Neonatal hypoxic/ischemic (H/I) brain injury causes neurological impairment, including cognitive and motor dysfunction as well as seizures. However, the molecular mechanisms regulating neuron death after H/I injury are poorly defined and remain controversial. Here we show that Atg7, a gene essential for autophagy induction, is a critical mediator of H/Iinduced neuron death. Neonatal mice subjected to H/I injury show dramatically increased autophagosome formation and extensive hippocampal neuron death that is regulated by both caspase-3-dependent and -independent execution. Mice deficient in Atg7 show nearly complete protection from both H/I-induced caspase-3 activation and neuron death indicating that Atg7 is critically positioned upstream of multiple neuronal death executioner pathways. Adult H/I brain injury also produces a significant increase in autophagy, but unlike neonatal H/I, neuron death is almost exclusively caspase-3-independent. These data suggest that autophagy plays an essential role in triggering neuronal death execution after H/I injury and Atg7 represents an attractive therapeutic target for minimizing the neurological deficits associated with H/I brain injury.

Hemodialysis patients with foot lesions have a poor prognosis, with high rates of mortality and amputation. Prompt assessments of the severity of systemic conditions, such as cardiac ischemia, and focal wound conditions, such as ischemia and infection, are necessary to treat hemodialysis patients with foot lesions.

Brachiocephalic artery dissection and no tear resection are potential predictors of patent false lumen of the aortic arch after hemiarch replacement.

We concluded that AAAs over 6 cm in diameter were an appropriate indication for surgery in octogenarians.

Although the instructions for use of most commercially available stent grafts provide for a PN angulation of ≤ 60°, PN angulation was not a major issue in a midterm follow-up of AAAs with adequate PN length for patients in this series who received a Zenith or Excluder graft.