The CaSR is broadly expressed in the CNS and colocalized with the

The CaSR is broadly expressed in the CNS and colocalized with the inhibitory gamma-aminobutyric acid-B receptor 1 (GABA-B-R1). In hippocampal neurons, GABA-B-R1 heterodimerizes with CaSR and suppresses CaSR expression. To study the interplay between these two receptors in the development of ischemic cell death and neuroprotection

by hypothermia, we subjected C57/BL6 mice to global cerebral ischemia by performing bilateral carotid artery occlusion (10 min) followed by reperfusion for 1-3 days with or without therapeutic hypothermia (33 degrees C for 3 h at the onset of reperfusion). Terminal deoxynucleotidyl transferase dUTP nick end labeling staining MI-503 supplier and immunohistochemistry showed that fore-brain ischemia increased CaSR expression, decreased GABA-B-R1 expression, and promoted cell death.

These changes were particularly evident in hippocampal neurons and could be reversed by mild hypothermia. The induction of CaSR, 3-deazaneplanocin A along with reciprocal decreases in GABA-B-R1 expression, may together potentiate ischemic neuronal death, suggesting a new therapeutic target for treatment of ischemic brain injury.”
“Purpose: The aim of this study was to provide an overview of a single-institution, 30-year surgical experience with the soft tissue management of orbitotemporal neurofibromatosis. Lessons learned are highlighted in case presentations.

Methods: Selleck VX-661 From 1981 to 2011, all patients who presented to the Chang Gung Memorial Hospital Craniofacial Center with craniofacial neurofibromatosis and orbitotemporal involvement were retrospectively reviewed. The medical records of those patients who underwent surgical correction were reviewed for age, extent of involvement, procedures performed, histologic confirmation, and acute complications. All patients were grouped according to the Jackson Classification.

The electronic photobank was queried to evaluate results.

Results: Thirty-five patients presented to our center with orbitotemporal neurofibromatosis during the study period. Thirty-one patients underwent surgical management of their disease. The average age was 25 years (range 4 to 57 years). Over half of our patients (n = 18) presented with concomitant disease of the cheek. The 2 most common procedures performed were lateral canthopexy (n = 24) and upper eyelid excision (n = 24). The only acute complication recorded was a postoperative hematoma on the fourth postoperative day following simultaneous lateral canthopexy and upper eyelid excision which required operative evacuation.

Conclusions: In orbitotemporal neurofibromatosis, tissue hyperextensibility and tumor weight adversely affect outcomes. Treatment of concomitant disease of the cheek should be prioritized in order to provide periorbital support prior to addressing the delicate structures of the eyelids.

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