Visible-light-promoted cascade cyclization of -arylacrylamides with bromomethyl sulfone: access to sulfonylmethylated phenanthridines.

We present a visible-light-promoted radical cascade cyclization reaction sulfonylmethylation, cyano insertion, and radical cyclization of unactivated alkenes bearing cyano groups. This strategy enables the rapid synthesis of sulfonylmethylated phenanthridines under mild conditions with broad substrate compatibility, operational simplicity, and mild reaction conditions. The developed approach provides a novel pathway for assembling complex polycyclic nitrogen-containing frameworks, addressing a critical synthetic challenge and expanding the toolbox of photochemical transformations in organic synthesis.

A meta-analysis of randomized controlled trials: evaluating the efficacy of isokinetic muscle strengthening training in improving knee osteoarthritis outcomes.

Background: Knee osteoarthritis (KOA) is a prevalent degenerative joint disease. The primary pathological manifestations of KOA include articular cartilage degeneration, joint space narrowing, and osteophyte formation, leading to a spectrum of symptoms, including joint pain, stiffness, reduced mobility, diminished muscle strength, and severe disability. We aimed to utilize a meta-analysis to evaluate the efficacy of isokinetic muscle strengthening training (IMST) as a rehabilitation treatment for KOA in lowland areas.

ACOX1 activates autophagy via the ROS/mTOR pathway to suppress proliferation and migration of colorectal cancer.

Acyl-CoA oxidase 1 (ACOX1), a member of the acyl-coenzyme A oxidase family, is considered a crucial regulator whose dysregulation is implicated in the occurrence and progression of various cancers. This study aims to elucidate the impact of ACOX1 in CRC, shedding light on its potential as a therapeutic target. Through analysis of the GEO dataset, it was found that ACOX1 is significantly downregulated in colorectal cancer (CRC), and this lower expression level is associated with a worse prognosis.

Intranasal iron administration induces iron deposition, immunoactivation, and cell-specific vulnerability in the olfactory bulb of C57BL/6 mice.

Iron is the most abundant transition metal in the brain and is essential for brain development and neuronal function; however, its abnormal accumulation is also implicated in various neurological disorders. The olfactory bulb (OB), an early target in neurodegenerative diseases, acts as a gateway for environmental toxins and contains diverse neuronal populations with distinct roles. This study explored the cell-specific vulnerability to iron in the OB using a mouse model of intranasal administration of ferric ammonium citrate (FAC).