Vacuum-Deposited Organometallic Halide Perovskite Light-Emitting Devices

In this work, a sequential vacuum deposition process of bright, highly crystalline, and smooth methylammonium lead bromide and phenethylammonium lead bromide perovskite thin films are investigated and the first vacuum-deposited organometallic halide perovskite light-emitting devices (PeLEDs) are demonstrated. Exceptionally low refractive indices and extinction coefficients in the emission wavelength range are obtained for these films, which contributed to a high light out-coupling efficiency of the PeLEDs. By utilizing these perovskite thin films as emission layers, the vacuum-deposited PeLEDs exhibit a very narrow saturated green electroluminescence at 531 nm, with a spectral full width at half-maximum bandwidth of 18.6 nm, a promising brightness of up to 6200 cd/m², a current efficiency of 1.3 cd/A, and an external quantum efficiency of 0.36%

Genome and Infection Characteristics of Human Parechovirus Type 1: The Interplay between Viral Infection and Type I Interferon Antiviral System

<div><p>Human parechoviruses (HPeVs), members of the family <i>Picornaviridae</i>, are associated with severe human clinical conditions such as gastrointestinal disease, encephalitis, meningitis, respiratory disease and neonatal sepsis. A new contemporary strain of HPeV1, KVP6 (accession no. KC769584), was isolated from a clinical specimen. Full-genome alignment revealed that HPeV1 KVP6 shares high genome homology with the German strain of HPeV1, 7555312 (accession no. FM178558) and could be classified in the clade 1B group. An intertypic recombination was shown within the P2-P3 genome regions of HPeV1. Cell-type tropism test showed that T84 cells (colon carcinoma cells), A549 cells (lung carcinoma cells) and DBTRG-5MG cells (glioblastoma cells) were susceptible to HPeV1 infection, which might be relevant clinically. A facilitated cytopathic effect and increased viral titers were reached after serial viral passages in Vero cells, with viral genome mutation found in later passages. HPeV1 is sensitive to elevated temperature because 39C incubation impaired virion production. HPeV1 induced innate immunity with phosphorylation of interferon (IFN) regulatory transcription factor 3 and production of type I IFN in A549 but not T84 cells. Furthermore, type I IFN inhibited HPeV1 production in A549 cells but not T84 cells; T84 cells may be less responsive to type I IFN stimulation. Moreover, HPeV1-infected cells showed downregulated type I IFN activation, which indicated a type I IFN evasion mechanism. The characterization of the complete genome and infection features of HPeV1 provide comprehensive information about this newly isolated HPeV1 for further diagnosis, prevention or treatment strategies.</p></div

Baseline characteristics of the patients.

a<p>Data presented as mean +/− standard deviation.</p><p>AFP: alpha-fetoprotein, CLIP: Cancer of the Liver Italian Program, BCLC: Barcelona-Clinic Liver Cancer.</p

Adverse events of patients who received HAIC according to NCI-CTC AE grading.

<p>Adverse events of patients who received HAIC according to NCI-CTC AE grading.</p

HPeV1 KVP6 full-genome analysis.

<p><b>(A)</b> SimPlot analysis of complete genome sequence of HPeV1 KVP6 with other strains or types of HPeV genomes. <b>(B)</b> Phylogenetic analysis of HPeV1 KVP6 full-length polypeptide with other HPeVs. <b>(C)</b> Phylogenetic analysis of VP1 nucleotide fragment of HPeV KVP6 with other strains of HPeV1. The clade of HPeV1 is indicated. The genome or protein accession number in GenBank is indicated.</p

HPeV1 downregulates type I IFN activity.

<p><b>(A)</b> A549 and T84 cells (3×10⁵) were infected with mock or HPeV1 at MOI = 5 for 6 h, then treated with IFNβ (1000 U/ml) for 18 h; untreated cells are indicated as ctrl. Immunoblotting of levels of phospho-STAT1 and total STAT1 in whole cell extracts. HPeV1 VP0 indicates viral infection and β-actin is a loading control. <b>(B)</b> Interferon-stimulated response element (ISRE) reporter assay was performed in A549 and T84 cells (3×10⁵) transfected with ISRE-luciferase reporter plasmids (400 ng) and control vector pRL-TK (40 ng) for 24 h, then infected with HPeV1 for 6 h. After 24 h of IFNβ (1000 U/ml) stimulation, ISRE luciferase activity was measured by dual-luciferase assay and <b>(C)</b> RT-qPCR of mRNA expression. Data are mean ± SD of at least 3 independent experiments. Student <i>t</i> test, * <i>p</i><0.05, *** <i>p</i><0.005.</p

Comparison of the overall survival rate between the HAIC and symptomatic treatment group.

<p>The HAIC group had significantly better survival than the symptomatic treatment group (P<0.001).</p

Hepatitis B reactivation during systemic cytotoxic chemotherapy in solid tumor patients with a baseline HBV DNA level equal to or more than 2000 IU/mL and using prophylactic entecavir and lamivudine.

<p>Hepatitis B reactivation during systemic cytotoxic chemotherapy in solid tumor patients with a baseline HBV DNA level equal to or more than 2000 IU/mL and using prophylactic entecavir and lamivudine.</p

Demographic data of solid tumor patients undergoing systemic cytotoxic chemotherapy and using prophylactic entecavir or lamivudine.

<p>^<i>a</i>Entecavir group included 6 head and neck cancers, 4 gynecologic cancers, and 7 genitourinary cancers. Lamivudine group included 31 head and neck cancers, 15 gynecologic cancers, and 11 genitourinary cancers.</p><p>^<i>b</i>SCC: systemic cytotoxic chemotherapy</p><p>^<i>c</i>ALT: alanine aminotransferase.</p><p>^<i>d</i>INR: international normalized ratio.</p><p>Demographic data of solid tumor patients undergoing systemic cytotoxic chemotherapy and using prophylactic entecavir or lamivudine.</p

Cell tropism of HPeV1.

<p>Vero, T84, A549, DBTRG-5MG, BHK21, HeLa and J774A.1 cells at 2×10⁵ were infected with HPeV1 for 6 h at multiplicity of infection (MOI) = 1; HPeV1 VP0 was detected by immunofluorescence assay with anti-VP0 antibody; images show the red fluorescence of VP0 staining in susceptible cell types. DAPI staining indicated cell nucleus.</p