ObjectiveTo determine whether a change in editorial policy, including the implementation of a checklist, has been associated with improved reporting of measures which might reduce the risk of bias.MethodsThe study protocol has been published at doi: 10.1007/s11192-016-1964-8.DesignObservational cohort study.PopulationArticles describing research in the life sciences published in Nature journals, submitted after 1 May 2013.InterventionMandatory completion of a checklist during manuscript revision.Comparators(1) Articles describing research in the life sciences published in Nature journals, submitted before May 2013; and (2) similar articles in other journals matched for date and topic.Primary outcomeThe primary outcome is change in the proportion of Nature articles describing in vivo research published before and after May 2013 reporting the ‘Landis 4’ items (randomisation, blinding, sample size calculation and exclusions). We included 448 Nature Publishing Group (NPG) articles (223 published before May 2013, and 225 after) identified by an individual hired by NPG for this specific task, working to a standard procedure; and an independent investigator used PubMed ‘Related Citations’ to identify 448 non-NPG articles with a similar topic and date of publication from other journals; and then redacted all articles for time-sensitive information and journal name. Redacted articles were assessed by two trained reviewers against a 74-item checklist, with discrepancies resolved by a third.Results394 NPG and 353 matching non-NPG articles described in vivo research. The number of NPG articles meeting all relevant Landis 4 criteria increased from 0/203 prior to May 2013 to 31/181 (16.4%) after (two-sample test for equality of proportions without continuity correction, Χ²=36.2, df=1, p=1.8×10−9). There was no change in the proportion of non-NPG articles meeting all relevant Landis 4 criteria (1/164 before, 1/189 after). There were more substantial improvements in the individual prevalences of reporting of randomisation, blinding, exclusions and sample size calculations for in vivo experiments, and less substantial improvements for in vitro experiments.ConclusionThere was an improvement in the reporting of risks of bias in in vivo research in NPG journals following a change in editorial policy, to a level that to our knowledge has not been previously observed. However, there remain opportunities for further improvement.
Chronic kidney disease (CKD) is a major public health problem worldwide and is associated with spatial learning deficits. The aim of the present study was to evaluate the protective effects of hydrogen sulfide (H2S) on CKD-mediated behavioral deficits with emphasis to the role of nitric oxide (NO) in these effects. Fifty rats were randomly allocated to five experimental groups including: sham, Five-sixth (5/6) nephrectomy (Nx), 5/6Nx + NaHS, 5/6Nx + NaHS+L-nitroarginine methyl ester (L-NAME), and 5/6Nx + NaHS+aminoguanidine (AMG). Twelve weeks after 5/6Nx, we evaluated proteinuria, creatinine clearance (CrCl), oxidative/antioxidant status, and hippocampus neuro-inflammation and NO synthase genes in all groups. Furthermore, training trials of all animals were conducted in the Morris water maze (MWM) task one day before animal euthanizing. As predicted, 5/6Nx induced several injuries, including enhancement of proteinuria and reduction of CCr, oxidant/antioxidant imbalance and up-regulation of TNF-α and IL-1β gene expressions in the hippocampus tissues. As predicted, 5/6Nx resulted in learning and memory impairments, and increased escape latency during acquisition trials in the MWM task. Interestingly, NaHS (H2S donor) improved behavioral deficits, renal dysfunction, accelerated anti-oxidant/anti-inflammatory responses and increased eNOS and decreased iNOS. Moreover, these effects of NaHS were prevented by L-NAME but not AMG co-administration. In conclusion, H2S ameliorates CKD-mediated brain dysfunctions, through interaction with NO signaling in the hippocampus.
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