Pay-for-performance programs are growing, but little evidence exists on their effectiveness or on their potential unintended consequences and effects on the patient-physician relationship. Pay-for-performance has the potential to help improve the quality of care, if it can be aligned with the goals of medical professionalism. Initiatives that provide incentives for a few specific elements of a single disease or condition, however, may neglect the complexity of care for the whole patient, especially the elderly patient with multiple chronic conditions. Such programs could also result in the deselection of patients, "playing to the measures" rather than focusing on the patient as a whole, and misalignment of perceptions between physicians and patients. The primary focus of the quality movement in health care should not be on "pay for" or "performance" based on limited measures, but rather on the patient. The American College of Physicians hopes to move the pay-for-performance debate forward with a patient-centered focus--one that puts the needs and interests of the patient first--as these programs evolve.
Radioactive DNA complementary to nucleotide sequences in Moloney murine sarcoma virus (MSV) and Moloney leukemia virus (M-MuLV) complex was made by the endogenous reverse transcriptase reaction. These virus stocks contained a threefold excess of MSV over M-MuLV as measured by biological assay. The complementary DNA was an accurate copy of the viral RNA in that 86% of 35S viral RNA hybridized with complementary (cDNA) DNA at a 1.5 to 1 cDNA-RNA molar ratio. The complementary DNA, of a 4-6S size, was fractionated by sequential absorptions with MulV and the feline leukemia virus pseudotype of MSV, [MSV(FeLV)] RNA. In this manner three sets of nucleotide sequences whichrepresent different portions of the MSV viral complex were obtained: a sarcoma virus-specific fraction (cDNAsarc) with sequences that had no homology to M-MuLV RNA but which hybridized to MSV (FeLV) RNA, a sarcoma-leukemia fraction (cDNA common) with sequences common to MSV as well as M-MuLV viral RNA, and a cDNAleuk representing those nucleotide sequences found only in M-MuLV. Hybridization of MSV-MuLV viral 35S RNA with a threefold molar excess of cDNA's revealed that approximately 20% was hybridized with cDNAsarc, whereas approximately 75% was hybridized with cDNAcommon. M-MuLV 35S RNA alone did not hybridize with cDNAsarc but did hybridize 40 and 50% with cDNAleuk and cDNAcommon, respectively. The cDNAsarc represents about 25% of the total MSV sequences, whereas the cDNAcommon represents the remainder of the MSV virus genome. Some cDNAcommon sequences were shared by two other sarcoma viruses and several distinctly different isolates of MulV. In contrast, the MSV "sarc" sequences had little or no homology with two other murine sarcoma virus isolates.
Cat cells transformed by Moloney murine sarcoma virus contain virus-specific sequences in their RNA and DNA. Cloned, spontaneous revertant cell lines derived from clones of these cells had no evidence of the sarcoma genome in the cell RNA or DNA as judged by RNA-complementary DNA or DNA-complementary DNA hybridizations. ?This is apparently the first report of loss of a transforming genome in a revertant cell line.
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