Thermal homeostasis can maintain body temperature of warm-blooded organisms in a narrow range to avoid hypothermia, ensuring the normal operation of life activities. Thermal homeostasis can make the internal temperature of target relatively insensitive to temperature changes of surrounding environment, which is of great significance to the efficient operation of equipment and the service life of material. The current systems that maintain thermal homeostasis need to consume electricity, which is very detrimental to energy consumption and global warming. Here, we propose a novel thermal homeostasis program by means of tunable sunlight-scattering behaviors of thermochromic hydrogel, without external energy input such as electrical energy and mechanical energy. A sandwich structure thermal homeostasiser (SSTH) generated by the thermal homeostasis program consists of three parts: the radiative cooling part at the top, the thermochromic part in the middle and the solar heating part at the bottom. The feasibility of thermal homeostasis based on SSTH has been verified theoretically and experimentally. With the ambient air temperature difference of more than 6 °C, SSTH can maintain its own temperature difference within 1.2 °C. The SSTH is a simple-feasible paradigm for achieving thermal homeostasis. This new thermal homeostasis method we proposed can fill the vacancy of the current thermal homeostasis control means and show great potential as a complementary mean of the existing building environment control system to go a step further toward zero-energy building.

ABSTRACT. Bladder cancer is a highly heterogeneous neoplasm. We examined the gene expression profile in 3 bladder cancer stages (Ta, T1, T2) using expression microarray analysis of 40 bladder tumors. Differentially expressed genes were found by the t-test, with <0.005 as the significance threshold. KEGG pathway-enrichment analysis was used to study the signaling pathways of the genes. We found 36 genes that could be used as molecular markers for predicting the transition from Ta-T1 to T1-T2. Among these, 11 overlapped between Ta-T1 and T1-T2 stages. Six genes were downregulated at the Ta-T1 stage, but were up-regulated at the T1-T2 stage (ANXA5, ATP6V1B2, CTGF, GEM, IL13RA1, and LCP1); 5 genes were up-regulated at the Ta-T1 stage, but down-regulated at the T1-T2 stage (ACPP, GNL1, RIPK1, RAPGEF3, and ZER1). Another 25 genes changed relative expression levels at the T1-T2 stage. These genes (including COL1A1, COL1A2, FN1, ITGA5, LGALS1, SPP1, VIM, POSTN, and COL18A1) may be involved in bladder cancer progression by affecting extracellular matrix-receptor interaction and focal adhesion. The cytokine-cytokine receptor interaction, neuroactive ligandreceptor interaction, and calcium-signaling pathway were associated with bladder cancer progression at both the Ta-T1 and T1-T2 stages.

Long non-coding RNA plasmacytoma variant translocation 1 (PVT1) is up-regulated in various human cancers, and our results indicated that PVT1 was up-regulated in clear cell renal cell carcinoma tissues. The Cancer Genome Atlas cohort analysis revealed that in clear cell renal cell carcinoma, higher PVT1 expression correlated with advanced TNM stage, histological grade, and poor survival. PVT1 knockdown promoted apoptosis, inhibited renal cancer cell proliferation, decreased Mcl-1, and increased cleaved caspase-3 and cleaved PARP. PVT1 increased Mcl-1 mRNA levels in renal cancer cells by promoting mRNA stability without influencing its transcription. in vitro, the enhanced apoptosis arising from PVT1 suppression was attenuated by overexpressing Mcl-1. In addition, in vivo experiments showed that PVT1 knockdown repressed xenograft tumor growth, while Mcl-1 overexpression partially rescued xenograft tumor growth. These results indicate the PVT1/Mcl-1 pathway inhibits renal cancer cell apoptosis in vitro and in vivo. PVT1 may thus serve as a novel biomarker, and the PVT1/Mcl-1 pathway may be a useful therapeutic target for clear cell renal cell carcinoma.

Results show that the targeting delivery system consisting of collagen binding domain basic fibroblast growth factor and collagen membranes induced better bladder regeneration at the injury site. Thus, this targeting delivery system may be an effective strategy for bladder regeneration with potential clinical applications.

Passive radiative cooling includes using the atmospheric window to emit heat energy to the cold outer space and hence reduce the temperature of objects on Earth. In most cases, radiative cooling is required in summer and suppressed in winter for thermal comfort. Recent radiative cooling materials cannot self-adjust cooling capacity according to season and environment, thus limiting their applications. In this study, we have designed a temperature-controlled phase change structure (TCPCS). The TCPCS benefits radiative coolers to adjust their cooling ability according to the ambient temperature. In the outdoor test, the TCPCS can help the cooler to turn off at low temperatures and turn on at high temperatures automatically; the coolers with and without TCPCS have maximal temperature differences of 9.7 and 19.6 °C, respectively, in a whole day. Furthermore, we have further improved and designed a V-shaped TCPCS that can simultaneously achieve the dual functions of cooling in summer and heating in winter. The TCPCS assembled here is a simple, feasible, and scalable structure for self-adaptive cooling.

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Ischemia and subsequent reperfusion (I ⁄ R) damage kidney tubular cells and consequently impair renal function. Rabbit bone marrow mesenchymal stem cells (BM-MSCs) expressing human bone morphogenic protein-7 (hBMP-7) regenerated tubular cells and improved renal function in a kidney I ⁄ R model. Rabbits were injected immediately after I ⁄ R with one of the following: (i) hBMP-7-transduced BM-MSCs (BM-MSCs hBMP-7 ); (ii) enhanced green fluorescent protein-transduced BM-MSCs (BM-MSCs EGFP ); or (iii) PBS. The activity of superoxide dismutase (SOD) was higher, and the amount of malondialdehyde (MDA) was lower in the BM-MSCs hBMP-7 group than in the BM-MSCs EGFP group. Both the BM-MSCs hBMP-7 group and the BM-MSCs EGFP group had higher SOD activity and lower amounts of MDA than the PBS group. Bcl-2-and Bcl-2-associated X protein levels, and other variables, indicated the regeneration of the kidney in both experimental groups. However, the BM-MSCs hBMP-7 group showed higher activity than the BM-MSCs EGFP group, indicating that the combined strategy of BM-MSC transplantation with hBMP-7 gene therapy could be a useful approach for the treatment of renal IRI.

Background/Aims: Treatment options for metastatic castrate-resistant prostate cancer (mCRPC) are limited and typically centered on paclitaxel-based chemotherapy. In this study, we aimed to evaluate whether miR-34a attenuates chemoresistance to paclitaxel by regulating target genes associated with drug resistance. Methods: We used data from The Cancer Genome Atlas to compare miR-34a expression levels in prostate cancer (PC) tissues with normal prostate tissues. The effects of miR-34a inhibition and overexpression on PC proliferation were evaluated in vitro via Cell Counting Kit-8 (CCK-8) proliferation, colony formation, apoptosis, and cell-cycle assays. A luciferase reporter assay was employed to identify the interactions between miR-34a and specific target genes. To determine the effects of up-regulation of miR-34a on tumor growth and chemo-resistance in vivo, we injected PC cells overexpressing miR-34a into nude mice subcutaneously and evaluated the rate of tumor growth during paclitaxel treatment. We examined changes in the expression levels of miR-34a target genes JAG1 and Notch1 and their downstream genes via miR-34a transfection by quantitative reverse transcription PCR (qRT-PCR) and western blot assay. Results: miR-34a served as an independent predictor of reduced patient survival. MiR-34a was down-regulated in PC-3PR cells compared with PC-3 cells. The CCK-8 assay showed that miR-34a overexpression resulted in increased sensitivity to paclitaxel while miR-34a down-regulation resulted in chemoresistance to paclitaxel in vitro. A study of gain and loss in a series of functional assays revealed that PC cells expressing miR-34a were chemosensitive. Furthermore, the overexpression of miR-34a increased the sensitivity of PC-3PR cells to chemotherapy in vivo. The luciferase reporter assay confirmed that JAG1 and Notch1 were directly targeted by miR-34a. Interestingly, western blot analysis and qRT-PCR confirmed that miR-34a inhibited the Notch1 signaling pathway. We found that miR-34a increased the chemosensitivity of PC-3PR cells by directly repressing the TCF1/ LEF1 axis. Conclusion: Our results showed that miR-34a is involved in the development of chemosensitivity to paclitaxel. By regulating the JAG1/Notch1 axis, miR-34a or its target genes JAG1 or Notch1 might serve as potential predictive biomarkers of response to paclitaxel-based chemotherapy and/or therapeutic targets that will help to overcome chemoresistance at the mCRPC stage.