Present-day estimations of global nitrogen loss (N-loss) are underestimated. Commonly, N-loss from rivers is thought to be caused by denitrification only in bed-sediments. However, coupled nitrification-denitrification occurring in overlying water with suspended sediments (SPS) where oxic and anoxic/low oxygen zones may coexist is ignored for N-loss in rivers. Here the Yellow and Yangtze Rivers were taken as examples to investigate the effect of SPS, which exists in many rivers of the world, on N loss through coupled nitrification-denitrification with nitrogen stable (N) isotopic tracer simulation experiments and in-situ investigation. The results showed even when SPS was surrounded by oxic waters, there were redox conditions that transitioned from an oxic surface layer to anoxic layer near the particle center, enabling coupled nitrification-denitrification to occur around SPS. The production rate of N from NH-N (R) increased with increasing SPS concentration ([SPS]) as a power function (R=a·[SPS]) for both the SPS-water and bed sediment-SPS-water systems. The power-functional increase of nitrifying and denitrifying bacteria population with [SPS] accounted for the enhanced coupled nitrification-denitrification rate in overlying water. SPS also accelerated denitrification in bed-sediment due to increased NO concentration caused by SPS-mediated nitrification. For these two rivers, 1gL SPS will lead to N-loss enhancement by approximately 25-120%, and the enhancement increased with organic carbon content of SPS. Thus, we conclude that SPS in overlying water is a hot spot for nitrogen loss in river systems and current estimates of in-stream N-loss are underestimated without consideration of SPS; this may partially compensate for the current imbalance of global nitrogen inputs and sinks.

Suspended sediment (SPS) is ubiquitous in rivers, and SPS with different particle sizes and compositions may affect coupled nitrification-denitrification (CND) occurring on SPS significantly. However, there is no related research report. In this work, N isotope tracer technique was adopted to explore the CND in systems containing SPS (8 g L and 1 g L) collected from the Yellow River with various particle sizes, including <2, 2-20, 20-50, 50-100, and 100-200 μm. The results showed that the CND occurred on SPS and the CND rate was negatively related to particle size; both nitrification and denitrification rate constants increased with decreasing SPS particle size. For instance, SPS (8 g L) with a particle size below 2 μm had the highest N emission rate of 1.15 mg-N/(m·d), which was 2.9 times that of 100-200 μm. This is because SPS with a smaller particle size had a larger specific surface area and a higher organic carbon content, which is beneficial for bacteria growth. Both the nitrifying and denitrifying bacteria population were positively correlated with CND rate (p < 0.05). Different from the N production, NO emission rate did not decrease with increasing SPS particle size. For the system containing 8 g L SPS, NO emission rate reached the highest of 1.05 μg-N/(m·d) in the 50-100 μm SPS system, which was 17.5 times that of 100-200 μm. Similar results could be found from the system with 1 g L SPS. This is due to the fact that the oxygen concentration at the SPS-water interface increased with SPS particle size, and the oxygen conditions might be most suitable for the production of NO in the 50-100 μm system. This study suggests that SPS size and composition play an important role in nitrogen cycle of river systems, especially for the production of NO.

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Although observational studies have reported a positive association between obstructive sleep apnea syndrome (OSAS) and breast cancer (BC) risk, causality remains inconclusive. We aim to explore whether OSAS is associated with etiology of BC by conducting a two-sample Mendelian randomization (MR) study in a Chinese population and Asian population from the Breast Cancer Association Consortium (BCAC). We found a detrimental causal effect of OSAS on BC risk in the primary analysis of our samples (IVW OR, 2.47 for BC risk per log-odds increment in OSAS risk, 95% CI = 1.86-3.27; P = 3.6×10-10). This was very similar to results of the direct observational case-control study between OSAS and BC risk (OR = 2.80; 95% CI = 2.24-3.50; P =1.4×10-19). Replication in the Asian population of the BCAC study also supported our results (IVW OR, 1.33 for BC risk per log-odds increment in OSAS risk, 95% CI = 1.13-1.56; P = 0.0006). Sensitivity analyses confirmed the robustness of our findings. We provide novel evidence that genetically determined higher risk of OSAS has a causal effect on higher risk of BC. Further studies focused on the mechanisms of the relationship between OSAS and breast carcinogenesis are needed.