Halogen-bonding boosting the high performance X-ray imaging of organic scintillators.

Organic scintillators with efficient X-ray excited luminescence are essential for medical diagnostics and security screening. However, achieving excellent organic scintillation materials is challenging due to low X-ray absorption coefficients and inferior radioluminescence (RL) intensity. Herein, supramolecular interactions are incorporated, particularly halogen bonding, into organic scintillators to enhance their radioluminescence properties. By introducing heavy atoms (X = Cl, Br, I) into 9,10-bis(4-pyridyl)anthracene (BPA), the formation of halogen bonding (BPA-X) enhances their X-ray absorption coefficient and restricts the molecular vibration and rotation, which boosts their RL intensity. The RL intensity of BPA-Cl and BPA-Br fluorochromes increased by over 2 and 6.3 times compared to BPA, respectively. Especially, BPA-Br exhibits an ultrafast decay time of 8.25 ns and low detection limits of 25.95 ± 2.49 nGy s-1. The flexible film constructed with BPA-Br exhibited excellent X-ray imaging capabilities. Furthermore, this approach is also applicable to organic phosphors. The formation of halogen bonding in bromophenyl-methylpyridinium iodide (PYI) led to a fourfold increase in RL intensity compared to bromophenyl-methyl-pyridinium (PY). It suggests that halogen bonding serves as a promising and effective molecular design strategy for the development of high-performance organic scintillator materials, presenting new opportunities for their applications in radiology and security screening.

Naphthalenediimide/Iodobismuthate Hybrid Heterostructures: Water Resistance and Long-Lived Charge-Separated States.

Organic-inorganic hybrid iodobismuthate perovskites have become promising semiconductive materials for their environmentally friendly and light-harvesting characteristics. However, their low-dimensional bismuth-iodide skeletons result in poor charge-separation efficiency, limiting their application in optoelectronic devices. To address this issue, the donor-acceptor (D-A) heterostructures have been introduced to the iodobismuthate hybrid materials by incorporating an electron-deficient N,N'-bis(4-aminoethyl)-1,4,5,8-naphthalene diimide (NDIEA) as the electron acceptor and organic counterpart. Five naphthalenediimide/iodobismuthate hybrid heterostructures, named (H2NDIEA)1.5·Bi2I9·3DMF (1), H2NDIEA·[Bi2I8(DMF)2]·2DMF (2), (H2NDIEA)2·Bi4I16·2H2O·4MeOH (3), (H2NDIEA)2·Bi4I16·8H2O (4), and [(H2NDIEA)2·Bi6I22]n·4nH2O (5) (DMF = N,N-dimethylformamide), were synthesized. Their crystal structures, water stabilities, charge-separated behaviors, and electrical properties have been studied through experimental and computational investigations. The results revealed that hybrids 3-5 exhibited high water resistance attributed to their tightly packed structures and robust H-bonds between solvent molecules and organic-inorganic supramolecular frameworks. Density functional theory calculations confirmed characteristic type-IIa band alignments of all the five hybrids, facilitating to the photoinduced charge separation. Moreover, the closer contact caused by the strong anion-π interactions between electron donors and acceptors in hybrid 5 leads to the long-lived charge-separated states and improved electrical properties compared to the other hybrids.

Three Semiconductive 1D Naphthalene Diimide/Iodoplumbate Perovskites with High Moisture Tolerance and Long-Lived Charge Separation States.

Low-dimensional inorganic-organic hybrid perovskites with high moisture tolerance and long-lived charge separation states have captured significant attention in the field of optoelectronic devices. To further achieve the relationship between crystal structures and stability, as well as charge separation behaviors, three one-dimensional hybrid perovskites containing electron-deficient naphthalene diimide ammonium (NDIEA) and electron-rich iodoplumbate chains, [(H2NDIEA)Pb2I6]·2DMF (1), [(H2NDIEA)2Pb5I14·(DMF)2]·4DMF (2), and [(HNDIEA)2Pb2I6]·3H2O (3), were synthesized. Crystal structure determinations revealed various synthesis conditions leading to different stacking modes, especially the inorganic lead iodide fraction, which resulted in different water resistances and charge-separated behaviors. The comprehensive analysis found that strong intermolecular interactions (anion-π interactions and π-π interactions), and matching energy levels between protonated NDIEA and iodoplumbate chains, can facilitate the generation of long-lived charge separation states and extraordinary moisture stability, even in the water environment. In addition, the conductivity behavior of 3 was also explored in detail.

CDC25A inhibition suppresses cell proliferation and induces G1/S­phase cell cycle arrest in nasopharyngeal carcinoma.

Nasopharyngeal carcinoma (NPC) is a primary malignancy that originates from the nasopharyngeal region. It has been demonstrated that a decrease in the expression level of cell division cycle gene 25A (CDC25A) suppresses cell viability and induces apoptosis in a variety of different types of cancer. However, at present, the role of CDC25A in NPC has yet to be fully elucidated. Therefore, the aim of the present study was to investigate the role of CDC25A in NPC progression and to explore the potential underlying mechanism. Reverse transcription­quantitative PCR was performed to detect the relative mRNA levels of CDC25A and E2F transcription factor 1 (E2F1). Western blot analysis was subsequently used to determine the expression levels of CDC25A, Ki67, proliferating cell nuclear antigen (PCNA) and E2F1. CCK8 assay was employed to measure cell viability and flow cytometric analysis was employed to analyze the cell cycle. The binding sites between the CDC25A promoter and E2F1 were predicted using bioinformatics tools. Finally, luciferase reporter gene and chromatin immunoprecipitation assays were performed to verify the interaction between CDC25A and E2F1. The results obtained suggested that CDC25A is highly expressed in NPC cell lines and CDC25A silencing was found to inhibit cell proliferation, reduce the protein expression levels of Ki67 and PCNA and induce G1 arrest of NPC cells. Furthermore, E2F1 could bind CDC25A and positively regulate its expression at the transcriptional level. In addition, CDC25A silencing abolished the effects of E2F1 overexpression on cell proliferation and the cell cycle in NPC. Taken together, the findings of the present study showed that CDC25A silencing attenuated cell proliferation and induced cell cycle arrest in NPC and CDC25A was regulated by E2F1. Hence, CDC25A may be a promising therapeutic target for treatment of NPC.

Ginkgolic Acid Suppresses Nasopharyngeal Carcinoma Growth by Inducing Apoptosis and Inhibiting AKT/NF-κB Signaling.

Even though nasopharyngeal carcinoma (NPC) is not common worldwide, it is a major public health burden in endemic areas. Distant metastasis often leads to a poor prognosis for NPC; therefore, new and effective anticancer strategies are needed. Ginkgolic acid (GA) is small-molecule compound existing in Ginkgo biloba that has various biologically relevant activities, including antitumor properties; however, its effects and mechanism of action in NPC are unknown. The effects of GA on NPC and such underlying mechanisms were investigated using 5-8F and CNE2 cells and NP69 human immortalized nasopharyngeal epithelial cells in this study. Moreover, the xenograft models were built to examine GA's effection in vivo. GA treatment decreased the survival and invasive capacity of 5-8F and CNE2 and induced their apoptosis, which varied with dose; this was accompanied by downregulation of B cell lymphoma (Bcl)2, upregulation of Bcl2-associated X protein, and activation of poly-ADP ribose polymerase, and caspase-9/-3. G0/G1 phase arrest was induced by GA in NPCs. It also reduced the expression of cyclin-dependent kinase 6 and its regulators cyclin D2 and cyclin D3. GA inhibited the activation of protein kinase B/nuclear factor signaling; this effect was potentiated with GA and 5-fluorouracil (5-FU), which also enhanced 5-FU-induced apoptosis. In summary, GA may be effective as an adjuvant to conventional chemotherapy drugs in preventing the progression of NPC.

Synthesis, Transfer, and Properties of Layered FeTe2 Nanocrystals.

Different from layered two-dimensional (2D) transition metal dichalcogenides (TMDs), iron dichalcogenides crystallize in the most common three-dimensional pyrite or marcasite structures. Layered iron dichalcogenides are rarely reported and little is known about their structures and properties. Here, layered hexagonal phase iron ditelluride FeTe2 (h-FeTe2) nanocrystals are grown on mica by atmospheric pressure chemical vapor deposition (APCVD) method and are fully characterized by various methods. Like other 2D layered TMD materials, the FeTe2 nanoflakes exhibit regular hexagon, half hexagon, or triangle shapes with a controllable thickness of 6-95 nm and lateral length from a few to tens of micrometers. A simple and effective method is used to transfer the FeTe2 nanoflakes from the mica substrate onto any other substrates without quality deterioration by using polystyrene (PS) as a support polymer, which can also be operated in ethanol or ethylene glycol in a glovebox to avoid contact with water and air. Temperature-dependent electrical transport demonstrates that the FeTe2 nanoflake is a semiconductor with a variable range hopping (VRH) conduction, and its nonsaturated linear magnetoresistance (MR) reaches up to 10.4% under magnetic field of 9 T at 2 K, both probably due to its structure disorders. No signature of magnetic ordering is observed down to 2 K. The CVD growth of this layered FeTe2 represents an addition to the extensive library of 2D materials, particularly iron chalcogenides or alloys. Synthesis, properties, and even doping of phase pure h-FeTe2 call for further study in the future.

In vivo and in vitro investigation of KIN-193 anti-tumor effects on nasopharyngeal carcinoma.

BACKGROUND: The PI3K signaling pathway has important roles in nasopharyngeal carcinoma (NPC) tumorigenesis and progression. Inhibition of the PI3K pathway effectively inhibits NPC growth; however, the toxic side effects of PI3K inhibitors limit their clinical application. This study aimed to investigate the effects of the selective PI3K p110ß inhibitor, KIN-193, on proliferation and apoptosis in NPC. METHODS: Cell counting Kit-8, colony formation, flow cytometry, and western blotting experiments were conducted in CNE2Z NPC cells treated with various concentrations of KIN-193 to determine its effects on cell proliferation and apoptosis. Additionally, xenograft tumor models were established in nude mice and the anti-tumor effects of KIN-193 and the classical P110α inhibitor, PIK-75, compared in vivo. Hematoxylin-eosin (HE) staining, immunohistochemical staining, and western blotting were also conducted to detect the protein expression levels of proliferation and apoptosis markers. RESULTS: The results of both in vivo and in vitro experiments demonstrated that KIN-193 can dramatically inhibit cell proliferation and promote apoptosis in NPC. In addition, KIN-193 showed stronger antitumor effects, with fewer side effects, than PIK-75 in vivo. CONCLUSIONS: We conclude that KIN-193 exhibits considerable anti-tumor effects in NPC.

Screening and identification of potential target genes in head and neck cancer using bioinformatics analysis.

Head and neck cancer (HNC) is the sixth most common cancer worldwide. Recent studies on the pathogenesis of HNC have identified some biochemical associations of this disease, but the molecular mechanisms are not clear. To explore the genetic alterations in head and neck tumors, to identify new high-specificity and high-sensitivity tumor markers, and to investigate potentially effective therapeutic targets, in silico methods were used to study HNC. The GSE58911 microarray dataset was downloaded from the Gene Expression Omnibus online database to identify potential target genes in the carcinogenesis and progression of HNC. Differentially expressed genes (DEGs) were identified and functional enrichment analysis was performed. In addition, a protein-protein interaction network was also constructed, and gene analysis was undertaken using Search Tool for the Retrieval of Interacting Genes and Cytoscape. A total of 648 differentially expressed genes were identified. Kyoto Encyclopedia of Genes and Genomes pathway and Gene Ontology functional enrichment analysis of DEGs included muscle system process, extracellular matrix organization, actin binding, structural molecule activity, structural constituent of muscle, extracellular region part, ECM-receptor interaction, amoebiasis, focal adhesion, drug metabolism-cytochrome P450, and chemical carcinogenesis. There were 26 hub genes identified and biological process analysis revealed that these genes were mainly enriched in extracellular matrix organization, serine-type endopeptidase activity, extracellular matrix, and complement and coagulation cascades. Survival analysis revealed that interleukin (IL)-8 (C-X-C motif chemokine ligand 8), IL1B, and serpin family A member 1 may be involved in the carcinogenesis of HNC. In summary, the DEGs and hub genes identified in the present study may increase understanding of the molecular mechanisms of development of HNC and provide potential target genes for clinical diagnosis and targeted therapy.

PD­L1 promotes head and neck squamous cell carcinoma cell growth through mTOR signaling.

Programmed death­ligand 1 (PD­L1), an immune co­stimulatory molecule, is expressed on various cancer cells and the surface of immune cells. Its overexpression on tumor cells suppresses the immune response to promote tumor cell immune escape. The present study demonstrated that PD­L1 was critical in head and neck squamous cell carcinoma (HNSCC) carcinogenesis. Immunohistochemical analysis of HNSCC tissue microarrays revealed that PD­L1 was overexpressed in tumor tissue, and its expression increased as tumor malignancy progressed (from grade I to IV). Subsequently, the expression of PD­L1 was knocked down or overexpressed in the HNSCC cell lines Cal­27 and Fadu. It was demonstrated that PD­L1 significantly induced HNSCC cell proliferation and colony forming ability. Cell proliferation was also promoted in Cal­27 cell xenograft BALB/c nude mice. In addition, it was determined by western blotting that the PD­L1­mediated increase in HNSCC cell proliferation may have been associated with the activation of mammalian target of rapamycin (mTOR) signaling pathway. Furthermore, mTOR inhibitor (rapamycin) prevented the increase in proliferation. Based on these results, it was concluded that PD­L1 promoted cell proliferation of HNSCC cells through mTOR signaling, and blocking PD­L1 may be conducive in HNSCC therapy.