The impact of APOE4 on neurological symptoms after exposure to K. brevis neurotoxin.

Introduction: The harmful alga Karenia brevis (K. brevis) releases brevetoxins (PbTx) that cause respiratory and neurological symptoms. The apolipoprotein E (APOE) ε4 allele has been linked to poor neurological outcomes after exposure to environmental toxicants.

Securing Commercial Nucleic Acid Synthesis.

On-demand gene synthesis is a growing industry that has democratized access to customized synthetic deoxyribonucleic acid (DNA) and ribonucleic acid (RNA) products used in biological research. However, the increasing availability and decreasing cost of custom synthetic nucleic acids presents a risk of misuse that could allow nefarious actors to obtain sequences of dangerous organisms or novel-engineered pathogens to construct a biological weapon. Securing nucleic acid synthesis is a policy priority for the U.

PPARγ activation ameliorates cognitive impairment and chronic microglial activation in the aftermath of r-mTBI.

Chronic neuroinflammation and microglial activation are key mediators of the secondary injury cascades and cognitive impairment that follow exposure to repetitive mild traumatic brain injury (r-mTBI). Peroxisome proliferator-activated receptor-γ (PPARγ) is expressed on microglia and brain resident myeloid cell types and their signaling plays a major anti-inflammatory role in modulating microglial responses. At chronic timepoints following injury, constitutive PPARγ signaling is thought to be dysregulated, thus releasing the inhibitory brakes on chronically activated microglia.