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Schneider, M. D.

Publications and source records attributed to Schneider, M. D..

Correspondence of NNGP Kernel and the Matérn Kernel

Kernels representing limiting cases of neural network architectures have recently gained popularity. However, the application and performance of these new kernels compared to existing options, such as the Matérn kernel, is not well studied. We take a practical approach to explore the neural network Gaussian process (NNGP) kernel and its application to data in Gaussian process regression. We first demonstrate the necessity of normalization to produce valid NNGP kernels and explore related numerical challenges. We further demonstrate that the predictions from this model are quite inflexible, and therefore do not vary much over the valid hyperparameter sets. We then demonstrate a surprising result that the predictions given from the NNGP kernel correspond closely to those given by the Matérn kernel under specific circumstances, which suggests a deep similarity between overparameterized deep neural networks and the Matérn kernel. Finally, we demonstrate the performance of the NNGP kernel as compared to the Matérn kernel on three benchmark data cases, and we conclude that for its flexibility and practical performance, the Matérn kernel is preferred to the novel NNGP in practical applications.

97 MATHEMATICS AND COMPUTING↗

Blending and obscuration in weak-lensing magnification

ABSTRACT We test the impact of some systematic errors in weak-lensing (WL) magnification measurements with the COSMOS 30-band photo-z Survey flux limited to Iauto < 25.0 using correlations of both source galaxy counts and magnitudes. Systematic obscuration effects are measured by comparing counts and magnification correlations. We use the Advanced Camera for Survey-Hubble Space Telescope catalogues to identify potential blending objects (close pairs) and perform the magnification analyses with and without blended objects. We find that blending effects start to be important (∼0.04-mag obscuration) at angular scales smaller than 0.1 arcmin. Extinction and other systematic obscuration effects can be as large as 0.10 mag (U band) but are typically smaller than 0.02 mag depending on the band. After applying these corrections, we measure a 3.9σ magnification signal that is consistent for both counts and magnitudes. The corresponding projected mass profiles of galaxies at redshift z ≃ 0.6 (MI ≃ −21) is Σ = 25 ± 6 M⊙ h3 pc–2 at 0.1 Mpc h–1, consistent with NFW type profile with M200 ≃ 2 × 1012 M⊙h pc–2. Tangential shear and flux-size magnification over the same lenses show similar mass profiles. We conclude that magnification from counts and fluxes using photometric redshifts has the potential to provide complementary WL information in future wide-field surveys once we carefully take into account systematic effects, such as obscuration and blending.

79 ASTRONOMY AND ASTROPHYSICS↗

TAK1 is activated in the myocardium after pressure overload and is sufficient to provoke heart failure in transgenic mice

The transforming-growth-factor-beta-activated kinase TAK1 is a member of the mitogen-activated protein kinase kinase kinase family, which couples extracellular stimuli to gene transcription. The in vivo function of TAK1 is not understood. Here, we investigated the potential involvement of TAK1 in cardiac hypertrophy. In adult mouse myocardium, TAK1 kinase activity was upregulated 7 days after aortic banding, a mechanical load that induces hypertrophy and expression of transforming growth factor beta. An activating mutation of TAK1 expressed in myocardium of transgenic mice was sufficient to produce p38 mitogen-activated protein kinase phosphorylation in vivo, cardiac hypertrophy, interstitial fibrosis, severe myocardial dysfunction, 'fetal' gene induction, apoptosis and early lethality. Thus, TAK1 activity is induced as a delayed response to mechanical stress, and can suffice to elicit myocardial hypertrophy and fulminant heart failure.

NASA Discipline Cardiopulmonary↗

Genetic dissection of cardiac growth control pathways

Cardiac muscle cells exhibit two related but distinct modes of growth that are highly regulated during development and disease. Cardiac myocytes rapidly proliferate during fetal life but exit the cell cycle irreversibly soon after birth, following which the predominant form of growth shifts from hyperplastic to hypertrophic. Much research has focused on identifying the candidate mitogens, hypertrophic agonists, and signaling pathways that mediate these processes in isolated cells. What drives the proliferative growth of embryonic myocardium in vivo and the mechanisms by which adult cardiac myocytes hypertrophy in vivo are less clear. Efforts to answer these questions have benefited from rapid progress made in techniques to manipulate the murine genome. Complementary technologies for gain- and loss-of-function now permit a mutational analysis of these growth control pathways in vivo in the intact heart. These studies have confirmed the importance of suspected pathways, have implicated unexpected pathways as well, and have led to new paradigms for the control of cardiac growth.

NASA Program Biomedical Research and Countermeasur↗