Moiré superlattices in twisted two-dimensional halide perovskites.

Moiré superlattices have emerged as a new platform for studying strongly correlated quantum phenomena, but these systems have been largely limited to van der Waals layer two-dimensional materials. Here we introduce moiré superlattices leveraging ultrathin, ligand-free halide perovskites, facilitated by ionic interactions. Square moiré superlattices with varying periodic lengths are clearly visualized through high-resolution transmission electron microscopy. Twist-angle-dependent transient photoluminescence microscopy and electrical characterizations indicate the emergence of localized bright excitons and trapped charge carriers near a twist angle of ~10°. The localized excitons are accompanied by enhanced exciton emission, attributed to an increased oscillator strength by a theoretically predicted flat band. This research showcases the promise of two-dimensional perovskites as unique room-temperature moiré materials.

Direct Observation of Transient Structural Dynamics of Atomically Thin Halide Perovskite Nanowires.

Halide perovskite is a unique dynamical system, whose structural and chemical processes happening across different timescales have significant impact on its physical properties and device-level performance. However, due to its intrinsic instability, real-time investigation of the structure dynamics of halide perovskite is challenging, which hinders the systematic understanding of the chemical processes in the synthesis, phase transition, and degradation of halide perovskite. Here, we show that atomically thin carbon materials can stabilize ultrathin halide perovskite nanostructures against otherwise detrimental conditions. Moreover, the protective carbon shells enable atomic-level visualization of the vibrational, rotational, and translational movement of halide perovskite unit cells. Albeit atomically thin, protected halide perovskite nanostructures can maintain their structural integrity up to an electron dose rate of 10,000 e-/Å2·s while exhibiting unusual dynamical behaviors pertaining to the lattice anharmonicity and nanoscale confinement. Our work demonstrates an effective method to protect beam-sensitive materials during in situ observation, unlocking new solutions to study new modes of structure dynamics of nanomaterials.

Single-Cell Landscape of Lungs Reveals Key Role of Neutrophil-Mediated Immunopathology during Lethal SARS-CoV-2 Infection.

Due to the limitation of human studies with respect to individual difference or the accessibility of fresh tissue samples, how severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection results in pathological complications in lung, the main site of infection, is still incompletely understood. Therefore, physiologically relevant animal models under realistic SARS-CoV-2 infection conditions would be helpful to our understanding of dysregulated inflammation response in lung in the context of targeted therapeutics. Here, we characterized the single-cell landscape in lung and spleen upon SARS-CoV-2 infection in an acute severe disease mouse model that replicates human symptoms, including severe lung pathology and lymphopenia. We showed a reduction of lymphocyte populations and an increase of neutrophils in lung and then demonstrated the key role of neutrophil-mediated lung immunopathology in both mice and humans. Under severe conditions, neutrophils recruited by a chemokine-driven positive feedback produced elevated "fatal signature" proinflammatory genes and pathways related to neutrophil activation or releasing of granular content. In addition, we identified a new Cd177high cluster that is undergoing respiratory burst and Stfahigh cluster cells that may dampen antigen presentation upon infection. We also revealed the devastating effect of overactivated neutrophil by showing the highly enriched neutrophil extracellular traps in lung and a dampened B-cell function in either lung or spleen that may be attributed to arginine consumption by neutrophil. The current study helped our understanding of SARS-CoV-2-induced pneumonia and warranted the concept of neutrophil-targeting therapeutics in COVID-19 treatment. IMPORTANCE We demonstrated the single-cell landscape in lung and spleen upon SARS-CoV-2 infection in an acute severe disease mouse model that replicated human symptoms, including severe lung pathology and lymphopenia. Our comprehensive study revealed the key role of neutrophil-mediated lung immunopathology in SARS-CoV-2-induced severe pneumonia, which not only helped our understanding of COVID-19 but also warranted the concept of neutrophil targeting therapeutics in COVID-19 treatment.

ScRNA-seq identified the metabolic reprogramming of human colonic immune cells in different locations and disease states.

Different regions and states of the human colon are likely to have a distinct influence on immune cell functions. Here we studied the immunometabolic mechanisms for spatial immune specialization and dysregulated immune response during ulcerative colitis at single-cell resolution. We revealed that the macrophages and CD8+ T cells in the lamina propria of the human colon possessed an effector phenotype and were more activated, while their lipid metabolism was suppressed compared with those in the epithelial. Also, IgA+ plasma cells accumulated in lamina propria of the sigmoid colon were identified to be more metabolically activated versus those in the cecum and transverse colon, and the improved metabolic activity was correlated with the expression of CD27. In addition to the immunometabolic reprogramming caused by spatial localization colon, we found dysregulated cellular metabolism was related to the impaired immune functions of macrophages and dendritic cells in patients with ulcerative colitis. The cluster of OSM+ inflammatory monocytes was also identified to play its role in resistance to anti-TNF treatment, and we explored targeted metabolic reactions that could reprogram them to a normal state. Altogether, this study revealed a landscape of metabolic reprogramming of human colonic immune cells in different locations and disease states, and offered new insights into treating ulcerative colitis by immunometabolic modulation.

The HDAC3 inhibitor RGFP966 ameliorated ischemic brain damage by downregulating the AIM2 inflammasome.

Histone deacetylases 3 (HDAC3) modulates the acetylation state of histone and non-histone proteins and could be a powerful regulator of the inflammatory process in stroke. Inflammasome activation is a ubiquitous but poorly understood consequence of acute ischemic stroke. Here, we investigated the potential contributions of HDAC3 to inflammasome activation in primary cultured microglia and experimental stroke models. In this study, we documented that HDAC3 expression was increased in microglia of mouse experimental stroke model. Intraperitoneal injection of RGFP966 (a selective inhibitor of HDAC3) decreased infarct size and alleviated neurological deficits after the onset of middle cerebral artery occlusion (MCAO). In vitro data indicated that LPS stimulation evoked a time-dependent increase of HDAC3 and absent in melanoma 2 (AIM2) inflammasome in primary cultured microglia. Interestingly, AIM2 was subjected to spatiotemporal regulation by RGFP966. The ability of RGFP966 to inhibit the AIM2 inflammasome was confirmed in an experimental mouse model of stroke. As expected, AIM2 knockout mice also demonstrated significant resistance to ischemia injury compared with their wild-type littermates. RGFP966 failed to exhibit extra protective effects in AIM2-/- stroke mice. Furthermore, we found that RGFP966 enhanced STAT1 acetylation and subsequently attenuated STAT1 phosphorylation, which may at least partially contributed to the negative regulation of AIM2 by RGFP966. Together, we initially found that RGFP966 alleviated the inflammatory response and protected against ischemic stroke by regulating the AIM2 inflammasome.

NOD1/RIP2 signalling enhances the microglia-driven inflammatory response and undergoes crosstalk with inflammatory cytokines to exacerbate brain damage following intracerebral haemorrhage in mice.

BACKGROUND: Secondary brain damage caused by the innate immune response and subsequent proinflammatory factor production is a major factor contributing to the high mortality of intracerebral haemorrhage (ICH). Nucleotide-binding oligomerization domain 1 (NOD1)/receptor-interacting protein 2 (RIP2) signalling has been reported to participate in the innate immune response and inflammatory response. Therefore, we investigated the role of NOD1/RIP2 signalling in mice with collagenase-induced ICH and in cultured primary microglia challenged with hemin. METHODS: Adult male C57BL/6 mice were subjected to collagenase for induction of ICH model in vivo. Cultured primary microglia and BV2 microglial cells (microglial cell line) challenged with hemin aimed to simulate the ICH model in vitro. We first defined the expression of NOD1 and RIP2 in vivo and in vitro using an ICH model by western blotting. The effect of NOD1/RIP2 signalling on ICH-induced brain injury volume, neurological deficits, brain oedema, and microglial activation were assessed following intraventricular injection of either ML130 (a NOD1 inhibitor) or GSK583 (a RIP2 inhibitor). In addition, levels of JNK/P38 MAPK, IκBα, and inflammatory factors, including tumour necrosis factor-α (TNF-α), interleukin (IL)-1ß, and inducible nitric oxide synthase (iNOS) expression, were analysed in ICH-challenged brain and hemin-exposed cultured primary microglia by western blotting. Finally, we investigated whether the inflammatory factors could undergo crosstalk with NOD1 and RIP2. RESULTS: The levels of NOD1 and its adaptor RIP2 were significantly elevated in the brains of mice in response to ICH and in cultured primary microglia, BV2 cells challenged with hemin. Administration of either a NOD1 or RIP2 inhibitor in mice with ICH prevented microglial activation and neuroinflammation, followed by alleviation of ICH-induced brain damage. Interestingly, the inflammatory factors interleukin (IL)-1ß and tumour necrosis factor-α (TNF-α), which were enhanced by NOD1/RIP2 signalling, were found to contribute to the NOD1 and RIP2 upregulation in our study. CONCLUSION: NOD1/RIP2 signalling played an important role in the regulation of the inflammatory response during ICH. In addition, a vicious feedback cycle was observed between NOD1/RIP2 and IL-1ß/TNF-α, which could to some extent result in sustained brain damage during ICH. Hence, our study highlights NOD1/RIP2 signalling as a potential therapeutic target to protect the brain against secondary brain damage during ICH.

Dectin-1/Syk signaling triggers neuroinflammation after ischemic stroke in mice.

BACKGROUND: Dendritic cell-associated C-type lectin-1 (Dectin-1) receptor has been reported to be involved in neuroinflammation in Alzheimer's disease and traumatic brain injury. The present study was designed to investigate the role of Dectin-1 and its downstream target spleen tyrosine kinase (Syk) in early brain injury after ischemic stroke using a focal cortex ischemic stroke model. METHODS: Adult male C57BL/6 J mice were subjected to a cerebral focal ischemia model of ischemic stroke. The neurological score, adhesive removal test, and foot-fault test were evaluated on days 1, 3, 5, and 7 after ischemic stroke. Dectin-1, Syk, phosphorylated (p)-Syk, tumor necrosis factor-α (TNF-α), and inducible nitric oxide synthase (iNOS) expression was analyzed via western blotting in ischemic brain tissue after ischemic stroke and in BV2 microglial cells subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) injury in vitro. The brain infarct volume and Iba1-positive cells were evaluated using Nissl's and immunofluorescence staining, respectively. The Dectin-1 antagonist laminarin (LAM) and a selective inhibitor of Syk phosphorylation (piceatannol; PIC) were used for the intervention. RESULTS: Dectin-1, Syk, and p-Syk expression was significantly enhanced on days 3, 5, and 7 and peaked on day 3 after ischemic stroke. The Dectin-1 antagonist LAM or Syk inhibitor PIC decreased the number of Iba1-positive cells and TNF-α and iNOS expression, decreased the brain infarct volume, and improved neurological functions on day 3 after ischemic stroke. In addition, the in vitro data revealed that Dectin-1, Syk, and p-Syk expression was increased following the 3-h OGD and 0, 3, and 6 h of reperfusion in BV2 microglial cells. LAM and PIC also decreased TNF-α and iNOS expression 3 h after OGD/R induction. CONCLUSION: Dectin-1/Syk signaling plays a crucial role in inflammatory activation after ischemic stroke, and further investigation of Dectin-1/Syk signaling in stroke is warranted.

HDAC3 inhibition prevents oxygen glucose deprivation/reoxygenation-induced transendothelial permeability by elevating PPARγ activity in vitro.

Histone deacetylase 3 (HDAC3), a member of class I HDAC, regulates a wide variety of normal and abnormal physiological functions. Recent experimental studies suggested that inhibition of HDAC3 may increase acetylation of certain key signaling regulating proteins such as peroxisome proliferator-activated receptor γ (PPARγ), which plays a crucial role in modulating cerebrovascular function and integrity. However, the role of HDAC3 inhibition in cerebrovascular endothelium function under pathological condition has not been fully investigated. In this study, we tested the hypothesis that inhibition of HDAC3 by RGFP966, a highly selective HDAC3 inhibitor, promotes PPARγ activation by enhancing its protein acetylation, resulting in protection of oxygen glucose deprivation and reoxygenation (OGD/R)-induced increase of transendothelial cell permeability. In cultured primary human brain microvascular endothelial cells, our experimental results show that OGD/R increases transendothelial cell permeability and down-regulates junction protein expression. While we also detected HDAC3 activity increase and PPARγ activity decline after OGD/R. However, treatment with RGFP966 significantly attenuated the OGD/R-induced increase of transendothelial cell permeability and down-regulation of tight junction protein Claudin-5. These effects were observed to be dependent on HDAC3 activity inhibition-mediated PPARγ protein acetylation/activation. Lastly, HDAC3 small interfering RNA mimics the protective effects of RGFP966 on human brain microvascular endothelial cells. Taken together, our data indicate that HDAC3 inhibition might comprise a new therapeutic target for reducing blood-brain barrier integrity disruption and vascular dysfunctions in neurological disorders.

HDAC3 inhibition prevents blood-brain barrier permeability through Nrf2 activation in type 2 diabetes male mice.

BACKGROUND: Type 2 diabetes mellitus (T2DM) is a chronic metabolic dysfunction characterized by progressive insulin resistance and hyperglycaemia. Increased blood-brain barrier (BBB) permeability is a critical neurovascular complication of T2DM that adversely affects the central nervous system homeostasis and function. Histone deacetylase 3 (HDAC3) has been reported to be elevated in T2DM animals and may promote neuroinflammation; however, its involvement in the BBB permeability of T2DM has not been investigated. In this study, we tested our hypothesis that HDAC3 expression and activity are increased in the T2DM mouse brain. Inhibition of HDAC3 may ameliorate T2DM-induced BBB permeability through Nrf2 activation. METHODS: T2DM (db/db, leptin receptor-deficient), genetic non-hyperglycemic control (db/+), and wild-type male mice at the age of 16 weeks were used in this study. HDAC3 expression and activity, Nrf2 activation, and BBB permeability and junction protein expression were examined. The effects of HDAC3 activity on BBB permeability were tested using highly selective HDAC3 inhibitor RGFP966. In primary cultured human brain microvascular endothelial cells (HBMEC), hyperglycemia (25 mM glucose) plus interleukin 1 beta (20 ng/ml) (HG-IL1ß) served as T2DM insult in vitro. The effects of HDAC3 on transendothelial permeability were investigated by FITC-Dextran leakage and trans-endothelial electrical resistance, and the underlying molecular mechanisms were investigated using Western blot, q-PCR, co-immunoprecipitation, and immunocytochemistry for junction protein expression, miR-200a/Keap1/Nrf2 pathway regulation. RESULTS: HDAC3 expression and activity were significantly increased in the hippocampus and cortex of db/db mice. Specific HDAC3 inhibition significantly ameliorated BBB permeability and junction protein downregulation in db/db mice. In cultured HBMEC, HG-IL1ß insult significantly increased transendothelial permeability and reduced junction protein expression. HDAC3 inhibition significantly attenuated the transendothelial permeability and junction protein downregulation. Moreover, we demonstrated the underlying mechanism was at least in part attributed by HDAC3 inhibition-mediated miR-200a/Keap1/Nrf2 signaling pathway and downstream targeting junction protein expression in T2DM db/db mice. CONCLUSIONS: Our experimental results show that HDAC3 might be a new therapeutic target for BBB damage in T2DM.

Proteomic Analysis of HDAC3 Selective Inhibitor in the Regulation of Inflammatory Response of Primary Microglia.

HDAC3 has been shown to regulate inflammation. However, the role of HDAC3 in primary microglia is largely unknown. RGFP966 is a newly discovered selective HDAC3 inhibitor. In this study, we used protein mass spectrometry to analyze protein alterations in LPS-treated primary microglia with the application of RGFP966. Generally, about 2000 proteins were studied. 168 of 444 (37.8%) LPS-induced proteins were significantly reduced with the treatment of RGFP966, which mainly concentrated on Toll-like receptor signaling pathway. In this regard, we selected Toll-like receptor 2 (TLR2), TLR3, TLR6, MAPK p38, CD36, and spleen tyrosine kinase (SYK) for further validation and found that they were all significantly upregulated after LPS stimulation and downregulated in the presence of RGFP966. Additionally, RGFP966 inhibited supernatant tumor necrosis factor (TNF)-α and Interleukin 6 (IL-6) concentrations. Activation of STAT3 and STAT5 was partially blocked by RGFP966 at 2 h after LPS-stimulation. The fluorescence intensity of CD16/32 was significantly decreased in LPS + RGFP966-treated group. In conclusion, our data provided a hint that RGFP966 may be a potential therapeutic medication combating microglia activation and inflammatory response in central nervous system, which was probably related to its repressive impacts on TLR signaling pathways and STAT3/STAT5 pathways.

Dual effects of heme oxygenase-1 on astrocyte injury induced by hemin in vitro.

PRIMARY OBJECTIVE: The purpose of this study was to investigate the effects of heme oxygenase-1 (HO-1) on astrocyte injury induced by hemin. RESEARCH DESIGN: Primary astrocytes were isolated from Sprague Dawley rat pups and cultured in vitro. The expression of HO-1 was induced by hemin in a quantitative fashion and the effects of HO-1 on hemin-induced astrocyte injury were estimated by cell viability, cell membrane permeability and apoptosis. METHODS AND PROCEDURES: Astrocytes were divided into control group, hemin 5 µM group, hemin 5 µM + Zn-PPIX group, hemin 30 µM group and hemin 30 µM + Zn-PPIX group. Survival quality of astrocyte was measured by WST-8 assay, LDH assay, Hoechst 33258 Staining and annexin V-FITC/PI assay and apoptotic-related proteins were measured using Western blotting. MAIN OUTCOME AND RESULTS: Hemin could dose-dependently up-regulate the expression of HO-1. HO-1 exerted a protective role on astrocyte damage induced by 5 µM hemin, including increased cell survival rate and anti-apoptotic proteins expression (Bcl-2 and p-AKT), as well as decreased LDH release, apoptosis ratio and apoptotic protein expression (Bax, p-ERK and cleaved-caspase3). However, the effect of HO-1 on astrocyte injury between 30 µM hemin-treated groups was opposite of the protective role in 5 µM hemin-treated groups. CONCLUSIONS: There were dual effects of HO-1 in 5 µM and 30 µM hemin-induced astrocyte injuries.

Growth of close-packed semiconducting single-walled carbon nanotube arrays using oxygen-deficient TiO2 nanoparticles as catalysts.

For the application of single-walled carbon nanotubes (SWNTs) in nanoelectronic devices, techniques to obtain horizontally aligned semiconducting SWNTs (s-SWNTs) with higher densities are still in their infancy. We reported herein a rational approach for the preferential growth of densely packed and well-aligned s-SWNTs arrays using oxygen-deficient TiO2 nanoparticles as catalysts. Using this approach, a suitable concentration of oxygen vacancies in TiO2 nanoparticles could form by optimizing the flow rate of hydrogen and carbon sources during the process of SWNT growth, and then horizontally aligned SWNTs with the density of ∼ 10 tubes/µm and the s-SWNT percentage above 95% were successfully obtained on ST-cut quartz substrates. Theoretical calculations indicated that TiO2 nanoparticles with a certain concentration of oxygen vacancies have a lower formation energy between s-SWNT than metallic SWNT (m-SWNT), thus realizing the preferential growth of s-SWNT arrays. Furthermore, this method can also be extended to other semiconductor oxide nanoparticles (i.e., ZnO, ZrO2 and Cr2O3) for the selective growth of s-SWNTs, showing clear potential to the future applications in nanoelectronics.

Selective scission of C-O and C-C bonds in ethanol using bimetal catalysts for the preferential growth of semiconducting SWNT arrays.

For the application of single-walled carbon nanotubes (SWNTs) to electronic and optoelectronic devices, techniques to obtain semiconducting SWNT (s-SWNT) arrays are still in their infancy. We have developed herein a rational approach for the preferential growth of horizontally aligned s-SWNT arrays on a ST-cut quartz surface through the selective scission of C-O and C-C bonds of ethanol using bimetal catalysts, such as Cu/Ru, Cu/Pd, and Au/Pd. For a common carbon source, ethanol, a reforming reaction occurs on Cu or Au upon C-C bond breakage and produces C(ads) and CO, while a deoxygenating reaction occurs on Ru or Pd through C-O bond breaking resulting in the production of O(ads) and C2H4. The produced C2H4 by Ru or Pd can weaken the oxidative environment through decomposition and the neutralization of O(ads). When the bimetal catalysts with an appropriate ratio were used, the produced C(ads) and C2H4 can be used as carbon source for SWNT growth, and O(ads) promotes a suitable and durable oxidative environment to inhibit the formation of metallic SWNTs (m-SWNTs). Finally, we successfully obtained horizontally aligned SWNTs on a ST-cut quartz surface with a density of 4-8 tubes/µm and an s-SWNT ratio of about 93% using an Au/Pd (1:1) catalyst. The synergistic effects in bimetallic catalysts provide a new mechanism to control the growth of s-SWNTs.

Macroscopic Carbon Nanotube-based 3D Monoliths.

Carbon nanotubes (CNTs) are one of the most promising carbon allotropes with incredible diverse physicochemical properties, thereby enjoying continuous worldwide attention since their discovery about two decades ago. From the point of view of practical applications, assembling individual CNTs into macroscopic functional and high-performance materials is of paramount importance. For example, multiscaled CNT-based assemblies including 1D fibers, 2D films, and 3D monoliths have been developed. Among all of these, monolithic 3D CNT architectures with porous structures have attracted increasing interest in the last few years. In this form, theoretically all individual CNTs are well connected and fully expose their surfaces. These 3D architectures have huge specific surface areas, hierarchical pores, and interconnected conductive networks, resulting in enhanced mass/electron transport and countless accessible active sites for diverse applications (e.g. catalysis, capacitors, and sorption). More importantly, the monolithic form of 3D CNT assemblies can impart additional application potentials to materials, such as free-standing electrodes, sensors, and recyclable sorbents. However, scaling the properties of individual CNTs to 3D assemblies, improving use of the diverse, structure-dependent properties of CNTs, and increasing the performance-to-cost ratio are great unsolved challenges for their real commercialization. This review aims to provide a comprehensive introduction of this young and energetic field, i.e., CNT-based 3D monoliths, with a focus on the preparation principles, current synthetic methods, and typical applications. Opportunities and challenges in this field are also presented.

Characterizing the chiral index of a single-walled carbon nanotube.

The properties of single-walled carbon nanotubes (SWCNTs) mainly depend on their geometry. However, there are still formidable difficulties to determine the chirality of SWCNTs accurately. In this review, some efficient methods to characterize the chiral indices of SWCNTs are illuminated. These methods are divided into imaging techniques and spectroscopy techniques. With these methods, diameter, helix angle, and energy states can be measured. Generally speaking, imaging techniques have a higher accuracy and universality, but are time-consuming with regard to the sample preparation and characterization. The spectroscopy techniques are very simple and fast in operation, but these techniques can be applied only to the particular structure of the sample. Here, the principles and operations of each method are introduced, and a comprehensive understanding of each technique, including their advantages and disadvantages, is given. Advanced applications of some methods are also discussed. The aim of this review is to help readers to choose methods with the appropriate accuracy and time complexity and, furthermore, to put forward an idea to find new methods for chirality characterization.

Slow wave activity disruptions and memory impairments in a mouse model of aging.

The aging population suffers from memory impairments. Slow-wave activity (SWA) is composed of slow (0.5-1 Hz) and delta (1-4 Hz) oscillations, which play important roles in long-term memory and working memory function respectively. SWA disruptions might lead to memory disturbances often experienced by older adults. We conducted behavioral tests in young and older C57BL/6 J mice. SWA was monitored using wide-field imaging with voltage sensors. Cell-specific calcium imaging was used to monitor the activity of excitatory and inhibitory neurons in these mice. Older mice exhibited impairments in working memory but not memory consolidation. Voltage-sensor imaging revealed aberrant synchronization of neuronal activity in older mice. Notably, we found older mice exhibited no significant alterations in slow oscillations, whereas there was a significant increase in delta power compared to young mice. Calcium imaging revealed hypoactivity in inhibitory neurons of older mice. Combined, these results suggest that neural activity disruptions might correlate with aberrant memory performance in older mice.

An Overview on Fatigue of High-Entropy Alloys.

Due to their distinct physical, chemical, and mechanical features, high-entropy alloys have significantly broadened the possibilities of designing metal materials, and are anticipated to hold a crucial position in key engineering domains such as aviation and aerospace. The fatigue performance of high-entropy alloys is a crucial aspect in assessing their applicability as a structural material with immense potential. This paper provides an overview of fatigue experiments conducted on high-entropy alloys in the past two decades, focusing on crack initiation behavior, crack propagation modes, and fatigue life prediction models.

Integrated metabolic profiling and transcriptome analysis of Lonicera japonica flowers for chlorogenic acid, luteolin and endogenous hormone syntheses.

The active ingredients of many medicinal plants are the secondary metabolites associated with the growth period. Lonicera japonica Thunb. is an important traditional Chinese medicine, and the flower development stage is an important factor that influences the quality of medicinal ingredients. In this study, transcriptomics and metabolomics were performed to reveal the regulatory mechanism of secondary metabolites during flowering of L. japonica. The results showed that the content of chlorogenic acid (CGA) and luteolin gradually decreased from green bud stage (Sa) to white flower stage (Sc), especially from white flower bud stage (Sb) to Sc. Most of the genes encoding the crucial rate-limiting enzymes, including PAL, C4H, HCT, C3'H, F3'H and FNSII, were down-regulated in three comparisons. Correlation analysis identified some members of the MYB, AP2/ERF, bHLH and NAC transcription factor families that are closely related to CGA and luteolin biosynthesis. Furthermore, differentially expressed genes (DEGs) involved in hormone biosynthesis, signalling pathways and flowering process were analysed in three flower developmental stage.

Strong Dipolar Repulsion of One-Dimensional Interfacial Excitons in Monolayer Lateral Heterojunctions.

Repulsive and long-range exciton-exciton interactions are crucial for the exploration of one-dimensional (1D) correlated quantum phases in the solid state. However, the experimental realization of nanoscale confinement of a 1D dipolar exciton has thus far been limited. Here, we demonstrate atomically precise lateral heterojunctions based at transitional-metal dichalcogenides (TMDCs) as a platform for 1D dipolar excitons. The dynamics and transport of the interfacial charge transfer excitons in a type II WSe2-WS1.16Se0.84 lateral heterostructure were spatially and temporally imaged using ultrafast transient reflection microscopy. The expansion of the exciton cloud driven by dipolar repulsion was found to be strongly density dependent and highly anisotropic. The interaction strength between the 1D excitons was determined to be ∼3.9 × 10-14 eV cm-2, corresponding to a dipolar length of 310 nm, which is a factor of 2-3 larger than the interlayer excitons at two-dimensional van der Waals vertical interfaces. These results suggest 1D dipolar excitons with large static in-plane dipole moments in lateral TMDC heterojunctions as an exciting system for investigating quantum many-body physics.

Exciton annihilation in molecular aggregates suppressed through quantum interference.

Exciton-exciton annihilation (EEA), an important loss channel in optoelectronic devices and photosynthetic complexes, has conventionally been assumed to be an incoherent, diffusion-limited process. Here we challenge this assumption by experimentally demonstrating the ability to control EEA in molecular aggregates using the quantum phase relationships of excitons. We employed time-resolved photoluminescence microscopy to independently determine exciton diffusion constants and annihilation rates in two substituted perylene diimide aggregates featuring contrasting excitonic phase envelopes. Low-temperature EEA rates were found to differ by more than two orders of magnitude for the two compounds, despite comparable diffusion constants. Simulated rates based on a microscopic theory, in excellent agreement with experiments, rationalize this EEA behaviour based on quantum interference arising from the presence or absence of spatial phase oscillations of delocalized excitons. These results offer an approach for designing molecular materials using quantum interference where low annihilation can coexist with high exciton concentrations and mobilities.