The increased mitochondrial DNA damage leads to altered functional capacities of retinal pigment epithelial (RPE) cells. A previous study showed the increased autophagy in RPE cells caused by low concentrations of rotenone, a selective inhibitor of mitochondrial complex I. However, the mechanism by which autophagy regulates RPE cell death is still unclear. In the present study, we examined the mechanism underlying the regulation of RPE cell death through the inhibition of mitochondrial complex I. We report herein that rotenone induced mitotic catastrophe (MC) in RPE cells. We further observed an increased level of autophagy in the RPE cells undergoing MC (RPE-MC cells). Importantly, autophagy inhibition induced nonapoptotic cell death in RPE-MC cells. These findings indicate that autophagy has a pivotal role in the survival of RPE-MC cells. We next observed PINK1 accumulation in the mitochondrial membrane and parkin translocation into the mitochondria from the cytosol in the rotenone-treated RPE-MC cells, which indicates that increased mitophagy accompanies MC in ARPE-19 cells. Noticeably, the mitophagy also contributed to the cytoprotection of RPE-MC cells. Although there might be a significant gap in the roles of autophagy and mitophagy in the RPE cells in vivo, our in vitro study suggests that autophagy and mitophagy presumably prevent the RPE-MC cells from plunging into cell death, resulting in the prevention of RPE cell loss.

Kernohan's notch phenomenon is the ipsilateral hemiplegia caused by compression of the contralateral cerebral peduncle against the tentorial edge by a supratentorial mass. Diffusion tensor imaging (DTI) and transcranial magnetic stimulation (TMS) could be useful for exploring the state of the corticospinal tract (CST). This report attempts to demonstrate Kernohan's notch phenomenon in a patient with subdural haematoma by using DTI and TMS. One patient and six normal control subjects were recruited. The patient showed severe right hemiplegia even though the subdural haematoma was located in the right hemisphere. Brain CT at the time of onset showed right transtentorial herniation, and T2 weighted images at 6 weeks after onset showed a leucomalacic lesion on the left cerebral peduncle. DTI and TMS were performed at 6 weeks after onset. The fractional anisotrophy value of the left midbrain and medulla of the patient was found to be decreased in comparison with that of the control subjects. On fibre tractography for the CST, an interruption was observed in the left midbrain and medulla. The motor evoked potential obtained from the right hand muscle showed delayed latency, low amplitude and a higher excitatory threshold, thus indicating that the CST of the left hemisphere had been damaged. It seems that the CST had been damaged at the left midbrain, although subdural haematoma and transtentorial herniation had occurred in the right hemisphere in this patient. This report demonstrates Kernohan's notch phenomenon in this patient using DTI and TMS.

The LTBI rate in the present study was much higher than that estimated from other contact investigations. To minimise the risk of nosocomial TB transmission to neonates, screening and management of TB in health care workers should be strengthened.