Soil rhizospheric metaproteomics is a powerful scientific tool to uncover the interactions between plants and microorganisms in the soil ecosystem. The present study established an extraction method ...suitable for different soils that could increase the extracted protein content. Close to 1000 separate spots with high reproducibility could be identified in the stained 2-DE gels. Among the spots, 189 spots representing 122 proteins on a 2-DE gel of rice soil samples were successfully identified by MALDI-TOF/TOF-MS. These proteins mainly originated from rice and microorganisms. They were involved in protein, energy, nucleotide, and secondary metabolisms, as well as signal transduction and resistance. Three characteristics of the crop rhizospheric metaproteomics seemed apparent: (1) approximately one-third of the protein spots could not be identified by MALDI-TOF/TOF/MS, (2) the conservative proteins from plants formed a feature distribution of crop rhizospheric metaproteome, and (3) there were very complex interactions between plants and microorganisms existing in a crop rhizospheric soil. Further functional analysis on the identified proteins unveiled various metabolic pathways and signal transductions involved in the soil biotic community. This study provides a paradigm for metaproteomic research on soil biology.
Growth-regulating factors (GRFs) are a unique family of transcription factors with well-characterized functions in plant growth and development. However, few studies have evaluated their roles in the ...absorption and assimilation of nitrate. In this study, we characterized the
family genes of flowering Chinese cabbage (
), an important vegetable crop in South China. Using bioinformatics methods, we identified
genes and analyzed their evolutionary relationships, conserved motifs, and sequence characteristics. Through genome-wide analysis, we identified 17
genes distributed on seven chromosomes. A phylogenetic analysis revealed that the
genes could be categorized into five subfamilies. RT-qPCR analysis showed that
,
,
, and
expression clearly increased in response to nitrogen (N) deficiency, particularly at 8 h after treatment.
expression was the most sensitive to N deficiency and was significantly correlated with the expression patterns of most key genes related to N metabolism. Using yeast one-hybrid and dual-luciferase assays, we discovered that BcGRF8 strongly enhances the driving activity of the
gene promoter. Next, we investigated the molecular mechanism by which
participates in nitrate assimilation and N signaling pathways by expressing it in Arabidopsis. BcGRF8 was localized in the cell nucleus and
overexpression significantly increased the shoot and root fresh weights, seedling root length, and lateral root number in Arabidopsis. In addition,
overexpression considerably reduced the nitrate contents under both nitrate-poor and -rich conditions in Arabidopsis. Finally, we found that BcGRF8 broadly regulates genes related to N uptake, utilization, and signaling. Our results demonstrate that BcGRF8 substantially accelerates plant growth and nitrate assimilation under both nitrate-poor and -rich conditions by increasing the number of lateral roots and the expression of genes involved in N uptake and assimilation, providing a basis for crop improvement.
Brain computer interfaces (BCIs) are valuable tools that expand the nature of communication through bypassing traditional neuromuscular pathways. The non-invasive, intuitive, and continuous nature of ...sensorimotor rhythm (SMR) based BCIs enables individuals to control computers, robotic arms, wheel-chairs, and even drones by decoding motor imagination from electroencephalography (EEG). Large and uniform datasets are needed to design, evaluate, and improve the BCI algorithms. In this work, we release a large and longitudinal dataset collected during a study that examined how individuals learn to control SMR-BCIs. The dataset contains over 600 hours of EEG recordings collected during online and continuous BCI control from 62 healthy adults, (mostly) right hand dominant participants, across (up to) 11 training sessions per participant. The data record consists of 598 recording sessions, and over 250,000 trials of 4 different motor-imagery-based BCI tasks. The current dataset presents one of the largest and most complex SMR-BCI datasets publicly available to date and should be useful for the development of improved algorithms for BCI control.
The jasmonate family of phytohormones plays central roles in plant development and stress acclimation. However, the architecture of their signaling circuits remains largely unknown. Here we describe ...a jasmonate family binding protein, cyclophilin 20-3 (CYP20-3), which regulates stress-responsive cellular redox homeostasis. (+)-12-oxo-phytodienoic acid (OPDA) binding promotes CYP20-3 to form a complex with serine acetyltransferase 1, which triggers the formation of a hetero-oligomeric cysteine synthase complex with O -acetylserine(thiol)lyase B in chloroplasts. The cysteine synthase complex formation then activates sulfur assimilation that leads to increased levels of thiol metabolites and the buildup of cellular reduction potential. The enhanced redox capacity in turn coordinates the expression of a subset of OPDA-responsive genes. Thus, we conclude that CYP20-3 is a key effector protein that links OPDA signaling to amino acid biosynthesis and cellular redox homeostasis in stress responses.
To address the limitations of traditional photothermal therapy (PTT)/ photodynamic therapy (PDT) and real-time cancer metastasis detection, a pH-responsive nanoplatform (NP) with dual-modality ...imaging capability was rationally designed. Herein, 1 H,1 H-undecafluorohexylamine (PFC), served as both an oxygen carrier and a
F magnetic resonance imaging (MRI) probe, and photosensitizer indocyanine green (ICG) were grafted onto the pH-responsive peptide hexahistidine (H
) to form H
-PFC-ICG (HPI). Subsequently, the heat shock protein 90 inhibitor, gambogic acid (GA), was incorporated into hyaluronic acid (HA) modified HPI (HHPI), yielding the ultimate HHPI@GA NPs. Upon self-assembly, HHPI@GA NPs passively accumulated in tumor tissues, facilitating oxygen release and HA-mediated cell uptake. Once phagocytosed by lysosomes, protonation of H
was triggered due to the low pH, resulting in the release of GA. With near-infrared laser irradiation, GA-mediated decreased HSP90 expression and PFC-mediated increased ROS generation amplified the PTT/PDT effect of HHPI@GA, leading to excellent in vitro and in vivo anticancer efficacies. Additionally, the fluorescence and
F MRI dual-imaging capabilities of HHPI@GA NPs enabled effective real-time primary cancer and lung metastasis monitoring. This work offers a novel approach for enhanced cancer phototherapy, as well as precise cancer diagnosis.
Epidemiological studies have unveiled a robust link between exposure to repetitive mild traumatic brain injury (r-mTBI) and elevated susceptibility to develop neurodegenerative disorders, notably ...chronic traumatic encephalopathy (CTE). The pathogenic lesion in CTE cases is characterized by the accumulation of hyperphosphorylated tau in neurons around small cerebral blood vessels which can be accompanied by astrocytes that contain phosphorylated tau, the latter termed tau astrogliopathy. However, the contribution of tau astrogliopathy to the pathobiology and functional consequences of r-mTBI/CTE or whether it is merely a consequence of aging remains unclear. We addressed these pivotal questions by utilizing a mouse model harboring tau-bearing astrocytes, GFAP
mice, subjected to our r-mTBI paradigm. Despite the fact that r-mTBI did not exacerbate tau astrogliopathy or general tauopathy, it increased phosphorylated tau in the area underneath the impact site. Additionally, gene ontology analysis of tau-bearing astrocytes following r-mTBI revealed profound alterations in key biological processes including immunological and mitochondrial bioenergetics. Moreover, gene array analysis of microdissected astrocytes accrued from stage IV CTE human brains revealed an immunosuppressed astroglial phenotype similar to tau-bearing astrocytes in the GFAP
model. Additionally, hippocampal reduction of proteins involved in water transport (AQP4) and glutamate homeostasis (GLT1) was found in the mouse model of tau astrogliopathy. Collectively, these findings reveal the importance of understanding tau astrogliopathy and its role in astroglial pathobiology under normal circumstances and following r-mTBI. The identified mechanisms using this GFAP
model may suggest targets for therapeutic interventions in r-mTBI pathogenesis in the context of CTE.
Objective
To predict the risk of dystrophinopathy in fetal carriers of dystrophin gene (DMD) mutations.
Methods
Twenty‐three pregnant women, with a total of 25 female fetuses carrying DMD mutations, ...were recruited. Among them, 13 pregnant women who participated in this study were only used to analyse the incidence of induced abortion after fetuses were diagnosed as dystrophinopathy carriers. Eleven fetal carriers from 10 pregnant women were tested to analyse X‐chromosome inactivation (XCI) using amniocytes to assess the risk of dystrophinopathy. Follow‐ups were conducted on all cases.
Results
Approximately one‐third of fetuses were aborted before assessing the risk of dystrophinopathy. XCI analysis of amniocytes showed that 10 fetuses had random XCI patterns, and one fetus exhibited a highly skewed XCI pattern (100:0) with primary expression of the maternal X chromosome that carried the mutant allele. These 11 fetal carriers were born, and follow‐up showed that the girl who showed the skewed XCI pattern as a fetus was diagnosed with Duchenne muscular dystrophy (DMD) at the age of four. The others did not present with dystrophinopathy‐associated symptoms.
Conclusions
XCI was significantly implicated in symptomatic female carriers of dystrophinopathies, and XCI pattern analysis of amniocytes may be useful in predicting the risk of dystrophinopathy in fetal carriers.
Social media benign envy, an upward comparison-based and painful emotions associated with the motivation to improve oneself, has attracted increasing attention from researchers due to its ubiquitous ...and significant impact on social network users' intentions and behavior. However, the results of previous studies on whether material or experiential consumption is more likely to cause social media envy (treated as a single construct) have been inconsistent, and there is a lack of research on what triggers social media users to experience more intense benign envy and thus inspiring their consumption intentions. The purpose of this study is to investigate how the type and luxuriousness of shared consumption and viewer's social comparison orientation jointly affect social media users' consumption intentions through benign envy.
A 2 (type of consumption sharing: experiential vs. material) × 2 (luxuriousness of consumption sharing: luxury vs. non-luxury) × 2 (social comparison orientation: high vs. low) mixed-design experiment was conducted to test theoretical model with data from 544 undergraduates in China. SPSS 26.0 and the Process macro were used to test the model.
The results revealed that luxury experiential consumption information shared on social media triggered more benign envy compared with other types of shared consumption information. When social media users shared non-luxury consumption, experiential consumption was more likely to inspire benign envy among users with high social comparison orientation than material consumption. However, when luxury consumption was shared, benign envy acted as a mediator between purchase type and participants' purchase intention regardless of whether participants' social comparison orientation was high or low.
This study revealed that whether and how social comparison orientation of social media users who read the shared content influences the mechanism by which the type of consumption sharing on social media affects social media users' consumption intentions through benign envy as a mediator is dependent on the luxuriousness of the shared consumption. The findings not only provide new insights for researchers to better understand social media envy and the underlying psychological mechanism for social media readers' consumption intention, but also have practical implications for practitioners.
The ongoing global pandemic of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has caused devastating impacts on the public health and the ...global economy. Rapid viral antigenic evolution has led to the continual generation of new variants. Of special note is the recently expanding Omicron subvariants that are capable of immune evasion from most of the existing neutralizing antibodies (nAbs). This has posed new challenges for the prevention and treatment of COVID-19. Therefore, exploring broad-spectrum antiviral agents to combat the emerging variants is imperative. In sharp contrast to the massive accumulation of mutations within the SARS-CoV-2 receptor-binding domain (RBD), the S2 fusion subunit has remained highly conserved among variants. Hence, S2-based therapeutics may provide effective cross-protection against new SARS-CoV-2 variants. Here, we summarize the most recently developed broad-spectrum fusion inhibitors (e.g., nAbs, peptides, proteins, and small-molecule compounds) and candidate vaccines targeting the conserved elements in SARS-CoV-2 S2 subunit. The main focus includes all the targetable S2 elements, namely, the fusion peptide, stem helix, and heptad repeats 1 and 2 (HR1-HR2) bundle. Moreover, we provide a detailed summary of the characteristics and action-mechanisms for each class of cross-reactive fusion inhibitors, which should guide and promote future design of S2-based inhibitors and vaccines against new coronaviruses.
•LPS induced inflammation autophagy in primary brain cell model.•Collagenase injection caused autophagy in rat CPSP model.•EA inhibited autophagy by reducing β-catenin/COX-2 expression.
To explore ...the underlying mechanism of electroacupuncture (EA) treatment on central post-stroke pain (CPSP), and provide basic evidence for the EA treatment on CPSP.
Firstly, 40 male SD rats were successfully established with a model of CPSP, under the intervention of different EA frequencies (2 Hz and 15 Hz) and fluoxetine (5 ml/kg and 0.4 mg/ml), whose brain tissue was then removed for paraffin-embedded sectioning; secondly, LPS induced the primary brain cells in the hippocampus to cause inflammation model which were added NS398 (inhibitor of COX-2) and DKK-1 (inhibitor of β-catenin) later. The lesion sites of brain tissue were observed by Nissl staining and Transmission Electron Microscope (TEM) and autophagy-related proteins (LC3B, p62, LAMP-1), COX-2 and β-catenin were detected by Western Blot and immunohistochemical staining. Finally, the correlation between LC3B, COX-2, and β-catenin was calculated by multispectral quantification.
(1) In the EA group (15 Hz), the number of Nissl bodies increased, autophagy-related protein LC3B-Ⅱ/Ⅰ, LAMP-1, COX-2, and β-catenin was lowly expressed, p62 was highly expressed; (2) COX-2, β-catenin and LC3B are positively correlated with each other (COX-2 & β-catenin: r = 0.923; COX-2 & LC3B: r = 0.818; β-catenin & LC3B: r = 0.801); (3) Nissl bodies of primary brain cells of the hippocampus under LPS were like animal experiments; after addition of DKK-1, high expression of β-catenin and COX-2 induced by LPS was significantly down-regulated, and LC3B-II/I was significantly down-regulated, and p62 protein only had up-regulation trend; after addition of NS398, COX-2 and LC3B-II/I was significantly down-regulated.
EA may inhibit autophagy in the hippocampus by reducing β-catenin/COX-2 protein expression and effectively alleviating CPSP.
Previous studies have found that EA can reduce the expression of NK-1R in damaged rats by inhibition of COX-2 and β-catenin loops, which controls the activation of glial cells in the damaged area and the apoptosis of neuronal cells, and alleviated pain. In the male SD rat model, we evaluated this effect that EA inhibits autophagy in the hippocampus by reducing β-catenin/COX-2 protein expression in the brain tissue. In addition, we assessed expression levels of autophagy-related proteins and genes on the inflammatory primary brain cells model. From the experiment, we found EA may inhibit autophagy in the hippocampus by reducing β-catenin/COX-2 protein expression. These findings provide a foundation for the interpretation of the mechanism of EA on relieving CPSP in clinical practice.
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