The tearing instability of resistive magnetohydrodynamics

In this chapter we explore the linear onset of one of the most important instabilities of resistive magnetohydrodynamics, the tearing instability. In particular, we focus on two important aspects of the onset of tearing: asymptotic (modal) stability and transient (non-modal) stability. We discuss the theory required to understand these two aspects of stability, both of which have undergone significant development in recent years

Effect on Wall Shear Rates of Taylor Vortex Instabilities Induced by Progressive Variation of the Inner Cylinder

International audienc

Spatial resolution and dissipation rate estimation in Taylor–Couette flow for tomographic PIV

Process and EnergyMechanical, Maritime and Materials Engineerin

Clinical activity and molecular correlates of response to atezolizumab alone or in combination with bevacizumab versus sunitinib in renal cell carcinoma

We describe results from IMmotion150, a randomized phase 2 study of atezolizumab (anti-PD-L1) alone or combined with bevacizumab (anti-VEGF) versus sunitinib in 305 patients with treatment-naive metastatic renal cell carcinoma. Co-primary endpoints were progression-free survival (PFS) in intent-to-treat and PD-L1+ populations. Intent-to-treat PFS hazard ratios for atezolizumab + bevacizumab or atezolizumab monotherapy versus sunitinib were 1.0 (95% confidence interval (CI), 0.69-1.45) and 1.19 (95% CI, 0.82-1.71), respectively; PD-L1+ PFS hazard ratios were 0.64 (95% CI, 0.38-1.08) and 1.03 (95% CI, 0.63-1.67), respectively. Exploratory biomarker analyses indicated that tumor mutation and neoantigen burden were not associated with PFS. Angiogenesis, T-effector/IFN-gamma response, and myeloid inflammatory gene expression signatures were strongly and differentially associated with PFS within and across the treatments. These molecular profiles suggest that prediction of outcomes with anti-VEGF and immunotherapy may be possible and offer mechanistic insights into how blocking VEGF may overcome resistance to immune checkpoint blockade