The service dominant logic:an MC21 project view

Vargo and Lusch propose a very exciting framework that aims in expanding the boundaries of the marketing discipline by moving away from the existing exchange paradigm towards a Service Dominant (S-D) logic. This new S-D logic has the potential to strengthen the theoretical grounds of marketing by establishing links to other disciplines. This commentary attempts to discuss some aspects of the foundational premises of the S-D logic from the perspective of the MC21 group with special emphases on innovation, value creation, and resource allocation.

Q parameter scaling in scalar and vector models with dominant signal-noise and noise-noise beating terms

The Q parameter scales differently with the noise power for the signal-noise and the noise-noise beating terms in scalar and vector models. Some procedures for including noise in the scalar model largely under-estimate the Q parameter.

Defective peroxisomal proliferators activated receptor gamma activity due to dominant-negative mutation synergizes with hypertension to accelerate cardiac fibrosis in mice

Aims: Humans with inactivating mutations in peroxisomal proliferators activated receptor gamma (PPAR?) typically develop a complex metabolic syndrome characterized by insulin resistance, diabetes, lipodystrophy, hypertension, and dyslipidaemia which is likely to increase their cardiovascular risk. Despite evidence that the activation of PPAR? may prevent cardiac fibrosis and hypertrophy, recent evidence has suggested that pharmacological activation of PPAR? causes increased cardiovascular mortality. In this study, we investigated the effects of defective PPAR? function on the development of cardiac fibrosis and hypertrophy in a murine model carrying a human dominant-negative mutation in PPAR?. Methods and results: Mice with a dominant-negative point mutation in PPAR? (P465L) and their wild-type (WT) littermates were treated with either subcutaneous angiotensin II (AngII) infusion or saline for 2 weeks. Heterozygous P465L and WT mice developed a similar increase in systolic blood pressure, but the mutant mice developed significantly more severe cardiac fibrosis to AngII that correlated with increased expression of profibrotic genes. Both groups similarly increased the heart weight to body weight ratio compared with saline-treated controls. There were no differences in fibrosis between saline-treated WT and P465L mice. Conclusion: These results show synergistic pathogenic effects between the presence of defective PPAR? and AngII-induced hypertension and suggest that patients with PPAR? mutation and hypertension may need more aggressive therapeutic measures to reduce the risk of accelerated cardiac fibrosis. © The Author 2009.