene expression profiles over a course of up to 2 years in patients starting treatment with interferon beta-1b (IFNB-1b) after a clinically isolated syndrome. MS disease activity was assessed by the number of gadolinium-enhancing lesions present on repeated magnetic resonance imaging (MRIs). Results: The number of gadolinium-enhancing lesions was highly significantly associated with 25(OH)D levels. Conducting various systems-level analyses on the molecular level, multiple lines of evidence indicated that 25(OH)D regulates expression dynamics of a large gene–gene interaction system which primarily regulates immune modulatory processes modulating MS activity. The vitamin D response element was significantly enriched in this system, indicating a direct regulation of this gene interaction network through the vitamin D receptor. With increasing 25(OH)D levels, resulting regulation of this system was associated with a decrease in MS activity. Within the complex network of genes that are regulated by 25(OH)D, well-described targets of IFNB-1b and a regulator of sphingosine-1-phosphate bioavailability were found. The 25(OH)D effects on MS activity were additively enhanced by IFNB-1b. Interpretation Here, we provide mechanistic evidence that an unbalanced 25(OH)D gene expression system may affect MS activity. Our findings support a potential benefit of monitoring and managing vitamin D levels (e.g., through supplementation) in early MS patients treated with IFN-beta-1b

Long-term Impact of Early MS Treatment with Interferon Beta-1b (IFNB-1b): Clinical, MRI, Employment, and Patient-Reported Outcomes (PROs) at the 11-Year Follow-up of BENEFIT (BENEFIT 11) (P7.012)

International audienceOBJECTIVE:To study long-term outcomes in patients treated with IFNB-1b after clinically isolated syndrome (CIS). BACKGROUND:In BENEFIT, patients with CIS were randomized to IFNB-1b or placebo (PL) treatment. After the second clinical event or after 2 years, all patients were treated with IFNB-1b. Mean delay of IFNB-1b in PL was 1.33 years. Comprehensive clinical, MRI, and PROs at 11 years post-randomization are reported. DESIGN/METHODS:All originally randomized patients were asked to undergo clinical, MRI, laboratory, and PRO assessments 11 years after randomization. RESULTS:281 patients were identified (60[percnt] of originally randomized, 72.6[percnt] of eligible patients at participating sites); 278 enrolled. Baseline characteristics were similar to the original BENEFIT population. At Year 11, patients randomized to IFNB-1b still had lower overall annualized relapse rate (p=0.0018) and longer time to first relapse (p=0.0005) and clinically definite MS (p=0.0012). Median EDSS score was 2.0 (change from baseline 0.5) in both groups. PASAT scores remained high (overall median 56 [IQR 10]). Of the 81.3[percnt] working at CIS start, 73.4[percnt] were still employed (64.4[percnt] fulltime). 12.2[percnt] retired early or were on long-term disability (2.9[percnt] at baseline). 64.0[percnt] did not report any sick leave during the past 12 months. Health-related quality of life remained stable (median [IQR] change from baseline EQ-5D: 0.000 [0.209], FAMS TOI: -7.54 [27.17]. Median (IQR) fatigue (FSMC) score: 45.00 (40.00), 46[percnt] of patients without fatigue (cut-off score\textless43), median (IQR) depression (CES-D) score: 9.00 (15.00). MRI findings were similar across groups: 86.4[percnt] had no gadolinium-enhancing lesions; median (IQR) number of new T2 lesions since 5-year MRI: 2.0 (6.0), T2 volume: 1760.0mm³ (3963.0mm³), cortical lesions: 2.0 (5.0), brain volume 1519.0cm³ (152.0mm³), mean cortical thickness 2.64mm³ (0.56mm³). CONCLUSIONS:Results from BENEFIT11 support a long-term impact of early treatment with IFNB-1b on clinical measures, including cognition and fatigue, and health economic and MRI outcomes. Study Supported by:Bayer HealthCare Pharmaceuticals Disclosure: Dr. Edan has received personal compensation for activities with LFB, Biogenidec, speaking from Serono, Inc., Sanofi, Teva, and Bayer Pharmaceuticals Corporation as a consultant and/or scientific advisory board member. Dr. Freedman has received personal compensation for activities with Bayer Healthcare, Biogen Idec, Chugai, EMD Canada, Genzyme, Novartis, Sanofi-Aventis, and Teva Canada Innovation. Dr. Montalban has received personal compensation for activities with Bayer, Biogen Idec, EMD, Genentech, Genzyme, Merck Serono, Neurotec, Novartis, Sanofi-Aventis, Teva Pharmaceuticals, and Almirall. Dr. Miller has received personal compensation for activities with UCL Institute of Neurology, Biogen Idec, GlaxoSmithKline Inc., Novartis, Merck & Co. Inc., Chugai, and Mitsubishi Pharma. Dr. Miller has received personal compensation in an editorial capac Dr. Hartung has holds stock and/or stock options from Opexa Therapeutics. Dr. Hemmer has received personal compensation for activities with Roche, Novartis, Bayer Schering, Merck Serono, Biogen Idec, GlaxoSmithKline, Chugai Pharmaceutical, Micromet, and Genzyme as a scientific advisory board member. Dr. Fox has received personal compensation for activities Acorda Therapeutics, Bayer Pharmaceuticals Corporation, Biogen Idec, Eli Lilly & Company, EMD Serono, Genzyme Corporation, GlaxoSmithKline, and Novartis. Dr. Barkhof has received personal compensation for activities with Bayer Schering Pharma, Sanofi, Genzyme, Biogen Idec, Teva, Merck Serono, Novartis, Roche, Synthon BV, and Janssen Research as a consultant. Dr. Schippling has received personal compensation for activities with Novartis. Dr. Schippling has received research support from Bayer Schering and Biogen Idec. Dr. Schulze has received personal compensation for activities with PAREXEL International as an employee. Dr. Pleimes has received personal compensation for activities with Myelo Therapeutics GmbH as an employee, and with Bayer Pharmaceuticals Corp. as an employee and consultant. Dr. Pohl has received personal compensation for activities with Bayer Pharmaceuticals Corporation as an employee. Dr. Pohl owns stock and/or stock options in Bayer Pharmaceuticals Corporation. Dr. Sandbrink has received personal compensation for activities with Bayer Pharmaceuticals Corporation as an employee. Dr. Sandbrink holds stock and/or stock options in Bayer Pharmaceuticals Corporation. Dr. Suarez has received personal compensation for activities with Bayer Pharmaceuticals Corporation as an employee. Dr. Wicklein has received personal compensation for activities with Bayer Pharmaceuticals Corporation as an employee. Dr. Kappos has received personal compensation for activities with Actelion Pharmaceutical

The 11-year long-term follow-up study from the randomized BENEFIT CIS trial

To assess outcomes for patients treated with interferon beta-1b immediately after clinically isolated syndrome (CIS) or after a short delay.status: publishe

The 11-year long-term follow-up study from the randomized BENEFIT CIS trial

OBJECTIVE To assess outcomes for patients treated with interferon beta-1b immediately after clinically isolated syndrome (CIS) or after a short delay. METHODS Participants in BENEFIT (Betaferon/Betaseron in Newly Emerging MS for Initial Treatment) were randomly assigned to receive interferon beta-1b (early treatment) or placebo (delayed treatment). After conversion to clinically definite multiple sclerosis (CDMS) or 2 years, patients on placebo could switch to interferon beta-1b or another treatment. Eleven years after randomization, patients were reassessed. RESULTS Two hundred seventy-eight (59.4%) of the original 468 patients (71.3% of those eligible at participating sites) were enrolled (early: 167 [57.2%]; delayed: 111 [63.1%]). After 11 years, risk of CDMS remained lower in the early-treatment arm compared with the delayed-treatment arm (p = 0.0012), with longer time to first relapse (median [Q1, Q3] days: 1,888 [540, not reached] vs 931 [253, 3,296]; p = 0.0005) and lower overall annualized relapse rate (0.21 vs 0.26; p = 0.0018). Only 25 patients (5.9%, overall; early, 4.5%; delayed, 8.3%) converted to secondary progressive multiple sclerosis. Expanded Disability Status Scale scores remained low and stable, with no difference between treatment arms (median [Q1, Q3]: 2.0 [1.0, 3.0]). The early-treatment group had better Paced Auditory Serial Addition Task-3 total scores (p = 0.0070). Employment rates remained high, and health resource utilization tended to be low in both groups. MRI metrics did not differ between groups. CONCLUSIONS Although the delay in treatment was relatively short, several clinical outcomes favored earlier treatment. Along with low rates of disability and disease progression in both groups, this supports the value of treatment at CIS. CLINICALTRIALSGOV IDENTIFIER NCT01795872. CLASSIFICATION OF EVIDENCE This study provides Class IV evidence that early compared to delayed treatment prolongs time to CDMS in CIS after 11 years

Interferon beta-1b reduces black holes in a randomised trial of clinically isolated syndrome.

TRIAL REGISTRATION NUMBER: NCT00544037International audienc

Vitamin D as an early predictor of multiple sclerosis activity and progression.

International audienc

Subtraction MR Images in a Multiple Sclerosis Multicenter Clinical Trial Setting

Purpose: To explore the applicability of subtraction magnetic resonance (MR) images to (a) detect active multiple sclerosis (MS) lesions, (b) directly quantify lesion load change, and (c) detect treatment effects (distinguish treatment arms) in a placebo-controlled multicenter clinical trial by comparing the subtraction scheme with a conventional pair-wise comparison of nonregistered MR images