Effects of 2,3,7,8-tetrachlorodibenzo-<em>p</em>-dioxin (TCDD) on liver phosphoenolpyruvate carboxykinase (PEPCK) activity, glucose homeostasis and plasma amino acid concentrations in the most TCDD-susceptible and the most TCDD-resistant rat strains.

Reduced gluconeogenesis due to decreased activity of key gluconeogenic enzymes in liver, together with feed refusal, has been suggested to play an important role in 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD)-induced lethality in rats. This study was carried out to further analyse the toxicological significance of reduced gluconeogenesis by comparing dose-responses and time-courses of effects of TCDD on the activity of phosphoenolpyruvate carboxykinase (PEPCK) in liver, liver glycogen concentration as well as plasma concentrations of glucose and amino acids in both genders of TCDD-sensitive Long-Evans (L-E) rats and TCDD-resistant Han/Wistar (H/W) rats. A dose-dependent decrease in PEPCK activity was observed in H/W rats, but in L-E rats the activity was not decreased. However, TCDD impaired the strong increase in liver PEPCK activity observed in pair-fed controls of the L-E strain. Liver glycogen concentrations were severely decreased in L-E rats and moderately in H/W rats. This effect seems to be secondary to reduced feed intake, since a similar decrease was seen in pair-fed controls. Decreases in plasma glucose concentrations were also more profound in L-E rats than in H/W rats, but pair-fed controls were generally less affected. Circulating concentrations of amino acids were markedly increased in TCDD-treated L-E rats, which is likely to reflect increased mobilization of amino acids and their decreased metabolism in liver. Reduction of liver PEPCK activity cannot account for the sensitivity difference of these two strains of rats in terms of mortality. Nevertheless, the response of both strains of TCDD-treated rats regarding gluconeogenesis is different from that seen in pair-fed controls and suggesting that impairment of this pathway contributes to the development of the wasting syndrome

Health effects caused by primary fine particulate matter (PM2.5) emitted from buses in the Helsinki metropolitan area, Finland

Fine particle (PM2.5) emissions from traffic have been associated with premature mortality. The current work compares PM2.5 induced mortality in alternative public bus-transportation strategies as being considered by the Helsinki Metropolitan Area Council, Finland. The current bus fleet and transportation volume is compared to four alternative hypothetical bus fleet strategies for the year 2020: (i) the current bus fleet for 2020 traffic volume; (ii) modern diesel buses without particle traps, (iii) diesel buses with particle traps, and (iv) buses using natural gas engines. Average population PM2.5 exposure level attributable to the bus emissions was determined for the 1996-97 situation using PM2.5 exposure measurements including elemental composition from the EXPOLIS-Helsinki study and similar element-based source apportionment of ambient PM2.5 concentrations observed in the ULTRA-study. Average population exposure to particles originating from the bus traffic in the year 2020 is assumed to be proportional to the bus emissions in each strategy. Associated mortality was calculated using dose-response relationships from two large cohort studies on PM2.5 mortality from the U.S. Estimated number of deaths per year (90 % confidence intervals in parenthesis) associated with primar

Liver Tumor-promoting Activity of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD-sensitive and TCDD- resistant Rat Strains1.

Risk assessment of dioxins is currently based on induction of liver tumors in rats. The toxicity of dioxins is characterized by large sensitivity differences among animal species and even strains of the same species, which complicates the risk assessment. The significance of these differences in dioxin-induced carcinogenicity is not known. We therefore studied the liver tumor-promoting activity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the sensitive Long-Evans (L-E) and the resistant Han/Wistar (H/W) rats differing &gt;1000-fold in their sensitivity to the acute lethality of TCDD. Female rats were partially hepatectomized, initiated with nitrosodiethylamine, and treated with TCDD for 20 weeks. Altered hepatic foci (AHF) were stereologically quantitated using glutathione S-transferase P as a marker. AHF were significantly (P &lt; 0.001) and dose dependently increased in L-E rats at 10 and 100 ng/kg/day, but in H/W rats only at 1000 ng/kg/day and above, indicating a remarkable (&sim;100-fold) sensitivity difference between L-E and H/W rats. The same sensitivity difference but 10-fold less foci were observed between nonhepatectomized/noninitiated L-E and H/W rats. Induction of AHF was related to hepatotoxicity but not to cytochrome P4501A1 activity in the liver. Liver TCDD concentrations were similar in both strains. H/W rats are exceptionally resistant to induction of AHF by TCDD, and the resistance is associated with an altered transactivation domain of the aryl hydrocarbon receptor. Genetic differences may account for significant interindividual/intraspecies sensitivity differences in dioxin-induced carcinogenesis. Understanding the role of transactivation domain of the aryl hydrocarbon receptor in carcinogenesis is therefore likely to improve dioxin risk assessment

Assessment of Dickeya and Pectobacterium spp. on vegetables and ornamentals (Soft rot)

Dickeya and Pectobacterium belonging to the group of soft rot Pectobacteriaceae (SRP) are causing emerging problems in a wide range of vegetable and ornamental crops in Europe, including potato, carrot, cabbage, Chinese cabbage, celery, leek, pepper, parsley, Zantedeschia, hyacinth, Dahlia, Chrysanthemum, Philodendron, Freesia, Saintpaulia, Iris, Aglaonema, Crocus, Campanula and Phalaenopsis. The phytopathogens in both genera are genetically and phenotypically highly diverse. Disease problems in the different hosts are associated with the introduction of new variants or by spread of groups already present in Europe. Within this Euphresco project we aimed to identify and assess the risks of these new variants, and to develop management strategies, including reliable diagnostic methods to prevent introductions and further spread of SRP. To reach our goals, meetings were organized and collaborations were established with specialists worldwide. All information on meetings, protocols and activities of the Euphresco group are published on the Dickeya/Pectobacterium website, conveyed by the James Hutton Institute in Invergowrie (Scotland) (https://engage.hutton.ac.uk, contact person Dr I. Toth/Dr J. Fairly).During the project, 1.5 days meetings were held in 2015 in Gdansk (Poland), in 2016 in Helsinki (Finland), in 2017 in Edinburgh (Scotland) and in 2018 in Emmeloord (The Netherlands). Meetings were attended by an average of 30 participants from organizations in EU member states, North- and Latin America, Africa, Asia and Australia.One project’s objective was to develop methods for the detection and identification of Pectobacterium and Dickeya species in different matrices. For this, a panel of reference strains has been compiled for Dickeya and Pectobacterium species. Most strains have been deposited in international collections. For most strains also whole genome sequence data are available. During the course of this project, several diagnostic tests were developed and evaluated, often based on the TaqMan technology.In several countries, surveys in potato and ornamental crops were conducted, but also in other matrices of the potato ecosystem, including water used for irrigation. In addition, new taxonomic groups that have been identified, are now new species including: P. versatile, P. aquaticum, P. fontis and P. polonicum. In potato, P. brasiliense became dominant as blackleg causing organism and has largely outcompeted D. solani in the last five years. In surface water in Europe, D. zeae was found to be the dominant SRP. In other continents, serious outbreaks of potato blackleg with other SRP has been reported, such as D. dianthicola in the USA and Australia. Various new SRP have been described, namely P. punjabense, P. peruviense, P. polaris, D. lacustris and D. zantedeschia. For the first time, D. fangzhongdai was described in Phalaenopsis. Not all species can cause potato blackleg.Studies on various virulence factors were conducted for SRP, such as on chemoreceptors, small phenolic plant compounds interacting with signal molecules of Pectobacterium involved in the quorum sensing mechanism of the pathogen. A Tn-seq approach was developed and used to identify new virulence factors.Information was exchanged on disease management strategies which include cultivation practices, resistance breeding, hygiene and the use of (bio-) control agents. A strict hygiene and an intensive monitoring of seed lots was found to be associated with a significant reduction of infections with blackleg causing SRP. A phage therapy has been developed to protect (seed) potato tubers against soft rot during storage. Various bacteriophages and bacterial antagonists were characterized and some evaluated for control of potato soft rot and/or blackleg. Steam treatments for seed tubers were found to decrease the blackleg incidence. Cold plasma treatment was found to kill SRP grown in vitro. Similarly, stabilized silver nanostructures killed SRP. It was found that seed potato lots can differ in suppressiveness against D. solani. Indications were found that the microbiome in tuber tissue plays a role in this.<br/