Interface Dipole Management of D-A-Type Molecules for Efficient Perovskite Solar Cells.

Interfacial engineering of perovskite films has been the main strategies in improving the efficiency and stability of perovskite solar cells (PSCs). In this study, three new donor-acceptor (D-A)-type interfacial dipole (DAID) molecules with hole-transporting and different anchoring units are designed and employed in PSCs. The formation of interface dipoles by the DAID molecules on the perovskite film can efficiently modulate the energy level alignment, improve charge extraction, and reduce non-radiative recombination. Among the three DAID molecules, TPA-BAM with amide group exhibits the best chemical and optoelectrical properties, achieving a champion PCE of 25.29 % with the enhanced open-circuit voltage of 1.174 V and fill factor of 84.34 %, due to the reduced defect density and improved interfacial hole extraction. Meanwhile, the operational stability of the unencapsulated device has been significantly improved. Our study provides a prospect for rationalized screening of interfacial dipole materials for efficient and stable PSCs.

Self-Polymerized Spiro-Type Interfacial Molecule toward Efficient and Stable Perovskite Solar Cells.

In the pursuit of highly efficient perovskite solar cells, spiro-OMeTAD has demonstrated recorded power conversion efficiencies (PCEs), however, the stability issue remains one of the bottlenecks constraining its commercial development. In this study, we successfully synthesize a novel self-polymerized spiro-type interfacial molecule, termed v-spiro. The linearly arranged molecule exhibits stronger intermolecular interactions and higher intrinsic hole mobility compared to spiro-OMeTAD. Importantly, the vinyl groups in v-spiro enable in situ polymerization, forming a polymeric protective layer on the perovskite film surface, which proves highly effective in suppressing moisture degradation and ion migration. Utilizing these advantages, poly-v-spiro-based device achieves an outstanding efficiency of 24.54 %, with an enhanced open-circuit voltage of 1.173 V and a fill factor of 81.11 %, owing to the reduced defect density, energy level alignment and efficient interfacial hole extraction. Furthermore, the operational stability of unencapsulated devices is significantly enhanced, maintaining initial efficiencies above 90 % even after 2000 hours under approximately 60 % humidity or 1250 hours under continuous AM 1.5G sunlight exposure. This work presents a comprehensive approach to achieving both high efficiency and long-term stability in PSCs through innovative interfacial design.

A DFT prediction of two-dimensional MB3 (M = V, Nb, and Ta) monolayers as excellent anode materials for lithium-ion batteries.

Transition metal borides (MBenes) have recently drawn great attention due to their excellent electrochemical performance as anode materials for lithium-ion batteries (LIBs). Using the structural search code and first-principles calculations, we identify a group of the MB3 monolayers (M = V, Nb and Ta) consisting of multiple MB4 units interpenetrating with each other. The MB3 monolayers with non-chemically active surfaces are stable and have metal-like conduction. As the anode materials for Li-ion storage, the low diffusion barrier, high theoretical capacity, and suitable average open circuit voltage indicate that the MB3 monolayers have excellent electrochemical performance, due to the B3 chain exposed on the surface improving the Li atoms' direct adsorption. In addition, the adsorbed Li-ions are in an ordered hierarchical arrangement and the substrate structure remains intact at room temperature, which ensures excellent cycling performance. This work provides a novel idea for designing high-performance anode materials for LIBs.

Gemcitabine resistance of pancreatic cancer cells is mediated by IGF1R dependent upregulation of CD44 expression and isoform switching.

Chemoresistance in pancreatic cancer cells may be caused by the expansion of inherently resistant cancer cells or by the adaptive plasticity of initially sensitive cancer cells. We investigated how CD44 isoforms switching contributed to gemcitabine resistance. Treating CD44 null/low single-cell clones with increasing amounts of gemcitabine caused an increase in expression of CD44 and development of gemcitabine resistant (GR) cells. Drug sensitivity, invasiveness, and EMT process was evaluated by MTT, Matrigel invasion assays, and western blots. Genetic knockdown and pharmacological inhibitors were used to examine the roles of CD44 and IGF1R in mediating gemcitabine resistance. CD44 promoter activity and its interactive EMT-related transcription factors were evaluated by luciferase reporter assay and chromatin immunoprecipitation assay. Kaplan-Meier curve was created by log-rank test to reveal the clinical relevance of CD44 and IGF1R expression in patients. We found silence of CD44 in GR cells partially restored E-cadherin expression, reduced ZEB1 expression, and increased drug sensitivity. The gemcitabine-induced CD44 expressing and isoform switching were associated with an increase in nuclear accumulation of phosphor-cJun, Ets1, and Egr1 and binding of these transcription factors to the CD44 promoter. Gemcitabine treatment induced phosphorylation of IGF1R and increased the expression of phosphor-cJun, Ets1, and Egr1 within 72 h. Stimulation or suppression of IGF1R signaling or its downstream target promoted or blocked CD44 promoter activity. Clinically, patients whose tumors expressed high levels of CD44/IGF1R showed a poor prognosis. This study suggests that IGF1R-dependent CD44 isoform switching confers pancreatic cancer cells to undergo an adaptive change in response to gemcitabine and provides the basis for improved targeted therapy of pancreatic cancer.

Percutaneous BCG enhances innate effector antitumor cytotoxicity during treatment of bladder cancer: a translational clinical trial.

Background: Intravesical bacillus Calmette-Guérin (BCG) is the gold standard immunologic agent for treating patients with high-grade non-muscle invasive bladder cancer (NMIBC). Nevertheless, relapse rates remain high and BCG unresponsive NMIBC often requires bladder removal. Preclinical data suggest that priming with percutaneous BCG vaccine could improve response to intravesical BCG. Methods: A single-arm trial (NCT02326168) was performed to study the safety, immunogenicity, and preliminary efficacy of priming. Percutaneous BCG was given 21 days prior to intravesical BCG instillation in patients (n = 13) with high-risk NMIBC. Immune responses were monitored and compared to a sequentially enrolled cohort of nine control patients receiving only intravesical BCG. The effect of BCG on natural killer (NK) and γδ T cell in vitro cytotoxicity was tested. γδ T cell subsets were determined by T cell receptor gene expression with NanoString. Results: Priming was well tolerated and caused no grade ≥3 adverse events. The 3-month disease-free rate for prime patients was 85% (target goal ≥ 75%). Priming boosted BCG-specific immunity at 3 months and increased the activation status of in vitro expanded circulating NK and γδ T cells and their cytotoxicity against bladder cancer cells through receptor NKG2D. BCG enhanced the cytotoxicity of NK and γδ T cells against K562, RT4, and UM-UC6 but not against T24, UM-UC-3, or UM-UC-14 cells. Infiltrating γδ T cell subsets identified in the bladder includes γ9δ2 and γ8δ2. Conclusions: BCG priming is safe and tolerable. Poor sensitivity to NK and γδ T cell cytotoxicity by some bladder tumors represents a potential BCG-resistance mechanism.

Synchrony of telomere length among hematopoietic cells.

OBJECTIVE: Little is known about the relationship of telomere length among leukocyte subsets and cells up the hematopoietic hierarchy. This information is relevant because telomere dynamics in granulocytes were postulated to mirror those of hematopoietic stem cells (HSCs). MATERIALS AND METHODS: In newborn umbilical cord blood (UCB), we examined the relationships of telomere length in hematopoietic progenitor cells (HPCs) (CD34(+)CD45(-)) with those in T lymphocytes and granulocytes. In addition, we correlated telomere length in granulocytes with those in whole leukocyte samples of individuals ranging in age from birth to 100 years. RESULTS: In the UCB, we found strong correlations of telomere length in HPCs with telomere length in T lymphocytes (r ranging from 0.882 to 0.935; p ranging from 0.0038 to 0.0007) and in granulocytes (r = 0.930; p = 0.0072). At birth, strong correlations were also observed between telomere length in granulocytes and those in all leukocytes (r = 0.979; p = 0.0003). Throughout the human lifespan, the relationship between telomere length in granulocytes and that in all leukocytes was r > 0.980 and p < 0.0001. CONCLUSIONS: Robust synchrony exists among leukocyte subsets throughout the human lifespan; individuals with relatively long (or short) telomeres in one leukocyte subset have long (or short) telomeres in other leukocyte subsets. Moreover, telomere length in leukocytes reflects its length in cells up the hematopoietic hierarchy, i.e., HPCs and, by inference, HSCs. Strong links have been found by many studies between leukocyte telomere length and a host of aging-related diseases. Our findings suggest, therefore, that these links might be traced to telomere dynamics in HSCs.