Molecular Engineered Hole-Extraction Materials to Enable Dopant-Free, Efficient p-i-n Perovskite Solar Cells

Two hole-extraction materials (HEMs), TPP-OMeTAD and TPP-SMeTAD, have been developed to facilitate the fabrication of efficient p-i-n perovskite solar cells (PVSCs). By replacing the oxygen atom on HEM with sulfur (from TPP-OMeTAD to TPP-SMeTAD), it effectively lowers the highest occupied molecular orbital of the molecule and provides stronger Pb-S interaction with perovskites, leading to efficient charge extraction and surface traps passivation. The TPP-SMeTAD-based PVSCs exhibit both improved photovoltaic performance and reduced hysteresis in p-i-n PVSCs over those based on TPP-OMeTAD. This work not only provides new insights on creating perovskite-HEM heterojunction but also helps in designing new HEM to enable efficient organic–inorganic hybrid PVSCs

The impact of monthly air pollution exposure and its interaction with individual factors: Insight from a large cohort study of comprehensive hospitalizations in Guangzhou area

BackgroundAlthough the association between short-term air pollution exposure and certain hospitalizations has been well documented, evidence on the effect of longer-term (e. g., monthly) air pollution on a comprehensive set of outcomes is still limited.MethodA total of 68,416 people in South China were enrolled and followed up during 2019–2020. Monthly air pollution level was estimated using a validated ordinary Kriging method and assigned to individuals. Time-dependent Cox models were developed to estimate the relationship between monthly PM10 and O3 exposures and the all-cause and cause-specific hospitalizations after adjusting for confounders. The interaction between air pollution and individual factors was also investigated.ResultsOverall, each 10 μg/m3 increase in PM10 concentration was associated with a 3.1% (95%CI: 1.3%−4.9%) increment in the risk of all-cause hospitalization. The estimate was even greater following O3 exposure (6.8%, 5.5%−8.2%). Furthermore, each 10 μg/m3 increase in PM10 was associated with a 2.3%-9.1% elevation in all the cause-specific hospitalizations except for those related to respiratory and digestive diseases. The same increment in O3 was relevant to a 4.7%−22.8% elevation in the risk except for respiratory diseases. Additionally, the older individuals tended to be more vulnerable to PM10 exposure (Pinteraction: 0.002), while the alcohol abused and those with an abnormal BMI were more vulnerable to the impact of O3 (Pinteraction: 0.052 and 0.011). However, the heavy smokers were less vulnerable to O3 exposure (Pinteraction: 0.032).ConclusionWe provide comprehensive evidence on the hospitalization hazard of monthly PM10 and O3 exposure and their interaction with individual factors

IL-17C Mitigates Murine Acute Graft-vs.-Host Disease by Promoting Intestinal Barrier Functions and Treg Differentiation

Acute graft-vs.-host disease (aGVHD) is one of the major complications and results in high mortality after allogeneic hematopoietic stem cell transplantation (allo-HSCT). IL-17C is involved in many inflammatory immune disorders. However, the role of IL-17C in aGVHD remains unknown. Here we demonstrated that IL-17C deficiency in the graft significantly promoted alloreactive T cell responses and induced aggravated aGVHD compared with wildtype donors in a fully MHC-mismatched allo-HSCT model. In contrast, IL-17C overexpression ameliorated aGVHD. IL-17C deficiency increased intestinal epithelial permeability and elevated inflammatory cytokine production, leading to an enhanced aGVHD progression. Tregs was reduced in recipients of IL-17C−/− graft, whilst restored after IL-17C overexpression. Decreased Treg differentiation was abrogated after neutralizing IFN-γ, but not IL-6. Moreover, depletion of Tregs diminished the protective effect of IL-17C. Of note, patients with low IL-17C expression displayed higher aGVHD incidence together with poor overall survival, thereby IL-17C could be an independent risk factor for aGVHD development. Our results are the first demonstrating the protective role of IL-17C in aGVHD by promoting intestinal barrier functions and Treg differentiation in a MHC fully mismatched murine aGVHD model. IL-17C may serve as a novel biomarker and potential therapeutic target for aGVHD

Overexpressed Gαi1 exerts pro-tumorigenic activity in nasopharyngeal carcinoma

Abstract The current study tested the expression and potential functions of Gαi1 in nasopharyngeal carcinoma (NPC). The Cancer Genome Atlas (TCGA) database results demonstrate that Gαi1 transcripts’ number in NPC tissues is significantly higher than that in the normal nasal epithelial tissues. Its overexpression correlates with poor survival in certain NPC patients. Moreover, Gαi1 is significantly upregulated in NPC tissues of local primary patients and in different primary human NPC cells. Whereas its expression is relatively low in cancer-surrounding normal tissues and in primary nasal epithelial cells. Genetic silencing (via shRNA strategy) or knockout (via CRISPR-sgRNA method) of Gαi1 substantially suppressed viability, proliferation, cell cycle progression, and migration in primary NPC cells, causing significant caspase-apoptosis activation. Contrarily, ectopic Gαi1 expression exerted pro-tumorigenic activity and strengthened cell proliferation and migration in primary NPC cells. Gαi1 is important for Akt-mTOR activation in NPC cells. Akt-S6K phosphorylation was downregulated after Gαi1 shRNA or KO in primary NPC cells, but strengthened following Gαi1 overexpression. In Gαi1-silenced primary NPC cells, a S473D constitutively-active mutant Akt1 (caAkt1) restored Akt-S6K phosphorylation and ameliorated Gαi1 shRNA-induced proliferation inhibition, migration reduction and apoptosis. Bioinformatics analyses proposed zinc finger protein 384 (ZNF384) as a potential transcription factor of Gαi1. In primary NPC cells, ZNF384 shRNA or knockout (via CRISPR-sgRNA method) decreased Gαi1 mRNA and protein expression, whereas ZNF384 overexpression upregulated it. Importantly, there was an increased binding between ZNF384 protein and the Gαi1 promoter in human NPC tissues and different NPC cells. In vivo studies showed that intratumoral injection of Gαi1-shRNA-expressing adeno-associated virus (AAV) impeded subcutaneous NPC xenograft growth in nude mice. Gαi1 downregulation, Akt-mTOR inactivation, and apoptosis induction were detected in Gαi1-silenced NPC xenograft tissues. Gαi1 KO also effectively inhibited the growth of NPC xenografts in nude mice. Together, overexpressed Gαi1 exerts pro-tumorigenic activity in NPC possibly by promoting Akt-mTOR activation

Genome-Wide Identification and Characterization of the TCP Gene Family in Cucumber (Cucumis sativus L.) and Their Transcriptional Responses to Different Treatments

TCP proteins are plant-specific transcription factors widely implicated in leaf morphogenesis and senescence, flowering, lateral branching, hormone crosstalk, and stress responses. However, the relationship between the transcription pattern of TCPs and organ development in cucumber has not been systematically studied. In this study, we performed a genome-wide identification of putative TCP genes and analyzed their chromosomal location, gene structure, conserved motif, and transcript expression. A total of 27 putative TCP genes were identified and characterized in cucumber. All 27 putative CsTCP genes were classified into class I and class II. Class I comprised 12 CsTCPs and Class II contained 15 CsTCPs. The 27 putative CsTCP genes were randomly distributed in five of seven chromosomes in cucumber. Four putative CsTCP genes were found to contain putative miR319 target sites. Quantitative RT-PCR revealed that 27 putative CsTCP genes exhibited different expression patterns in cucumber tissues and floral organ development. Transcript expression and phenotype analysis showed that the putative CsTCP genes responded to temperature and photoperiod and were induced by gibberellin (GA)and ethylene treatment, which suggested that CsTCP genes may regulate the lateral branching by involving in multiple signal pathways. These results lay the foundation for studying the function of cucumber TCP genes in the future

In Situ Interfacial Conjugation of Chitosan with Cinnamaldehyde during Homogenization Improves the Formation and Stability of Chitosan-Stabilized Emulsions

The emulsifying properties of a natural cationic polysaccharide (chitosan) were improved by in situ conjugation with a natural essential oil (cinnamaldehyde, CA) during homogenization. In the absence of CA, chitosan-coated medium-chain triglyceride droplets were highly susceptible to creaming and coalescence at pH values ranging from 1 to 6.5. However, incorporation of relatively low levels of CA in the oil phase greatly improved the formation and stability of oil-in-water emulsions. These effects were attributed to two main factors: (i) covalent binding of lipophilic CA moieties to hydrophilic chitosan chains leading to conjugates with a good surface activity and (ii) interfacial cross-linking of adsorbed chitosan layers by CA leading to the formation of a rigid polymeric coating around the lipid droplets, which improved their stability against coalescence. The encapsulation technique developed in this study may be useful for applications in a range of commercial products; regulatory and flavor issues associated with chitosan and CA would have to be addressed

How long-term PM exposure may affect all-site cancer mortality: Evidence from a large cohort in southern China

Background: Evidence of a potential causal link between long-term exposure to particulate matter (PM) and all-site cancer mortality from large population cohorts remained limited and suffered from residual confounding issues with traditional statistical methods. Aims: We aimed to examine the potential causal relationship between long-term PM exposure and all-site cancer mortality in South China using causal inference methods. Methods: We used a cohort in southern China that recruited 580,757 participants from 2009 through 2015 and tracked until 2020. Annual averages of PM1, PM2.5, and PM10 concentrations were generated with validated spatiotemporal models. We employed a causal inference approach, the Marginal Structural Cox model, based on observational data to evaluate the association between long-term exposure to PM and all-site cancer mortality. Results: With an increase of 1 µg/m³ in PM1, PM2.5, and PM10, the hazard ratios (HRs) and 95% confidence interval (CI) for all-site cancer were 1.033 (95% CI: 1.025–1.041), 1.032 (95% CI: 1.027–1.038), and 1.020 (95% CI: 1.016–1.025), respectively. The HRs (95% CI) for digestive system and respiratory system cancer mortality associated with each 1 µg/m³ increase in PM1 were 1.022 (1.009–1.035) and 1.053 (1.038–1.068), respectively. In addition, inactive participants, who never smoked, or who lived in areas of low surrounding greenness were more susceptible to the effects of PM exposure, the HRs (95% CI) for all-site cancer mortality were 1.042 (1.031–1.053), 1.041 (1.032–1.050), and 1.0473 (1.025–1.070) for every 1 µg/m³ increase in PM1, respectively. The effect of PM1 tended to be more pronounced in the low-exposure group than in the general population, and multiple sensitivity analyses confirmed the robustness of the results. Conclusion: This study provided evidence that long-term exposure to PM may elevate the risk of all-site cancer mortality, emphasizing the potential health benefits of improving air quality for cancer prevention