Myeloid-specific deletion of autotaxin inhibits rheumatoid arthritis and osteoclastogenesis.

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by joint swelling, pain, and bone remodeling. We previously reported that autotaxin (ATX) deficiency disrupts lipid rafts in macrophages. Lipid raft disruption results in the dysregulation of RANK signaling, which is crucial for osteoclastogenesis and the pathogenesis of RA.

Microtubule acetylation and PERK activation facilitate eribulin-induced mitochondrial calcium accumulation and cell death.

Over the past few decades, microtubules have been targeted by various anticancer drugs, including paclitaxel and eribulin. Despite their promising effects, the development of drug resistance remains a challenge. We aimed to define a novel cell death mechanism that targets microtubules using eribulin and to assess its potential in overcoming eribulin resistance.

Effects of Stigmatizing Language on Trainees' Clinical Decision-Making in Substance Use Disorders: A Randomized Controlled Trial.

Objectives: Substance use disorder (SUD) continues to be one of the most stigmatized and under-treated conditions in the United States. Stigmatizing language used by healthcare workers can transmit bias to others within healthcare, including medical trainees. This study investigates how stigmatizing language and undergraduate medical education (UME) curricula may influence trainees' clinical decision-making for patients with SUD.

CKAP4 is a potential therapeutic target to overcome resistance to EGFR-TKIs in lung adenocarcinoma.

Background: Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) are standard treatments for non-small cell lung cancer (NSCLC) patients with EGFR mutations; however, drug resistance limits their efficacy. Cytoskeleton-associated protein 4 (CKAP4) has been linked to cancer progression, but its role in EGFR-TKI resistance remains unclear.

Objective: This study investigates the clinical relevance of CKAP4 as a therapeutic target to overcome EGFR-TKI resistance in lung adenocarcinoma (LUAD) patients.