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Semiconducting two-dimensional (2D) materials have potential applications as ultrathin optoelectronic materials. Therefore, being able to precisely modulate the band gap is useful to improving their applicability. Electron doping of the semiconducting materials is one of the successful techniques used to modulate their band gap. Silver nanoclusters (AgNCs) or gold nanoclusters (AuNCs) a few nanometers in size can generate a high density of highly energetic hot electrons with relatively long lifetimes when photoexcited. The optical band gap of 2D MoS 2 nanosheets shows different responses when integrated with different amounts of AgNCs or AuNCs due to the electron doping effect. Introducing a small amount of the nanoclusters to the surface of a MoS 2 nanosheet lowered its optical band gap. Further reduction of the optical band gap of MoS 2 is obtained upon tripling the amount of integrated nanoclusters. Conversely, the optical band gap of MoS 2 was increased when integrated with 5 times the concentration of AuNCs and AgNCs. The optical band gap of the MoS 2 nanosheets was significantly increased when integrated with an even higher concentration of AuNCs or AgNCs. The magnitude of the shift of the optical band gap of MoS 2 induced by AgNCs is higher than that induced by AuNCs because the energy of LUMO of the AgNCs is higher than that of the AuNCs.

The two characteristic absorption peaks of semiconducting two-dimensional tungsten disulfide (WS 2 ) are red-shifted after integrating with gold nanocube (AuNC) arrays. The amount of the red shift is reduced when the AuNCs are coated with a high concentration of Pd. A negligible shift was observed in the absorption peaks of WS 2 when smaller amounts of Pd are introduced to the surface of AuNCs. Conversely, the photoluminescence (PL) of WS 2 is blue-shifted when measured on top of AuNCs and AuNCs coated with different amounts of Pd. AuNC-Pd Janus nanoparticles are prepared by depositing Pd atoms asymmetrically on AuNCs assembled into 2-D arrays on the surface of a glass substrate by the chemical reduction of Pd ions. Due to the large AuNC or AuNC-Pd/WS 2 Schottky barrier, the plasmon-induced hot electron transfer (PHET) from AuNCs and AuNCs coated with a high concentration of Pd is responsible for the red shift of the absorption spectrum of WS 2 . Introducing a lower concentration of Pd to AuNCs increases the Schottky barrier further due to the formation of the Au-Pd equilibrium Fermi level of lower energy, reducing the efficiency of PHET. The effect of Pd on the Fermi level of AuNCs vanishes at high Pd deposition. Pauli blocking and phase-space filling are responsible for the blue shift of PL of WS 2 on top of AuNCs and AuNCs coated with Pd. The Pauli blocking effect is directly proportional to the PHET efficiency. This explains the significant blue shift of PL of WS 2 after integrating with AuNCs and AuNCs coated with a high concentration of Pd. Additionally, depositing Pd onto AuNCs elongates the lifetime of the hot electrons and enhances the PHET efficiency.

Abnormal expression of dermatan sulfate epimerase (DSE) has been found in many types of cancer, while its expression and biological functions in hepatocellular carcinoma (HCC) progression remains obscure. Here we report that DSE, the enzyme that catalyzes the conversion of chondroitin sulfate (CS) to dermatan sulfate (DS), is a critical mediator of malignant character in HCC, through regulation of CCL5 signaling. DSE mRNA and protein were downregulated frequently in HCC tumors, where these events were associated with advanced tumor stages, metastases, and poor survival. DSE-mediated tumor growth was evaluated in immune-deficient and immune-complement mice models. Restoring DSE expression in HCC cells suppressed tumor growth, as well as decreased IL-1β and CCL5 levels in transplanted tumor tissue. Mechanistic investigations revealed that the expression of DSE altered CCL5 signaling and cell surface binding in HCC cells. Accordingly, DSE suppressed CCL5-induced cell growth, migration, and invasion, whereas silencing of DSE enhanced CCL5-triggered malignant phenotypes. Inhibiting CCR1 activity with BX471 decreased CCL5-induced malignant characters caused by siRNA-mediated knockdown of DSE in HCC cells, establishing the critical role of the CCL5/CCR1 axis in mediating the effects of DSE expression. Taken together, our results suggest that DSE dysregulation contributes to the malignant behavior of HCC cells. This provides novel insight into the significance of DSE in CCL5 signaling and HCC pathogenesis., Competing Interests: None.

A major complication in continuous, ambulatory peritoneal dialysis in patients with end-stage renal disease who are undergoing long-term peritoneal dialysis (PD) is peritoneal fibrosis, which can result in peritoneal structural changes and functional ultrafiltration failure. Human umbilical mesenchymal stem cells (HUMSCs) in Wharton's jelly possess stem cell properties and are easily obtained and processed. This study focuses on the effects of HUMSCs on peritoneal fibrosis in in vitro and in vivo experiments. After 24-hour treatment with mixture of Dulbecco's modified Eagle's medium and PD solution at a 1:3 ratio, primary human peritoneal mesothelial cells became susceptible to PD-induced cell death. Such cytotoxic effects were prevented by coculturing with primary HUMSCs. In a rat model, intraperitoneal injections of 20 mM methylglyoxal (MGO) in PD solution for 3 weeks (the PD/MGO 3W group) markedly induced abdominal cocoon formation, peritoneal thickening, and collagen accumulation. Immunohistochemical analyses indicated neoangiogenesis and significant increase in the numbers of ED-1- and α-smooth muscle actin (α-SMA)-positive cells in the thickened peritoneum in the PD/MGO 3W group, suggesting that PD/MGO induced an inflammatory response. Furthermore, PD/MGO treatment for 3 weeks caused functional impairments in the peritoneal membrane. However, in comparison with the PD/MGO group, intraperitoneal administration of HUMSCs into the rats significantly ameliorated the PD/MGO-induced abdominal cocoon formation, peritoneal fibrosis, inflammation, neoangiogenesis, and ultrafiltration failure. After 3 weeks of transplantation, surviving HUMSCs were found in the peritoneum in the HUMSC-grafted rats. Thus, xenografts of HUMSCs might provide a potential therapeutic strategy in the prevention of peritoneal fibrosis. Significance: This study demonstrated that direct intraperitoneal transplantation of human umbilical mesenchymal stem cells into the rat effectively prevented peritoneal dialysis/methylglyoxal-induced abdominal cocoon formation, ultrafiltration failure, and peritoneal membrane alterations such as peritoneal thickening, fibrosis, and inflammation. These findings provide a basis for a novel approach for therapeutic benefits in the treatment of encapsulating peritoneal sclerosis., (©AlphaMed Press.)