The interaction of tPA with NMDAR1 drives neuroinflammation and neurodegeneration in α-synuclein-mediated neurotoxicity.

The thrombolytic protease tissue plasminogen activator (tPA) is expressed in the CNS, where it regulates diverse functions including neuronal plasticity, neuroinflammation, and blood-brain-barrier integrity. However, its role in different brain regions such as the substantia nigra (SN) is largely unexplored. In this study, we characterize tPA expression, activity, and localization in the SN using a combination of retrograde tracing and β-galactosidase tPA reporter mice.

Juno Observations of Jupiter's Magnetodisk Plasma: Implications for Equilibrium and Dynamics.

The Jovian magnetodisk plays an essential role in the dynamics of the Jupiter system by coupling its various components. Here, we investigate the Juno (JADE, JEDI, and MAG) observations of the magnetodisk within 20-80 Jupiter radii ( ) in the 0-6 hr local time sector. JADE and JEDI data are combined to generate equatorial plane distributions of density, pressure, temperature, and anisotropy of electrons, protons, and heavy ions.

Chromosome-Scale Genomes of the Flightless Caterpillar Hunter Beetles Calosoma tepidum and Calosoma wilkesii From British Columbia (Coleoptera: Carabidae).

The giant ground beetle genus Calosoma (Coleoptera, Carabidae) comprises ca. 120 species distributed worldwide. About half of the species in this genus are flightless due to a process of wing reduction likely resulting from the colonization of remote habitats such as oceanic islands, highlands, and deserts.

Loss of embryonically-derived Kupffer cells during hypercholesterolemia accelerates atherosclerosis development.

Hypercholesterolemia is a major risk factor for atherosclerosis and associated cardiovascular diseases. The liver plays a key role in the regulation of plasma cholesterol levels and hosts a large population of tissue-resident macrophages known as Kupffer cells (KCs). KCs are located in the hepatic sinusoids where they ensure key functions including blood immune surveillance.

Bax Inhibitor-1 preserves pancreatic β-cell proteostasis by limiting proinsulin misfolding and programmed cell death.

The prevalence of diabetes steadily increases worldwide mirroring the prevalence of obesity. Endoplasmic reticulum (ER) stress is activated in diabetes and contributes to β-cell dysfunction and apoptosis through the activation of a terminal unfolded protein response (UPR). Our results uncover a new role for Bax Inhibitor-One (BI-1), a negative regulator of inositol-requiring enzyme 1 (IRE1α) in preserving β-cell health against terminal UPR-induced apoptosis and pyroptosis in the context of supraphysiological loads of insulin production.