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Biomedical subjects

L C Dearden

Publications and source records attributed to L C Dearden.

At least 37 records · Page 2Linked to original sources
PubMed1978

Cortisone induced alterations of costal cartilage in single and in parabiosed rats.

Cortisone-treated Buffalo rats have been parabiosed with untreated controls of the same age. The optical and electron microscopy, including histochemistry, of costal cartilage of these rats has been compared with that in single cortisone treated rats, single controls, and control parabiosed with control rats, at 14 and 28 days after parabiosis. Single cortisone-treated rats, in comparison to controls, have shown the greatest alteration in cellular morphology and in the extracellular matrix both at 14 and at 28 days. Cortisone-treated parabiosed rats demonstrate a gradation of these alterations. Cellular alterations include enhancement of lipid and glycogen deposition concrurently with the presence of numerous large cytoplasmic vacuoles containing beaded irregularly-shaped filaments, banded or unbanded collagen-like fibrils, and/or electron dense lamellar bodies. In the extracellular matrix, matrix vesicles, amianthoid fibers, randomly oriented unbanded fibrillar materials, and filament-like materials are most prominent in the single cortisone-treated rats and they are progressively less prominent in the cortisone-treated parabiosed rats, and in the parabiosed and single controls. Calcification of the extracellular matrix follows a similar pattern and is observed initially in pericellular halos of the single cortisone and in cortisone-treated rats parabiosed with controls. Histochemical techniques have shown that chondroitin sulfate is less demonstrable in the single cortisone and in the cortisone-treated parabiosed rats than it is in the single or parabiosed controls at 14 days but, at 28 days, all untreated or treated rats, single or parabiosed are basically comparable. Glycoproteins are prominent in the single cortisone-treated rats both at 14 and at 28 days and, at these same times, they are progressively less prominent in the cortisone-treated parabiosed rats and in the single or parabiosed controls. Many of the cortisone induced alterations in costal cartilage are suggestive of enhancement of the aging process.

Animals↗
PubMed1978

Deposits of immunoglobulin and complement in the pulmonary tissue of patients with "heroin lung".

Pulmonary tissues from six patients who died with a clinical diagnosis of "heroin lung" (heroin-induced pulmonary edema) were examined with the light microscope and electron microscope. Immunofluorescent microscopic analysis revealed multifocal granular alveolar septal deposits of IgM in all patients, C3 complement in five patients, IgG in four patients, fibrinogen in three patients, and IgA in two patients. IgM, IgG, IgA, and C3 complement were eluted from the lungs of these addicts with citrate buffer with a low pH. No deposition of albumin was found in any of the specimens. These findings are believed to represent the first report of immune complexes in the alveolar capillary membrane in patients with heroin-induced pulmonary edema. Electron-microscopic studies revealed a proteinaceous plasma-like fluid in the alveolar spaces, thereby confirming the heroin induced pulmonary edema. Mechanisms of transport of edematous fluids from alveolar capillaries to alveolar spaces in lungs from heroin addicts are considered.

Adult↗
PubMed1978

Pulmonary ultrastructure of the late aspects of human paraquat poisoning.

The pulmonary ultrastructure of the late aspects of a case of human paraquat poisoning is investigated and compared with normal human pulmonary ultrastructure. Alveoli in the paraquat patient are numerically reduced in comparison to the control. They are filled with edematous proteinaceous plasma-like fluid containing erythrocytes, macrophages, leukocytes, fibroblast-like cells, platelets, and fibrin. These alveoli are lined by granular pneumocytes. Interstitial areas in the paraquat patient are greatly expanded and there are no alveolar septums. Interstitial areas contain proteinaceous plasma-like material, collagen, fibrin, platelets, mature fibroblasts, plasma cells, many leukocytes, numerous erythrocytes, and capillaries. Capillary permeability seems to be enhanced in the paraquat patient either by vesicles forming transendothelial channels or pores or by disruption of endothelial cells.

Adolescent↗
PubMed1977

Growth hormone, somatomedin and cartilage sulfation in failure of catch-up growth after propylthiouracil-induced hypothyroidism in the rat.

Male Long-Evans rats 36 to 39 days of age were fed a diet containing 0.1% propylthiouracil (PTU) for 17 to 20 days followed by the resumption of normal diet. Growth rates of body weight and tail length decreased during PTU treatment and increased during recovery; yet only slight catch-up (compensatory) growth occurred in either body weight or tail length. Although serum thyroxine and triiodothyronine concentrations (radioimmunoassay) decreased significantly during PTU treatment, they returned to normal by recovery day 14. Pituitary immunoassayable growth hormone (GH) content and concentration dropped during PTU-feeding. By recovery day 14 there was significant, but incomplete, repletion of the gland. Serum GH during ether anesthesia was increased significantly during PTU treatment; it remained elevated (NS) and showed greater variability during recovery than in controls. Bioassayable serum somatomedin (Sm) activity decreased during PTU treatment in one of two experiments but returned to a normal level by recovery day 7. The addition of PTU to normal rat serum in concentrations used during PTU treatment failed to alter Sm activity. The addition of L-triiodothyronine and/or L-thyroxine to hypothyroid serum also did not alter Sm activity. In vitro and in vivo cartilage sulfate incorporation decreased during PTU treatment but it rose to greater than control values during the recovery period. The difference in sulfate incorporation between treated and control rats was maintained throughout the observation periods. The results indicate that incomplete catch-up growth following transient hypothyroidism is the result of factors other than deficient GH or Sm production. The implications of the persistent changes in cartilage sulfate metabolism are not clear, but these findings during recovery suggest the possibility that a disturbance of intrinsic cartilage function is a limiting factor preventing full catch-up growth after PTU-induced hypothyroidism.

Animals↗
PubMed1977

The effect of ethchlorvynol on pulmonary ultrastructure in dogs.

The ultrastructure of alveolar septae in dogs is investigated at times ranging from 30 seconds to 60 minutes after intravenous injection of ethchlorvynol (Placidyl). Pulmonary edematous fluid first appears in alveolar spaces 5 minutes after injection and becomes progressively more prominent with increasing time. Alveolar septae are initially somewhat fibrotic, and subsequently, most interstitial spaces become swollen and hydrated. Vesicles in endothelial cells increase with postinjectional time, and they seem to form channels or pores interconnecting capillaries and interstitial spaces. Similar vesicles in epithelial cells (Type 1) show an increase after 30 minutes, and they also seem to form channels or pores interconnecting interstitial spaces and the alveolus. Vesicles, whether in endothelial or epithelial cells, contain a flocculent filamentous material similar to plasma protein and the filamentous proteinaceous material in edematous fluid in alveolar spaces. Ethchlorvynol injection rapidly induces a non-hemodynamic form of pulmonary edema. Since cell junctions of both endothelial and epithelial cells remained intact, it is proposed that transalveolar transport of edematous proteinaceous fluid is mediated by means of endothelial and epithelial vesicles.

Animals↗
PubMed1976

Cartilage sulfation and serum somatomedin in rats during and after cortisone-induced growth arrest.

The uptake of sulfate by rib cartilage in vitro and in vivo and the serum somatomedin activity by bioassay were determined in male rats during and after cortisone-induced growth arrest. Experimental treatment consisted of subcutaneous injections of cortisone acetate in a dose of 2.5 mg/rat/day for 4 days, beginning at 29 to 30 days of age in Buffalo rats, or 5 mg/rat/day for 4 or 5 days, beginning at 39 to 41 days of age in Long-Evans rats. Groups of hypophysectomized rats were studied in parallel in one experiment. The sulfate uptake in the controls declined linearly with increasing age in both the in vitro and the in vivo studies. Hypophysectomy resulted in a constant low level of sulfate uptake in vitro. At the end of cortisone treatment, the in vitro sulfate uptake was approximately midway between that of the hypophysectomized rats and that of controls; at 7 days recovery, it was at the control level; at 14 days it showed an additional rise above the control value; from 14 days to 35 days it declined parallel with but above the sulfate uptake of controls. The in vivo sulfate uptake was depressed by cortisone treatment. During recovery it approximately control values at recovery day 21. In succeeding recovery periods in vivo sulfate uptake remained at control levels. Serum somatomedin activity was significantly reduced during cortisone treatment; it returned to the control level by 21 days of recovery. The incubation of the cartilage of controls and cortisone-treated rats at 14 days of recovery with and without the presence of normal rat serum, cortisone recovery serum, or hypophysectomy serum resulted in significantly higher sulfate uptake in the cortisone-treated rat cartilage in each medium. These sera did not differ significantly in their stimulation of sulfate uptake in either cortisone recovery cartilage or control cartilage. Both treated and control cartilage had greater sulfate uptake with larger doses of serum added to the medium. The dose-response curves were parallel during treatment and early recovery; but the slopes of the dose-response curves of the cartilage of cortisone-treated rats were greater than those of the controls during late recovery. It is concluded that the increased in vitro sulfation after 14 days of recovery in cortisone-treated rats signifies a persistent alteration in cartilage metabolism. Normal in vivo sulfate uptake during that time may be the result of humoral controls. A mechanism other than the impairment of somatomedin production is probably involved in the failure of catch-up growth after glucocorticoid treatment in the rat.

Animals↗
PubMed1976

Matrix vesicles in aging cartilage.

The calcification process that occurs in aging has been studied with the electron microscope in costal and tracheal cartilage of rats and in human costal cartilage. In these tissues, the early stage of the calcification process is induced and regulated by matrix vesicles in the same way as it occurs in epiphyseal cartilage, bone, and dentine. However, the spreading of inorganic substance from vesicles into the surrounding matrix is frequently impaired in aged cartilage, either because of a too low concentration of calcium ions, or because the structure of the cartilage matrix is not suitable for inorganic substance deposition. This shows that matrix vesicles have a calcium affinity and calcium-binding potentiality greater than that of other components of the cartilage matrix. Most matrix vesicles are produced by "Verdämmerung der Zellen." This degenerative process of the chondrocytes leads also to the formation of pericellular halos consisting of aggregates of amorphous substance and thin filaments. Part of the material that forms these aggregates seems to be produced by disruption of matrix vesicles. Within this disruptive material, thick collagen fibrils can be formed. Moreover, this material seems capable of inducing calcification. These findings suggest that matrix vesicles, by releasing their content into the matrix, can be involved in some way in collagen formation, and that the released material maintains the calcium affinity and calcium-binding property it has within the vesicles.

Adolescent↗
PubMed1975

Filaments and granules in mitochondrial vacuoles in chondrocytes.

As chondrocytes degenerate mitochondria frequently become vacuolated. Vacuoles seem to form by an invagination of mitochondria into their own matrix followed by cytoplasmic invasion. The bounding membrane of vacuoles and the electron dense granules which are intermittently dispersed around its periphery are positive when stained with phosphotungstic acid and with silver nitrate methenamine after periodic acid oxidation, indicating the presence of glycoprotein; they are also positive after staining with colloidal iron and bismuth nitrate, indicating the presence of acid proteoglycans. Within vacuoles and apparently arising from their glycoprotein proteoglycan boundary are small filaments composed of granular and filamentous protions. Vacuoles and their contents are exocytosed thus accounting for the presence of granules and filaments in pericellular lacunae. In pericellular lacunae and in the extracellular matrix, filaments interconnect with granules or with collagen fibrils, or both. Filaments decrease in number as the distance from the cell increases, while granules decrease in size but remain numerous. Filaments and granules decrease in the extracellular matrix as collagen fibrils aggregate and as the matric calcifies. Thus, they may play a role in aggregation of collagen fibrils. Filaments and granules also decrease with increasing age. Filaments and granules do not seem to be derived from Golgi vacuoles. They are present in costal, tracheal, and epiphyseal cartilage in three different species of animals.

Aging↗
PubMed1975

Periodic fibrillar material in intracellular vesicles and in electron-dense bodies in chondrocytes of rat costal and tracheal cartilage at various ages.

The occurrence of intracellular fibrillar material (frequently banded) has been studied in normal costal and tracheal chondrocytes of rats at various ages ranging from 1 to 90 days. The study methods have included digestion with collagenase, electron histochemical techniques and routine electron microscopy. Banded fibrillar material has been observed intracellularly in vesicles or in electron-dense bodies in perichondrial and subperichondrial chondrocytes from rats of all ages. These fibrils and extracellular collagen fibrils are partially and equally degradable by collagenase, they are positive after staining with phosphotungstic acid or with silver nitrate methenamine, and their lucency corresponds with that of collagen when they are stained only with lead citrate. They have not been observed in intracellular clefts. They, therefore, seem to be formed intracellularly and to be exocytosed subsequently. Large vesicles and electron-dense bodies seem to be derived from Golgi saccules. A mechanism whereby banded intracellular fibrils could be formed from tropocollagen molecules is postulated. The frequency of occurrence and the diameter of intracellular fibrils seems to increase with increasing age.

Age Factors↗
PubMed1975

The effect of prolonged prednisone treatment on human costal cartilage.

Costal cartilage (biopsy) from a 13-year-old boy receiving prolonged prednisone treatment (discontinuously from 2 6/12 to 13 11/12 years) for hepatosplenomegaly and lymphadenopathy has been studied and compared with costal cartilage from untreated individuals. Optical and electron microscopic studies including histochemistry have been employed. Chondrocyte degeneration characterized by lipidic material and glycogen in cells is enhanced following prednisone treatment. Acid proteoglycans are reduced in comparison to those in the untreated controls. Amianthoid (asbestoid) collagen fibers, derived from electron-dense bodies which represent remnants of degenerating chondrocytes, occur in all cartilages. A type of collagen similar to fibrous long-spacing collagen has been observed and is prominent in cartilage from the prednisone-treated individual. Evidence suggests that this type of collagen is cellular in origin and represents a transitional form of native collagen. Morphologic changes suggestive of aging are present following prolonged prednisone treatment.

Adolescent↗