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Biomedical subjects

H C Anderson

Publications and source records attributed to H C Anderson.

At least 19 recordsLinked to original sources
PubMed1992

Familial syndrome of endocrine and neuroectodermal abnormalities.

We report on a previously undescribed combination of endocrine and neuroectodermal abnormalities in four sibs from Burma. These abnormalities include low growth hormone levels in response to provocative stimuli, delayed puberty associated with prepubertal levels of gonadotropins in the males and pubertal levels of gonadotropins in the females, type II diabetes mellitus with elevated insulin levels, mild mental retardation, sensori-neural deafness, and alopecia without pili torti. They also had a characteristic facial appearance and fleshy hands and feet. This family appears to have a previously undescribed combination of endocrine and neuroectodermal abnormalities.

Adolescent↗
PubMed1992

Comparison of normal and rachitic rat matrix vesicles.

Accumulated information about MVs in PO4-deficient rachitic rats shows them to be normal in most aspects. Both normal and rachitic MVs show the same ultrastructural features and selective spatial distribution in the growth plate, and both contain a nearly identical array of major proteins. Rachitic and normal MVs show the same avidity to calcify in vivo and in vitro. A slightly greater specific activity of ALP in rachitic MVs may enhance their calcifiability. We conclude that rachitic rat MVs are essentially 'normal' and can be used as an adequate model to study the mechanism of biological calcification.

Alkaline Phosphatase↗
PubMed1992

Presence and specific concentration of carbonic anhydrase II in matrix vesicles.

Matrix vesicles were isolated from the epiphyseal growth plates of normal weanling rats, and the presence of carbonic anhydrase II was demonstrated by Western blotting and ultrastructural immunolocalization using the immunogold technique. Total carbonic anhydrase activity was assayed and showed a statistically significant increase in matrix vesicles as compared to normal rat chondrocytes derived from the same growth plates. These results are the first to establish the presence of carbonic anhydrase in matrix vesicles.

Animals↗
PubMed1992

Bone-inducing agent (BIA) from cultured human Saos-2 osteosarcoma cells.

The Saos-2 line of human osteosarcoma cells was established in culture in 1975. These cells produce a large amount of alkaline phosphatase but little or no matrix in vitro, and are unable to grow when transplanted into athymic mice. We decided to test our local strain of Saos-2 cells for bone-inducing ability in the skeletal muscle of athymic mice by implanting freeze-dried, acetone-defatted cells, with and without a collagen carrier. A bone-inducing activity (BIA) thus was demonstrated in 88% of 90 implants of devitalized Saos-2 cells. In further studies, we have used guanidinium hydrochloride (Gu-HCl) to extract, solubilize, and remove the Saos bone-inducing agent(s) in an active state which when reprecipitated by aqueous dialysis was able to induce ultrastructurally typical endochondrial bone formation in nude mouse muscle in 92% of 48 implants. This preliminary report is offered to alert investigators to the presence of an extractable BIA in Saos-2 cells.

Animals↗
PubMed1992

Immunolocalization of alkaline phosphatase in osteoblasts and matrix vesicles of human fetal bone.

A monoclonal antibody raised against alkaline phosphatase (ALP) of human osteosarcoma was used to localize this enzyme in human fetal bone tissue. For light microscopy, the presence of alkaline phosphatase in osteoblasts and osteocytes was demonstrated by use of an avidin-biotin immunoperoxidase procedure. Electron microscopic immunolocalization was accomplished with an indirect immunoperoxidase method which revealed a concentration of the enzyme on matrix vesicle and osteoblast plasma membranes. In addition, many vesicular protrusions arising from areas of plasma membrane on the lateral surfaces of adjacent osteoblasts were strongly immunolabeled. Immunostaining for ALP was absent in vesicles which contained fine crystallites. Alkaline-phosphatase-rich matrix vesicles may play a significant role in the mineralization of the extracellular matrix.

Alkaline Phosphatase↗
PubMed1991

Monoclonal antibody against human bone alkaline phosphatase.

A monoclonal antibody which reacts preferentially with human bone alkaline phosphatase (AP) has been developed using human osteosarcoma bone AP as an immunogen. The antibody with the highest selectivity shows about three- and a-half fold greater binding to bone than to liver AP. The selectivity was confirmed using mixtures of authentic samples of the bone and liver isoenzymes. Its selectivity was also shown by measurements of bone AP in sera from patients with either bone or liver diseases. Such a selective antibody could lead to the development of a monoclonal antibody highly specific for bone AP which can be used for a more sensitive approach for quantitative analysis of the isoenzyme.

Alkaline Phosphatase↗
PubMed1991

Cardiovascular implant calcification: a survey and update.

Calcification of cardiovascular prosthetic implants is a common and important problem. This review provides an update based upon the Conference on Cardiovascular Implant Calcification held as part of the 13th World Congress of the International Society for Heart Research, 1989. A variety of cardiovascular prostheses are affected clinically by calcification, including bioprosthetic heart valves, aortic homografts and trileaflet polymeric valve prostheses. In addition, experimental studies have demonstrated calcification of artificial heart devices in ventricular assist systems in long-term calf studies. The pathophysiology of this disease process is incompletely understood. A common element between the various types of cardiovascular implant calcification is the localization of calcific deposits to devitalized cells and membranous debris. Prevention of cardiovascular implant calcification by either biomaterial modifications or regional drug therapy (controlled release) is being investigated.

Animals↗
PubMed1991

Increased matrix vesicle protein in rachitic rat epiphyseal growth plates.

Extracellular, membrane-bound vesicles are widely regarded to be the initial site of calcification in a variety of tissues under normal and pathological conditions. Alkaline phosphatase is believed to play a vital role in this process by hydrolysing ester phosphates or mineral inhibitors, e.g. inorganic phosphates. In the present study, matrix vesicles from normal and rachitic rat growth plates were compared with regard to specific activity of alkaline phosphatase, total vesicle protein and ultrastructural distribution of alkaline phosphatase activity. Matrix vesicles were released from normal or rachitic growth plates by collagenase digestion and isolated by differential centrifugation. Enzyme cytochemical localization involving a cerium capture method was performed on vesicles collected by vacuum filtration on Millipore filters. SDS gels and Western blots on fractions of both normal and rachitic matrix vesicles showed major proteins to be almost identical and confirmed the presence of alkaline phosphatase in both. Total matrix vesicle protein ((mg total matrix vesicle protein/rat) x 10(2)) per rat was significantly greater for the rachitic animals (9.0 +/- 2.0 vs. 4.0 +/- 1.0), P less than 0.0001. Alkaline phosphatase specific activity (units alkaline phosphatase/mg vesicle protein) in the rachitic and normal matrix vesicles was 25.29 +/- 9.36 and 18.78 +/- 3.37, respectively (0.05 less than P less than 0.1). Electron dense cerium phosphate deposits were localized to the outer membrane surface of matrix vesicles derived from both types of rats. This data, the first to quantify the relationship between rickets, matrix vesicle protein and alkaline phosphatase specific activity, suggests that matrix vesicles from rachitic and normal rats have biochemical and morphological similarity.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗
PubMed1991

The effect of a stiff spinal implant on the bone-mineral content of the lumbar spine in dogs.

The response of canine lumbar vertebral bone to the application of a stiff transpedicular screw-plate implant from the third to the fifth lumbar vertebra, without arthrodesis, was investigated. Five groups of six dogs each were studied: dogs that had not had an operation (control group); dogs that had had a sham operation, with survival periods of three and six months; and dogs that had received an implant, with survival periods of three and six months. The results were the same in specimens from the control group and the group that had had a sham operation. In the groups that had received an implant, dual-photon absorptiometry revealed an insignificant decrease in bone-mineral content at the bypassed fourth lumbar segment (17 per cent at three months and 12 per cent at six months). When the data for the three and six-month intervals were pooled, the mean decrease in bone-mineral content of 14 per cent was significant. Histomorphic study yielded similar results; the mean decrease in bone-mineral content for the pooled three and six-month specimens was significant (16 per cent). Losses were similar for the ventral and dorsal columns. Histomorphometric analysis also showed a significant (13 per cent) loss of bone-mineral content at the adjacent caudad (sixth lumbar) vertebra for the pooled three and six-month groups. The results of the methods of analysis of loss of bone-mineral content correlated strongly. Under these experimental conditions, a stiff spinal implant caused loss of bone-mineral content of the bypassed vertebral segment, although the loss was less than anticipated and did not increase between three and six months.

Absorptiometry, Photon↗
PubMed1990

Matrix vesicle calcification of ectopically induced osteoid tissue in 1-hydroxethylidene-1,1-bisphosphonate (HEBP)-treated mice.

The effects of 1 hydroxethylidene-1, 1-bisphosphonate (HEBP) on the mineralization of osteoid induced ectopically by a murine, osteosarcoma-derived, bone-inducing substance was examined at the ultrastructural level. Samples of Dunn osteosarcoma were chemically processed, lyophilized into pellets of uniform dimensions and protein content, and implanted into the back muscles of male, 4 week old, ddY mice. In control animals injected intraperitoneally (i.p.) with saline each day for 30 days, the pellets exhibited ectopic cartilage and bone formation in a sequential manner consistent with endochondral ossification. Daily administration of HEBP (30 mg/kg i.p. per day) to animals over the same period produced wide anastomosing strands of osteoid and haematopoietic marrow in the pellets. Electron microscopical examination revealed a tightly packed organization of collagen fibrils with many membrane bounded organelles or matrix vesicles (0.05-0.3 micron diameter) dispersed throughout this nonmineralized matrix. After withdrawal of HEBP, mineralization proceeded initially within matrix vesicles and secondarily by involvement of the surrounding collagen fibrils. In pellets retrieved at 30 days after HEBP withdrawal, most of the matrix had been mineralized and remodeled to reveal thin bony trabeculae and an overall histologic appearance similar to that seen in the control pellets. This model of ectopic bone formation permits clear visualization of the sequence of mineral nucleating events in osteoid in the absence of an established mineralizing front. The results add further support to the hypothesis that matrix vesicles are directly responsible for the initiation of mineralization in bone.

Animals↗
PubMed1990

Enzyme cytochemical localization of alkaline phosphatase in cultures of chondrocytes derived from normal and rachitic rats.

Epiphyseal growth plate cartilages were removed from rats which had been maintained on normal laboratory chow or a rachitogenic diet. Chondrocytes were released from the growth plates by collagenase digestion and cultured in tissue chamber slides. After 7, 10 and 12 days of culture, the chondrocytes were removed as intact multilayers and processed for electron microscopical enzyme cytochemical studies. Alkaline phosphatase activity in the cultures was visualized by means of a cerium based capture method. Electron-dense cerium phosphate deposits were localized on the membrane of matrix vesicles and plasma membranes of chondrocytes derived from normal and rachitic animals. The appearance of first crystals within matrix vesicles was characterized by a concomitant decrease in alkaline phosphatase activity in the membrane of these structures. Calcification was initiated at approximately the same time in cultures of chondrocytes derived from normal or rachitic animals. The results suggest that rickets has no serious effects on the capacity of chondrocytes to support matrix calcification in vitro. Additionally, the evidence indicates that alkaline phosphatase-positive matrix vesicles play a significant role in the initiation of this process.

Alkaline Phosphatase↗
PubMed1990

The role of cells versus matrix in bone induction.

Earlier observations indicated that epithelial cells of urinary bladder, and transformed epithelial cells from human amnion (FL), epidermal carcinoma (HeLa), etc. can induce ectopic endochondral bone formation when implanted into the skeletal muscle of immunosuppressed or autologous animals. Such epithelial cells are associated with little matrix. Bone-inducing activity was also demonstrated in cultured osteosarcoma cells of murine and human origin or extracts thereof, and it is notable that these bone-inducing osteosarcoma cells grow in vitro with little matrix production. Finally, electron microscopy of in vitro cartilage induction showed that decalcified rodent bone that had been extensively extracted to remove cells still contained devitalized cells and cell fragments some of which made contact with inducible, cartilage-forming mesenchymal cells that had migrated in from cocultured muscle. Suggestions: These observations suggest that: 1) the bone-inducing agent(s) of both epithelial and mesenchymal cells may reside mostly in cells rather than matrix. Thus it may be premature to assume that bone "matrix" is the major source of bone-inducing agent in decalcified bone until the osteoinductive activity of residual bone cells has been assessed; and 2) that the osteoinductive agent, whether residing in epithelial cells or bone cells, may be the same or a similar factor operating through the same mechanism.

Animals↗
PubMed1990

Matrix vesicle biogenesis in vitro by rachitic and normal rat chondrocytes.

Calcifying matrix vesicles (MVs) are released from chondrocytes and osteoblasts in monolayer culture. In the present studies, we tested the ability of rachitic versus normal rat growth plate chondrocytes in micromass or monolayer primary cultures to produce MVs. Unlike earlier reports of in vitro MV biogenesis by chicken chondrocytes in which most MVs were released into the medium, we found that most of the released rat matrix vesicles were entrapped in a newly formed cartilaginous matrix enveloping the cells. These matrix-associated MVs could be isolated by mild collagenase treatment and concentrated by differential centrifugation. Vesicle production slowed in the older 2- to 4-week-old cultures and, unlike vesicle release from cultured chicken chondrocytes, active vesicle production did not show a second burst of activity at 3 to 4 weeks. Alkaline phosphatase (ALP) activity diminished with time in culture in cells and matrix vesicles, suggesting a decrease in differentiative expression. Protein profiles on SDS polyacrylamide gels of native matrix vesicles and culture-derived MVs from rachitic and normal cells were quite similar and showed a typical simplified protein pattern as compared to chondrocyte plasma membrane proteins. There were distinctive proteins migrating at 130, 80 to 95, 66, 43, 20, and 14 kd. Culture-derived MVs showed vigorous in vitro calcifying activity that was ALP related. We conclude that 1) rachitic chondrocytes are essentially normal in their matrix vesicle production; 2) matrix entrapment of MVs is a characteristic of rat chondrocyte cultures; and 3) culture-produced MVs are similar to native MVs in protein profile and calcifiability, and thus can be studied as a model for normal MV composition and calcification.

Animals↗
PubMed1989

The isolation and partial sequencing of human bone alkaline phosphatase gene.

1. A charon 4A human fetal liver genomic library was screened for human alkaline phosphatase sequences using the cloned human bone cDNA as a hybridization probe. 2. A positive clone was obtained and then characterized by restriction endonuclease cleavage analysis, hybridization experiments and partial DNA sequencing.

Alkaline Phosphatase↗
PubMed1989

Heterotopic ossification: a case report and immunohistochemical observations.

This report describes the case of a 69-year-old man with adenocarcinoma of the transverse colon who developed heterotopic ossification in a metastatic axillary lymph node. The areas of pathologic bone formation were characterized by the appearance of osteoblast-like cells at the surfaces of the mineral deposits. Immunostaining for alkaline phosphatase revealed a significant concentration of this enzyme in these cells and, to a lesser degree, on the apical membrane of the glandular cells of the adenocarcinoma adjacent to the ossification centers. Proliferating mesenchymal cells in close proximity to the areas of osteogenesis also showed significant immunolabeling. We conclude that metastatic colonic carcinoma can promote heterotopic ossification, and that alkaline phosphatase is intimately associated with bone formation under these pathologic conditions.

Adenocarcinoma↗