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Conventional static radiative coolers have an unadjustable cooling capacity, which often results in overcooling in low temperature environment. Therefore, there is a great need for an adaptive dynamic radiative cooler. However, such adaptive coolers usually require complex preparation processes. This paper proposes an adaptive radiative cooler based on a Fabry–Perot resonant cavity. By optimizing the structural parameters of the radiative cooler, this adaptive radiative cooler achieves a modulation rate of 0.909 in the atmospheric window band. The net radiative cooling performance difference between low and high temperatures is nearly eight times. Meanwhile, the device is easily prepared, has a high tolerance, and can effectively prevent W–VO2 oxidation. This study provides new insights into adaptive radiative cooling with potential for large-scale applications.

Ubiquitination plays an essential role in protein stability, subcellular localization, and interactions. Crosstalk between different types of ubiquitination results in distinct biological outcomes for proteins. However, the role of ubiquitinationrelated crosstalk in lymph node (LN) metastasis and the key regulatory factors controlling this process have not been determined. Using high-throughput sequencing, we found that ubiquitin-conjugating enzyme E2 C (UBE2C) was overexpressed in bladder cancer (BCa) and was strongly associated with an unfavorable prognosis. Overexpression of UBE2C increased BCa lymphangiogenesis and promoted LN metastasis both in vitro and in vivo. Mechanistically, UBE2C mediated sodium-coupled neutral amino acid transporter 2 (SNAT2) monoubiquitination at lysine 59 to inhibit K63-linked polyubiquitination at lysine 33 of SNAT2. Crosstalk between monoubiquitination and K63-linked polyubiquitination increased SNAT2 membrane protein levels by suppressing epsin 1-mediated (EPN1-mediated) endocytosis. SNAT2 facilitated glutamine uptake and metabolism to promote VEGFC secretion, ultimately leading to lymphangiogenesis and LN metastasis in patients with BCa. Importantly, inhibition of UBE2C significantly attenuated BCa lymphangiogenesis in a patient-derived xenograft model. Our results reveal the mechanism by which UBE2C mediates crosstalk between the monoubiquitination and K63-linked polyubiquitination of SNAT2 to promote BCa metastasis and identify UBE2C as a promising target for treating LN-metastatic BCa., Introduction Lymph node (LN) metastasis is the predominant route of metastasis for most solid tumors and promotes distant metastasis (1, 2). Patients with LN involvement have shorter distant metastasis-free survival [...]

Perineural invasion (PNI) is a biological characteristic commonly observed in pancreatic cancer. Although PNI plays a key role in pancreatic cancer metastasis, recurrence, and poor postoperative survival, its mechanism is largely unclarified. Clinical sample analysis and endoscopic ultrasonographic elasticity scoring indicated that cancer-associated fibroblasts (CAFs) were closely related to the occurrence of PNI. Furthermore, CAF-derived extracellular vesicles (EVs) were involved in PNI in dorsal root ganglion coculture and mouse sciatic nerve models. Next, we demonstrated that CAFs promoted PNI through extracellular vesicle transmission of PNI-associated transcript (PIAT). Mechanistically, PIAT specifically bound to YBX1 and blocked the YBX1-Nedd4l interaction to inhibit YBX1 ubiquitination and degradation. Furthermore, PIAT enhanced the binding of YBX1 and PNI-associated mRNAs in a 5-methylcytosine (m5C)–dependent manner. Mutation of m5C recognition motifs in YBX1 or m5C sites in downstream target genes reversed PIAT-mediated PNI. Consistent with these findings, analyses using a KPC mouse model demonstrated that the PIAT/YBX1 axis enhanced PNI through m5C modification. Clinical data suggested that the PIAT expression in the serum EVs of patients with pancreatic cancer was associated with the degree of neural invasion and prognosis. Our study revealed the important role of the PIAT/YBX1 signaling axis in the tumor microenvironment (TME) in promoting tumor cell PNI and provided a new target for precise interference with CAFs and RNA methylation in the TME to suppress PNI in pancreatic cancer. Editor's summary: Pancreatic cancer has a very poor prognosis and is often characterized by perineural invasion (PNI); however, the role that PNI plays in postoperative survival has been unexplored. Here, Zheng et al. evaluate the role PNI plays in pancreatic cancer prognosis and show that cancer-associated fibroblasts (CAFs) induce PNI in tumors through CAF-derived extracellular vesicles (EVs). They show that these EVs are packaged with PNI-associated transcript (PIAT) that enhances PNI in mouse models and induces worse survival. PIAT represents a potential target for reducing PNI in pancreatic cancer and perhaps improving survival for patients that requires further study. —Dorothy Hallberg [ABSTRACT FROM AUTHOR]

The creep behavior of composite wing leading edges resulting from nonequilibrium residual stresses and material viscoelasticity needs to be evaluated comprehensively as it significantly affects assembly. In this study, long-term creep monitoring of a composite wing leading edge used in an actual airplane for 710 h is conducted using embedded fiber Bragg grating arrays and a creep extraction algorithm. The spectra and Bragg wavelength shifts of two embedded arrays, which involve temperature, thermal expansion, and creep, are recorded and analyzed. The creep curve of the composite wing leading edge is reconstructed and further predicted using the creep extraction algorithm based on multiparameter decoupling and the Burgers model. This study elucidates the enlargement of the opening size in the composite wing leading edge by measuring the tensile strain above the neutral axis. The predicted creep time serves as a valuable reference for determining the appropriate assembly timing. [ABSTRACT FROM AUTHOR]

Wang He, Guangzheng Zhong, Ning Jiang, Bo Wang, Xinxiang Fan, Changhao Chen, Xu Chen, Jian Huang, and Tianxin Lin Original citation: J Clin Invest. 2018;128(2):861-875. https://doi.org/10.1172/JCI96218. Citation for this corrigendum: [...]

Patients with bladder cancer (BCa) with clinical lymph node (LN) metastasis have an extremely poor prognosis. VEGF-C has been demonstrated to play vital roles in LN metastasis in BCa. However, approximately 20% of BCa with LN metastasis exhibits low VEGF-C expression, suggesting a VEGF-C-independent mechanism for LN metastasis of BCa. Herein, we demonstrate that BCa cell-secreted exosome-mediated lymphangiogenesis promoted LN metastasis in BCa in a VEGF-C-independent manner. We identified an exosomal long noncoding RNA (lncRNA), termed lymph node metastasis-associated transcript 2 (LNMAT2), that stimulated human lymphatic endothelial cell (HLEC) tube formation and migration in vitro and enhanced tumor lymphangiogenesis and LN metastasis in vivo. Mechanistically, LNMAT2 was loaded to BCa cell-secreted exosomes by directly interacting with heterogeneous nuclear ribonucleoprotein A2B1 (hnRNPA2B1). Subsequently, exosomal LNMAT2 was internalized by HLECs and epigenetically upregulated prospero homeobox 1 (PROX1) expression by recruitment of hnRNPA2B1 and increasing the H3K4 trimethylation level in the PROX1 promoter, ultimately resulting in lymphangiogenesis and lymphatic metastasis. Therefore, our findings highlight a VEGF-C-independent mechanism of exosomal lncRNA-mediated LN metastasis and identify LNMAT2 as a therapeutic target for LN metastasis in BCa., Introduction Bladder cancer (BCa), one of the most commonly diagnosed malignancies worldwide, is the leading cause of cancer-related death among men, with an estimated 550,000 new cases and 20,000 deaths [...]

Lymph node (LN) metastasis occurs frequently in pancreatic ductal adenocarcinoma (PDAC) and predicts poor prognosis for patients. The [KRAS.sup.G12D] mutation confers an aggressive PDAC phenotype that is susceptible to lymphatic dissemination. However, the regulatory mechanism underlying [KRAS.sup.G12D] mutation-driven LN metastasis in PDAC remains unclear. Herein, we found that PDAC with the [KRAS.sup.G12D] mutation ([KRAS.sup.G12D] PDAC) sustained extracellular vesicle-mediated (EV-mediated) transmission of heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1) in a SUMOylation-dependent manner and promoted lymphangiogenesis and LN metastasis in vitro and in vivo. Mechanistically, hnRNPA1 bound with SUMO2 at the lysine 113 residue via [KRAS.sup.G12D]-induced hyperactivation of SUMOylation, which enabled its interaction with TSG101 to enhance hnRNPA1 packaging and transmission via EVs. Subsequently, SUMOylation induced EV-packaged-hnRNPA1 anchoring to the adenylateand uridylate-rich elements of PROX1 in lymphatic endothelial cells, thus stabilizing PROX1 mRNA. Importantly, impeding SUMOylation of EV-packaged hnRNPA1 dramatically inhibited LN metastasis of [KRAS.sup.G12D] PDAC in a genetically engineered [Kras.sup.G12D/+] [Trp53.sup.R172H/+] Pdx-1-Cre (KPC) mouse model. Our findings highlight the mechanism by which KRAS mutant-driven SUMOylation triggers EV-packaged hnRNPA1 transmission to promote lymphangiogenesis and LN metastasis, shedding light on the potential application of hnRNPA1 as a therapeutic target in patients with [KRAS.sup.G12D] PDAC., Introduction Pancreatic ductal adenocarcinoma (PDAC) is one of the most malignant digestive system cancers and represents the seventh leading cause of cancer-related death worldwide (1, 2). Accumulating reports have shown [...]

PbSn solders are used in semiconductor devices for aerospace or military purposes with high levels of reliability requirements. Microalloying has been widely adopted to improve the reliability for Pb-free solders, but its application in PbSn solders is scarce. In this article, the optimization of PbSn solder reliability with Ge microalloying was investigated using both experimental and calculation methods. Intermetallic compounds (IMC) growth and morphologies evolution during reliability tests were considered to be the main factors of device failure. Through first-principle calculation, the growth mechanism of interfacial Ni3Sn4 was discussed, including the formation of vacancies, the Ni-vacancies exchange diffusion and the dominant Ni diffusion along the [1 0 0] direction. The doping of Ge in the cell increased the exchange energy barrier and thus inhibited the IMC development and coarsening trend. In three reliability tests, only 0.013 wt% Ge microalloying in Pb60Sn40 was able to reduce IMC thickness by an increment of 22.6~38.7%. The proposed Ge microalloying method in traditional PbSn solder could yield a prospective candidate for highly reliable applications. [ABSTRACT FROM AUTHOR]