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Biomedical subjects

R Pollack

Publications and source records attributed to R Pollack.

At least 19 recordsLinked to original sources
PubMed1992

Health care for all: comparing proposals for reform. A roundtable discussion: Part 2.

Part 1 of this roundtable discussion [Geriatrics 1992; 47(Sept):34-48] examined the flaws in our current healthcare system and factors that are interfering with our nation's ability to achieve reforms. This month, the panelists discuss the benefits and drawbacks of the major healthcare reform proposals, including managed care, single-payer systems, and so-called "play or pay." The practical aspects of any redistribution of healthcare resources are considered as each panelist outlines a favored approach. The influence of special interests, such as the insurance industry, is also discussed.

Health Policy↗
PubMed1992

Health care for all: long-term care, the missing piece. A roundtable discussion: Part 3.

Long-term care has been described as the "missing piece" in many healthcare reform proposals. Yet the cost of nursing home care often exceeds that of acute care, especially for the elderly with Alzheimer's disease. In this final installment of a three-part roundtable discussion, panelists discuss the options for providing long-term care, such as social insurance, a single-payer system, play or pay, or private insurance models. Alternatives to nursing home care, such as community service centers and home care, are discussed. The panelists conclude with an examination of how these proposed reforms might affect the practices of physicians and the U.S. economy.

Community Health Services↗
PubMed1990

Perineal endometriosis. A case report.

Perineal endometriosis was found unexpectedly in a 32-year-old woman with primary infertility. Since there had been no prior perineal trauma, the transport of endometrium through a venous or lymphatic route could have accounted for the location of the endometriosis.

Adult↗
PubMed1988

Multiple insertions and tandem repeats of origin-minus simian virus 40 DNA in transformed rat and mouse cells.

Stable simian virus 40 (SV40) transformation requires integration and expression of the early region of the SV40 genome. We have examined the amount and state of integrated viral DNA of SV40-transformed NIH 3T3 mouse and F2408 rat fibroblast lines generated by transfection with either wild-type or origin-defective SV40 DNA. A functional SV40 replication origin was not required for multiple inserts and partial-repeat structures to form in NIH 3T3 mouse transformants. In contrast, partial repeats in F2408 rat transformants were rare when the SV40 replication origin was intact and not detected at all when it was defective.

Animals↗
PubMed1986

Expression of 100,000-Mr simian virus 40 (SV40) tumor antigen in mouse fibroblasts transfected with replication-defective SV40 genomes.

Simian virus 40 early region mutants which are partially or completely replication defective were tested for their ability to transform postcrisis mouse fibroblasts. All mutants tested were capable of generating anchorage-independent transformants. We have previously reported the presence of a variant tumor antigen of 100,000 Mr (100K protein) generated upon transformation by wild-type simian virus 40 virions which correlates with anchorage-independent growth (Chen et al., Mol. Cell. Biol. 1:994-1006, 1981). In this study, none of the mutants tested produced the 100K variant protein at early (before the fifth) passage. Long-term passage (greater than 20 weeks) permitted the expression of this 100K variant in half of the transformants. Thus the phenotype of these mutants is different from both wild-type simian virus 40 (frequently production of 100K by the third passage, and always by the tenth passage) and the origin-minus class of mutants (no production of 100K at any passage).

Animals↗
PubMed1985

Altered actin cytoskeletal patterns in two premalignant stages in human colon carcinoma development.

Primary culture of human colonic biopsies converts the single cell thick epithelial layer from a highly indented sheet in vivo into a flat patch on the surface of a Petri dish. Migration of cells from biopsies in a continuous sheet to form the patch cultures allows the cultured cells in large part to retain the junctional complexes and membrane interdigitations which connect adjacent cells in vivo and therefore to maintain their spatial relationships to neighboring cells. Migration of the cells onto a flat surface also allows visualization of their actin cables (E. Friedman, M. Verderame, S. Winawer, and R. Pollack, Cancer Res., 44: 3040-3050, 1984). Actin organization patterns have been studied in primary patch cultures of colonic epithelial cells from four stages in the development of colon cancer: normal tissue, normal-appearing but preneoplastic cells characteristic of familial polyposis patients, benign tumors or adenomas from familial polyposis patients, and benign and malignant tumors from patients in the general population. Carcinomas exhibited the least number of actin cables, while adenomas contained the greatest concentration. Similar actin patterns were seen in both familial polyposis and nonpolyposis adenomas. The preneoplastic prebenign tumor stage characteristic of familial polyposis patients had less actin cables than either normal cells or benign tumor cells. Thus actin organization loss characterized the transition from the normal colonic epithelial cell to the preneoplastic nontumor cell. The ability to form actin cables was then regained with the transition from the preneoplastic pretumor cell to the benign tumor cell and lost again with the benign tumor to malignant tumor transition. The complexity of these changes in actin organization during the step-wise transformation of colonic epithelial cells was not predicted from the simple model of actin cable loss accompanying fibroblast transformation.

Actins↗
PubMed1979

Tumorigenicity of revertant from an SV40-transformed line.

A syndrome of in vitro properties correlates with the tumorigenicity of SV40-transformed rodent cells. These properties are: plasminogen activator production, loss of large actin cables, and anchorage-independent growth. An established rat fibroblast line, its SV40 transformant, several T-antigen negative revertants, and a spontaneous retransformant isolated from one of the revertants were analyzed in vivo for their tumorigenicity and in vitro for the syndrome. The two transformed lines were highly tumorigenic, and had clearly abnormal in vitro properties. The parental rat line was weakly tumorigenic in nude mice and demonstrated a slightly transformed response in the in vitro assays. The revertants were completely nontumorigenic. Expression of the in vitro syndrome was not uniform for all revertants; however, most cell lines maintained the correlation of the syndrome and tumorigenicity.

Animals↗
PubMed1979

Tumor promoters induce changes in the chick embryo fibroblast cytoskeleton.

We have examined the effect of the tumor promoter, 12-0-tetradecanoyl phorbol-13-acetate (TPA), on the actin-containing elements of the cytoskeleton of chick embryo fibroblasts (CEF). TPA at concentrations as low as 7.3 times 10-10M indices a reversible change in the cytoskeleton as visualized by indirect immunofluorescence using anti-actin antibodies. Cells incubated with TPA lose the ordered actin-containing structures found in normal cells and resemble Rous sarcoma virus-transformed cells in that the immunofluorescent actin pattern is diffuse. The TPA effects are both dose-and time-dependent. Analogs of TPA which are inactive as tumor promoters do not induce cytoskeletal changes at the concentrations tested, while a second tumor promoter, PDD, is also able to cause alterations in actin-containing structures. The action of TPA requires de novo synthesis of both RNA and protein. The direct cytoskeletal changes are neither plasmin-dependent nor subject to inhibition by incubating the cells with high levels of protease inhibitors during the exposure to TPA. However, plasminogen does increase the sensitivity of cells to TPA.

Actins↗
PubMed1979

Correlation of in vitro growth properties and tumorigenicity of Syrian hamster cell lines.

Several in vitro phenotypic characteristics frequently associated with neoplastic cells were examined in a series of spontaneous and benzo(a)pyrene-induced Syrian hamster clonal cell lines which differed in their degree of tumorigenicity. Nonparametric statistical analysis demonstrated cloning efficiency in semisolid agar, enhanced fibrinolytic activity, decreased serum requirement for growth, decreased organization of intracellular actin, and increased cloning efficiency in liquid medium to be correlated with tumorigenicity. These correlations were not only qualitative but also quantitative. This suggests that the factors determining the degree of tumorigenicity of a cell can be cellular growth properties.

Actins↗
PubMed1978

2-amino-isobutyric acid and 3-O-methyl-D-glucose transport in 3T3, SV 40-transformed 3T3 and revertant cell lines.

In order to further investigate the connection between transport and growth control, 3T3 cells, SV40 transformed 3T3 cells (SV101), and three revertant cell lines derived from SV101 which have regained certain manifestations of growth control were used. Transport rates of 2-amino-isobutyric acid and 3-O-methyl-D-glucose were measured in sparse, confluent, serum-starved, and serum-stimulated cultures. As shown before, cessation of 3T3 cell growth in G0 under conditions of confluence or serum deprivation was associated with reduced rates of transport for both compounds, whereas the density and serum dependence of growth and transport was largely eliminated in SV101. The density revertant F1SV101, which has regained density regulation of growth similar to 3T3 cells, has also regained density regulation of transport. Neither growth nor transport were serum dependent. The serum revertants AgammaSV7 and LsSV6 have regained both density and serum regulation of growth, but not according to the original mechanism of 3T3 cells of entry into a Go state. Transport was high under conditions of confluence or serum deprivation. Thus for these cells rates of transport were not reduced simply as a consequences of slower cell growth nor were low transport rates responsible for growth arrest. The data are consistent with the possibility that growth arrest specifically in the G0 state could shut off a number of cellular activities, including transport.

Aminoisobutyric Acids↗