ABSTRACT
BACKGROUND: Metamorphopsia includes a broad spectrum of visual perceptual distortions, such as alteration of perceived object size or, rarely, altered perception of faces, termed prosopometamorphopsia. CASE REPORT: This report describes a patient who complained of metamorphopsia restricted to the center of the face, particularly the lower part of the face (nose and mouth), following infarction of the right medial temporooccipital lobe that included the fusiform face area. CONCLUSIONS: The fusiform face area is commonly believed to be a face-selective cortical region dedicated to the visual analysis of face stimuli. We speculate that any injury to this brain area could bring about prosopometamorphopsia involving whole or unilateral face perception, or very rarely, as in our case, distortion restricted to the central area of the face. Furthermore, there could be topographical correspondences between facial structures and the fusiform face area.
Subject(s)
Humans , Brain , Infarction , Mouth , Nose , Perceptual Distortion , Vision DisordersABSTRACT
BACKGROUND: Defects in mitochondrial function have been shown to participate in the induction of neuronal cell injury. The extracellular-signal-regulated kinase (ERK) signaling pathway plays a crucial role in almost all cell functions, including proliferation, differentiation, survival, and death. However, the effect of ERK inhibition on oxysterol-induced apoptosis remains uncertain. METHODS: This study assessed the effect of ERK inhibition on the apoptotic effect of 7-ketocholesterol. RESULTS: Treatment with 7-ketocholesterol increased phosphorylated-ERK1/2 levels in differentiated PC12 cells, while the total amount of ERK was not altered. 7-Ketocholesterol decreased Bid and Bcl-2 levels, increased Bax and p53 levels, and promoted cytochrome c release, which elicits the activation of caspases (-8, -9, and -3), nuclear damage, and cell death. ERK and farnesyltransferase inhibitors inhibited the 7-ketocholesterol-induced phosphorylation of ERK1/2, activation of apoptosis-related proteins, and cell death in PC12 cells. CONCLUSIONS: The ERK and farnesyltransferase inhibitors, which did not exhibit toxicity, may inhibit the 7-ketocholesterol toxicity on differentiated PC12 cells by suppressing the activation of the caspase-8-dependent pathway as well as activation of the mitochondria-mediated cell-death pathway, leading to the activation of caspases. The inhibition of ERK may confer a beneficial protective effect against the neuronal cell injury induced by cholesterol oxidation products.
Subject(s)
Animals , Apoptosis , Caspases , Cell Death , Cholesterol , Cytochromes c , Farnesyltranstransferase , Ketocholesterols , Neurons , PC12 Cells , Phosphorylation , Phosphotransferases , ProteinsABSTRACT
No abstract available.
Subject(s)
Humans , Diplopia , Isaacs Syndrome , Neoplasm Metastasis , OrbitABSTRACT
Spontaneous remission in untreated primary central nervous system lymphoma is rare. A 66-year-old man was admitted with dizziness and gait disturbance. Initial fluid-attenuated inversion-recovery images revealed hyperintensities in the upper brainstem, left temporal lobe, and right occipital lobe. The patient's symptoms and lesions disappeared spontaneously after 1 month. However, he was readmitted after 4 months with right hemiparesis. Magnetic resonance imaging revealed a homogenous enhanced lesion in the left basal ganglia with a vasogenic pattern. This disease warranted biopsy, which revealed large B-cell lymphoma.
Subject(s)
Aged , Humans , Basal Ganglia , Biopsy , Brain Stem , Central Nervous System , Dizziness , Gait , Lymphoma , Lymphoma, B-Cell , Magnetic Resonance Imaging , Occipital Lobe , Paresis , Remission, Spontaneous , Temporal LobeABSTRACT
BACKGROUND: Protein casein kinase 2 is involved in signal transduction, cell growth, and apoptosis. However, it has not been elucidated whether parkinsonian toxin 1-methyl-4-phenylpyridinium (MPP+)-induced neuronal cell death is mediated by a casein-kinase-2-mediated pathway. METHODS: We monitored apoptosis-related protein activation, changes in the level of casein kinase 2, nuclear damage, and apoptosis in differentiated PC12 cells exposed to MPP+ in combination with casein kinase 2 inhibitor. RESULTS: Casein kinase 2 inhibitors [4,5,6,7-tetrabromobenzotriazole (TBB), 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole, and apigenin] reduced MPP+- and rotenone-induced cell death in differentiated PC12 cells. TBB inhibited the MPP+-induced activation of apoptosis-related proteins (decreases in Bid and Bcl-2 levels, increase in Bax levels, cytochrome c release, and caspase-3 activation), increase in casein kinase 2 levels, and nuclear damage. CONCLUSIONS: Administering casein kinase 2 inhibitor TBB at concentrations that do not induce toxic effects may reduce MPP+-induced cell death in differentiated PC12 cells by suppressing the apoptosis-related protein activation that leads to cytochrome c release and subsequent activation of caspase-3. The results suggest that MPP+-induced cell death process is mediated by a casein kinase 2 pathway.
Subject(s)
Animals , 1-Methyl-4-phenylpyridinium , Apoptosis , Casein Kinase II , Casein Kinases , Caseins , Caspase 3 , Cell Death , Cytochromes c , Neurons , PC12 Cells , Proteins , Signal Transduction , TriazolesABSTRACT
No abstract available.