2,829 research outputs found
Interchange reconnection associated with a confined filament eruption: Implications for the source of transient cold-dense plasma in solar winds
The cold-dense plasma is occasionally detected in the solar wind with in situ
data, but the source of the cold-dense plasma remains illusive. Interchange
reconnections (IRs) between closed fields and nearby open fields are well known
to contribute to the formation of solar winds. We present a confined filament
eruption associated with a puff-like coronal mass ejection (CME) on 2014
December 24. The filament underwent successive activations and finally erupted,
due to continuous magnetic flux cancellations and emergences. The confined
erupting filament showed a clear untwist motion, and most of the filament
material fell back. During the eruption, some tiny blobs escaped from the
confined filament body, along newly-formed open field lines rooted around the
south end of the filament, and some bright plasma flowed from the north end of
the filament to remote sites at nearby open fields. The newly-formed open field
lines shifted southward with multiple branches. The puff-like CME also showed
multiple bright fronts and a clear southward shift. All the results indicate an
intermittent IR existed between closed fields of the confined erupting filament
and nearby open fields, which released a portion of filament material (blobs)
to form the puff-like CME. We suggest that the IR provides a possible source of
cold-dense plasma in the solar wind
Genetic liability between COVID-19 and heart failure: Evidence from a bidirectional mendelian randomization study
Background: Previous studies have observed inconsistent associations between coronavirus disease 2019 (COVID-19) and heart failure (HF), but these studies were prone to bias based on reverse causality and residual confounding factors. We aimed to investigate genetic liability between COVID-19 and heart failure using a bidirectional Mendelian randomization study. Methods: The causal relationship between COVID-19 (including COVID-19, hospitalized COVID-19 compared with the general population, and severe COVID-19) and HF are determined by using a bidirectional Mendelian randomization analysis. We drew on summary statistics from the largest HF genome-wide association study (GWAS) meta-analysis on individuals of European ancestry, which included 47,309 HF patients and 930,014 controls. The inverse variance weighted (IVW), an adaption of the Egger regression (MR-Egger), the weighted median, and weighted model were conducted for the Mendelian randomization analysis to estimate a causal effect. To confirm the stability, we performed a “leave-one-out” approach for the sensitivity analysis. Results: Genetically predicted severe COVID-19 was not significantly associated with the risk of HF [odds ratio (OR), 1.003; 95% confidence interval (CI), 0.969–1.037; p = 0.867]. The IVW demonstrated that there was no association between genetically hospitalized COVID-19 infection and HF risk [OR, 1.009; 95% CI, 0.939–1.085; p = 0.797]. There was no evidence to support the association between genetically determined COVID-19 and the risk of HF [OR, 1.066; 95% CI, 0.955–1.190; p = 0.253]. In addition, genetically predicted HF was also not causally associated with COVID-19 [OR, 1.162; 95% CI, 0.824–1.639; p = 0.393]. MR-Egger analysis indicated no evidence of directional pleiotropy. Conclusion: The current bidirectional Mendelian randomization analysis overcomes the limitations of observational studies. Our findings indicated that there is no causal association between COVID-19 and HF
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