Correction to 'A modified formulation of quasi-linear viscoelasticity for transversely isotropic materials under finite deformation'.

[This corrects the article DOI: 10.1098/rspa.2018.

Mechanics of human brain organoids.

Organoids are prototypes of human organs derived from cultured human stem cells. They provide a reliable and accurate experimental model to study the physical mechanisms underlying the early developmental stages of human organs and, in particular, the early morphogenesis of the cortex. Here we propose a mathematical model to elucidate the role played by two mechanisms which have been experimentally proven to be crucial in shaping human brain organoids: the contraction of the inner core of the organoid and the microstructural remodeling of its outer cortex.

Poynting effect of brain matter in torsion.

We investigate experimentally and model theoretically the mechanical behaviour of brain matter in torsion. Using a strain-controlled rheometer, we perform torsion tests on fresh porcine brain samples. We quantify the torque and the normal force required to twist a cylindrical sample at constant twist rate.

A modified formulation of quasi-linear viscoelasticity for transversely isotropic materials under finite deformation.

The theory of quasi-linear viscoelasticity (QLV) is modified and developed for transversely isotropic (TI) materials under finite deformation. For the first time, distinct relaxation responses are incorporated into an integral formulation of nonlinear viscoelasticity, according to the physical mode of deformation. The theory is consistent with linear viscoelasticity in the small strain limit and makes use of relaxation functions that can be determined from small-strain experiments, given the time/deformation separability assumption.

Evidence for sub-haplogroup h5 of mitochondrial DNA as a risk factor for late onset Alzheimer's disease.

Background: Alzheimer's Disease (AD) is the most common neurodegenerative disease and the leading cause of dementia among senile subjects. It has been proposed that AD can be caused by defects in mitochondrial oxidative phosphorylation. Given the fundamental contribution of the mitochondrial genome (mtDNA) for the respiratory chain, there have been a number of studies investigating the association between mtDNA inherited variants and multifactorial diseases, however no general consensus has been reached yet on the correlation between mtDNA haplogroups and AD.