The role of alternative anastomosis sites in occipital artery-posterior inferior cerebellar artery bypass in the absence of the caudal loop using the far-lateral approach.

OBJECTIVE Occipital artery-posterior inferior cerebellar artery (OA-PICA) bypass is a technically challenging procedure for posterior fossa revascularization. The caudal loop of the PICA is considered the optimal site for OA-PICA anastomosis, however its absence can increase the technical difficulty associated with this procedure. The use of the far-lateral approach for accessing alternative anastomosis sites in OA-PICA bypass in patients with absent or unavailable caudal loops of PICA is evaluated.

Stent-assisted coil embolization for anterior cerebral artery dissection presented with cerebral infarction.

Background: Compared to those found in the vertebrobasilar system, intracranial dissection in the anterior circulation is relatively rare, especially in the anterior cerebral artery (ACA). Moreover, only several cases of ACA dissection that underwent endovascular treatment have been reported. Here we present a rare case of gradually developing ACA dissecting aneurysm causing cerebral infarction, successfully treated by stent-assisted coil embolization.

Does thioredoxin-1 prevent mitochondria- and endoplasmic reticulum-mediated neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine?

We show that 1-methyl-4-phenylpyridinium ion (MPP(+)), an active metabolite of 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP), induces cytotoxicity via endoplasmic reticulum (ER)- and mitochondria-mediated pathways, and thioredoxin-1 (TRX-1), a redox-active protein, prevents MPTP-induced neurotoxicity. TRX-1 overexpression suppressed reactive oxygen species and the ATP decline caused by MPP(+) in HepG2 cells. MPP(+) activated caspase-12 in PC12 cells and induced cytotoxicity in HeLa-rho(0) cells lacking mitochondrial DNA, as well as in the parental HeLa-S3 cells.

[Treatment of a ruptured giant internal carotid artery pseudoaneurysm following transsphenoidal surgery: case report and literature review].

We report here a case of giant internal carotid artery (ICA) pseudoaneurysm as a complication of transsphenoidal surgery. This 50-year-old acromegalic male presented to our clinic with a status of hypovolemic shock due to serious epistaxis. Neuroradiological examinations at his admission revealed a giant aneurysm in the right cavernous portion projecting into the sphenoid sinus.

[A case of bow hunter's stroke treated with endovascular surgery].

Bow hunter's stroke results from vertebrobasilar insufficiency due to a mechanical occlusion or stenosis of the vertebral artery caused by head rotation. We report here a case of bow hunter's stroke that was successfully treated with endovascular surgery. A 69-year-old male complained of intractable vertigo when he rotated his head to the right side.

Stent-supported coil embolization for carotid artery pseudoaneurysm as a complication of endovascular surgery--case report.

A 57-year-old male presented with right amaurosis fugax and left transient ischemic attack caused by stenosis of the intracranial segment of the right internal carotid artery (ICA). Percutaneous transluminal angioplasty with stenting was successfully performed to dilate the stenosis. However, serial angiography revealed the development of a large pseudoaneurysm in the cervical ICA, probably as a result of carotid wall injury caused by the guiding catheter during the procedures.

Intravenous administration of thioredoxin decreases brain damage following transient focal cerebral ischemia in mice.

Thioredoxin (TRX) is induced by a variety of oxidative stimuli and shows cytoprotective roles against oxidative stress. To clarify the possibility of clinical application, we examined the effects of intravenously administered TRX in a model of transient focal cerebral ischemia in this study. Mature male C57BL/6j mice received either continuous intravenous infusion of recombinant human TRX (rhTRX) over a range of 1-10 mg/kg, bovine serum albumin, or vehicle alone for 2 h after 90-min transient middle cerebral artery occlusion (MCAO).

Activation of p38 kinase in the gerbil hippocampus showing ischemic tolerance.

Ischemic tolerance is a phenomenon in which brief episodes of ischemia protect against the lethal effects of subsequent periods of prolonged ischemia. The authors investigated the activation of p38 mitogen-activated protein kinase (p38) in the gerbil hippocampus by Western blotting and immunohistochemistry to clarify the role of p38 kinase in ischemic tolerance. After the 2-minute global ischemia, immunoreactivity indicating active p38 was enhanced at 6 hours of reperfusion and continuously demonstrated 72 hours after ischemia in CA1 and CA3 neurons.

Hypoxia-ischemia induces thioredoxin expression and nitrotyrosine formation in new-born rat brain.

Thioredoxin (TRX) is a 13 kDa protein with antioxidant effect and redox regulating functions. Peroxynitrite is a strong oxidizing and nitrating agent which can react with all classes of biomolecules. In the present study, we focused on the association between TRX and nitrotyrosine, which served as a marker of peroxynitrite formation, in the neonatal hypoxia-ischemia (HI) rat brain.

Critical roles of thioredoxin in nerve growth factor-mediated signal transduction and neurite outgrowth in PC12 cells.

Thioredoxin (TRX) has a role in a variety of biological processes, including cytoprotection and the activation of transcription factors. Nerve growth factor (NGF) is a major survival factor of sympathetic neurons and promotes neurite outgrowth in rat pheochromocytoma PC12 cells. In this study, we showed that NGF induces TRX expression at protein and mRNA levels.

Thioredoxin suppresses 1-methyl-4-phenylpyridinium-induced neurotoxicity in rat PC12 cells.

Thioredoxin (TRX) is a redox-active protein which plays a cytoprotective role against oxidative stress. Geranylgeranylacetone (GGA), used widely as an anti-ulcer drug, has been reported to induce TRX as well as heat shock protein 70 (HSP70) in hepatocytes and other cells. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), causes dopaminergic denervation and Parkinsonism in humans.