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World Journal of Gastroenterology 2006年第15期12卷 2406-2411页

作者： Manuel Romero-Gómez María Jover Daniel Díaz-Gómez Laura Collantes de Terán Regina Rodrigo Inés Camacho Miriam Echevarría Vicente Felipo Juan D Bautista Unit for the Clinical Management of Digestive Diseases Hospital Universitario de Valme SevillaSpain department of Biochemistry Bromatology and Toxicology Faculty of PharmacyUniversity of SevilleSpain Laboratory of Neurobiology Fundación Valenciana de Investigaciones Biomédicas ValenciaSpain Biochemistry Unit Hospital Universitario de Valme SevillaSpain Instituto de investigaciones biomédicas departament of Physiology University of SevilleSpain Laboratory of Neurobiology Fundación Valenciana de Investigaciones Biomédicas ValenciaSpain

瞄准：估计在老鼠的门腔静脉吻合(PCA ) 是否在肾影响蛋白质表示或谷酰胺酶的活动，肠并且在外皮的三个大脑区域，基础轧了神经胶质和小脑并且解释在肝的脑病发现的神经病学的改变(他) 。方法：称 250-350 g 的十六只男 Wistar 老鼠被... 详细信息

瞄准：估计在老鼠的门腔静脉吻合(PCA ) 是否在肾影响蛋白质表示或谷酰胺酶的活动，肠并且在外皮的三个大脑区域，基础轧了神经胶质和小脑并且解释在肝的脑病发现的神经病学的改变(他) 。方法：称 250-350 g 的十六只男 Wistar 老鼠被组织进假冒操作的控制(n=8 ) 或 portacaval (n=8 ) 。在过程以后的 28 天，动物被牺牲。十二指肠，肾和大脑被移开， homogenised 和线粒体被孤立。氨在大脑和血被测量。激活磷酸盐的谷酰胺酶(PAG ) 活动被与 O-phthalaldehyde (OPA ) 和每蛋白质(蛋白质的 mukat/g ) 的克以单位表示的特殊活动在 37 摄氏度测量氨生产追随者孵化一个小时决定。蛋白质表示被弄污的免疫测量。结果：十二指肠并且和蛋白质内容的肾 PAG 活动比在 PCA 组是显著地更高的在控制或假冒操作老鼠(十二指肠 PAG 活动是在 PCA 老鼠对在假冒操作老鼠的蛋白质的 429.19+/-126.92mukat/g 的蛋白质的 976.95+/-268.87 mukat/g；肾 PAG 活动是在 PCA 老鼠对在控制的蛋白质的 669.67+/-400.8 mukat/g 的 1259.18+/-228.79 mukat/g 蛋白质， Pns ) 。结论：在肾和十二指肠的增加的 PAG 活动能在 PCA 老鼠显著地作出贡献到 hyperammonaemia，脑病的动物模型。PAG 从外皮在 non-synaptic 线粒体被增加并且基础轧了神经胶质并且能在肝的脑病的致病被含有。因此， PAG 能是为处理的一个可能的目标他或肝机能障碍。

关键词：磷酸谷氨酰胺酶酶活性脑疾病门腔静脉吻合术

neurotoxicity of the pesticide rotenone on neuronal polarization: a mechanistic approach

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neural Regeneration Research 2019年第5期14卷 762-766页

作者： Mariano Bisbal Mónica Sanchez laboratory of neurobiology Instituto Mercedes y Martín Ferreyra (INIMEC-CONICET) Universidad nacional de Córdoba Instituto Universitario Ciencias biomédicas Córdoba

neurons are the most extensive and polarized cells that display a unique single long axon and multiple dendrites, which are compartments exhibiting structural and functional differences. Polarity occurs early in neuronal development and it is maintained by complex subcellular mechanisms throughout cell life. A well-defined and controlled spatio-temporal program of cellular and molecular events strictly regulates the formation of the axon and dendrites from a non-polarized cell. This event is critical for an adequate neuronal wiring and therefore for the normal functioning of the nervous system. neuronal polarity is very sensitive to the harmful effects of different factors present in the environment. In this regard, rotenone is a crystalline, colorless and odorless isoflavone used as insecticide, piscicide and broad spectrum pesticide commonly used earlier in agriculture. In the present review we will summarize the toxicity mechanism caused by this pesticide in different neuronal cell types, focusing on a particular biological mechanism whereby rotenone could impair neuronal polarization in cultured hippocampal neurons. Recent advances suggest that the inhibition of axonogenesis produced by rotenone could be related with its effect on microtubule dynamics, the actin cytoskeleton and their regulatory pathways, particularly affecting the small RhoGTPase RhoA. Unveiling the mechanism by which rotenone produces neurotoxicity will be instrumental to understand the cellular mechanisms involved in neurodegenerative diseases influenced by this environmental pollutant, which may lead to research focused on the design of new therapeutic strategies.

关键词： rotenone environmental pollutants toxicity neuronal polarity RhoGTPase RhoA Lfc Arhgef1

Relation of COVID-19 with liver diseases and their impact on healthcare systems:The Portuguese case

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World Journal of Gastroenterology 2023年第6期29卷 1109-1122页

作者： Sara Fernandes Milaydis Sosa-napolskij Graça Lobo Isabel Silva Instituto de Ciências biomédicas Abel Salazar da Universidade do Porto(ICBAS-UP) Porto 4050-313Portugal CInTESIS@RISE Center for Health Technology and Services Research at The Associate Laboratory RISE–Health Research NetworkFaculty of Medicine of The University of PortoPorto 4200-219Portugal laboratory of Pharmacology and neurobiology–department of Immuno-physiology and Pharmacology Instituto de Ciências Biomédicas Abel Salazar da Universidade do Porto(ICBAS-UP)Porto 4050-313Portugal Center for Drug Discovery and Innovative Medicines(MedInUP) Instituto de Ciências Biomédicas Abel Salazar da Universidade do Porto(ICBAS-UP)Porto 4050-313Portugal

BACKGROUnD The impact caused by the coronavirus disease 2019(COVID-19)on the Portuguese population has been addressed in areas such as clinical manifestations,frequent comorbidities,and alterations in consumption habits.However,comorbidities like liver conditions and changes concerning the Portuguese population's access to healthcare-related services have received less attention.AIM To(1)Review the impact of COVID-19 on the healthcare system;(2)examine the relationship between liver diseases and COVID-19 in infected individuals;and(3)investigate the situation in the Portuguese population concerning these topics.METHODS For our purposes,we conducted a literature review using specific keywords.RESULTS COVID-19 is frequently associated with liver damage.However,liver injury in COVID-19 individuals is a multifactor-mediated effect.Therefore,it remains unclear whether changes in liver laboratory tests are associated with a worse prognosis in Portuguese individuals with COVID-19.COnCLUSIOn COVID-19 has impacted healthcare systems in Portugal and other countries;the combination of COVID-19 with liver injury is common.Previous liver damage may represent a risk factor that worsens the prognosis in individuals with COVID-19.

关键词： COVID-19 Healthcare systems Liver Portuguese individuals Comorbidities Clinical outcomes

IKKβ overexpression together with a lack of tumour suppressor genes causes ameloblastic odontomas in mice

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International Journal of Oral Science 2020年第1期12卷 31-39页

作者： Angustias Page Ana Bravo Cristian Suarez-Cabrera Raquel Sanchez-Baltasar Marta Oteo Miguel Angel Morcillo MLlanos Casanova Jose CSegovia Manuel navarro Angel Ramirez Molecular Oncology Unit.Centro de investigaciones Energéticas Medioambientales y Tecnológicas(CIEMAT)MadridSpain Instituto de Investigación 12 de Octubre i+12 MadridSpain Centro de Investigación biomédica en Red de Cáncer(CIBEROnC) MadridSpain department of Anatomy Animal Production and Veterinary Clinical SciencesLaboratory of Pathology Phenotyping of Genetically Engineered MiceFaculty of Veterinary MedicineUniversity of Santiago de CompostelaLugoSpain biomedical Applications and Pharmacokinetics Unit Centro de Investigaciones EnergéticasMedioambientales y Tecnológicas(CIEMAT)MadridSpain Hematopoietic Innovative Therapies Division.Centro de investigaciones Energéticas Medioambientales y Tecnológicas(CIEMAT).Centro de Investigación Biomédica en Red de Enfermedades Raras(CIBERER)MadridSpain Unidad Mixta de Terapias Avanzadas Fundación Instituto de Investigaciones Sanitarias Fundación Jiménez DíazMadridSpain

Odontogenic tumours are a heterogeneous group of lesions that develop in the oral cavity region and are characterized by the formation of tumoural structures that differentiate as teeth. Due to the diversity of their histopathological characteristics and clinical behaviour, the classification of these tumours is still under debate. Alterations in morphogenesis pathways such as the Hedgehog,MAPK and WnT/β-catenin pathways are implicated in the formation of odontogenic lesions, but the molecular bases of many of these lesions are still unknown. In this study, we used genetically modified mice to study the role of IKKβ(a fundamental regulator of nF-κB activity and many other proteins) in oral epithelial cells and odontogenic tissues. Transgenic mice overexpressing IKKβ in oral epithelial cells show a significant increase in immune cells in both the oral epithelia and oral submucosa. They also show changes in the expression of several proteins and mi RnAs that are important for cancer development. Interestingly, we found that overactivity of IKKβ in oral epithelia and odontogenic tissues, in conjunction with the loss of tumour suppressor proteins(p53, or p16 and p19), leads to the appearance of odontogenic tumours that can be classified as ameloblastic odontomas, sometimes accompanied by foci of secondary ameloblastic carcinomas. These tumours show nF-κB activation and increased β-catenin activity.These findings may help to elucidate the molecular determinants of odontogenic tumourigenesis and the role of IKKβ in the homoeostasis and tumoural transformation of oral and odontogenic epithelia.

关键词： IKKβ tumour suppressor

Promotion of structural plasticity in area V2 of visual cortex prevents against object recognition memory deficits in aging and Alzheimer's disease rodents

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neural Regeneration Research 2024年第8期19卷 1835-1841页

作者： Irene navarro-Lobato Mariam Masmudi-Martín Manuel F.López-Aranda Juan F.López-Téllez Gloria delgado Pablo Granados-Durán Celia Gaona-Romero Marta Carretero-Rey Sinforiano Posadas María E.Quiros-Ortega Zafar U.Khan laboratory of neurobiology Centro de Investigaciones Médico Sanitarias(CIMES)University of MalagaMalagaSpain department of Medicine Faculty of MedicineUniversity of MalagaMalagaSpain Centro de Investigación biomédica en Red de Enfermedades neurodegenerativas(CIBERnED) Institute of Health Carlos IIIMadridSpain the Donders Institute for Brain Cognition and Behaviour Radboud UniversityNijmegenThe Netherlands the Brain Metastasis Group National Cancer Research Centre(CNIO)MadridSpain the department of neurobiology University of California-Los AngelesLos AngelesCAUSA

Memory deficit,which is often associated with aging and many psychiatric,neurological,and neurodegenerative diseases,has been a challenging issue for treatment.Up till now,all potential drug candidates have failed to produce satisfa ctory effects.Therefore,in the search for a solution,we found that a treatment with the gene corresponding to the RGS14414protein in visual area V2,a brain area connected with brain circuits of the ventral stream and the medial temporal lobe,which is crucial for object recognition memory(ORM),can induce enhancement of ORM.In this study,we demonstrated that the same treatment with RGS14414in visual area V2,which is relatively unaffected in neurodegenerative diseases such as Alzheimer s disease,produced longlasting enhancement of ORM in young animals and prevent ORM deficits in rodent models of aging and Alzheimer’s disease.Furthermore,we found that the prevention of memory deficits was mediated through the upregulation of neuronal arbo rization and spine density,as well as an increase in brain-derived neurotrophic factor(BDnF).A knockdown of BDnF gene in RGS14414-treated aging rats and Alzheimer s disease model mice caused complete loss in the upregulation of neuronal structural plasticity and in the prevention of ORM deficits.These findings suggest that BDnF-mediated neuronal structural plasticity in area V2 is crucial in the prevention of memory deficits in RGS14414-treated rodent models of aging and Alzheimer’s disease.Therefore,our findings of RGS14414gene-mediated activation of neuronal circuits in visual area V2 have therapeutic relevance in the treatment of memory deficits.

关键词： behavioral performance brain-derived neurotrophic factor cognitive dysfunction episodic memory memory circuit activation memory deficits memory enhancement object recognition memory prevention of memory loss regulator of G protein signaling

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小胶质细胞在卒中中的作用

神经损伤与功能重建 2024年第2期19卷 F0003-F0003页

作者： Anna M Planas 唐颖馨(编译) Cerebrovascular Research laboratory Department of Neuroscience and Experimental TherapeuticsInstituto de Investigaciones Biomédicas de Barcelona(IIBB)Consejo Superior de Investigaciones Científicas(CSIC)BarcelonaSpain Cerebrovascular Diseases Area of Clinical and Experimental NeuroscienceInstitut d'Investigacions Biomèdiques August Pi i Sunyer(IDIBAPS)-Hospital ClínicBarcelonaSpain 不详

小胶质细胞在缺血后的炎症反应和受损组织的清除中扮演关键角色,它们对缺血引起的干扰反应迅速,致力于恢复失去的稳态。然而,被修改的环境,包括离子失衡、关键的神经元-小胶质细胞相互作用的中断、去极化传播以及来自坏死神经元的危险... 详细信息

小胶质细胞在缺血后的炎症反应和受损组织的清除中扮演关键角色,它们对缺血引起的干扰反应迅速,致力于恢复失去的稳态。然而,被修改的环境,包括离子失衡、关键的神经元-小胶质细胞相互作用的中断、去极化传播以及来自坏死神经元的危险信号的产生,诱导了小胶质细胞的形态和表型转变。这导致它们表现为促炎表型并增加吞噬活动。从缺血后的第3天开始,巨噬细胞渗透到坏死组织核心,而小胶质细胞则在病灶周边聚集。此外,炎症促使代谢转向有利于糖酵解、戊糖磷酸途径和脂质合成。这些转变与吞噬脂质的摄入相结合,促进了脂滴生成、合成代谢,并使小胶质细胞增殖。增殖的小胶质细胞释放营养因子,有助于神经保护和修复。然而,一些小胶质细胞持续积累脂质,并转变为功能失调且可能有害的泡沫细胞。研究还表明,有些小胶质细胞要么清除凋亡细胞能力的受损,要么消除突触、活神经元或内皮细胞。然而,阐明被吞噬细胞的生存能力、局部环境特征、组织损伤程度和时间序列将是至关重要的。缺血为小胶质细胞提供了丰富多样的、依赖于区域和损伤的刺激,随着时间演变导致出现不同的小胶质细胞表型,包括表现为促炎性或功能失调特征的细胞,以及显示出促进修复功能的细胞。准确分析小胶质细胞表型,以及更精确地了解相关的缺血后组织条件,是对卒中进行针对性干预的必要步骤。

关键词：脑缺血危险信号异质性炎症脂质吞噬作用修复

How to protect liver graft with nitric oxide

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World Journal of Gastroenterology 2011年第24期17卷 2879-2889页

作者： Hassen Ben Abdennebi Mohamed Amine Zaoualí Izabel Alfany-Fernandez Donia Tabka Joan Roselló-Catafau laboratory of Human Physiology Faculty of PharmacyUniversity of Monastir Unit of Experimental Hepatic IschemiaReperfusion Institut of d'Investigacions Biomèdiques de BarcelonaConsejo Superior de Investigaciones Científicas Unitat de Transplantament de Fetge i Viabilitat de l'Empelt Institut d'Investigacions Biomèdiques August Pi i Sunyer

Organ preservation and ischemia reperfusion injury as- sociated with liver transplantation play an important role in the induction of graft injury. One of the earliest events associated with the reperfusion injury is en- dothelial cell dysfunction. It is generally accepted that endothelial nitric oxide synthase (e-nOS) is cell-pro- tective by mediating vasodilatation, whereas inducible nitric oxide synthase mediates liver graft injury after transplantation. We conducted a critical review of the literature evaluating the potential applications of regu- lating and promoting e-nOS activity in liver preservation and transplantation, showing the most current evidenceto support the concept that enhanced bioavailability of nO derived from e-nOS is detrimental to ameliorate graft liver preservation, as well as preventing subse- quent graft reperfusion injury. This review deals mainly with the beneficial effects of promoting "endogenous" pathways for nO generation, via e-nOS inducer drugs in cold preservation solution, surgical strategies such as ischemic preconditioning, and alternative "exogenous" pathways that focus on the enrichment of cold storage liquid with nO donors. Finally, we also provide a basic bench-to-bed side summary of the liver physiology and cell signalling mechanisms that account for explaining the e-nOS protective effects in liver preservation and transplantation. ? 2011 Baishideng. All rights reserved.

关键词：一氧化氮合成酶保护作用肝移植缺血再灌注损伤 nOS活性内皮细胞一氧化氮合酶生物利用度

Omics-based biomarkers as useful tools in metabolic dysfunctionassociated steatotic liver disease clinical practice:How far are we?

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World Journal of Gastroenterology 2024年第14期30卷 1982-1989页

作者： Julieta Trinks María F Mascardi Adrián Gadano Sebastián Marciano Instituto de Medicina Traslacional e Ingeniería biomédica-Consejo nacional de investigaciones Científicas y Técnicas-Instituto Universitario del Hospital Italiano-Hospital Italiano de Buenos Aires Ciudad Autónoma de Buenos Aires C1199ACLArgentina Consejo nacional de investigaciones Científicas y Técnicas Ciudad Autónoma de Buenos Aires C1425FQBArgentina Liver Unit Hospital Italiano de Buenos AiresCiudad Autónoma de Buenos Aires C1199DFArgentina department of Research Hospital Italiano de Buenos AiresCiudad Autónoma de Buenos Aires C1199DFArgentina

Unmet needs exist in metabolic dysfunction-associated steatotic liver disease(MASLD)risk stratification.Our ability to identify patients with MASLD with advanced fibrosis and at higher risk for adverse outcomes is still limited.Incorporating novel biomarkers could represent a meaningful improvement to current risk predictors.With this aim,omics technologies have revolutionized the process of MASLD biomarker discovery over the past decades.While the research in this field is thriving,much of the publication has been haphazard,often using single-omics data and specimen sets of convenience,with many identified candidate biomarkers but lacking clinical validation and utility.If we incorporate these biomarkers to direct patients’management,it should be considered that the roadmap for translating a newly discovered omics-based signature to an actual,analytically valid test useful in MASLD clinical practice is rigorous and,therefore,not easily accomplished.This article presents an overview of this area’s current state,the conceivable opportunities and challenges of omics-based laboratory diagnostics,and a roadmap for improving MASLD biomarker research.

关键词： Metabolic dysfunction-associated steatotic liver disease non-alcoholic steatohepatitis biomarker Risk stratification Omics

nanoscale interactions between the nicotinic acetylcholine receptor and cholesterol

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BIOCELL 2021年第6期45卷 1479-1484页

作者： FRAnCISCO J.BARRAnTES laboratory of Molecular neurobiology Institute of Biomedical Research(BIOMED)UCA-CONICETFaculty of Medical SciencesBuenos AiresArgentina

Cholesterol is a major lipid in biological membranes.It not only plays a structural role but also modulates a wide range of functional properties of neurotransmitter and hormone receptors and ion channels.The membraneembedded segments of the paradigm neurotransmitter receptor for acetylcholine(nAChR)contain linear sequences of amino acids with the capacity to recognize cholesterol.These cholesterol consensus domains have been designated as“CARC”and its mirror sequence“CRAC”.CARC preferentially occurs in the exoplasmic-facing membrane leaflet,and CRAC,in the cytoplasmic-facing hemilayer.Both motifs are highly conserved among ion-channel and neurotransmitter receptor proteins in vertebrate nervous systems,where they recognize cholesterol,and in prokaryotic homologues in bacteria,where they recognize hopanoids.This phylogenetically conserved trait is an indication that the hopanoids in some bacteria and cholesterol in eukaryotes subserve analogous functions,probably contributing to the stability of membrane-embedded protein domains.Structural studies from our laboratory using superresolution optical microscopy(“nanoscopy”)have disclosed other interrelated functional and structural properties exerted by cholesterol on the nAChR.The neutral lipid content at the cell surface influences both the macromolecular organization of the receptor and its translational mobility(diffusion)in the plane of the membrane.

关键词： Cholesterol Pentameric ligand-gated ion channel nicotinic acetylcholine receptor Membrane proteins Evolution nanoscopy Cholesterol-recognition domains

Glutathione metabolism is essential for self-renewal and chemoresistance of pancreatic cancer stem cells

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World Journal of Stem Cells 2020年第11期12卷 1410-1428页

作者： Petra Jagust Sonia Alcala Bruno Sainz Jr Christopher Heeschen Patricia Sancho Molecular Pathology Programme Spanish National Cancer Research Centre(CNIO)Madrid 28029Spain department of Biochemistry Autónoma University of MadridInstituto de Investigaciones Biomédicas"Alberto Sols"CSIC-UAMMadrid 28029Spain Center for Single-Cell Omics&Key laboratory of Oncogenes and Related Genes Shanghai Cancer InstituteShanghai Jiao Tong University School of MedicineShanghai 200025China Hospital Universitario Miguel Servet IIS AragonZaragoza 50009Spain

BACKGROUnD Cellular metabolism regulates stemness in health and disease.A reduced redox state is essential for self-renewal of normal and cancer stem cells(CSCs).However,while stem cells rely on glycolysis,different CSCs,including pancreatic CSCs,favor mitochondrial metabolism as their dominant energy-producing pathway.This suggests that powerful antioxidant networks must be in place to detoxify mitochondrial reactive oxygen species(ROS)and maintain stemness in oxidative CSCs.Since glutathione metabolism is critical for normal stem cell function and CSCs from breast,liver and gastric cancer show increased glutathione content,we hypothesized that pancreatic CSCs also rely on this pathway for ROS detoxification.AIM To investigate the role of glutathione metabolism in pancreatic CSCs.METHODS Primary pancreatic cancer cells of patient-derived xenografts(PDXs)were cultured in adherent or CSC-enriching sphere conditions to determine the role of glutathione metabolism in stemness.Real-time polymerase chain reaction(PCR)was used to validate RnAseq results involving glutathione metabolism genes in adherent vs spheres,as well as the expression of pluripotency-related genes following treatment.Public TCGA and GTEx RnAseq data from pancreatic cancer vs normal tissue samples were analyzed using the webserver GEPIA2.The glutathione-sensitive fluorescent probe monochlorobimane was used to determine glutathione content by fluorimetry or flow cytometry.Pharmacological inhibitors of glutathione synthesis and recycling[buthionine-sulfoximine(BSO)and 6-Aminonicotinamide(6-An),respectively]were used to investigate the impact of glutathione depletion on CSC-enriched cultures.Staining with propidium iodide(cell cycle),Annexin-V(apoptosis)and CD133(CSC content)were determined by flow cytometry.Self-renewal was assessed by sphere formation assay and response to gemcitabine treatment was used as a readout for chemoresistance.RESULTS Analysis of our previously published RnAseq dataset E-MTAB-3808 revealed upregulation of genes involved in

关键词： Pancreatic cancer Cancer stem cells Glutathione Self-renewal Chemoresistance Redox