'Yeah, this is my donation': An application of psychological ownership in blood donation.

To meet the priority healthcare needs of any population there must be a consistently available blood supply donated by willing donors. Due to this universal need for blood, retaining blood donors remains an ongoing challenge for blood services internationally. Encouraging psychological ownership, or the feeling of ownership one experiences over a possession, provides a potential novel solution to donor retention.

Microglial inflammation in genome instability: A neurodegenerative perspective.

The maintenance of genome stability is crucial for cell homeostasis and tissue integrity. Numerous human neuropathologies display chronic inflammation in the central nervous system, set against a backdrop of genome instability, implying a close interplay between the DNA damage and immune responses in the context of neurological disease. Dissecting the molecular mechanisms of this crosstalk is essential for holistic understanding of neuroinflammatory pathways in genome instability disorders.

Psychological ownership and identity motives in blood donation.

Background And Objectives: Interventions to retain existing donors are essential to increase the blood supply. Blood donor self-identity is proposed to motivate sustained donation behaviour. However, interventions to develop self-identity in the absence of donating blood are scarce.

Comparison of tumor-informed and tumor-naïve sequencing assays for ctDNA detection in breast cancer.

Analysis of circulating tumor DNA (ctDNA) to monitor cancer dynamics and detect minimal residual disease has been an area of increasing interest. Multiple methods have been proposed but few studies have compared the performance of different approaches. Here, we compare detection of ctDNA in serial plasma samples from patients with breast cancer using different tumor-informed and tumor-naïve assays designed to detect structural variants (SVs), single nucleotide variants (SNVs), and/or somatic copy-number aberrations, by multiplex PCR, hybrid capture, and different depths of whole-genome sequencing.

CRISPR-Cas9 genetic screen leads to the discovery of L-Moses, a KAT2B inhibitor that attenuates Tunicamycin-mediated neuronal cell death.

Accumulation of aggregated and misfolded proteins, leading to endoplasmic reticulum stress and activation of the unfolded protein response, is a hallmark of several neurodegenerative disorders, including Alzheimer's and Parkinson's disease. Genetic screens are powerful tools that are proving invaluable in identifying novel modulators of disease associated processes. Here, we performed a loss-of-function genetic screen using a human druggable genome library, followed by an arrayed-screen validation, in human iPSC-derived cortical neurons.