Strategically leveraging corporate social responsibility

orporate social responsibility (CSR) is changing the rules of branding but it is unclear how. While the literature offers a range of approaches seeking insight to how to manage CSR-related issues, practitioners are left in a state of confusion when having to decide on how to tackle CSR in a way that benefits both the corporate brand and society at large. based on qualitative empirical research, this article offers a framework for companies to address CSR and their brands strategically, whether as entrepreneurs, performers, vocal converts, or quietly conscientious. We define these categories according to the level of involvement, integration, and the key initiator of the CSR focus. This article concludes with suggestions practitioners should keep in mind when aiming to balance stakeholder tensions and to achieve consistency in their corporate branding and CSR efforts

Intergenerational Effects of Nicotine in an Animal Model of Paternal Nicotine Exposure

Environmental conditions imposed onto organisms during certain phases of their life cycles such as embryogenesis or puberty can not only impact the organisms’ own health, but also affect subsequent generations. The underlying mechanisms causing intergenerational phenotypes are not encoded in the genome, but the result of reversible epigenetic modifications. This work investigates in a mouse model the impact of paternal nicotine exposure on the next generation regarding addictive behavior modulation, metabolic changes, and molecular mechanisms. It provides evidence that male offspring from nicotine-exposed fathers (NIC offspring) is more resistant to lethal doses of nicotine. This phenotype is gender-specific and depends on short-term environmental challenges with low doses of nicotine prior to the LD50 application. The observed survival phenotype is not restricted to nicotine as drug of abuse, but also presents itself, when NIC offspring is challenged with a cocaine LD50 after acclimatization to low doses of either nicotine or cocaine. Functionally, NIC offspring metabolizes nicotine faster than control. Mechanistically, NIC offspring livers show global up-regulation of xenobiotic processing genes (XPG), an effect that is even more pronounced in primary hepatocyte cultures. Being known targets of Constitutive Androstane Receptor (CAR) and Pregnane X Receptor (PXR), these XPGs show higher baseline expression in naïve NIC offspring livers. Nicotine’s action on the brain’s reward circuitry does not appear to be of biological significance in our model system. Taken together, paternal nicotine exposure leads to a non-specific and conditional phenotype in male NIC offspring that may provide a general survival advantage against xenobiotic challenges