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Solar absorber is the key component to realize efficient utilization of solar energy. In this paper, only titanium nitride (TiN) is used to create a broadband, wide-angle, polarization insensitivity solar absorber. The average absorption of the absorber in the spectral range of 300-2500 nm is 91.3%. The distributions of electric and magnetic fields indicate that the strong absorption is caused by the coupling effect of surface plasmon resonance and guided mode resonance. Investigate the effects of the geometric parameters of the absorber on the spectral absorption performance. Moreover, we also discuss the absorption performance of the solar absorber at different incidence angles. It is demonstrated that even at a large incidence angle of 60°, the average spectral absorption can exceed more than 70%. The proposed solar energy absorber is also insensitive to polarization. The research results in this work could benefit the applications in solar thermophotovoltaic system. [ABSTRACT FROM AUTHOR]

Solar absorber is a key device that converts solar irradiation into heat via photothermal conversion, which has potential applications in solar thermal power systems, and seawater desalination. In this paper, we propose a wide-angle, broadband and polarization insensitivity metamaterial solar absorber based on titanium nitride (TiN). Numerical results show that this solar absorber has a total average spectrum absorption of up to 97.5% at wavelength of 300–2500 nm. Based on the distributions of the electric and magnetic field, it is believed that the coupling resonance of surface plasmon resonance, guided mode resonance and cavity resonance is responsible for its excellent absorption of solar energy. Furthermore, we discuss the effects of incidence angle on the solar absorber and demonstrate that the average spectrum absorption of more than 85% can be obtained even at a large incidence angle of 60°, and it is insensitive to the change of polarization angle. The effect of geometric parameters of the solar absorber on spectrum absorption performance was investigated. This research will provide new ideas for the design of solar thermophotovoltaic and thermal conversion systems. [ABSTRACT FROM AUTHOR]

Delirium is an acute brain dysfunction. As one of the common psychiatric disorders in ICU, it can seriously affect the prognosis of patients. Hormones are important messenger substances found in the human body that help to regulate and maintain the function and metabolism of various tissues and organs. They are also one of the most commonly used drugs in clinical practice. Recent evidences suggest that aberrant swings in cortisol and non-cortisol hormones might induce severe cognitive impairment, eventually leading to delirium. However, the role of hormones in the pathogenesis of delirium still remains controversial. This article reviews the recent research on risk factors of delirium and the association between several types of hormones and cognitive dysfunction. These mechanisms are expected to offer novel ideas and clinical relevance for the treatment and prevention of delirium. • The mechanisms of glucocorticoid-induced delirium are thoroughly discussed. • The highest incidence of delirium is in the ICU with multiple kinds of risk factors. • Hormone therapy may be an option for preventing and treating delirium. [ABSTRACT FROM AUTHOR]

Abstract: Condylomata acuminata (CA) caused by human papillomavirus (HPV) is a common sexually transmitted disease with half a million new cases diagnosed in the United States per year and the annual increase in incidence in China. Recurrence is a major challenge for CA treatment. Recently, we demonstrated that FOXP3+ regulatory T (Treg) cells mediate the immunosuppression in large genital warts. Here, we further report that low-dose cyclophosphamide (CY), a conventional chemotherapy drug, can effectively prevent the recurrence of large CA in clinical patients after laser therapy. Surprisingly, although 9 out of 52 patients recur six weeks after the combination treatment, the re-administration of low-dose CY alone completely eliminates most recurred lesions. We provide evidence that low-dose CY not only depletes patients'' Treg cells and enhances function of HPV-specific T cells and NK cells in the periphery, but also ameliorates the immune milieu of the lesion site, leading to the elimination of remnant viruses. These findings have important clinical significance, and potentially lead to a therapeutic breakthrough for the treatment of CA. [Copyright &y& Elsevier]

Graphene modified dye sensitized solar cells (DSSCs) show high photovoltaic performances due to the fast electron transport capacity and the large BET area of the additive. However, the corresponding research on how to further improve the properties of DSSCs by optimizing the adopted graphene is insufficient. In this study, reduced graphene oxide (RGO) nanosheets and three-dimensional graphene networks (3DG) are employed to build high performance photoanodes with a two-layer structure by taking full advantages of them, simultaneously. Residual functional groups of RGO support preconditions to construct an electron transport layer between conducting substrate and work layer of photoanode, which is beneficial to depress dark current on the interface. On the other hand, high integrity and continuity of 3DG provide a fast electrons transport network in the work layer, which suppresses the recombination of electron–hole pairs in the photoanode. After optimizing the structure of photoanode, the energy conversion efficiency reaches 8.87%. [ABSTRACT FROM AUTHOR]

Background: It has been reported that programmed death‐ligand 1 (PD‐L1) is highly expressed in cells during viral infection, which helps the virus escape host immunity. However, the relationship between human papillomavirus (HPV) and PD‐L1 in condyloma acuminatum and whether they participate in immunosuppression have not been reported. In this paper, we aimed to explore the expression and significance of PD‐L1 in condyloma acuminatum. Methods: The expression of PD‐L1 in the wart of condyloma acuminatum patients and the foreskin of healthy individuals was evaluated. Lentivirus transfection was used to introduce the HPV11‐E7 gene into HaCaT cells to investigate whether HPV infection could affect the expression of PD‐L1. The successfully constructed HPV11‐E7 HaCaT cells were cocultured with Jurkat cells, and Jurkat cell apoptosis and proliferation as well as the Jurkat cell cycle were evaluated by flow cytometry and cell counting kit‐8 (CCK‐8) assays. Results: PD‐L1 was highly expressed in keratinocytes of genital warts. Through the construction of a cell model, we found that HPV11‐E7 could upregulate the expression of PD‐L1 in HaCaT cells. Furthermore, HPV11‐E7 HaCaT cells can promote the apoptosis of Jurkat cells, inhibit the proliferation of Jurkat cells and mediate the cell cycle arrest of Jurkat cells through the PD‐1/PD‐L1 signalling pathway. Conclusions: HPV infection may upregulate PD‐L1 expression in the keratinocytes of genital warts and participate in the inhibition of local T‐cell function. [ABSTRACT FROM AUTHOR]

IFN-ε is essential in combating viral infections, particularly in epithelial cells and protected mucosal tissues. Its protective effects have been demonstrated against HSV2, Zika virus, HIV and SARS-COV2. However, the specific expression and role of IFN-ε in skin keratinocytes and HPV infection are still not fully understood and require further investigation. In this study, we aimed to investigate the functions and expression mechanism of IFN-ε in keratinocytes during HPV infection and the progression of condyloma acuminata. Keratinocytes isolated from biopsied CA warts and normal skins samples were analyzed by MeRIP-seq analysis. IFN-ε and WTAP in CA warts and normal skins were analyzed by immunostaining and qPCR. In this study, we identified IFN-ɛ was markedly upregulated in CA warts and HPV-infected keratinocytes. IFN-ɛ expression also showed negatively correlation with the size of CA warts (R=−0.4646, P = 0.009). IFN-ɛ suppressed the susceptibility of HPV infection directly. m6A analysis reveals WTAP is a key m6A writer promoting the m6A modification of IFNE mRNA. Our research suggests that IFN-ɛ is an important Type I IFN cytokine involved in the development of genital warts. Furthermore, we found that HPV infection affects the m6A modifications of IFNE through a mechanism dependent on WTAP. This study provides insights into the innate immune response of the host to HPV infection and may contribute to the development of future strategies for regulating innate immunity to treat genital warts. • HPV infection induces IFN-ɛ expression in keratinocytes. • IFN-ɛ shows negative correlation with the development of condyloma acuminata. • IFN-ɛ suppressed the susceptibility of HPV infection. • WTAP regulates the expression of IFN-ɛ by m6A modification. [ABSTRACT FROM AUTHOR]

Background: Human papillomavirus (HPV) infected keratinocyte dysfunction results in the formation of genital warts, and the specific role of Sonic hedgehog (SHh) signaling in genital warts remains elusive. Thus, this study aimed to identify the correlation between wart formation and SHh signaling. Materials and methods: In this study, nine male patients with genital warts were recruited, and the expression of SHh and its downstream signal molecules Patched‐1 and GLI family zinc finger 1 (Ptch1 and Gli1) was detected. Moreover, G2‐phase cells in the collected genital warts samples were assessed with normal foreskin samples as a comparison. HPV6/11 were detected via in situ hybridization (ISH), and SHh expression of the corresponding paraffin sections was determined via immunohistochemical staining (IHC). In addition, an in vitro down‐regulated SHh model was constructed by siRNA transfection of the HaCaT cell line, and the cell cycle was detected at 36 h by flow cytometry with propidium iodide staining. Results: SHh, Ptch1, and Gli1 in warts were significantly downregulated in the condyloma acuminatum (CA) group compared to the normal foreskin group. G2‐phase cells in the middle section of the spinous layer of CA wart tissues were significantly increased. Moreover, the expression of HPV‐DNA was amplified and negatively correlated with SHh activity in CA wart tissues. Lastly, the downregulation of SHh‐induced G2 arrest in vitro. Conclusions: The downregulation of the SHh signaling promotes HPV replication and the formation of warts by inducing G2/M arrest in the keratinocytes of CA. [ABSTRACT FROM AUTHOR]

Patients with metastatic melanoma have a poorer prognosis. Prion protein (PrP) in melanoma is known to play an important role in cancer cell migration and invasion by interacting with filamin A (FLNa), a cytolinker protein. To investigate if PrP may contribute to cancer cell mobility independent of its binding to FLNa, we knocked out PRNP in M2 melanoma cell, which lacked FLNa expression. We found that deletion of PRNP in M2 significantly reduced its motility. When PRNP was deleted, the level of Akt was decreased. As a consequence, phosphorylation of small heat shock protein (hsp27) was also reduced, which resulted in polymerization of F-actin rendering the cells less migratory. Accordingly, when PrP was re-expressed in PRNP null M2 cells, the mobility of the recurred cells was rescued, so were the expression levels of Akt and phosphorylated hsp27, resulting in a decrease in the polymerization of F-actin. These results revealed that PrP can play a FLNa independent role in cytoskeletal organization and tumor cell migration by modulating Akt-hsp27-F-actin axis. • Filamin A (FLNa) independent cell migration has not been thoroughly studied. • Prion protein (PrP) modulates actin polymerization and mediates M2 melanoma cell migration independent of FLNa. • Expression of PrP stabilizes protein kinase B (Akt), enhances interaction between Akt and heat shock protein 27 (hsp27). • Akt phosphorylates hsp27 to reduce polymerization of F-actin, which in turn to enhance cancer cell migration. [ABSTRACT FROM AUTHOR]

Previous studies have identified neuron navigator 2(NAV2) as an oncogene in several human tumors. However, the NAV2 gene expression changes and its role in the pathogenesis of cutaneous melanoma have not been clearly illustrated. Further investigations of NAV2 in cutaneous melanoma may provide new mechanistic insight and treatment strategy for this disease. Through immunohistochemistry assay and bioinformatics analysis, we found that melanoma tissues showed an upregulated expression of NAV2 which correlated with poor prognosis of cutaneous melanoma. To investigate the effect of NAV2 on the proliferation and invasion of melanoma, shNAV2 and NAV2-cDNA were transfected into melanoma cell lines. NAV2 overexpression significantly promoted melanoma cell proliferation, migration and invasion, while NAV2 silencing effectively inhibited this process. The potential underlying mechanisms were investigated using bioinformatics analysis, qRT-PCR, and western blot. Results showed that NAV2-mediated invasion of melanoma cells was driven by enhanced epithelial–mesenchymal transition, which was resulted from SNAI2 upregulation via the GSK-3β/β-catenin pathway. This study suggested that NAV2 could induce melanoma proliferation and invasion by epithelial–mesenchymal transition through the GSK-3β/β-catenin-SNAI2 pathway. Our findings on the pathological mechanisms of NAV2-associated cutaneous melanoma may contribute to the development of potential therapeutic strategy for melanoma. [ABSTRACT FROM AUTHOR]