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Biomedical subjects

D Boyd

Publications and source records attributed to D Boyd.

At least 163 records · Page 9Linked to original sources
PubMed1977

Quantitative aspects of computed tomography of the blood and cerebrospinal fluid.

Computed tomographic (CT) scans of fresh and coagulated blood in vitro as well as calcium and iron solutions demonstrate that the increased absorption seen in hematomas is primarily a reflection of hemoconcentration: calcium plays essentially no role in this increased absorption, while iron makes a minimal contribution. In vitro studies of cerebrospinal fluid (CSF) indicate that CT scanning is insensitive to pathological elevations of CSF protein.

Blood↗
PubMed1968

Screening of Escherichia coli temperature-sensitive mutants by pretreatment with glucose starvation.

A system for screening Escherichia coli temperature-sensitive mutants is described. The system involves glucose starvation and minimizes ambiguities introduced by the interdependencies of macromolecular synthesis during balanced growth. The system permits the quick recognition of protein synthesis mutants and their classification into two general catagories. Complete protein synthesis mutants are unable to make any polypeptide material, whereas partial protein synthesis mutants are able to produce inactive proteins. The phenotypes of several mutants are described.

Bacterial Proteins↗
PubMedDate not supplied

Quantitative bone mineral analysis using dual energy computed tomography.

This preliminary evaluation indicates that CT scanning permits measurement of cancellous, cortical or integral bone. With the single energy technique, precision is high and with mode, CT scanning may prove an important tool for assessing the axial skeleton is osteoporotic conditions.

Bone and Bones↗
PubMedDate not supplied

Socio-economic and behavioural risk factors for tooth loss from age 18 to 26 among participants in the Dunedin Multidisciplinary Health and Development Study.

OBJECTIVE: To determine the risk factors associated with tooth loss between the ages of 18 and 26. METHODS: Dental examinations at ages 18 and 26 were conducted on Study members in the Dunedin Multidisciplinary Health and Development Study, and sociodemographic and dental service use data were collected using a self-report questionnaire. At age 15, an estimate of socio-economic status (SES) for each Study member had been obtained by classifying the occupation of the male parent. A case of tooth loss was defined as an individual who had lost one or more teeth (excluding third molars) due to caries between ages 18 and 26. Logistic regression and Poisson analysis were used to model the occurrence of tooth loss. RESULTS: Among the 821 study members who were examined at both ages, one or more teeth were lost because of caries by 85 (10.3%). After controlling for sex, SES and visiting pattern, baseline caries experience predicted subsequent tooth loss, with the odds increasing by 2.8 for every increase by 1 in the number of decayed surfaces present at age 18. Episodic dental visitors had 3.1 times the odds of their routine visiting counterparts of losing a tooth over the observation period. The number of teeth lost was, on average, 2.3 times higher among episodic dental visitors. CONCLUSIONS: Socio-economic inequalities in tooth loss appear to begin early in the life course, and are modified by individuals' SES and dental visiting patterns.

Adolescent↗
PubMedDate not supplied

Macrophage oxidation of low density lipoprotein generates a modified form recognized by the scavenger receptor.

Incubation of low density lipoprotein (LDL) with endothelial cells or smooth muscle cells overnight has resulted in an oxidative modification of LDL that results in its recognition by macrophages by way of the acetyl LDL receptor. In the present study, we examined whether macrophages themselves can oxidize and modify LDL in a manner similar to that of endothelial cells. Incubation of 125I-labeled LDL with resident or thioglycollate-elicited macrophages for 24 hours in Ham's F-10 medium resulted in the appearance of thiobarbituric acid (TBA) reactive materials and trichloroacetic acid (TCA) soluble radioactivity in the medium. The LDL harvested from these incubations showed increased electrophoretic mobility and was degraded rapidly when added to fresh macrophages as compared to LDL previously incubated in the absence of cells. These macrophage-induced modifications could be prevented if the first incubation was carried out in the presence of the antioxidant butylated hydroxytoluene (BHT) or in Dulbecco's modified Eagle's medium (DMEM). The degradation of 125I-labeled macrophage-modified LDL by macrophages was competitively inhibited by unlabeled acetyl LDL or unlabeled endothelial cell-modified LDL but not by native LDL, indicating that the degradation was mediated by the acetyl LDL receptor.

Animals↗
PubMedDate not supplied

Simultaneous spontaneous dissections in three coronary arteries.

A 61-year-old man who sustained separate spontaneous coronary artery dissections involving each of the three epicardial coronary arteries is described. Hyperestrinism related to hepatic cirrhosis may have been important in the pathogenesis of this unusual case.

Coronary Disease↗
PubMedDate not supplied

Up-regulation of urokinase-type plasminogen activator expression by the HER2/neu proto-oncogene.

The HER2/neu (c-erbB2) protooncogene, which encodes a transmembrane receptor (p185neu), contributes to tumor cell invasion/metastasis through mechanism(s) which are, at present, poorly defined. Since basement membrane degradation is a prerequisite for tumor progression, we undertook a study to determine if the expression of urokinase, a key protease implicated in extracellular matrix proteolysis, was regulated by this oncogene. Stable overexpression of a cDNA encoding HER2/neu in H460 lung cancer cells led to elevated secretion of urokinase which was a consequence of a higher level of protease mRNA. Transfection of the HER2/neu-overexpressing B 104-1 cells with a CAT reporter construct driven by the urokinase promoter, gave rise to increased CAT activity when compared with parental NIH3T3 cells, which have low levels of HER2/neu, suggesting that the protooncogene can enhance urokinase promoter activity. Since the enhanced expression of HER2/neu results in increased tumor invasion/metastasis (1), these data suggest that, at least in vitro, HER2/neu-induced expression of urokinase may contribute to tumor progression in p185neu-positive cancers.

3T3 Cells↗