By mimicking natural photosynthesis, generating hydrogen through visible-light-driven splitting of water would be an almost ideal process for converting abundant solar energy into a usable fuel in an environmentally friendly and high-energy-density manner. In a search for efficient photocatalysts that mimic such a function, here we describe a series of cycloplatinated polymer dots (Pdots), in which the platinum complex unit is presynthesized as a comonomer and then covalently linked to a conjugated polymer backbone through Suzuki–Miyaura cross-coupling polymerization. On the basis of our design strategy, the hydrogen evolution rate (HER) of the cycloplatinated Pdots can be enhanced by 12 times in comparison to that of pristine Pdots under otherwise identical conditions. In comparison to the Pt-complex-blended counterpart Pdots, the HER of cycloplatinated Pdots is over 2 times higher than that of physically blended Pdots. Furthermore, enhancement of the photocatalytic reaction time with high eventual hydrogen production and low efficiency rolloff are observed by utilizing the cycloplatinated Pdots as photocatalysts. On the basis of their performance, our cyclometallic Pdot systems appear to be alternative types of promising photocatalysts for visible-light-driven hydrogen evolution.

This article describes the design and synthesis of donor-bridge-acceptor-based semiconducting polymer dots (Pdots) that exhibit narrow-band emissions, ultrahigh brightness, and large Stokes shifts in the near-infrared (NIR) region. We systematically investigated the effect of π-bridges on the fluorescence quantum yields of the donor-bridge-acceptor-based Pdots. The Pdots could be excited by a 488 or 532 nm laser and have a high fluorescence quantum yield of 33% with a Stokes shift of more than 200 nm. The emission full width at half-maximum of the Pdots can be as narrow as 29 nm, about 2.5 times narrower than that of inorganic quantum dots at the same emission wavelength region. The average per-particle brightness of the Pdots is at least 3 times larger than that of the commercially available quantum dots. The excellent biocompatibility of these Pdots was demonstrated in vivo, and their specific cellular labeling capability was also approved by different cell lines. By taking advantage of the durable brightness and remarkable stability of these NIR fluorescent Pdots, we performed in vivo microangiography imaging on living zebrafish embryos and long-term tumor monitoring on mice. We anticipate these donor-bridge-acceptor-based NIR-fluorescent Pdots with narrow-band emissions to find broad use in a variety of multiplexed biological applications.

This study investigated the oral status and dental complications in patients with both anorexia and bulimia nervosa. Results revealed that prolonged periods of dietary restraint in anorexic patients did not result in changes to bacteria associated in dental caries. Furthermore, patients did not have lower decay rates or salivary flow but did have more acidic saliva. Moreover, both groups of patients revealed changes indicative of gingivitis and gingival recession but not necessarily of periodontitis when compared to control subjects. © 1993 by John Wiley & Sons, Inc.

BackgroundThe antiparasitic agent niclosamide has been demonstrated to inhibit the arthropod-borne Zika virus. Here, we investigated the antiviral capacity of niclosamide against dengue virus (DENV) serotype 2 infection in vitro and in vivo.Principle findingNiclosamide effectively retarded DENV-induced infection in vitro in human adenocarcinoma cells (A549), mouse neuroblastoma cells (Neuro-2a), and baby hamster kidney fibroblasts (BHK-21). Treatment with niclosamide did not retard the endocytosis of DENV while niclosamide was unable to enhance the antiviral type I interferon response. Furthermore, niclosamide did not cause a direct effect on viral replicon-based expression. Niclosamide has been reported to competitively inhibit the mTOR (mammalian target of rapamycin), STAT3 (signal transducer and activator of transcription 3), and NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) signaling pathways; however, selective inhibitors of those pathways did not reduce DENV infection. Similar to the vacuolar-type H+-ATPase inhibitor bafilomycin A1, both niclosamide and other protonophores, such as CCCP (carbonyl cyanide m-chlorophenyl hydrazone), and FCCP (carbonyl cyanide-p-trifluoromethoxyphenylhydrazone), effectively reduced endosomal acidification and viral dsRNA replication. Co-administration of a single dose of niclosamide partially decreased viral replication, viral encephalitis, and mortality in DENV-infected ICR suckling mice.SignificanceThese results demonstrate that niclosamide diminishes viral infection by hindering endosomal acidification.

Immune interferon (IFN), also known as IFN-γ, promotes not only immunomodulation but also antimicrobial and anticancer activity. After IFN-γ binds to the complex of IFN-γ receptor (IFNGR) 1-IFNGR2 and subsequently activates its downstream signaling pathways, IFN-γ immediately causes transcriptional stimulation of a variety of genes that are principally involved in its biological activities. Regarding IFN-γ-dependent immunosurveillance, IFN-γ can directly suppress tumorigenesis and infection and/or can modulate the immunological status in both cancer cells and infected cells. Regarding the anticancer effects of IFN-γ, cancer cells develop strategies to escape from IFN-γ-dependent cancer immunosurveillance. Immune evasion, including the recruitment of immunosuppressive cells, secretion of immunosuppressive factors, and suppression of cytotoxic T lymphocyte responses, is speculated to be elicited by the oncogenic microenvironment. All of these events effectively downregulate IFN-γ-expressing cells and IFN-γ production. In addition to these extrinsic pathways, cancer cells may develop cellular tolerance that manifests as hyporesponsiveness to IFN-γ stimulation. This review discusses the potential escape mechanisms from IFN-γ-dependent immunosurveillance in tumorigenesis.