Tremendous efforts have been dedicated toward minimizing the open-circuit voltage deficits on perovskite solar cells (PSCs), and the fill factors are still relatively low. This hinders their further application in large scalable modules. Herein, we employ a newly designed ammonium salt, cyclohexylethylammonium iodide (CEAI), for interfacial engineering between the perovskite and hole-transporting layer (HTL), which enhanced the fill factor to 82.6% and consequent PCE of 23.57% on the target device. This can be associated with a reduction of the trap-assisted recombination rate at the 3D perovskite surface, via formation of a 2D perovskite interlayer. Remarkably, the property of the 2D perovskite interlayer along with the cyclohexylethyl group introduced by CEAI treatment also determines a pronounced enhancement in the surface hydrophobicity, leading to an outstanding stability of over 96% remaining efficiency of the passivated devices under maximum power point tracking with one sun illumination under N 2 atmosphere at room temperature after 1500 h.

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Integrin α v β 6 , a member of the integrin family, is specifically expressed in many malignancies but not in normal organs. Overexpression of integrin α v β 6 is usually correlated with malignant potential and poor prognosis. In this study, we describe the synthesis and evaluation of a 99m Tc-labeled integrin α v β 6 -targeting peptide as a SPECT radiotracer for the in vivo imaging of integrin α v β 6 expression. Methods: An integrin α v β 6 -targeting peptide (denoted as the HK peptide) was conjugated with 6-hydrazinonicotinyl (HYNIC) and radiolabeled with 99m Tc using tricine and TPPTS (trisodium triphenylphosphine-3,3′,3″-trisulfonate) as coligands. The in vitro and in vivo characteristics of 99m Tc-HYNIC(tricine)(TPPTS)-HK ( 99m Tc-HHK) were investigated in BxPC-3 (integrin α v β 6 -positive) and HEK293 (integrin α v β 6 -negative) models. The ability of 99m Tc-HHK to detect liver metastasis of pancreatic cancer was evaluated using small-animal SPECT/CT. Results: 99m Tc-HHK showed high integrin α v β 6 -binding specificity both in vitro and in vivo. 99m Tc-HHK was cleared rapidly from the blood and normal organs except for the kidneys. The highest uptake (0.88 ± 0.12 percentage injected dose per gram) of 99m Tc-HHK in BxPC-3 tumors was observed at 0.5 h after injection. High-contrast images of integrin α v β 6 -positive tumors were obtained using 99m Tc-HHK. The minimum nonspecific activity accumulation in normal liver tissues rendered high-quality SPECT/CT images of metastatic lesions. Conclusion: 99m Tc-HHK is a promising SPECT radiotracer for the noninvasive imaging of integrin α v β 6 expression in vivo. SPECT/ CT with 99m Tc-HHK could provide an effective approach for the noninvasive detection of primary and metastatic lesions of integrin α v β 6 -positive tumors.

Significant evidence has indicated that tumor-associated macrophages (TAMs) play a critical role in the proliferation, invasion, angiogenesis, and metastasis of a variety of human carcinomas. In this study, we investigated whether near-infrared fluorescence (NIRF) imaging using a macrophage mannose receptor (MMR; CD206)-targeting agent could be used to noninvasively visualize and quantify changes in TAMs in vivo. The CD206-targeting NIRF agent, Dye-anti-CD206, was prepared and characterized in vitro and in vivo. By using NIRF imaging, we were able to noninvasively image tumor-infiltrating macrophages in the 4T1 mouse breast cancer model. Importantly, longitudinal NIRF imaging revealed the depletion of macrophages in response to zoledronic acid (ZA) treatment. However, ZA alone did not lead to the inhibition of 4T1 tumor growth. We therefore combined anti-macrophage ZA therapy and tumor cytotoxic docetaxel (DTX) therapy in the mouse model. The results demonstrated that this combination strategy could significantly inhibit tumor growth as well as tumor metastasis to the lungs. Based on these findings, we concluded that CD206-targeted molecular imaging can sensitively detect the dynamic changes in tumor-infiltrating macrophages, and that the combination of macrophage depletion and cytotoxic therapy is a promising strategy for the effective treatment of solid tumors.

Epidermal growth factor receptor (EGFR) has been well characterized as an important target for cancer therapy. Immunotherapy based on EGFR-specific antibodies (e.g., panitumumab and cetuximab) has shown great clinical promise. However, increasing evidence has indicated that only a subgroup of patients receiving these antibodies will benefit from them, and even patients who do initially experience a major response may eventually develop therapeutic resistance. In this study, we investigated whether panitumumab and cetuximab can serve as delivery vehicles for tumor-targeted radionuclide therapy in a preclinical tumor model that did not respond to immunotherapy. The in vitro toxicity and cell binding properties of panitumumab and cetuximab were characterized. Both antibodies were conjugated with 1,4,7,10-tetraazadodecane-N,N',N",N"'-tetraacetic acid (DOTA) and radiolabeled with (177)Lu. Small-animal SPECT/CT, biodistribution, and radioimmunotherapy (RIT) studies of (177)Lu-DOTA-panitumumab ((177)Lu-Pan) and (177)Lu-DOTA-cetuximab ((177)Lu-Cet) were performed in the UM-SCC-22B tumor model. Both (177)Lu-Pan and (177)Lu-Cet exhibited favorable tumor targeting efficacy. The tumor uptake was 20.92 ± 4.45, 26.10 ± 5.18, and 13.27 ± 1.94% ID/g for (177)Lu-Pan, and 15.67 ± 3.84, 15.72 ± 3.49, and 7.82 ± 2.36% ID/g for (177)Lu-Cet at 24, 72, and 120 h p.i., respectively. RIT with a single dose of 14.8 MBq of (177)Lu-Pan or (177)Lu-Cet significantly delayed tumor growth. (177)Lu-Pan induced more effective tumor growth inhibition due to a higher tumor uptake. Our results suggest that panitumumab and cetuximab can function as effective carriers for tumor-targeted delivery of radiation, and that RIT is promising for targeted therapy of EGFR-positive tumors, especially for those tumors that are resistant to antibody-based immunotherapy.

Achieving high power conversion efficiencies with Cu(In,Ga)Se2 (CIGS) solar cells grown at low temperature is challenging because of insufficient thermal energy for grain growth and defect annihilation, resulting in poor crystallinity, higher defect concentration, and degraded device performance. Herein, the possibilities for high‐performing devices produced at very low temperatures (≤450 °C) are explored. By alloying CIGS with Ag by the precursor layer method, (Ag,Cu)(In,Ga)Se2 (ACIGS) solar cells grown at about 450 °C reach an efficiency of 20.1%. Only a small efficiency degradation (0.5% and 1.6% absolute) is observed for ACIGS absorbers deposited at 60 and 110 °C lower substrate temperature. CIGS devices exhibit a stronger efficiency degradation, driven by a decrease in the open‐circuit voltage (VOC). The root cause of the VOC difference between ACIGS and CIGS devices is investigated by advanced characterization techniques, which show improved morphology, reduced tail states, and higher doping density in ACIGS absorbers. The proposed approach offers several benefits in view of depositions on temperature‐sensitive substrates. Increased Cu diffusion promoted by Ag allows end‐point detection in the three‐stage process at the substrate temperatures below 300 °C. The modified process requires minimal modification of existing processes and equipment and shows the potential for the use of different flexible substrates and device architectures.

Epidermal growth factor receptor (EGFR) expression is upregulated in many types of tumors, and the EGFR tyrosine kinase inhibitor gefitinib has high potential as an anticancer drug. However, accumulating clinical evidence has indicated that only a subset of patients benefit from gefitinib treatment. This study aimed to determine whether optical imaging of vascular endothelial growth factor (VEGF) expression can be an early biomarker for tumor response to gefitinib therapy. Methods: A VEGF-targeting fluorescent probe Dye-BevF(ab′) 2 was prepared and tested in vivo. Longitudinal optical imaging studies using Dye-BevF(ab′) 2 were performed in both 22B (gefitinib-resistant) and A549 (gefitinib-responsive) tumor models at different times (days 0, 2, and 5) before and after gefitinib treatment. The imaging results were validated by ex vivo immunofluorescence staining and enzymelinked immunosorbent assay. Results: Dye-BevF(ab′) 2 exhibited high specificity for VEGF in vivo. There was no significant change in the Dye-BevF(ab′) 2 uptake in gefitinib-treated 22B tumors, compared with the control group. In contrast, the A549 tumor uptake of DyeBevF(ab′) 2 in the gefitinib-treated group was significantly lower on days 2 and 5 than that in the control group and at the baseline. An in vivo gefitinib treatment study confirmed that 22B tumors were gefitinibresistant, whereas A549 tumors were gefitinib-responsive. Immunofluorescence staining and enzyme-linked immunosorbent assay confirmed that changes in the Dye-BevF(ab′) 2 uptake were correlated with VEGF expression levels in tumors. Conclusion: Optical imaging of VEGF expression with Dye-BevF(ab′) 2 can be used for the early assessment of tumor response to gefitinib therapy. This approach may also be valuable for preclinical high-throughput screening of novel antiangiogenic drugs.

Forming good metal/graphene contact is of significance in making graphene devices, while tuning the graphene work function is a valid approach to decrease the contact barrier and then achieve electrodes with low contact resistance. A strain device has been fabricated to apply uniaxial strain to graphene grown by chemical vapor deposition method, and Kelvin probe force microscopy was used to measure the work function of the graphene under strain. The work function of the graphene is found to increase as strain increases. By applying a uniaxial strain of 7%, the work function can be adjusted as large as 0.161 eV. Such a result can be explained by strain induced increase of the density of states in graphene.