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Biomedical subjects

R A Clasen

Publications and source records attributed to R A Clasen.

At least 19 recordsLinked to original sources
PubMed1994

Recurrent intracranial epithelioid hemangioendothelioma associated with multicentric disease of liver and heart: case report.

Epithelioid hemangioendothelioma is an unusual vascular neoplasm with prominent cytoplasmic vacuolization representing primitive lumen formation. A case is presented of this unique vascular neoplasm in a woman with a seizure disorder who had cardiac, hepatic, and recurrent nervous system lesions. To our knowledge, this is the third known case of intracranial epithelioid hemangioendothelioma. Emphasis is placed on the indolent course of this rare neoplasm, with a recommendation for aggressive surgical treatment and diligent follow-up.

Adult↗
PubMed1992

Adenocarcinoma metastatic to a growth-hormone-secreting pituitary adenoma: case report.

Although the pituitary gland is known to harbor metastatic deposits, it is a rare occurrence for a metastatic deposit to appear in a pituitary adenoma. A case is presented of an adenocarcinoma metastatic in an acromegalic patient with a pituitary adenoma. This report adds to the literature of the unusual phenomenon of neoplasm-to-neoplasm metastasis.

Adenocarcinoma↗
PubMed1987

Cortical biopsy results in Alzheimer's disease: correlation with cognitive deficits.

Neuropsychologic and pathologic data are presented for a group of 11 patients with a clinical diagnosis of probable Alzheimer's disease (AD) according to recently proposed criteria. In all cases, the diagnosis was verified by cortical biopsy. In addition, increased cortical plaque counts were associated with greater deficits in language production and comprehension and poorer performance on an index of global mental status. These results suggest that a clinical diagnosis of AD is very accurate when patient selection is restricted to typical cases and that language deficits may provide a useful indicator of severity of disease in AD patients.

Aged↗
PubMed1982

Protein and electrolyte changes in experimental cerebral edema.

Analysis of protein and electrolyte data in cryogenic cerebral edema in the rhesus monkey has led to the conclusion that, in the first 24 hours (h) after injury, the edematous process is not homogenous, but compartmentalized. This involves, first of all, a division into intra- and extracellular compartments. The intracellular compartment is further divided into a compartment containing water, electrolytes, and serum proteins, and a compartment containing only excess sodium. The extracellular compartment is also subdivided into a compartment containing albumin, globulin, and electrolytes, and a compartment containing only albumin and electrolytes. Anatomically, the latter is most likely the pre-existing normal extracellular space.

Albumins↗
PubMed1981

A correlative study of computed tomography and histology in human and experimental vasogenic cerebral edema.

The computed tomography (CT) scans of nine patients with vasogenic cerebral edema and five monkeys with cryogenic lesions were correlated with histologic findings. The areas of diminished density on the CT scan corresponded to foci of histologically recognizable edema. The attenuation number of the edematous tissue in the human varied from 18.0 to 28.8 Hounsfield units (HU: 1,000 scale) and in the monkey from 27.0 to 34.7 HU. There was a rough correlation between the extent of decrease in the attenuation number and the degree of staining of edematous tissue by the periodic acid-Schiff method. The decreased attenuation number of edematous tissue signifies dilution by edema fluid only when it is above 20 HU or represents a change of less than 12 HU. Lower numbers imply an additional process, possibly transformation of complex into neutral lipids. It is our belief that cerebral edema in the human can be quantitatively studied with the presently available CT scanners.

Adult↗
PubMed1974

Experimental acute lead encephalopathy in the juvenile rhesus monkey.

Lead subacetate (0.5g) and 1000 units of vitamin D were given three times a week to four newly-weaned rhesus monkeys. In addition, two animals received only the vitamin D. The poisoned animals had an increase in the urinary excretion of delta-aminolevulinic acid, an elevated content of lead in the blood, and a fall in hemoglobin concentration. Between 6 and 18 weeks the animals suddenly developed ataxia, nystagmus, generalized weakness, and convulsions. At this time the animals were killed by perfusion of fixative and the brain prepared for light and electron microscopic studies. Definite morphological evidence of disease was confined to the central nervous system, except for one animal which showed the characteristic renal inclusions of lead poisoning. All animals showed PAS-positive globules associated with blood vessels and an exudative edema involving the white matter of the cerebral hemispheres and cerebellum. Ultra-structurally, this appeared as a granular precipitate within an expanded extracellular space. Alterations of nerve fibers were not seen in the white matter but axonal swelling was observed in the cerebral cortex. The perikaryon and neuropil appeared normal. The control animals showed no significant cerebral changes.

Acute Disease↗
PubMed1974

Electron microscopic and chemical studies of the vascular changes and edema of lead encephalopathy. A comparative study of the human and experimental disease.

Lead encephalopathy was induced in suckling rats by administering lead to the mother. The brains were studied by light and electron microscopy, and the results were compared with observations in the human disease as well as in cases of cerebral ischemia in children. In their severe forms, both human and experimental lead encephalopathies are characterized by exudative extracellular edema and perivascular PAS-positive globules. The latter consist of osmiophilic non-membrane-limited cytoplasmic inclusions located, in the rat exclusively and in the human predominantly, in perivascular astrocytes. Intervascular strands are also found in both forms of the disease. In the rat these consist of basement membrane surrounding endothelial cytoplasm. Chemically, experimental lead encephalopathy with morphologically demonstrable edema is associated with an increase in brain water, sodium and serum albumin. Relative to the serum concentration, the increase in water is disproportionately greater than the sodium or albumin. There were no demonstrable changes in chloride or potassium.

Adult↗