scott and szewczyk in technometrics, 2001, have introduced a similarity measure for twodensities f1 and f2 , by1, 21 21 1 2 2( , ), ,f fsim f ff f f f< >=< >< >wheref1, f2 f1(x, θ1)f2(x, θ2)dx.+∞−∞< >=∫sim(f1, f2) has some appropriate properties that can be suitable measures for the similarity of f1 and f2 .however, due to some restrictions on the value of parameters and the kind of densities, ...

Worker Preferences Firm Preferences w1 : [f1] f2 f3 f4 f5 f6 f7 f8 f1 : [w1] w2 w3 w4 w5 w6 w7 w8 w2 : f1 [f2] f3 f4 f5 f6 f7 f8 f2 : w1 [w2] w3 w4 w5 w6 w7 w8 w3 : f1 f2 [f3] f4 f5 f6 f7 f8 f3 : w1 w2 [w3] w4 w5 w6 w7 w8 w4 : f1 f2 f3 [f4] f5 f6 f7 f8 f4 : w1 w2 w3 [w4] w5 w6 w7 w8 w5 : f1 f2 f3 f4 [f5] f6 f7 f8 f5 : w1 w2 w3 w4 [w5] w6 w7 w8 w6 : f1 f2 f3 f4 f5 [f6] f7 f8 f6 : w1 w2 w3 w4 w5 ...

UNLABELLED Influenza A viruses (IAVs) express the PB1-F2 protein from an alternate reading frame within the PB1 gene segment. The roles of PB1-F2 are not well understood but appear to involve modulation of host cell responses. As shown in previous studies, we find that PB1-F2 proteins of mammalian IAVs frequently have premature stop codons that are expected to cause truncations of the protein, ...

Superinfection by phage T4 of cells infected by the ribonucleic acid (RNA) phage f2 results in inhibition of further f2 production. Experiments using rifampin show that the exclusion of f2 requires T4 gene function soon after T4 infection. By using a sensitive new peptide-mapping procedure to identify f2 coat protein in infected cells, we show that synthesis of the f2 coat occurs at a reduced l...

PB1-F2 is a 90 amino acid protein that is expressed from the +1 open reading frame in the PB1 gene of some influenza A viruses and has been shown to contribute to viral pathogenicity. Notably, a serine at position 66 (66S) in PB1-F2 is known to increase virulence compared to an isogenic virus with an asparagine (66N) at this position. Recently, we found that an influenza virus expressing PB1-F2...

The PB1-F2 protein of influenza A virus has been considered a virulence factor, but its function in inducing apoptosis may be of disadvantage to viral replication. Host mechanisms to regulate PB1-F2-induced apoptosis remain unknown. We generated a PB1-F2-deficient avian influenza virus (AIV) H9N2 and found that the mutant virus replicated less efficiently in human lung epithelial cells. The PB1...