Background Antenatal depression can have harmful consequences for the mother and fetus. Exercise may be a useful intervention to prevent and treat antenatal depression.Objectives This systematic review aims to establish whether there is sufficient evidence to conclude that exercise is an effective intervention for preventing and treating antenatal depression.Search strategy Searches using electronic databases from MEDLINE, Cochrane Library, CINAHL, EMBASE, AMED and PsycINFO were performed.Selection criteria Randomised controlled trials (RCT) that compared any type of exercise intervention with any comparator in pregnant women were eligible for inclusion.Data collection and analysis Meta-analysis was performed calculating standardised mean differences (SMD).Main results Six trials (seven comparisons) were eligible for inclusion. Meta-analysis showed a significant reduction in depression scores (SMD À0.46, 95% CI À0.87 to À0.05, P = 0.03, I 2 = 68%) for exercise interventions relative to comparator groups.The test for subgroup differences in women who were non-depressed (one trial) (SMD À0.74, 95%CI À1.22 to À0.27, P = 0.002) and depressed (five trials) (SMD À0.41, 95% CI À0.88 to 0.07, P = 0.09) at baseline was not significant (P = 0.32). The test for subgroup differences between aerobic (one trial) and non-aerobic exercise (five trials) was also nonsignificant (P = 0.32).Authors' conclusions We found some evidence that exercise may be effective in treating depression during pregnancy but this conclusion is based on a small number of low-moderate quality trials with significant heterogeneity and wide confidence intervals.
Diatoms are one of the most successful phytoplankton groups in our oceans, being responsible for over 20% of the Earth’s photosynthetic productivity. Their chimeric genomes have genes derived from red algae, green algae, bacteria and heterotrophs, resulting in multiple isoenzymes targeted to different cellular compartments with the potential for differential regulation under nutrient limitation. The resulting interactions between metabolic pathways are not yet fully understood.We previously showed how acclimation to Cu limitation enhanced susceptibility to overreduction of the photosynthetic electron transport chain and its reorganization to favor photoprotection over light-harvesting in the oceanic diatom Thalassiosira oceanica (Hippmann et al., 2017). In order to understand the overall metabolic changes that help alleviate the stress of Cu limitation, we generated comprehensive proteomic datasets from the diatom Thalassiosira oceanica grown under Cu-limiting and -replete conditions. The datasets were used to identify differentially expressed proteins involved in carbon, nitrogen and oxidative stress-related metabolic pathways and to predict the proteins cellular location.Metabolic pathway analysis showed integrated responses to Cu limitation in diatoms. The up-regulation of ferredoxin (Fdx) was correlated with up-regulation of plastidial Fdx-dependent isoenzymes involved in nitrogen assimilation as well as enzymes involved in glutathione synthesis thus integrating nitrogen uptake and metabolism with photosynthesis and oxidative stress resistance. The differential regulation of glycolytic isoenzymes located in the chloroplast and mitochondria enables them to channel both excess electrons and/or ATP between these compartments. Additional evidence for chloroplast-mitochondrial cross-talk is shown by up-regulation of chloroplast and mitochondrial proteins involved in the proposed malate shunt.One sentence summaryDiatoms adapt to Cu limitation by regulating their large repertoire of isoenzymes to channel electrons away from the chloroplast, enhance nitrogen uptake, and integrate the oxidative stress response. 123
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.