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This study aimed to evaluate whether there is a causal relationship between autoimmune thyroid disorders (AITDs) and telomere length (TL) in the European population and whether there is reverse causality. In this study, Mendelian randomization (MR) and colocalization analysis were conducted to assess the potential causal relationship between AITDs and TL using summary statistics from large‐scale genome‐wide association studies, followed by analysis of the relationship between TL and thyroid stimulating hormone and free thyroxine (FT4) to help interpret the findings. The inverse variance weighted (IVW) method was used to estimate the causal estimates. The weighted median, MR‒Egger and leave‐one‐out methods were used as sensitivity analyses. The IVW method results showed a significant causal relationship between autoimmune hyperthyroidism and TL (β = −1.93 × 10−2; p = 4.54 × 10−5). There was no causal relationship between autoimmune hypothyroidism and TL (β = −3.99 × 10−3; p = 0.324). The results of the reverse MR analysis showed that genetically TL had a significant causal relationship on autoimmune hyperthyroidism (IVW: odds ratio (OR) = 0.49; p = 2.83 × 10−4) and autoimmune hypothyroidism (IVW: OR = 0.86; p = 7.46 × 10−3). Both horizontal pleiotropy and heterogeneity tests indicated the validity of our bidirectional MR study. Finally, colocalization analysis suggested that there were shared causal variants between autoimmune hyperthyroidism and TL, further highlighting the robustness of the results. In conclusion, autoimmune hyperthyroidism may accelerate telomere attrition, and telomere attrition is a causal factor for AITDs. [ABSTRACT FROM AUTHOR]

Benchmarking of evaluated neutron nuclear data libraries was performed for ∼14.8 MeV neutrons on the several targets, such as gallium, graphite, silicon carbide, uranium and tungsten samples. The experiments were performed at China Institute of Atomic Energy (CIAE). The neutron leakage spectra from the samples were measured at 60◦ and 120◦ by a TOF technique with a BC501A scintillation detector. The measured spectra are rather well reproduced by MCNP-4C simulations with the CENDL3.1, JENDL-4.0 and the new release ENDF/B-VIII.0, JEFF-3.3 evaluated nuclear data libraries and so on. There have some difference between experiments and simulations for the elastic and inelastic contributions in the partial energy range. And the discrepancies of the neutron leakage spectra in the MCNP simulations originate simply from the differences in the spectra distributions of the neutron reaction channels in the evaluated nuclear data libraries.

Introduction: Systemic lupus erythematosus (SLE) and hypothyroidism often coexist in observational studies; however, the causal relationship between them remains controversial., Methods: Complementary genetic approaches, including genetic correlation, Mendelian randomization (MR), and colocalization analysis, were conducted to assess the potential causal association between SLE and primary hypothyroidism using summary statistics from large-scale genome-wide association studies. The association between SLE and thyroid-stimulating hormone (TSH) was further analyzed to help interpret the findings. In addition, findings were verified using a validation data set, as well as through different MR methods with different model assumptions., Results: The linkage disequilibrium score regression revealed a shared genetic structure between SLE and primary hypothyroidism, with the significant genetic correlation estimated to be 0.2488 (P = 6.00 × 10-4). MR analysis with the inverse variance weighted method demonstrated a bidirectional causal relationship between SLE and primary hypothyroidism. The odds ratio (OR) of SLE on primary hypothyroidism was 1.037 (95% CI, 1.013-1.061; P = 2.00 × 10-3) and that of primary hypothyroidism on SLE was 1.359 (95% CI, 1.217-1.520; P < 0.001). The OR of SLE on TSH was 1.007 (95% CI, 1.001-1.013; P = 0.032). However, TSH was not causally associated with SLE (P = 0.152). Similar results were found using different MR methods. In addition, colocalization analysis suggested that shared causal variants existed between SLE and primary hypothyroidism. The results of the validation analysis indicated a bidirectional causal relationship between SLE and primary hypothyroidism, as well as shared loci., Conclusion: In summary, a bidirectional causal relationship between SLE and primary hypothyroidism was observed with complementary genetic approaches., Competing Interests: Conflict of Interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© The Author(s) 2022. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)