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The colon is the largest compartment of the immune system, with innate immune cells exposed to antigens in the environment. However, the mechanisms by which the innate immune system is instigated are poorly defined in colorectal cancer (CRC). Here, a population of CD16+ neutrophils that specifically accumulate in CRC tumor tissues by imaging mass cytometry (IMC), immune fluorescence, and flow cytometry, which demonstrated pro‐tumor activity by disturbing natural killer (NK) cells are identified. It is found that these CD16+ neutrophils possess abnormal cholesterol accumulation due to activation of the CD16/TAK1/NF‐κB axis, which upregulates scavenger receptors for cholesterol intake including CD36 and LRP1. Consequently, these region‐specific CD16+ neutrophils not only competitively inhibit cholesterol intake of NK cells, which interrupts NK lipid raft formation and blocks their antitumor signaling but also release neutrophil extracellular traps (NETs) to induce the death of NK cells. Furthermore, CD16‐knockout reverses the pro‐tumor activity of neutrophils and restored NK cell cytotoxicity. Collectively, the findings suggest that CRC region‐specific CD16+ neutrophils can be a diagnostic marker and potential therapeutic target for CRC. [ABSTRACT FROM AUTHOR]

Throughout the evolution of fish nutrition science, the importance of dietary arachidonic acid (ARA, 20:4n‐6) has been somewhat overlooked, likely due to the polarizing research focus on docosahexaenoic (DHA, 22:6n‐3) and eicosapentaenoic (EPA, 20:5n‐3) acids. Nevertheless, especially during the past two decades, increasing attention has been paid to the requirements and functions of ARA in fish nutrition, and a number of relevant studies have now been conducted on a series of fish species, including both marine and freshwater species. Those studies revealed important and diverse functions of ARA in various physiological processes, such as growth, reproduction, stress resistance, pigmentation, immunity, lipid deposition and bone development. The results of the present review, in addition to providing a state‐of‐the‐art summary of current knowledge, also revealed the complexity of ARA functions in terms of dosages, species, development stage, sex and feeding period, as well as in terms of interaction between ARA and other nutritional or non‐nutritional factors. [ABSTRACT FROM AUTHOR]

Pleckstrin homology‐like domain family A, member 3 (PHLDA3) has a particularly critical role in regulating cell survival under stress conditions. However, whether PHLDA3 plays a role in myocardial ischemia/reperfusion injury has not been studied. We aimed to assess the possible role of PHLDA3 in myocardial ischemia/reperfusion (I/R) injury. PHLDA3 expression was increased in myocardial tissue from rats with myocardial I/R injury and rat cardiomyocytes with hypoxia/reoxygenation (H/R) injury. PHLDA3 knockdown protected against myocardial I/R injury in vivo and H/R injury in vitro. Inhibition of PHLDA3 increased the activation of nuclear factor erythroid‐derived 2‐related factor 2 (Nrf2) associated with regulation of the Akt/glycogen synthase kinase‐3β (GSK‐3β) axis. Repression of Nrf2 reversed PHLDA3‐inhibition‐mediated cardioprotective effects. Taken together, our work demonstrates that PHLDA3 inhibition exerts a protective role in myocardial I/R injury via regulation of the Akt/GSK‐3β/Nrf2 axis. We suggest PHLDA3 as an attractive target for developing treatments against myocardial I/R injury. [ABSTRACT FROM AUTHOR]