Multicomponent Solar Cells with High Fill Factors and Efficiencies Based on Non-Fullerene Acceptor Isomers.

Multicomponent organic solar cells (OSCs), such as the ternary and quaternary OSCs, not only inherit the simplicity of binary OSCs but further promote light harvesting and power conversion efficiency (PCE). Here, we propose a new type of multicomponent solar cells with non-fullerene acceptor isomers. Specifically, we fabricate OSCs with the polymer donor J71 and a mixture of isomers, ITCF, as the acceptors. In comparison, the ternary OSC devices with J71 and two structurally similar (not isomeric) NFAs (IT-DM and IT-4F) are made as control. The morphology experiments reveal that the isomers-containing blend film demonstrates increased crystallinity, more ideal domain size, and a more favorable packing orientation compared with the IT-DM/IT-4F ternary blend. The favorable orientation is correlated with the balanced charge transport, increased exciton dissociation and decreased bimolecular recombination in the ITCF-isomer-based blend film, which contributes to the high fill factor (FF), and thus the high PCE. Additionally, to evaluate the generality of this method, we examine other acceptor isomers including IT-M, IXIC-2Cl and SY1, which show same trend as the ITCF isomers. These results demonstrate that using isomeric blends as the acceptor can be a promising approach to promote the performance of multicomponent non-fullerene OSCs.

Simple Solvent Treatment Enabled Improved PEDOT:PSS Performance toward Highly Efficient Binary Organic Solar Cells.

PEDOT: PSS is the most popular hole-transporting material (HTM) for conventional structural organic solar cell (OSC) devices, whose performance is of great importance for realizing high power conversion efficiency (PCE). However, its performance in OSC devices has been continuously challenged by various replacing materials and different doping strategies, for better conductivity, work function, and surface property. Here, we report a simple dopant-free method to tune the phase separation of the PEDOT:PSS layer, which results in better charge transport and extraction in devices. Specifically, high PCEs for binary polymer-small-molecule (>18%) and polymer-polymer (>17%) systems are simultaneously achieved. This work engineeringly provides encouraging improvement for OSC device performance with easy modification and scientifically offers insights into tuning the property of the PEDOT:PSS layer.

Spontaneously immortalised bovine mammary epithelial cells exhibit a distinct gene expression pattern from the breast cancer cells.

BACKGROUND: Spontaneous immortalisation of cultured mammary epithelial cells (MECs) is an extremely rare event, and the molecular mechanism behind spontaneous immortalisation of MECs is unclear. Here, we report the establishment of a spontaneously immortalised bovine mammary epithelial cell line (BME65Cs) and the changes in gene expression associated with BME65Cs cells. RESULTS: BME65Cs cells maintain the general characteristics of normal mammary epithelial cells in morphology, karyotype and immunohistochemistry, and are accompanied by the activation of endogenous bTERT (bovine Telomerase Reverse Transcriptase) and stabilisation of the telomere. Currently, BME65Cs cells have been passed for more than 220 generations, and these cells exhibit non-malignant transformation. The expression of multiple genes was investigated in BME65Cs cells, senescent BMECs (bovine MECs) cells, early passage BMECs cells and MCF-7 cells (a human breast cancer cell line). In comparison with early passage BMECs cells, the expression of senescence-relevant apoptosis-related gene were significantly changed in BME65Cs cells. P16INK4a was downregulated, p53 was low expressed and Bax/Bcl-2 ratio was reversed. Moreover, a slight upregulation of the oncogene c-Myc, along with an undetectable level of breast tumor-related gene Bag-1 and TRPS-1, was observed in BME65Cs cells while these genes are all highly expressed in MCF-7. In addition, DNMT1 is upregulated in BME65Cs. These results suggest that the inhibition of both senescence and mitochondrial apoptosis signalling pathways contribute to the immortality of BME65Cs cells. The expression of p53 and p16INK4a in BME65Cs was altered in the pattern of down-regulation but not "loss", suggesting that this spontaneous immortalization is possibly initiated by other mechanism rather than gene mutation of p53 or p16INK4a. CONCLUSIONS: Spontaneously immortalised BME65Cs cells maintain many characteristics of normal BMEC cells and exhibit non-malignant transformation. Although this cell line displays altered patterns of gene expression, it is clearly distinct from malignant breast cancer cell line. It showed that co-inhibition of cellular senescence and mitochondrial apoptosis pathways coordinates BME65Cs cells immortalisation. Additionally, mechanisms other than gene mutation are likely to be involved in regulation of cellular functions. This study provides an insight into the relationship between cell senescence and immortalisation. BME65Cs cells will be useful in future studies of cellular senescence and tumorigenesis.

Immortalization of bovine mammary epithelial cells alone by human telomerase reverse transcriptase.

Immortal bovine mammary epithelial cell lines are useful for providing an efficient indicator for transgene expression and for the technological improvement of genetic modification. The preparation of hTERT (human telomerase reverse transcriptase)-mediated immortalized MECs (mammary epithelial cells) requires a down-regulation of p16(INK4a). Here, we report the establishment of two immortal bovine MEC lines by expression of hTERT gene alone under serum-containing culture conditions. This two cell lines maintain the general characteristics of MECs and have been stably passed more than 200 generations accompanying telomere extension, and were identified as non-malignant transformation. Investigation on transcriptional profile showed a similar down-regulation in both p16(INK4a) and p53. By comparing with non-immortal hTERT-positive MECs, we speculated that there are some spontaneous p16(INK4a)-reduced cells under normal culture conditions and the immortalization required for a co-ordinate repression of p53 and p16(INK4a) signalling pathways. Interestingly, two immortal cell lines showed a significant distinction in proliferation rate, implying that other mechanisms might be involved in proliferation control.

[The relationship of angiotensin I-converting enzyme gene polymorphism with diabetic retinopathy and diabetes myocardial infarction].

OBJECTIVE: To investigate the relationship of angiotensin I-converting enzyme (ACE) gene polymorphism to diabetic retinopathy and diabetes myocardial infarction. METHODS: ACE insertion/deletion(I/D) polymorphism was determined by PCR. RESULTS: No evidence showed that ACE gene was associated with diabetic retinopathy. By comparison of the type 2 diabetes patients with myocardial infarction versus those without-myocardial infarction, it was found that the frequencies of homozygote DD (41.2% versus 33.2%) and of allele D (64.7% versus 55.0%) increased remarkably; the difference was statistically significant (P<0.05). CONCLUSION: Allele D(RR=1.50) and genotype DD(RR=1.33) seemed to be a genetic risk factor for type 2 diabetes myocardial infarction.

[Studies on the genetic diathesis of asthma bronchial].

To study the association of genes polymorphisms in glutathione S-transferase M1 and T1 with asthma bronchial. The distribute frequency of allele(+) and allele(o) between GSTM1 and GSTT1 of 60 patients asthma bronchial and 60 control groups in Tangshan was studied with PCR. The result shown GSTM1 deficiency allele(0/0) frequency of asthma bronchial was 81.2%, which showed significantly higher(chi(2)=32.46, P<0.001; wchi(2)=28.75,P<0.001) than the control groups; GSTT1 was similar to GSTM1. But GSTT1 zero allele(0/0) frequency of asthma bronchial were 71.7%, which were significantly higher (chi(2)=26.72, P<0.001; wchi(2)=35.75, P<0.001) than the control groups(11.7%). Zero allele of GSTM1 and GSTT1 were showed the most features in the asthma bronchial. Associated significantly in the genes polymorphisms of GSTM1 and GSTT1 with asthma bronchial, their genes mutation may be the genetic risk factor of asthma bronchial.

Identification and distribution of rRNH1, a gene upregulated after spinal cord primary neuron injury.

Our previous study identified and characterized one differentially expressed gene, Rattus norvegicus ribonuclease/angiogenin inhibitor 1 (rRNH1). Transcriptional activity of lots of genes involves in spinal cord injury (SCI) and regeneration, but the mechanisms remain unknown. In the present study, we analyzed the sequences of rRNH1 and examined the expression pattern of rRNH1 in different adult rat tissues. We found the sequences of rRNH1 show high homology to Homo sapiens ribonuclease/angiogenin inhibitor 1; it encoded a protein of 461 amino acid residues and contained 13 leucine-rich repeat motifs. Using real-time quantitative PCR (q-PCR), rRNH1 mRNA was widely expressed in adult rat tissues, especially in the central nervous system. Moreover, rRNH1 protein was found to be upregulated after SCI. Although the precise function of rRNH1 is unknown, its unique expression pattern and upregulation after SCI suggest that rRNH1 might be involved in the succeeding injury and/or regeneration processes of injured spinal cord. All these data make rRNH1 a new interesting start to study the mechanisms of SCI and neuron regeneration.

Oct-4B isoform is differentially expressed in breast cancer cells: hypermethylation of regulatory elements of Oct-4A suggests an alternative promoter and transcriptional start site for Oct-4B transcription.

The human Oct-4 gene has three isoforms, Oct-4A, Oct-4B and Oct-4B1, which are thought to be derived from alternative splicing. It remains controversial whether the Oct-4 gene is expressed in cancer cells. Expression of Oct-4A is regulated by two elements, the PE (proximal enhancer) and DE (distal enhancer), but the expression and regulation of Oct-4B are not well known. Here, we firstly report that Oct-4B is expressed at low levels in MCF-7 cells, while the Oct-4A gene is inactivated. By analysing the function of different promoter constructs and the DNA methylation status of three regulatory regions, we demonstrate that the Oct-4A gene in MCF-7 cells is repressed by epigenetic control rather than transcriptional control. In addition, we speculate that the transcription of Oct-4B in MCF-7 cells is differentially regulated by additional regulatory elements. This work will enhance the understanding of Oct-4 gene in differential regulation.