Intermittent cyclic mechanical compression promotes endplate chondrocytes degeneration by disturbing Nrf2/PINK1 signaling pathway-dependent mitophagy.

An abnormal mechanical load is a pivotal inducer of endplate cartilage degeneration, which subsequently promotes intervertebral disc degeneration. Our previous study indicated that intermittent cyclic mechanical compression (ICMC) promotes endplate chondrocyte degeneration, but the mechanism underlying this effect is unclear. In this study, we investigated PTEN-induced kinase 1(PINK1) dependent mitophagy during ICMC-induced endplate chondrocyte degeneration.

Exposure of the hidden anti-ferromagnetism in paramagnetic CdSe:Mn nanocrystals.

We present theoretical and experimental investigations of the magnetism of paramagnetic semiconductor CdSe:Mn nanocrystals and propose an efficient approach to the exposure and analysis of the underlying anti-ferromagnetic interactions between magnetic ions therein. A key advance made here is the development of an analysis method with the exploitation of group theory technique that allows us to distinguish the anti-ferromagnetic interactions between aggregative Mn(2+) ions from the overall pronounced paramagnetism of magnetic-ion-doped semiconductor nanocrystals. By using the method, we clearly reveal and identify the signatures of anti-ferromagnetism from the measured temperature-dependent magnetisms and furthermore determine the average number of Mn(2+) ions and the fraction of aggregative ones in the measured CdSe:Mn nanocrystals.

Gamma Knife surgery for hemifacial spasm related to cerebellopontine angle tumors.

Object: Most cases of tumor-related hemifacial spasm (HFS) are treated by open surgery. The authors report the effects of Gamma Knife surgery (GKS) on benign tumor-related HFS at a mean follow-up time of 84 months.

Methods: Between 2000 and 2011, 6 patients (5 women and 1 man) harboring single tumors of the cerebellopontine angle (4 meningiomas and 2 vestibular schwannomas [VSs]) and experiencing HFS underwent GKS as a primary treatment.

Cooking oil fumes improve lung adenocarcinoma cell survival through c-IAP2 induction.

Cooking oil fumes (COF) exposure was demonstrated to be associated with lung cancer development in Taiwanese nonsmoking women. Previous studies identified Cox-2 overexpression and oxidative DNA damage in lung adenocarcinoma cells after exposure to COF. Involvement of COF in lung tumorigenesis may be associated with cell survival, as well as proliferation of lung adenocarcinoma.