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Biomedical subjects

R E Weiss

Publications and source records attributed to R E Weiss.

121 records · Page 7Linked to original sources
PubMed1981

Influence of high protein diets on cartilage and bone formation in rats.

The influence of diets containing combinations of high protein and low calcium on discrete stages of bone formation was investigated in 28-day-old rats. A bone matrix-induced bone forming system was utilized to determine the stages of endochondral ossification that were being affected. Mesenchymal cell proliferation as assessed by [3H]-thymidine incorporation and ornithine decarboxylase activity were unchanged in animals fed a high protein (80% casein)/normal calcium (0.61% Ca; 0.40% P) diet. However, osteogenesis was reduced by 78% in the rats fed high protein/normal calcium as measured by 45Ca incorporation. Alkaline and acid phosphatase activities in bone were increased 2.5 and 2.3 times, respectively, reflecting increased matrix turnover induced by the high protein availability. Bone that did form was not remodeled nor was there evidence of marrow formation. The animals were normocalcemic and normophosphatemic and showed no evidence of acidosis. A combination diet of high protein and low calcium resulted in a 62% reduction of cell proliferation and chondrogenesis and a 98% inhibition of bone formation. High dietary protein-induced osteoporosis in animals is due to a failure of osteogenesis of the stage of ossification possibly a result of restricted availability of calcium at the site of mineralization.

Acid Phosphatase↗
PubMed1981

Calcitonin stimulates bone formation when administered prior to initiation of osteogenesis.

The influence of calcitonin (CT) on various stages of bone formation was investigated. A demineralized collagenous bone matrix-induced bone forming system in rats was used to temporally segregate chondrogenesis and osteogenesis. Administration of CT (15 Medical Research Council Units [MRCU]) daily) at the initiation of matrix-induced bone formation (BF) resulted in a 76% stimulation of BF as measured by 45Ca incorporation and alkaline phosphatase activity. This increase was due, in part, to a stimulation of cartilage and bone precursor cell proliferation monitored by the rate of [3H]thymidine incorporation and ornithine decarboxylase activity. Chondrogenesis on day 7 as measured by 35SO4 incorporation was increased by 52% with CT treatment. To rule out the possibility of a secondary response due to parathyroid hormone, similar studies were done in parathyroidectomized animals and CT stimulation of BF was still observed. However, when CT injections were started after cartilage formation (day 8) there was no stimulation of BF but a significant decrease in 45Ca incorporation was observed. These results indicate CT has two actions: (a) when CT is administered during the initial phases of bone formation, it increases BF due to a stimulation of proliferation of cartilage and bone precursor cells; and (b) when CT is administered after bone formation has been initiated, subsequent bone formation is suppressed.

Acid Phosphatase↗
PubMed1981

Abnormalities in the biosynthesis of cartilage and bone proteoglycans in experimental diabetes.

Proteoglycans synthesized in developing cartilage and bone were investigated in control and streptozotocin-induced (65 mg/kg, i.v.) diabetic rats. Ten days after streptozotocin injection, animals were implanted subcutaneously with demineralized bone matrix particles. This system induces formation of cartilage and bone on days 7 and 14, respectively. Two hours before they were killed, animals were injected with 35SO4 and the labeled proteoglycans were extracted from the explants and metaphyses by either a direct associative extraction (0.5 M GuCl2) or a direct dissociative extraction (4.0 M GuCl2). These procedures extract 80-90% of the total counts incorporated. To characterize the proteoglycans, extracts were subjected to cesium chloride density gradient centrifugation and molecular sieve chromatography. These data showed that (1) there is less proteoglycan made in diabetic bone; (2) the proteoglycan aggregate is of a smaller molecular weight in bone than in cartilage; (3) 10% of the proteoglycan synthesized in diabetic bone was in the form of aggregates compared with 48% of the control bone; (4) aggregates did form in the diabetic cartilage, and their molecular weight was smaller than in normal cartilage. This investigation shows that proteoglycans, structurally important macromolecules of cartilage and bone, are altered in experimental diabetes. This metabolic abnormality may be an important factor contributing to decreased bone formation observed in diabetes.

Animals↗
PubMed1981

The role of fibronectin and substrate size in attachment of rat bone marrow cells to an osteoinductive matrix.

Culturing bone marrow cells in the presence of osteoinductive demineralized bone matrix particles results in increased cell proliferation. We have previously reported that this response is substrate specific and is not observed when cells are cultured with glass beads or collagenous tail tendon particles. In the present investigation, we show that a bone matrix particle size of less than 70 micrometers or greater then 420 micrometers is not supportive of cell attachment, as observed by the scanning electron microscope and that subsequent cell proliferation, as measured by DNA content, does not occur. The attachment of the bone marrow cells to bone matrix particles is dependent upon fibronectin, a serum glycoprotein. When serum was absent in the culture medium, cell attachment was still observed. Fibronectin was detected by an enzyme linked immunoabsorbent assay in cultures grown in the absence of serum. Therefore, fibronectin may be synthesized by bone marrow cells. When bone marrow cells were cultured in the presence of anti-fibronectin antibodies, the number of cells attaching to the matrix particles was greatly decreased. When cell attachment was reduced, the rate of cell proliferation as measured by DNA synthesis was also reduced. This study demonstrated that substrate size and fibronectin are important for the interaction of bone marrow cells with an osteoinductive matrix.

Animals↗
PubMed1980

Synthesis and localization of fibronectin during collagenous matrix-mesenchymal cell interaction and differentiation of cartilage and bone in vivo.

The biosynthesis of fibronectin during the in vivo development of matrix-induced endochondral bone was investigated by using [35S]methionine in rats. The dmineralized bone matrix that was implanted subcutaneously to induce local bone formation bound circulating fibronectin. This may be an important initial requirement for cell attachment to the matrix. Fibronectin was present throughout the development of bone but accounted for the largest percentage of total protein synthesized during mesenchymal cell proliferation and hematopoiesis. Fibronectin was identified in tissue extracts by its (i) comigration on electrophoretic NaDodSO4/polyacrylamide gels with human and rat plasma fibronectin, (ii) affinity for denatured collagen, (iii) crossreactivity with purified antibody of rat plasma fibronectin, and (iv) insensitivity to collagenase digestion. Fibronectin was localized by immunofluorescence in the extracellular matrix during the period of mesenchymal cell proliferation. During chondrogenesis, fibronectin was demonstrated in the differentiating chondrocytes. Fibronectin was detectable in the cartilage matrix only after hyaluronidase treatment. During vascular invasion, prior to osteogenesis, fibronectin was localized in association with endothelial cells. These observations demonstrate a possible role of fibronectin in collagenous matrix-mesenchymal cell interaction in vivo.

Animals↗
PubMed1980

Influence of experimental diabetes and insulin on matrix-induced cartilage and bone differentiation.

The influence of streptozotocin-induced diabetes on discrete stages of matrix-induced endochondral bone formation has been investigated. Mesenchymal cell proliferation was inhibited in diabetic rats as evidenced by a 65% reduction of ornithine decarboxylase (ODC) activity and a 56% reduction of [3H]thymidine incorporation per microgram DNA compared to nondiabetic controls; the inhibition was prevented by insulin treatment. In diabetic animals, chondrogenesis on day 7 was reduced by 49% compared to control animals as assessed by 35SO4 incorporation. Exogenous insulin was stimulatory to cartilage development when present during days 0 through 4 (mesenchymal cell proliferation). Calcification of cartilage and osteogenesis were reduced by more than 50% in diabetic rats and corrected by insulin as measured by alkaline phosphatase activity and 45Ca incorporation. Decreased in vivo endochondral bone growth and development during diabetes is the result of 1) inhibition of insulin-dependent mesenchymal cell proliferation, 2) decreased and delayed cartilage formation due to impaired mesenchymal cell proliferation, 3) decreased and delayed vascular invasion prior to chondrolysis and osteogenesis, and 4) reduced insulin-dependent calcification and ossification.

Absorption↗
PubMed1979

Studies on the biology of fish bone. III. Ultrastructure of osteogenesis and resorption in osteocytic (cellular) and anosteocytic (acellular) bones.

The comparative ultrastructure of fish bone osteogenesis and resorption induced by scale removal was described in the osteocytic (cellular-boned) Carassius auratus and the anosteocytic (acellular-boned) Tilapia macrocephala. Osteocytes, present in osteocytic bone, were lacking in anosteocytic bone. In osteocytic bone the osteoblast secreted a collagenous preosseous matrix in which it became enmeshed and then was termed a preosteocyte. When the preosseous matrix mineralized, the preosteocyte was termed an osteocyte and was completely surrounded by bone. In anosteocytic bone the osteoblasts receded from the mineralizing front and never became trapped as osteocytes. During resorption, types A and B resorptive cells, present in both bone types, invaded the matrix and demineralized the osseous zone. These cells were characterized by large amounts of granular endoplasmic reticulum and intracellular inclusions containing crystal-like material. Although functionally similar to mammalian osteoclasts, these cells lacked a characteristic ruffled border and were not multinucleated. The osteocytes of cellular bone did not appear to be involved during demineralization.

Animals↗
PubMedDate not supplied

Biology of metastasis: clinical implications.

Bladder tumor has a spectrum of neoplastic activity. Some behave in a benign fashion, and others are highly aggressive and lead rapidly to metastatic disease and death. The processes of metastasis can be described as a sequence of interrelated steps. The processes involve 1) tumor cell adhesion to basement membranes, 2) the degradation of basement membranes, and 3) the migration of tumor cells through the destroyed stroma into blood and lymphatic vessels. Each of these processes involves the expression of molecular factors unique to tumor cells. With better understanding of the molecular basis of these factors, novel prognostic and potential therapeutic agents can be generated and applied to the clinical arena.

BCG Vaccine↗
PubMedDate not supplied

The syndrome of resistance to thyroid hormone, misdiagnosed and treated as thyrotoxicosis.

OBJECTIVE: To report two cases of resistance to thyroid hormone and to promote increased awareness of this syndrome, which is frequently misdiagnosed and incorrectly treated. METHODS: We describe a young woman and her father, both of whom were diagnosed at a younger age as having thyrotoxicosis and were treated with thyroidectomy and radioactive iodine. Both patients later proved to have resistance to thyroid hormone and required supraphysiologic doses of levothyroxine to normalize the thyroid-stimulating hormone (TSH) while remaining euthyroid. RESULTS: Laboratory evaluation revealed increased serum total thyroxine and triiodothyronine levels as well as normal to increased TSH levels. The free alpha sub-unit/TSH ratio was normal, and magnetic resonance imaging of the pituitary gland showed no tumor. Metabolic studies in the daughter, with use of graded doses of triiodothyronine, supported the diagnosis. CONCLUSION: Both patients shown to have resistance to thyroid hormone were misdiagnosed and inappropriately treated in the past. The resultant hypothyroidism has been difficult to treat, particularly in the father who has coronary artery disease.

Journal Article↗