The spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has already taken on pandemic proportions, affecting over 100 countries in a matter of weeks. A global response to prepare health systems worldwide is imperative. Although containment measures in China have reduced new cases by more than 90%, this reduction is not the case elsewhere, and Italy has been particularly affected. There is now grave concern regarding the Italian national health system's capacity to effectively respond to the needs of patients who are infected and require intensive care for SARS-CoV-2 pneumonia. The percentage of patients in intensive care reported daily in Italy between March 1 and March 11, 2020, has consistently been between 9% and 11% of patients who are actively infected. The number of patients infected since Feb 21 in Italy closely follows an exponential trend. If this trend continues for 1 more week, there will be 30 000 infected patients. Intensive care units will then be at maximum capacity; up to 4000 hospital beds will be needed by mid-April, 2020. Our analysis might help political leaders and health authorities to allocate enough resources, including personnel, beds, and intensive care facilities, to manage the situation in the next few days and weeks. If the Italian outbreak follows a similar trend as in Hubei province, China, the number of newly infected patients could start to decrease within 3-4 days, departing from the exponential trend. However, this cannot currently be predicted because of differences between social distancing measures and the capacity to quickly build dedicated facilities in China.

We present a modeling framework designed for patient-specific computational hemodynamics to be performed in the context of large-scale studies. The framework takes advantage of the integration of image processing, geometric analysis and mesh generation techniques, with an accent on full automation and high-level interaction. Image segmentation is performed using implicit deformable models taking advantage of a novel approach for selective initialization of vascular branches, as well as of a strategy for the segmentation of small vessels. A robust definition of centerlines provides objective geometric criteria for the automation of surface editing and mesh generation. The framework is available as part of an open-source effort, the Vascular Modeling Toolkit, a first step towards the sharing of tools and data which will be necessary for computational hemodynamics to play a role in evidence-based medicine.

The incidence of chronic kidney diseases is increasing worldwide, and these conditions are emerging as a major public health problem. While genetic factors contribute to susceptibility and progression of renal disease, proteinuria has been claimed as an independent predictor of outcome. Reduction of urinary protein levels by various medications and a low-protein diet limits renal function decline in individuals with nondiabetic and diabetic nephropathies to the point that remission of the disease and regression of renal lesions have been observed in experimental animals and even in humans. In animal models, regression of glomerular structural changes is associated with remodeling of the glomerular architecture. Instrumental to this discovery were 3D reconstruction studies of the glomerular capillary tuft, which allowed the quantification of sclerosis volume reduction and capillary regeneration upon treatment. Regeneration of capillary segments might result from the contribution of resident cells, but progenitor cells of renal or extrarenal origin may also have a role. This review describes recent advances in our understanding of the mechanisms and mediators underlying renal tissue repair ultimately responsible for regression of renal injury.

The effects of hemodynamic forces upon vascular endothelial cell turnover were studied by exposing contact-inhibited confluent cell monolayers to shear stresses of varying amplitude in either laminar or turbulent flow. Laminar shear stresses (range, 8-15 dynes/cm2; 24 hr) induced cell alignment in the direction of flow without initiating the cell cycle. In contrast, turbulent shear stresses as low as 1.5 dynes/cm2 for as short a period as 3 hr stimulated substantial endothelial DNA synthesis in the absence of cell alignment, discernible cell retraction, or cell loss. The results of these in vitro experiments suggest that in atherosclerotic lesion-prone regions of the vascular system, unsteady blood flow characteristics, rather than the magnitude ofwall shear stressperse, may be the major determinant of hemodynamically induced endothelial cell turnover.Hemodynamic forces have been implicated in the initiation, localization, and development of atherosclerotic vascular disease (1, 2). Little is known, however, about the effects of such forces upon the endothelial cell lining of blood vessels, the integrity of which is essential for normal vascular function. In certain areas ofthe aorta and its main branches, blood flow characteristics are both variable and complex. In locations such as the descending thoracic aorta and distal carotid arteries, pulsatile laminar flow is prevalent (3), whereas in other regions, such as coronary arteries and the carotid bifurcation, secondary flows, vortices, and intermittently changing flow directions are encountered (4). The distribution of atherosclerotic lesions in susceptible species, including humans, is closely correlated with the location of disturbed flow in the major vessels (5). Time-dependent flow separation and unsteady secondary flow typically occur in localized regions that are usually well defined and of limited size. Furthermore, turbulence will occur in the largest arteries under conditions of increased flow velocity and cardiac output (4). Thus, shear stresses, which are the direct tractive forces acting on the endothelial cell surface as a result of blood flow, are highly variable in magnitude, frequency, and direction in such regions.Autoradiographic studies in vivo have demonstrated increased endothelial DNA synthesis in localized areas of the aorta and its major branches, suggesting that locally increased endothelial cell turnover, perhaps as a result of injury, may occur near branches and bifurcations (6, 7). Increased cell turnover need not imply denudation of the endothelium and indeed during the initiation and early development of atherosclerotic lesions the endothelium remains a confluent monolayer of cells (8).The role of fluid shear stress in promoting endothelial cell injury and/or turnover is uncertain: both high and low shear stresses have been implicated. High shear stress has been linked to alignment of endothelial cells (9), cell loss (10), increased arterial permeability (11), and enhanced endothelial biosynthetic capabilities (12). Ath...