Search results for "pathology [Aging]"

showing 10 items of 1700 documents

Mothers who killed or attempted to kill their child: life circumstances, childhood abuse, and types of killing.

1999

The objectives of the present study were to examine the life circumstances, childhood abuse, and types of homicidal acts of 48 mothers who killed/attempted to kill their children) under age 12 between 1970-96 in Finland. Data on the mothers’ life stresses, psychological problems, and childhood abuse were collected from mental state examination (MSE) reports. The cases were divided into 15 neonaticides and 33 mothers who killed an older child. Childhood abuse was documented in 63% of the mothers’ MSE reports. Qualitative analysis identified neonaticides, joint homicide-suicide attempts, impulsive aggression, psychotic acts, postpartum depression, and abusive acts. Nonlinear principal compone…

Postpartum depressionMalePediatricsmedicine.medical_specialtyHealth (social science)Poison controlMothersCycle of violenceNeonaticideSuicide preventionOccupational safety and healthPathology and Forensic MedicineDepression PostpartumLife Change EventsAge DistributionRisk FactorsInjury preventionmedicineHumansChild AbuseSex DistributionPsychiatryChildFinlandInfant NewbornInfantGeneral Medicinemedicine.diseaseMother-Child RelationsAggressionNonlinear DynamicsChild PreschoolFemalePsychologyFactor Analysis StatisticalHomicideMental Status ScheduleLawPsychosocialViolence and victims
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The predictive and incremental validity of the German adaptation of the Static-2002 in a sexual offender sample released from the prison system

2015

Purpose The aim of this study was to examine the predictive validity of the German adaptation of the Static-2002 and to compare it with the results of the Static-99. Method The predictive validity of Static-2002 was investigated in a sample of n = 452 sexual offenders released from the Austrian Prison System. The instrument was coded retrospectively using file information. Afterwards, the predictive estimates of the Static-2002 were related to officially documented reconviction data. Results The Static-2002 was found to have large effect sizes for predicting sexual, violent, and general recidivism (area under the receiver operating characteristic curve [AUC] = .78, .75, .75, respectively) f…

Predictive validityReceiver operating characteristicRecidivismmedia_common.quotation_subject05 social sciencesSample (statistics)Prisonlanguage.human_languagePathology and Forensic MedicineGermanStatistical significance050501 criminologylanguagePsychologySocial psychologyIncremental validityApplied Psychology0505 lawClinical psychologymedia_commonLegal and Criminological Psychology
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Molecular Alterations of the RBI, TP53, and MDM2 Genes in Primary and Xenografted Human Osteosarcomas

1997

We report the status of the RBI, TP53, and MDM2 genes in human osteosarcomas and cell lines established from surgical specimens and transplanted into athymic naked mice. By using reverse transcriptase-polymerase chain reaction (RT-PCR) as a prescreening technique and posterior sequencing, we observe

Primary (chemistry)Cell cultureCancer researchbiology.proteinMdm2Cell BiologyBiologyneoplasmsMolecular BiologyGenePathology and Forensic MedicineDiagnostic Molecular Pathology
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Ischemic Preconditioning: Postischemic Structural Changes in the Brain

2008

Ischemic brain damage can be prevented or at least significantly reduced when there is a preceding brief ischemic period that does not exceed the threshold for tissue damage--a phenomenon termed "ischemic preconditioning" (ischemic PC). Experimental PC in rodents is now considered to be a model for transient ischemic attacks in humans, and there is increasing hope for translating the knowledge of underlying mechanisms in the animal models into the clinic to enhance endogenous neuroprotective mechanisms in patients with stroke. However, although PC was originally defined as a subtoxic stimulus without any morphologic damage, there is a growing body of evidence from studies using sensitive te…

Programmed cell deathCentral nervous systemIschemiaStimulus (physiology)NeuroprotectionPathology and Forensic MedicineBrain ischemiaCellular and Molecular NeuroscienceIschemiamedicineAnimalsHumansIschemic PreconditioningStrokebusiness.industryBrainGeneral Medicinemedicine.diseaseReceptors NeurotransmitterDisease Models Animalmedicine.anatomical_structureGene Expression RegulationNeurologyIschemic preconditioningNeurology (clinical)businessNeuroscienceJournal of Neuropathology & Experimental Neurology
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Differentiation-associated apoptosis of neural stem cells is effected by Bcl-2 overexpression: impact on cell lineage determination

2001

Apoptosis is an integral part of neural development. To elucidate the importance of programmed cell death on cell lineage determination we utilized murine PCC7-Mzl cells, a model system for neural differentiation. Treatment of pluripotent PCC7-Mzl stem cells with 0.1 microM all-trans retinoic acid (RA) causes a cease of proliferation and an initiation of differentiation into neurons, glial cells and fibroblasts. Simultaneously, a fraction of the cell culture (ca. 25%) dies within 24 h by apoptosis. We transfected PCC7-Mzl cells with the human bcl-2 cDNA and generated PCC7-Mz-Bcl-2 cell lines expressing two- to tenfold higher levels of Bcl-2 than parental cells. Overexpression of Bcl-2 resul…

Programmed cell deathDNA ComplementaryHistologyCellular differentiationApoptosisTretinoinBiologyCeramidesTransfectionPathology and Forensic MedicineMiceNeurosphereTumor Cells CulturedAnimalsCell LineageElectrophoresis Agar GelNeuronsCaspase 8Stem CellsCell DifferentiationCell BiologyGeneral MedicineFibroblastsMolecular biologyCaspase 9Neural stem cellCell biologyP19 cellProto-Oncogene Proteins c-bcl-2Cell cultureCaspasesStem cellNeurogliaBiomarkersCell DivisionAdult stem cellEuropean Journal of Cell Biology
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Knockout of myeloid cell leukemia-1 induces liver damage and increases apoptosis susceptibility of murine hepatocytes

2008

Apoptosis, or programmed cell death, regulates tissue development and homeostasis in multi-cellular organisms. Extrinsic or intrinsic death signals activate pro-apoptotic pathways, resulting in the activation of caspases and finally in cell death. An important event during apoptosis process is the permeabilization of the outer mitochondrial membrane (OMM). Integrity of the OMM is regulated by the Bcl-2 protein family, which is divided into three groups: anti-apoptotic members Bcl-2, Bcl-xL and myeloid cell leukemia-1 (Mcl-1), pro-apoptotic multidomain members Bax and Bak, and pro-apoptotic BH3-only proteins. Mitochondrial activation is regulated by selective interactions of Bcl-2 proteins v…

Programmed cell deathGenotypeCellular differentiation610 Medicine & healthApoptosisBiologyPolymerase Chain ReactionArticleMiceimmune system diseases10049 Institute of Pathology and Molecular Pathologyhemic and lymphatic diseasesmedicineAnimalsAspartate AminotransferasesneoplasmsDNA PrimersHepatologyCaspase 3Alanine TransaminaseCell DifferentiationDNAFas receptorCell biologyMyeloid Cell Leukemia Sequence 1 ProteinHaematopoiesisGene Expression RegulationLiverProto-Oncogene Proteins c-bcl-2ApoptosisHepatocytesMyeloid Cell Leukemia Sequence 1 ProteinRNA2721 HepatologyHepatocyte growth factorStem cellmedicine.drugHepatology
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Characterization of cells with different mitochondrial membrane potential during apoptosis.

2005

Background Until now, the simultaneous analysis of several parameters during apoptosis, including DNA content and mitochondrial membrane potential (ΔΨ), has not been possible because of the spectral characteristics of the commonly used dyes. Using polychromatic flow cytometry based upon multiple laser and UV lamp excitation, we have characterized cells with different ΔΨ during apoptosis. Methods U937 cells were treated with the flavonoid quercetin (Qu) and stained with JC-1 to detect ΔΨ, propidium iodide (PI) for cell viability, Hoechst 33342 for DNA content, Annexin V conjugated with Alexa Fluor-647 for detection of phosphatidilserine (PS) exposure, marker of early apoptosis, or Mitotracke…

Programmed cell deathHistologyCell Membrane PermeabilityCell Survivalpolychromatic flow cytometry • mitochondrial membrane potential • apoptosis • JC-1 • propidium iodide • Hoechst • Annexin-VPopulationApoptosisHL-60 CellsDNA FragmentationPhosphatidylserinesBiologyPathology and Forensic MedicineFlow cytometryMembrane Potentialschemistry.chemical_compoundAnnexinCell Line TumormedicineHumansViability assayPropidium iodideeducationFluorescent Dyeseducation.field_of_studymedicine.diagnostic_testDaunorubicinCell BiologyDNAIntracellular MembranesU937 CellsCarbocyaninesFlow CytometryMolecular biologyMitochondriachemistryApoptosisCell cultureDoxorubicinLeukocytes MononuclearBenzimidazolesQuercetinCytometry. Part A : the journal of the International Society for Analytical Cytology
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Hypoxia inducible factor-1alpha inactivation unveils a link between tumor cell metabolism and hypoxia-induced cell death.

2008

Hypoxia and the acquisition of a glycolytic phenotype are intrinsic features of the tumor microenvironment. The hypoxia inducible factor-1alpha (HIF-1alpha) pathway is activated under hypoxic conditions and orchestrates a complex transcriptional program that enhances cell survival. Although the consequences of HIF-1alpha inactivation in cancer cells have been widely investigated, only a few studies have addressed the role of HIF-1alpha in the survival of cancer cells endowed with different glycolytic capacities. In this study, we investigated this aspect in ovarian cancer cells. Hypoxia-induced toxicity was increased in highly glycolytic cells compared with poorly glycolytic cells; it was a…

Programmed cell deathMice SCIDBiologyPathology and Forensic MedicineMiceCell Line TumormedicineAnimalsHumansGene SilencingRNA Small InterferingCell ProliferationOvarian NeoplasmsTumor microenvironmentCell DeathCell growthLentivirusHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaCell biologyPhenotypeHypoxia-inducible factorsApoptosisCell cultureCancer cellFemalemedicine.symptomRegular ArticlesThe American journal of pathology
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Differential Roles of JNK in ConA/GalN and ConA-Induced Liver Injury in Mice

2008

Tumor necrosis factor-alpha-mediated liver injury can be induced by several different means; however, the signaling events and mechanisms of cell death are likely different. We investigated the mechanism of both apoptotic and necrotic hepatocyte cell death as well as the role of c-Jun NH2-terminal kinase (JNK) in the ConA and ConA/D-galactosamine (GalN) models of murine liver injury. ConA alone induced primarily necrotic cell death with no caspase activation, whereas ConA/GalN induced apoptosis in addition to necrotic cell death. The bi-modal death pattern in the ConA/GalN model was confirmed by the use of transgenic mice expressing a dominant-negative form of Fas-associated death domain in…

Programmed cell deathNecrosisFas-Associated Death Domain ProteinApoptosisGalactosamineMitochondria Liverchemical and pharmacologic phenomenaCaspase 8Pathology and Forensic MedicineMiceNecrosisConcanavalin AmedicineAnimalsPhosphorylationDeath domainLiver injuryCaspase 8biologyLiver DiseasesJNK Mitogen-Activated Protein Kinasesmedicine.diseaseMolecular biologyEnzyme ActivationMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureConcanavalin AApoptosisHepatocytebiology.proteinMutant ProteinsChemical and Drug Induced Liver Injurymedicine.symptomGene DeletionRegular ArticlesBH3 Interacting Domain Death Agonist ProteinThe American Journal of Pathology
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Hepatocyte-specific deletion of the antiapoptotic protein myeloid cell leukemia-1 triggers proliferation and hepatocarcinogenesis in mice

2010

Regulation of hepatocellular apoptosis is crucial for liver homeostasis. Increased sensitivity of hepatocytes toward apoptosis results in chronic liver injury, whereas apoptosis resistance is linked to hepatocarcinogenesis and nonresponsiveness to therapy-induced cell death. Recently, we have demonstrated an essential role of the antiapoptotic Bcl-2 family member Myeloid cell leukemia-1 (Mcl-1) in hepatocyte survival. In mice lacking Mcl-1 specifically in hepatocytes (Mcl-1Δhep), spontaneous apoptosis caused severe liver damage. Here, we demonstrate that chronically increased apoptosis of hepatocytes coincides with strong hepatocyte proliferation resulting in hepatocellular carcinoma (HCC).…

Programmed cell deathPathologymedicine.medical_specialty10208 Institute of NeuropathologyApoptosis610 Medicine & health10071 Functional Genomics Center ZurichBiologyArticleMiceLiver Neoplasms Experimental10049 Institute of Pathology and Molecular PathologySurvivinmedicineAnimalsneoplasmsCell ProliferationChromosome AberrationsMice KnockoutHepatologyCell growthLiver cellmedicine.diseaseMyeloid Cell Leukemia Sequence 1 ProteinLeukemiamedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2ApoptosisHepatocyteHepatocytesCancer researchMyeloid Cell Leukemia Sequence 1 Protein570 Life sciences; biology2721 HepatologyU7 Systems Biology / Functional GenomicsHepatology
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