The microRNA miR-21 conditions the brain to protect against ischemic and traumatic injuries.

Ischemic and traumatic injuries to CNS remain leading causes of death and disability worldwide, despite decades of research into risk factors, therapies, and preventative measures. Recent studies showed that CNS injuries significantly alter the cerebral microRNAome that impact the secondary brain damage as well as plasticity and recovery. Many microRNA based therapies are currently in various clinical trials for different pathologic conditions indicating their therapeutic potential.

Retromandibular fossa approach to the high cervical internal carotid artery: an anatomic study.

Objective: Access to the high cervical internal carotid artery (ICA) is technically challenging for the treatment of lesions in and around this region. The aims of this study were to analyze the efficacy of approaching the high cervical ICA through the retromandibular fossa and to compare preauricular and postauricular incisions. In addition, the relevant neural and vascular structures of this region are demonstrated in cadaveric dissections.

Inhibition of calcium-induced insulin secretion from intact HIT-T15 or INS-1 beta cells by GTP depletion.

Using intact rat islets, we previously observed that GTP depletion (achieved through the use of mycophenolic acid or other synthesis inhibitors) impedes nutrient- but not K+-induced insulin secretion. It was concluded that a proximal nutrient-dependent step in stimulus-secretion coupling (but not the process of Ca2+-induced exocytosis itself) is modulated by ambient GTP levels. To examine Ca2+-dependent steps further in intact beta cells, INS-1 cells (which synthesize GTP and ATP similarly to rat islets) and HIT-T15 cells (whose synthesis of purine nucleotides is different) were studied following cell culture for 1-18 hr in various concentrations of mycophenolic acid (MPA) or mizoribine (MZ).

Dual functional effects of interleukin-1beta on purine nucleotides and insulin secretion in rat islets and INS-1 cells.

Interleukin-1beta (IL-1beta) has been shown to inhibit glucose-induced insulin secretion from rat islets and purified beta-cells, primarily through the generation of nitric oxide (NO). However, the mechanisms by which NO exerts its effects remain unclear. To examine the role of purine nucleotides, we cultured intact rat islets or INS-1 (glucose-responsive transformed rat) beta-cells for 18 h in the presence or absence of IL-1beta.