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Quorum sensing (QS) can regulate the production of multiple functional factors in bacteria, but the process of identifying its regulatory targets is very complex and labor-intensive. In this study, an efficient and rapid method to find QS targets through prediction was used. The genome of Lactiplantibacillus plantarum (L. plantarum) L3 was sequenced and characterized, and then linked the L. plantarum L3 genome to the STRING database for QS system regulatory target prediction. A total of 3,167,484 base pairs (bps) were examined from the genome of L. plantarum L3, and 30 QS-related genes were discovered (including luxS). The STRING database prediction indicated that the 30 QS-related genes are mainly involved in the regulation of nine metabolic pathways. Furthermore, metE, metK, aroB, cysE, and birA1 were predicted to be regulatory targets of the LuxS/AI-2 QS system, and these five targets were validated based on quantitative real-time PCR and content determination. Successful elucidation of the LuxS/AI-2 QS system's key targets and regulation mechanism in L. plantarum L3 demonstrated the effectiveness of the new approach for predicting QS targets and provides a scientific basis for future work on improving regulation of functional factor production.
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Proteínas de Bactérias , Biofilmes , Regulação Bacteriana da Expressão Gênica , Lisina , Percepção de Quorum , Proteínas de Bactérias/genética , Proteínas de Bactérias/metabolismo , Biofilmes/crescimento & desenvolvimento , Lisina/metabolismo , Lactobacillus plantarum/genética , Lactobacillus plantarum/metabolismo , Lactobacillus plantarum/fisiologia , Genoma Bacteriano , Liases de Carbono-EnxofreRESUMO
With the rapid development of bridge construction, the service life of bridges and traffic volume continue to increase, leading to the gradual appearance of diseases such as potholes and cracks in bridge deck pavements under repeated external loads. These issues severely impact the safety and service life of bridges. The repair of bridge deck potholes and cracks is crucial for ensuring the integrity and safety of bridge structures. Rapid repair materials designed for this purpose play a critical role in effectively and efficiently addressing these issues. In order to address the issues of pavement diseases, this study focuses on the rapid repair of epoxy concrete for bridge deck pavements and its performance is studied using experimental methods. Firstly, carbon black, rubber powder, and other materials were used to improve the elastic modulus and aging resistance of the epoxy concrete. Secondly, the addition of solid asphalt particles provided thermal sensitivity to the repair material. Finally, various properties of the rapid repair epoxy concrete for bridge deck pavements were tested through experiments including compressive strength testing, elastic modulus measurement, thermal sensitivity testing, and anti-UV aging testing. The experimental results show that adding carbon black and rubber powder reduces the elastic modulus of epoxy concrete by 25% compared to normal epoxy concrete, while increasing its aging resistance by 1.8%. The inclusion of solid asphalt particles provided thermal sensitivity to the repair material, contributing to better stress coordination between the repair material and the original pavement material under different temperature conditions. The epoxy concrete has early strength, toughness, and anti-aging properties, making it suitable for rapid repair of bridge deck pavement.
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The special particle grading properties of silt lead to the strong water sensitivity and low soil strength of silt sites, many of which are severely damaged and urgently need to be repaired. This article takes the powder soil from a certain burial site area in Xizhu Village, Luoyang as the research object, which is improved by adding nanosilica and potassium methylsilicate. The modified soil is studied through mechanical and waterproof performance tests, and the mechanism of action of the modified material is analyzed through SEM and XRD. The experimental results show that the mechanical properties and waterproof properties of the composite modified soil were improved when the nanosilica content was 2% and the potassium methylsilicate content was 0.5%; the durability of the composite modified soil is improved, making this the optimum ratio. The mechanical properties and water resistance of the silty soil were significantly improved by adding the appropriate amount of nanosilica and potassium methylsilicate. Nanosilica can be evenly dispersed in the soil matrix, absorb a small amount of water to form a gel state, fill the pores in the silt aggregates, and improve soil compactness. In addition, nanosilica aggregates can attach to the surface of the soil particles and extend from the particle surface to the particle edge. By increasing the contact between soil particles and increasing the particle size, the mechanical properties of the modified soil are improved. When potassium methylsilicate solution is added to the soil, it reacts with water and carbon dioxide, decomposes into methylsilicate, and quickly generates a polymethylsiloxane film to cover the surface of soil particles, forming a waterproof film on the surface and thereby improving the waterproof performance of modified soil. Our research results can provide a reference for the restoration and protection of silty and silt-like sites. The next step is to apply the composite modified soil in engineering restoration through field tests in order to study the repairing ability of composite modified soil and its actual protective effects.
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The surfactant-macromolecule interactions (SMI) are one of the most critical topics for scientific research and industrial application. Small-angle X-ray scattering (SAXS) is a powerful tool for comprehensively studying the structural and conformational features of macromolecules at a size ranging from Angstroms to hundreds of nanometers with a time-resolve in milliseconds scale. The SAXS integrative techniques have emerged for comprehensively analyzing the SMI and the structure of their complex in solution. Here, the various types of emerging interactions of surfactant with macromolecules, such as protein, lipid, nuclear acid, polysaccharide and virus, etc. have been systematically reviewed. Additionally, the principle of SAXS and theoretical models of SAXS for describing the structure of SMI as well as their complex has been summarized. Moreover, the recent developments in the applications of SAXS for charactering the structure of SMI have been also highlighted. Prospectively, the capacity to complement artificial intelligence (AI) in the structure prediction of biological macromolecules and the high-throughput bioinformatics sequencing data make SAXS integrative structural techniques expected to be the primary methodology for illuminating the self-assembling dynamics and nanoscale structure of SMI. As advances in the field continue, we look forward to proliferating uses of SAXS based upon its abilities to robustly produce mechanistic insights for biology and medicine.
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This paper proposes a self-learning sliding mode control (SlSMC) strategy with stability guarantee for the trajectory tracking of nonholonomic mobile robots (NMRs) under matched uncertainties, which improves the control performance of NMRs by optimizing the reaching law and the sliding mode surface of SMC as well as retaining the finite-time convergence and the robustness to uncertainties. In the presence of adverse factors such as skidding, slipping and environmental noise, the kinematic model of NMRs is reconstructed and an integral terminal sliding mode controller is designed for the trajectory tracking of NMRs. Then, based on the sliding mode controller, the proposed control strategy formulates the optimization of the SMC's reaching law and the sliding mode surface under stability constraints as two asynchronous optimal control problems with control constraints. Meanwhile, an online continuous-time receding-horizon optimization mechanism based on an actor-critic algorithm is proposed to solve the optimal problems asynchronously and improve online learning efficiency. The stability and the convergence of the proposed strategy are validated both in theory and simulations. Furthermore, extensive contrastive simulation results illustrate that the proposed receding horizon learning-based control strategy outperforms three recent methods in control performance. Finally, experiments of the proposed self-learning SMC strategy are carried out based on a real intelligent vehicle, and the experimental results also verify that the proposed method can meet the actual control needs of NMRs.
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A novel wild-type Lactiplantibacillus plantarum (L. plantarum) L3 with good fermentation characteristics and protein degradation capacity was isolated from raw milk samples. In this study, the metabolites in milk fermented with L. plantarum L3 were investigated by metabolomic and peptidomics analyses. The metabolomics results revealed that the metabolites in milk fermented with L. plantarum L3 were Thr-Pro, Val-Lys, l-creatine, pyridoxine, and muramic acid, which improved the taste and nutritional qualities of the milk. Moreover, the water-soluble peptides derived from L3 fermented milk exhibited high antioxidant properties and angiotensin I-converting enzyme inhibitory (ACEI) activities. Additionally, 152 peptides were found using liquid chromatography-mass spectrometry (LC-MS/MS). Furthermore, endogenous enzymes secreted by L. plantarum L3 cleaved ß- and α-casein to release six ACEI peptides (ACEIPs), nineteen antioxidant peptides (AOPs), and five antimicrobial peptides (AMPS). Overall, these findings could be valuable in improving the quality of fermented milk.
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The phenyllactic acid (PLA) produced by lactic acid bacteria (LAB) inhibits fungi and facilitates the quality control of fermented milk. A strain of Lactiplantibacillus plantarum L3 (L. plantarum L3) with high PLA production was screened in the pre-laboratory, but the mechanism of its PLA formation is unclear. The amount of autoinducer-2 (AI-2) increased with increasing culture time, as did cell density and PLA. The results in this study suggest that PLA production in L. plantarum L3 may be regulated by the LuxS/AI-2 Quorum Sensing (QS) system. Tandem mass tag (TMT) quantitative proteomics analysis showed that a total of 1291 differentially expressed proteins (DEPs) were quantified in the incubated for 24 h compared with the incubated for 2 h, of which 516 DEPs were up-regulated and 775 DEPs were down-regulated. Among them, S-ribosomal homocysteine lyase (luxS), aminotransferase (araT), and lactate dehydrogenase (ldh) are the key proteins for PLA formation. The DEPs were mainly involved in the QS pathway and the core pathway of PLA synthesis. Furanone effectively inhibited the production of L. plantarum L3 PLA. In addition, Western blot analysis demonstrated that luxS, araT, and ldh were the key proteins regulating PLA production. This study reveals the regulatory mechanism of PLA based on the LuxS/AI-2 QS system, which provides a theoretical basis for the efficient and large-scale production of PLA in industries in the future.
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Proteínas de Bactérias , Percepção de Quorum , Proteínas de Bactérias/metabolismo , Lactatos/metabolismo , PoliésteresRESUMO
Lung homeostasis and regeneration depend on lung epithelial progenitor cells. Lkb1 (Liver Kinase B1) has known roles in the differentiation of airway epithelial cells during embryonic development. However, the effects of Lkb1 in adult lung epithelial progenitor cell regeneration and its mechanisms of action have not been determined. In this study, we investigated the mechanism by which Lkb1 regulates lung epithelial progenitor cell regeneration. Organoid culture showed that loss of Lkb1 significantly reduced the proliferation of club cells and alveolar type 2 (AT2) cells in vitro. In the absence of Lkb1, there is a slower recovery rate of the damaged airway epithelium in naphthalene-induced airway epithelial injury and impaired expression of surfactant protein C during bleomycin-induced alveolar epithelial damage. Moreover, the expression of autophagy-related genes was reduced in club cells and increased in AT2 cells, but the expression of Claudin-18 was obviously reduced in AT2 cells after Lkb1 knockdown. On the whole, our findings indicated that Lkb1 may promote the proliferation of lung epithelial progenitor cells via a niche-dependent pathway and is required for the repair of the damaged lung epithelium.
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Pulmão , Células-Tronco , Pulmão/metabolismo , Células-Tronco/metabolismo , Proteínas Serina-Treonina Quinases/genética , Proteínas Serina-Treonina Quinases/metabolismo , Células Epiteliais Alveolares/metabolismo , Diferenciação Celular/genética , Células Epiteliais/metabolismo , Proliferação de Células/fisiologiaRESUMO
OBJECTIVES: Early embryo development is dependent on the regulation of maternal messages stored in the oocytes during the maternal-to-zygote transition. Previous studies reported variability of oocyte competence among different inbred mouse strains. The present study aimed to identify the maternal transcripts responsible for early embryonic development by comparing transcriptomes from oocytes of high- or low- competence mouse strains. MATERIALS AND METHODS: In vitro fertilization embryos from oocytes of different mouse strains were subject to analysis using microarrays, RNA sequencing, real-time quantitative PCR (RT-qPCR) analysis, Western blotting, and immunofluorescence. One candidate gene, Prkce, was analysed using Prkce knockout mice, followed by a cRNA rescue experiment. RESULTS: The fertilization and 2-cell rate were significantly higher for FVB/NJ (85.1% and 82.0%) and DBA/2J (79.6% and 76.7%) inbred mouse strains than those for the MRL/lpr (39.9% and 35.8%) and 129S3 (35.9% and 36.6%) strains. Thirty-nine differentially expressed genes (DEGs) were noted, of which nine were further verified by RT-qPCR. Prkce knockout mice showed a reduced 2-cell rate (Prkce+/+ 80.1% vs. Prkce-/- 32.4%) that could be rescued by Prkce cRNA injection (2-cell rate reached 76.7%). Global transcriptional analysis revealed 143 DEGs in the knockout mice, which were largely composed of genes functioning in cell cycle regulation. CONCLUSIONS: The transcription level of maternal messages such as Prkce in mature oocytes is associated with different 2-cell rates in select inbred mouse strains. Prkce transcript levels could serve as a potential biomarker to characterize high-quality mature oocytes.
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Embrião de Mamíferos/metabolismo , Oócitos , Proteína Quinase C-épsilon/metabolismo , Zigoto , Animais , Embrião de Mamíferos/citologia , Feminino , Regulação da Expressão Gênica no Desenvolvimento , Camundongos , Camundongos Endogâmicos DBA , Camundongos Endogâmicos MRL lpr , Camundongos Knockout , Oócitos/metabolismo , Gravidez , RNA Complementar/metabolismo , Zigoto/metabolismoRESUMO
(1) Background: Abnormal repair after alveolar epithelial injury drives the progression of idiopathic pulmonary fibrosis (IPF). The maintenance of epithelial integrity is based on the self-renewal and differentiation of alveolar type 2 (AT2) cells, which require sufficient energy. However, the role of glutamine metabolism in the maintenance of the alveolar epithelium remains unclear. In this study, we investigated the role of glutamine metabolism in AT2 cells of patients with IPF and in mice with bleomycin-induced fibrosis. (2) Methods: Single-cell RNA sequencing (scRNA-seq), transcriptome, and metabolomics analyses were conducted to investigate the changes in the glutamine metabolic pathway during pulmonary fibrosis. Metabolic inhibitors were used to stimulate AT2 cells to block glutamine metabolism. Regeneration of AT2 cells was detected using bleomycin-induced mouse lung fibrosis and organoid models. (3) Results: Single-cell analysis showed that the expression levels of catalytic enzymes responsible for glutamine catabolism were downregulated (p < 0.001) in AT2 cells of patients with IPF, suggesting the accumulation of unusable glutamine. Combined analysis of the transcriptome (p < 0.05) and metabolome (p < 0.001) revealed similar changes in glutamine metabolism in bleomycin-induced pulmonary fibrosis in mice. Mechanistically, inhibition of the key enzymes involved in glucose metabolism, glutaminase-1 (GLS1) and glutamic-pyruvate transaminase-2 (GPT2) leads to reduced proliferation (p < 0.01) and differentiation (p < 0.01) of AT2 cells. (4) Conclusions: Glutamine metabolism is required for alveolar epithelial regeneration during lung injury.
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Fibrose Pulmonar Idiopática , Lesão Pulmonar , Células Epiteliais Alveolares , Animais , Bleomicina/toxicidade , Glutamina/metabolismo , Humanos , Fibrose Pulmonar Idiopática/induzido quimicamente , Fibrose Pulmonar Idiopática/metabolismo , Lesão Pulmonar/induzido quimicamente , CamundongosRESUMO
The lung is the primary site of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced immunopathology whereby the virus enters the host cells by binding to angiotensin-converting enzyme 2 (ACE2). Sophisticated regeneration and repair programs exist in the lungs to replenish injured cell populations. However, known resident stem/progenitor cells have been demonstrated to express ACE2, raising a substantial concern regarding the long-term consequences of impaired lung regeneration after SARS-CoV-2 infection. Moreover, clinical treatments may also affect lung repair from antiviral drug candidates to mechanical ventilation. In this review, we highlight how SARS-CoV-2 disrupts a program that governs lung homeostasis. We also summarize the current efforts of targeted therapy and supportive treatments for COVID-19 patients. In addition, we discuss the pros and cons of cell therapy with mesenchymal stem cells or resident lung epithelial stem/progenitor cells in preventing post-acute sequelae of COVID-19. We propose that, in addition to symptomatic treatments being developed and applied in the clinic, targeting lung regeneration is also essential to restore lung homeostasis in COVID-19 patients.
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COVID-19 , Enzima de Conversão de Angiotensina 2 , Humanos , Pulmão , Regeneração , SARS-CoV-2RESUMO
The prevalence of staphylococcal infection and the emergence of multidrug resistance of Staphylococcus aureus (S. aureus) are major concerns in food safety and public health. This study aimed to investigate the prevalence of S. aureus isolated from traditional Chinese Rubing and Rushan cheese, antimicrobial resistance profiles, genomic characteristics, and predict antimicrobial resistance genes (ARGs). From 124 samples, 18 of 62 (29.03%) of Rubing and 5 of 62 (8.06%) of Rushan cheese were confirmed to be S. aureus positive by standard culture-based methods. Twenty-three coagulase-positive staphylococci isolates were grouped into 16 clusters by pulsed-field gel electrophoresis and subjected to routine susceptibility testing to 12 antibiotics. Those isolates exhibited high resistance to penicillin (100%), erythromycin, trimethoprim-sulphamethoxazole (34.78%), oxacillin, clindamycin, and cefoxitin (21.74%). Multidrug-resistant (MDR) S. aureus was found in 34.78% (8 of 23) of isolates. Further, S. aureus strain DC.RB_015 isolated from Rubing cheese, recognized as the most resistant to six antibiotics, was selected for whole-genome sequencing (WGS), continued with in silico approaches. S. aureus DC.RB_015 had a single chromosome size of 2,794,578 bp and a plasmid size of 22,961 bp. The strain harbored 18 predicted ARGs, including eight efflux pump genes (mepA, tet(K), arlR, arlS, norA, mgrA, tet(38), LmrS), one peptidoglycan biosynthesis gene (bacA), two ß-lactams resistance genes (mecA, blaZ), and seven genes conferring other antimicrobial resistance (APH(3')-IIIa, aad(6), ErmB, SAT-4, mecR1, GlpT, murA). The results of this study expand the knowledge of S. aureus strain DC.RB_015, increase food safety awareness, and will be helpful in establishing therapeutic therapy. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13205-021-03072-4.
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ß654-thalassemia is a prominent Chinese subtype of b-thalassemia, representing 17% of all cases of ß-thalassemia in China. The molecular mechanism underlying this subtype involves the IVS-2-654 CâT mutation leading to aberrant ß-globin RNA splicing. This results in an additional 73-nucleotide exon between exons 2 and 3 and leads to a severe thalassemia syndrome. Herein, we explored a CRISPR/Cas9 genome editing approach to eliminate the additional 73- nucleotide by targeting both the IVS-2-654 CâT and a cryptic acceptor splice site at IVS-2-579 in order to correct aberrant b-globin RNA splicing and ameliorate the clinical ß-thalassemia syndrome in ß654 mice. Gene-edited mice were generated by microinjection of sgRNA and Cas9 mRNA into one-cell embryos of ß654 or control mice: 83.3% of live-born mice were gene-edited, 70% of which produced correctly spliced RNA. No off-target events were observed. The clinical symptoms, including hematologic parameters and tissue pathology of all of the edited ß654 founders and their offspring were significantly improved compared to those of the non-edited ß654 mice, consistent with the restoration of wild-type b-globin RNA expression. Notably, the survival rate of gene-edited heterozygous ß654 mice increased significantly, and liveborn homozygous ß654 mice were observed. Our study demonstrated a new and effective gene-editing approach that may provide groundwork for the exploration of ß654-thalassemia therapy in the future.
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Down's syndrome (DS) is one of the most commonly known disorders with multiple congenital disabilities. Besides severe cognitive impairment and intellectual disability, individuals with DS also exhibit additional phenotypes of variable penetrance and severity, with one or more comorbid conditions, including Alzheimer's disease, congenital heart disease, or leukemia. Various vital genes and regulatory networks had been studied to reveal the pathogenesis of the disease. Nevertheless, very few studies have examined alternative splicing. Alternative splicing (AS) is a regulatory mechanism of gene expression when making one multi-exon protein-coding gene produce more than one unique mature mRNA. We employed the GeneChip Human Transcriptome Array 2.0 (HTA 2.0) for the global gene analysis with hiPSCs from DS and healthy individuals. Examining differentially expressed genes (DEGs) in these groups and focusing on specific transcripts with AS, 466 up-regulated and 722 down-regulated genes with AS events were identified. These genes were significantly enriched in biological processes, such as cell adhesion, cardiac muscle contraction, and immune response, through gene ontology (GO) analysis of DEGs. Candidate genes, such as FN1 were further explored for potentially playing a key role in DS. This study provides important insights into the potential role that AS plays in DS.
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Inflammation and fibrosis in human liver are often precursors to hepatocellular carcinoma (HCC), yet none of them is easily modeled in animals. We previously generated transgenic mice with hepatocyte-specific expressed herpes simplex virus thymidine kinase (HSV-tk). These mice would develop hepatitis with the administration of ganciclovir (GCV)(Zhang, 2005 #1). However, our HSV-tk transgenic mice developed hepatitis and HCC tumor as early as six months of age even without GCV administration. We analyzed the transcriptome of the HSV-tk HCC tumor and hepatitis tissue using microarray analysis to investigate the possible causes of HCC. Gene Ontology (GO) enrichment analysis showed that the up-regulated genes in the HCC tissue mainly include the immune-inflammatory and cell cycle genes. The down-regulated genes in HCC tumors are mainly concentrated in the regions related to lipid metabolism. Gene set enrichment analysis (GSEA) showed that immune-inflammatory-related signals in the HSV-tk mice are up-regulated compared to those in Notch mice. Our study suggests that the immune system and inflammation play an important role in HCC development in HSV-tk mice. Specifically, increased expression of immune-inflammatory-related genes is characteristic of HSV-tk mice and that inflammation-induced cell cycle activation maybe a precursory step to cancer. The HSV-tk mouse provides a suitable model for the study of the relationship between immune-inflammation and HCC, and their underlying mechanism for the development of therapeutic application in the future.
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Down syndrome (DS), trisomy chromosome 21 (Hsa21), is the most common genetic disease caused by chromosome aberration in the human genome. Modeling DS in mice has been challenging since the orthologs of Hsa21 genes map to separate segments of three mouse chromosomes, Mmu16, Mmu17, and Mmu10. Although the early Ts65Dn mouse model exhibited various DS phenotypes, the duplicated fragments were randomly generated by ionizing radiation and did not include all Hsa21 orthologs. In 2004, the successful use of the Cre/LoxP recombination technique in chromosomal engineering in the construction of the Ts1Rhr mouse strain solved the problem of duplication of specific chromosome segment, resulting in the establishment of specific DS mouse models with accurate triplication of particular genes and associated phenotypes. In this review, we briefly introduce the different DS mouse models and discuss their advantages and limitations by focusing on the triplication of Hsa21 orthologs and manifestations of DS phenotypes, thereby providing some references for the selection of specific mouse models in DS research.
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Modelos Animais de Doenças , Síndrome de Down/genética , Animais , Cromossomos/genética , Patrimônio Genético , Humanos , Camundongos , TrissomiaRESUMO
OBJECTIVE: To explore the disease-causing mutations in a patient suspected for giant axonal neuropathy(GAN). METHODS: Target sequence capture sequencing was used to screen potential mutations in genomic DNA extracted from peripheral blood sample of the patient. Sanger sequencing was applied to confirm the detected mutation. The mutation was verified among 400 GAN alleles from 200 healthy individuals by Sanger sequencing. The function of the mutations was predicted by bioinformatics analysis. RESULTS: The patient was identified as a compound heterozygote carrying two novel pathogenic GAN mutations, i.e., c.778G>T (p.Glu260Ter) and c.277G>A (p.Gly93Arg). Sanger sequencing confirmed that the c.778G>T (p.Glu260Ter) mutation was inherited from his father, while c.277G>A (p.Gly93Arg) was inherited from his mother. The same mutations was not found in the 200 healthy individuals. Bioinformatics analysis predicted that the two mutations probably caused functional abnormality of gigaxonin. CONCLUSION: Two novel GAN mutations were detected in a patient with GAN. Both mutations are pathogenic and can cause abnormalities of gigaxonin structure and function, leading to pathogenesis of GAN. The results may also offer valuable information for similar diseases.
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Proteínas do Citoesqueleto/genética , Neuropatia Axonal Gigante/genética , Mutação , Sequência de Aminoácidos , Criança , Biologia Computacional , Humanos , Masculino , Dados de Sequência Molecular , Análise de Sequência de DNAAssuntos
Diferenciação Celular , Fator de Crescimento de Hepatócito/metabolismo , Proteínas de Membrana/metabolismo , Células-Tronco Embrionárias Murinas/metabolismo , Precursores de Proteínas/metabolismo , Serina Endopeptidases/metabolismo , Animais , Fator de Crescimento de Hepatócito/genética , Proteínas de Membrana/genética , Camundongos , Células-Tronco Embrionárias Murinas/citologia , Precursores de Proteínas/genética , Serina Endopeptidases/genéticaRESUMO
Thuja, a genus of Cupressaceae comprising five extant species, presently occurs in both East Asia (3 species) and North America (2 species) and has a long fossil record from Paleocene to Pleistocene in the Northern Hemisphere. Two distinct hypotheses have been proposed to account for the origin and present distribution of this genus. Here we recognize and describe T. sutchuenensis Franch., a new fossil Thuja from the late Pliocene sediments of Zhangcun, Shanxi, North China, based on detailed comparisons with all living species and other fossil ones, integrate the global fossil records of this genus plotted in a set of paleomaps from different time intervals, which show that Thuja probably first appeared at high latitudes of North America in or before the Paleocene. This genus reached Greenland in the Paleocene, then arrived in eastern Asia in the Miocene via the land connection between East Asia and western North America. In the late Pliocene, it migrated into the interior of China. With the Quaternary cooling and drying, Thuja gradually retreated southwards to form today's disjunctive distribution between East Asia and North America.
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Fósseis , Epiderme Vegetal/anatomia & histologia , Thuja/anatomia & histologia , Thuja/fisiologia , China , Europa (Continente) , Ásia Oriental , Geografia , América do Norte , Dispersão Vegetal/fisiologia , Epiderme Vegetal/citologia , Especificidade da Espécie , Thuja/classificação , Fatores de TempoRESUMO
Vasovagal syncope (VVS) causes accidental harm for susceptible patients. However, pathophysiology of this disorder remains largely unknown. In an effort to understanding of molecular mechanism for VVS, genome-wide gene expression profiling analyses were performed on VVS patients at syncope state. A total of 66 Type 1 VVS child patients and the same number healthy controls were enrolled in this study. Peripheral blood RNAs were isolated from all subjects, of which 10 RNA samples were randomly selected from each groups for gene expression profile analysis using Gene ST 1.0 arrays (Affymetrix). The results revealed that 103 genes were differently expressed between the patients and controls. Significantly, two G-proteins related genes, GPR174 and GNG2 that have not been related to VVS were among the differently expressed genes. The microarray results were confirmed by qRT-PCR in all the tested individuals. Ingenuity pathway analysis and gene ontology annotation study showed that the differently expressed genes are associated with stress response and apoptosis, suggesting that the alteration of some gene expression including G-proteins related genes is associated with VVS. This study provides new insight into the molecular mechanism of VVS and would be helpful to further identify new molecular biomarkers for the disease.