PubMed Health⌕ Search

Biomedical subjects

J H McMaster

Publications and source records attributed to J H McMaster.

29 records · Page 2Linked to original sources
PubMedDate not supplied

Growth and hormone control mechanisms in osteosarcoma. Evidence for a new therapeutic approach.

The association between osteosarcoma and growth, including altered carbohydrate metabolism has been investigated in 5 osteosarcoma patients. Serum from an adolescent osteosarcoma patient has been noted to consistently enhance 3-H-thymidine uptake in cultured chondrocytes and tumor cells. Females survive osteosarcoma more frequently than males. In vitro serum-enhanced proliferation of osteosarcoma cells is suppressed by estradiol.

Adolescent↗
PubMedDate not supplied

On the nature of stress fractures.

It is felt that stress fractures are caused by excessive, repetitive muscle forces acting across the affected bone. These fractures should be suspected in participants of athletic endeavors who present with a history of persistent, focal, activity-related pain regardless of their stage of physical conditioning. Associated physical findings are localized tenderness and swelling without evidence of a generalized systemic response. Bone scans and serial roentgenograms including specialized views may be required for documentation. Limitation of the athletic activity is the hallmark of the treatment program.

Adolescent↗
PubMedDate not supplied

Repair of acromioclavicular separation using a dacron prosthesis graft.

Twenty patients were treated for acute acromioclavicular separation using a Dacron vascular prosthesis and followed for an average period of 13.1 months. None demonstrated loss of motion, or muscle weakness. All resumed their prior level of athletic activity. Satisfactory results were obtained in 18 patients. Residual deformity was the primary reason for an unsatisfactory rating. Recurrence of deformity can be minimized by technical skill and perfection of the surgical reduction.

Acromioclavicular Joint↗
PubMedDate not supplied

Acquisition of resistance to 6-azauridine through DNA amplification in neoplastic but not normal osteoblasts.

In this communication, we have characterized the resistance to AZUrd in tumorigenic mouse C3H-OS osteosarcoma cells and non-tumorigenic MC3T3-E1 osteoblast cells. DNA and RNA blot analysis showed a 30-fold increase in UMP synthase specific DNA and a 10-fold increase in mRNA, respectively, in resistant versus non-resistant C3H-OS cells. No corresponding increases in either UMP synthetase DNA or mRNA were evident in resistant MC3T3-E1 osteoblasts. Karyotype analysis of MC3T3-E1 and C3H-OS cells revealed translocations in the resistant cells. Regardless of drug-sensitive or resistant phenotype, the normal and neoplastic cells exhibited aneuploidy which was significantly more pronounced in the non-resistant tumor cells. Additionally, the number of chromosomes decreased in all resistant cells whether normal or neoplastic. We conclude that genomic instability in neoplastic cells is a prerequisite for the generation of drug resistant variants via the process of gene amplification.

Animals↗