0000000001310636

AUTHOR

Fei Cheng

showing 16 related works from this author

Synthesis and structural characterisation of germanium(II) halide complexes with neutral N-donor ligands.

2010

The Ge(II) complexes [GeX(2)(L-L)] (L-L = 1,10-phen (X = Cl, Br); L-L = Me(2)N(CH(2))(2)NMe(2), 2,2'-bipy (X = Cl)), [GeX(L-L)][GeX(3)] (L-L = 2,2'-bipy (X = Br); L-L = pmdta (MeN(CH(2)CH(2)NMe(2))(2)) (X = Cl, Br)) have been prepared and their crystal structures determined. The crystal structure of [GeCl(2){Me(2)N(CH(2))(2)NMe(2)}] shows a weakly associated centrosymmetric dimer based upon distorted square-pyramidal coordination at Ge(II) and containing asymmetrically chelating diamine ligands. The structure of [GeCl(2)(2,2'-bipy)] contains a chelating 2,2'-bipy ligand and forms a zig-zag chain polymer via long-range intermolecular Ge...Cl bridging interactions, leading to a very distorted…

PMDTAStereochemistryLigandgermanium(II) complexes structure identificationDimerCrystal structureInorganic Chemistrychemistry.chemical_compoundCrystallographychemistryTetramerCovalent bondDiamineMoleculeDalton transactions (Cambridge, England : 2003)
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No effect of C-reactive protein on early atherosclerosis in LDLR-/- / human C-reactive protein transgenic mice

2008

summaryThe association between increased concentrations of C-reactive protein (CRP) and future cardiovascular events is well established. However, it is currently unclear whether this clinical observation represents an epiphenomenon or whether the pentraxin may actively promote the development of atherosclerosis. Experimental studies with knockout mice with a defect in apolipoprotein E (ApoE-/-) have been used to investigate the role of CRP in atherogenesis, but the results obtained have been contradictory so far. Since knockout mice with a defect in low density lipoprotein receptor (LDLR-/-) may represent a better model of atherogenesis compared to ApoE-/- animals, we undertook experiments…

Genetically modified mouseApolipoprotein ETime FactorsGenotypeLipoproteinsTransgeneMice TransgenicBiologyLesionMicemedicineAnimalsHumansComplement ActivationAortaCrosses GeneticMice KnockoutC-reactive proteinAcute-phase proteinHematologyAtherosclerosisDietary FatsLipidsDisease Models AnimalC-Reactive ProteinPhenotypeReceptors LDLImmunologyLDL receptorKnockout mousebiology.proteinlipids (amino acids peptides and proteins)medicine.symptomThrombosis and Haemostasis
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Overexpression of TGF-ß1 in macrophages reduces and stabilizes atherosclerotic plaques in ApoE-deficient mice.

2011

Although macrophages represent the hallmark of both human and murine atherosclerotic lesions and have been shown to express TGF-ß1 (transforming growth factor β1) and its receptors, it has so far not been experimentally addressed whether the pleiotropic cytokine TGF-ß1 may influence atherogenesis by a macrophage specific mechanism. We developed transgenic mice with macrophage specific TGF-ß1 overexpression, crossed the transgenics to the atherosclerotic ApoE (apolipoprotein E) knock-out strain and quantitatively analyzed both atherosclerotic lesion development and composition of the resulting double mutants. Compared with control ApoE(-/-) mice, animals with macrophage specific TGF-ß1 overe…

Genetically modified mouseApolipoprotein Emedicine.medical_specialtyPathologyHistologyMouseSciencemedicine.medical_treatmentImmune CellsImmunologyAntigen-Presenting CellsMice TransgenicBiologyCardiovascularLesionTransforming Growth Factor beta1MiceApolipoproteins EModel OrganismsVascular BiologyInternal medicinemedicineGeneticsMacrophageAnimalsReceptorBiologyMice KnockoutMultidisciplinaryMacrophagesQRAnimal ModelsAtherosclerosisImmunohistochemistryPlaque AtheroscleroticCytokineEndocrinologyImmunohistochemistryMedicineFemalemedicine.symptomGene FunctionTransforming growth factorResearch ArticlePloS one
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Investigation of Sudan IV staining areas in aortas of infants and children: Possible prelesional stages of atherogenesis

2009

Although atherosclerosis in infants and children is generally acknowledged, the temporal and spatial sequence of LDL insudation, modification and intimal monocyte accumulation has not been systematically studied. We have investigated herein very early stages of lesion formation in human aortas of individuals up to the age of 15 years. Aortic specimens from 61 cases (37 male, 24 female) were examined. 34 cases were1 year old, 16 cases were between 1 and 5 years old, and 11 cases were between 6 and 15 years old. Areas preselected under a dissection microscope after Sudan IV staining were investigated in depth by immunohistochemical staining for apolipoprotein B, monocytes/macrophages, smooth …

MalePathologymedicine.medical_specialtyLipoprotein modificationAdolescentAorta ThoracicMonocytesmedicine.arterymedicineHumansMacrophageChildAortaApolipoproteins BAortabiologyVascular diseaseMacrophagesC-reactive proteinInfant NewbornInfantAtherosclerosismedicine.diseaseC-Reactive Proteinmedicine.anatomical_structureChild PreschoolImmunologybiology.proteinFemaleTunica IntimaCardiology and Cardiovascular MedicineAzo CompoundsBlood vesselArteryLipoproteinAtherosclerosis
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Combined B, T and NK Cell Deficiency Accelerates Atherosclerosis in BALB/c Mice.

2016

This study focused on the unique properties of both the Ldlr knockout defect (closely mimicking the human situation) and the BALB/c (C) inbred mouse strain (Th-2 slanted immune response). We generated two immunodeficient strains with severe combined B- and T-cell immunodeficiency with or without a complete lack of natural killer cells to revisit the role of adaptive immune responses on atherogenesis. C-Ldlr-/- Rag1-/- mice, which show severe combined B- and T-cell immunodeficiency and C-Ldlr-/- Rag1-/- Il2rg-/- mice, which combine the T- and B-cell defect with a complete lack of natural killer cells and inactivation of multiple cytokine signalling pathways were fed an atherogenic Western ty…

0301 basic medicineT-Lymphocyteslcsh:MedicineNK cellsAdaptive ImmunityBiochemistryVascular MedicineMicechemistry.chemical_compoundCellular typesReceptorlcsh:ScienceImmunodeficiencyMice KnockoutB-LymphocytesMice Inbred BALB CMultidisciplinarybiologyT CellsImmune cellsAcquired immune systemLipidsPlaque AtheroscleroticKiller Cells NaturalCholesterolPhenotypeWhite blood cellsFemalelipids (amino acids peptides and proteins)Research ArticleCell biologyBlood cellsLipoproteinsImmunologyResearch and Analysis MethodsBALB/cImmune Deficiency03 medical and health sciencesImmune systemmedicineAnimalsImmunohistochemistry TechniquesTriglyceridesMedicine and health sciencesBiology and life sciencesCholesterolMacrophageslcsh:RImmunologic Deficiency SyndromesWild typeProteinsAtherosclerosisbiology.organism_classificationmedicine.diseaseMolecular biologyHistochemistry and Cytochemistry Techniques030104 developmental biologyAnimal cellsReceptors LDLchemistryImmune SystemMutationImmunologyLDL receptorImmunologic TechniquesClinical Immunologylcsh:QClinical MedicinePLoS ONE
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Selective p38α MAP kinase/MAPK14 inhibition in enzymatically modified LDL-stimulated human monocytes: implications for atherosclerosis.

2016

The first ATP-competitive p38α MAPK/MAPK14 inhibitor with excellent in vivo efficacy and selectivity, skepinone-L, is now available. We investigated the impact of selective p38α MAPK/MAPK14 inhibition on enzymatically modified LDL (eLDL) stimulated human monocytes with its implications for atherosclerosis. Among the different p38 MAPK isoforms, p38α/MAPK14 was the predominantly expressed and activated isoform in isolated human peripheral blood monocytes. Moreover, eLDL colocalized with macrophages positive for p38α MAPK/MAPK14 in human carotid endarterectomy specimens. Using the human leukemia cell line THP-1 and/or primary monocyte-derived macrophages, skepinone-L inhibited eLDL-induced ac…

0301 basic medicineAdultMaleChemokineMAP Kinase Signaling Systemp38 mitogen-activated protein kinasesCD36CCL4Dibenzocycloheptenes030204 cardiovascular system & hematologyBiochemistryGene Expression Regulation EnzymologicMonocytesMitogen-Activated Protein Kinase 1403 medical and health sciences0302 clinical medicineCell Line TumorGeneticsHumansInterleukin 8Molecular BiologyFoam cellMAPK14AgedAged 80 and overCaspase 7biologyChemistryCaspase 3Cholesterol LDLAtherosclerosisMolecular biology030104 developmental biologyBiochemistryMitogen-activated protein kinasebiology.proteinFemaleBiotechnologyFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Impact of Glutathione Peroxidase-1 Deficiency on Macrophage Foam Cell Formation and Proliferation: Implications for Atherogenesis

2013

Clinical and experimental evidence suggests a protective role for the antioxidant enzyme glutathione peroxidase-1 (GPx-1) in the atherogenic process. GPx-1 deficiency accelerates atherosclerosis and increases lesion cellularity in ApoE(-/-) mice. However, the distribution of GPx-1 within the atherosclerotic lesion as well as the mechanisms leading to increased macrophage numbers in lesions is still unknown. Accordingly, the aims of the present study were (1) to analyze which cells express GPx-1 within atherosclerotic lesions and (2) to determine whether a lack of GPx-1 affects macrophage foam cell formation and cellular proliferation. Both in situ-hybridization and immunohistochemistry of l…

CD36 AntigensMAPK/ERK pathwayMouseMitogen-Activated Protein Kinase 3lcsh:MedicineGene ExpressionSignal transductionCardiovascularMiceMolecular cell biologyGlutathione Peroxidase GPX1lcsh:ScienceIn Situ HybridizationFoam cellMice KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MultidisciplinaryReverse Transcriptase Polymerase Chain ReactionKinaseSignaling cascadesScavenger Receptors Class AAnimal ModelsImmunohistochemistryLipoproteins LDLMedicineFemaleSignal transductionResearch ArticleMacrophage colony-stimulating factorMAPK signaling cascadesBlotting WesternBiologyCell GrowthModel OrganismsApolipoproteins EVascular BiologyAnimalsHumansProtein kinase ABiologyCell ProliferationGlutathione PeroxidaseMacrophage Colony-Stimulating Factorlcsh:RAtherosclerosisMolecular biologyMacrophages Peritoneallcsh:QMacrophage proliferationFoam CellsPLoS ONE
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Deficiency of glutathione peroxidase-1 accelerates the progression of atherosclerosis in apolipoprotein E-deficient mice.

2007

Background— We have recently demonstrated that activity of red blood cell glutathione peroxidase-1 is inversely associated with the risk of cardiovascular events in patients with coronary artery disease. The present study analyzed the effect of glutathione peroxidase-1 deficiency on atherogenesis in the apolipoprotein E-deficient mouse. Methods and Results— Female apolipoprotein E-deficient mice with and without glutathione peroxidase-1 deficiency were placed on a Western-type diet for another 6, 12, or 24 weeks. After 24 weeks on Western-type diet, double-knockout mice (GPx-1 −/− ApoE −/− ) developed significantly more atherosclerosis than control apolipoprotein E-deficient mice. Moreover…

Apolipoprotein Emedicine.medical_specialtyGPX1AntioxidantApolipoprotein Bmedicine.medical_treatmentLipoproteinsApoptosisBlood Pressuremedicine.disease_causeNitric OxideMitochondria HeartMonocyteschemistry.chemical_compoundMiceApolipoproteins EGlutathione Peroxidase GPX1SuperoxidesInternal medicinePeroxynitrous AcidmedicineAnimalsAortaCell Proliferationchemistry.chemical_classificationMice KnockoutReactive oxygen speciesGlutathione PeroxidaseMembranesbiologyGlutathione peroxidaseGlutathioneAtherosclerosisEndocrinologyPhenotypechemistryImmunologybiology.proteinDisease ProgressionFemaleCardiology and Cardiovascular MedicineReactive Oxygen SpeciesOxidation-ReductionOxidative stressArteriosclerosis, thrombosis, and vascular biology
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T Cell-Specific Overexpression of TGFß1 Fails to Influence Atherosclerosis in ApoE-Deficient Mice

2013

Clinical data have indicated a negative correlation between plasma TGFß1 concentrations and the extent of atherosclerosis and have thus led to the hypothesis that the pleiotropic cytokine may have anti-atherogenic properties. T-cells are currently discussed to significantly participate in atherogenesis, but the precise role of adaptive immunity in atherogenesis remains to be elucidated. TGFß1 is known to strongly modulate the function of T-cells, however, inhibition of TGFß1 signalling in T-cells of atherosclerosis-prone knock-out mice failed to unequivocally clarify the role of the cytokine for the development of atherosclerosis. In the present study, we thus tried to specify the role of T…

Genetically modified mouseApolipoprotein ELipoproteinsT-LymphocytesScienceCD3medicine.medical_treatmentT cellTransgeneMutantGene ExpressionMice TransgenicBiologyTransforming Growth Factor beta1MiceApolipoproteins EmedicineAnimalsHumansMultidisciplinaryQRAtherosclerosisAcquired immune systemCytokinemedicine.anatomical_structureImmunologyDisease Progressionbiology.proteinMedicineFemaleResearch ArticlePLoS ONE
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CCDC 724642: Experimental Crystal Structure Determination

2010

Related Article: Fei Cheng, J.M.Dyke, F.Ferrante, A.L.Hector, W.Levason, G.Reid, M.Webster, Wenjian Zhang|2010|Dalton Trans.|39|847|doi:10.1039/b911016j

Space GroupCrystallographyCrystal SystemBromo-(NNN'N''N''-pentamethyldiethylenetriamine-NN'N'')-germanium(ii) tribromogermanate(ii)Crystal StructureCell ParametersExperimental 3D Coordinates
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CCDC 724632: Experimental Crystal Structure Determination

2010

Related Article: Fei Cheng, J.M.Dyke, F.Ferrante, A.L.Hector, W.Levason, G.Reid, M.Webster, Wenjian Zhang|2010|Dalton Trans.|39|847|doi:10.1039/b911016j

Space GroupCrystallographyCrystal SystemCrystal StructureCell Parameters(22'-Bipyridine-NN')-dichloro-germanium(ii)Experimental 3D Coordinates
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CCDC 724631: Experimental Crystal Structure Determination

2010

Related Article: Fei Cheng, J.M.Dyke, F.Ferrante, A.L.Hector, W.Levason, G.Reid, M.Webster, Wenjian Zhang|2010|Dalton Trans.|39|847|doi:10.1039/b911016j

Space GroupCrystallographyCrystal SystemCrystal StructureDichloro-(12-bis(dimethylamino)ethane-NN')-germanium(ii)Cell ParametersExperimental 3D Coordinates
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CCDC 724634: Experimental Crystal Structure Determination

2010

Related Article: Fei Cheng, J.M.Dyke, F.Ferrante, A.L.Hector, W.Levason, G.Reid, M.Webster, Wenjian Zhang|2010|Dalton Trans.|39|847|doi:10.1039/b911016j

Space GroupCrystallographyCrystal SystemCrystal StructureCell ParametersDichloro-(110-phenanthroline-NN')-germanium(ii) chlorideExperimental 3D Coordinates
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CCDC 724636: Experimental Crystal Structure Determination

2010

Related Article: Fei Cheng, J.M.Dyke, F.Ferrante, A.L.Hector, W.Levason, G.Reid, M.Webster, Wenjian Zhang|2010|Dalton Trans.|39|847|doi:10.1039/b911016j

Chloro-(NNN'N''N''-pentamethyldiethylenetriamine-NN'N'')-germanium(ii) trichlorogermanate(ii)Space GroupCrystallographyCrystal SystemCrystal StructureCell ParametersExperimental 3D Coordinates
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CCDC 724633: Experimental Crystal Structure Determination

2010

Related Article: Fei Cheng, J.M.Dyke, F.Ferrante, A.L.Hector, W.Levason, G.Reid, M.Webster, Wenjian Zhang|2010|Dalton Trans.|39|847|doi:10.1039/b911016j

Space GroupCrystallography(22'-Bipyridine)-bromo-germanium(ii) tribromogermanate(ii)Crystal SystemCrystal StructureCell ParametersExperimental 3D Coordinates
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CCDC 724635: Experimental Crystal Structure Determination

2010

Related Article: Fei Cheng, J.M.Dyke, F.Ferrante, A.L.Hector, W.Levason, G.Reid, M.Webster, Wenjian Zhang|2010|Dalton Trans.|39|847|doi:10.1039/b911016j

Dibromo-(110-phenanthroline-NN')-germanium(ii)Space GroupCrystallographyCrystal SystemCrystal StructureCell ParametersExperimental 3D Coordinates
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