Adaptive responses in Chlamydomonas reinhardtii

The photosynthetic single cellular alga Chlamydomonas reinhardtii has been used as a model organism to examine in detail the physiological, biochemical and molecular processes of photosynthesis, flagella synthesis and movement, mineral stress, interactions between nucleus, chloroplasts and mitochondria and other processes. In this review we summarize part of the current knowledge on adaptive responses in C. reinhardtii when it is exposed to oxidative stress and to changes in light intensity, concentration of minerals, herbicides and metals. The individual responses are linked in order to understand the response of the cell, which is continuously subjected to fluctuations, as a whole

Gonadal Malformations in Whitefish from Lake Thun: Defining the Case and Evaluating the Role of EDCs

The objectives of this project were to evaluate i) whether the gonad alterations of whitefish (Coregonus lavaretus spp.) in Lake Thun represent abnormal morphological variations specific to this lake, and, if so, ii) whether the malformations are related to chemical exposure, in particular to exposure to endocrine-disrupting compounds (EDCs). Large-scale monitoring data revealed that, although whitefish in other lakes display some background variation of gonad morphology, the situation in Lake Thun, is unique because of the significantly higher prevalence of gonad malformations. The abnormal variations of whitefish gonad morphology include aplasias, compartmentations, fusions, and intersex. In the search for the factor(s) causing the gonad malformations, coregonids were exposed from fertilization up to maturity to Lake Thun water and plankton or to contaminants possibly being present in the lake, including trinitrotoluenes, and naphtalene sulfonates. Since these experiments are still ongoing, a conclusive answer cannot be given yet, but initial observations point to a role of the lake plankton. The possible presence of EDCs in Lake Thun was assessed using bioanalytics and biomarkers. The bioanalytical studies found estrogenic activities in concentrated plankton extracts of Lake Thun, however, estrogenic activities occurred also in plankton extracts of reference lakes. Bioassay-directed fractionation of the plankton samples points to degradation products of natural substances as a cause of the estrogenic activity. Examination of Lake Thun whitefish for EDC biomarkers such as vitellogenin, sex steroid levels or intersex frequency yielded no indications of exposure to EDCs, neither in fish with normal nor in fish with abnormal gonad morphology. Long-term laboratory exposure of developing coregonids to the prototype estrogenic compound, 17?-estradiol, resulted in an increased frequency of intersex gonads, but did not induce the other gonad malformations typical for Lake Thun coregonids. In summing up, the currently available evidence does not support an EDC or chemical etiology of the gonad malformations, however, this preliminary conclusion needs to be substantiated in the ongoing investigations. The project also highlights the need for more detailed knowledge of natural variation in wildlife populations to be able to recognize anthropogenically caused variation

Barriers to evidence use for sustainability: Insights from pesticide policy and practice.

Calls for supporting sustainability through more and better research rest on an incomplete understanding of scientific evidence use. We argue that a variety of barriers to a transformative impact of evidence arises from diverse actor motivations within different stages of evidence use. We abductively specify this variety in policy and practice arenas for three actor motivations (truth-seeking, sense-making, and utility-maximizing) and five stages (evidence production, uptake, influence on decisions, effects on sustainability outcomes, and feedback from outcome evaluations). Our interdisciplinary synthesis focuses on the sustainability challenge of reducing environmental and human health risks of agricultural pesticides. It identifies barriers resulting from (1) truth-seekers' desire to reduce uncertainty that is complicated by evidence gaps, (2) sense-makers' evidence needs that differ from the type of evidence available, and (3) utility-maximizers' interests that guide strategic evidence use. We outline context-specific research-policy-practice measures to increase evidence use for sustainable transformation in pesticides and beyond

Barriers to evidence use for sustainability: Insights from pesticide policy and practice

Calls for supporting sustainability through more and better research rest on an incomplete understanding of scientific evidence use. We argue that a variety of barriers to a transformative impact of evidence arises from diverse actor motivations within different stages of evidence use. We abductively specify this variety in policy and practice arenas for three actor motivations (truth-seeking, sense-making, and utility-maximizing) and five stages (evidence production, uptake, influence on decisions, effects on sustainability outcomes, and feedback from outcome evaluations). Our interdisciplinary synthesis focuses on the sustainability challenge of reducing environmental and human health risks of agricultural pesticides. It identifies barriers resulting from (1) truth-seekers’ desire to reduce uncertainty that is complicated by evidence gaps, (2) sense-makers’ evidence needs that differ from the type of evidence available, and (3) utility-maximizers’ interests that guide strategic evidence use. We outline context-specific research–policy–practice measures to increase evidence use for sustainable transformation in pesticides and beyond

Health in the 2030 Agenda for Sustainable Development : from framework to action, transforming challenges into opportunities

The critically important role of health for development was underlined in the 16th World Development Report entitled “Investing in health”, published in 1993 [1]. Put forth by the World Bank and enhanced with input from the World Health Organization (WHO), the report examined the interplay between human health, health policy, and economic development. In the period 2000-2015, health for development was strongly emphasized in the Millennium Development Goals (MDGs). Indeed, three of the eight MDGs explicitly featured health [2]. Meanwhile, major achievements have been made in population health. For instance, average global life expectancy has increased by more than 20 years between 1950 and 2010 [3]. Yet, there are areas of unfinished business, such as reducing child mortality and improving maternal health [4]. Key vulnerable groups, such as the poorest and most isolated populations, have been left excluded and marginalized [4,5]. In addition, there are new challenges, as for instance non-communicable diseases have surpassed infectious diseases in terms of global burden [6], novel infectious threats from zoonoses [7] and anti-microbial resistance [8] have emerged, there are toxic mixtures of chemicals compromising human, animal, and ecosystem health, while climate change, urbanization, and migration have amplified health problems and vulnerabilities [9]. Taken together, there are multifactorial stresses that ask for innovative, multi-partner, integrated approaches.ISSN:2047-298

Correction:How the COVID-19 pandemic highlights the necessity of animal research (vol 30, pg R1014, 2020)

(Current Biology 30, R1014–R1018; September 21, 2020) As a result of an author oversight in the originally published version of this article, a number of errors were introduced in the author list and affiliations. First, the middle initials were omitted from the names of several authors. Second, the surname of Dr. van Dam was mistakenly written as “Dam.” Third, the first name of author Bernhard Englitz was misspelled as “Bernard” and the surname of author B.J.A. Pollux was misspelled as “Pullox.” Finally, Dr. Keijer's first name was abbreviated rather than written in full. These errors, as well as various errors in the author affiliations, have now been corrected online

In vitro assessment of modes of toxic action of pharmaceuticals in aquatic life

An ecotoxicological test battery based on a mode-of-action approach was designed and applied to the hazard identification and classification of modes of action of six pharmaceuticals (carbamazepine, diclofenac, ethinyl estradiol, ibuprofen, propranolol, and sulfamethoxazole). The rationale behind the design of the battery was to cover the relevant interactions that a compound may have with biological targets. It is thus not comprehensive but contains representative examples of each category of mode of toxic action including nonspecific, specific, and reactive toxicity. The test battery consists of one test system for nonspecific toxicity (baseline toxicity or narcosis), two test systems for specific effects, and two test systems for reactive toxicity. The baseline toxicity was quantified with the Kinspec test, which detects membrane leakage via measurements of membrane potential. This test system may also be used to detect the specific effects on energy transduction, although this was not relevant to any compound investigated in this study. As examples of specific receptor-mediated toxicity, we chose the yeast estrogen screen (YES) as a specific test for estrogenicity, and the inhibition of chlorophyll fluorescence in algae to assess specific effects on photosynthesis. Reactive modes of action were assessed indirectly by measuring the relevance of cellular defense systems. Differences in growth inhibition curves between a mutant of Escherichia coli that could not synthesize glutathione and its parent strain indicate the relevance of conjugation with glutathione as a defense mechanism, which is an indirect indicator of protein damage. DNA damage was assessed by comparing the growth inhibition in a strain that lacks various DNA repair systems with that in its competent parent strain. Most compounds acted merely as baseline toxicants in all test systems. As expected, ethinylestradiol was the only compound showing estrogenic activity. Propranolol was baseline-toxic in all test systems except for the photosynthesis inhibition assay, where it surprisingly showed a 100-fold excess toxicity over the predicted baseline effect. The exact mode of toxic action could not be confirmed, but additional chlorophyll fluorescence induction experiments excluded the possibility of direct interference with photosynthesis through photosystem II inhibition. Mixture experiments were performed as a diagnostic tool to analyze the mode of toxic action. Compounds with the same mode of toxic action showed the expected concentration addition. In the photosynthesis inhibition assay, agreement between experimental results and prediction was best for two-stage predictions considering the assigned modes of action. In a two-stage prediction, concentration addition was used as a model to predict the mixture effect of the baseline toxicants followed by their independent action as a single component combined with the specifically acting compound propranolol and the reference compound diuron. A comparison with acute toxicity data for algae, daphnia, and fish showed generally good agreement for the nonspecifically acting compounds but also that the proposed test battery offered better diagnostic value in the case of the specifically acting compounds