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Core Ideas Throughfall was statistically different among five measurement locations. Cumulative throughfall of 24 to 36 cm from row exceeded that of 0 to 12 cm and 48 to 60 cm by 46 to 88%. Coefficient of variation of throughfall decreased with rainfall amount and increased with leaf area index and plant height. Understanding throughfall (TF) and its influencing factors at crop row scale is a key step to reveal the mechanisms of soil water recharging, soil erosion, and evaporation of intercepted rainfall. The objective of this study was to determine the amount and the variation of TF in relation to plant canopy and rainfall. In this study, TF was measured by a rectangular plexiglass collector at five measurement locations (MLs) with the distances of the (A) 0 to 12 cm, (B) 12 to 24 cm, (C) 24 to 36 cm, (D) 36 to 48 cm, and (E) 48 to 60 cm from corn (Zea mays L.) row during the period of corn plant height growth (HT) approximately from 50 to 250 cm when the leaf area index (LAI) increases from 0.4 to 4.0 in 2013 and 2014. Throughfall increased with total rainfall amount (RA) but decreased with LAI and HT values. The lowest TF values were recorded at the MLs of 0 to 12 cm and 48 to 60 cm near the corn row, and the highest TF values occurred at the ML of 24 to 36 cm at the center of between row areas. The cumulative TF at the ML of 24 to 36 cm exceeded that at the MLs of 0 to 12 cm and 48 to 60 cm by approximately 88 and 46% in 2013 and 2014, respectively. These results have potential values in irrigation scheduling and agrochemical application in the Corn Belt of Northeast China (CBNC).

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Background The expression of Kelch-like protein 18 (KLHL18) in non-small cell lung cancer (NSCLC) is lower than that in normal lung tissue according to the Gene Expression Profiling Interactive Analysis database. KLHL18 is a BTB domain protein and binds cullin 3 (CUL3). However, whether this complex participates in ubiquitination-mediated protein degradation in NSCLC is unclear. Therefore, we aimed to investigate the role of KLHL18 in human NSCLC cells. Results We found that KLHL18 is downregulated in cancer cells and is associated with poor prognosis. Further, its expression was significantly associated with tumor node metastasis (TNM) stage, lymph node metastasis, and tumor size. In vitro analysis of NSCLC cells showed that overexpressing KLHL18 inhibited cell proliferation, migration, and invasion. We found that the tumor-inhibitory effect of the KLHL18 protein was achieved by promoting the ubiquitination and degradation of phosphatidylinositol 3-kinase (PI3K) p85α and inhibiting the expression of PD-L1 protein, ultimately preventing tumor cell immune escape. Conclusions Our results identified the tumor-suppressive mechanism of KLHL18 and suggested that it is closely related to NSCLC occurrence and development. Further investigation of the underlying mechanism may provide new targets for NSCLC treatment.