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Biomedical subjects

D E Woolley

Publications and source records attributed to D E Woolley.

At least 109 records · Page 6Linked to original sources
PubMed1984

Mast cells at sites of cartilage erosion in the rheumatoid joint.

Cartilage-pannus junctions of the rheumatoid lesion have been examined by histochemical and ultrastructural techniques in an attempt to identify the cells responsible for cartilage degradation. Mast cells have been identified at sites of cartilage erosion in 3 specimens of rheumatoid joint. It is known that mast cells participate in immunological reactions, produce the vasoactive and proteinase-modulating agents histamine and heparin as well as their own degradative proteinases. The close association of mast cells with sites of cartilage erosion suggests they may play an important role in the pathophysiology of joint destruction in rheumatoid arthritis.

Arthritis, Rheumatoid↗
PubMed1984

A perspective of lead poisoning in antiquity and the present.

Seen in perspective, it is evident that lead poisoning is one of the earliest occupational diseases, described already thousands of years ago. The first major upswing in the history of anthropogenic production of lead was associated with the development of the Greco-Roman culture and the most recent followed the Industrial Revolution. At the peak of the power of the Roman Empire, lead production was about 80,000 tons per year, lead and its compounds were used with great inventiveness in numerous ways, and lead poisoning was pandemic, with the severity of poisoning proportional to the power and status of the class. Intake of lead by the aristocracy may have been as much as 1 mg/day. The resultant mental incompetence and especially the rapidly declining birth rate among the ruling class are now believed to have been major factors in the decline of the Roman Empire. Epidemic outbreaks of lead poisoning have occurred repeatedly throughout history and still occur today. The estimated 3.5 million tons of lead produced annually during peak production in the 1970's included about 0.4 million tons of organoleads. Such intense production has increased global contamination with lead enormously. Even under relatively ideal conditions the daily intake of lead is so much higher than in prehistoric times that investigators must pause to ask themselves what a proper control group really is. Are investigators merely determining the effects of additional lead exposure on systems already greatly perturbed by lead? If so, how can we find out?

Egypt↗
PubMed1984

Morphometric effects of preweaning lead exposure on the hippocampal formation of adult rats.

We previously observed that lead exposure beginning at parturition reduced or retarded neuropil development and synaptogenesis in specific regions of the hippocampal formation in 15-day-old rats. To determine if morphologic effects of perinatal lead exposure persist into adulthood, the hippocampus of rats exposed to lead from parturition to weaning via the milk of dams drinking 0.2% lead acetate was analyzed by light and electron microscopy at 90-97 days of age. Preweaning lead exposure did not cause obvious hippocampal cytotoxicity, edema, damaged vasculature or altered numerical density (number per unit area) of dentate granule or hippocampal pyramidal neurons. However, lead exposure increased the area of the hilar portion of stratum pyramidale, increased the number of blood vessels per section in the dentate stratum granulosum and tended to increase the number of glial cells per section in the non-hilar CA3 stratum pyramidale. Effects of early postnatal lead exposure on synaptic profiles in the suprapyramidal mossy fiber zone (MFZ) were limited to the proximal (close to the dentate gyrus) region of the extrahilar zone. Both numerical density and areal density (proportion of neuropil covered) of complex invaginated (Ci) profiles, typical of mature mossy fiber boutons, were increased by lead exposure in the deep (close to stratum pyramidale) subfield of the proximal portion of the suprapyramidal MFZ. Lead exposure tended to increase the mean cross-sectional area of Cl profiles in the superficial (distant from stratum pyramidale) subfield of the proximal portion, and reduced the cross-sectional area of complex noninvaginated (CN) synaptic profiles in some subfields. Although lead exposure reduced or delayed neuropil development in selected late developing hippocampal regions examined at 15 days of age, it appeared to allow normal growth or to induce compensatory hypertrophy in these same regions in the adult.

Animals↗
PubMed1984

Acetylcholinesterase activity in the brain of rat pups and dams after exposure to lead via the maternal water supply.

Acetylcholinesterase (AChE) activity was measured in 11 brain areas of control and lead-exposed pups and dams. Lead exposure of pups was by way of the milk of dams drinking 0.2% lead acetate solution as drinking water starting at parturition. Of the brain areas studied, the cerebellum showed the greatest increase in weight (11-fold) and AChE activity per brain area (42-fold per cerebellum) from birth to 20 days, and was the only area in the pups in which AChE activity was consistently affected by the treatment. AChE activity in the cerebellum was 13% less at 10 days of age and 8% less at 20 days in lead-exposed than in control rats. This agrees with observations by others that the developing cerebellum is particularly sensitive to the effects of lead, and may be consistent with our previous report of an effect on motor coordination, i.e., slightly delayed appearance of the air righting reflex, in similarly treated pups. At weaning AChE activity in septum and olfactory tubercles was lower in lead-exposed than in control dams by 15% and 29%, respectively, and the increase in activity in the hypothalamus expected in lactating dams was attenuated by the lead exposure. Thus, lead exposure may affect AChE activity in brain areas of dams, as well as in pups, and so the potential for effects of lead exposure on the dam should not be discounted.

Acetylcholinesterase↗
PubMed1983

Dopaminergic agonists increase [3H]estradiol binding in hypothalamus of female rats, but not of males.

Specific nuclear binding of [3H]estradiol in the hypothalamus was increased by acute dopaminergic treatment in female, but not in male, gonadectomized-adrenalectomized rats. In the female this increase could be blocked by the dopaminergic receptor blocker perphenazine and was noted from 1 to 3 hours after injection of [3H]estradiol. Binding was not different in male and female rats in the absence of dopaminergic treatment. These results suggest that acute dopaminergic stimulation may modulate estradiol binding in neural areas known to be important in endocrine function.

Animals↗
PubMed1983

Histamine H2 receptors on foetal-bovine articular chondrocytes.

The dose-response curve of histamine-induced cyclic AMP elevation in monolayer cultures of primary foetal-bovine articular chondrocytes was displaced to the right by cimetidine. In addition, H2 but not H1 antagonists prevented the histamine-induced cyclic AMP elevation, suggesting histamine activates chondrocyte adenylate cyclase through an H2 receptor.

Animals↗
PubMed1983

Catecholamine synthesis inhibitors acutely modulate [3H]estradiol binding by specific brain areas and pituitary in ovariectomized rats.

Drugs known to alter endogenous levels of catecholamines were administered to adult ovariectomized rats to assess catecholaminergic effects on estradiol (E2) uptake and binding in nuclear and supernatant fractions of pituitary and specific brain regions and on cytoplasmic E2 receptor numbers and affinities. Specific (i.e. diethylstilbestrol-blockable) binding in vivo was measured 1 h after the iv injection of [3H]E2 (1 micrograms/kg). Administration of the tyrosine hydroxylase inhibitor alpha-methyl-p-tyrosine (alpha MPT) 2 h before [3H]E2, to reduce levels of dopamine (DA), norepinephrine (NE), and epinephrine (Ep), decreased total and specific [3H]E2 binding by 36-56% in the nuclear fraction of the anterior pituitary, basal hypothalamus, and anterior hypothalamus. The dopamine-beta-hydroxylase inhibitor diethyldithiocarbamate (DDC), administered 2 h before [3H]E2 to reduce levels of only NE and Ep, increased the total and specific uptake of [3H]E2 by 62-140% in nuclear and supernatant fractions of the anterior pituitary and also increased uptake in several brain areas. In vitro analysis of hypothalamic and pituitary cytoplasms showed that in vivo administration of DDC increased E2 binding. Scatchard analysis showed that DDC increased receptor numbers 18-29%, with no change in the dissociation constant in pituitary cytoplasms. At the same time, plasma PRL levels were reduced by DDC treatment, indicating that DDC had increased DA output. Phenoxybenzamine (a blocking agent at alpha 1 postsynaptic binding sites) and a high dose of clonidine (a pre- and postsynaptic alpha-receptor agonist) did not significantly alter specific uptake in the cell nuclear fraction of any tissue, suggesting that postsynaptic alpha-receptors do not play a major role in modulating [3H]E2 uptake. No drug altered plasma levels of radioactivity. Because alpha-methyl-p-tyrosine and DDC both inhibit synthesis of NE and Ep, it is suggested that their opposite effects on uptake of [3H]E2 are related to their opposite effects on DA output. This interpretation is compatible with our previous observations that DA agonists increase [3H]E2 uptake in brain and pituitary in ovariectomized rats.

Animals↗
PubMed1982

Morphometric effects of postnatal lead exposure on hippocampal development of the 15-day-old rat.

Neurotoxic sequelae of developmental lead exposure suggest that the hippocampus may be affected. Therefore, rats received low-level exposure via the milk of dams drinking 0.2% lead acetate beginning at parturition, and mid-dorsal sections of the hippocampus and dentate gyrus (DG) from 15-day-old pups were examined by light and electron microscopy. Lead exposure did not reduce body weight nor produce obviously abnormal vascularity or signs of cytotoxicity in the hippocampal formation, and total numbers per section of dentate granule cells or CA3 pyramidal cells were not reduced. On the other hand, lead exposure reduced neuropil development as evidenced both by reduced areas of the dentate hilus and dentate infrapyramidal stratum moleculare and by increased number of hilar CA3 pyramidal cells per unit area. Also, lead exposure reduced numbers of several types of synaptic profiles per unit area in the suprapyramidal mossy fiber zone. Complex invaginated (CI) profiles, assumed to be mature mossy fiber boutons, were characterized by multiple membrane densities and deep invaginations around dendritic spines of pyramidal cells. Complex noninvaginated (CN) boutons exhibited bag-like profiles with multiple membrane densities. Smaller, less numerous, simple (S) profiles contacted either dendritic trunks (ST) or spines (SS). Lead exposure reduced the numerical density of any of the profiles in the deep (close to stratum pyramidale) part of the proximal (close to DG) region of the suprapyramidal mossy fiber zone, but did not alter the numerical density of any of the profiles in the superficial (distal to stratum pyramidale) parts of either proximal or distal (close to CA1) regions. Average size of CN profiles in the distal region was increased by lead exposure. The pattern of effects suggests that low-level lead exposure during development preferentially affects later developing structures within the hippocampal formation, rather than affecting mature structures.

Animals↗
PubMed1981

Motor development, tissue weights and seizure susceptibility in perinatally lead-exposed rats.

Motor impairments and seizures are frequent neurologic sequelae of excess lead exposure in children. To evaluate the relative significance of such symptoms in an animal model, Long-Evans rats were lead-exposed from parturition to weaning by adulteration of the dams' drinking water with 0.02% or 0.2% lead acetate. Ontogeny of swimming ability from 6 through 24 days of age was not altered by postnatal lead exposure. Rotorod performance was tested on 21, 30, 60, 90, 150 and 440 days of age and was maximal in rats 30 through 150 days of age, with the poorest performance by 440-day-old rats. Rotorod performance was decreased by both levels of lead exposure and this effect was most evident at 60 and 150 days of age. Both levels of lead exposure increased kidney weights of dams at weaning and the 0.2% lead acetate exposure decreased hematocrit of dams. Kidney weights of lead-exposed pups were not increased at 10 days of age, but pups in the 0.2% lead acetate group had increased kidney weights at 20, 90 and 150 days of age. Hematocrit values of pups in the 0.2%, but not in the 0.02%, lead acetate exposure group were decreased at 20 days of age. No effects of lead exposure on hematocrits were found at 10, 90 or 150 days of age. Wet weight of brain, cerebellum, adrenals, spleen and thymus were not altered at any age by postnatal lead treatment. In a second study, Sprague-Dawley rats exposed to lead via dams drinking 0.2% lead acetate throughout gestation and lactation. Pre- and postnatal lead exposure did not alter the ontogeny of electro-shock seizure thresholds in rats tested on 8 through 20 days of age. The results suggest that the lead exposure levels used were at or near a no-effect level for several common neurobehavioral tasks and that kidney weight may be a more discriminative index of excess lead exposure than some simple neurobehavioral indices.

Animals↗
PubMed1980

Collagenase immunolocalization studies of cutaneous secondary melanomas.

Immunoreactive collagenase has been demonstrated in 5/14 specimens of cutaneous secondary melanomas. In contrast, very little enzyme was seen in 10 specimens of normal human skin. All specimens were fixed within minutes of excision. These findings support the hypothesis that collagenase facilitates connective-tissue breakdown which is associated with tumour invasiveness and metastatic spread.

Fluorescent Antibody Technique↗