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In the working-age population worldwide, diabetic retinopathy (DR), a prevalent complication of diabetes, is the main cause of vision impairment. Chronic low-grade inflammation plays an essential role in DR development. Recently, concerning the pathogenesis of DR, the Nod-Like Receptor Family Pyrin Domain Containing 3 (NLRP3) inflammasome in retinal cells has been determined as a causal factor. In the diabetic eye, the NLRP3 inflammasome is activated by several pathways (such as ROS and ATP). The activation of NPRP3 leads to the secretion of inflammatory cytokines interleukin-1β (IL-1β) and interleukin-18 (IL-18), and leads to pyroptosis, a rapid inflammatory form of lytic programmed cell death (PCD). Cells that undergo pyroptosis swell and rapture, releasing more inflammatory factors and accelerating DR progression. This review focuses on the mechanisms that activate NLRP3 inflammasome and pyroptosis leading to DR. The present research highlighted some inhibitors of NLRP3/pyroptosis pathways and novel therapeutic measures concerning DR treatment.

Passive radiative cooling draws heat from surfaces and radiates it into space as infrared radiation to which the atmosphere is transparent. However, the energy density mismatch between solar irradiance and the low infrared radiation flux from a near-ambient-temperature surface requires materials that strongly emit thermal energy and barely absorb sunlight. We embedded resonant polar dielectric microspheres randomly in a polymeric matrix, resulting in a metamaterial that is fully transparent to the solar spectrum while having an infrared emissivity greater than 0.93 across the atmospheric window. When backed with a silver coating, the metamaterial shows a noontime radiative cooling power of 93 watts per square meter under direct sunshine. More critically, we demonstrated high-throughput, economical roll-to-roll manufacturing of the metamaterial, which is vital for promoting radiative cooling as a viable energy technology.

The heating and cooling energy consumption of buildings accounts for about 15% of national total energy consumption in the United States. In response to this challenge, many promising technologies with minimum carbon footprint have been proposed. However, most of the approaches are static and monofunctional, which can only reduce building energy consumption in certain conditions and climate zones. Here, we demonstrate a dual-mode device with electrostatically-controlled thermal contact conductance, which can achieve up to 71.6 W/m 2 of cooling power density and up to 643.4 W/m 2 of heating power density (over 93% of solar energy utilized) because of the suppression of thermal contact resistance and the engineering of surface morphology and optical property. Building energy simulation shows our dual-mode device, if widely deployed in the United States, can save 19.2% heating and cooling energy, which is 1.7 times higher than cooling-only and 2.2 times higher than heating-only approaches. Future zero-energy buildings require smart and dynamic utilization of renewable energy for efficient indoor temperature control. Here the authors show that the dual-mode device enables building envelopes to switch between solar heating and radiative cooling to save HVAC energy for all seasons and all climate zones.

Abstract This study investigated possible therapeutic effect mechanisms of exosomes from bone marrow-derived mesenchymal stem cells (BMSC) in neuronal and microglial cells and in a Parkinson disease (PD) model. Neuronal SH-SY5Y cells and microglial HMC3 cells were subjected to 1-methyl-4-phenylpyridinium (MPP+) or LPS, respectively. The mRNA and protein expression was assessed using qRT-PCR, Western blotting, and enzyme-linked immunosorbent assay. Cell viability and apoptosis of SH-SY5Y cells were examined using the MTT assay and flow cytometry. Chromatin immunoprecipitation assays were performed to assess the binding relationship between glioma-associated oncogene homolog 1 (Gli1) and the Sp1 transcription factor promoter. BMSC-derived exosomes promoted cell proliferation and inhibited apoptosis in MPP+-treated SH-SY5Y cells and suppressed inflammatory markers in LPS-treated HMC3 cells. Sp1 knockdown decreased SH-SY5Y cell damage and HMC3 immune activation. Gli1 carried by BMSC exosomes directly bound with Sp1 to inhibit Sp1-mediated LRRK2 activation whereas exosomes secreted by Gli1-knockdown in BMSC did not. In a PD mouse model induced with MPTP, BMSC exosomes decreased neuron loss injury and the inflammatory response by inhibiting Sp1 signaling. Thus, BMSC-derived exosomal Gli1 alleviates inflammatory damage and neuronal apoptosis by inhibiting Sp1 in vitro and in vivo. These findings provide the basis for the potential clinical use of BMSC-derived exosomes in PD.

Background Metabolic disturbance, particularly of glucose metabolism, is a hallmark of tumors, including non-small cell lung cancer. This study mainly analyzed the role of multiple inositol polyphosphate phosphatase 1 (MINPP1) in regulating glycolysis in lung adenocarcinoma (LUAD) in vitro and in vivo. Methods First, the differential expression of ten-eleven translocation (TET)1/TET3, WD repeat and HMG-box DNA-binding protein 1 (WDHD1), and MINPP1 in tumors and paracancerous tissues of LUAD patients was measured using RT-qPCR and western blot assays. The effects of the WDHD1/MINPP1 axis on the proliferation and glycolysis of LUAD were explored by lentivirus-mediated gene intervention techniques or treatment with the glycolysis inhibitor 2-deoxyglucose (2-DG). The transcriptional regulation of WDHD1 and MINPP1 was probed using ChIP-qPCR, dual-luciferase assay, RT-qPCR, and western blot analyses. The association of TET1/TET3 with WDHD1 promoter demethylation was assessed using qMSP, RT-qPCR, and western blot assay. Results TET1, TET3, WDHD1, and MINPP1 are all expressed at high levels in tumor tissues of patients with LUAD. TET1/TET3 upregulated WDHD1 expression through demethylation and further mediated MINPP1 transcriptional activation. Administration of the glycolysis inhibitor 2-DG reversed the LUAD glycolytic program, and progression was inhibited by the knockdown of MINPP1. Restoration of MINPP1 also reversed glycolysis and proliferation suppressed by the knockdown of WDHD1. Finally, reactivation of WDHD1 promoted LUAD cell glycolysis and growth, curtailed by knockdown of TET1/TET3. Conclusion The demethylases TET1/TET3 mediate the demethylation of the WDHD1 promoter to upregulate WDHD1 expression, thereby activating MINPP1 transcription to promote LUAD glycolysis and progression.

Background Acquired resistance to sorafenib greatly limits its therapeutic efficiency in the treatment of hepatocellular carcinoma (HCC). Increasing evidence indicates that long noncoding RNAs (lncRNAs) play important roles in the resistance to anti-cancer drugs. The present study aims to explore the involvement of lncRNA SNHG1 (small nucleolar RNA host gene 1) in sorafenib resistance and how SNHG1 is associated with overexpressed microRNA-21 (miR-21) and the activated Akt pathway, which have been demonstrated to mediate this resistance in HCC cells. Methods Sorafenib-resistant HCC (SR-HCC) cells were generated and their sorafenib-resistant properties were confirmed by cell viability and apoptosis assays. Potential lncRNAs were screened by using multiple bioinformatics analyses and databases. The expression of genes and proteins was detected by qRT-PCR, Western blot and in situ hybridization. Gene silencing was achieved by specific siRNA or lncRNA Smart Silencer. The effects of anti-SNHG1 were evaluated in vitro and in experimental animals by using quantitative measures of cell proliferation, apoptosis and autophagy. The binding sites of miR-21 and SNHG1 were predicted by using the RNAhybrid algorithm and their interaction was verified by luciferase assays. Results The Akt pathway was highly activated by overexpressed miR-21 in SR-HCC cells compared with parental HCC cells. Among ten screened candidates, SNHG1 showed the largest folds of alteration between SR-HCC and parental cells and between vehicle- and sorafenib-treated cells. Overexpressed SNHG1 contributes to sorafenib resistance by activating the Akt pathway via regulating SLC3A2. Depletion of SNHG1 enhanced the efficacy of sorafenib to induce apoptosis and autophagy of SR-HCC cells by inhibiting the activation of Akt pathway. Sorafenib induced translocation of miR-21 to the nucleus, where it promoted the expression of SNHG1, resulting in upregulation of SLC3A2, leading to the activation of Akt pathway. In contrast, SNHG1 was shown to have little effect on the expression of miR-21, which downregulated the expression of PTEN, leading to the activation of the Akt pathway independently of SNHG1. Conclusions The present study has demonstrated that lncRNA SNHG1 contributes to sorafenib resistance by activating the Akt pathway and its nuclear expression is promoted by miR-21, whose nuclear translocation is induced by sorafenib. These results indicate that SNHG1 may represent a potentially valuable target for overcoming sorafenib resistance for HCC.

Background Primary macronodular adrenal hyperplasia (PMAH), previously termed ACTH-independent macronodular adrenal hyperplasia (AIMAH), is a rare cause of Cushing’s syndrome usually characterized by functioning adrenal macronodules and increased cortisol production. Methods To screen and analyse the microRNA (miRNA) profile of PMAH in order to elucidate its possible pathogenesis, a miRNA microarray was used to test tissue samples from patients with familial PMAH, patients with sporadic PMAH and normal control samples of other nontumour adrenocortical tissues and identify characteristic microRNA expression signatures. Randomly selected miRNAs were validated by quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). Furthermore, the key signalling pathways and miRNAs involved in PMAH pathogenesis were determined by gene ontology and pathway analysis. Results Characteristic microRNA expression signatures were identified for patients with familial PMAH (16 differentially expressed microRNAs) and patients with sporadic PMAH (8 differentially expressed microRNAs). The expression of the selected miRNAs was confirmed by qRT-PCR, suggesting the high reliability of the miRNA array analysis results. Pathway analysis showed that the most enriched pathway was the renal cell carcinoma pathway. Overexpression of miR-17, miR-20a and miR-130b may inhibit glucocorticoid-induced apoptosis in PMAH pathogenesis. Conclusion We identified the miRNA signatures in patients with familial and sporadic PMAH. The differentially expressed miRNAs may be involved in the mechanisms of PMAH pathogenesis. Specific miRNAs, such as miR-17, miR-20a and miR-130b, may be new targets for further functional studies of PMAH.

In this study, we explored the effects of particulate matter 2.5 (PM 2 . 5 ) eye drops on the ocular surface structure and tear function in mice and established a novel animal model for dry eye research. We found that, following treatment with PM 2.5 , the tear volume and, the tear film break-up time showed statistical differences at each time point (P < 0.05). The FL score of the PM 2.5 -treated group was higher than that of others (P < 0.05). The average number of corneal epithelial layer cells in groups A and B was significantly lower than that in group C (P < 0.05). Scanning electron microscopy and transmission electron microscopy revealed that the number of corneal epithelial microvilli and corneal desmosomes was drastically reduced in group C. PM 2.5 induced apoptosis in the corneal superficial and basal epithelium and led to abnormal differentiation and proliferation of the ocular surface with higher expression levels of Ki67 and a reduced number of goblet cells in the conjunctival fornix in group C. PM 2.5 significantly increased the levels of TNF-α, NF-κB p65 (phospho S536), and NF-κB in the cornea. Thus, the topical administration of PM 2.5 in mice induces ocular surface changes that are similar to those of dry eye in humans, representing a novel model of dry eye.

Thermal error monitoring technology is the key technological support to solve the thermal error problem of heavy-duty CNC （computer numerical control） machine tools. Currently, there are many review literatures intro- ducing the thermal error research of CNC machine tools, but those mainly focus on the thermal issues in small and medium-sized CNC machine tools and seldom introduce thermal error monitoring technologies. This paper gives an overview of the research on the thermal error of CNC machine tools and emphasizes the study of thermal error of the heavy-duty CNC machine tool in three areas. These areas are the causes of thermal error of heavy-duty CNC machine tool and the issues with the temperature moni- toring technology and thermal deformation monitoring technology. A new optical measurement technology called the ＂fiber Bragg grating （FBG） distributed sensing tech- nology＂ for heavy-duty CNC machine tools is introduced in detail. This technology forms an intelligent sensing and monitoring system for heavy-duty CNC machine tools. This paper fills in the blank of this kind of review articlesto guide the development of this industry field and opens up new areas of research on the heavy-duty CNC machine tool thermal error.