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Biomedical subjects

C L White

Publications and source records attributed to C L White.

At least 73 records · Page 4Linked to original sources
PubMed1993

Neuronal and glial gene expression in neocortex of Down's syndrome and Alzheimer's disease.

The association cortex of Down's syndrome (DS) predictably and prematurely undergoes neurofibrillary degeneration of Alzheimer type. Hence studies of DS are potentially useful in defining the earliest pathogenetic events in Alzheimer's disease (AD). Previous reports have described altered expression of several mRNAs in AD cortex; but the pathogenetic stage at which expression of these mRNAs begins to deviate from the norm has not been defined. We have examined this issue in neocortex of DS. Expression of mRNAs, known to be altered in AD cortex, was studied by Northern analysis, comparing frontal cortex of DS (15-45 years) with age-matched controls and with AD. Chromosome 21- and non-21-encoded mRNAs were studied, including transcripts expressed preferentially in neurons (neurofilament light subunit and amyloid precursor transcripts) and in glia (glial fibrillary acidic protein [GFAP] and S100 beta). Chromosome 21-encoded mRNAs were increased in DS cortex as expected. Except in the DS case with extensive neurofibrillary degeneration, GFAP was expressed at levels significantly below the control, suggesting that trisomy 21 exerts a suppressive effect on GFAP gene expression. We found no instance in which AD-type changes of transcript expression preceded the appearance of neurofibrillary degeneration. The findings indicate that in trisomy 21, certain changes of mRNA prevalence previously described for AD neocortex are not a necessary antecedent to neurofibrillary degeneration.

Adolescent↗
PubMed1993

Brain blood flow in the dementias: SPECT with histopathologic correlation.

Single photon emission computed tomography (SPECT) of regional cerebral blood flow (RCBF) has been employed experimentally in the assessment of patients with dementia. The standard with which the SPECT diagnosis has been compared previously has been the initial clinical diagnosis. Recognizing that histopathologic diagnosis would be a more reliable standard, the authors compared SPECT diagnoses and clinical diagnoses with histopathologic diagnoses in a series of 18 patients who had been referred by the Alzheimer Disease Research Center. SPECT RCBF studies were carried out prospectively in 15 patients with an inhaled xenon-133 SPECT technique and in three patients with technetium-99m hexamethyl-propylene-amine oxime and triple-camera-scanner SPECT. When compared with histopathologic diagnosis, clinical diagnosis was correct in 15 of 18 patients; visual scanning diagnosis, in 13 of 18; and Xe-133-SPECT diagnosis based on quantitative ratios in regions of interest, in 14 of 15 (13 of 13 with Alzheimer disease).

Adult↗
PubMed1992

Disease-specific patterns of locus coeruleus cell loss.

Computer visualization techniques were used to map and to quantitatively reconstruct the entire locus coeruleus, including the nucleus subcoeruleus, to compare the topographic patterns of cell loss in postmortem brains from patients with Parkinson's disease, Alzheimer's disease, and Down syndrome. There was comparable cell loss in all three diseases (approximately 60%) compared with aged normal subjects, and there was a significant loss of nucleus subcoeruleus cells specifically in patients with Parkinson's disease (63%). There was a significant positive correlation between the magnitude of locus coeruleus cell loss and the duration of Alzheimer's disease, but no such correlation was found for Parkinson's disease. In patients with Parkinson's disease, there was comparable cell loss throughout the rostral-caudal extent of the nucleus; however, in patients with Alzheimer's disease and Down syndrome, the greatest cell loss always occurred within the rostral portion of the nucleus, with a relative sparing of caudal cells. These data are consistent with the hypothesis that cell loss in Parkinson's disease is the result of a pathological process that attacks the catecholaminergic cells of the locus coeruleus and the subcoeruleus in general; in Alzheimer's disease and Down syndrome, however, the pathological process only affects the rostral, cortical-projecting locus coeruleus cells and spares the caudal, noncortical-projecting cells.

Aged↗
PubMed1992

MRI evaluation of amyloid myopathy.

Amyloid myopathy is a rare complication of primary amyloidosis. The magnetic resonance imaging (MRI) features of two patients with amyloid myopathy were studied. Slight prolongation of muscle T1 and T2 relaxation times was evident but the striking abnormality was marked reticulation of the subcutaneous fat. The clinical findings of indurated extremities far exceeds the minimal signal intensity alteration seen in the muscles. The MR appearance of amyloid myopathy differs from that of other neuromuscular conditions in the minimal changes found in muscle, but the striking abnormality seen in subcutaneous fat makes it distinct from many neuromuscular conditions.

Amyloid↗
PubMed1992

Postoperative pain incidence related to the type of emergency treatment of symptomatic pulpitis.

Some endodontic emergencies occur as a result of attempts to relieve symptoms of pulpitis. The aim of this study was to identify any predictor of postoperative pain in a patient population treated by dental students. Patients who reported for treatment of symptomatic pulpitis were subjected to three different emergency treatment regimens. Clinical data was collected on those patients who reported in the emergency service with severe postoperative pain within 24 hours of emergency endodontic treatment. Statistical analysis of these data suggested that the type of endodontic emergency procedure carried out was a significant predictor of severe postoperative pain.

Adolescent↗
PubMed1992

Symptom assessment and management of outpatients receiving biotherapy: the application of a symptom report form.

Patients treated with high doses of biologic response modifiers (BRMs) often require hospitalization for monitoring and management of toxicities. However, with careful symptom assessment and management, patients can be treated safely with low-dose, long-term BRM regimens in an outpatient setting. Quantifiable, consistent, and accurate symptom assessment sets the groundwork for regular, effective symptom management. A symptom report form or nursing care flow sheet is a helpful daily assessment tool for recording and quantifying the most common side effects experienced by patients receiving BRMs. Parameters can be established and converted to a numerical code to provide a consistent guide for evaluating a patient's toxicities during treatment. Additional space on the report form allows for narrative comments about symptoms or concerns not addressed elsewhere. To be safe and effective, outpatient therapy of this kind requires excellent patient education and compliance, with easy access to a health care professional when necessary.

Activities of Daily Living↗
PubMed1992

Effects of dietary zinc deficiency on gonadotrophin secretion and testicular growth in young male sheep.

The hypothesis that the secretion of gonadotrophins would be reduced by zinc deficiency was tested in five groups of four young Merino rams (initial liveweight 22 kg). Four groups were fed ad libitum with diets containing 4, 10, 17 or 27 micrograms Zn g-1. The effects of loss of appetite on the deficient diet was controlled by feeding a fifth group (pair-fed control) at a rate of 27 micrograms Zn g-1, but the amount of feed offered was restricted to that eaten voluntarily by the deficient (4 micrograms Zn g-1) group. Blood was sampled every 20 min for 32 h on two occasions before the treatments were imposed and 96 days later, at the end of the experiment. The rams were injected with gonadotrophin-releasing hormone (GnRH; 10 ng kg-1 i.v.) after each serial sampling, and with naloxone (1 mg kg-1 i.v.) 24 h after the end of the final GnRH test. In the group that were fed the diet with the lowest zinc content, the concentration of zinc in blood plasma was reduced to 18% of that in the pair-fed controls (P < 0.05) and was within the deficient range. The appetite of the deficient rams was half that of the controls fed 27 micrograms Zn g-1 ad libitum and there was no increase in liveweight or testicular diameter during pubertal development. Similar, but smaller, effects were observed in the pair-fed controls. There were no significant differences between pair-fed and deficient groups in the frequency of the luteinizing hormone (LH) pulses or in the concentration of follicle-stimulating hormone (FSH), but the secretion of gonadotrophins was markedly lower in both groups than in the control rams fed ad libitum. The response to GnRH was not affected by treatment, but the increase in LH pulse frequency evoked by naloxone was lower in the deficient animals than in other groups. The animals fed zinc at intermediate rates (10-17 micrograms g-1) showed similar responses to the controls fed ad libitum. It is concluded that the specific effects of zinc deficiency on testicular function were small. Most of the reduction in testicular growth in rams fed a deficient diet was not specifically related to the trace element, but was due to the fall in energy and protein intake caused by the loss of appetite. This leads to a reduction in the frequency of GnRH pulses secreted by the hypothalamus, and to low rates of gonadotrophin secretion by the pituitary gland.

Analysis of Variance↗
PubMed1992

Protecting workers from pathogens. Employers must act now to comply with OSHA's new standard on bloodborne pathogens.

A new standard set forth by the Occupational Safety and Health Administration (OSHA) requires healthcare employers to implement sweeping new controls in areas such as record keeping, engineering, hazard prevention, and work practice. Through the bloodborne pathogen standard, which went into effect on March 6, OSHA acknowledges that healthcare workers face significant health risks as a result of occupational exposure to blood and other infectious materials. Although most prudent healthcare providers already adhere to the Centers for Disease Control's universal precautions, the OSHA regulations include several additional mandatory measures that are more specific and stringent. The additional measures include the development of an exposure control plan, procedures for responding to an employee's exposure to bloodborne pathogens, the implementation of certain engineering and work practice controls to eliminate or minimize on-the-job exposure risks, and the provision of personal protective equipment and information and training programs. OSHA estimates that the greatest cost component of implementing procedures to bring a facility into compliance is attributable to the purchase of personal protective equipment. Although the costs of compliance are substantial, OSHA has estimated that these costs represent less than 1 percent of the healthcare industry's annual revenues. Violation of the bloodborne pathogen standard may result in penalties of up to $70,000, depending on the severity of the infraction. Criminal penalties are also possible for willful violations that result in worker death.

Blood↗
PubMed1991

Alzheimer disease paired helical filament core structures contain glycolipid.

The core structures of sodium dodecyl sulfate extracted, pronase digested paired helical filaments of Alzheimer disease were solubilized by heating in dimethyl sulfoxide. Electron microscopy revealed that after heating in dimethyl sulfoxide, intact paired helical filaments were no longer present in the dimethyl sulfoxide soluble fractions or in the insoluble lipofuscin-containing fractions. Enzyme-linked immunosorbent assays of the various fractions with the monospecific antibody A128 to paired helical filaments demonstrated 96% of the immunoreactivity to be in the dimethyl sulfoxide soluble fraction, and only 4% in the dimethyl sulfoxide insoluble fractions. Lyophilization of the dimethyl sulfoxide soluble supernatant and resuspension in water failed to reassociate the paired helical filaments, but did result in an insoluble precipitate. Analysis of the dimethyl sulfoxide solubilized paired helical filament fraction by nuclear magnetic resonance revealed it to be composed of glycolipid in a form that was distinct from similar fractions isolated from normal aged control brains. The aggregation of an altered glycolipid to form paired helical filaments in Alzheimer disease could explain their insolubility.

Alzheimer Disease↗
PubMed1991

Receptor-stimulated death pathway is opened by antigen in mature T cells.

Clonal deletion provides an important mechanism for the elimination of autoreactive T cells. Deletion is accomplished by programmed cell death directed by interaction of the T-cell receptor (TCR) of the developing thymocyte with major histocompatibility complex elements in the thymic environment. In this report we present evidence to support the hypothesis that the activation and the maturation state of the T cell may be important in coupling the TCR to the "death program." We show that coupling of the TCR to the death program is open during maturation but closed in naive mature T cells. However, during primary antigenic stimulation, coupling between the TCR and the death program is reopened, as demonstrated by the stimulation of the death of these cells by immobilized anti-TCR. Our results suggest that further examination of mature cells that are either resistant or sensitive to receptor-stimulated death may lead to the identification of the components of the death pathway and may provide clues to the regulation of their coupling to TCR signals.

Animals↗
PubMed1991

Transplants of mouse trisomy 16 hippocampus provide a model of Alzheimer's disease neuropathology.

Alzheimer's disease, which is characterized by amyloid plaques and neurofibrillary tangles, may be attributed to the abnormal expression of gene(s) located on human chromosome 21. Genetic linkage studies have narrowed the region of candidate genes to 21q11.2-21q22 of the long arm of this chromosome. Several single copy sequences within this region, including the amyloid precursor protein (APP), have been mapped to mouse chromosome 16. Reliable strategies exist for breeding Trisomy 16 mice. However, the consequences of developmental overexpression of genes on chromosome 16 have not been previously investigated, because of the lethal effects of this aneuploidy during gestation. In the present report, we employ neural transplantation to study long-term survival and pathogenesis in Trisomy 16 central nervous system tissues. Immunocytochemical staining with antiserum raised against the synthetic APP, beta-A4 and alpha 1-antichymotrypsin revealed numerous densely stained cells within hippocampal grafts of Trisomy 16 mice. Similarly, a population of grafted cells were positively stained following incubation with an antiserum raised against components of the pathological neurofibrillary tangle and with the monoclonal antibodies Tau 6.423 and ubiquitin.

Alzheimer Disease↗