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The inverse temperature layer (ITL) beneath water‐atmosphere interface within which temperature increases with depth has been observed from measurement of water temperature profile at an inland lake. Strong solar radiation combined with moderate wind‐driven near‐surface turbulence leads to the formation of a pronounced diurnal cycle of the ITL predicted by a physical heat transfer model. The ITL only forms during daytime when solar radiation intensity exceeds a threshold while consistently occurs during nighttime. The largest depth of the ITL is comparable to the e‐fold penetration depth of solar radiation during daytime and at least one order of magnitude deeper during nighttime. The dynamics of the ITL depth variation simulated by a physical model forced by observed water surface solar radiation and temperature is confirmed by the observed water temperature profile in the lake. Plain Language Summary: An idealized one‐dimensional heat transfer equation reveals the physical mechanisms of water temperature increasing with depth beneath the water‐atmosphere interface known as inverse temperature layer (ITL). Solar radiation is the dominant forcing of water temperature profile while wind‐driven turbulent mixing is a critical process determining whether the ITL forms. The limited depth of the ITL poses a constraint on the rate of heat transfer from the water body into the atmosphere. The dynamics of the ITL plays an important role in the water and energy cycle of large water bodies such as lakes and oceans. Key Points: The formation of inverse temperature layer (ITL) is driven by strong solar radiation and moderate wind‐driven turbulenceThe ITL depth has pronounced diurnal cycle shallower during daytime than during nighttimeA physical model using observed solar radiation and water surface temperature captures the ITL dynamics [ABSTRACT FROM AUTHOR]

The prevalence of colorectal cancer (CRC) continues to increase. Treatment of CRC remains a significant clinical challenge, and effective therapies for advanced CRC are desperately needed. Increasing attention and ongoing research efforts have focused on krill oil that may provide health benefits to the human body. Here we report that krill oil exerts in vitro anticancer activity through a direct inhibition on proliferation, colony formation, migration, and invasion of mouse colon cancer cells. Krill oil inhibited the proliferation and colony formation of CT‐26 colon cancer cells by causing G0/G1 cell cycle arrest and apoptosis. Cell cycle arrest was attributable to reduction of cyclin D1 levels in krill oil‐treated cells. Further studies revealed that krill oil induced mitochondrial‐dependent apoptosis of CT‐26 cells, including loss of mitochondrial membrane potential, increased cytosolic calcium levels, activation of caspase‐3, and downregulation of anti‐apoptotic proteins MCL‐1 and BCL‐XL. Krill oil suppressed migration of CT‐26 cells by disrupting the microfilaments and microtubules. Extracellular signal‐regulated protein kinase (ERK) plays crucial roles in regulating proliferation and migration of cancer cells. We found that krill oil attenuated the activation of ERK signaling pathway to exert the effects on cell cycle, apoptosis, and migration of colon cancer cells. We speculate that polyunsaturated fatty acids of krill oil may dampen ERK activation by decreasing the phospholipid saturation of cell membrane. Although findings from in vitro studies may not necessarily translate in vivo, our study provides insights into the possibility that krill oil or its components could have therapeutic potential in colon cancer. [ABSTRACT FROM AUTHOR]

The immune landscape of bladder cancer progression is not fully understood, and effective therapies are lacking in advanced bladder cancer. Here, we visualized that bladder cancer cells recruited neutrophils by secreting interleukin-8 (IL-8); in turn, neutrophils played dual functions in bladder cancer, including hepatocyte growth factor (HGF) release and CCL3 high PD-L1 high super-immunosuppressive subset formation. Mechanistically, c-Fos was identified as the mediator of HGF up-regulating IL-8 transcription in bladder cancer cells, which was central to the positive feedback of neutrophil recruitment. Clinically, compared with serum IL-8, urine IL-8 was a better biomarker for bladder cancer prognosis and clinical benefit of immune checkpoint blockade (ICB). Additionally, targeting neutrophils or hepatocyte growth factor receptor (MET) signaling combined with ICB inhibited bladder cancer progression and boosted the antitumor effect of CD8 + T cells in mice. These findings reveal the mechanism by which tumor-neutrophil cross talk orchestrates the bladder cancer microenvironment and provide combination strategies, which may have broad impacts on patients suffering from malignancies enriched with neutrophils., Competing Interests: Competing interests statement:The authors declare no competing interest.