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C Massey

Publications and source records attributed to C Massey.

5 recordsLinked to original sources
PubMed2001

A 2-year efficacy study of Not On Tobacco in Florida: an overview of program successes in changing teen smoking behavior.

BACKGROUND: Adolescent smoking has been an issue of major concern in the United States. This has led to a need for the development, evaluation, and dissemination of effective youth cessation programs. The purpose of this paper is to report the results of a 2-year demonstration study (1999-2000) of the American Lung Association's teen smoking cessation program, the Not On Tobacco (NOT) program. METHODS: The study used a "matched" design wherein each NOT school was matched to a brief intervention (BI) school. The study consisted of 20 NOT and 20 BI Florida high schools encompassing 627 students. The primary outcome measures were carbon monoxide-validated quit and reduction rates for NOT and BI schools at 5.2 months postprogram. RESULTS: NOT smoking cessation and reduction outcomes were significantly better than those of the brief intervention. Further, data indicate that NOT was more effective than the brief intervention for females compared with males; males showed successful quit attempts in both intervention groups. Overall, more NOT youth either quit or reduced smoking than did BI youth. CONCLUSIONS: These positive smoking behavior changes suggest that NOT is an effective teen smoking cessation option.

Adolescent↗
PubMed2001

Recent developments in the evolution of morphologies and controllers for physically simulated creatures.

Karl Sims' work on evolving body shapes and controllers for three-dimensional, physically simulated creatures generated wide interest on its publication in 1994. The purpose of this article is threefold: (a) to highlight a spate of recent work by a number of researchers in replicating, and in some cases extending, Sims' results using standard PCs (Sims' original work was done on a Connection Machine CM-5 parallel computer). In particular, a re-implementation of Sims' work by the authors will be described and discussed; (b) to illustrate how off-the-shelf physics engines can be used in this sort of work, and also to highlight some deficiencies of these engines and pitfalls when using them; and (c) to indicate how these recent studies stand in respect to Sims' original work.

Anatomy↗
PubMed1993

Targeting of the rasT24 oncogene to the proximal convoluted tubules in transgenic mice results in hyperplasia and polycystic kidneys.

Five families of transgenic mice were derived from one-cell-stage embryos injected with gamma GT-rasT24, a fusion gene consisting of the gamma-glutamyl transpeptidase (gamma GT) 5' flanking region containing promoter I linked to a mutated (codon 12) human H-ras oncogene. The transgene was expressed selectively in the kidneys, eyes, and brains of all families as determined by reverse transcription-polymerase chain reaction, nuclease protection assays, and in situ hybridization. In two of five families, kidney lesions consisting of proximal tubular hyperplasia, renal cysts, and microadenomas developed in male animals; males also expressed higher levels of gamma GT/rasT24 RNA. Early lesions consisted of proximal tubular hyperplasia as defined by alkaline phosphatase histochemistry, gamma GT immunohistochemistry, and electron microscopy and could be correlated with the presence of rasT24 RNA within the cystic proximal tubular epithelium by in situ hybridization. Advanced lesions also involved other segments of the nephron and consisted of cysts lined by a flattened unicellular layer of attenuated epithelium. No rasT24 could be identified within cystic lesions of the distal nephron and collecting tubules by in situ hybridization, and they most likely arise by external compression. Animals from the two transgenic strains exhibiting cystic lesions die of renal failure beginning at 8 months of age. No difference in cell-cycle parameters or DNA ploidy between transgenic and control kidneys was identified by flow cytometric analysis. No renal carcinomas developed. The primary renal effects of the H-rasT24 oncogene in this model system consist of proximal tubular hyperplasia and polycystic kidneys. This model appears to provide a useful in vivo system for the study of ras oncogene function and control of renal cell proliferation.

Animals↗
PubMed1990

Protein kinase C inhibits Ca2+ accumulation in cardiac sarcoplasmic reticulum.

It is now recognized that phorbol esters are negative inotropic agents in mammalian heart which presumably act via stimulation of Ca2(+)-activated phospholipid-dependent protein kinase (PKC). The goal in the present study was to identify the underlying cellular processes. Digitonin-permeabilized cultured neonatal rat ventricular myocytes were used to study biochemical and functional effects of phorbol esters on cardiac sarcoplasmic reticulum (SR). These cells contracted spontaneously at 3 microM Ca2+. Beating was inhibited by 10 microM ryanodine and was insensitive to 1 microM nifedipine. Thus, beating behavior results from the phasic oscillation of Ca2+ transport by SR in this preparation. Phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), decreased frequency by 30%, suggesting that Ca2+ transport by SR had been reduced. Whereas cAMP stimulated the rate of oxalate-supported 45Ca2+ uptake 2-fold, phorbol esters, TPA, and phorbol 12,13-dibutyrate inhibited this process by about 45%. The effects of phorbols were specific: (a) the alpha-analogues of TPA and phorbol 12,13-dibutyrate were inactive; and (b) the phorbol esters had no effect on Ca2+ transport in cells that had been depleted of PKC. TPA decreased oxalate-stimulated Ca2+ uptake over the entire range of Ca2+ concentrations, from 0.1 to 10 microM, by at least 70% without shifting the half-maximal effective Ca2+ concentration. Taken together these results indicate that the effects of phorbol ester on cardiac contraction are due to decreased Ca2+ transport by the SR and that these responses are mediated by PKC. These studies support the interpretation that the negative inotropic effects of phorbol esters are due, in part, to decreased SR function.

Animals↗