Precision Lattice Calculation of SU(2) 't Hooft loops

The [dual] string tension of a spatial 't Hooft loop in the deconfined phase of Yang-Mills theory can be formulated as the tension of an interface separating different Z_N deconfined vacua. We review the 1-loop perturbative calculation of this interface tension in the continuum and extend it to the lattice. The lattice corrections are large. Taking these corrections into account, we compare Monte Carlo measurements of the dual string tension with perturbation theory, for SU(2). Agreement is observed at the 2% level, down to temperatures O(10) T_c.Comment: 17 pages, 7 figures; reference added, typos correcte

't Hooft loops and perturbation theory

We show that high-temperature perturbation theory describes extremely well the area law of SU(N) spatial 't Hooft loops, or equivalently the tension of the interface between different Z_N vacua in the deconfined phase. For SU(2), the disagreement between Monte Carlo data and lattice perturbation theory for sigma(T)/T^2 is less than 2%, down to temperatures O(10) T_c. For SU(N), N>3, the ratios of interface tensions, (sigma_k/sigma_1)(T), agree with perturbation theory, which predicts tiny deviations from the ratio of Casimirs, down to nearly T_c. In contrast, individual tensions differ markedly from the perturbative expression. In all cases, the required precision Monte Carlo measurements are made possible by a simple but powerful modification of the 'snake' algorithm.Comment: presented at Lattice 2005 (topology and confinement), 6 pages, 7 figure

MSSM Higgs Couplings to Bottom Quarks: Two-Loop Corrections

We present the two-loop SUSY-QCD corrections to the effective bottom Yukawa couplings within the minimal supersymmetric extension of the Standard Model. The effective Yukawa couplings include the resummation of the non-decoupling corrections Delta m_b for large values of tg(beta). We have derived the two-loop SUSY-QCD corrections to the leading SUSY-QCD and top-induced SUSY-electroweak contributions to Delta m_b. The scale dependence of the resummed Yukawa couplings is reduced from O(10%) to the per-cent level. These results reduce the theoretical uncertainties of the MSSM Higgs branching ratios to the accuracy which can be achieved at a future linear e+e- collider.Comment: 5 pages, 4 figure

Peripheral Blood Gene Expression as a Novel Genomic Biomarker in Complicated Sarcoidosis

Sarcoidosis, a systemic granulomatous syndrome invariably affecting the lung, typically spontaneously remits but in ∼20% of cases progresses with severe lung dysfunction or cardiac and neurologic involvement (complicated sarcoidosis). Unfortunately, current biomarkers fail to distinguish patients with remitting (uncomplicated) sarcoidosis from other fibrotic lung disorders, and fail to identify individuals at risk for complicated sarcoidosis. We utilized genome-wide peripheral blood gene expression analysis to identify a 20-gene sarcoidosis biomarker signature distinguishing sarcoidosis (n = 39) from healthy controls (n = 35, 86% classification accuracy) and which served as a molecular signature for complicated sarcoidosis (n = 17). As aberrancies in T cell receptor (TCR) signaling, JAK-STAT (JS) signaling, and cytokine-cytokine receptor (CCR) signaling are implicated in sarcoidosis pathogenesis, a 31-gene signature comprised of T cell signaling pathway genes associated with sarcoidosis (TCR/JS/CCR) was compared to the unbiased 20-gene biomarker signature but proved inferior in prediction accuracy in distinguishing complicated from uncomplicated sarcoidosis. Additional validation strategies included significant association of single nucleotide polymorphisms (SNPs) in signature genes with sarcoidosis susceptibility and severity (unbiased signature genes - CX3CR1, FKBP1A, NOG, RBM12B, SENS3, TSHZ2; T cell/JAK-STAT pathway genes such as AKT3, CBLB, DLG1, IFNG, IL2RA, IL7R, ITK, JUN, MALT1, NFATC2, PLCG1, SPRED1). In summary, this validated peripheral blood molecular gene signature appears to be a valuable biomarker in identifying cases with sarcoidoisis and predicting risk for complicated sarcoidosis.</p

Supersymmetric Higgs Yukawa Couplings to Bottom Quarks at next-to-next-to-leading Order

The effective bottom Yukawa couplings are analyzed for the minimal supersymmetric extension of the Standard Model at two-loop accuracy within SUSY-QCD. They include the resummation of the dominant corrections for large values of tg(beta). In particular the two-loop SUSY-QCD corrections to the leading SUSY-QCD and top-induced SUSY-electroweak contributions are addressed. The residual theoretical uncertainties range at the per-cent level.Comment: 25 pages, 9 figures, added comments and references, typos corrected, results unchanged, published versio

Genome-Wide Association Study of Susceptibility to Idiopathic Pulmonary Fibrosis

Rationale: Idiopathic pulmonary fibrosis (IPF) is a complex lung disease characterised by scarring of the lung that is believed to result from an atypical response to injury of the epithelium. Genome-wide association studies have reported signals of association implicating multiple pathways including host defence, telomere maintenance, signalling and cell-cell adhesion. Objectives: To improve our understanding of factors that increase IPF susceptibility by identifying previously unreported genetic associations. Methods and measurements: We conducted genome-wide analyses across three independent studies and meta-analysed these results to generate the largest genome-wide association study of IPF to date (2,668 IPF cases and 8,591 controls). We performed replication in two independent studies (1,456 IPF cases and 11,874 controls) and functional analyses (including statistical fine-mapping, investigations into gene expression and testing for enrichment of IPF susceptibility signals in regulatory regions) to determine putatively causal genes. Polygenic risk scores were used to assess the collective effect of variants not reported as associated with IPF. Main results: We identified and replicated three new genome-wide significant (P<5×10−8) signals of association with IPF susceptibility (associated with altered gene expression of KIF15, MAD1L1 and DEPTOR) and confirmed associations at 11 previously reported loci. Polygenic risk score analyses showed that the combined effect of many thousands of as-yet unreported IPF susceptibility variants contribute to IPF susceptibility. Conclusions: The observation that decreased DEPTOR expression associates with increased susceptibility to IPF, supports recent studies demonstrating the importance of mTOR signalling in lung fibrosis. New signals of association implicating KIF15 and MAD1L1 suggest a possible role of mitotic spindle-assembly genes in IPF susceptibility

Leveraging global multi-ancestry meta-analysis in the study of idiopathic pulmonary fibrosis genetics

The research of rare and devastating orphan diseases, such as idiopathic pulmonary fibrosis (IPF) has been limited by the rarity of the disease itself. The prognosis is poor—the prevalence of IPF is only approximately four times the incidence, limiting the recruitment of patients to trials and studies of the underlying biology. Global biobanking efforts can dramatically alter the future of IPF research. We describe a large-scale meta-analysis of IPF, with 8,492 patients and 1,355,819 population controls from 13 biobanks around the globe. Finally, we combine this meta-analysis with the largest available meta-analysis of IPF, reaching 11,160 patients and 1,364,410 population controls. We identify seven novel genome-wide significant loci, only one of which would have been identified if the analysis had been limited to European ancestry individuals. We observe notable pleiotropy across IPF susceptibility and severe COVID-19 infection and note an unexplained sex-heterogeneity effect at the strongest IPF locus MUC5B.publishedVersionPeer reviewe

Association study of human leukocyte antigen (HLA) variants and idiopathic pulmonary fibrosis

IntroductionIdiopathic pulmonary fibrosis (IPF) is a chronic interstitial pneumonia marked by progressive lung fibrosis and a poor prognosis. Recent studies have highlighted the potential role of infection in the pathogenesis of IPF and a prior association of theHLA-DQB1gene with idiopathic fibrotic interstitial pneumonia (including IPF) has been reported. Due to the important role that the Human Leukocyte Antigen (HLA) region plays in the immune response, here we evaluated if HLA genetic variation was associated specifically with IPF risk.MethodsWe performed a meta-analysis of associations of the HLA region with IPF risk in individuals of European ancestry from seven independent case-control studies of IPF (comprising a total of 5159 cases and 27 459 controls, including the prior study of fibrotic interstitial pneumonia). Single nucleotide polymorphisms, classical HLA alleles and amino acids were analysed and signals meeting a region-wide association thresholdp&lt;4.5×10−4and a posterior probability of replication &gt;90% were considered significant. We sought to replicate the previously reportedHLA-DQB1association in the subset of studies independent of the original report.ResultsThe meta-analysis of all seven studies identified four significant independent single nucleotide polymorphisms associated with IPF risk. However, none met the posterior probability for replication criterion. TheHLA-DQB1association was not replicated in the independent IPF studies.ConclusionVariation in the HLA region was not consistently associated with risk in studies of IPF. However, this does not preclude the possibility that other genomic regions linked to the immune response may be involved in the aetiology of IPF

Supersymmetric precision calculations of Bottom Yukawa couplings

Wir haben die Zwei-Schleifen SUSY-QCD Korrekturen zu effektiven Bottom Yukawa Kopplungen in der minimalen, supersymmetrischen Erweiterung des Standardmodells berechnet. Diese effektiven Kopplungen beinhalten die Resummation der nicht entkoppelnden Korrekturen $\Delta m_b$ für große Werte von $tg\beta$. Wir haben die Zwei-Schleifen SUSY-QCD Korrekturen zu den führenden SUSY-QCD und top-induzierten SUSY-elektroschwachen Beiträgen zu $\Delta m_b$ berechnet. Die Skalenabhängigkeit der resummierten Yukawa Kopplungen wurde von $\mathcal{O}$ (10%) auf den Prozentbereich reduziert. Folglich reduzieren unsere Resultate die theoretische Unsicherheit der MSSM Verzweigungsverhältnisse erheblich. Darüber hinaus profitieren alle Prozesse, die von den Bottom Yukawa Kopplungen vermittelt werden, von der nun erreichten, hohen Präzision, wie z.B. Higgs Boson Strahlung von Bottom Quarks, einem wichtigen Produktionskanal an allen Kollidern. Die neuen NNLO Korrekturen für die Bottom Yukawa Kopplungen können daher als Basis für experimentelle Analysen am Tevatron und am LHC, sowie am zukünftigen, linearen $e^{+}e^{−}$ Kollider genutzt werden. We present the two-loop SUSY-QCD corrections to the effective bottom Yukawa couplings within the minimal supersymmetric extension of the Standard Model. These effective Yukawa couplings include the resummation of the non-decoupling corrections $\Delta m_b$ for large values of $tg\beta$. We have derived the two-loop SUSY-QCD corrections to the leading SUSY-QCD and top-induced SUSY-electroweak contributions to $\Delta m_b$. The scale dependence of the resummed Yukawa couplings is reduced from $\mathcal{O}$ (10%) to the percent level. Consequently, our results reduce the theoretical uncertainties of the MSSM Higgs branching ratios to a high accuracy. Moreover, all processes which are mediated by the bottom Yukawa couplings are directly affect by the now reached high precision, as e.g. Higgs boson radiation off bottom quarks which is a very important production process at all colliders. The improved NNLO predictions for the bottom Yukawa couplings can thus be taken as a base for experimental analysis at the Tevatron and the LHC as well as a future linear $e^{+}e^{−}$ collider