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Structural variations of lead halide perovskites (LHPs) upon light illumination play an important role in their photovoltaic applications. However, density functional theory (DFT)-based simulations have often been performed to unveil the nature of defects in LHPs without light illumination. So far, the nature of traps in LHPs triggered by the light remains largely unexplored. In this work, hole traps induced by the halogen interstitial in LHPs are studied by combining DFT and time-dependent DFT approaches, the latter of which treats electron-hole and electron-nuclei interactions on the same footing. Both a semilocal exchange functional and hybrid functional are adopted to relax the ground-state and excited-state geometries followed by the calculations of energy levels of hole traps. The effect of the self-interaction corrections on the light-triggered geometric deformation and the electronic structure of hole traps is analyzed. Relaxation energies that correspond to the light-triggered geometric deformation are also calculated with different functionals. The relationship between the hole traps and light-triggered geometric variations are then explored.

The role of organic cations in A-sites of lead halide perovskites (LHPs) on carrier dynamics has been debated in an effort to understand the remarkable properties in these materials. However, the change of A-site species in LHPs often leads to the variation of crystalline phases at room temperature. Herein, we combine density functional theory (DFT) and time-dependent DFT methods to study electron traps in CH

The defect properties at surfaces or grain boundaries of metal halide perovskites are largely unexplored due to the complexity of surface structures stirred by the rotational A-site cations with varied dipole moments. Using a combination of density functional theory (DFT) and time-dependent DFT methods, we study the nature of iodine vacancies at the surfaces of lead iodide perovskites (APbI

NUT carcinoma (NC) is a rare, highly invasive and fatal tumor and often misdiagnosed. It typically arises from the mediastinum and midline organs and has complicated pathogenesis and poor outcome. Genetically, its pathogenesis is related to a chromosomal rearrangement involving the NUTM1 gene. In most cases, the main oncoprotein is BRD4-NUT with a translocation between NUTM1 and BRD4 genes, but in a few cases, the oncoprotein is BRD3-NUT, or NSD3-NUT. Studies have shown that the histone hyperacetylation and BRD4 hyperphosphorylation may lead to the activation of cancer circuits. Abnormal production of microRNA, inactivation of tumor suppressor genes and abnormal activation of several signaling pathways are proposed as potential mechanisms underlying the pathogenesis of NC. Currently, there is no consensus on its standard treatment for NC. Extent of surgical resection with negative margins, initial radiotherapy and part of chemotherapy regimens may significantly associated with the improvement of progression-free survival (PFS) rate and overall survival (OS) rate. Some bromodomain and extraterminal inhibitors (BETis) have shown encouraging results in the clinical trials on NC, but delayed drug resistance is still an important issue that needs to be resolved. Histone deacetylase inhibitors are also found to possess the potential in the treatment of NC. Herein, we summarize recent advances in the pathogenesis and treatment of NC.

Background The ginsenosides have been reported to possess a variety of biological activities. Synthesized from the ginsenoside Protopanaxadiol (PPD), the octanone Pseudoginsengenin DQ (PDQ) may have stronger pharmacological effects as a secondary ginsenoside. Nevertheless, its antitumor activity and molecular mechanism against hypopharyngeal cancer cells remains unclear. Methods Cell Counting Kit-8, cell cycle assay and cell apoptosis assay were conducted to detect FADU cells proliferation, cell phase and apoptosis. The interactions between PDQ and HIF-1α were investigated by a molecular docking study. The expression of HIF-1α, GLUT1, apoptosis related proteins was tested by western blotting, direct stochastic optical reconstruction microscopy (dSTORM) and qRT-PCR. Glucose uptake assay was used to assess the glucose uptake capacity of FADU cells. Results PDQ was found to suppress the proliferation, reduce glucose uptake, induce the cell cycle arrest and apoptosis of FaDu cells. Molecular docking study demonstrated that PDQ could interact with the active site of HIF-1α. PDQ decreased the expression and mRNA levels of HIF-1α and its downstream factor GLUT1. Moreover, dSTORM results showed that PDQ reduced GLUT1 expression on the cell membrane but also inhibited its clustering. Conclusion Our work elucidated that the antitumor effect of PDQ is related to its downregulation of HIF-1α-GLUT1 pathway, suggesting that PDQ could be a potential therapeutic agent for hypopharyngeal cancer treatment.

Laryngeal carcinoma (LC) is one of the most prevalent malignant tumors in the head and neck area. Due to its high morbidity and mortality, LC poses a serious threat to human life and health. Even with surgical removal, some patients were not sensitive to radiotherapy or experienced transfer or recurrence. 20(s)-Protopanaxadiol (PPD), a natural product from Panax ginseng, has been reported to have cytotoxic effects against several cancer cell lines. However, whether it can improve the radiation sensitivity and the underlying mechanism of PPD's sensitization effect is still unknown. Herein, from in vitro and in vivo experiments, we found that the combination of PPD and radiation not only significantly inhibited proliferation and induced apoptosis, but also suppressed the tumor growth in mouse models. These findings confirmed the role of PPD in enhancing the sensitivity of radiotherapy. Moreover, our work showed that the expression levels of mTOR and its downstream effectors decreased remarkably after PPD addition when compared to radiation only. This result suggested that PPD's excellent synergistic effects with radiation might be associated with the down-regulation of the mTOR signaling pathway in Hep-2 cells.

Eukaryotic translation initiation factor (eIF) 4E is a valuable marker in cancer prognostics in many human cancers. Silencing eIF4E via delivery of siRNA may be able to overcome chemoresistance. Cisplatin, used as a first-line anti-cancer reagent, has been widely accepted for its great success in clinical applications but it is restricted due to severe side effects such as nephrotoxicity, peripheral neuropathy, and hearing loss. Moreover, platinum drug resistance is a major obstacle to its use. Platinum(iv) prodrugs (denoted as Pt(iv)) which could be reduced to Pt(ii) by various reductants, including mercaptan and glutathione, within cancer cells have very limited toxicity and might overcome platinum resistance because of their chemical inertness. Moreover, combinational therapies that could sensitize the cancer cells to Pt drugs have received great attention nowadays around the world. Here we report a simple and effective upconversion nanoparticle carrier system loaded with both eIF4E siRNA and Pt(iv). We find that this theranostic system could sensitize laryngeal cancer cells to cisplatin based chemotherapy and allow bioimaging both in vitro and in vivo.

In this work, 20( S )-protopanaxadiol (PPD)-loaded polycaprolactone (PCL) nanofibres were successfully fabricated by the electrospinning technique using Tween 80 as a solubilizer. Firstly, smooth and continuous nanofibres were collected using suitable solvents and appropriate spinning conditions. Secondly, nanofibre mats were characterized by scanning electron microscopy, thermogravimetric (TG) analysis, Fourier transform infrared spectroscopy and mechanical testing. Finally, nanofibrous membranes were evaluated using water contact angle, in vitro drug release, biodegradation test, in vitro and in vivo anti-tumour activity and cell apoptosis assay. Scanning electron microscopic observations indicated that the diameter of the drug-loaded nanofibres increased with the increase of drug concentration. TG analysis and mechanical test showed that nanofibres were equipped with great thermal and mechanical properties. Biodegradation test exhibited that the structure of fabricated nanofibres had a certain degree of change after 15 days. An in vitro release study showed that PPD from drug-loaded nanofibres could be released in a sustained and prolonged mode. The cytotoxic effect of drug-loaded nanofibre mats examined on human laryngeal carcinoma cells (Hep-2 cells) demonstrated that the prepared nanofibres had a remarkable anti-tumour effect. Meanwhile, the drug-loaded fibre mats showed a super anti-tumour effect in an in vivo anti-tumour study. All in all, PCL nanofibres could be a potential carrier of PPD for cancer treatment.

To assess the effect of CPAP therapy on sleep quality and quality of life in patients with moderate or severe OSAHS.Seventy-two patients diagnosed as OSAHS by polysomnography (PSG) were assigned to receive CPAP therapy for 3 months. At baseline and three months after treatment patients underwent polysomnography (PSG). Analyze the results of PSG, sleep quality, excessive daytime sleepiness, quality of life and the general well-being.The lowest average oxygen saturation and the average blood oxygen saturation improved significantly after CPAP therapy, and the longest sleep apnea time and AHI decreased obviously (P0.01). Except body pain, the other seven dimensions of SF-36 improved obviously (P0.01); ESS, PSQI and GWB also improved (P0.05).For patients with moderate or severe OSAHS, CPAP therapy can obviously improve the sleep quality, excessive daytime sleepiness, improve patients' life quality and the general well-being.

The mammalian target of rapamycin (mTOR) kinase forms two multiprotein complexes, mTORC1 and mTORC2, which regulate cell growth, survival, and autophagy. Allosteric inhibitors of mTORC1, such as rapamycin, have been extensively used to study tumor cell growth, proliferation, and autophagy but have shown only limited clinical utility. Here, we describe AZD8055, a novel ATP-competitive inhibitor of mTOR kinase activity, against all class I phosphatidylinositol3-kinase (PI3K) and other members of the PI3K-like kinase family. The study was to determine the effect of AZD8055 on proliferation and apoptosis on Hep-2, a human laryngeal cancer cell line and to investigate the underlying mechanism(s) of action. Hep-2 cells were treated with AZD8055 for 24, 48 or 72 h. MTT was used to determine cell proliferation. Rhodamine 123 and TUNEL staining were used to determine mitochondrial membrane potential and cell apoptosis analyzed by fluorescence-activated cell sorting (FACS). Protein expressions were examined by western blotting. Treatment with AZD8055 inhibited proliferation and induced apoptosis in Hep-2 cells in a dose- and time-dependent manner. During the prolonged treatment with AZD8055, AZD8055 inhibits the mammalian target of rapamycin mTOR. Further experiments showed which signaling cascade p-4EBP1 and substrate EIF4E as well as downstream proteins were down regulated. Furthermore, our study showed that the expression profiles of various BH3-only proteins including Bid, Bad, and Bim, apoptosis regulatory protein cleaved caspase3 was up regulated in a time-dependent manner in Hep-2 cells treated with AZD8055. Thus, in vitro, AZD8055 potently inhibits proliferation and induces apoptosis in head and neck squamous cell carcinoma.

A 12-year-old boy presented to our emergency department after being shot in the face. A computed tomographic scan revealed a bullet through the posterolateral wall of the maxillary sinus into the right infratemporal area, just adjacent to the skull base. We elected transantral approach with the help of endoscopy and C-arm. The bullet was successfully removed. Little is known on the best strategy for removing the infratemporal foreign body. Our experience in this case provides a safe and effective way for such injury.