According to palaeoenvironmental analysis on the fossil fauna dominated by Foraminifera and Ostracoda, core QC2 contains 8 marine transgressive beds, called (from up to bottom) Transgressive Beds Ⅰ,Ⅱ, Ⅲ, …,Ⅷ resp...According to palaeoenvironmental analysis on the fossil fauna dominated by Foraminifera and Ostracoda, core QC2 contains 8 marine transgressive beds, called (from up to bottom) Transgressive Beds Ⅰ,Ⅱ, Ⅲ, …,Ⅷ respectively. Together with dating data, the transgressive sequence since 1. 7 Ma B. P. has been established, indicating that the core went through middle and late Early Pleistocene, early and late Middle Pleistocene, early and late (Substages A and B) Late Pleistocene and the Holocene transgressions. Within these 8 transgressions, late Middle Pleistocene, early Late Pleistocene and the Holocene transgressions-had rather strong activities proved by shallow sea (of 50 or 20-50 m water depth) deposits in the prime, while 2 of the 8, during middle Early Pleistocene and late Late Pleistocene (Substage A), were much weaker only with supratidal deposits. The transgressive cycles also differ from each other. Transgressions in the Holocene and in Substage B of late Late Pleistocene are made up of 3 and 2 subcycles of marine ingressions and regressions respectively, but most transgressions only have a single ingressive or regressive sequence. With the core, some important problems concerning, the study of Quaternary transgression such as correlation of transgressive beds and climatic periods and dating of the transgressive beds are discussed in this paper.展开更多
目的探讨动脉粥样硬化(AS)患者口腔菌群多样性与炎症因子水平的特征及关联。方法纳入AS患者50例与健康对照50例,采集唾液和血样进行16S rRNA测序、IL-6、IL-1β、TNF-α、CRP检测;比较两组菌群结构与炎症指标差异,并进行Spearman相关和...目的探讨动脉粥样硬化(AS)患者口腔菌群多样性与炎症因子水平的特征及关联。方法纳入AS患者50例与健康对照50例,采集唾液和血样进行16S rRNA测序、IL-6、IL-1β、TNF-α、CRP检测;比较两组菌群结构与炎症指标差异,并进行Spearman相关和多因素回归分析。结果AS组IL-6、IL-1β、TNF-α、CRP水平均显著高于对照组(IL-6:8.24±2.15 vs 6.15±1.76,P<0.01;CRP:7.42±2.41 vs 3.98±1.57,P<0.01);口腔菌群Shannon指数低于对照组(4.38±0.55 vs 4.61±0.52,P=0.040);Fusobacterium与CRP、IL-6正相关(r=0.41、0.36,均P<0.05)。多因素回归提示Fusobacterium丰度及IL-6、CRP水平均为AS潜在危险因素。结论AS患者口腔菌群多样性下降伴随炎症显著增高,二者或通过免疫和代谢途径相互作用,为AS的风险评估与干预策略提供新的思路。展开更多
采用常规检测方法检测南阳市西峡县奎文村(KW)、屈原岗村(QYG)、王营村(WY)猕猴桃根际土壤样品的基本理化指标,采用Illumina Mi Seq高通量测序技术分析其微生物群落多样性,并分析两者间的相关性。结果表明,3个样品的pH、有效磷含量、速...采用常规检测方法检测南阳市西峡县奎文村(KW)、屈原岗村(QYG)、王营村(WY)猕猴桃根际土壤样品的基本理化指标,采用Illumina Mi Seq高通量测序技术分析其微生物群落多样性,并分析两者间的相关性。结果表明,3个样品的pH、有效磷含量、速效钾含量、碱解氮含量差异显著(P<0.05)。3个样品细菌群落多样性及物种丰度无显著差异(P>0.05),QYG样品真菌群落多样性最高,KW样品最低,但3个样品真菌群落的物种丰度无显著差异(P>0.05)。从3个样品中共注释到51个细菌门和16个真菌门,包括16个优势细菌门和6个优势真菌门,其中芽孢杆菌门(Bacillota)和放线菌门(Actinomycetota)作为潜在的猕猴桃溃疡病生防细菌,在3个样品中均为优势菌门。土壤理化性质对猕猴桃根际土壤微生物群落分布具有显著影响,其中,芽孢杆菌门与速效钾含量呈极显著负相关(P<0.01),放线菌门与速效钾含量呈显著正相关(P<0.05),与p H呈显著负相关(P<0.05);pH与罗兹菌门(Rozellomycota)呈高度显著正相关(P<0.001)。该研究结果为猕猴桃溃疡病生防细菌的筛选鉴定了基础。展开更多
【目的】本研究旨在扩增丽江猪清道夫受体B族成员2(scavenger receptor class B member 2,SCARB2)基因序列并进行生物信息学分析,检测其在丽江猪各组织中的表达情况,为后续探究该基因的功能提供理论依据。【方法】采集6月龄丽江猪脂肪组...【目的】本研究旨在扩增丽江猪清道夫受体B族成员2(scavenger receptor class B member 2,SCARB2)基因序列并进行生物信息学分析,检测其在丽江猪各组织中的表达情况,为后续探究该基因的功能提供理论依据。【方法】采集6月龄丽江猪脂肪组织,参考GenBank中野猪(Sus scrofa)的SCARB2基因mRNA序列(登录号:NM_001244155.1)设计引物扩增SCARB2基因CDS区序列并测序,利用生物信息学软件分析SCARB2基因的序列特征和密码子偏好性,分析多个物种与丽江猪、中外猪种与丽江猪SCARB2基因序列的相似性并构建系统进化树,预测SCARB2蛋白理化性质和蛋白结构。使用实时荧光定量PCR检测SCARB2基因在2、4、6月龄丽江猪和6月龄杜洛克猪背部脂肪、心脏、肝脏、肺脏、肾脏等组织中的表达情况。【结果】丽江猪SCARB2基因CDS区序列总长为1437 bp,编码478个氨基酸。丽江猪与山羊、绵羊、牛、马、大鼠、小鼠、人和原鸡的相似性分别为91.3%、91.2%、91.0%、89.8%、82.6%、82.5%、76.0%和66.0%;在6个地方猪种中,除巴马小型猪外,丽江猪与中国地方猪的相似性均为99.4%,与外种猪的相似性为99.1%~99.3%。系统进化树分析显示,丽江猪与野猪、牛、山羊、绵羊聚为一支,原鸡形成单独分支。丽江猪SCARB2蛋白属于亲水蛋白,有2个跨膜螺旋和1个信号肽切割位点,包含10个N-糖基化位点和39个磷酸化位点;其二级结构与三级结构均以无规则卷曲为主。SCARB2基因在6月龄丽江猪背部脂肪和肝脏组织中的表达量极显著高于其他组织(P<0.01);随着月龄增长,SCARB2基因在丽江猪腹部脂肪、背部脂肪和肩部脂肪组织中的表达量逐渐升高,且在2、6月龄间达显著或极显著水平(P<0.05;P<0.01);6月龄丽江猪背部脂肪组织中SCARB2基因表达量极显著高于杜洛克猪(P<0.01)。【结论】本研究成功扩增了丽江猪SCARB2基因序列并分析了其分子特征,其在皮下脂肪、肝脏和肺脏等多个组织中均有表达,且随月龄增长在皮下脂肪组织中的表达量呈显著增加。因此,SCARB2可作为研究丽江猪脂肪沉积性状的候选基因,研究结果可为进一步探究猪脂肪沉积的分子机制提供参考。展开更多
Border-associated macrophages are located at the interface between the brain and the periphery, including the perivascular spaces, choroid plexus, and meninges. Until recently, the functions of border-associated macro...Border-associated macrophages are located at the interface between the brain and the periphery, including the perivascular spaces, choroid plexus, and meninges. Until recently, the functions of border-associated macrophages have been poorly understood and largely overlooked. However, a recent study reported that border-associated macrophages participate in stroke-induced inflammation, although many details and the underlying mechanisms remain unclear. In this study, we performed a comprehensive single-cell analysis of mouse border-associated macrophages using sequencing data obtained from the Gene Expression Omnibus(GEO) database(GSE174574 and GSE225948). Differentially expressed genes were identified, and enrichment analysis was performed to identify the transcription profile of border-associated macrophages. CellChat analysis was conducted to determine the cell communication network of border-associated macrophages. Transcription factors were predicted using the ‘pySCENIC' tool. We found that, in response to hypoxia, borderassociated macrophages underwent dynamic transcriptional changes and participated in the regulation of inflammatory-related pathways. Notably, the tumor necrosis factor pathway was activated by border-associated macrophages following ischemic stroke. The pySCENIC analysis indicated that the activity of signal transducer and activator of transcription 3(Stat3) was obviously upregulated in stroke, suggesting that Stat3 inhibition may be a promising strategy for treating border-associated macrophages-induced neuroinflammation. Finally, we constructed an animal model to investigate the effects of border-associated macrophages depletion following a stroke. Treatment with liposomes containing clodronate significantly reduced infarct volume in the animals and improved neurological scores compared with untreated animals. Taken together, our results demonstrate comprehensive changes in border-associated macrophages following a stroke, providing a theoretical basis for targeting border-associated macrophages-induced neuroinflammation in stroke treatment.展开更多
Global brain ischemia and neurological deficit are consequences of cardiac arrest that lead to high mortality.Despite advancements in resuscitation science,our limited understanding of the cellular and molecular mecha...Global brain ischemia and neurological deficit are consequences of cardiac arrest that lead to high mortality.Despite advancements in resuscitation science,our limited understanding of the cellular and molecular mechanisms underlying post-cardiac arrest brain injury have hindered the development of effective neuroprotective strategies.Previous studies primarily focused on neuronal death,potentially overlooking the contributions of non-neuronal cells and intercellular communication to the pathophysiology of cardiac arrest-induced brain injury.To address these gaps,we hypothesized that single-cell transcriptomic analysis could uncover previously unidentified cellular subpopulations,altered cell communication networks,and novel molecular mechanisms involved in post-cardiac arrest brain injury.In this study,we performed a single-cell transcriptomic analysis of the hippocampus from pigs with ventricular fibrillation-induced cardiac arrest at 6 and 24 hours following the return of spontaneous circulation,and from sham control pigs.Sequencing results revealed changes in the proportions of different cell types,suggesting post-arrest disruption in the blood-brain barrier and infiltration of neutrophils.These results were validated through western blotting,quantitative reverse transcription-polymerase chain reaction,and immunofluorescence staining.We also identified and validated a unique subcluster of activated microglia with high expression of S100A8,which increased over time following cardiac arrest.This subcluster simultaneously exhibited significant M1/M2 polarization and expressed key functional genes related to chemokines and interleukins.Additionally,we revealed the post-cardiac arrest dysfunction of oligodendrocytes and the differentiation of oligodendrocyte precursor cells into oligodendrocytes.Cell communication analysis identified enhanced post-cardiac arrest communication between neutrophils and microglia that was mediated by neutrophil-derived resistin,driving pro-inflammatory microglial polarization.Our findings provide a comprehensive single-cell map of the post-cardiac arrest hippocampus,offering potential novel targets for neuroprotection and repair following cardiac arrest.展开更多
文摘According to palaeoenvironmental analysis on the fossil fauna dominated by Foraminifera and Ostracoda, core QC2 contains 8 marine transgressive beds, called (from up to bottom) Transgressive Beds Ⅰ,Ⅱ, Ⅲ, …,Ⅷ respectively. Together with dating data, the transgressive sequence since 1. 7 Ma B. P. has been established, indicating that the core went through middle and late Early Pleistocene, early and late Middle Pleistocene, early and late (Substages A and B) Late Pleistocene and the Holocene transgressions. Within these 8 transgressions, late Middle Pleistocene, early Late Pleistocene and the Holocene transgressions-had rather strong activities proved by shallow sea (of 50 or 20-50 m water depth) deposits in the prime, while 2 of the 8, during middle Early Pleistocene and late Late Pleistocene (Substage A), were much weaker only with supratidal deposits. The transgressive cycles also differ from each other. Transgressions in the Holocene and in Substage B of late Late Pleistocene are made up of 3 and 2 subcycles of marine ingressions and regressions respectively, but most transgressions only have a single ingressive or regressive sequence. With the core, some important problems concerning, the study of Quaternary transgression such as correlation of transgressive beds and climatic periods and dating of the transgressive beds are discussed in this paper.
文摘目的探讨动脉粥样硬化(AS)患者口腔菌群多样性与炎症因子水平的特征及关联。方法纳入AS患者50例与健康对照50例,采集唾液和血样进行16S rRNA测序、IL-6、IL-1β、TNF-α、CRP检测;比较两组菌群结构与炎症指标差异,并进行Spearman相关和多因素回归分析。结果AS组IL-6、IL-1β、TNF-α、CRP水平均显著高于对照组(IL-6:8.24±2.15 vs 6.15±1.76,P<0.01;CRP:7.42±2.41 vs 3.98±1.57,P<0.01);口腔菌群Shannon指数低于对照组(4.38±0.55 vs 4.61±0.52,P=0.040);Fusobacterium与CRP、IL-6正相关(r=0.41、0.36,均P<0.05)。多因素回归提示Fusobacterium丰度及IL-6、CRP水平均为AS潜在危险因素。结论AS患者口腔菌群多样性下降伴随炎症显著增高,二者或通过免疫和代谢途径相互作用,为AS的风险评估与干预策略提供新的思路。
文摘采用常规检测方法检测南阳市西峡县奎文村(KW)、屈原岗村(QYG)、王营村(WY)猕猴桃根际土壤样品的基本理化指标,采用Illumina Mi Seq高通量测序技术分析其微生物群落多样性,并分析两者间的相关性。结果表明,3个样品的pH、有效磷含量、速效钾含量、碱解氮含量差异显著(P<0.05)。3个样品细菌群落多样性及物种丰度无显著差异(P>0.05),QYG样品真菌群落多样性最高,KW样品最低,但3个样品真菌群落的物种丰度无显著差异(P>0.05)。从3个样品中共注释到51个细菌门和16个真菌门,包括16个优势细菌门和6个优势真菌门,其中芽孢杆菌门(Bacillota)和放线菌门(Actinomycetota)作为潜在的猕猴桃溃疡病生防细菌,在3个样品中均为优势菌门。土壤理化性质对猕猴桃根际土壤微生物群落分布具有显著影响,其中,芽孢杆菌门与速效钾含量呈极显著负相关(P<0.01),放线菌门与速效钾含量呈显著正相关(P<0.05),与p H呈显著负相关(P<0.05);pH与罗兹菌门(Rozellomycota)呈高度显著正相关(P<0.001)。该研究结果为猕猴桃溃疡病生防细菌的筛选鉴定了基础。
文摘【目的】本研究旨在扩增丽江猪清道夫受体B族成员2(scavenger receptor class B member 2,SCARB2)基因序列并进行生物信息学分析,检测其在丽江猪各组织中的表达情况,为后续探究该基因的功能提供理论依据。【方法】采集6月龄丽江猪脂肪组织,参考GenBank中野猪(Sus scrofa)的SCARB2基因mRNA序列(登录号:NM_001244155.1)设计引物扩增SCARB2基因CDS区序列并测序,利用生物信息学软件分析SCARB2基因的序列特征和密码子偏好性,分析多个物种与丽江猪、中外猪种与丽江猪SCARB2基因序列的相似性并构建系统进化树,预测SCARB2蛋白理化性质和蛋白结构。使用实时荧光定量PCR检测SCARB2基因在2、4、6月龄丽江猪和6月龄杜洛克猪背部脂肪、心脏、肝脏、肺脏、肾脏等组织中的表达情况。【结果】丽江猪SCARB2基因CDS区序列总长为1437 bp,编码478个氨基酸。丽江猪与山羊、绵羊、牛、马、大鼠、小鼠、人和原鸡的相似性分别为91.3%、91.2%、91.0%、89.8%、82.6%、82.5%、76.0%和66.0%;在6个地方猪种中,除巴马小型猪外,丽江猪与中国地方猪的相似性均为99.4%,与外种猪的相似性为99.1%~99.3%。系统进化树分析显示,丽江猪与野猪、牛、山羊、绵羊聚为一支,原鸡形成单独分支。丽江猪SCARB2蛋白属于亲水蛋白,有2个跨膜螺旋和1个信号肽切割位点,包含10个N-糖基化位点和39个磷酸化位点;其二级结构与三级结构均以无规则卷曲为主。SCARB2基因在6月龄丽江猪背部脂肪和肝脏组织中的表达量极显著高于其他组织(P<0.01);随着月龄增长,SCARB2基因在丽江猪腹部脂肪、背部脂肪和肩部脂肪组织中的表达量逐渐升高,且在2、6月龄间达显著或极显著水平(P<0.05;P<0.01);6月龄丽江猪背部脂肪组织中SCARB2基因表达量极显著高于杜洛克猪(P<0.01)。【结论】本研究成功扩增了丽江猪SCARB2基因序列并分析了其分子特征,其在皮下脂肪、肝脏和肺脏等多个组织中均有表达,且随月龄增长在皮下脂肪组织中的表达量呈显著增加。因此,SCARB2可作为研究丽江猪脂肪沉积性状的候选基因,研究结果可为进一步探究猪脂肪沉积的分子机制提供参考。
基金supported by Qingdao Key Medical and Health Discipline ProjectThe Intramural Research Program of the Affiliated Hospital of Qingdao University,No. 4910Qingdao West Coast New Area Science and Technology Project,No. 2020-55 (all to SW)。
文摘Border-associated macrophages are located at the interface between the brain and the periphery, including the perivascular spaces, choroid plexus, and meninges. Until recently, the functions of border-associated macrophages have been poorly understood and largely overlooked. However, a recent study reported that border-associated macrophages participate in stroke-induced inflammation, although many details and the underlying mechanisms remain unclear. In this study, we performed a comprehensive single-cell analysis of mouse border-associated macrophages using sequencing data obtained from the Gene Expression Omnibus(GEO) database(GSE174574 and GSE225948). Differentially expressed genes were identified, and enrichment analysis was performed to identify the transcription profile of border-associated macrophages. CellChat analysis was conducted to determine the cell communication network of border-associated macrophages. Transcription factors were predicted using the ‘pySCENIC' tool. We found that, in response to hypoxia, borderassociated macrophages underwent dynamic transcriptional changes and participated in the regulation of inflammatory-related pathways. Notably, the tumor necrosis factor pathway was activated by border-associated macrophages following ischemic stroke. The pySCENIC analysis indicated that the activity of signal transducer and activator of transcription 3(Stat3) was obviously upregulated in stroke, suggesting that Stat3 inhibition may be a promising strategy for treating border-associated macrophages-induced neuroinflammation. Finally, we constructed an animal model to investigate the effects of border-associated macrophages depletion following a stroke. Treatment with liposomes containing clodronate significantly reduced infarct volume in the animals and improved neurological scores compared with untreated animals. Taken together, our results demonstrate comprehensive changes in border-associated macrophages following a stroke, providing a theoretical basis for targeting border-associated macrophages-induced neuroinflammation in stroke treatment.
基金supported by the National Science Foundation of China,Nos.82325031(to FX),82030059(to YC),82102290(to YG),U23A20485(to YC)Noncommunicable Chronic Diseases-National Science and Technology Major Project,No.2023ZD0505504(to FX),2023ZD0505500(to YC)the Key R&D Program of Shandong Province,No.2022ZLGX03(to YC).
文摘Global brain ischemia and neurological deficit are consequences of cardiac arrest that lead to high mortality.Despite advancements in resuscitation science,our limited understanding of the cellular and molecular mechanisms underlying post-cardiac arrest brain injury have hindered the development of effective neuroprotective strategies.Previous studies primarily focused on neuronal death,potentially overlooking the contributions of non-neuronal cells and intercellular communication to the pathophysiology of cardiac arrest-induced brain injury.To address these gaps,we hypothesized that single-cell transcriptomic analysis could uncover previously unidentified cellular subpopulations,altered cell communication networks,and novel molecular mechanisms involved in post-cardiac arrest brain injury.In this study,we performed a single-cell transcriptomic analysis of the hippocampus from pigs with ventricular fibrillation-induced cardiac arrest at 6 and 24 hours following the return of spontaneous circulation,and from sham control pigs.Sequencing results revealed changes in the proportions of different cell types,suggesting post-arrest disruption in the blood-brain barrier and infiltration of neutrophils.These results were validated through western blotting,quantitative reverse transcription-polymerase chain reaction,and immunofluorescence staining.We also identified and validated a unique subcluster of activated microglia with high expression of S100A8,which increased over time following cardiac arrest.This subcluster simultaneously exhibited significant M1/M2 polarization and expressed key functional genes related to chemokines and interleukins.Additionally,we revealed the post-cardiac arrest dysfunction of oligodendrocytes and the differentiation of oligodendrocyte precursor cells into oligodendrocytes.Cell communication analysis identified enhanced post-cardiac arrest communication between neutrophils and microglia that was mediated by neutrophil-derived resistin,driving pro-inflammatory microglial polarization.Our findings provide a comprehensive single-cell map of the post-cardiac arrest hippocampus,offering potential novel targets for neuroprotection and repair following cardiac arrest.
