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204 result(s) for "Lin, Ziyan"
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Identification and analysis of VOCs released by Rhodococcus ruber GXMZU2400 to promote plant growth and inhibit pathogen growth
A strain of Rhodococcus ruber was isolated from the rhizosphere of Spartina alterniflora . The VOCs released by this strain effectively promote the growth of Arabidopsis thaliana and inhibit several plant pathogenic fungi, including Bipolaris sorokiniana , Cryphonectria parasitica , Fusarium oxysporum , Fusarium pseudograminearum , and Plectosphaerella cucumerina . SPME/GC–MS analysis revealed that the strain produces dimethyl disulfide (DMDS) and dimethyl trisulfide (DMTS), with DMDS being the predominant component of the volatile organic compounds (VOCs). It was observed that the growth of A. thaliana was enhanced under fumigation with DMDS and DMTS. Furthermore, these compounds effectively inhibited the aforementioned plant pathogenic fungi, with DMTS demonstrating a lethal effect on plant pathogenic fungi. Previous studies have confirmed that DMDS and DMTS promote the growth of A. thaliana . In this study, we found that DMTS could significantly enhance plant growth and inhibit plant pathogenic fungi even at low dosages. Transcriptome analysis indicated that the growth-related genes of A. thaliana were significantly upregulated in response to treatment with VOCs from R. ruber . Additionally, VOCs induced changes in multiple plant defense response genes and promoted the C4 pathway.
Transcriptome profiling and weighted gene co-expression network analysis reveal changes of hub genes and molecular pathways in rat lungs following deep hypothermic circulatory arrest
The incidence of acute lung injury (ALI) following aortic dissection repair surgery that involves deep hypothermic circulatory arrest (DHCA) is notably high. We analyzed hub genes and signaling pathways in rat lung tissues post-DHCA using transcriptome sequencing and weighted gene co-expression network analysis (WGCNA). A rat model of DHCA was established, and lung tissues were collected after the procedure. High-throughput transcriptome sequencing was employed to assess gene expression differences between the DHCA group and the non-DHCA group. The DESeq2 method was utilized to analyze differentially expressed genes (DEGs) between these two groups, with further screening for hub genes and their upstream molecules conducted using WGCNA, protein-protein interaction (PPI) networks, and the iRegulon plugin. Biological functions of hub genes were examined via Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses. The changes in mRNA and protein levels of hub genes across both groups were evaluated through experimental verification. A total of 438 DEGs were identified when comparing the DHCA group to the control group. WGCNA further revealed 197 key genes. Subsequent PPI analysis led to the identification of eight hub genes: FOS, FOSB, JUN, EGR1, ATF3, NR4A1, CCN1, and ZFP36. The hub genes were primarily associated with inflammation, cell apoptosis, and cellular immune responses. ATF3 and SRF may serve as potential upstream regulators. The experimental findings further corroborated that substantial alterations took place in these hub genes, accompanied by significant injury of lung tissue during DHCA. DHCA significantly altered gene expression patterns in rat lung tissues. The identified hub genes and signaling pathways related to inflammation and apoptosis may serve as potential therapeutic targets for lung injury following DHCA.
Gpr125 is a unifying hallmark of multiple mammary progenitors coupled to tumor latency
Gpr125 is an orphan G-protein coupled receptor, with homology to cell adhesion and axonal guidance factors, that is implicated in planar polarity and control of cell movements. By lineage tracing we demonstrate that Gpr125 is a highly specific marker of bipotent mammary stem cells in the embryo and of multiple long-lived unipotent basal mammary progenitors in perinatal and postnatal glands. Nipple-proximal Gpr125+ cells express a transcriptomic profile indicative of chemo-repulsion and cell movement, whereas Gpr125+ cells concentrated at invasive ductal tips display a hybrid epithelial-mesenchymal phenotype and are equipped to bind chemokine and growth factors and secrete a promigratory matrix. Gpr125 progenitors acquire bipotency in the context of transplantation and cancer and are greatly expanded and massed at the pushing margins of short latency MMTV-Wnt1 tumors. High Gpr125 expression identifies patients with particularly poor outcome within the basal breast cancer subtype highlighting its potential utility as a factor to stratify risk. Gpr125 has emerged as a specific marker of mammary stem cells and basal progenitors. Here they show that Gpr125 cells congregate at ductal tips during morphogenesis and amass at tumor margins, and that high Gpr125 predicts early tumor onset and poor outcome in basal breast cancer.
Series-Parallel Reconfigurable Electric Double-Layer Capacitor Module with Cell Equalization Capability, High Energy Utilization Ratio, and Good Modularity
Voltages of electric double-layer capacitor (EDLC) modules vary rather wider than traditional secondary batteries. Although EDLCs should desirably be cycled in a voltage range as wide as possible to achieve a high energy utilization ratio, the wide voltage variation of EDLC modules impairs the performance of DC–DC converters. To address such issues, previous works reported series-parallel reconfiguration techniques, which are roughly divided into balance- and unbalance-shift circuits. However, conventional balance-shift circuits are not applicable to modules comprising odd number cells, impairing modularity. Unbalance-shift circuits, on the other hand, unavoidably cause cell voltage imbalance that reduces energy utilization ratio. This paper proposes a novel series-parallel reconfigurable EDLC module with cell voltage equalization capability. The proposed reconfigurable EDLC module is applicable to any number of cells, realizing good modularity. Furthermore, all cells in the proposed module can be charged and discharged uniformly without generating cell voltage imbalance, achieving an improved energy utilization ratio compared with conventional techniques. A five-cell module prototype was built for experimental verification. While the module voltage varied between 1.04 and 2.83 V, all cells discharged from 2.5 to 0.3 V. The result is equivalent to a 98.6% energy utilization ratio.
Causal relationship between mitochondrial proteins and risks of aortic aneurysms and aortic dissection: a Mendelian randomization study
Background Mitochondrial dysfunction may be linked to the development of aortic aneurysm (AA) and aortic dissection (AD). This study aimed to evaluate the potential associations between proteins related to mitochondrial function and the risks of AA/AD using Mendelian randomization (MR). Methods Large-scale publicly available genome-wide association studies (GWAS) and FinnGen summary data were utilized for MR analysis. The causal relationship between mitochondrial proteins and AA/AD was assessed using inverse-variance weighted (IVW) as the primary method. Sensitivity analyses were conducted to detect heterogeneity and pleiotropy by Cochran’s Q test, MR-Egger test, MR-PRESSO global test, and “leave-one-out” analysis. Results There were potential causal relationships between several mitochondrial proteins and AA/AD. Specifically, the iron-sulfur cluster assembly enzyme ISCU (OR = 1.165, 95% CI: 1.051–1.291, P  = 0.004) and NFU1 iron-sulfur cluster scaffold homolog (OR = 1.184, 95% CI: 1.056–1.329, P  = 0.004) were identified as potential risk factors for AA; whereas the 39 S ribosomal protein L14 (OR = 0.868, 95% CI: 0.764–0.987, P  = 0.031) was found to be a protective factor for AA. Furthermore, 39 S ribosomal protein L33 (OR = 1.134, 95% CI: 1.010–1.274, P  = 0.033) and cytochrome C oxidase subunit 5B (OR = 1.330, 95% CI: 1.037–1.706, P  = 0.025) were associated with increased risks of AD; whereas the 39 S ribosomal protein L52 (OR = 0.736, 95% CI: 0.550–0.984, P  = 0.038) and mitochondrial ubiquitin ligase activator of NFKB 1 (OR = 0.806, 95% CI: 0.656–0.989, P  = 0.039) were identified as potential protective factors for AD. Sensitivity analysis confirmed the stability of the results. Conclusions This study identified potential genetic associations between mitochondrial proteins and AA/AD. Targeting these mitochondrial proteins may help prevent the occurrence of AA/AD.
Deletion of sf3b4 causes splicing defects and gene dysregulation that disrupt craniofacial development and survival
Nager and Rodriguez syndromes are rare craniofacial and limb disorders characterized by midface retrusion, micrognathia, absent thumbs and radial hypoplasia. These disorders result from haploinsufficiency of SF3B4 (splicing factor 3b, subunit 4), a component of the pre-mRNA spliceosomal machinery. Although the spliceosome is present and functions in all cells of the body, most spliceosomopathies – including Nager and Rodriguez syndromes – are cell- or tissue-specific in their pathology. To understand the pathomechanism underlying these conditions, we generated a Xenopus tropicalis sf3b4 mutant line using CRISPR/Cas9 gene-editing technology. Homozygous deletion of sf3b4 is detrimental to the development of cranial neural crest (NC)-derived cartilage progenitors. Temporal RNA-sequencing analyses of mutant embryos identified an increase in exon-skipping events, followed by important transcriptional changes associated with an enrichment for terms consistent with defects in NC cell migration and survival. We propose that disruption of these processes may underly the pathogenesis of Nager and Rodriguez syndromes.
The Fabrication and Function of Strontium-modified Hierarchical Micro/Nano Titanium Implant
Relying on surface topography alone to enhance the osteointegration of implants is still inadequate. An effective way to combine long-term ion release and surface topography to enhance osteogenic property is urgently needed. The objective of this study is to fabricate a long-term strontium ion release implant system and confirm the biological function in vitro and in vivo. The biomimic surface was fabricated through alkali-heat treatment and magnetron sputtering. The in vitro biological function assays were determined by MTT, fluorescence staining, alkaline phosphatase activity, extracellular mineralization, and quantitative real-time polymerase chain reaction assays. The in vivo experiments were detected by micro-CT, HE staining and Masson staining. The biomimic surface structure has been successfully fabricated. The in vitro cell assays determined that AH-Ti/Sr90 possessed the best biological function. The in vivo experiments demonstrated that AH-Ti/Sr90 could promote osteointegration significantly under both in normal and osteoporotic conditions. We determined that AH-Ti/Sr90 possesses the best osteogenic property, long-term ion release capacity and osteointegration promotion ability. It has potential clinic application prospects.
Ectopic expression of an AtBMI1a homolog from Vitis vinifera accelerates flowering time in transgenic Arabidopsis
BMI1 is the main component of the Polycomb Group Complex 1 (PRC1), which functions as an important epigenetic inhibitor of various regulatory genes associated with shoot apical meristem, embryonic development, flowering, senescence and so on. However, its role in the regulation of grapevine development is still unclear. In order to explore the function of VvBMI1a gene in the regulation of flowering in Vitis vinifera ‘Cabernet Sauvignon’, the subcellular localization, expression pattern, yeast two-hybrid, two-molecule fluorescence complementation and flowering time of transgenic Arabidopsis were analyzed. The results showed that VvBMI1a , a member of RING domain-containing proteins family from grapevine (Vitis vinifera) , is involved in controlling plant flowering time. Expression of VvBMI1a was abundant in the shoot tips and inflorescence meristems of grapevine. VvBMI1a protein is localized in the nucleus. VvBMI1a could interact with VvRING1a protein which belonged to PRC1. Phenotypic analysis showed that VvBMI1a over-expression lines had earlier flowering time than wild-type plants under long-day (LD) conditions. Further analysis by qRT-PCR and transcriptome suggests that both the suppression of FLC and activation of FT , SOC1 , SQUAMOSA PROMOTER BINDING PROTEIN-LIKE 5 ( SPL5 ), AGL8 were observed in VvBMI1a -overexpressing lines, resulting in early flowering. Our results provide the evidence demonstrating the effectiveness of manipulating VvBMI1a to alter the flowering time of plants. In a word, ectopic overexpression of VvBMI1a inhibited the expression of FLC , activated the expression of FT , SPL5 , AGL8 to alter the flowering time of Arabidopsis plants. Key message • VvBMI1a is a ubiquitously expressed nuclear protein. • VvBMI1a can interact with VvRING1a. • Ectopic overexpression of VvBMI1a induced the early flowering via inhibition of FLC , activation of FT , SPL5 , AGL8 expression.
Using gross ecosystem product to harmonize biodiversity conservation and economic development in Southwestern China
Gross ecosystem product (GEP) is the aggregate economic value of the final goods and services of the ecosystem produced within a given area, providing a potentially effective means of linking nature protection and restoration to development. In this study, we calculated the values and distribution of biodiversity, GEP and gross domestic product (GDP) in the 547 counties of Southwestern China, a biodiversity hotspot. We then divided the region into nine types of area based on spatial correlations between the three indicators. Areas with high biodiversity, GEP per km2 and GDP per capita were mainly found in and around the large cities of Kunming, Chengdu and Guiyang, reflecting a reasonably high degree of coupling coordination between ecosystems and the local economy. Contrary to our hypotheses, areas with high biodiversity do not necessarily have high GEP, and regions with high GDP do not inherently have low biodiversity. This suggests that synergies exist between biodiversity conservation and economic development, and that increasing the value of material and non‐material services in GEP could improve this alignment. Based on our findings, we argue that GEP can act as a bridge between biodiversity conservation and economic development. Understanding the interactions between biodiversity, GEP and GDP can inform the design of effective policies. In particular, we suggest that sustainable agricultural intensification and forestry along with ecotourism offer promising pathways for advancing nature‐positive development in this ecologically critical region. Read the free Plain Language Summary for this article on the Journal blog. Read the free Plain Language Summary for this article on the Journal blog.
Electronic Cigarette Use Promotes a Unique Periodontal Microbiome
Electronic cigarette (e-cig) use is gaining in popularity and is often perceived as a healthier alternative to conventional smoking. Yet there is little evidence of the effects of long-term use of e-cigs on oral health. Electronic cigarettes (e-cigs) have become prevalent as an alternative to conventional cigarette smoking, particularly in youth. E-cig aerosols contain unique chemicals which alter the oral microbiome and promote dysbiosis in ways we are just beginning to investigate. We conducted a 6-month longitudinal study involving 84 subjects who were either e-cig users, conventional smokers, or nonsmokers. Periodontal condition, cytokine levels, and subgingival microbial community composition were assessed, with periodontal, clinical, and cytokine measures reflecting cohort habit and positively correlating with pathogenic taxa (e.g., Treponema , Saccharibacteria , and Porphyromonas ). α-Diversity increased similarly across cohorts longitudinally, yet each cohort maintained a unique microbiome. The e-cig microbiome shared many characteristics with the microbiome of conventional smokers and some with nonsmokers, yet it maintained a unique subgingival microbial community enriched in Fusobacterium and Bacteroidales (G-2). Our data suggest that e-cig use promotes a unique periodontal microbiome, existing as a stable heterogeneous state between those of conventional smokers and nonsmokers and presenting unique oral health challenges. IMPORTANCE Electronic cigarette (e-cig) use is gaining in popularity and is often perceived as a healthier alternative to conventional smoking. Yet there is little evidence of the effects of long-term use of e-cigs on oral health. Conventional cigarette smoking is a prominent risk factor for the development of periodontitis, an oral disease affecting nearly half of adults over 30 years of age in the United States. Periodontitis is initiated through a disturbance in the microbial biofilm communities inhabiting the unique space between teeth and gingival tissues. This disturbance instigates host inflammatory and immune responses and, if left untreated, leads to tooth and bone loss and systemic diseases. We found that the e-cig user’s periodontal microbiome is unique, eliciting unique host responses. Yet some similarities to the microbiomes of both conventional smokers and nonsmokers exist, with strikingly more in common with that of cigarette smokers, suggesting that there is a unique periodontal risk associated with e-cig use.