Biomedical subjects
Publications and source records attributed to H W Sampson.
One way to increase medical students' awareness of anatomical variability is the dissection of different cadavers throughout laboratory coursework. This report covers such a procedure successfully instituted in a human gross anatomy course.
Factors that influence tissue copper concentration include age, diet, hormones, and pregnancy. In this study we altered diet independently, hormone (estrogen) independently, and various combinations of diet and hormone in animals of the same age to study the effects of ovariectomy complicated with dietary copper deficiency; a deficiency that has been demonstrated to cause bone defects. Sprague-Dawley rats were placed on various combinations of copper deficient or enriched diets before and/or after ovariectomy to determine if copper deficiency aggravated osteoporosis and if return to a copper-adequate diet alleviated it. In this study, ovariectomy did induce an osteopenia that was characterized by decreased trabecular bone. This osteopenia was slightly more severe with copper deficiency, but was not necessarily alleviated by the return of normal copper levels to the diet.
It has been hypothesized that boron (B) is an essential element for animals, but its action will vary greatly depending on the nutriture of the organism. One of the nutrients implicated as having an interaction with boron is cholecalciferol (Vit D3). This study was carried out to determine if such an interaction exists. The study was conducted utilizing vitamin D-deficient chicken embryos that were injected through the shell at 8 d of embryogenesis with carrier (NaCl and/or acetone), B (0.5 mg), B + Vit D3 (0.5 mg and 0.3 microgram, respectively), or Vit D3 (0.3 or 1.5 micrograms). The in ovo concomitant administration of boron and vitamin D enhanced (p less than 0.05) the hatchability of the vitamin D-deficient embryos. Furthermore, boron and/or vitamin D3 increased (p less than 0.05) the percent of bone ash and decreased (p less than 0.05) the exaggerated height of the proliferative zone of the epiphyseal growth plate normally observed in vitamin D deficiency, suggesting a more rapid bone formation. The results provide further evidence supporting the hypothesis that boron plays a role in bone mineralization through an interaction with vitamin D.
It has been hypothesized that boron (B) is an essential element for animals, especially in bone metabolism. In this study, the influence of in ovo boron administration was assessed in the chicken. At 8 d of embryogenesis, carrier or B (0.1, 0.5, or 1.0 mg) was injected on to the chorioallantoic membrane of fertile eggs. At hatching, body weights were recorded and tissue samples collected. Although boron failed to alter bone mineralization, it decreased (p less than 0.05) dried bone weight, suggesting a reduction in the bone organic matrix. Furthermore, 1 mg boron decreased (p less than 0.05) hatchability and increased (p less than 0.05) the height of the proliferative zone in the growth plate, indicating an unfavorable effect on bone elongation of the developing chick.
Progressive ankylosis mice (ank/ank) spontaneously develop a joint disorder characterized by calcium hydroxyapatite deposition and bony ankylosis of the joints of the axial and the appendicular skeleton. Mice in this study were used to determine the extent of mineralization of the intervertebral disks and to determine their suitability as a model for ankylosing spondyloarthropathies. Intervertebral disks taken from affected mice from 4 to 18 weeks of age were studied by electron-microscopic, electron energy-dispersive X-ray microanalysis and selected-area electron diffraction techniques. Necrotic foci seen in light microscope studies were found to be massive accumulations of calcium hydroxyapatite crystals deposited within the extracellular matrix. Chondrocytes of older animals demonstrated what appeared to be postmortem changes and contained numerous large vacuoles.
The objective of this study was to quantitate the increasing mineral content of the intervertebral disk of progressive ankylosis mice and to identify changes in serum and bone mineral levels that might occur concurrent with the rapid mineralization of the disk. Serum calcium (8.43 +/- 1.01 mg/dl vs. 7.48 +/- 2.07) and phosphorus (6.66 +/- 1.32 mg/dl vs. 5.53 +/- 2.19) levels were within normal limits. Ankylosing mice had a 5.2% decrease in water content, a 24% increase in calcium content and a 29% decrease in phosphorus content of the intervertebral disks. The magnitude of these changes increased with age. There was no significant difference in mineral or water content of the vertebral bodies. The mineral levels per gram of tissue were much greater in ankylosing disks than in the vertebral bodies. No correlation was identified between ankylosing disks and serum or bone mineral levels.
Adult rats were subjected to midthoracic spinal cord transections. Three segments of spinal cord, each approximately 5 mm in length, were removed from each animal at intervals from 5 min to 48 h postlesion; one from the lesion site and one each immediately rostral and caudal to the transection. Total tissue calcium concentrations ([Ca]t) for each spinal cord segment were determined using atomic absorption spectrophotometry and compared to control segments from untransected animals. [Ca]t levels in the segment at the lesion site was significantly elevated above control values at 30 min post-lesion, but decreased to control levels by 1 h. All other segments remained at control levels for the duration of the postlesion period. The rapid rise and fall of [Ca]t at the lesion site differs from spinal cord contusion studies in which [Ca]t remains at elevated levels for extended periods. It is postulated that the "open" transection injury permits the rapid clearance of calcium from the injury site.
The metacarpophalangeal joint of the progressive ankylosis mouse was examined at 4, 6 and 8 weeks of age by using electron microscopy and electron probe microanalysis. These studies describe the progression of the disorder, and they reveal three overlapping phases: pannus proliferation, chondrophyte formation and mineralization, and articular cartilage mineralization. The chondrophyte mineralized in a manner fairly similar to endochondrial bone, whereas articular cartilage mineralized by advancement of a calcification front across the cartilage. Synovial crystal phagocytosis was also observed. The progressive ankylosis mouse should be an important model for studying both crystal deposition and abnormal articular cartilage calcification.
Three questions are asked regarding the toxin kainic acid (KA). Does it destroy specific glial cells as well as neurons? Does KA gain access to the cytoplasm in intact cells and to which organelles does it bind? Intracerebral injections of tritiated KA into the pigeon (Columba livia) paleostriatal complex (basal ganglia) coupled with electron microscopic autoradiography revealed the following major points. Kainic acid destroyes oligodendrocytes, with pathophysiology apparent by 30 min after challenge with KA leading to cell destruction by 4 h. The response of astrocytes at the longest observation period (4 h) involves swelling of perivascular endfeet and processes in the neuropil. Reactive microglial-like cells show an accumulation of label in their cytoplasm, but no apparent morphological changes. The label appears in the cytoplasm of intact cells, both glia and neurons early after challenge with the toxin. Label is associated (bound) with mitochondria at an incidence significantly above chance at 30 min, 2 and 4 h after challenge with KA. Two hours after exposure to KA is the critical period where metabolic, physiological and morphological changes occur that lead to cell death. Cell destruction may be a consequence of KA-induced energy depletion. Kainate may interfere with adequate energy production by uncoupling glycolysis and the Krebs cycle in the mitochondria.
Progressive ankylosis mice rapidly develop an ankylosing spondyloarthropathy that rapidly affects all of the articulations of the vertebral column. The disorder symmetrically affects the nonsynovial synchondroses and symphyses of the intervertebral spaces, the diarthrodial synovial apophyseal and costovertebral joints, and the sacroiliac joint. These joints present a clear progression from syndesmophyte formation through joint bridging to total fusion. The similarities and differences of the disorder identified in this mouse and human spondyloarthropathies are discussed.
The intervertebral disks of progressive ankylosis mice were examined at successive periods in order to describe the pathologic lesions involved and to explore possible relationships with any known human disorder. The techniques employed in this study showed the presence of necrotic foci of calcification that ultimately obliterated the anulus fibrosus. Following the appearance of these lesions, peripheral proliferation of hyaline cartilage appeared that eventually bridged adjacent vertebral bodies, calcified, and was replaced with bone. The results of this study support the hypothesis that the progressive ankylosis mouse has a disorder affecting mineralization. Although it does not exactly resemble any known human disorder, it should be an important model for studying both crystal deposition and abnormal mineralization of hyaline cartilage and fibrocartilage since many vertebral ankylosis disorders, as well as the normal aging process, involve increased mineralization.
In an effort to reduce contact of tissue with silicone gel, it has become popular to use double-lumen prostheses in mammaplasty. We report a case of silicon incorporation by human tissue after insertion of a double-lumen implant.
The project described in this article used in vitro tissue culture techniques and flow cytometry to determine if there are alterations in cell morphology in those cells that have been placed in contact with a commercially available medical-grade silicone gel used in mammary implants. We were unable to demonstrate significant changes in cell cycle characteristics following in vitro exposure for 1 to 12 days using human fibroblasts, mouse fibroblasts, and Chinese hamster ovary cells.
Articular-epiphyseal cartilage from the femur of New Zealand rabbits was subjected to histochemistry for determination of the presence of metabolic enzymes along its zonal stratification. Glycolytic enzymes were strongly reactive in all of the zones. Krebs cycle enzymes, enzymes of the hexose monophosphate shunt and the respiratory chain enzymes showed a progressive increase in reactivity from the tangential zone through the top half of the epiphyseal zone. Indicators of lipid metabolism were fairly high in all regions of the cartilage.
Oral administration of L-tryptophan at 250 mg/(kg X d) for 3 consecutive days to rats produced enlarged hepatic sinusoids and vacuolated cells, many of which contained lipid. These changes persisted for at least 2 wk. Since the hepatic metabolism of L-tryptophan is very similar in rats and humans, these data suggest that people who self-administer large doses of L-tryptophan for the purpose of decreasing sleep latency may be inducing hepatic pathology.
Young, male mice (25 to 30 g) were given oral doses of hymenoxon, a sesquiterpene lactone, for 5, 10, or 20 days. Hymenoxon, isolated from Hymenoxys odorata DC, was dissolved in dimethyl sulfoxide (DMSO) and water (1:1, v/v) and was administered daily at a dosage level of 100 mg/kg of body weight for 5, 10, or 20 days. Two control groups were maintained; 1 group was given DMSO and water, and 1 group was given water only. Twenty-four hours after the last dosing, the mice were euthanatized and their livers were processed for transmission electron microscopy. Hepatocyte organelles of hymenoxon-treated mice appeared normal although the bile canaliculi contained a fine granular material and membranous structures, including myelin figures. The canaliculi of hymenoxon-treated mice were also markedly dilated, compared with bile canaliculi in the control groups. The mean area of bile canaliculi of the 5-, 10-, and 20-day mice was 14.08 microns2, 15.65 microns2, and 17.56 microns2, respectively, compared with 7.73 microns2 for the canaliculi of DMSO + water-treated mice. The P values were less than 0.001, 0.02, and 0.05 for the 5-, 10-, and 20-day hymenoxon-treated mice, respectively. Seemingly, the mouse was not a good model for studying hepatic ultrastructural changes produced by hymenoxon, using dosages less than or equal to 100 mg/kg/day for 20 days.
Parotid gland tissue from carbachol-treated and isoproterenol-treated rats was studied cytochemically by pyroantimonate precipitation and x-ray microanalysis in an effort to identify any intracellular calcium reservoirs that might be available for use in a stimulus-secretion coupling mechanism, and to determine any differences that might exist in terms of calcium utilization due to the cholinergic or beta-adrenergic receptor mechanisms. Stimulation by either secretagogue results in a reduction of mitochondrial and plasma membrane calcium, but the reduction in mitochondrial calcium deposits of carbachol-treated animals is only one-half that of the beta-adrenergic-treated animals. This could possibly suggest a greater dependency on mitochondrial calcium for beta-adrenergic stimulated animals.
Experiments were carried out to investigate the nature of the calcium homeostatic mechanisms in neoplastic GH3 rat pituitary cells. GH3 cells grown and maintained in Ham's F10 culture medium contained 35 nmoles calcium/mg cell protein. When stimulated by thyrotropin releasing hormone (TRH) or elevated K+ concentrations, only the latter caused cell calcium levels to rise although both resulted in hormone release. When exposed to EGTA, the GH3 cells lost calcium. When the temperature was lowered to 4 degrees C, the cells gained calcium and when rewarmed were able to extrude the previously accumulated calcium. The increased cell calcium following cold exposure could be blocked by prior treatment with rotenone. If rotenone was added subsequent to the cold exposure, it did not block the extrusion seen upon rewarming. In the absence of glucose in the medium, the GH3 cells took up more calcium upon exposure to 4 degrees C, and upon rewarming the cells could not return to their previous low levels. There are thus significant differences in calcium homeostasis between the neoplastic GH3 cells and their normal pituitary counterparts. When intracellular calcium was localized with the potassium pyroantimonate technique, there was calcium found in/on mitochondria, membrane bound vesicles and plasma membrane. Nuclear staining was sparse, and nucleolar staining was virtually absent. Upon stimulation with TRH, there was a decrease in mitochondrial calcium along with increases in both plasma membrane and nucleolar calcium levels. Since total calcium is unchanged, this indicates a significant calcium redistribution in response to TRH. The increased nucleolar calcium may reflect a calcium dependent increase in mRNA synthesis as has been reported. Since TRH presumably acts at a surface receptor, the increased plasma membrane calcium might be functionally related to receptor activation.