The role of computed tomography and magnetic resonance imaging in diagnosing clear cell ameloblastoma: A case report.

Ameloblastoma is the most common and clinically relevant type of odontogenic tumor. Clear cell odontogenic carcinoma is histologically characterized by solid sheets and nests of clear cells, whereas clear cell ameloblastoma (CCAM) is histologically characterized by an ameloblastomatous component intermixed with an extensive clear cell component. A total of 12 reports have been published on the histological etiology for CCAM; however, no reports have made regarding the detailed computed tomography and/or magnetic resonance imaging features of tumors of this type. The present study describes a case of a well-circumscribed 20-mm radiolucent lesion of the anterior mandible that was misdiagnosed as a clear cell odontogenic carcinoma. The study describes the detailed radiological characteristics of a case of CCAM.

Ketamine reduces amyloid ß-protein degradation by suppressing neprilysin expression in primary cultured astrocytes.

Pathological accumulation of cortical amyloid ß-protein (Aß) is an early and consistent feature of Alzheimer's disease (AD). Aß levels in the brain are determined by production and catabolism. Previous studies have suggested that deficits in the brain expression of neprilysin (NEP) and the insulin-degrading enzyme (IDE), which are both proteases involved in amyloid degradation, may promote Aß deposition in patients with sporadic late-onset AD. Because the incidence of AD increases after surgical intervention, we examined whether ketamine, which is a general anaesthetic with neuroprotective properties for excitotoxic ischaemic damage, is associated with Aß degradation by inducing NEP and IDE expression. The non-competitive N-methyl-d-aspartate receptor antagonist ketamine and MK801 significantly decreased the expression of NEP, but not IDE, in a concentration- and time-dependent manner through the dephosphorylation of p38 mitogen-activated protein kinase (MAPK) in cultured rat astrocytes. Furthermore, NEP-reduced reagents significantly suppressed the degradation of exogenous Aß in cultured astrocytes. These results suggested that ketamine suppresses the Aß degradation of NEP by reducing p38 MAPK-mediated pathway activity.

Brain insulin resistance accelerates Aß fibrillogenesis by inducing GM1 ganglioside clustering in the presynaptic membranes.

Type 2 diabetes mellitus is thought to be a significant risk factor for Alzheimer's disease. Insulin resistance also affects the central nervous system by regulating key processes, such as neuronal survival and longevity, learning and memory. However, the mechanisms underlying these effects remain uncertain. To investigate whether insulin resistance is associated with the assembly of amyloid ß-protein (Aß) at the cell surface of neurons, we inhibited insulin-signalling pathways of primary neurons. The treatments of insulin receptor (IR)-knockdown and a phosphatidylinositol 3-kinase inhibitor (LY294002), but not an extracellular signal-regulated kinase inhibitor, induced an increase in GM1 ganglioside (GM1) levels in detergent-resistant membrane microdomains of the neurons. The aged db/db mouse brain exhibited reduction in IR expression and phosphorylation of Akt, which later induced an increase in the high-density GM1-clusters on synaptosomes. Neurons treated with IR knockdown or LY294002, and synaptosomes of the aged db/db mouse brains markedly accelerated an assembly of Aßs. These results suggest that ageing and peripheral insulin resistance induce brain insulin resistance, which accelerates the assembly of Aßs by increasing and clustering of GM1 in detergent-resistant membrane microdomains of neuronal membranes.