There is increasing awareness that the value of peer-reviewed scientific literature is not consistent, resulting in a growing desire to improve the practice and reporting of studies. This is especially important in the field of ecotoxicology, where regulatory decisions can be partly based on data from the peer-reviewed literature, with wide-reaching implications for environmental protection. Our objective is to improve the reporting of ecotoxicology studies so that they can be appropriately utilized in a fair and transparent fashion, based on their reliability and relevance. We propose a series of nine reporting requirements, followed by a set of recommendations for adoption by the ecotoxicology community. These reporting requirements will provide clarity on the the test chemical, experimental design and conditions, chemical identification, test organisms, exposure confirmation, measurable endpoints, how data are presented, data availability and statistical analysis. Providing these specific details will allow for a fuller assessment of the reliability and relevance of the studies, including limitations. Recommendations for the implementation of these reporting requirements are provided herein for practitioners, journals, reviewers, regulators, stakeholders, funders, and professional societies. If applied, our recommendations will improve the quality of ecotoxicology studies and their value to environmental protection.

Background Fatigue is one of the most debilitating side effects of cancer therapy. Identifying biomarkers early during cancer therapy may help us understand the biologic underpinnings of the persistence of fatigue following therapy. Objective We aimed to identify early biomarkers of fatigue by examining correlations of levels of cytokines during external beam radiation therapy (EBRT) with persistence of fatigue one year following treatment completion in men with non-metastatic prostate cancer (NM-PC). Methods A sample of 34 men with NM-PC scheduled to receive EBRT were followed at baseline (T1), midpoint of EBRT (T2), and one year following EBRT (T3). Demographic and clinical data were obtained by chart review. The Functional Assessment of Cancer Therapy-Fatigue (FACT-F) was administered to measure fatigue levels. Plasma cytokine levels were determined at T1 and T2 using the Bio-Rad Bio-Plex Cytokine Assay Kits. Results Significant correlations were observed between levels of IL-3, IL-8, IL-9, IL-10, IL-16, IP10, IFNα2, IFNγ, and SDF1α at T2 with worsening of fatigue from T1 to T3. Conclusions Immunological changes prior to chronic fatigue development may reflect the long term response to radiation therapy-induced damage. Implications for Practice Early biomarkers for chronic fatigue related to cancer therapy will help advance our understanding of the etiology of this distressing symptom and will help nurses identify patients at risk for developing chronic fatigue after cancer treatment. This information will also aide in patient education, as well as symptom management.

Site-directed mutagenesis has been performed in the human transforming growth factor alpha gene. When tyrosine 38 is mutated into phenylalanine or tryptophane, biological activity is retained. In contrast, other alterations between cysteine 34 and cysteine 43 and disruption of disulfide bonds 8 to 21 and 34 to 43 resulted in loss of activities. The presence of an aromatic side chain at position 38 of transforming growth factor alpha seems to be essential for its activity.

Cancer-related fatigue (CRF) is a common burden in cancer patients and little is known about its underlying mechanism. The primary aim of this study was to identify gene signatures predictive of post-radiotherapy fatigue in prostate cancer patients. We employed Fisher Linear Discriminant Analysis (LDA) to identify predictive genes using whole genome microarray data from 36 men with prostate cancer. Ingenuity Pathway Analysis was used to determine functional networks of the predictive genes. Functional validation was performed using a T lymphocyte cell line, Jurkat E6.1. Cells were pretreated with metabotropic glutamate receptor 5 (mGluR5) agonist (DHPG), antagonist (MPEP), or control (PBS) for 20 min before irradiation at 8 Gy in a Mark-1 γ-irradiator. NF-κB activation was assessed using a NF-κB/Jurkat/GFP Transcriptional Reporter Cell Line. LDA achieved 83.3% accuracy in predicting post-radiotherapy fatigue. “Glutamate receptor signaling” was the most significant (p = 0.0002) pathway among the predictive genes. Functional validation using Jurkat cells revealed clustering of mGluR5 receptors as well as increased regulated on activation, normal T cell expressed and secreted (RANTES) production post irradiation in cells pretreated with DHPG, whereas inhibition of mGluR5 activity with MPEP decreased RANTES concentration after irradiation. DHPG pretreatment amplified irradiation-induced NF-κB activation suggesting a role of mGluR5 in modulating T cell activation after irradiation. These results suggest that mGluR5 signaling in T cells may play a key role in the development of chronic inflammation resulting in fatigue and contribute to individual differences in immune responses to radiation. Moreover, modulating mGluR5 provides a novel therapeutic option to treat CRF.

Endangered and endemic June sucker (JS, Chasmistes liorus) have been stocked for many years to prevent extinction in Utah Lake, Utah. When unmarked fish appeared in the lake at higher rates than expected from tag loss, we sought to determine if 87 Sr/ 86 Sr and Sr/Ca (signatures) in otoliths, fin rays, and scales could be used to identify whether stocking had created a naturally reproducing population. Signatures from otoliths and fin rays suggested that approximately 38% (12 of 31) of unmarked JS probably came from the Fisheries Experimental Station (FES) hatchery in Logan, Utah, and a minimum of 13% (four of 31) of unmarked JS had signatures that strongly indicated that they were of wild origin. The remaining JS (15 of 31) could not be assigned to any particular location because of signature overlap. While scales were not useful for determining fish provenance, we found a nearly 1:1 relationship between pelvic fin and otolith 87 Sr/ 86 Sr. Thus, fin sections appear to provide a nonlethal structure for laser ablation microchemical analysis to determine origins of unknown origin JS in the future.Résumé : L'empoissonnement du Chasmistes liorus, un poisson endémique en voie de disparition, se poursuit depuis de nombreuses années afin d'en prévenir la disparition dans le lac Utah (Utah, États-Unis). Quand des poissons non marqués ont commencé à apparaître dans ce lac à des fréquences plus grandes que ce que la perte d'étiquettes permet de prévoir, nous avons tenté de déterminer si les rapports 87 Sr/ 86 Sr et Sr/Ca (signatures) dans les otolites, les rayons de nageoire et les écailles pouvaient être utilisés pour établir si l'empoissonnement avait produit une population issue de la reproduction naturelle. Les signatures d'otolites et de rayons semblent indiquer qu'environ 38 % (12 sur 31) des C. liorus non marqués proviennent probablement de l'écloserie de la Fisheries Experimental Station (FES) à Logan (Utah) et au moins 13 % (quatre sur 31) des C. liorus non marqués ont des signatures indiquant fortement qu'ils seraient issus de la reproduction à l'état sauvage. Les autres C. liorus (15 sur 31) ne peuvent être affectés à un endroit précis en raison de la superposition de signatures. Si les écailles ne se sont pas avérées utiles pour déterminer la provenance des poissons, nous avons noté un rapport avoisinant 1:1 des valeurs de 87 Sr/ 86 Sr des nageoires pelviennes et des otolites. Les sections de nageoire semblent donc constituer une structure se prêtant à l'analyse microchimique non létale par ablation laser pour la détermination des origines de C. liorus d'origine inconnue. [Traduit par la Rédaction]