The Impact of Patenting on New Product Introductions in the Pharmaceutical Industry

Since Comanor and Scherer (1969), researchers have been using patents as a proxy for new product development. In this paper, we reevaluate this relationship by using novel new data. We demonstrate that the relationship between patenting and new FDA-approved product introductions has diminished considerably since the 1950s, and in fact no longer holds. Moreover, we also find that the relationship between R&D expenditures and new product introductions is considerably smaller than previously reported. While measures of patenting remain important in predicting the arrival of product introductions, the most important predictor is the loss of exclusivity protection on a current product. Our evidence suggests that pharmaceutical firms are acting strategically with respect to new product introductions. Finally, we find no relationship between firm size and new product introductions.Patenting; Pharmaceutical industry; New product management; Research productivity

The Impact of Patenting on New Product Introductions in the Pharmaceutical Industry

Since Comanor and Scherer (1969), researchers have been using patents as a proxy for new product development. In this paper, we reevaluate this relationship by using novel new data. We demonstrate that the relationship between patenting and new FDA-approved product introductions has diminished considerably since the 1950s, and in fact no longer holds. Moreover, we also find that the relationship between R&D expenditures and new product introductions is considerably smaller than previously reported. While measures of patenting remain important in predicting the arrival of product introductions, the most important predictor is the loss of exclusivity protection on a current product. Our evidence suggests that pharmaceutical firms are acting strategically with respect to new product introductions. Finally, we find no relationship between firm size and new product introductions

The Impact of Patenting on New Product Introductions in the Pharmaceutical Industry

Since Comanor and Scherer (1969), researchers have been using patents as a proxy for new product development. In this paper, we reevaluate this relationship by using novel new data. We demonstrate that the relationship between patenting and new FDA-approved product introductions has diminished considerably since the 1950s, and in fact no longer holds. Moreover, we also find that the relationship between R&D expenditures and new product introductions is considerably smaller than previously reported. While measures of patenting remain important in predicting the arrival of product introductions, the most important predictor is the loss of exclusivity protection on a current product. Our evidence suggests that pharmaceutical firms are acting strategically with respect to new product introductions. Finally, we find no relationship between firm size and new product introductions

High Aspect Ratio-Nanostructured Surfaces as Biological Metamaterials

Materials patterned with high-aspect-ratio nanostructures have features on similar lengthscales to cellular components. These surfaces are an extreme topography on the cellular level and have become useful tools for perturbing and sensing the cellular environment. Motivation comes from the ability of high-aspect-ratio nanostructures to deliver cargoes into cells and tissues, access the intracellular environment, and control cell behavior. These structures directly perturb cells’ ability to sense and respond to external forces, influencing cell fate and enabling new mechanistic studies. Through careful design of their nanoscale structure, these systems act as biological metamaterials, eliciting unusual biological responses. While predominantly used to interface eukaryotic cells, there is growing interest in non-animal and prokaryotic cell interfacing. Both experimental and theoretical studies have attempted to develop a mechanistic understanding for the observed behaviors, predominantly focusing on the cell – nanostructure interface. Here, we consider how high-aspect-ratio nanostructured surfaces are used to both stimulate and sense biological systems and discuss remaining research questions

The #ebooksos campaign in Ireland

Against the backdrop of COVID-19, this article outlines the ebooksos campaign. The origin and rationale for the campaign is described. Development of the campaign and possible future developments are considered

Threshold values for the protection of marine ecosystems from NORM in subsea oil and gas infrastructure

Acknowledgements The authors thank Professor Claus Otto (Curtin University) and Professor Richard Neilson (National Decommissioning Centre, Aberdeen, UK.) for comments and support to the project team; and, Sam Jarvis (National Environment Resources Australia), Professor Peter Macreadie, Dr Rick Tinker, and the industry partners of the National Decommissioning Research Initiative for helpful comments to this project. Funding This research was funded by the Australian Government’s Industry Growth Centre National Energy Resources Australia (NERA) through a National Decommissioning Research Initiative (NDRI) grant to Curtin University. The NDRI project was funded by eight industry partners including Shell Australia, Esso Australia, Chevron Australia, BHP Petroleum, Woodside Energy, Santos Limited, ConocoPhillips Pipeline Australia, and Vermilion Oil and Gas Australia. AH is partly funded by the National Decommissioning Centre, Scotland, and the University of Aberdeen.Peer reviewedPublisher PD

Current understanding of the ecological risk of mercury from subsea oil and gas infrastructure to marine ecosystems

Funding Information: This research was funded by the Australian Government’s Industry Growth Centre National Energy Resources Australia (NERA) through a National Decommissioning Research Initiative (NDRI) grant to Curtin University (grant number 13266). The NDRI project was funded by eight industry partners including Shell Australia, Esso Australia, Chevron Australia, BHP Petroleum, Woodside Energy, Santos Limited, ConocoPhillips Pipeline Australia, and Vermilion Oil and Gas Australia. Astley Hastings is funded by the National Decommissioning Centre, Scotland, and the University of Aberdeen. Funding Information: The authors thank Professor Claus Otto (Curtin University) and Professor Richard Neilson (National Decommissioning Centre, Aberdeen, UK.) for comments and support to the project team; and Samantha Jarvis (National Environment Resources Australia), Professor Peter Macreadie, Dr Rick Tinker, and the industry partners of the National Decommissioning Research Initiative for helpful comments to this project. This research was funded by the Australian Government's Industry Growth Centre National Energy Resources Australia (NERA) through a National Decommissioning Research Initiative (NDRI) grant to Curtin University (grant number 13266). The NDRI project was funded by eight industry partners including Shell Australia, Esso Australia, Chevron Australia, BHP Petroleum, Woodside Energy, Santos Limited, ConocoPhillips Pipeline Australia, and Vermilion Oil and Gas Australia. Astley Hastings is funded by the National Decommissioning Centre, Scotland, and the University of Aberdeen. Past research has shown that mercury associates with offshore oil and gas pipelines as well as other products associated with the infrastructure, deeming such materials “hazardous”. However, the current environmental risk assessments for decommissioning activities of such contaminated materials does not take into account the complexity of the compound's nature and the potential harmful effects on e.g. marine food webs. This review paper has outlined these gaps in our current understanding, as well as providing advice on addressing these gaps to ensure that the marine environmental risk assessments reflect the hazardous nature of mercury-contaminated offshore infrastructure. Publisher Copyright: © 2022 The AuthorsPeer reviewedPublisher PD

Intra- and interspecific polymorphisms ofLeishmania donovani andL. tropica minicircle DNA

A pair of degenerate polymerase chain reaction (PCR) primers (LEI-1, TCG GAT CC[C,T] [G,C]TG GGT AGG GGC GT; LEI-2, ACG GAT CC[G,C] [G,C][A,C]C TAT [A,T]TT ACA CC) defining a 0.15-kb segment ofLeishmania minicircle DNA was constructed. These primers amplified not only inter- but also intraspecifically polymorphic sequences. Individual sequences revealed a higher intraspecific than interspecific divergence. It is concluded that individual sequences are of limited relevance for species determination. In contrast, when a data base of 19 different sequences was analyzed in a dendrographic plot, an accurate species differentiation was feasible

A review of the potential risks associated with mercury in subsea oil and gas pipelines in Australia

Peer reviewedPublisher PD

Nrf2 is activated by disruption of mitochondrial thiol homeostasis but not by enhanced mitochondrial superoxide production

The transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) regulates the expression of genes involved in antioxidant defenses to modulate fundamental cellular processes such as mitochondrial function and glutathione metabolism. Previous reports proposed that mitochondrial ROS production and disruption of the glutathione pool activate the Nrf2 pathway, suggesting that Nrf2 senses mitochondrial redox signals and/or oxidative damage and signals to the nucleus to respond appropriately. However, until now it has not been possible to disentangle the overlapping effects of mitochondrial superoxide/ hydrogen peroxide production as a redox signal from changes to mitochondrial thiol homeostasis on Nrf2. Recently, we developed mitochondria-targeted reagents that can independently induce mitochondrial superoxide and hydrogen peroxide production (MitoPQ), or selectively disrupt mitochondrial thiol homeostasis (MitoCDNB). Using these reagents, here we have determined how enhanced generation of mitochondrial superoxide and hydrogen peroxide, or disruption of mitochondrial thiol homeostasis affect activation of the Nrf2 system in cells, which was assessed by Nrf2 protein level, nuclear translocation and expression of its target genes. We found that selective disruption of the mitochondrial glutathione pool and inhibition of its thioredoxin system by MitoCDNB led to Nrf2 activation, while using MitoPQ to enhance production of mitochondrial superoxide and hydrogen peroxide alone did not. We further showed that Nrf2 activation by MitoCDNB requires cysteine sensors of Kelch-like ECH-associated protein 1 (Keap1). These findings provide important information on how disruption to mitochondrial redox homeostasis is sensed in the cytoplasm and signaled to the nucleus