Impacts of climate change on plant diseases – opinions and trends

There has been a remarkable scientific output on the topic of how climate change is likely to affect plant diseases in the coming decades. This review addresses the need for review of this burgeoning literature by summarizing opinions of previous reviews and trends in recent studies on the impacts of climate change on plant health. Sudden Oak Death is used as an introductory case study: Californian forests could become even more susceptible to this emerging plant disease, if spring precipitations will be accompanied by warmer temperatures, although climate shifts may also affect the current synchronicity between host cambium activity and pathogen colonization rate. A summary of observed and predicted climate changes, as well as of direct effects of climate change on pathosystems, is provided. Prediction and management of climate change effects on plant health are complicated by indirect effects and the interactions with global change drivers. Uncertainty in models of plant disease development under climate change calls for a diversity of management strategies, from more participatory approaches to interdisciplinary science. Involvement of stakeholders and scientists from outside plant pathology shows the importance of trade-offs, for example in the land-sharing vs. sparing debate. Further research is needed on climate change and plant health in mountain, boreal, Mediterranean and tropical regions, with multiple climate change factors and scenarios (including our responses to it, e.g. the assisted migration of plants), in relation to endophytes, viruses and mycorrhiza, using long-term and large-scale datasets and considering various plant disease control methods

Do Stress Responses Promote Leukemia Progression? An Animal Study Suggesting a Role for Epinephrine and Prostaglandin-E2 through Reduced NK Activity

In leukemia patients, stress and anxiety were suggested to predict poorer prognosis. Oncological patients experience ample physiological and psychological stress, potentially leading to increased secretion of stress factors, including epinephrine, corticosteroids, and prostaglandins. Here we tested whether environmental stress and these stress factors impact survival of leukemia-challenged rats, and studied mediating mechanisms. F344 rats were administered with a miniscule dose of 60 CRNK-16 leukemia cells, and were subjected to intermittent forced swim stress or to administration of physiologically relevant doses of epinephrine, prostaglandin-E2 or corticosterone. Stress and each stress factor, and/or their combinations, doubled mortality rates when acutely applied simultaneously with, or two or six days after tumor challenge. Acute administration of the β-adrenergic blocker nadolol diminished the effects of environmental stress, without affecting baseline survival rates. Prolonged β-adrenergic blockade or COX inhibition (using etodolac) also increased baseline survival rates, possibly by blocking tumor-related or normal levels of catecholamines and prostaglandins. Searching for mediating mechanisms, we found that each of the stress factors transiently suppressed NK activity against CRNK-16 and YAC-1 lines on a per NK basis. In contrast, the direct effects of stress factors on CRNK-16 proliferation, vitality, and VEGF secretion could not explain or even contradicted the in vivo survival findings. Overall, it seems that environmental stress, epinephrine, and prostaglandins promote leukemia progression in rats, potentially through suppressing cell mediated immunity. Thus, patients with hematological malignancies, which often exhibit diminished NK activity, may benefit from extended β-blockade and COX inhibition

Soil respiration in northern forests exposed to elevated atmospheric carbon dioxide and ozone

The aspen free-air CO 2 and O 3 enrichment (FACTS II–FACE) study in Rhinelander, Wisconsin, USA, is designed to understand the mechanisms by which young northern deciduous forest ecosystems respond to elevated atmospheric carbon dioxide (CO 2 ) and elevated tropospheric ozone (O 3 ) in a replicated, factorial, field experiment. Soil respiration is the second largest flux of carbon (C) in these ecosystems, and the objective of this study was to understand how soil respiration responded to the experimental treatments as these fast-growing stands of pure aspen and birch + aspen approached maximum leaf area. Rates of soil respiration were typically lowest in the elevated O 3 treatment. Elevated CO 2 significantly stimulated soil respiration (8–26%) compared to the control treatment in both community types over all three growing seasons. In years 6–7 of the experiment, the greatest rates of soil respiration occurred in the interaction treatment (CO 2  + O 3 ), and rates of soil respiration were 15–25% greater in this treatment than in the elevated CO 2 treatment, depending on year and community type. Two of the treatments, elevated CO 2 and elevated CO 2  + O 3 , were fumigated with 13 C-depleted CO 2 , and in these two treatments we used standard isotope mixing models to understand the proportions of new and old C in soil respiration. During the peak of the growing season, C fixed since the initiation of the experiment in 1998 (new C) accounted for 60–80% of total soil respiration. The isotope measurements independently confirmed that more new C was respired from the interaction treatment compared to the elevated CO 2 treatment. A period of low soil moisture late in the 2003 growing season resulted in soil respiration with an isotopic signature 4–6‰ enriched in 13 C compared to sample dates when the percentage soil moisture was higher. In 2004, an extended period of low soil moisture during August and early September, punctuated by a significant rainfall event, resulted in soil respiration that was temporarily 4–6‰ more depleted in 13 C. Up to 50% of the Earth’s forests will see elevated concentrations of both CO 2 and O 3 in the coming decades and these interacting atmospheric trace gases stimulated soil respiration in this study.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/45867/1/442_2006_Article_381.pd

Brain microvascular endothelial cell association and distribution of a 5 nm ceria engineered nanomaterial

Mo Dan,1,2 Michael T Tseng,3 Peng Wu,4 Jason M Unrine,5 Eric A Grulke,4 Robert A Yokel1,21Department of Pharmaceutical Sciences, College of Pharmacy, 2Graduate Center for Toxicology, University of Kentucky, Lexington, KY, USA; 3Departments of Anatomical Sciences and Neurobiology, University of Louisville, Louisville, KY, USA; 4Chemical and Materials Engineering Department, 5Department of Plant and Soil Science, University of Kentucky, Lexington, KY, USAPurpose: Ceria engineered nanomaterials (ENMs) have current commercial applications and both neuroprotective and toxic effects. Our hypothesis is that ceria ENMs can associate with brain capillary cells and/or cross the blood–brain barrier.Methods: An aqueous dispersion of ~5 nm ceria ENM was synthesized and characterized in house. Its uptake space in the Sprague Dawley rat brain was determined using the in situ brain perfusion technique at 15 and 20 mL/minute flow rates; 30, 100, and 500 µg/mL ceria perfused for 120 seconds at 20 mL/minute; and 30 µg/mL perfused for 20, 60, and 120 seconds at 20 mL/minute. The capillary depletion method and light and electron microscopy were used to determine its capillary cell and brain parenchymal association and localization.Results: The vascular space was not significantly affected by brain perfusion flow rate or ENM, demonstrating that this ceria ENM did not influence blood–brain barrier integrity. Cerium concentrations, determined by inductively coupled plasma mass spectrometry, were significantly higher in the choroid plexus than in eight brain regions in the 100 and 500 µg/mL ceria perfusion groups. Ceria uptake into the eight brain regions was similar after 120-second perfusion of 30, 100, and 500 µg ceria/mL. Ceria uptake space significantly increased in the eight brain regions and choroid plexus after 60 versus 20 seconds, and it was similar after 60 and 120 seconds. The capillary depletion method showed 99.4% ± 1.1% of the ceria ENM associated with the capillary fraction. Electron microscopy showed the ceria ENM located on the endothelial cell luminal surface.Conclusion: Ceria ENM association with brain capillary endothelial cells saturated between 20 and 60 seconds and ceria ENM brain uptake was not diffusion-mediated. During the 120-second ceria ENM perfusion, ceria ENM predominately associated with the surface of the brain capillary cells, providing the opportunity for its cell uptake or redistribution back into circulating blood.Keywords: ceria engineered nanomaterial, brain microvascular endothelial cell association, in situ brain perfusion, capillary depletio