Three Isomeric Non-Fullerene Acceptors Comprising a Mono-Brominated End-Group for Efficient Organic Solar Cells.

Non-fullerene acceptors (NFAs) carrying a 1,1-dicyanomethylene-3-indanone (IC) end-group are the most powerful ones to boost the power conversion efficiency of organic solar cells (OSCs). However, the well-known Knoevenagel condensation of the mono-halogenated IC end-group will result in an NFA isomeric effect, a chemical issue that needs to be addressed. Herein, facile preparations and separations of three well-defined mono-brominated isomers BTzIC-2Br-δ, BTzIC-2Br-γ, and BTzIC-2Br-δγ via column chromatography with a well-chosen mixing solvent were demonstrated for Knoevenagel condensation, and their structures were verified by NMR spectra and matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF) mass spectra. It is the first time that an asymmetric isomer BTzIC-2Br-δγ is reported, and the regioisomeric effect on optoelectronic properties can be investigated based on all three isomers. Moreover, the single-crystal structure was successfully achieved for the symmetric molecule BTzIC-2Br-γ. With benzodithiophene (BDT)-free PFBT4T-T20 as an easily accessible and low-cost polymer donor, the three isomers could show differentiated device performances, with a power conversion efficiency order of BTzIC-2Br-γ (16.00%) > BTzIC-2Br-δγ (15.81%) > BTzIC-2Br-δ (15.29%). The best efficiency of 16.00% achieved with BTzIC-2Br-γ is among the highest ones for binary OSCs based on the low-cost BDT-free donors. The facile and complete synthesis of isomeric NFAs with mono-halogenated IC end-groups would promote the elucidation of the structure-property relationship.

Identification of LINC00654-NINL Regulatory Axis in Diffuse Large B-Cell Lymphoma In Silico Analysis.

Background: The long non-coding RNA (lncRNA)-mRNA regulation network plays an important role in the development of diffuse large B-cell lymphoma (DLBCL). This study uses bioinformatics to find an innovative regulation axis in DLBCL that will provide a positive reference for defining the mechanism of disease progression. Methods: Batch Cox regression was used to screen prognosis-related lncRNAs, and a random forest model was used to identify hub lncRNA. The clinical value of the lncRNA was evaluated and Spearman correlation analysis was used to predict the candidate target genes. Gene Oncology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment were used to define the biological function of the lncRNA. A batch Cox regression model, expression validation, and Spearman correlation analysis were used to select the best downstream target genes. The expression and prognostic value validation of this gene was conducted using public data. Gene Set Enrichment Analysis (GSEA) was performed to explore potential mechanisms for this gene in DLBCL. Results: LINC00654 was identified as the hub lncRNA and 1443 mRNAs were selected as downstream target genes of the lncRNA. The target genes were enriched in the regulation of GTPase and Notch signaling pathways. After validation, the ninein-like (NINL) gene was selected as the potential target of LINC00654 and the LINC00654-NINL axis was constructed. Patients with better responses to therapy were shown to have high NINL gene expression (p-value = 0.036). NINL also had high expression in the DB cell line and low expression in the OCILY3 cell line. Survival analysis showed that high NINL expression was a risk factor for overall survival (OS) and disease-specific survival (DSS) within older patients and those with advanced-stage cancer. GSEA results showed that NINL may be involved in neutrophil-mediated immunity and NF-κB signaling. Conclusion: This study identified a novel LncRNA00654-NINL regulatory axis in DLBCL, which could provide a favorable reference for exploring the possible mechanisms of disease progression.

Expression of MAGE--A restricted to testis and ovary or to various cancers in dogs.

Expression of MAGE-A protein, a family of cancer/testis antigens, was investigated in normal and neoplastic canine tissues. Immunohistochemical analysis of cross-reactions between a mouse anti-human MAGE-A proteins including MAGE-A1, -A2, -A3, -A4, -A6, -A10, and -A12 monoclonal antibody and canine proteins, showed positive immunoreactivity only in testicular spermatogonia and spermatocytes, and ovary oocytes. The immunoreaction was negative in all other tissues tested, including normal tissues of the skin, gingiva, muscle, adipose, connective, salivary gland, lymph node, intestinal mucosa, mammary gland, liver, cartilage, oviduct, endometrium, cerebrum and cerebellum. Use of a scoring system in the investigated tumors showed positive immunoreactivity in 75% (21/28) of melanomas including oral, cutaneous, eyelid, and interdigital melanomas; in 68.7% (22/32) of oral and nasal tumors; in 52.5% (21/40) discrete round cell tumors; and in 40.5% (15/37) of soft tissue sarcomas. Different tumor types also showed large difference in percentage of MAGE-A expression. Although oral squamous cell carcinomas, multicentric lymphomas and extraosseous osteosarcomas showed no expression, overexpression occurred in oral melanomas (81.82%, 18/21), malignant nasal tumors (100%, 3/3) and in transmissible venereal tumors (100%, 10/10). Based on the characteristic expression of MAGE-A in canine germ cells and in various neoplasms, MAGE-A has potential use as an indicator of malignancy but is probably unsuitable for strictly diagnostic purposes (i.e., diagnosis of tumor type).

Recruitment of Rpd3 to the telomere depends on the protein arginine methyltransferase Hmt1.

In the yeast Saccharomyces cerevisiae, the establishment and maintenance of silent chromatin at the telomere requires a delicate balance between opposing activities of histone modifying enzymes. Previously, we demonstrated that the protein arginine methyltransferase Hmt1 plays a role in the formation of yeast silent chromatin. To better understand the nature of the Hmt1 interactions that contribute to this phenomenon, we carried out a systematic reverse genetic screen using a null allele of HMT1 and the synthetic genetic array (SGA) methodology. This screen revealed interactions between HMT1 and genes encoding components of the histone deacetylase complex Rpd3L (large). A double mutant carrying both RPD3 and HMT1 deletions display increased telomeric silencing and Sir2 occupancy at the telomeric boundary regions, when comparing to a single mutant carrying Hmt1-deletion only. However, the dual rpd3/hmt1-null mutant behaves like the rpd3-null single mutant with respect to silencing behavior, indicating that RPD3 is epistatic to HMT1. Mutants lacking either Hmt1 or its catalytic activity display an increase in the recruitment of histone deacetylase Rpd3 to the telomeric boundary regions. Moreover, in such loss-of-function mutants the levels of acetylated H4K5, which is a substrate of Rpd3, are altered at the telomeric boundary regions. In contrast, the level of acetylated H4K16, a target of the histone deacetylase Sir2, was increased in these regions. Interestingly, mutants lacking either Rpd3 or Sir2 display various levels of reduction in dimethylated H4R3 at these telomeric boundary regions. Together, these data provide insight into the mechanism whereby Hmt1 promotes the proper establishment and maintenance of silent chromatin at the telomeres.

Proteomic analysis of interactors for yeast protein arginine methyltransferase Hmt1 reveals novel substrate and insights into additional biological roles.

Protein arginine methylation is a PTM catalyzed by an evolutionarily conserved family of enzymes called protein arginine methyltransferases (PRMTs), with PRMT1 being the most conserved member of this enzyme family. This modification has emerged to be an important regulator of protein functions. To better understand the role of PRMTs in cellular pathways and functions, we have carried out a proteomic profiling experiment to comprehensively identify the physical interactors of Hmt1, the budding yeast homolog for human PRMT1. Using a dual-enzymatic digestion linear trap quadrupole/Orbitrap proteomic strategy, we identified a total of 108 proteins that specifically copurify with Hmt1 by tandem affinity purification. A reverse coimmunoprecipitation experiment was used to confirm Hmt1's physical association with Bre5, Mtr4, Snf2, Sum1, and Ssd1, five proteins that were identified as Hmt1-specific interactors in multiple biological replicates. To determine whether the identified Hmt1-interactors had the potential to act as an Hmt1 substrate, we used published bioinformatics algorithms that predict the presence and location of potential methylarginines for each identified interactor. One of the top hits from this analysis, Snf2, was experimentally confirmed as a robust substrate of Hmt1 in vitro. Overall, our data provide a feasible proteomic approach that aid in the better understanding of PRMT1's roles within a cell.

Protein arginine methylation facilitates cotranscriptional recruitment of pre-mRNA splicing factors.

Cotranscriptional recruitment of pre-mRNA splicing factors to their genomic targets facilitates efficient and ordered assembly of a mature messenger ribonucleoprotein particle (mRNP). However, how the cotranscriptional recruitment of splicing factors is regulated remains largely unknown. Here, we demonstrate that protein arginine methylation plays a novel role in regulating this process in Saccharomyces cerevisiae. Our data show that Hmt1, the major type I arginine methyltransferase, methylates Snp1, a U1 small nuclear RNP (snRNP)-specific protein, and that the mammalian Snp1 homolog, U1-70K, is likewise arginine methylated. Genome-wide localization analysis reveals that the deletion of the HMT1 gene deregulates the recruitment of U1 snRNP and its associated components to intron-containing genes (ICGs). In the same context, splicing factors acting downstream of U1 snRNP addition bind to a reduced number of ICGs. Quantitative measurement of the abundance of spliced target transcripts shows that these changes in recruitment result in an increase in the splicing efficiency of developmentally regulated mRNAs. We also show that in the absence of either Hmt1 or of its catalytic activity, an association between Snp1 and the SR-like protein Npl3 is substantially increased. Together, these data support a model whereby arginine methylation modulates dynamic associations between SR-like protein and pre-mRNA splicing factor to promote target specificity in splicing.

Quantum yield of conversion of the photoinitiator camphorquinone.

The primary absorber in dental resins is the photoinitiator, which starts the photo polymerization process. We studied the quantum yield of conversion of camphorquinone (CQ), a blue light photoinitiator, in dental resin composites using a LED lamp (3M FreeLight) and a Quartz Tungsten Halogen (QTH) lamp (VIP) as the light curing units at five different irradiances. The molar extinction coefficient, epsilon(469), of CQ was 46+/-2 cm(-1)/(mol/L) at 469 nm. The reciprocity of irradiance and exposure time holds for changes of CQ absorption coefficient, that is, irradiance x exposure time (=radiant exposure)=constant. Both LED and QTH lamps yielded the same curing threshold (the radiant exposure when CQ absorption drops to 1/e) and the same quantum yield conversion under different irradiances. In our dental resin formulation (0.7 wt.% CQ with reducing agents 0.35 wt.% dimethylaminoethyl methacrylate (DMAEMA) and 0.05 wt.% butylated hydroxytoluene (BHT)) the quantum yield was measured as 0.07+/-0.01 CQ conversion per absorbed photon.

Preparation and characterization of polyurethane optical phantoms.

We describe a method for the preparation of a polyurethane phantom to simulate the optical properties of biologic tissues at two wavelengths in the visible and near-infrared spectral range. We characterize the addition of added molecular absorbers with relatively narrow absorption bands [full width at half maximum (FWHM) 32 and 76 nm for Epolight 6084 and 4148, respectively] for independent absorption at 690 nm for absorption up to 5 cm(-1), and 830 nm for absorptions up to 3 cm(-1). Absorption by both dyes is linear with concentration in these respective regions and is consistent in polyurethane both before and after curing. The dyes are stable over long durations with no more than 4% change. The absorption of visible light by polyurethane decreases with time and is stable by one year with a drop of 0.03+/-0.003 cm(-1) from 500 to 830 nm. The scattering properties are selected by the addition of TiO2 particles to the polyurethane, which we functionally describe for the 690- and 830-nm wavelengths as related to the weight per volume. We demonstrate that the variation in absorption and scattering properties for large batch fabrication (12 samples) is +/-3%. The optical properties of the phantoms have not significantly changed in a period of exceeding one year, which makes them suitable for use as a reference standard.

Fluorescence anisotropy studies of molecularly imprinted polymers.

A molecularly imprinted polymer (MIP) is a biomimetic material that can be used as a biochemical sensing element. We studied the steady-state and time-resolved fluorescence and fluorescence anisotropy of anthracene-imprinted polyurethane. We compared MIPs with imprinted analytes present, MIPs with the imprinted analytes extracted, MIPs with rebound analytes, non-imprinted control polymers (non-MIPs) and non-MIPs bound with analytes to understand MIP's binding behaviour. MIPs and non-MIPs had similar steady-state fluorescence anisotropy in the range 0.11-0.24. Anthracene rebound in MIPs and non-MIPs had a fluorescence lifetime of tau = 0.64 ns and a rotational correlation time of phi(F) = 1.2-1.5 ns, both of which were shorter than that of MIPs with imprinted analytes present (tau = 2.03 ns and phi(F) = 2.7 ns). The steady-state anisotropy of polymer solutions increased exponentially with polymerization time and might be used to characterize the polymerization extent in situ.

A pilot study of a simple photon migration model for predicting depth of cure in dental composite.

OBJECTIVES: The purpose of this study was to build a photo migration model to calculate the radiant exposure (irradiancextime) in dental composite and to relate the radiant exposure with extent of cure using polymer kinetics models. METHODS: A composite (Z100, Shade A2) cylinder (21 mm diameter by 15 mm deep) was cured with a tungsten-halogen lamp emitting 600 mW/cm2, 1 mm above the composite for 60s. For each of the 2x1 mm grids along the longitudinal cross section (diameter versus depth), the degree of conversion (DC) and hardness (KHN) were measured to construct the curing extent distribution. The inverse adding-doubling method was used to characterize the optical properties of the composite for the Monte Carlo model simulating the photon propagation within the composite cylinder. The calculated radiant exposure (H) distribution along the cross section was related to the curing extent DC/DC(max) distribution and fitted with two polymer curing kinetics models, the exponential model DC=DC(max)[1-exp((ln0.5)H/H(dc)(50%))] and Racz's model [Formula: see text] , where H(dc)(50%) is a fitting parameter representing the threshold for 50% of the maximum curing level. RESULTS AND SIGNIFICANCE: The absorption and scattering coefficients of uncured composite were higher than that of cured composite at wavelengths between 420 and 520 nm. A roughly hemi-spheric distribution of radiant exposure in the Monte Carlo simulation result was comparable with the curing profiles determined by both DC and KHN. The relationship between DC (or KHN) and H agreed with the Racz model (r2=0.95) and the exponential model (r2=0.93). The H(dc)(50%) was 1.5(0.1), equal for the two models (P<0.05). The estimated radiant exposure threshold for 80% of the maximum curing level was between 3.8 and 8.8 J/cm2. The simulation results verify that the radiant exposure extends to a greater depth and width for composite with lower absorption and scattering coefficients. Given the optical properties and the geometry of the composite, and the spectrum and the geometry of the light source, the Monte Carlo simulation can accurately describe the radiant exposure distribution in a composite material to predict the extent of cure.