Biomedical subjects
Publications and source records attributed to C Araoz.
A case of primary nasal meningioma in a 69-year-old women is described. The pathologic, radiologic and clinical characteristics are described. A summary of previously published articles on the subject is given.
Apolipoprotein D (apoD) levels were examined in the temporal cortex as well as an assessment of the location of apoD positive cells within the brain by immunohistochemical and biochemical methods in young control (YC), aged control (AC), and Alzheimer's demented (AD) probands. Scattered apoD positive astrocytes and oligodendrocytes were found throughout the white matter by immunohistochemistry. ApoD immunoreactivity was also observed in the cerebellar oligodendrocytes of the YC group. There was faint positive apoD staining in scattered cortical astrocytes and a few neurons in the same group. In contrast, some of the AC and all of the AD probands had intense and frequent apoD immunostained cortical astrocytes and pyramidal neurons. The cortical senile plaques and neurofibrillary tangles were apoD immunonegative. No quantitative differences were found between the cortical apoD levels in the AC and AD groups, determined by immunoblotting. ApoD detected in the brain tissue was different in molecular weight (29 kDal) from that seen in CSF or in the serum (32 kDal). Our results indicate apoD is present in the human brain, especially in glial cells, and has increased abundance in the elderly and AD subjects.
Interleukin 1, an immune response-generated cytokine that stimulates astrocyte proliferation and reactivity (astrogliosis), was present in up to 30 times as many glial cells in tissue sections of brain from patients with Down syndrome and Alzheimer disease compared with age-matched control subjects. Most interleukin 1-immunoreactive glia in Down syndrome and Alzheimer disease were classified as microglia. The number of interleukin 1 immunoreactive neurons did not appear to differ in Down syndrome and Alzheimer disease compared with control brain. Numerous temporal lobe astrocytes in Alzheimer disease and postnatal Down syndrome were intensely interleukin 1-, S-100-, and glial fibrillary acidic protein-immunoreactive and had reactive structure. Interleukin 1 levels in Alzheimer disease temporal lobe homogenates were elevated, as were the levels of S-100 and glial fibrillary acidic protein, two proteins reportedly elevated in reactive astrocytes. These data suggest that increased expression of S-100 in Down syndrome, resulting from duplication of the gene on chromosome 21 that encodes the beta subunit of S-100, may be augmented by elevation of interleukin 1. As a corollary, the astrogliosis in Alzheimer disease may be promoted by elevation of interleukin 1.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Patients with treated head and neck cancer may have focal neurologic symptoms and personality changes due to delayed cerebral radionecrosis. A history of past treatment should direct the physician to consider these lesions in the differential diagnosis. Craniotomy is the management recommended. Histopathologic changes include fibrotic response of the meninges with pleomorphic and vacuolated fibroblasts, capillary hyperplasia, reactive astrocytes, and fibrosis of the blood vessels. Amyloid is deposited in the arteriolar walls and extracellular space. Ischemic, autoimmune, or vascular mechanisms, and glial alterations have all been considered in the pathogensis of delayed cerebral radionecrosis. Some researchers have concluded that chemotherapeutic agents, such as methotrexate, may contribute to its production.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Postmortem light and electron microscopic studies of a 52 year old black male who died 17 months after the onset of upper and lower motor neuron signs showed: (1) degeneration of cortico-spinal tracts, (2) loss of spinal neurons and gliosis and (3) cellular inclusions with neurotubules, neurofilaments and granular material. Although these cellular inclusions resemble Lafora bodies, they differ in that, to the authors' knowledge, the latter were not reported to have microtubules. Review of the literature revealed no previous report of these inclusions in cases of amyotrophic lateral sclerosis. Tissue cultures of cord, hindbrain and cerebrum did not show cytopathic effect during a three-week observation period.
The mitochondrial anomalies observed in the skeletal muscle of a patient with dermatomyositis included paracrystalline inclusions, dense bodies and stacks of lamellae. Virions were not found. These anomalies are similar to those noted in other myopathies.