404 research outputs found
Location of the albumin gainesville mutation in the N-terminal quarter of the albumin molecule
Two Cases of Primary Osteolytic Intraosseous Meningioma of the Skull Metastasizing to Whole Skull and the Spine
We report here two cases of primary intraosseous meningioma with aggressive behavior. A 68-year-old man presented with a one year history of a soft, enlarging mass in the right parietal region. Magnetic resonance image (MRI) revealed a 6 cm sized, heterogeneously-enhancing, bony expansile mass in the right parietal bone, and computed tomograph (CT) showed a bony, destructive lesion. The tumor, including the surrounding normal bone, was totally resected. Dural invasion was not apparent. Diagnosis was atypical meningioma, which extensively metastasized within the skull one year later. A 74-year-old woman presented with a 5-month history of a soft mass on the left frontal area. MRI revealed a 4 cm sized, multilobulated, strongly-enhancing lesion on the left frontal bone, and CT showed a destructive lesion. The mass was adhered tightly to the scalp and dura mater. The lesion was totally removed. Biopsy showed a papillary meningioma. The patient refused adjuvant radiation therapy and later underwent two reoperations for recurred lesions, at 19 and at 45 months postoperative. The patient experienced back pain 5 years later, and MRI showed an osteolytic lesion on the 11th thoracic vertebra. After her operation, a metastatic papillary meningioma was diagnosed. These osteolytic intraosseous meningiomas had atypical/malignant pathologies, which metastasized to whole skull and the spine
The molecular defect of albumin Tagliacozzo: 313 Lys ā Asn
AbstractAlbumin Tagliacozzo is a fast-moving genetic variant of human serum albumin found in 19 unrelated families. The protein was isolated from the serum of a heterozygous healthy subject. Analysis of CNBr fragments by isoelectric focusing allowed us to localize the mutation to CNBr fragment IV (residues 299ā329). This fragment was isolated on a preparative scale and subjected to tryptic digestion. Sequential analysis of the abnormal tryptic peptide, purified by RP-HPLC, revealed the variant was caused by 313 Lys ā Asn substitution, probably due to a point mutation in the structural gene. The lack of a lysine residue accounts for the electrophoretic behavior of albumin Tagliacozzo
Oculopalatal tremor explained by a model of inferior olivary hypertrophy and cerebellar plasticity
The inferior olivary nuclei clearly play a role in creating oculopalatal tremor, but the exact mechanism is unknown. Oculopalatal tremor develops some time after a lesion in the brain that interrupts inhibition of the inferior olive by the deep cerebellar nuclei. Over time the inferior olive gradually becomes hypertrophic and its neurons enlarge developing abnormal soma-somatic gap junctions. However, results from several experimental studies have confounded the issue because they seem inconsistent with a role for the inferior olive in oculopalatal tremor, or because they ascribe the tremor to other brain areas. Here we look at 3D binocular eye movements in 15 oculopalatal tremor patients and compare their behaviour to the output of our recent mathematical model of oculopalatal tremor. This model has two mechanisms that interact to create oculopalatal tremor: an oscillator in the inferior olive and a modulator in the cerebellum. Here we show that this dual mechanism model can reproduce the basic features of oculopalatal tremor and plausibly refute the confounding experimental results. Oscillations in all patients and simulations were aperiodic, with a complicated frequency spectrum showing dominant components from 1 to 3 Hz. The modelās synchronized inferior olive output was too small to induce noticeable ocular oscillations, requiring amplification by the cerebellar cortex. Simulations show that reducing the influence of the cerebellar cortex on the oculomotor pathway reduces the amplitude of ocular tremor, makes it more periodic and pulse-like, but leaves its frequency unchanged. Reducing the coupling among cells in the inferior olive decreases the oscillationās amplitude until they stop (at ā¼20% of full coupling strength), but does not change their frequency. The dual-mechanism model accounts for many of the properties of oculopalatal tremor. Simulations suggest that drug therapies designed to reduce electrotonic coupling within the inferior olive or reduce the disinhibition of the cerebellar cortex on the deep cerebellar nuclei could treat oculopalatal tremor. We conclude that oculopalatal tremor oscillations originate in the hypertrophic inferior olive and are amplified by learning in the cerebellum
Fractional anisotropy in the centrum semiovale as a quantitative indicator of cerebral white matter damage in the subacute phase in patients with carbon monoxide poisoning: correlation with the concentration of myelin basic protein in cerebrospinal fluid
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