Humidity-tolerant porous polymer coating for passive daytime radiative cooling.

Coating building envelopes with a passive daytime radiative cooling (PDRC) material has attracted enormous attention as an alternative cooling technique with minimal energy consumption and carbon footprint. Despite the exceptional performance and scalability of porous polymer coating (PPC), achieving consistent performance over a wide range of drying environments remains a major challenge for its commercialization as a radiative cooling paint. Herein, we demonstrate the humidity vulnerability of PPC during the drying process and propose a simple strategy to greatly mitigate the issue. Specifically, we find that the solar reflectance of the PPC rapidly decreases with increasing humidity from 30% RH, and the PPC completely losses its PDRC ability at 45% RH and even become a solar-heating material at higher humidity. However, by adding a small amount of polymer reinforcement to the PPC, it maintains its PDRC performance up to 60% RH, resulting in a 950% increase in estimated areal coverage compared to PPC in the United States. This study sheds light on a crucial consistency issue that has thus far been rarely addressed, and offers engineering guidance to handle this fundamental threat to the development of dependable PDRC paint for industrial applications.

PLK1/vimentin signaling facilitates immune escape by recruiting Smad2/3 to PD-L1 promoter in metastatic lung adenocarcinoma.

The prerequisite function of vimentin for the epithelial-mesenchymal transition (EMT) is not clearly elucidated yet. Here, we show that vimentin phosphorylated by PLK1, triggers TGF-ß-signaling, which consequently leads to metastasis and PD-L1 expression for immune suppression in lung adenocarcinoma. The clinical correlation between expression of both vimentin and PLK1, and overall survival rates of patients was significant in lung adenocarcinoma but not in squamous cell carcinoma. The phosphorylation of vimentin was accompanied by the activation of PLK1 during TGF-ß-induced EMT in lung adenocarcinoma. Among the several phosphorylation sites determined by phospho-proteomic analysis and the site-specific mutagenesis, the phosphorylation at S339 displayed the most effective metastasis and tumourigenesis with the highest expression of PD-L1, compared with that of wild-type and other versions in both 3D cell culture and tail-vein injection metastasis models. Phosphomimetic vimentin at S339 interacted with p-Smad2 for its nuclear localization, leading to the expression of PD-L1. Clinical relevance revealed the inverse correlation between the survival rates of patients and the expressions of VIM, PLK1, and CD274 in primary and metastatic lung adenocarcinoma. Thus, PLK1-mediated phosphorylation of vimentin activates TGF-ß signaling pathway, leading to the metastasis and immune escape through the expression of PD-L1, functioning as a shuttling protein in lung adenocarcinoma.

Effects of disusing closed suction drainage in simultaneous bilateral total hip arthroplasty: A retrospective cohort study.

PURPOSE: Increased blood loss remains a major drawback of simultaneous bilateral total hip arthroplasty (SBTHA). We examined the effects of disusing closed suction drainage (CSD) on postoperative blood loss and transfusion requirement in cementless SBTHA. METHODS: A retrospective cohort study was conducted with a consecutive series of cementless SBTHAs performed by a single surgeon between January 2014 and March 2017. The surgeon routinely used CSD until May 2015 and refrained from CSD in all primary THAs thereafter. This study included SBTHAs with intravenous administration of tranexamic acid (TXA). Postoperative hemoglobin drop, blood loss, transfusion rate, pain scores, complication rates, and implant survivorships were compared between the groups of SBTHA with and without CSD. The minimum follow-up duration was 1 year. RESULTS: Among the 110 patients (220 hips), 46 (92 hips) and 64 (128 hips) underwent SBTHA with and without CSD, respectively. Maximum hemoglobin drop (mean, 4.8 vs. 3.9 g/dL; P = 0.001), calculated blood loss (mean, 1530 vs. 1190 mL; P<0.001), transfusion rate (45.7% vs. 21.9%; P = 0.008), and length of hospital stay (mean, 6.6 vs. 5.8 days; P = 0.004) were significantly lower in patients without CSD. There were no significant differences in postoperative pain scales and wound complication rates. The mean Harris Hip scores at final follow-up (92.5 vs. 92.1; P = 0.775) and implant survivorships with an end-point of any revision at 4 years (98.9% vs. 98.4%; log-rank, P = 0.766) were similar between groups. CONCLUSIONS: Disusing CSD significantly reduced postoperative blood loss and transfusion requirement without increasing postoperative pain and surgical wound complications in cementless SBTHA with concurrent administration of intravenous TXA.

Clinical outcome of ultrasound-guided atelocollagen injection for patients with partial rotator cuff tear in an outpatient clinic: a preliminary study.

BACKGROUND: Atelocollagen has been studied for restoration of rotator cuff tendon. In this study, we attempted to evaluate the clinical outcome of ultrasound-guided atelocollagen injection in an outpatient clinic for patients with partial rotator cuff tear. METHODS: We recruited 42 outpatients who visited our hospital from May 2019 to September 2019. Atelocollagen injection was performed in patients with partial rotator cuff tear diagnosed by magnetic resonance imaging and ultrasound. American Shoulder and Elbow Surgeons (ASES), Constant, Korean Shoulder Score (KSS) and Simple Shoulder Test (SST) scores, and range of motion were assessed before injection and after 2 months. Statistically, we analyzed the clinical results using the Wilcoxon signed-rank test. RESULTS: Finally, 15 patients were enrolled for analysis. There was no significant difference between pre- and post-injection in terms of range of motion, ASES (57.0 vs. 60.4), Constant (56.4 vs. 58.9), KSS (64.6 vs. 68.5), and pain-visual analog scale (4.2 vs. 3.7), except function-visual analog scale (F-VAS; 6.3 vs. 7.1) and SST (6.6 vs. 6.9). A significant difference was found in SST (P=0.046) and F-VAS (P=0.009). According to the ultrasound results at 2 months, we found hyperechoic materials in three of seven patients. The most common complication of atelocollagen injection was post-injection pain (53%, 8/15). CONCLUSIONS: Ultrasound-guided atelocollagen injection for partial rotator cuff tear showed no significant change in terms of clinical outcomes, except for F-vas and SST score. Tendon regeneration was not clear due to the remnants of atelocollagen present at 2-month follow-up ultrasound. There seems to be alarming post-injection pain for 2 to 3 days in the patients who received atelocollagen injection in an outpatient clinic.

Active PLK1-driven metastasis is amplified by TGF-ß signaling that forms a positive feedback loop in non-small cell lung cancer.

Early findings that PLK1 is highly expressed in cancer have driven an exploration of its functions in metastasis. However, whether PLK1 induces metastasis in vivo and its underlying mechanisms in NSCLC have not yet been determined. Here, we show that the expression of active PLK1 phosphorylated at T210, abundant in TGF-ß-treated lung cells, potently induced metastasis in a tail-vein injection model. Active PLK1 with intact polo-box and ATP-binding domains accelerated cell motility and invasiveness by triggering EMT reprogramming, whereas a phosphomimetic version of p-S137-PLK1 did not, indicating that the phosphorylation status of PLK1 may determine the cell traits. Active PLK1-driven invasiveness upregulated TGF-ß signaling and TSG6 encoded by TNFAIP6. Loss of TNFAIP6 disturbed the metastatic activity induced by active PLK1 or TGF-ß. Clinical relevance shows that PLK1 and TNFAIP6 are strong predictors of poor survival rates in metastatic NSCLC patients. Therefore, we suggest that active PLK1 promotes metastasis by upregulating TGF-ß signaling, which amplifies its metastatic properties by forming a positive feedback loop and that the PLK1/TGF-ß-driven metastasis is effectively blocked by targeting PLK1 and TSG6, providing PLK1 and TSG6 as negative markers for prognostics and therapeutic targets in metastatic NSCLC.

Correction: Active PLK1-driven metastasis is amplified by TGF-ß signaling that forms a positive feedback loop in non-small cell lung cancer.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Roles of the Phosphorylation of Transcriptional Factors in Epithelial-Mesenchymal Transition.

Epithelial-to-mesenchymal transition (EMT) is the first step in the development of the invasive and migratory properties of cancer metastasis. Since the transcriptional reprogramming of a number of genes occurs in EMT, the regulation of EMT transcription factors has been intensively investigated. EMT transcriptional factors are commonly classified by the direct or indirect repression of E-cadherin because one of hallmarks of EMT is the loss of E-cadherin. This facilitates the expression of genes for EMT, tumor invasion, and metastasis. The posttranslational modification of EMT transcriptional factors, such as Snail and Slug, directly regulates their functions, including their stability, nuclear localization, protein-protein interaction, and ubiquitination for the promotion or termination of EMT at the specific points. Here, we discuss how posttranslational modifications regulate gene expression in a dynamic and reversible manner by modifying upstream signaling pathways, focusing in particular on the posttranslational modifications of Snail, Slug, ZEB1, ZEB2, and TWIST1. This review demonstrates that EMT transcription factors regulate metastasis through their posttranslational modifications and that the flexibility and reversibility of EMT can be modified by phosphorylation.

Molecular Targets of Genistein and Its Related Flavonoids to Exert Anticancer Effects.

Increased health awareness among the public has highlighted the health benefits of dietary supplements including flavonoids. As flavonoids target several critical factors to exert a variety of biological effects, studies to identify their target-specific effects have been conducted. Herein, we discuss the basic structures of flavonoids and their anticancer activities in relation to the specific biological targets acted upon by these flavonoids. Flavonoids target several signaling pathways involved in apoptosis, cell cycle arrest, mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase (PI3K)/AKT kinase, and metastasis. Polo-like kinase 1 (PLK1) has been recognized as a valuable target in cancer treatment due to the prognostic implication of PLK1 in cancer patients and its clinical relevance between the overexpression of PLK1 and the reduced survival rates of several carcinoma patients. Recent studies suggest that several flavonoids, including genistein directly inhibit PLK1 inhibitory activity. Later, we focus on the anticancer effects of genistein through inhibition of PLK1.