Data from: Shorebirds-driven trophic cascade helps restore coastal wetland multifunctionality

<p>Ecosystem restoration has traditionally focused on re-establishing vegetation and other foundation species at basal trophic levels, with mixed outcomes. Here, we show that threatened shorebirds could be important to restoring coastal wetland multifunctionality. We carried out surveys and manipulative field experiments in a region along the Yellow Sea affected by the invasive cordgrass Spartina alterniflora. We found that planting native plants alone failed to restore wetland multifunctionality in a field restoration experiment. Shorebird exclusion weakened wetland multifunctionality, whereas mimicking higher predation before shorebird population declines by excluding their key prey – crab grazers – enhanced wetland multifunctionality. The mechanism underlying these effects is a simple trophic cascade, whereby shorebirds control crab grazers that otherwise suppress native vegetation recovery and destabilize sediments (via bioturbation). Our findings suggest that harnessing the top-down effects of shorebirds – through habitat conservation, rewilding, or temporary simulation of consumptive or non-consumptive effects – should be explored as a nature-based solution to restoring the multifunctionality of degraded coastal wetlands.  </p><p> </p><p>This ZIP file contains the following datasets and code for the above paper:</p><p>1.  Focal study site_shorebird trends.xlsx This file contains data on shorebird abundance at the focal study site between 1996 and 2021</p><p>2.  Regional crab grazing effects.xlsx This file contains data used in the meta-analysis of studies on the effect of crab grazers on native wetland plants</p><p>3.  Regional predation intensity.xlsx This file contains data on shorebird predation on crabs at five native marsh sites</p><p>4.  Restoration experiment_bird abundance.xlsx This file contains data on bird abundance in three camera traps installed at the restoration site</p><p>5.  Restoration experiment_bird species richness.xlsx This file contains data on bird species richness in three camera traps installed at the restoration site</p><p>6.  Restoration experiment_crab abundance.xlsx This file contains data on crab abundance in different treatments of the restoration experiment</p><p>7. Restoration experiment_ecosystem functions.xlsx This file contains data for the 12 ecosystem functions measured in different treatments of the restoration experiment</p><p>8. Restoration experiment_for meta-regression of bird effect sizes on crab abundance This file contains the calculated effect sizes of birds on crab abundance for meta-regression against bird abundance</p><p>9. Restoration experiment_for regression of ecosystem functions This file contains data for regression of ecosystem functions and multifunctionality against crab abundance and primary production  </p><p>10.  Restoration experiment_plant abundance.xlsx This file contains data on plant abundance in different treatments of the restoration experiment</p><p>11.  Restoration experiment_predation intensity.xlsx This file contains data on shorebird predation on tethered crabs in different treatments of the restoration experiment</p><p>12. Restoration experiment_the rate of plant abundance change.xlsx This file contains data on the rate of plant abundance change in different treatments of the restoration experiment  </p><p>13. Shorebird non-consumptive effects experiment.xlsx This file contains data on crab abundance in different treatments of the shorebird non-consumptive effects simulation experiment</p><p>14. Code_Li_Shorebirds_Ms.R This file contains the R code used for data analysis. </p&gt

Is coral richness related to community resistance to and recovery from disturbance?

More diverse communities are thought to be more stable-the diversity-stability hypothesis-due to increased resistance to and recovery from disturbances. For example, high diversity can make the presence of resilient or fast growing species and key facilitations among species more likely. How natural, geographic biodiversity patterns and changes in biodiversity due to human activities mediate community-level disturbance dynamics is largely unknown, especially in diverse systems. For example, few studies have explored the role of diversity in tropical marine communities, especially at large scales. We tested the diversity-stability hypothesis by asking whether coral richness is related to resistance to and recovery from disturbances including storms, predator outbreaks, and coral bleaching on tropical coral reefs. We synthesized the results of 41 field studies conducted on 82 reefs, documenting changes in coral cover due to disturbance, across a global gradient of coral richness. Our results indicate that coral reefs in more species-rich regions were marginally less resistant to disturbance and did not recover more quickly. Coral community resistance was also highly dependent on pre-disturbance coral cover, probably due in part to the sensitivity of fast-growing and often dominant plating acroporid corals to disturbance. Our results suggest that coral communities in biodiverse regions, such as the western Pacific, may not be more resistant and resilient to natural and anthropogenic disturbances. Further analyses controlling for disturbance intensity and other drivers of coral loss and recovery could improve our understanding of the influence of diversity on community stability in coral reef ecosystems

Adult body mass index and risk of ovarian cancer by subtype: a Mendelian randomization study

Background: Observational studies have reported a positive association between body mass index (BMI) and ovarian cancer risk. However, questions remain as to whether this represents a causal effect, or holds for all histological subtypes. The lack of association observed for serous cancers may, for instance, be due to disease-associated weight loss. Mendelian randomization (MR) uses genetic markers as proxies for risk factors to overcome limitations of observational studies. We used MR to elucidate the relationship between BMI and ovarian cancer, hypothesizing that genetically predicted BMI would be associated with increased risk of non-high grade serous ovarian cancers (non-HGSC) but not HGSC. Methods: We pooled data from 39 studies (14 047 cases, 23 003 controls) in the Ovarian Cancer Association Consortium. We constructed a weighted genetic risk score (GRS, partial F-statistic = 172), summing alleles at 87 single nucleotide polymorphisms previously associated with BMI, weighting by their published strength of association with BMI. Applying two-stage predictor-substitution MR, we used logistic regression to estimate study-specific odds ratios (OR) and 95% confidence intervals (CI) for the association between genetically predicted BMI and risk, and pooled these using random-effects meta-analysis. Results: Higher genetically predicted BMI was associated with increased risk of non-HGSC (pooled OR = 1.29, 95% CI 1.03-1.61 per 5 units BMI) but not HGSC (pooled OR = 1.06, 95% CI 0.88-1.27). Secondary analyses stratified by behaviour/subtype suggested that, consistent with observational data, the association was strongest for low-grade/borderline serous cancers (OR = 1.93, 95% CI 1.33-2.81). Conclusions: Our data suggest that higher BMI increases risk of non-HGSC, but not the more common and aggressive HGSC subtype, confirming the observational evidence

Adult height is associated with increased risk of ovarian cancer: a Mendelian randomisation study

Observational studies suggest greater height is associated with increased ovarian cancer risk, but cannot exclude bias and/or confounding as explanations for this. Mendelian randomisation (MR) can provide evidence which may be less prone to bias.status: publishe

Adult height is associated with increased risk of ovarian cancer: a Mendelian randomisation study.

BACKGROUND: Observational studies suggest greater height is associated with increased ovarian cancer risk, but cannot exclude bias and/or confounding as explanations for this. Mendelian randomisation (MR) can provide evidence which may be less prone to bias. METHODS: We pooled data from 39 Ovarian Cancer Association Consortium studies (16,395 cases; 23,003 controls). We applied two-stage predictor-substitution MR, using a weighted genetic risk score combining 609 single-nucleotide polymorphisms. Study-specific odds ratios (OR) and 95% confidence intervals (CI) for the association between genetically predicted height and risk were pooled using random-effects meta-analysis. RESULTS: Greater genetically predicted height was associated with increased ovarian cancer risk overall (pooled-OR (pOR) = 1.06; 95% CI: 1.01-1.11 per 5 cm increase in height), and separately for invasive (pOR = 1.06; 95% CI: 1.01-1.11) and borderline (pOR = 1.15; 95% CI: 1.02-1.29) tumours. CONCLUSIONS: Women with a genetic propensity to being taller have increased risk of ovarian cancer. This suggests genes influencing height are involved in pathways promoting ovarian carcinogenesis