Non-esterified fatty acid palmitate facilitates oxidative endoplasmic reticulum stress and apoptosis of β-cells by upregulating ERO-1α expression.

Adipose tissue-derived non-esterified saturated long-chain fatty acid palmitate (PA) decisively contributes to β-cell demise in type 2 diabetes mellitus in part through the excessive generation of hydrogen peroxide (HO). The endoplasmic reticulum (ER) as the primary site of oxidative protein folding could represent a significant source of HO. Both ER-oxidoreductin-1 (ERO-1) isoenzymes, ERO-1α and ERO-1β, catalyse oxidative protein folding within the ER, generating equimolar amounts of HO for every disulphide bond formed.

Luminal H O promotes ER Ca dysregulation and toxicity of palmitate in insulin-secreting INS-1E cells.

The endoplasmic reticulum (ER) lumen is not only the major site for the assembly and folding of newly synthesized proteins but also the main intracellular Ca store. Ca ions are involved in versatile biochemical processes, including posttranslational processing and folding of nascent proteins. Disruption of ER Ca homeostasis is usually accompanied by an ER stress response that can ultimately lead to apoptosis if unresolved.

Carotid Endarterectomy Surgeries: A Multimodality Intraoperative Neurophysiological Monitoring Approach.

Patients with untreated carotid artery stenosis remain at high risk for stroke. Carotid endarterectomy (CEA) is a surgical procedure for the treatment of symptomatic and severe asymptomatic carotid stenosis. A small percentage of patients who do not have good collateral circulation are at high risk of cerebral ischemia during the cross-clamping of the carotid artery.