White Paper: Measuring Research Outputs Through Bibliometrics

The suggested citation for this white paper is: University of Waterloo Working Group on Bibliometrics, Winter 2016. White Paper: Measuring Research Outputs through Bibliometrics, Waterloo, Ontario: University of Waterloo.This White Paper provides a high-level review of issues relevant to understanding bibliometrics, and practical recommendations for how to appropriately use these measures. This is not a policy paper; instead, it defines and summarizes evidence that addresses appropriate use of bibliometric analysis at the University of Waterloo. Issues identified and recommendations will generally apply to other academic institutions. Understanding the types of bibliometric measures and their limitations makes it possible to identify both appropriate uses and crucial limitations of bibliometric analysis. Recommendations offered at the end of this paper provide a range of opportunities for how researchers and administrators at Waterloo and beyond can integrate bibliometric analysis into their practice

Inhibition of Programmed Cell Death in Tobacco Plants during a Pathogen-Induced Hypersensitive Response at Low Oxygen Pressure.

The hypersensitive response (HR) of plants to invading pathogens is thought to involve a coordinated activation of plant defense mechanisms and programmed cell death (pcd). To date, little is known about the mechanism underlying death of plant cells during this response. In addition, it is not known whether suppression of pcd affects the induction of other defense mechanisms during the HR. Here, we report that death of tobacco cells (genotype NN) infected with tobacco mosaic virus (TMV) is inhibited at low oxygen pressure. In contrast, virus replication and activation of defense mechanisms, as measured by synthesis of the pathogenesis-related protein PR-1a, were not inhibited at low oxygen pressure. Bacterium-induced pcd was also inhibited at low oxygen pressure. However, pcd induced by TMV or bacteria was not inhibited in transgenic tobacco plants expressing the mammalian anti-pcd protein Bcl-XL. Our results suggest that ambient oxygen levels are required for efficient pcd induction during the HR of plants and that activation of defense responses can be uncoupled from cell death. Furthermore, pcd that occurs during the interaction of tobacco with TMV or bacteria may be distinct from some cases of pcd or apoptosis in animals that are insensitive to low oxygen or inhibited by the Bcl-XL protein