Methamphetamine induces thoracic aortic aneurysm/dissection through C/EBPβ.

Aims: Thoracic aortic aneurysm/dissection (TAAD) is a life-threatening disease with diverse clinical manifestations. Although the association between methamphetamine (METH) and TAAD is frequently observed, the causal relationship between METH abuse and aortic aneurysm/dissection has not been established. This study was designed to determine if METH causes aortic aneurysm/dissection and delineate the underlying mechanism.

[Clinical observation on auricular magnetotherapy for convalescent stroke patients with depression].

Objective: To observe the effect of auricular magnetotherapy on depression and quality of life in stroke patients with depression after recovery.

Methods: Ninety-three stroke patients with depression were randomly divided into a conventional group(a control group), a conventional combined with magnetotherapy group (an observation 1 group), a conventional combined with vaccaria seed group (an observation 2 group), 31 cases in each group. Conventional treatments were applied in the three groups.

Methamphetamine exposure triggers apoptosis and autophagy in neuronal cells by activating the C/EBPβ-related signaling pathway.

Methamphetamine (Meth) is a widely abused psychoactive drug that primarily damages the nervous system, notably causing dopaminergic neuronal apoptosis. CCAAT-enhancer binding protein (C/EBPβ) is a transcription factor and an important regulator of cell apoptosis and autophagy. Insulin-like growth factor binding protein (IGFBP5) is a proapoptotic factor that mediates Meth-induced neuronal apoptosis, and Trib3 (tribbles pseudokinase 3) is an endoplasmic reticulum (ER) stress-inducible gene involved in autophagic cell death through the mammalian target of rapamycin (mTOR) signaling pathway.