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Solution-processed bathocuproine (BCP) has been widely used in fullerene (FA)-based organic solar cells (OSCs) for decades as an electron transport layer (ETL).

Despite the outstanding role of conjugated polyelectrolytes (CPEs) in organic solar cells, the use of CPEs in perovskite solar cells has rarely been reported due to instability issues of the material itself under operating conditions.

This work provides new insight into photoelectrochemical hydrogen production under real sunlight by developing a photoelectrochemical module system based on an organic semiconductor photoelectrode with a maximized performance by metal encapsulation.

A simpler and less expensive fabrication process is one of the essential demands for the commercialization of perovskite solar cells (PeSCs). Especially, inverted PeSCs (I-PeSCs) require a cathode buffer layer (CBL) for fabricating highly efficient and stable PeSCs. However, this increases the number of fabrication step. Here, we demonstrate highly stable and efficient cathode-buffer-layer-free I-PeSCs via additive engineering on an ETL, which is based on phenyl-C61-butyric acid methyl ester (PC61BM) with a small amount of poly(methyl methacrylate) (PMMA). This modified ETL shows not only a simplified fabrication process but also effective extraction of charge from the perovskite to a high work function copper electrode (Cu) by formation of an interfacial dipole at the interfaces between the ETL and the Cu. Additionally, it exhibits good passivation of the trap density existing along the grain boundaries and surface of the perovskite layer, reducing the non-radiative recombination and consistent with the increases in open-circuit voltage (Voc). As a result, I-PeSCs with a blend PC61BM : PMMA ETL demonstrate an enhancement in the power conversion efficiency (PCE) from 13.55% (without PMMA) to 18.38%. Furthermore, they exhibit both burn-in-free behaviour in photostability measurements by maximum power-point tracking (MPPT) method and long-term air-stability (30 days for T90) in ambient air. Lastly, we obtained PCE of 15.03% and 16.83% for large-area (1 cm2) I-PeSCs with PC61BM and PC61BM : PMMA, respectively. This method provides an alternative route to reduce the fabrication time and budget for commercialization of I-PeSCs without sacrificing device performance.

We report that sequential deposition of a highly crystalline polymer donor and a soluble fullerene acceptor leads to a well-defined interpenetrating network and enhanced power conversion efficiencies in bilayer polymer solar cells. Even without the use of solvent additives, layered thin films of poly[(5,6-difluoro-2,1,3-benzothiadiazol-4,7-diyl)-alt-(3,3‴-di(2-octyldodecyl)-2,2’; 5′,2’’; 5″,2‴-quaterthiophen-5,5‴-diyl)] (PffBT4T-2OD) and [6,6]-phenyl C71-butyric acid methyl ester (PC71BM), as electron donor and acceptor materials, respectively, showed bicontinuous networks similar to those of a PffBT4T-2OD:PC71BM bulk-heterojunction (BHJ) thin film processed with 1,8-diiodooctane (DIO) as a solvent additive. Transmission electron microscopy results confirmed the BHJ-like morphology of the bilayered PffBT4T-2OD/PC71BM thin films. Bilayer solar cells fabricated without the DIO additive produced a power conversion efficiency of η ≈ 7.65%, which is even higher than that of a BHJ solar cell fabricated with the DIO additive (η ≈ 7.04%). These results demonstrate that a highly crystalline polymer donor and an electron-accepting small molecule can be a good combination for efficient bilayer polymer solar cells.

Despite the promise of simple manufacturing via an entirely solution-based process at low temperature (

Background: Tamoxifen (tam) is widely used to treat estrogen-positive breast cancer. However, cancer recurrence after chemotherapy remains a major obstacle to achieve good patient prognoses. In this study, we aimed to identify genes responsible for epigenetic regulation of tam resistance in breast cancer. Methods: Methylation microarray data were analyzed to screen highly hypomethylated genes in tam resistant (tamR) breast cancer cells. Quantitative RT-PCR, Western blot analysis, and immunohistochemical staining were used to quantify expression levels of genes in cultured cells and cancer tissues. Effects of matrix metalloproteinase-1 (MMP1) expression on cancer cell growth and drug resistance were examined through colony formation assays and flow cytometry. Xenografted mice were generated to investigate the effects of MMP1 on drug resistance in vivo. Results: MMP1 was found to be hypomethylated and overexpressed in tamR MCF-7 (MCF-7/tamR) cells and in tamR breast cancer tissues. Methylation was found to be inversely associated with MMP1 expression level in breast cancer tissues, and patients with lower MMP1 expression exhibited a better prognosis for survival. Downregulating MMP1 using shRNA induced tam sensitivity in MCF-7/tamR cells along with increased apoptosis. The xenografted MCF-7/tamR cells that stably expressed short hairpin RNA (shRNA) against MMP1 exhibited retarded tumor growth compared to that in cells expressing the control shRNA, which was further suppressed by tam. Conclusions: MMP1 can be upregulated through promoter hypomethylation in tamR breast cancer, functioning as a resistance driver gene. MMP1 can be a potential target to suppress tamR to achieve better prognoses of breast cancer patients.

Suppressing nonradiative recombination at the interface between the organometal halide perovskite (PVK) and the charge-transport layer (CTL) is crucial for improving the efficiency and stability of PVK-based solar cells (PSCs). Here, a new bathocuproine (BCP)-based nonconjugated polyelectrolyte (poly-BCP) is synthesized and this is introduced as a "dual-side passivation layer" between the tin oxide (SnO

Correction for ‘A long-term stable organic semiconductor photocathode-based photoelectrochemical module system for hydrogen production’ by Sehun Seo et al., J. Mater. Chem. A, 2022, 10, 13247–13253, https://doi.org/10.1039/D2TA02322A.

Correction for ‘Conjugated polyelectrolytes for stable perovskite solar cells based on methylammonium lead triiodide’ by Yong Ryun Kim et al., J. Mater. Chem. A, 2022, 10, 3321–3329, https://doi.org/10.1039/D1TA10185D.

Background To comprehensively understand the molecular mechanism of tamoxifen resistance (TamR) acquisition by epigenetically regulated genes, it is essential to identify pivotal genes by genome-wide methylation analysis and verify their function in xenograft animal model and cancer patients. Methods The MCF-7/TamR breast cancer cell line was developed and a genome-wide methylation array was performed. The methylation and expression of ELOVL2 was validated in cultured cells, xenografted tumor tissue, and breast cancer patients by methylation-specific PCR, qRT-PCR, Western blot analysis, and immunohistochemistry. Deregulation of ELOVL2 and THEM4 was achieved using siRNA or generating stable transfectants. Tam sensitivity, cell growth, and apoptosis were monitored by colorimetric and colony formation assay and flow cytometric analysis. Pathway analysis was performed to generate networks for the differentially methylated genes in the MCF-7/TamR cells and for the differentially expressed genes in the ELOVL2-overexpressing cells. Results Genome-wide methylation analysis in the MCF-7/TamR cells identified elongation of very-long chain fatty acid protein 2 (ELOVL2) to be significantly hypermethylated and downregulated, which was further verified in the tumor tissues from TamR breast cancer patients (n = 28) compared with those from Tam-sensitive (TamS) patients (n = 33) (P THEM4, which plays crucial roles in drug resistance. Conclusions ELOVL2 was hypermethylated and downregulated in TamR breast cancer patients compared with TamS patients. ELOVL2 is responsible for the recovery of Tam sensitivity. AKT- and ERα-hubbed networks are pivotal in ELOVL2 signaling, where THEM4 contributes to the relaying ELOVL2 signaling. This study implies that deregulation of a gene in fatty acid metabolism can lead to drug resistance, giving insight into the development of a new therapeutic strategy for drug-resistant breast cancer.

Background: Ginsenoside Rg3, a derivative of steroidal saponins abundant in ginseng, has a range of effects on cancer cells, including anti-cell proliferation and anti-inflammation activity. Here, we investigate two long noncoding RNAs (lncRNAs), STXBP5-AS1 and RFX3-AS1, which are hypomethylated and hypermethylated in the promoter region by Rg3 in MCF-7 cancer cells. Methods: The lncRNAs epigenetically regulated by Rg3 were mined using methylation array analysis. The effect of the lncRNAs on the apoptosis and proliferation of MCF-7 cells was monitored in the presence of Rg3 or Korean Red Ginseng (KRG) extract after deregulating the lncRNAs. The expression of the lncRNAs and their target genes was examined using qPCR and Western blot analysis. The association between the expression of the target genes and the survival rate of breast cancer patients was analyzed using the Kaplan-Meier Plotter platform. Results: STXBP5-AS1 and RFX3-AS1 exhibited anti- and pro-proliferation effects, respectively, in the cancer cells, and the effects of Rg3 and KRG extract on apoptosis and cell proliferation were weakened after deregulating the lncRNAs. Of the genes located close to STXBP5-AS1 and RFX3-AS1 on the chromosome, STXBP5, GRM1, RFX3, and SLC1A1 were regulated by the lncRNAs on the RNA and protein level. Breast cancer patients that exhibited a higher expression of the target genes of the lncRNAs had a higher metastasis-free survival rate. Conclusion: The current study is the first to identify lncRNAs that are regulated by the presence of Rg3 and KRG extract and that subsequently contribute to inhibiting the proliferation of cancer cells. Keywords: CpG methylation, ginsenoside Rg3, long noncoding RNA, Korean Red Ginseng

Ginsenoside Rh2, a major bioactive ingredient abundant in red ginseng, has an antiproliferative effect on various cancer cells. In this study, we report a novel long noncoding RNA, C3orf67-AS1, which was identified as being hypermethylated at a CpG site of the promoter by Rh2 in MCF-7 cancer cells. Rh2-induced hypermethylation was responsible for the lower gene expression; the expression was recovered following treatment with a methyltransferase inhibitor, 5-aza-2′-deoxycytidine. When C3orf67-AS1 was downregulated by a siRNA, the cell growth rate was decreased, demonstrating the RNA’s oncogenic activity. Accordingly, breast cancer patients showed a lower methylation and higher expression level of C3orf67-AS1. Within 800 kb flanking C3orf67-AS1 on the chromosome, eight genes were found, and four genes including C3orf67 (the sense strand gene of C3orf67-AS1) were downregulated by Rh2. In particular, C3orf67 was downregulated when C3orf67-AS1 was suppressed by a siRNA; however, the expression of C3orf67-AS1 was not affected by C3orf67. Taken together, this study identifies a novel noncoding RNA, C3orf67-AS1, of which the expression could be suppressed by Rh2 via promoter methylation, thereby mediating the anti-proliferative effect of the ginsenoside.

Carbazole-based conjugated small molecule electrolytes (CSEs) containing different numbers of amine groups were synthesized and applied to bulk-heterojunction (BHJ) organic solar cells for the formation of a spontaneous self-assembled electron transporting layer (ETL). The active layer was spin-coated with a mixture solution containing the BHJ materials and a small amount of CSE, and a thin layer of CSE was formed underneath the active layer (CSE/BHJ bi-layer) via spontaneous phase separation, which is confirmed by the depth profile of the time of flight secondary ion mass spectroscopy (ToF-SIMS) spectrum. The amino groups in the CSEs form hydrogen-bonds with the surface of indium tin oxide (ITO), which acts as an ETL in BHJ solar cells. Moreover, the formed CSE layer is capable of changing the effective work function (WF) of ITO. An increasing number of amino groups in the CSEs (from Cz1N to Cz3N) provides more reduction of the effective WF of ITO, which results in a lower internal resistance and a higher power conversion efficiency (PCE). Furthermore, the enhanced hydrogen bonding between the amines and ITO with an increased number of amine groups has been studied by XPS. This result suggests that one-step processing provides a reduction of the manufacturing cost, which can provide an attractive design concept for ETL fabrication.

Ginsenoside Rg3 exerts antiproliferation activity on cancer cells by regulating diverse noncoding RNAs. However, little is known about the role of long noncoding RNAs (lncRNAs) or their relationship with competitive endogenous RNA (ceRNA) in Rg3-treated cancer cells. Here, a lncRNA (ATXN8OS) was found to be downregulated via Rg3-mediated promoter hypermethylation in MCF-7 breast cancer cells. SiRNA-induced downregulation of ATXN8OS decreased cell proliferation but increased apoptosis, suggesting that the noncoding RNA possessed proproliferation activity. An in silico search for potential ATXN8OS-targeting microRNAs (miRs) identified a promising candidate (miR-424-5p) based on its high binding score. As expected, miR-424-5p suppressed proliferation and stimulated apoptosis of the MCF-7 cells. The in silico miR-target-gene prediction identified 200 potential target genes of miR-424-5p, which were subsequently narrowed down to seven that underwent hypermethylation at their promoter by Rg3. Among them, three genes (EYA1, DACH1, and CHRM3) were previously known oncogenes and were proven to be oppositely regulated by ATXN8OS and miR-424-5p. When taken together, Rg3 downregulated ATXN8OS that inhibited the tumor-suppressive miR-424-5p, leading to the downregulation of the oncogenic target genes.

Kim and colleagues show that OCA-B in T cells is essential for the generation of type 1 diabetes. OCA-B loss leaves the pancreatic lymph nodes largely undisturbed but associates autoreactive CD4+ T cells in the pancreas with anergy while deleting potentially autoreactive CD8+ T cells., The transcriptional coregulator OCA-B promotes expression of T cell target genes in cases of repeated antigen exposure, a necessary feature of autoimmunity. We hypothesized that T cell–specific OCA-B deletion and pharmacologic OCA-B inhibition would protect mice from autoimmune diabetes. We developed an Ocab conditional allele and backcrossed it onto a diabetes-prone NOD/ShiLtJ strain background. T cell–specific OCA-B loss protected mice from spontaneous disease. Protection was associated with large reductions in islet CD8+ T cell receptor specificities associated with diabetes pathogenesis. CD4+ clones associated with diabetes were present but associated with anergic phenotypes. The protective effect of OCA-B loss was recapitulated using autoantigen-specific NY8.3 mice but diminished in monoclonal models specific to artificial or neoantigens. Rationally designed membrane-penetrating OCA-B peptide inhibitors normalized glucose levels and reduced T cell infiltration and proinflammatory cytokine expression in newly diabetic NOD mice. Together, the results indicate that OCA-B is a potent autoimmune regulator and a promising target for pharmacologic inhibition., Graphical Abstract

The establishment of durable immunological memory remains a poorly understood aspect of lymphocyte biology and a limiting factor in vaccine development. Using a T cell-conditional OCA-B (Pou2af1) knockout model and a mouse viral pathogen, we show that expression of the transcription cofactor OCA-B within T cells is necessary for proper CD4+ memory T cell formation. We also show that ectopic OCA-B expression is sufficient to drive T cells towards a memory fate while having no effect on primary antiviral effector response. Bulk and single-cell gene expression profiling comparing cells transduced with OCA-B and empty vector at peak primary viral response identifies changes in gene expression consistent with later memory formation. Intersecting differentially expressed genes in bulk RNA-seq with prior ChIP-seq identifies direct targets increased (Tbx21, Zeb2, Gadd45b, Socs2) and decreased (Zbtb16, Ccr1) by ectopic OCA-B expression. Single-cell RNA-seq reveals expansion of short-lived effector T cell compartments with increased expression of Gadd45b and Socs2, as well as increased expression of memory-associated genes such as Slamf6, Il7r and Tcf1 in smaller clusters of effector cells with memory potential. We also describe a new OCA-B-mCherry reporter mouse that efficiently labels B and T lymphocytes and that shows high expression in CD4+ TCM cells. Cumulatively, the results demonstrate that OCA-B expression in T cells is necessary and sufficient to promote CD4 T cell memory in vivo. Supported by grants from NIH (R01 AI100873)

Simple Summary Cold atmospheric plasma is being applied to treat cancer by virtue of its preferential anti-proliferative effect on cancer cells over normal cells. This study aimed to systemically determine the distribution of target genes regulated by the reactive oxygen species and non-reactive oxygen species constituents of the plasma. After analyzing genome-wide expression data for a leukemia and a melanoma cancer cell line from a public database followed by experimental approaches, PTGER3 and HSPA6 genes were found regulated by the non-reactive oxygen species and non-reactive nitrogen species constituents of the plasma in the cancer cells. This study could contribute to elucidate the molecular mechanism how each physicochemical constituent of the plasma induces the specific molecular changes in cancer cells. Abstract Cold atmospheric plasma (CAP) can induce cancer cell death. The majority of gene regulation studies have been biased towards reactive oxygen species (ROS) among the physicochemical components of CAP. The current study aimed to systemically determine the distribution of target genes regulated by the ROS and non-ROS constituents of CAP. Genome-wide expression data from a public database, which were obtained after treating U937 leukemia and SK-mel-147 melanoma cells with CAP or H2O2, were analyzed, and gene sets regulated by either or both of them were identified. The results showed 252 and 762 genes in H2O2-treated U937 and SK-mel-147 cells, respectively, and 112 and 843 genes in CAP-treated U937 and SK-mel-147 cells, respectively, with expression changes higher than two-fold. Notably, only four and two genes were regulated by H2O2 and CAP in common, respectively, indicating that non-ROS constituents were responsible for the regulation of the majority of CAP-regulated genes. Experiments using ROS and nitrogen oxide synthase (NOS) inhibitors demonstrated the ROS- and reactive nitrogen species (RNS)-independent regulation of PTGER3 and HSPA6 when U937 cancer cells were treated with CAP. Taken together, this study identified CAP-specific genes regulated by constituents other than ROS or RNS and could contribute to the annotation of the target genes of specific constituents in CAP.

The transcriptional coregulator OCA-B promotes expression of T cell target genes in cases of repeated antigen exposure, a necessary feature of autoimmunity. We hypothesized that T cell-specific OCA-B deletion and pharmacologic OCA-B inhibition would protect mice from autoimmune diabetes. We developed an Ocab conditional allele and backcrossed it onto a diabetes-prone NOD/ShiLtJ strain background. T cell-specific OCA-B loss protected mice from spontaneous disease. Protection was associated with large reductions in islet CD8+ T cell receptor specificities associated with diabetes pathogenesis. CD4+ clones associated with diabetes were present, but associated with anergic phenotypes. The protective effect of OCA-B loss was recapitulated using autoantigen-specific NY8.3 mice, but diminished in monoclonal models specific to artificial or neoantigens. Rationally-designed membrane-penetrating OCA-B peptide inhibitors normalized glucose levels, and reduced T cell infiltration and proinflammatory cytokine expression in newly-diabetic NOD mice. Together, the results indicate that OCA-B is a potent autoimmune regulator and a promising target for pharmacologic inhibition.~40-word summary statement for the online JEM table of contents and alertsKim and colleagues show that OCA-B in T cells is essential for the generation of type-1 diabetes. OCA-B loss leaves the pancreatic lymph nodes largely undisturbed, but associates autoreactive CD4+ T cells in the pancreas with anergy while deleting potentially autoreactive CD8+ T cells.SummaryKim et al. show that loss or inhibition of OCA-B in T cells protects mice from type-1 diabetes.

Cold atmospheric plasma (CAP) has been recognized as a potential alternative or supplementary cancer treatment tool, which is attributed by its selective antiproliferation effect on cancer cells over normal cells. Standardization of the CAP treatment in terms of biological outputs such as cell growth inhibition and gene expression change is essential for its clinical application. This study aims at identifying genes that show consistent expression profiles at a specific CAP condition, which could be used to monitor whether CAP is an appropriate treatment to biological targets. To do this, genes showing differential expression by two different CAP treatment conditions were screened in the MCF-7 breast cancer cells. As a result, ZNRD1 was identified as a potential marker with being consistently upregulated by 600 s but downregulated by the 10×30 s CAP treatment scheme. Expression of ZNRD1 was increased in breast cancer tissues compared to normal tissues, judged by cancer tissue database analysis, and supported by the antiproliferation after siRNA-induced downregulation in MCF-7. Interestingly, the antisense long noncoding RNA (lncRNA) of ZNRD1, ZNRD1-AS1, was regulated to the opposite direction of ZNRD1 by CAP. The siRNA-based qPCR analysis indicates that ZNRD1 downregulates ZNRD1-AS1, but not vice versa. ZNRD1-AS1 was shown to increase a few cis-genes such as HLA-A, HCG9, and PPP1R11 that were also regulated by CAP. Altogether, this study identified a pair of gene and its antisense lncRNA of which expression is precisely controlled by CAP in a dose-dependent manner. These genes could help elucidate the molecular mechanism how CAP regulates lncRNAs in cancer cells.

본 연구는 한국과 일본의 미혼모에 대한 원가족의 수용의 차이와 미혼모에 대한 인식의 역사적 배경을 알아보고 미혼모와 원가족 간 관계 개선을 위한 시사점을 발견하는데 목적이 있다. 이를 위해 미혼모와 원가족 관련 문헌을 고찰하고, 양국 미혼모 11명을 대상으로 심층면접을 하여 분석하였다. 연구결과, 미혼모가 되는 과정과 원가족의 수용 정도, 국가의 지원방식에서 양국 간 차이가 나타났다. 한국미혼모들은 출산과 양육 결정 과정에서 가족들로부터 출산과 양육에 대한 비난과 반대에 부딪치며 심리․사회적 고립과 관계의 단절을 경험하였다. 반면, 일본 미혼모들은 출산과 양육 과정에서 부모님 등 가족의 도움이 가장 중요한 지지체계로 작용하고 있었다. 한국과 일본 모두 미혼모에 대한 지원이 제한적이거나 차별적이어서 미혼모들의 탈빈곤이 어려운 공통점이 있었다. 특히 일본은 미혼모에 대한 사회적 인식이 한국보다 개방적이기는 하나 제도적 지원에서는 공식적인 결혼 여부를 기준으로 차별적인 지원을 하는 이중적인 경향이 있었다. 이와 같은 연구결과를 통해 본 연구에서는 가족과 개인의 다양화와 규범, 그리고 현실 간 괴리에 대한 재인식의 필요성을 포함하여, 적극적 인식개선 노력이 필요함을 제언하였다.

Solution-processable small molecule (SM) organic semiconductors for organic photovoltaics have been in the spotlight for several years. In particular, SM semiconductors have been developed in an attempt to control their film morphology, study their intermolecular interactions, and synthesize new electron donor and electron acceptor subunits. SMs have many advantages over polymers including well-defined molecular structures, monodispersity, and no batch-to-batch dependence. Although SM semiconductors can be designed by truncation from polymers, such examples have rarely been reported. Herein we designed SM semiconductors by truncating a representative polymer, Poly[4-(4,8-bis((2-hexyldecyl)oxy)benzo[1,2-b:4,5-b’]dithiophen-2-yl)-alt-benzo[c][1,2,5]thiadiazole] (PBDTBT). Based on density functional theory (DFT) calculations, 2,1,3-benzothiadiazole (BT) was chosen as an electron acceptor subunit instead of thieno[3,4-c]pyrrole-4,6-dione (TPD). The SM semiconductors were end-capped with pyridine derivatives. Thermal, optical and electrochemical properties of these materials were examined to confirm the degradation temperature, the highest occupied molecular orbital (HOMO), the lowest unoccupied molecular orbital (LUMO) energy levels, and the band gaps. In particular, the benzyloxyl pyridine-capped semiconductor (SM1) exhibited power conversion efficiency (PCE) of 1.92% which is higher than those shown by the corresponding polymer PBDTBT (0.90% and 1.71%).

Paclitaxel (Tx) is a widely used therapeutic chemical for breast cancer treatment, however, cancer recurrence remains an obstacle for improved prognosis of cancer patients. In this study, cold atmospheric plasma (CAP) was tested for its potential to overcome the drug resistance. After developing Tx-resistant MCF-7 (MCF-7/TxR) breast cancer cells, CAP was applied to the cells, and its effect on the recovery of drug sensitivity was assessed in both cellular and molecular aspects. Sensitivity to Tx in the MCF-7/TxR cells was restored up to 73% by CAP. A comparison of genome-wide expression profiles between the TxR cells and the CAP-treated cells identified 49 genes that commonly appeared with significant changes. Notably, 20 genes, such as KIF13B, GOLM1, and TLE4, showed opposite expression profiles. The protein expression levels of selected genes, DAGLA and CEACAM1, were recovered to those of their parental cells by CAP. Taken together, CAP inhibited the growth of MCF-7/TxR cancer cells and recovered Tx sensitivity by resetting the expression of multiple drug resistance&ndash, related genes. These findings may contribute to extending the application of CAP to the treatment of TxR cancer.

Elimination of charge trapping at defects is highly challenging for poly-crystalline organometal halide perovskites. Here, we report a new architecture for reinforcing the built-in electric field (Ein) across the photoactive layer with a pair of strong electric dipole layers (EDLs). The paired EDLs significantly intensify the Ein across the perovskite layer, resulting in suppressed charge trapping of photogenerated charges. As a result, our low-temperature processed P–I–N planar PeSC devices using the paired EDLs exhibit a higher power conversion efficiency (ηmax ∼ 19.4%) and a smaller device-to-device variation with a standard deviation (S.D.) of 0.70%, which far surpass those (ηmax ∼ 17.8%, S.D. ∼ 1.1%) of the devices with typical charge transport layers.

(E)-6,6′-Dibromo-1,1-bis(2-octyldodecyl)-(3,3′-biindolinylid-ene)-2,2′-dione and/or 2,5-bis(2-octyldodecyl)-3,6-di(5-bromothien-2-yl)pyrrolo[3,4-c]pyrrole-1,4-(2H,5H)-dione and their tBoc-counterparts were propagated with 2,5-bis(tributylstannyl)thiophene in a molar ratio of 0.8 : 0.2 : 1.0 to release P(ODIDT-BID), P(ODIDT·BDPP), P(ODDPPT·BID) and P(ODDPPT·BDPP) as a new series of random conjugated polymers (RCPs) bearing a large number of octyldodecyl chains to ensure solubility and a small number of thermocleavable tBoc function to cast H-bonding upon heating up to 220 °C. All new polymers were synthesised via Pd catalysed Stille cross-coupling methodology in high yields and reasonable average molecular weights. The cast polymer films exhibited considerable red-shifted UV-vis absorption spectra and a further red-shift was also obtained in the thermal annealed films (at 220 °C for 30 min), which reflected the increasing of crystalline structure. The formation of H-bonding in these polymers was investigated using X-ray diffractometry (XRD) measurements. The field-effect mobilities of these polymers were investigated in the configuration of bottom-gate and bottom-contact (BGBC) field-effect transistors (FETs). The results from FETs indicated that the crystalline structure of RCPs exhibited reasonable FET mobilities with 1.17 × 10−3 cm2 V−1 s−1 for P(ODDPPT·BID) and 1.41 × 10−3 cm2 V−1 s−1 for P(ODDPPT·BDPP).

We investigate a correlation between the type of solvent additives (SAs) with specific criteria such as aromatic additives (AAs) and non-aromatic additives (NAAs) and phase separation in the bulk heterojunction (BHJ) films comprising low-band gap polymer and fullerene derivatives. When AAs are used as SAs, the geometrical structures (π-π and lamellar stacking) of aggregated polymer chains do not significantly change. However, NAAs increase the lamellar stacking distance through a strong interaction with non-aromatic segments of polymers. Therefore, a well-phase separated BHJ morphology with the finer fibrils is developed, thereby leading to balanced charge mobilities and a reduced charge recombination in BHJ solar cells. Finally, the optimized solar cell exhibits a high power conversion efficiency of 7.9%.

A better understanding of the development and progression of acute myelogenous leukemia (AML) is necessary to improve patient outcome. Here we define roles for the transcription factor Oct1/Pou2f1 in AML and normal hematopoiesis. Inappropriate reactivation of the CDX2 gene is widely observed in leukemia patients and in leukemia mouse models. We show that Oct1 associates with the CDX2 promoter in both normal and AML primary patient samples, but recruits the histone demethylase Jmjd1a/Kdm3a to remove the repressive H3K9me2 mark only in malignant specimens. The CpG DNA immediately adjacent to the Oct1 binding site within the CDX2 promoter exhibits variable DNA methylation in healthy control blood and bone marrow samples, but complete demethylation in AML samples. In MLL-AF9-driven mouse models, partial loss of Oct1 protects from myeloid leukemia. Complete Oct1 loss completely suppresses leukemia but results in lethality from bone marrow failure. Loss of Oct1 in normal hematopoietic transplants results in superficially normal long-term reconstitution; however, animals become acutely sensitive to 5-fluorouracil, indicating that Oct1 is dispensable for normal hematopoiesis but protects blood progenitor cells against external chemotoxic stress. These findings elucidate a novel and important role for Oct1 in AML.