Correlations between East Asian monsoon indices and temperature/precipitation during the observed period.

<p>(a) winter monsoon index and winter temperature and (b) summer monsoon index and June–July precipitation. The shaded areas from red to yellow passed negative correlation at 99%, 95%, 90% confidence levels, and green color indicates positive correlated regions.</p

Variations of EAWM and EASM over the interdecadal–centennial scale: (a) EAWM and (b) EASM.

<p>Variations of EAWM and EASM over the interdecadal–centennial scale: (a) EAWM and (b) EASM.</p

East Asian Monsoon Signals Reflected in Temperature and Precipitation Changes over the Past 300 Years in the Middle and Lower Reaches of the Yangtze River

<div><p>Based on observational data and Asian monsoon intensity datasets from China, the relationships between the East Asian winter monsoon index and winter temperature, the East Asian summer monsoon index and Meiyu precipitation over the middle and lower reaches of the Yangtze River, were analyzed. We found that the monsoon signals were reflected in the temperature and Meiyu precipitation variations. Thus, we used the reconstructed Meiyu precipitation and winter temperature series for the past 300 years and detected the summer/winter monsoon intensity signals using multi-taper spectral estimation method and wavelet analysis. The main periodicities of Meiyu precipitation and winter temperature, such as interannual cycle with 2–7-year, interdecadal-centennial cycles with 30–40-year and 50–100-year, were found. The good relationships between the East Asian summer and winter monsoons suggested that they were in phase at 31-year cycle, while out of phase at 100-year cycle, but with 20-year phase difference. In addition, the winter monsoon intensity may be regulated by the North Atlantic Oscillation, the Arctic Oscillation and the Atlantic Multidecadal Oscillation, and the summer monsoon is closely related to the signal intensities of the Pacific Decadal Oscillation.</p></div

Standardized climate reconstructions and spectra analysis.

<p>(a) winter temperature and (b) Meiyu precipitation over the MLRYR. (1) Standardized climate reconstructions; (2) wavelet spectra analysis; region circled by black contours passing the 90% confidence level; cross-hatched areas represent the cone of influence calculated by the standard program from <a href="http://ion.researchsystems.com/" target="_blank">http://ion.researchsystems.com/</a> [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0131159#pone.0131159.ref041" target="_blank">41</a>]; (3) multi-taper method analysis with 90% and 95% confidence levels [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0131159#pone.0131159.ref042" target="_blank">42</a>].</p

Relationship between EAWM, NAO, AO and AMO at 50–100-year cycles, AO and AMO use the green and red color axes (a), and EASM and PDO at 30–40-year cycles (b).

<p>Relationship between EAWM, NAO, AO and AMO at 50–100-year cycles, AO and AMO use the green and red color axes (a), and EASM and PDO at 30–40-year cycles (b).</p

Image_4_The causal relationship between sarcoidosis and autoimmune diseases: a bidirectional Mendelian randomization study in FinnGen.tif

BackgroundSarcoidosis has been considered to be associated with many autoimmune diseases (ADs), but the cause-and-effect relationship between these two diseases has not been fully explored. Therefore, the objective of this study is to explore the possible genetic association between sarcoidosis and ADs.MethodsWe conducted a bidirectional Mendelian randomization (MR) study using genetic variants associated with ADs and sarcoidosis (4,041 cases and 371,255 controls) from the FinnGen study. The ADs dataset comprised 96,150 cases and 281,127 controls, encompassing 44 distinct types of autoimmune-related diseases. Subsequently, we identified seven diseases within the ADs dataset with a case size exceeding 3,500 and performed subgroup analyses on these specific diseases.ResultsThe MR evidence supported the causal association of genetic predictors of ADs with an increased risk of sarcoidosis (OR = 1.79, 95% CI = 1.59 to 2.02, P IVW-FE = 1.01 × 10-21), and no reverse causation (OR = 1.05, 95% CI 0.99 to 1.12, PIVW-MRE = 9.88 × 10-2). Furthermore, subgroup analyses indicated that genetic predictors of type 1 diabetes mellitus (T1DM), celiac disease, and inflammatory bowel disease (IBD) were causally linked to an elevated risk of sarcoidosis (All P -3). Conversely, genetic predictors of sarcoidosis showed causal associations with a higher risk of type 1 diabetes mellitus (P -3).ConclusionThe present study established a positive causal relationship between genetic predictors of ADs (e.g. T1DM, celiac disease, and IBD) and the risk of sarcoidosis, with no evidence of reverse causation.</p

Table_1_The causal relationship between sarcoidosis and autoimmune diseases: a bidirectional Mendelian randomization study in FinnGen.docx

BackgroundSarcoidosis has been considered to be associated with many autoimmune diseases (ADs), but the cause-and-effect relationship between these two diseases has not been fully explored. Therefore, the objective of this study is to explore the possible genetic association between sarcoidosis and ADs.MethodsWe conducted a bidirectional Mendelian randomization (MR) study using genetic variants associated with ADs and sarcoidosis (4,041 cases and 371,255 controls) from the FinnGen study. The ADs dataset comprised 96,150 cases and 281,127 controls, encompassing 44 distinct types of autoimmune-related diseases. Subsequently, we identified seven diseases within the ADs dataset with a case size exceeding 3,500 and performed subgroup analyses on these specific diseases.ResultsThe MR evidence supported the causal association of genetic predictors of ADs with an increased risk of sarcoidosis (OR = 1.79, 95% CI = 1.59 to 2.02, P IVW-FE = 1.01 × 10-21), and no reverse causation (OR = 1.05, 95% CI 0.99 to 1.12, PIVW-MRE = 9.88 × 10-2). Furthermore, subgroup analyses indicated that genetic predictors of type 1 diabetes mellitus (T1DM), celiac disease, and inflammatory bowel disease (IBD) were causally linked to an elevated risk of sarcoidosis (All P -3). Conversely, genetic predictors of sarcoidosis showed causal associations with a higher risk of type 1 diabetes mellitus (P -3).ConclusionThe present study established a positive causal relationship between genetic predictors of ADs (e.g. T1DM, celiac disease, and IBD) and the risk of sarcoidosis, with no evidence of reverse causation.</p

Image_6_The causal relationship between sarcoidosis and autoimmune diseases: a bidirectional Mendelian randomization study in FinnGen.tif

BackgroundSarcoidosis has been considered to be associated with many autoimmune diseases (ADs), but the cause-and-effect relationship between these two diseases has not been fully explored. Therefore, the objective of this study is to explore the possible genetic association between sarcoidosis and ADs.MethodsWe conducted a bidirectional Mendelian randomization (MR) study using genetic variants associated with ADs and sarcoidosis (4,041 cases and 371,255 controls) from the FinnGen study. The ADs dataset comprised 96,150 cases and 281,127 controls, encompassing 44 distinct types of autoimmune-related diseases. Subsequently, we identified seven diseases within the ADs dataset with a case size exceeding 3,500 and performed subgroup analyses on these specific diseases.ResultsThe MR evidence supported the causal association of genetic predictors of ADs with an increased risk of sarcoidosis (OR = 1.79, 95% CI = 1.59 to 2.02, P IVW-FE = 1.01 × 10-21), and no reverse causation (OR = 1.05, 95% CI 0.99 to 1.12, PIVW-MRE = 9.88 × 10-2). Furthermore, subgroup analyses indicated that genetic predictors of type 1 diabetes mellitus (T1DM), celiac disease, and inflammatory bowel disease (IBD) were causally linked to an elevated risk of sarcoidosis (All P -3). Conversely, genetic predictors of sarcoidosis showed causal associations with a higher risk of type 1 diabetes mellitus (P -3).ConclusionThe present study established a positive causal relationship between genetic predictors of ADs (e.g. T1DM, celiac disease, and IBD) and the risk of sarcoidosis, with no evidence of reverse causation.</p

Table_1_Radioiodine adjuvant therapy in differentiated thyroid cancer: An update and reconsideration.docx

Radioiodine (131I) therapy (RAI) has been utilized for treating differentiated thyroid cancer (DTC) for decades, and its uses can be characterized as remnant ablation, adjuvant therapy (RAT) or treatment for known diseases. Compared with the definite 131I treatment targets for remnant ablation and known disease, 131I adjuvant therapy (RAT) aims to reduce the risk of recurrence by destroying potential subclinical disease. Since it is merely given as a risk with no imaging confirmation of persistence/recurrence/metastases, the evidence is uncertain. With limited knowledge and substance, the indication for RAT remains poorly defined for everyday clinical practice, and the benefits of RAT remain controversial. This ambiguity results in a puzzle for clinicians seeking clarity on whether patients should receive RAT, and whether patients are at risk of recurrence/death from undertreatment or adverse events from overtreatment. Herein, we clarified the RAT indications in terms of clinicopathological features, postoperative disease status and response to therapy evaluation, and retrospectively examined the clinical outcomes of RAT as reported in current studies and guidelines. Furthermore, given the evolution of nuclear medicine imaging techniques, it can be expected that the future of RAT may be advanced by nuclear medicine theranostics (i.e., 131I whole-body scan, PET/CT) by accurately revealing the biological behaviors, as well as the underlying molecular background.</p

Image_2_The causal relationship between sarcoidosis and autoimmune diseases: a bidirectional Mendelian randomization study in FinnGen.tif

BackgroundSarcoidosis has been considered to be associated with many autoimmune diseases (ADs), but the cause-and-effect relationship between these two diseases has not been fully explored. Therefore, the objective of this study is to explore the possible genetic association between sarcoidosis and ADs.MethodsWe conducted a bidirectional Mendelian randomization (MR) study using genetic variants associated with ADs and sarcoidosis (4,041 cases and 371,255 controls) from the FinnGen study. The ADs dataset comprised 96,150 cases and 281,127 controls, encompassing 44 distinct types of autoimmune-related diseases. Subsequently, we identified seven diseases within the ADs dataset with a case size exceeding 3,500 and performed subgroup analyses on these specific diseases.ResultsThe MR evidence supported the causal association of genetic predictors of ADs with an increased risk of sarcoidosis (OR = 1.79, 95% CI = 1.59 to 2.02, P IVW-FE = 1.01 × 10-21), and no reverse causation (OR = 1.05, 95% CI 0.99 to 1.12, PIVW-MRE = 9.88 × 10-2). Furthermore, subgroup analyses indicated that genetic predictors of type 1 diabetes mellitus (T1DM), celiac disease, and inflammatory bowel disease (IBD) were causally linked to an elevated risk of sarcoidosis (All P -3). Conversely, genetic predictors of sarcoidosis showed causal associations with a higher risk of type 1 diabetes mellitus (P -3).ConclusionThe present study established a positive causal relationship between genetic predictors of ADs (e.g. T1DM, celiac disease, and IBD) and the risk of sarcoidosis, with no evidence of reverse causation.</p