Purification of human platelet-derived growth factor.

Human platelets contain a polypeptide growth factor that stimulates the proliferation of connective tissue cells. Purification of this platelet-derived growth factor (PDGF) was accomplished by heat (100 degrees C) treatment of washed platelets and subsequent ion-exchange chromatography, gel filtration in 1 M acetic acid, isoelectric focusing, and preparative sodium dodecyl sulfate/polyacrylamide gel electrophoresis. PDGF has an isoelectric point of 9.

Dual control of cell growth by somatomedins and platelet-derived growth factor.

Quiescent BALB/c 3T3 cells exposed briefly to a platelet-derived growth factor (PDGF) become "competent" to replicate their DNA but do not "progress" into S phase unless incubated with growth factors contained in platelet-poor plasma. Plasma from hypophysectomized rats is deficient in progression activity; it does not stimulate PDGF-treated competent cells to synthesize DNA, demonstrating that somatomedin C is required for progression. Various growth factors were tested for progression activity and competence activity by using BALB/c 3T3 tissue culture assays.

An ordered sequence of events is required before BALB/c-3T3 cells become committed to DNA synthesis.

An ordered sequence of events must be completed before cells become committed to synthesize DNA. A platelet-derived growth factor (PDGF), present in heated (100 degrees ) extracts of human platelets, induces density-inhibited BALB/c-3T3 cells to become competent to proliferate. Platelet-poor plasma induces these competent cells to leave the competence point, progress through G(0)/G(1), and enter the S phase.

Induction of DNA synthesis in BALB/c 3T3 cells by serum components: reevaluation of the commitment process.

Serum contains a growth factor derived from platelets and also growth factors derived from platelet-poor plasma. Extracts of heated (100 degrees ) human platelets function synergistically with platelet-poor plasma to induce DNA synthesis in quiescent, density-inhibited BALB/c 3T3 cells. Platelet-poor plasma alone did not induce DNA synthesis.

Relationship of cell growth behavior in vitro to tumorigenicity in athymic nude mice.

The serum requirements, anchorage requirements, saturation densities, and contact inhibition responses of a variety of mammalian cell lines were determined under uniform conditions. The serum requirement of both transformed and normal cells was a sensitive function of initial plating density. Cloning efficiency on irradiated mouse monolayers was found to be an invalid indicator of contact inhibition of growth, since most cell lines that failed to form visible colonies on cell monolayers nonetheless proliferated on these monolayers.

Differential degradation of messenger RNAs in mammalian cells.

Through the use of an assay that measures cellular capacity for specific enzyme synthesis, mRNA of alanine aminotransferase (EC 2.6.1.

Growth control of heterologous tissue culture cells in the congenitally athymic nude mouse.

A variety of heterologous mammalian cells were inoculated into nude mice and scored for tumorigenicity. The cells tested were from primary cell cultures, established cell lines of neoplastic origin, established cell lines of nontumor origin, and primary cell cultures transformed by oncogenic viruses. Regardless of the animal species of origin, every cell line that was tumorigenic in some other animal host and every cell line of neoplastic origin was tumorigenic in nude mice.

Failure of human cells transformed by simian virus 40 to form tumors in athymic nude mice.

Four individual lines and one subline of human cells, permanently established in tissue culture after infection with simian virus 40, failed to form tumors when inoculated into athymic nude mice. Under identical conditions, three established human cell lines of neoplastic origin and a spontaneously established human lymphocyte line formed tumors. Nude mice that failed to grow tumors from inocula of simian virus 40-transformed human cells, grew tumors from subsequent injections of authentic human cancer cells.

Evolution of treatment of paralytic scoliosis at Rancho Los Amigos Hospital.

Between 1954 and 1970, 351 patients with severe paralytic scoliosis were treated at Rancho Los Amigos Hospital. During this time the treatment evolved through five stages: body cast alone, halo cast, halo cast with buttons and traction wires, Harrington instrumentation, and finally preoperative halo-femoral traction and Harrington instrumentation. Coincident with this evolution, correction improved from 20 to 57 per cent, the incidence of curve progression dropped from 38 to 0 per cent, and curve extension decreased from 25 to 0 per cent, while postoperative recumbency was reduced from one year to about three weeks.