Comparative Advertising Wars: An Historical Analysis of Their Causes and Consequences

This historical study contributes to the extensive literature on comparative advertising by examining the causes and consequences of comparative advertising wars; that is, when one advertiser responds to a direct or implied attack by another advertiser. Primary and secondary sources consist of articles published in historic and contemporary marketing and advertising trade journals, such as Printers’ Ink, Advertising & Selling, and Advertising Age. The findings reveal that well-publicized advertising wars occurred frequently between major U.S. advertisers throughout the twentieth century and into the twenty-first, and that they most often occurred in product and service markets characterized by intense competition. Many, if not most, advertisers’ principal motive for responding to a comparative advertising attack has been emotional rather than rational. The findings also reveal that advertising wars often became increasingly hostile, leading to negative consequences for all combatants, as well as a broad and negative social consequence in the form of potentially misleading advertising.Yeshttps://us.sagepub.com/en-us/nam/manuscript-submission-guideline

Desmoglein-2 is important for islet function and β-cell survival

Type 1 diabetes is a complex disease characterized by the lack of endogenous insulin secreted from the pancreatic β-cells. Although β-cell targeted autoimmune processes and β-cell dysfunction are known to occur in type 1 diabetes, a complete understanding of the cell-to-cell interactions that support pancreatic function is still lacking. To characterize the pancreatic endocrine compartment, we studied pancreata from healthy adult donors and investigated a single cell surface adhesion molecule, desmoglein-2 (DSG2). Genetically-modified mice lacking Dsg2 were examined for islet cell mass, insulin production, responses to glucose, susceptibility to a streptozotocin-induced mouse model of hyperglycaemia, and ability to cure diabetes in a syngeneic transplantation model. Herein, we have identified DSG2 as a previously unrecognized adhesion molecule that supports β-cells. Furthermore, we reveal that DSG2 is within the top 10 percent of all genes expressed by human pancreatic islets and is expressed by the insulin-producing β-cells but not the somatostatin-producing δ-cells. In a Dsg2 loss-of-function mice (Dsg2lo/lo), we observed a significant reduction in the number of pancreatic islets and islet size, and consequently, there was less total insulin content per islet cluster. Dsg2lo/lo mice also exhibited a reduction in blood vessel barrier integrity, an increased incidence of streptozotocininduced diabetes, and islets isolated from Dsg2lo/lo mice were more susceptible to cytokine-induced β-cell apoptosis. Following transplantation into diabetic mice, islets isolated from Dsg2lo/lo mice were less effective than their wildtype counterparts at curing diabetes. In vitro assays using the Beta-TC-6 murine β-cell line suggest that DSG2 supports the actin cytoskeleton as well as the release of cytokines and chemokines. Taken together, our study suggests that DSG2 is an under-appreciated regulator of β-cell function in pancreatic islets and that a better understanding of this adhesion molecule may provide new opportunities to combat type 1 diabetes.Kay K. Myo Min, Darling Rojas-Canales, Daniella Penko, Mark DeNichilo, Michaelia P. Cockshell, Charlie B. Ffrench, Emma J. Thompson, Olof Asplund, Christopher J. Drogemuller, Rashmi B. Prasad, Leif Groop, Shane T. Grey, Helen E. Thomas, Thomas Loudovaris, Thomas W. Kay, My G. Mahoney, Claire F. Jessup, P. Toby Coates, and Claudine S. Bonde