Suicide vs medical assistance in dying (MAiD): A secondary qualitative analysis

Abstract

This is a secondary analysis of three qualitative studies about MAiD in which researchers asked about the differences between suicide and MAiD. In all, researchers interviewed 52 Canadians; 7 were people who had requested MAiD and had been found ineligible, 6 were MAiD providers and 39 were socially and economically marginalized. The overwhelming response was that MAiD is better than suicide in the context of suffering at the end of life. Whereas these people perceived suicide as uncertain, difficult, and something that was usually done alone and without support, they thought MAiD was certain, painless, and more socially acceptable.     

The Effects of Expressing Religious Support Online for Breast Cancer Patients

The growth of online support groups has led to an expression effects paradigm within the health communication literature. Although religious support expression is characterized as a typical subdimension of emotional support, we argue that in the context of a life-threatening illness, the inclusion of a religious component creates a unique communication process. Using data from an online group for women with breast cancer, we test a theoretical expression effects model. Results demonstrate that for breast cancer patients, religious support expression has distinct effects from general emotional support messages, which highlights the need to further theorize expression effects along these lines.     

Mutant C9orf72 human iPSC-derived astrocytes cause non-cell autonomous motor neuron pathophysiology

Mutations in C9orf72 are the most common genetic cause of amyotrophic lateral sclerosis (ALS). Accumulating evidence implicates astrocytes as important non-cell autonomous contributors to ALS pathogenesis, although the potential deleterious effects of astrocytes on the function of motor neurons remains to be determined in a completely humanized model of C9orf72-mediated ALS. Here, we use a human iPSC-based model to study the cell autonomous and non-autonomous consequences of mutant C9orf72 expression by astrocytes. We show that mutant astrocytes both recapitulate key aspects of C9orf72-related ALS pathology and, upon co-culture, cause motor neurons to undergo a progressive loss of action potential output due to decreases in the magnitude of voltage-activated Na⁺ and K⁺ currents. Importantly, CRISPR/Cas-9 mediated excision of the C9orf72 repeat expansion reverses these phenotypes, confirming that the C9orf72 mutation is responsible for both cell-autonomous astrocyte pathology and non-cell autonomous motor neuron pathophysiology.     

Longitudinal multi-modal muscle-based biomarker assessment in motor neuron disease

Journal of Neurology - Clinical phenotypic heterogeneity represents a major barrier to trials in motor neuron disease (MND) and objective surrogate outcome measures are required, especially for...