Compared to efficient green and near‐infrared light‐emitting diodes (LEDs), less progress has been made on deep‐blue perovskite LEDs. They suffer from inefficient domain various number of PbX6− ...layers (n) control, resulting in a series of unfavorable issues such as unstable color, multipeak profile, and poor fluorescence yield. Here, a strategy involving a delicate spacer modulation for quasi‐2D perovskite films via an introduction of aromatic polyamine molecules into the perovskite precursor is reported. With low‐dimensional component engineering, the n1 domain, which shows nonradiative recombination and retarded exciton transfer, is significantly suppressed. Also, the n3 domain, which represents the population of emission species, is remarkably increased. The optimized quasi‐2D perovskite film presents blue emission from the n3 domain (peak at 465 nm) with a photoluminescence quantum yield (PLQY) as high as 77%. It enables the corresponding perovskite LEDs to deliver stable deep‐blue emission (CIE (0.145, 0.05)) with an external quantum efficiency (EQE) of 2.6%. The findings in this work provide further understanding on the structural and emission properties of quasi‐2D perovskites, which pave a new route to design deep‐blue‐emissive perovskite materials.
A quasi‐two‐dimensional perovskite film with stable domain distribution is prepared based on a new spacer. The film containing pure bromide perovskite exhibits enhanced deep‐blue fluorescence with quantum yield of 77% by low‐dimensional component engineering. As a result, the corresponding light‐emitting diodes deliver stable deep‐blue emission with a peak external quantum efficiency of 2.6%.
Urbanization is increasing worldwide, with major impacts on biodiversity, species interactions and ecosystem functioning. Pollination is an ecosystem function vital for terrestrial ecosystems and ...food security; however, the processes underlying the patterns of pollinator diversity and the ecosystem services they provide in cities have seldom been quantified. Here, we perform a comprehensive meta‐analysis of 133 studies examining the effects of urbanization on pollinators and pollination. Our results confirm the widespread negative impacts of urbanization on pollinator richness and abundance, with Lepidoptera being the most affected group. Furthermore, pollinator responses were found to be trait‐specific, with below‐ground nesting and solitary Hymenoptera, and spring flyers more severely affected by urbanization. Meanwhile, cities promote non‐native pollinators, which may exacerbate conservation risks to native species. Surprisingly, despite the negative effects of urbanization on pollinator diversity, pollination service measured as seed set is enhanced in non‐tropical cities likely due to abundant generalists and managed pollinators therein. We emphasize that the richness of local flowering plants could mitigate the negative impacts of urbanization on pollinator diversity. Overall, the results demonstrate the varying magnitudes of multiple moderators on urban pollinators and pollination services and could help guide conservation actions for biodiversity and ecosystem function for a sustainable future.
Urbanization is increasing worldwide, with major impacts on biodiversity and ecosystem service. Our meta‐analysis of 133 studies examining urbanization effects on pollinators and pollination showed that the magnitudes of the effects were dependent on the taxonomic group of the pollinator, its origin and functional traits. Despite pollinator decline in non‐tropical cities, pollination services measured as seed sets are enhanced.
Solar energy is considered the most promising energy source for the future. Nanocomposites of TiO2 and CdS (denoted as TiO2/CdS) compose a class of materials with potential application in the ...photocatalysis and photovoltaic industry due to simple compositions, easily controlled microstructures and high extinction coefficients. TiO2/CdS nanocomposites with different microstructures have been designed and prepared over the past 30 years, and their performance for photocatalytic hydrogen production through water splitting and quantum-dot-sensitized solar cells was studied. This paper reviewed recent advances in the TiO2/CdS nanocomposite. The preparation, microstructure and application of the TiO2/CdS nanocomposite powder, TiO2/CdS nanocomposite film, and TiO2/CdS-based multiple nanocomposite and the interfacial charge transfer between TiO2 and CdS were introduced and summarized. Future developments of the TiO2/CdS nanocomposite were also discussed.
Nucleophosmin (NPM1) is the most commonly mutated gene in acute myeloid leukemia (AML) resulting in aberrant cytoplasmic translocation of the encoded nucleolar protein (NPM1c
). NPM1c
maintains a ...unique leukemic gene expression program, characterized by activation of HOXA/B clusters and MEIS1 oncogene to facilitate leukemogenesis. However, the mechanisms by which NPM1c
controls such gene expression patterns to promote leukemogenesis remain largely unknown. Here, we show that the activation of HOXBLINC, a HOXB locus-associated long non-coding RNA (lncRNA), is a critical downstream mediator of NPM1c
-associated leukemic transcription program and leukemogenesis. HOXBLINC loss attenuates NPM1c
-driven leukemogenesis by rectifying the signature of NPM1c
leukemic transcription programs. Furthermore, overexpression of HoxBlinc (HoxBlincTg) in mice enhances HSC self-renewal and expands myelopoiesis, leading to the development of AML-like disease, reminiscent of the phenotypes seen in the Npm1 mutant knock-in (Npm1
) mice. HoxBlincTg and Npm1
HSPCs share significantly overlapped transcriptome and chromatin structure. Mechanistically, HoxBlinc binds to the promoter regions of NPM1c
signature genes to control their activation in HoxBlincTg HSPCs, via MLL1 recruitment and promoter H3K4me3 modification. Our study reveals that HOXBLINC lncRNA activation plays an essential oncogenic role in NPM1c
leukemia. HOXBLINC and its partner MLL1 are potential therapeutic targets for NPM1c
AML.
Parkinson’s disease (PD) is one of the most common neurodegenerative diseases. Although its pathogenesis remains unclear, a number of studies indicate that microglia‐mediated neuroinflammation makes ...a great contribution to the pathogenesis of PD. Melatonin receptor 1 (MT1) is widely expressed in glia cells and neurons in substantia nigra (SN). Neuronal MT1 is a neuroprotective factor, but it remains largely unknown whether dysfunction of microglial MT1 is involved in the PD pathogenesis. Here, we found that MT1 was reduced in microglia of SN in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐induced PD mouse model. Microglial MT1 activation dramatically inhibited lipopolysaccharide (LPS)‐induced neuroinflammation, whereas loss of microglial MT1 aggravated it. Metabolic reprogramming of microglia was found to contribute to the anti‐inflammatory effects of MT1 activation. LPS‐induced excessive aerobic glycolysis and impaired oxidative phosphorylation (OXPHOS) could be reversed by microglial MT1 activation. MT1 positively regulated pyruvate dehydrogenase alpha 1 (PDHA1) expression to enhance OXPHOS and suppress aerobic glycolysis. Furthermore, in LPS‐treated microglia, MT1 activation decreased the toxicity of conditioned media to the dopaminergic (DA) cell line MES23.5. Most importantly, the anti‐inflammatory effects of MT1 activation were observed in LPS‐stimulated mouse model. In general, our study demonstrates that MT1 activation inhibits LPS‐induced microglial activation through regulating its metabolic reprogramming, which provides a mechanistic insight for microglial MT1 in anti‐inflammation.
A schematic diagram shows the involvement of metabolic reprogramming in MT1 activation‐mediated inhibition of LPS‐induced microglial activation. Once microglia suffered LPS insults, microglia would transfer into over‐activated state, accompanied by converting their metabolic status from OXPHOS to aerobic glycolysis. However, microglial MT1 activation could promote PDHA1 expression, leading to reverse LPS‐mediated microglial metabolic reprogramming, thereby, suppressing microglial activation.
...developmental stages of B cells, that is B220+CD43+IgM−IgD− (pro‐B), B220+CD43−IgM−IgD− (pre‐B), B220+CD43−IgM+IgD− (immature B) and B220+CD43−IgM+IgD+ (mature B), were detected in mouse BM, ...intestinal lamina propria (LPL) and Peyer's patches (PPs) by flow cytometry. ...the expression levels of CD40, CD80 and MHC‐Ⅱ on B cells were detected in mouse SPL, MLN and PPs. ...we examined the Secretory Immunoglobulin A (SIgA) level in intestinal lavage fluid and serum IgM, IgA and Immunoglobulin G (IgG) by ELISA. ...LGG intervention can promote the development and maturation of B lymphocytes, enhance the activation and antigen‐presentation ability of B lymphocytes, and regulate the secretion of immunoglobulin by B lymphocytes. ...LGG can regulate the mucosal immunity and humoural immunity of mice.
Shrimp white spot disease (WSD), which is caused by white spot syndrome virus (WSSV), is one of the world's most serious shrimp diseases. Our objective in this study was to use an immunomagnetic ...reduction (IMR) assay to develop a highly sensitive, automatic WSSV detection platform targeted against ICP11 (the most highly expressed WSSV protein). After characterizing the magnetic reagents (Fe3O4 magnetic nanoparticles coated with anti ICP11), the detection limit for ICP11 protein using IMR was approximately 2 x 10(-3) ng/ml, and the linear dynamic range of the assay was 0.1~1 x 10(6) ng/ml. In assays of ICP11 protein in pleopod protein lysates from healthy and WSSV-infected shrimp, IMR signals were successfully detected from shrimp with low WSSV genome copy numbers. We concluded that this IMR assay targeting ICP11 has potential for detecting the WSSV.
The grafts of fluorophores 9‐anthraldehyde (AD) and 9‐phenanthrenecarboxaldehyde (PD), respectively, on the one‐dimensional spin‐crossover compound Fe(L)3(ClO4)2 (FeL, L=4‐amino‐1,2,4‐triazole) by ...post‐synthetic aldimine condensation reactions produced two spin‐crossover (SCO)–fluorescent hybrid materials, that is, FeL‐AD and FeL‐PD. The spin‐crossover critical temperatures of the two materials both centered at Tc↓=254 and Tc↑=256 K, whereas the fluorescence intensities of the two materials featured functions of the temperature that strictly synchronized with the spin‐crossover processes, which showed that the ligand‐centered fluorescence was dominated by the spin states of the ferrous ions. The bifunctional entities (spin‐crossover centers and fluorophores) in FeL‐AD or FeL‐PD showed spectral band overlap that purported the Förster resonance energy transfer mechanism of such spin‐crossover–fluorescence correlation. The post‐synthetic modification of SCO materials and the relationship between the fluorescence and the SCO may be helpful in the development of multifunctional materials that can be sensitive to multiple stimuli.
Reciprocal conclusion: Two hybrid spin‐crossover–fluorescent (FL) materials made by post‐synthetic aldimine condensation reactions exhibit synchronization of changes in the spin states (hs=high spin, ls=low spin) and the fluorescence intensity, giving the possibility to reciprocally report spin states and fluorescence in one system (see figure).
The cell‐to‐cell transfer of α‐synuclein (α‐Syn) greatly contributes to Parkinson's disease (PD) pathogenesis and underlies the spread of α‐Syn pathology. During this process, extracellular α‐Syn can ...activate microglia and neuroinflammation, which plays an important role in PD. However, the effect of extracellular α‐Syn on microglia autophagy is poorly understood. In the present study, we reported that extracellular α‐Syn inhibited the autophagy initiation, as indicated by LC3‐II reduction and p62 protein elevation in BV2 and cultured primary microglia. The in vitro findings were verified in microglia‐enriched population isolated from α‐Syn‐overexpressing mice induced by adeno‐associated virus (AAV2/9)‐encoded wildtype human α‐Syn injection into the substantia nigra (SN). Mechanistically, α‐Syn led to microglial autophagic impairment through activating toll‐like receptor 4 (Tlr4) and its downstream p38 and Akt‐mTOR signaling because Tlr4 knockout and inhibition of p38, Akt as well as mTOR prevented α‐Syn‐induced autophagy inhibition. Moreover, inhibition of Akt reversed the mTOR activation but failed to affect p38 phosphorylation triggered by α‐Syn. Functionally, the in vivo evidence showed that lysozyme 2 Cre (Lyz2cre)‐mediated depletion of autophagy‐related gene 5 (Atg5) in microglia aggravated the neuroinflammation and dopaminergic neuron losses in the SN and exacerbated the locomotor deficit in α‐Syn‐overexpressing mice. Taken together, the results suggest that extracellular α‐Syn, via Tlr4‐dependent p38 and Akt‐mTOR signaling cascades, disrupts microglial autophagy activity which synergistically contributes to neuroinflammation and PD development.
Autophagy‐dependent and independent machinery synergistically contribute to hα‐Syn‐caused neuroinflammation in PD. The basal autophagy activity restricts microglia inflammation. Extracellular hα‐Syn interacts with and activates Tlr4, resulting in inflammatory responses, as well as autophagy suppression in microglia via Tlr4‐dependent p38 and Akt/mTOR signaling cascades. This impairs the inhibitory effect of autophagy on inflammation, and thus aggravating hα‐Syn‐induced inflammatory responses.
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