SnSe2 Quantum Dots and Chlorhexidine Acetate Suppress Synergistically Non-radiative Recombination Loss for High Efficiency and Stability Perovskite Solar Cells.

Non-radiative recombination losses limit the property of perovskite solar cells (PSCs). Here, a synergistic strategy of SnSe2QDs doping into SnO2 and chlorhexidine acetate (CA) coating on the surface of perovskite is proposed. The introduction of 2D SnSe2QDs reduces the oxygen vacancy defects and increases the carrier mobility of SnO2. The optimized SnO2 as a buried interface obviously improves the crystallization quality of perovskite. The CA containing abundant active sites of ─NH2/─NH─, ─C═N, CO, ─Cl groups passivate the defects on the surface and grain boundary of perovskite. The alkyl chain of CA also improves the hydrophobicity of perovskite. Moreover, the synergism of SnSe2QDs and CA releases the residual stress and regulates the energy level arrangement at the top and bottom interface of perovskite. Benefiting from these advantages, the bulk and interface non-radiative recombination loss is greatly suppressed and thereby increases the carrier transport and extraction in devices. As a result, the best power conversion efficiency (PCE) of 23.41% for rigid PSCs and the best PCE of 21.84% for flexible PSCs are reached. The rigid PSC maintains 89% of initial efficiency after storing nitrogen for 3100 h. The flexible PSCs retain 87% of the initial PCE after 5000 bending cycles at a bending radius of 5 mm.

Unexpected longer T1 lifetime of 6-sulfur guanine than 6-selenium guanine: the solvent effect of hydrogen bonds to brake the triplet decay.

The decay of the T1 state to the ground state is an essential property of photosensitizers because it decides the lifetime of excited states and, thus, the time window for sensitization. The sulfur/selenium substitution of carbonyl groups can red-shift absorption spectra and enhance the triplet yield because of the large spin-orbit coupling, modifying nucleobases to potential photosensitizers for various applications. However, replacing sulfur with selenium will also cause a much shorter T1 lifetime. Experimental studies found that the triplet decay rate of 6-seleno guanine (6SeGua) is 835 times faster than that of 6-thio guanine (6tGua) in aqueous solution. In this work, we reveal the mechanism of the T1 decay difference between 6SeGua and 6tGua by computing the activation energy and spin-orbit coupling for rate calculation. The solvent effect of water is treated with explicit microsolvation and implicit solvent models. We find that the hydrogen bond between the sulfur atom of 6tGua and the water molecule can brake the triplet decay, which is weaker in 6SeGua. This difference is crucial to explain the relatively long T1 lifetime of 6tGua in an aqueous solution. This insight emphasizes the role of solvents in modulating the excited state dynamics and the efficiency of photosensitizers, particularly in aqueous environments.

Knockdown of the prolyl isomerase Pin1 inhibits Hep-2 cell growth, migration, and invasion by targeting the ß-catenin signaling pathway.

There is increasing evidence indicating that peptidylprolyl cis/trans isomerase, NIMA-interacting 1 (Pin1) plays a decisive role in a variety of cancers. Nevertheless, its function in laryngeal squamous cell carcinoma (LSCC) has not been elaborated. The aim of this study is to determine the role of Pin1 in LSCC. Here, we established stably transfected Hep-2 cells with low expression of Pin1. Intriguingly, cell proliferation, migration, and invasion was significantly inhibited in Pin1-silenced Hep-2 cells. Similarly, knockdown of Pin1 induced apoptosis of Hep-2 cells, as evidenced by increased expression of cleaved-caspase-3, cleaved-PARP, and bax, and decreased expression of bcl2. We also demonstrated that silencing of Pin1 down-regulated ß-catenin and cyclin D1 expression. Inversely, over-expression of ß-catenin reversed the inhibiting effect of Pin1 silencing on Hep-2 cells. Moreover, we proved that knockdown of Pin1 inhibited tumorigenesis of Hep-2 cells in vivo. Taken together, we demonstrate that silencing of Pin1 effectively suppresses the growth of Hep-2 cells through ß-catenin, indicating that Pin1 possess the potential to serve as a therapeutic target for the treatment of LSCC.

Transcriptome Analysis of mfs2-Defective Penicillium digitatum Mutant to Reveal Importance of Pdmfs2 in Developing Fungal Prochloraz Resistance.

Demethylation inhibitors (DMIs), including prochloraz, are popular fungicides to control citrus postharvest pathogens such as Penicillium digitatum (green mold). However, many P. digitatum strains have developed prochloraz resistance, which decreases drug efficacy. Specific major facilitator superfamily (MFS) transporter gene mfs2, encoding drug-efflux pump protein MFS2, has been identified in P. digitatum strain F6 (PdF6) to confer fungal strain prochloraz resistance. However, except for the drug-efflux pump function of MFS2, other mechanisms relating to the Pdmfs2 are not fully clear. The present study reported a transcriptome investigation on the mfs2-defective P. digitatum strain. Comparing to the wild-type strain, the mfs2-defective strain showed 717 differentially expressed genes (DEGs) without prochloraz induction, and 1221 DEGs with prochloraz induction. The obtained DEGs included multiple isoforms of MFS transporter-encoding genes, ATP-binding cassette (ABC) transporter-encoding genes, and multidrug and toxic compound extrusion (MATE) family protein-encoding genes. Many of these putative drug-efflux pump protein-encoding genes had significantly lower transcript abundances in the mfs2-defective P. digitatum strain at prochloraz induction, as compared to the wild-type strain, including twenty-two MFS transporter-encoding genes (MFS1 to MFS22), two ABC transporter-encoding genes (ABC1 and ABC2), and three MATE protein-encoding genes (MATE1 to MATE3). The prochloraz induction on special drug-efflux pump protein genes in the wild-type strain was not observed in the mfs2-defective strain, including MFS21, MFS22, ABC2, MATE1, MATE2, and MATE3. On the other hand, the up-regulation of other drug-efflux pump protein genes in the mfs2-defective strain cannot recover the fungal prochloraz resistance, including MFS23, MFS26, MFS27, MFS31, MFS33, and ABC3 to ABC8. The functional enrichment of DEGs based on Kyoto Encyclopedia of Genes and Genomes (KEGG), Clusters of Orthologous Groups (COG), and euKaryotic Orthologous Groups (KOG) database resources suggested some essential contributors to the mfs2-relating prochloraz resistance, including ribosome biosynthesis-related genes, oxidative phosphorylation genes, steroid biosynthesis-related genes, fatty acid and lipid metabolism-related genes, and carbon- and nitrogen-metabolism-related genes. The results indicated that the MFS2 transporter might be involved in the regulation of multiple drug-efflux pump protein gene expressions and multiple metabolism-related gene expressions, thus playing an important role in developing P. digitatum prochloraz resistance.

Characterization and Functional Analysis of a New Calcium/Calmodulin-Dependent Protein Kinase (CaMK1) in the Citrus Pathogenic Fungus Penicillium italicum.

Calcium (Ca2+)/calmodulin-dependent protein kinases (CaMKs) act as a class of crucial elements in Ca2+-signal transduction pathways that regulate fungal growth, sporulation, virulence, and environmental stress tolerance. However, little is known about the function of such protein kinase in phytopathogenic Penicillium species. In the present study, a new CaMK gene from the citrus pathogenic fungus P. italicum, designated PiCaMK1, was cloned and functionally characterized by gene knockout and transcriptome analysis. The open reading frame of PiCaMK1 is 1209 bp in full length, which encodes 402 amino acid residues (putative molecular weight ~45.2 KD) with the highest homologous (~96.3%) to the P. expansum CaMK. The knockout mutant ΔPiCaMK1 showed a significant reduction in vegetative growth, conidiation, and virulence (i.e., to induce blue mold decay on citrus fruit). ΔPiCaMK1 was less sensitive to NaCl- or KCl-induced salinity stress and less resistant to mannitol-induced osmotic stress, indicating the functional involvement of PiCaMK1 in such environmental stress tolerance. In contrast, the PiCaMK1-complemented strain ΔPiCaMK1COM can restore all the defective phenotypes. Transcriptome analysis revealed that knockout of PiCaMK1 down-regulated expression of the genes involved in DNA replication and repair, cell cycle, meiosis, pyrimidine and purine metabolisms, and MAPK signaling pathway. Our results suggested the critical role of PiCaMK1 in regulating multiple physical and cellular processes of citrus postharvest pathogen P. italicum, including growth, conidiation, virulence, and environmental stress tolerance.

Preliminary study on the electromagnetic field treatment of osteoporosis in rats.

OBJECTIVE: In our study, the influence of PEMF on skeleton morphology and bone metabolism on rats with disuse osteoporosis was investigated, and the possibility of using it for the treatment of disuse osteoporosis was explored. METHODS: The rats in the ALN group were treated with alendronate, and the rats in the PEMF group were exposed to pulsed electromagnetic fields (3.82 mT, 10 Hz) for 40 mind-1. Rats were sacrificed by the end of 2, 4, 8 and 12 weeks, and serum and right leg bones were collected. Serum BMP-2, BGP concentrations and bone metabolism and biomechanical parameters were measured. RESULTS: The bone structural mechanical indices and material mechanical indices of the right femur in all groups of mice during weeks 2 and 4 were decreased. At week 8 the bone structural mechanical index and maximum stress of the right femur in the ALN group were markedly raised compared with the CON group (P< 0.01). Only maximum stress and strain were improved in the ALN group and had a significant difference (P< 0.05) at week 12. The serum BGP and BMP-2 concentration in the PEMF and ALN groups was increased (P< 0.05) at week 2, but this increase was not synchronized. After 8 weeks, BGP and BMP-2 level in the PEMF group was observably elevated (P<0.01) in contrast to the ALN group. CONCLUSION: From the experimental time interval analysis, PEMF can improve the mechanical stability of bone structure more gently and permanently than alendronate.

Decreased level of osteopontin in children with allergic rhinitis during sublingual immunotherapy.

OBJECTIVE: Sublingual immunotherapy (SLIT) is proven to be very effective in the treatment of allergic rhinitis (AR), but its regulatory mechanism and biomarkers for predicting efficacy are still unknown. Osteopontin (OPN), as a recently described Th2 inflammation related protein, plays key role in the pathogenesis of AR. The aim of this study was to identify the expression and role of OPN during SLIT in children. METHODS: Fifty house dust mite (HDM)-sensitized children with AR were enrolled in this study. AR children received HDM allergen extract or placebo for SLIT. Serum of different time points during treatment was collected and used for enzyme-linked immuno sorbent assay (ELISA) of OPN and related cytokines, respectively. Peripheral blood mononuclear cells from children after SLIT or placebo treatment were collected and stimulated with HDM with or without OPN/anti-OPN after one year's treatment. RESULTS: Our results showed that expression of OPN protein was decreased after one year's therapy. The decreased OPN expression was positively related to decreased Th2 cytokines and negatively related to enhanced IL-10 and TGF-ß expression. In vitro experiments confirmed that children received SLIT treatment showed decreased production of Th2 cytokines by PBMCs after HDM stimulation. CONCLUSION: During SLIT, decreased OPN expression was related to low Th2 cytokine expression and enhanced IL-10 and TGF-ß expression. High serum OPN expression predicts poor treatment efficacy. OPN may be used as a biomarker for SLIT treatment.