19 research outputs found

    Holonomy and submanifold geometry

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    We survey applications of holonomic methods to the study of submanifold geometry, showing the consequences of some sort of extrinsic version of de Rham decomposition and Berger's Theorem, the so-called Normal Holonomy Theorem. At the same time, from geometric methods in submanifold theory we sketch very strong applications to the holonomy of Lorentzian manifolds. Moreover we give a conceptual modern proof of a result of Kostant for homogeneous spaces

    On weak r-Helix submanifolds

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    In this paper, we investigate special curves on a weak r-helix submanifold in Euclidean n-space E^{n}. Also, we give the important relations between weak r-helix submanifolds and the special curves such as line of curvature, asymptotic curve and helix line.Comment: arXiv admin note: text overlap with arXiv:1203.160

    Surfaces in R4 with constant principal angles with respect to a plane

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    We study surfaces in R4 whose tangent spaces have constant principal angles with respect to a plane. Using a PDE we prove the existence of surfaces with arbitrary constant principal angles. The existence of such surfaces turns out to be equivalent to the existence of a special local symplectomorphism of R2\R^2. We classify all surfaces with one principal angle equal to 00 and observe that they can be constructed as the union of normal holonomy tubes. We also classify the complete constant angles surfaces in R4 with respect to a plane. They turn out to be extrinsic products. We characterize which surfaces with constant principal angles are compositions in the sense of Dajczer-Do Carmo. Finally, we classify surfaces with constant principal angles contained in a sphere and those with parallel mean curvature vector fiel

    Kahler submanifolds of Wolf Spaces

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    We classify the Kahler submanifolds of Wolf spaces i.e. Quaternionic Kahler symmetric spaces, with parallel second fundamental form

    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
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