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There are no obvious advantages in withholding fluid and food after cesarean. Indeed, EOF offers some short-term benefits.

A series of Dy Er-polyoxometalates (POMs) were successfully synthesized and characterized well by various physicochemical analysis. The structurally isolated compounds exhibit three characteristic emissions at 480 nm (blue, F → H transition), 573 nm (yellow, F → H transition), and 663 nm (red, F → H transition) whose luminescent color coordinates appear in the near-white area in the CIE 1931 chromaticity diagram. Time-resolved emission spectroscopy was used in Dy Er-POM to further authenticate energy transfer from the photoexcitation O → M ligand to the metal charge-transfer state of phosphotungstate components to active Dy/Er ions and energy transfer between Dy ion and Er ion via intramolecular energy transitions. The relative emission intensity of ∼32%, ∼53%, and ∼85% for Dy-POM, DyEr-POM, and DyEr-POM respectively, were obtained under 300 min of UV irradiation, which indicates better photostability of DyEr-POM. Furthermore, Dy Er-POM samples can emit macroscopic white light under blue irradiation.

Cell death after spinal cord ischemia/reperfusion (I/R) can occur through necrosis, apoptosis, and autophagy, resulting in changes to the immune environment. However, the molecular mechanism of this immune regulation is not clear. Accumulating evidence indicates that microRNAs (miRs) play a crucial role in the pathogenesis of spinal cord I/R injury. Here, we hypothesized miR‐22‐3p may be involved in spinal cord I/R injury by interacting with interferon regulatory factor (IRF) 5. Rat models of spinal cord I/R injury were established by 12‐min occlusion of the aortic arch followed by 48‐hr reperfusion, with L4‐6 segments of spinal cord tissues collected. MiR‐22‐3p agomir, a lentivirus‐delivered siRNA specific for IRF5, or a lentivirus expressing wild‐type IRF5 was injected intrathecally to rats with I/R injury to evaluate the effects of miR‐22‐3p and IRF5 on hindlimb motor function. Macrophages isolated from rats were treated with miR‐22‐3p mimic or siRNA specific for IRF5 to evaluate their effects on macrophage polarization. The levels of IL‐1β and TNF‐α in spinal cord tissues were detected by ELISA. miR‐22‐3p was down‐regulated, whereas IRF5 was up‐regulated in rat spinal cord tissues following I/R. IRF5 was a target gene of miR‐22‐3p and could be negatively regulated by miR‐22‐3p. Silencing IRF5 or over‐expressing miR‐22‐3p relieved inflammation, elevated Tarlov score, and reduced the degree of severity of spinal cord I/R injury. Increased miR‐22‐3p facilitated M2 polarization of macrophages and inhibited inflammation in tissues by inhibiting IRF5, thereby attenuating spinal cord I/R injury. Taken together, these results demonstrate that increased miR‐22‐3p can inhibit the progression of spinal cord I/R injury by repressing IRF5 in macrophages, highlighting the discovery of a promising new target for spinal cord I/R injury treatment.

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