Enhancing the Efficiency and Stability of Tin-Lead Perovskite Solar Cells via Sodium Hydroxide Dedoping of PEDOT:PSS.

Tin-lead (Sn-Pb) perovskite solar cells (PSCs) have gained interest as candidates for the bottom cell of all-perovskite tandem solar cells due to their broad absorption of the solar spectrum. A notable challenge arises from the prevalent use of the hole transport layer, PEDOT:PSS, known for its inherently high doping level. This high doping level can lead to interfacial recombination, imposing a significant limitation on efficiency. Herein, NaOH is used to dedope PEDOT:PSS, with the aim of enhancing the efficiency of Sn-Pb PSCs. Secondary ion mass spectrometer profiles indicate that sodium ions diffuse into the perovskite layer, improving its crystallinity and enlarging its grains. Comprehensive evaluations, including photoluminescence and nanosecond transient absorption spectroscopy, confirm that dedoping significantly reduces interfacial recombination, resulting in an open-circuit voltage as high as 0.90 V. Additionally, dedoping PEDOT:PSS leads to increased shunt resistance and high fill factor up to 0.81. As a result of these improvements, the power conversion efficiency is enhanced from 19.7% to 22.6%. Utilizing NaOH to dedope PEDOT:PSS also transitions its nature from acidic to basic, enhancing stability and exhibiting less than a 7% power conversion efficiency loss after 1176 h of storage in N2 atmosphere.

Chicken miR-126-5p negatively regulates antiviral innate immunity by targeting TRAF3.

Innate immunity plays an essential role in preventing the invasion of pathogenic microorganisms. However, innate immunity is a double-edged sword, whose excessive activation is detrimental to immune homeostasis and even leads to a "cytokine storm" of the infected host. The host develops a series of negative regulatory mechanisms to balance the immune response. Here, we report a negative regulatory mechanism of chicken innate immunity mediated by miRNA. In the GEO database, we found that miR-126-5p was markedly up-regulated in chickens infected by RNA viruses. Upregulation of miR-126-5p by RNA virus was then further shown via both a cell model and in vivo tests. Overexpression of miR-126-5p significantly inhibited the expression of interferon and inflammatory cytokine-related genes induced by RNA viruses. The opposite result was achieved after the knockdown of miR-126-5p expression. Bioinformatics analysis identified TRAF3 as candidate target gene of miR-126-5p. Experimentally, miR-126-5p can target TRAF3, as shown by the effects of miR-126-5p on the endogenous expression of TRAF3, and by the TRAF3 3'UTR driven luciferase reporter assay. Furthermore, we demonstrated that miR-126-5p negatively regulated innate immunity by blocking the MAVS-TRAF3-TBK1 axis, with a co-expression assay. Overall, our results suggest that miR-126-5p is involved in the negative regulation of chicken innate immunity, which might contribute to maintaining immune balance.

The identification of a shorter cyclic GMP-AMP synthase gene from chickens and bioinformatics analysis of its potential signaling in IFN regulation.

Chicken has an impaired innate immune system compared with mammals. Some key innate immune genes, such as Retinoic acid-inducible gene I (RIG-I), Toll like receptor 8 (TLR8), Absent in melanoma 2 (AIM2) and IFN regulatory factor 3 (IRF3), are inactivated or missing due to DNA Insertion, gene partial deletion, or gene total deletion. A predicted N-terminal deleted chicken Cyclic GMP-AMP synthase (chcGAS) gene, which is proven as the most essential cytosolic DNA sensor in other species, be obtained from the GenBank database. The large fragment deletion makes the sequence accuracy and functional integrity of the predicted chcGAS open to dispute. Here, the exact chcGAS gene was first experimentally determined by 5' and 3' rapid amplification of cDNA ends (RACE) PCR, which specifically lacked 83 amino acids in the DNA binding domain. In addition, the conservation and feasibility of cGAS-STING signaling among different species were conducted by bioinformatics to explore the possibility of the existence of the conserved pathway in chickens. The basic characteristics of the chcGAS, such as macroscopic and microscopic distribution patterns of chcGAS have been studied. In order to better research the function of chGAS, a chcGAS knockout chicken cell line has been generated by CRISPR/CAS9. Together, chicken owns an N-terminal deleted cGAS gene, and more experimental evidences are urgently needed to verify the functional integrity of chcGAS.

Chicken DDX1 Acts as an RNA Sensor to Mediate IFN-ß Signaling Pathway Activation in Antiviral Innate Immunity.

Chickens are the natural host of Newcastle disease virus (NDV) and avian influenza virus (AIV). The discovery that the RIG-I gene, the primary RNA virus pattern recognition receptor (PRR) in mammals, is naturally absent in chickens has directed attention to studies of chicken RNA PRRs and their functions in antiviral immune responses. Here, we identified Asp-Glu-Ala-Asp (DEAD)-box helicase 1 (DDX1) as an essential RNA virus PRR in chickens and investigated its functions in anti-RNA viral infections. The chDDX1 gene was cloned, and cross-species sequence alignment and phylogenetic tree analyses revealed high conservation of DDX1 among vertebrates. A quantitative RT-PCR showed that chDDX1 mRNA are widely expressed in different tissues in healthy chickens. In addition, chDDX1 was significantly upregulated after infection with AIV, NDV, or GFP-expressing vesicular stomatitis virus (VSV-GFP). Overexpression of chDDX1 in DF-1 cells induced the expression of IFN-ß, IFN-stimulated genes (ISGs), and proinflammatory cytokines; it also inhibited NDV and VSV replications. The knockdown of chDDX1 increased the viral yield of NDV and VSV and decreased the production of IFN-ß, which was induced by RNA analog polyinosinic-polycytidylic acid (poly[I:C]), by AIV, and by NDV. We used a chicken IRF7 (chIRF7) knockout DF-1 cell line in a series of experiments to demonstrate that chDDX1 activates IFN signaling via the chIRF7 pathway. Finally, an in-vitro pulldown assay showed a strong and direct interaction between poly(I:C) and the chDDX1 protein, indicating that chDDX1 may act as an RNA PRR during IFN activation. In brief, our results suggest that chDDX1 is an important mediator of IFN-ß and is involved in RNA- and RNA virus-mediated chDDX1-IRF7-IFN-ß signaling pathways.

Application of Thermosonication in Red Pitaya Juice Processing: Impacts on Native Microbiota and Quality Properties during Storage.

The effects of thermosonication (TS) on microbial safety and quality of red pitaya juice during storage were assessed in this study. Freshly prepared red pitaya juices were thermosonicated at 475 W and 56 °C for 20 min. Upon TS processing, native microbiota including aerobic bacteria, yeasts, and molds reduced to less than 10 CFU/mL. Their growth during storage were slow and equal to thermal-processed (83 °C, 1.5 min) samples. During storage at 4 °C for 28 days, soluble solid content, pH, activities of polyphenol oxidase and peroxidase, and browning degree remained unchanged. A visible color decay was observed in TS-processed samples at day 10, mainly resulting from decomposition of betacyanins and the growth of residual native microbiota. Compared to thermal-treated juices, better color retention was obtained by TS treatment. Therefore, TS is a promising alternative technology of thermal methods of juice processing, with equal shelf life and better quality retention effects.

Development of Environmentally Friendly Atom Transfer Radical Polymerization.

Atom transfer radical polymerization (ATRP) is one of the most successful techniques for the preparation of well-defined polymers with controllable molecular weights, narrow molecular weight distributions, specific macromolecular architectures, and precisely designed functionalities. ATRP usually involves transition-metal complex as catalyst. As the most commonly used copper complex catalyst is usually biologically toxic and environmentally unsafe, considerable interest has been focused on iron complex, enzyme, and metal-free catalysts owing to their low toxicity, inexpensive cost, commercial availability and environmental friendliness. This review aims to provide a comprehensive understanding of iron catalyst used in normal, reverse, AGET, ICAR, GAMA, and SARA ATRP, enzyme as well as metal-free catalyst mediated ATRP in the point of view of catalytic activity, initiation efficiency, and polymerization controllability. The principle of ATRP and the development of iron ligand are briefly discussed. The recent development of enzyme-mediated ATRP, the latest research progress on metal-free ATRP, and the application of metal-free ATRP in interdisciplinary areas are highlighted in sections. The prospects and challenges of these three ATRP techniques are also described in the review.

Functional Characterization of Duck STING in IFN-ß Induction and Anti-H9N2 Avian Influenza Viruses Infections.

The stimulator of interferon genes (STING) protein has been shown to play a pivotal role in response to both cytosolic RNA and dsDNA to elicit interferon (IFN) production in mammals. However, the role of duck STING (DuSTING) in antiviral innate immunity, especially in anti-RNA virus infection, has yet to be elucidated. In this study, the function of DuSTING in IFN induction and its role in anti-RNA virus infections were studied. DuSTING was amplified via reverse transcription-polymerase chain reaction (RT-PCR) from Pekin duck, showing that its cDNA sequence contains an open reading frame (ORF) of 1,149 bp and encodes 382 amino acids (aa). Sequence alignment showed that DuSTING protein shares 71.1, 43.4, and 33.3% identity with chickens, humans, and zebra fish, respectively. Overexpression of DuSTING in duck embryo fibroblasts (DEFs) strongly activated IFN-ß promotor activity. Deletion mutant analysis revealed that the first 42 aa containing the first transmembrane (TM) domains and the last 32 aa containing a part of the C-terminal tail (CTT) are essential for its IFN-ß activation. In vitro experiments showed that the mRNA levels of DuSTING and IFNs were all upregulated when the DEFs were infected with H9N2 avian influenza virus (AIV) SH010, while overexpression of DuSTING inhibited the replication of this virus. In vivo studies showed that DuSTING mRNA was widely expressed in different tissues, and was up-regulated in the spleen and lung of ducks challenged with SH010. In conclusion, our results indicate that DuSTING is an essential IFN mediator and plays a role in anti-RNA virus innate immunity.

IRF7 Is Involved in Both STING and MAVS Mediating IFN-ß Signaling in IRF3-Lacking Chickens.

IFN regulatory factor (IRF) 3 has been identified as the most critical regulator of both RNA and DNA virus-induced IFN production in mammals. However, ambiguity exists in research on chicken IRFs; in particular IRF3 seems to be missing in chickens, making IFN regulation in chickens unclear. In this study, we comprehensively investigated the potential IFN-related IRFs in chickens and showed that IRF7 is the most critical IFN-ß regulator in chickens. With a chicken IRF7 (chIRF7) knockout DF-1 cell line, we conducted a series of experiments to demonstrate that chIRF7 is involved in both chicken STING (chSTING)- and chicken MAVS (chMAVS)-mediated IFN-ß regulation in response to DNA and RNA viral infections, respectively. We further examined the mechanisms of chIRF7 activation by chSTING. We found that chicken TBK1 (chTBK1) is indispensable for chIRF7 activation by chSTING as well as that chSTING interacts with both chIRF7 and chTBK1 to function as a scaffold in chIRF7 activation by chTBK1. More interestingly, we discovered that chSTING mediates the activation of chIRF7 through a conserved SLQxSyS motif. In short, we confirmed that although IRF3 is missing in chickens, they employ IRF7 to reconstitute corresponding IFN signaling to respond to both DNA and RNA viral infections. Additionally, we uncovered a mechanism of chIRF7 activation by chSTING. The results will enrich and deepen our understanding of the regulatory mechanisms of the chicken IFN system.

Host immune responses of pigeons infected with Newcastle disease viruses isolated from pigeons.

Newcastle disease (ND), affecting over 250 bird species, is caused by the Newcastle disease virus (NDV). ND is one of the leading causes of morbidity and mortality in pigeons. Most studies investigating NDV in pigeons have focused on the epidemiology and pathogenicity of the virus. However, the host immune responses in pigeons infected with NDVs remains largely unclear. In this study, we investigated the host immune responses in pigeons infected with two NDV stains, a pigeon paramyxovirus type 1(PPMV-1) strain, GZH14, and a genotype II virus, KP08. Although no mortality was observed upon infection with either virus, obvious neurological effects were observed in the GZH14-infected pigeons but not in the KP08-infected pigeons. Both viruses could replicate in the examined tissues, namely brain, lung, spleen, trachea, kidney, and bursa of Fabricius. The expression level of RIG-I, IL-6, IL-1ß, CCL5, and IL-8 were up-regulated by both viruses in the brain, lung and spleen at 3 and 7 days post-infection. Notably, these proinflammatory cytokines and chemokines showed more intense expression in the brain, when induced by the GZH14 strain than with the KP08 strain. These results indicate that the intense inflammatory responses induced by PPMV-1 in the brain may be a critical determinant of neurological symptoms in pigeons infected with PPMV-1. Our study provides new insight into the pathogenicity of PPMV-1 in pigeons attributable to the host immune responses.

Immune responses of mature chicken bone-marrow-derived dendritic cells infected with Newcastle disease virus strains with differing pathogenicity.

Infection of chickens with virulent Newcastle disease virus (NDV) is associated with severe pathology and increased morbidity and mortality. The innate immune response contributes to the pathogenicity of NDV. As professional antigen-presenting cells, dendritic cells (DCs) play a unique role in innate immunity. However, the contribution of DCs to NDV infection has not been investigated in chickens. In this study, we selected two representative NDV strains, i.e., the velogenic NDV strain Chicken/Guangdong/GM/2014 (GM) and the lentogenic NDV strain La Sota, to investigate whether NDVs could infect LPS-activated chicken bone-derived marrow DCs (mature chicken BM-DCs). We compared the viral titres and innate immune responses in mature chicken BM-DCs following infection with those strains. Both NDV strains could infect mature chicken BM-DC, but the GM strain showed stronger replication capacity than the La Sota strain in mature chicken BM-DCs. Gene expression profiling showed that MDA5, LGP2, TLR3, TLR7, IFN-α, IFN-ß, IFN-γ, IL-1ß, IL-6, IL-18, IL-8, CCL5, IL-10, IL-12, MHC-I, and MHC-II levels were altered in mature DCs after infection with NDVs at all evaluated times postinfection. Notably, the GM strain triggered stronger innate immune responses than the La Sota strain in chicken BM-DCs. However, both strains were able to suppress the expression of some cytokines, such as IL-6 and IFN-α, in mature chicken DCs at 24 hpi. These data provide a foundation for further investigation of the role of chicken DCs in NDV infection.

S1PR1 expression correlates with inflammatory responses to Newcastle disease virus infection.

Newcastle disease virus (NDV) is the causative agent of Newcastle disease, which is characterized by inflammatory pathological changes in the organs of chickens. The inflammatory response to this disease has not been well characterized. Previous reports showed that the sphingosine-1-phosphate-1 receptor (S1PR1), a G protein-coupled receptor, is important to the activation of inflammatory responses. To understand better the viral pathogenesis and host inflammatory response, we analyzed S1PR1 expression during NDV infection. We observed a direct correlation between chicken embryo fibroblast (CEF) cellular inflammatory responses and S1PR1 expression. Virulent NDV-infected CEF cells also had elevated levels of pro-inflammatory cytokines (IL-1ß, IL-6 and IL-18). When S1PR1 was inhibited by using the specific antagonist W146, pro-inflammatory cytokine production declined. Overexpression of S1PR1 resulted in increased virus-induced IL-1ß production. S1PR1 expression levels did not impact significantly NDV replication. These findings highlight the important role of S1PR1 in inflammatory responses in NDV infection.

Meta-analysis of the association of brain-derived neurotrophic factor Val66Met polymorphism with obsessive-compulsive disorder.

OBJECTIVE: Brain-derived neurotrophic factor (BDNF) plays an important role in neural survival and was proposed to be related to psychiatric disorders. Val66Met (also known as rs6265 or G196A), the only known functional polymorphism of the BDNF gene, has been widely studied and considered to be associated with risk of some psychiatric disorders such as bipolar disorder and schizophrenia. However, studies evaluating its association with obsessive-compulsive disorder (OCD) obtained inconsistent results. The purpose of this study was to derive a more precise estimation of the association between BDNF Val66Met polymorphism and OCD susceptibility by a meta-analysis. METHOD: We carried a structured literature search in PubMed, Embase, PsycINFO and Chinese Biomedical Database up to December 2014; and retrieved all eligible case-control studies according to the including criteria. Meta-analysis was performed for four genetic models: allelic model: Met versus Val; additive model: Met/Met versus Val/Val; recessive model: Met/Met versus Val/Val+Val/Met; and dominant model: Val/Met+Met/Met versus Val/Val. Stratified analyses were performed by ethnicity and gender where appropriate. RESULTS: A total of eight articles with nine studies including 1632 OCD cases and 2417 controls were identified. No significant association was detected in any comparison when the whole data were pooled together or stratified by ethnicity or gender in all four genetic models (p>0.05 for each comparison). CONCLUSION: Despite some limitations, our meta-analysis suggests that no significant association exists between the BDNF Val66Met polymorphism and OCD susceptibility.

[Expressions of neurotransmitters in patients of insomnia differentiated as liver stagnation transforming into fire treated with acupuncture].

OBJECTIVE: To compare the difference in the efficacy between acupuncture and oral administration of trazodone and the expressions of neurotransmitters in patients of insomnia differentiated as liver stagnation transforming into fire. METHODS: Seventy patients of insomnia differentiated as liver stagnation transforming into fire were randomized into an observation group and a control group, 35 cases in each one. In the observation group, acupuncture therapy was adopted at Shenmen (HT 7), Baihui (GV 20), Yintang (GV 29), Hegu (LI 4), Taichong (LR 3), etc. The needles were retained for 20 min each time. The treatment was given once a day, the treatment of 2 weeks made one session. In the control group, trazodone, 100 mg, oral administration, once a day, the treatment of 2 weeks made one session. Two sessions were required in the two groups. The scores in Pittsburgh sleep quality index (PSQI) and Asberg rating scale for side effects (SERS), the levels of neurotransmitters such as 5-hydroxy tryptamine (5-HT) and norepinephrine (NE) and the expressions of protein kinase C (PKC) and brain-derived neurotrophic factor (BDNF) in peripheral blood were observed before and after treatment in the two groups. RESULTS: PSQI score and SERS score after treatment were all decreased compared with those in both groups before treatment (both P<0. 05). After treatment, PSQI score and SERS score in the observation group were lower apparently than those in the control group (both P<0. 05). After treatment NE content and PKC level were decreased; 5-HT content and BDNF mRNA were increased compared with those in both groups before treatment (all P<0. 05). NE content and PKC level in the observation group were lower apparently than those in the control group (both P<0. 05). The serum 5-HT content and BDNF mRNA expression in the observation group were higher than those in the control group separately (both P<0. 05). CONCLUSION: Acupuncture therapy improves the sleeping quality of patients of insomnia differentiated as liver stagnation transforming into fire, and reduces serum NE level and increases 5-HT content and BDNF expression, which achieves the better efficacy as compared with the oral administration of trazodone. It is one of the effective approaches to the treatment of insomnia differentiated as liver stagnation transforming into fire.

Olanzapine-induced weight gain plays a key role in the potential cardiovascular risk: evidence from heart rate variability analysis.

Patients with schizophrenia have a higher risk for cardiovascular disease (CVD) than the general population. Research has suggested that autonomic imbalance is a common pathway to increased morbidity and mortality for CVD. Heart rate variability (HRV) analysis is a non-invasive method that assesses autonomic imbalance, and low HRV is correlated with high cardiovascular risk. Olanzapine, a widely used antipsychotic drug, is considered to have good cardiac safety because of not causing significant corrected QT-interval (QTc) prolongation; however, it is still unclear whether olanzapine affects HRV. We recruited 83 patients with schizophrenia who were medication-free for at least 1 month and tested their HRV at the baseline and 4 weeks after treatment with olanzapine. We found that patients who had substantial weight gain (EWG) manifested significantly lower HRV than those who had non-substantial weight gain (NWG) and that HRV decrease was positively correlated to an increase in body mass index (BMI) and weight gain. Our results indicate that olanzapine-induced weight gain may play an important role in its potential cardiovascular risk. Since olanzapine has a very high potential for weight gain compared with other antipsychotics, further research is needed to explore its cardiovascular safety profile, specifically long-term cardiac safety.

Effect of astragalus injection on serious abdominal traumatic patients' cellular immunity.

OBJECTIVE: To explore the change of serious abdominal traumatic patients' cellular immunity and the effect of Astragalus Injection (AI) on it. METHODS: Sixty-three serious abdominal traumatic patients were randomly assigned into two groups, the conventional group and the treated group, patients in the conventional group were given conventional treatment, while others in the treated group were given conventional treatment as the basis, with AI 20 ml was added into 250 ml of 5% glucose solution given through intravenous dripping, and then on the first day and 14th day, their T cell activated antigens as well as that of 10 healthy subjects were monitored. RESULTS: On the first day, in the conventional group and treated group, the levels of CD(3)(+), CD(4)(+), CD(4)(+)/CD(8)(+), CD(16)(+), CD(69)(+) and CD(3)(+)/homologous leucocytic antigen-DR (HLA-DR(+)) were apparently lower than those in the healthy group (P < 0.05), while the CD(8)(+) was significantly higher than that in the healthy group (P < 0.05), and there was no significant difference between the conventional group and the treated group (P > 0.05); on the 14th days, the levels of CD(3)(+), CD(4)(+), CD(4)(+)/CD(8)(+), CD(16)(+), CD(69)(+) and CD(3)(+)/HLA-DR(+) of the treated group got closed to healthy subject value, and got even higher than those of conventional group (P < 0.05); CD(8)(+) got close to that of healthy subjects, while obviously lower than that of conventional group (P < 0.05). CONCLUSION: After serious abdominal trauma, cellular immunity lowered, auxiliary use of AI was beneficial to the restoration of cellular immunity.

[Correlation of the changes of T lymphocyte phenotype to tumor stage and operative pattern of gastric cancer].

BACKGROUND & OBJECTIVE: Immunity, especially cellular immunity, of patients with tumor is related to tumorigenesis. The correlation of changes of T Lymphocyte phenotype to tumor stage and operative pattern of gastric cancer is unclear. This study was to evaluate the perioperative immune state in patients with gastric cancer (GC) of different stage and accepted different operative pattern. METHODS: Six kinds of T lymphocyte phenotype in 33 GC patients were measured by flow cytometry before and after operation, and compared with that of benign disease patients. RESULTS: With progress of cancer stage, CD3, CD4, CD4/CD8, CD16, and CD69 gradually decreased, while CD8 gradually increased (P< 0.05). There was no significant difference of activated T cell CD3+/HLA-DR+ among patients of stage I,II,III. After radical resection, CD8 decreased, while CD3, CD4, CD4/CD8, CD16, CD69, and CD3+/HLA-DR+ increased significantly (P< 0.01). CD3, and CD4 unchanged after palliative operation. CD16, and CD4/CD8 further decreased in patients with unresectable tumor (P< 0.05). CONCLUSIONS: The preoperative immune state of GC patients is negatively related to cancer stage. Tumor removal may improve the cellular immunity of patients.