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Biomedical subjects

C L White

Publications and source records attributed to C L White.

At least 91 records · Page 5Linked to original sources
PubMed1991

A rapid one-step extraction procedure for the isolation of ubiquitin from human erythrocytes for antibody production.

A procedure is described that employs 5% perchloric acid extraction to isolate ubiquitin from human erythrocytes. The procedure is rapid and economical as it requires no specialized equipment. The extracted protein appeared to be highly purified as judged by electrophoresis and was identified as ubiquitin by immunoblotting and total amino acid analysis. The extraction yields about 78% of the ubiquitin in the hemolysate, which is a higher yield than is obtained with other procedures. The purified ubiquitin was used to make a polyclonal antiserum. As ubiquitin is a small and highly conserved protein, it is necessary to couple it to a larger immunogen to elicit an immune response. This ubiquitin antiserum was produced using an immunogen system that produces an immune response to the ubiquitin, but not to the carrier protein.

Electrophoresis, Polyacrylamide Gel↗
PubMed1991

The neuropathology of human immunodeficiency virus infection. The Dallas, Texas, experience.

Postmortem neuropathologic changes were evaluated in 141 consecutive patients dying with human immunodeficiency virus infection at publicly supported hospitals affiliated with the University of Texas Southwestern Medical Center in Dallas, between August 1984 and September 1990. Morphologic abnormalities were identified in 112 cases (79%). Cytomegalovirus was the most common opportunistic infection encountered, with characteristic viral inclusions identified in 23 patients, and presumptive evidence of infection in six additional patients. Progressive multifocal leukoencephalopathy was present in four patients. Gram-positive bacterial infections were identified in six patients, and mycobacterial infections in three patients. Opportunistic fungal infections included cryptococcosis (13 cases), histoplasmosis (two cases), and coccidioidomycosis (one case). Toxoplasmosis was uncommon, with active or quiescent lesions identified in five patients. Lymphoma was present in nine patients and was primary in the central nervous system in five patients. Multinucleate giant cell (human immunodeficiency virus) encephalitis was identified in 28 patients. In an additional 26 patients, microglial nodules and/or more generalized white-matter abnormalities were encountered in the absence of multinucleate giant cells, cytomegalovirus inclusions, or systemic cytomegalovirus infection. Vacuolar change was present in 21% of spinal cords, and was highly correlated with cytomegalovirus infection in the nervous system. Mixed infections and/or neoplasms were identified in 24 patients. This survey documents a high frequency of neuropathologic abnormalities in human immunodeficiency virus-infected individuals in a geographical region of the United States not represented in previous series. Variations noted in the frequencies of specific central nervous system disorders between this and other study populations reinforce the need for continuing documentation of geographical trends in human immunodeficiency virus-associated disorders.

Adult↗
PubMed1990

Paired helical filaments are not the major binding sites for wheat germ and Dolichos biflorus agglutinins in the neurofibrillary tangles of Alzheimer's disease.

The isolated paired helical filaments (PHF) that occur in the neurofibrillary tangles of Alzheimer's disease were assayed to determine if they contained N-acetyl-glucosamine and N-acetyl-galactosamine residues. The enzyme-linked lectin assay was used to detect their total content in the PHF preparation. The assay employed biotinylated Dolichos biflorus and wheat germ agglutinins and was developed with avidin-horseradish peroxidase. The total PHF preparation was shown to contain very little of these glycosyl groups compared to equal amounts of highly glycosylated control proteins. Colloidal gold-labeled lectins were used to study the PHF by electron microscopy to assess whether the minor amount of lectin binding in the total preparation was directly associated with the PHF. These studies showed no significant association of the colloidal gold-labeled lectins with the isolated filaments. We conclude that the PHF themselves contain few or no N-acetyl-glucosamine or N-acetyl-galactosamine residues.

Acetylglucosamine↗
PubMed1990

Production and characterization of a monospecific antiserum (A128) to disaggregated Alzheimer paired helical filaments.

Paired helical filaments (PHF), which constitute neurofibrillary tangles (NFT) and neuritic plaque (NP) neurites, serve as a useful marker for Alzheimer disease (AD). We have isolated AD PHF in a highly purified and disaggregated form for use as an immunogen to produce a heterologous polyclonal antiserum in rabbits. One rabbit was maintained long-term for the high quality of the antiserum it produced. Through absorptions with normal brain tissue, we were able to produce a monospecific antiserum which reacts only with NFT and NP neurites in AD brain tissue sections. We further demonstrated the specificity of this antiserum by electron microscopic immunohistochemistry, gel diffusion analysis, and immunoblotting. This antiserum also showed immunoreactivity to NFT of Down syndrome and progressive supranuclear palsy, and to the Pick bodies of Pick disease, but not to the Lewy bodies of idiopathic Parkinson disease. This well-characterized antiserum, all from one rabbit, offers several unique advantages to the study of the nature, origin, and interrelationships of filamentous protein abnormalities in AD and other neurodegenerative disorders.

Alzheimer Disease↗
PubMed1990

Intracarotid hydroxyethyl methacrylate solution causing stroke in dogs.

Hydroxyethyl methacrylate (HEMA) has been advocated as a polymerizing solution with which to prevent deflation of detachable balloons in interventional neuroradiology. It is pertinent to know if unpolymerized HEMA would have untoward effects if accidentally released into the carotid artery by balloon rupture or deflation. Seven mongrel dogs underwent transfemoral catheterization of the common carotid artery and subsequent injection of HEMA solution in volumes of 1 cc in five dogs, 2 cc in one, and 4 cc in one. Angiography performed at the time of injection revealed evidence of intravascular thrombosis as well as possible spasm. Three surviving animals were sacrificed at 48 hours; the brains were fixed and examined histopathologically. One brain was normal and one was autolyzed and could not be examined. Five of the seven animals had histopathologically documented cerebral infarctions of varying size. No foreign substance was seen within the blood vessels to suggest intravascular polymerization. The animals injected with 2 or 4 cc HEMA solution did not survive 48 hours. Literature review reveals little documentation of the toxicology of intravascular HEMA. With its increasing popularity as a compound for polymerization in detachable balloons introduced into the brain, further investigations are warranted to understand the physical properties of the compound and potential risks of its use.

Animals↗
PubMed1990

Polyadenylated messenger RNA in paired helical filament-immunoreactive neurons in Alzheimer disease.

An antibody raised against isolated paired helical filaments (PHF) was used to identify tangle-bearing (PHF+) neurons in autopsy brain tissue from six Alzheimer disease (AD) patients and six age-matched controls (AMC). A comparison of the levels of polyadenylated messenger RNA [poly(A)+ mRNA] in PHF+ and PHF- neurons of similar cross-sectional area in temporal and parietal lobe and cerebellum from four AD and four AMC brains was made by analysis of in situ hybridization of [3H] polyuridylate [poly(U)] to intracellular poly(A)+ mRNA. In PHF+ neurons, the level of poly(A)+ mRNA was approximately two-thirds that in similar-sized PHF- neurons in either AD or AMC. The level of poly(A)+ mRNA in PHF- neurons in regions of the brain that have more of the histopathologically defined effect in AD was similar to that in regions with less effects.

Aged↗
PubMed1989

Dominantly inherited dementia and parkinsonism, with non-Alzheimer amyloid plaques: a new neurogenetic disorder.

A family is described in which a dominant form of inheritance, probably autosomal dominant, expresses severe dementia and parkinsonism as the major clinical features. Neuropathological correlates in two autopsied members of this family consisted of extracellular hyaline eosinophilic, congophilic amyloid plaques in decreasing order of frequency in the cerebral cortex, basal ganglia, thalamus, and substantia nigra, and atrophy and gliosis of the basal ganglia and substantia nigra. The extracellular plaques did not stain with antibody raised against the prion protein nor with two separate anti-amyloid A4 antibodies. The combination of dominantly inherited dementia with parkinsonism and extracellular plaques in this distribution that are amyloid and prion protein antibody negative has not been previously reported and thus may represent a new neurological genetic disorder.

Alzheimer Disease↗
PubMed1989

Brain interleukin 1 and S-100 immunoreactivity are elevated in Down syndrome and Alzheimer disease.

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.

Adult↗
PubMed1989

Ribonuclease activities and distribution in Alzheimer's and control brains.

Levels of free and total alkaline ribonuclease, and levels of acidic ribonuclease, were measured postmortem in control brains and in the brains of patients with Alzheimer's disease. In each brain region assayed, whether control or Alzheimer's, there was a statistically significant difference between the levels of free and total alkaline ribonuclease. Between 59 and 90% of the enzyme activity was associated with alkaline ribonuclease inhibitor in an inactive complex. Levels of free and total alkaline ribonuclease varied widely among different brains and brain regions, and were always lower in cerebellum than in temporal cortex and occipital pole. There was no significant difference in the levels of total alkaline ribonuclease, free alkaline ribonuclease, or acidic ribonucleases between corresponding regions of Alzheimer's and control brains. There was also no qualitative difference in the subcellular distribution of the alkaline and acidic ribonucleases between Alzheimer's and control brain. No significant relationships were found between ribonuclease levels and age, neuritic plaque density, postmortem interval, or storage time.

Acids↗
PubMed1989

Microfibrillar collagen model of canine cerebral infarction.

A new canine model of focal cerebral ischemia has been developed employing intravascular delivery of microfibrillar collagen via femoral catheterization. In 13 dogs, dose-effect studies showed neurologic deficits (ranging from mild hemiparesis to death) related to the dose of microfibrillar collagen delivered. In another 10 dogs, 0.5 ml of 60 mg/ml microfibrillar collagen was injected into the common carotid artery; neurologic assessment over 48 hours revealed a survivable stroke syndrome in seven dogs, death at 40 hours in one dog and at less than 12 hours in another, and no clinical effect in one dog. The eight surviving dogs were sacrificed at 48 hours; nine of the 10 dogs had middle cerebral artery distribution infarcts (two grossly hemorrhagic and five grossly nonhemorrhagic) on histologic examination. Angiography in three dogs demonstrated no significant major vascular occlusion. All seven dogs with survivable strokes demonstrated a dense hemiparesis at 24 hours that improved to ambulatory status at 48 hours. The use of microfibrillar collagen to produce middle cerebral artery strokes in dogs provides a new opportunity to study cerebral ischemia without surgery involving the cervical or cranial vasculature. Dogs have larger brains than other common animal models and thus are more amenable to study with imaging modalities. A model with a measurable but survivable insult provides an opportunity for short- and long-term clinical follow-up and for the investigation of therapeutic interventions.

Animals↗
PubMed1989

Reversible middle cerebral artery embolization in dogs without intracranial surgery.

Using dogs, we developed an intravascular model for reversible middle cerebral artery occlusion that does not involve intracranial surgery or enucleation. Using silicone plastic plugs with a suture embedded within them, we embolized the middle cerebral artery in 19 dogs via the cervical carotid artery. The free end of the suture remained accessible in the neck, and after variable dwell times traction was placed on the suture and the plug was withdrawn. Placement of the plug in the middle cerebral artery produced ischemia in the basal ganglia. The degree and distribution of cortical ischemia were variable as evidence by the pathologically documented scattered nature of infarcts that resulted when the plug was left permanently in the middle cerebral artery and when it was removed after 1 or 2 hours. Angiography demonstrated occlusion of the middle cerebral artery with the plug in place as well as reperfusion when the plug was withdrawn. This modification of a previously described model of middle cerebral artery occlusion provides an opportunity to study structural, physiologic, and biochemical events occurring in acutely hypoperfused cerebral tissue as well as critical changes leading to irreversible injury without the disadvantages of surgical manipulation required by all previous models of reversible cerebral ischemia.

Animals↗
PubMed1989

Effects of copper and molybdenum supplements on the copper and selenium status of pregnant ewes and lambs.

The aim of this work was to investigate whether Cu, alone or in combination with Mo, reduces the Se status of sheep. Thirty-six Hampshire ewes were separated prior to mating into four treatment groups of nine sheep each. The four groups consisted of 1) basal (alfalfa hay or legume-grass low-moisture silage, corn, oats), 2) basal plus 10 mg Cu/kg diet, 3) basal plus 10 mg Mo/kg and 4) basal plus Cu and Mo (each 10 mg/kg). Copper and Mo were added to both ewe and lamb diets. Treatments continued until lambs were weaned at 10 wk postpartum. The basal ewe diet contained, in mg/kg, 5.6 Cu, .05 Se and 1.0 Mo. The basal lamb diet contained, in mg/kg, 6.1 Cu, .07 Se and less than 1.0 Mo. Sulfur concentrations in the ewe and lamb diets were .24% and .20%, respectively. Copper supplements increased, and Mo supplements decreased, the concentration of Cu in the livers of ewes and lambs (P less than .05). Despite this, there were no effects of treatment on Se concentration or glutathione peroxidase activity in blood or tissues. Selenium levels in plasma of all ewes declined throughout pregnancy and lactation, indicating that .05 mg/kg Se was insufficient for the maintenance of Se status during pregnancy in Hampshire ewes. Copper and Se levels (mg/kg fresh weight) in the liver of lambs at weaning for Treatments 1 through 4 were 48 and .13, 158 and .10, 11 and .11, and 136 and .13, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗
PubMed1989

The metabolism of 75Se-selenomethionine in sheep given supplementary copper and molybdenum.

Four groups of three ram lambs were fed, in group pens, the following diets from 4 to 19 wk of age: 1) control (6 mg Cu/kg and 1 mg Mo/kg); 2) control plus 10 mg Cu/kg; 3) control plus 10 mg Mo/kg and 4) control plus 10 mg/kg of both Cu and Mo. Copper and Mo were added to the diet as copper sulfate and sodium molybdate. The main ingredients of the diets were alfalfa hay (20%), oats (20%) and corn (59%). At 19 wk, the animals were allocated randomly to individual metabolism cages and received a single oral dose of 75Se-selenomethionine. Liver Cu concentrations at slaughter (22 wk) were 77, 259, 68 and 316 mg/kg fresh weight for treatments 1 through 4. There was clinical evidence of Cu poisoning in lambs on treatment 2. Sheep given Cu supplements without additional Mo had reduced (P less than .05) levels of 75Se activity in muscle compared with control animals. This decrease in muscle 75Se in Cu-supplemented lambs was associated with a nonsignificant increase in 75Se content of other tissues and a nonsignificant increase in fecal excretion of 75Se. Apparent absorption and net retention of 75Se was 80% and 74%, respectively. Long-term ingestion of moderate levels of Cu influenced the metabolism of Se fed as selenomethionine, possibly through effects of chronic Cu toxicity on liver function.

Analysis of Variance↗