Search results for "harm"

showing 10 items of 13866 documents

Posttraumatic Propofol Neurotoxicity Is Mediated via the Pro–Brain-Derived Neurotrophic Factor-p75 Neurotrophin Receptor Pathway in Adult Mice*

2016

Objectives:The gamma-aminobutyric acid modulator propofol induces neuronal cell death in healthy immature brains by unbalancing neurotrophin homeostasis via p75 neurotrophin receptor signaling. In adulthood, p75 neurotrophin receptor becomes down-regulated and propofol loses its neurotoxic effect. H

musculoskeletal diseases0301 basic medicineBrain-derived neurotrophic factorProgrammed cell deathbiologybusiness.industryNeurotoxicityCaspase 3PharmacologyCritical Care and Intensive Care Medicinemedicine.disease03 medical and health sciences030104 developmental biology0302 clinical medicinenervous systemAnesthesiamedicinebiology.proteinLow-affinity nerve growth factor receptorReceptorbusiness030217 neurology & neurosurgeryHomeostasisNeurotrophinCritical Care Medicine
researchProduct

RNA-mediated therapies in myotonic dystrophy

2018

Myotonic dystrophy 1 (DM1) is a multisystemic neuromuscular disease caused by a dominantly inherited 'CTG' repeat expansion in the gene encoding DM Protein Kinase (DMPK). The repeats are transcribed into mRNA, which forms hairpins and binds with high affinity to the Muscleblind-like (MBNL) family of proteins, sequestering them from their normal function. The loss of function of MBNL proteins causes numerous downstream effects, primarily the appearance of nuclear foci, mis-splicing, and ultimately myotonia and other clinical symptoms. Antisense and other RNA-mediated technologies have been applied to target toxic-repeat mRNA transcripts to restore MBNL protein function in DM1 models, such as…

musculoskeletal diseases0301 basic medicinePharmacologycongenital hereditary and neonatal diseases and abnormalitiesMessenger RNAMyotonin-protein kinaseRNABiologymedicine.diseaseMyotoniaMyotonic dystrophyMyotonin-Protein KinaseCell biology03 medical and health sciences030104 developmental biologyDrug DiscoverymedicineAnimalsHumansMyotonic DystrophyRNARNA MessengerTrinucleotide repeat expansionGeneLoss functionDrug Discovery Today
researchProduct

<p>Effects of losartan and atorvastatin on the development of early posttraumatic joint stiffness in a rat model</p>

2019

Background After a trauma, exuberant tissue healing with fibrosis of the joint capsule can lead to posttraumatic joint stiffness (PTJS). Losartan and atorvastatin have both shown their antifibrotic effects in different organ systems. Objective The purpose of this study was the evaluation of the influence of losartan and atorvastatin on the early development of joint contracture. In addition to joint angles, the change in myofibroblast numbers and the distribution of bone sialoprotein (BSP) were assessed. Study design and methods In this randomized and blinded experimental study with 24 rats, losartan and atorvastatin were compared to a placebo. After an initial joint injury, rat knees were …

musculoskeletal diseases0301 basic medicinePharmacologymedicine.medical_specialtyArticular capsule of the knee jointbusiness.industryAtorvastatinUrologyPharmaceutical SciencePlacebo03 medical and health sciences030104 developmental biology0302 clinical medicinemedicine.anatomical_structureLosartan030220 oncology & carcinogenesisJoint stiffnessDrug DiscoveryJoint capsulemedicineJoint Contracturemedicine.symptomContracturebusinessmedicine.drugDrug Design, Development and Therapy
researchProduct

Myotonic dystrophy: candidate small molecule therapeutics

2017

Myotonic dystrophy type 1 (DM1) is a rare multisystemic neuromuscular disorder caused by expansion of CTG trinucleotide repeats in the noncoding region of the DMPK gene. Mutant DMPK transcripts are toxic and alter gene expression at several levels. Chiefly, the secondary structure formed by CUGs has a strong propensity to capture and retain proteins, like those of the muscleblind-like (MBNL) family. Sequestered MBNL proteins cannot then fulfill their normal functions. Many therapeutic approaches have been explored to reverse these pathological consequences. Here, we review the myriad of small molecules that have been proposed for DM1, including examples obtained from computational rational …

musculoskeletal diseases0301 basic medicineTherapeutic gene modulationcongenital hereditary and neonatal diseases and abnormalitiesMutantComputational biologyBiologyMyotonic dystrophyMyotonin-Protein Kinase03 medical and health sciences0302 clinical medicineTrinucleotide RepeatsDrug DiscoveryGene expressionmedicineAnimalsHumansMyotonic DystrophyGenePharmacologyRegulation of gene expressionGeneticsDrug RepositioningRational designmedicine.diseaseSmall moleculeHigh-Throughput Screening Assays030104 developmental biologyGene Expression RegulationDrug Design030217 neurology & neurosurgeryDrug Discovery Today
researchProduct

A STAT4 variant increases liver fibrosis risk in Caucasian patients with chronic hepatitis B

2018

Background Host genetic modifiers of the natural history of chronic hepatitis B (CHB) remain poorly understood. Recently, a genome-wide association study (GWAS)-identified polymorphism in the STAT4 gene that contributes to the risk for hepatocellular carcinoma (HCC) was shown to be associated with the full spectrum of hepatitis B virus (HBV) outcomes in Asian patients. However, the functional mechanisms for this effect are unknown and the role of the variant in modulating HBV disease in Caucasians has not been investigated. Aims To determine whether STAT4 genetic variation is associated with liver injury in Caucasian patients with CHB and to investigate potential mechanisms mediating this e…

musculoskeletal diseases0301 basic medicinemedicine.medical_specialtyGenome-wide association studymedicine.disease_cause03 medical and health sciences0302 clinical medicineSDG 3 - Good Health and Well-beingimmune system diseasesInternal medicinemedicineGenetic predispositionPharmacology (medical)skin and connective tissue diseasesHepatitis B virusHepatologybusiness.industryGastroenterologyhemic and immune systemsHepatologyHepatitis Bmedicine.disease030104 developmental biologyHepatocellular carcinomaImmunologyInterleukin 12030211 gastroenterology & hepatologyViral hepatitisbusinessAlimentary Pharmacology & Therapeutics
researchProduct

The role of osteoprotegerin in the crosstalk between vessels and bone: Its potential utility as a marker of cardiometabolic diseases

2018

International audience; Among the numerous molecules that are being studied for their potential utility as biomarkers of cardiovascular diseases, much interest has been shown in the superfamily of tumor necrosis factor (TNF) receptors. Members of this family include osteoprotegerin (OPG) and its ligands, which are receptor activators of nuclear factor κB ligand (RANKL) and TNF-related apoptosis-inducing ligand (TRAIL). These signals may be expressed and regulated, and their functions could be involved in several physiological and pathological processes. The relationship between bone regulatory proteins and vascular biology has attracted attention, and it has been suggested that OPG may medi…

musculoskeletal diseases0301 basic medicinemedicine.medical_specialtyOsteoporosisInflammationDisease030204 cardiovascular system & hematologyBone remodeling03 medical and health sciences0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemOsteoprotegerinInternal medicinemedicineHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyPharmacology (medical)Vascular CalcificationReceptorPharmacologybiologyChemistryOsteoprotegerinmedicine.disease3. Good health030104 developmental biologyEndocrinologyCardiovascular DiseasesRANKLbiology.proteinTumor necrosis factor alphaBone Remodelingmedicine.symptomPharmacology & Therapeutics
researchProduct

FRI0150 Mtor blockade by rapamycin decreases arthritis and spondylitis development and severity in hla-b27 transgenic rats

2018

Career situation of first and presenting author Student for a master or a PhD. Introduction TNF and IL-17A have been demonstrated as key inflammatory cytokines in Spondyloarthritis (SpA), whereas targeting bone remodeling remains an unmet clinical need in SpA. The mammalian target of rapamycin (mTOR) regulates IL-17 expression and osteogenesis and could therefore be a promising therapeutic target in SpA. Objectives To investigate if blockade of mTOR with rapamycin inhibits the pathological processes in inflammation and bone in SpA. Methods Cytokines were measured by ELISA in the supernatant from SpA patient PBMCs stimulated with anti-CD3/CD28, with various concentrations of rapamycin. SpA F…

musculoskeletal diseases030203 arthritis & rheumatologyHLA-B27business.industryArthritis030209 endocrinology & metabolismInflammationPharmacologymedicine.diseaseBlockadeProinflammatory cytokineBone remodeling03 medical and health sciences0302 clinical medicinemedicineTumor necrosis factor alphamedicine.symptombusinessPI3K/AKT/mTOR pathwayFRIDAY, 15 JUNE 2018
researchProduct

HLA-B27-restricted cytotoxic T lymphocyte responses to arthritogenic enterobacteria or self-antigens are dominated by closely related TCRBV gene segm…

1996

Identification of the T-cell receptors (TCR) used by synovial cytotoxic T lymphocytes (CTL) of patients with reactive arthritis (ReA) may be crucial to better understanding the pathogenetic mechanism underlying the HLA-B27 association of spondylarthropathies. The authors, therefore, sequenced 25 TCRB chains from HLA-B27-restricted CD8+ CTL clones and two clonal lines specific for self- or Yersinia enterocolitica antigen isolated from synovial fluids of 3 HLA-B27+ patients with ReA and PBL of one healthy HLA-B27+ individual. Fourteen non-HLA-B27-restricted CTL served as controls. Both autoreactive and Y. enterocolitica specific HLA-B27-restricted CTL used a highly limited set of VB genes wit…

musculoskeletal diseasesAdultMaleSalmonella typhimuriumYersinia InfectionsReceptors Antigen T-Cell alpha-betaImmunologyMolecular Sequence Datachemical and pharmacologic phenomenaChlamydia trachomatisBiologyCD8-Positive T-LymphocytesArthritis ReactiveAutoantigensPolymerase Chain ReactionProhibitinsSynovial FluidCytotoxic T cellHumansAmino Acid SequenceGene Rearrangement beta-Chain T-Cell Antigen Receptorskin and connective tissue diseasesReceptorSpondylarthropathiesGeneHLA-B27 AntigenYersinia enterocoliticaHLA-B27Antigens BacterialT-cell receptorhemic and immune systemsGeneral MedicineDNAChlamydia InfectionsCTL*ImmunologySalmonella InfectionsCD8T-Lymphocytes CytotoxicScandinavian journal of immunology
researchProduct

Association of interleukin-10G microsatellite polymorphism with the susceptibility of ankylosing spondylitis

2013

Study suggests an association of IL10.G poly- morphisms with AS which might contribute to the increased or decreased susceptibility to AS. IL10.G8 and G7 microsatellites alleles appear as protective alleles against the development of AS in the German subjects investigated here. Allele IL10.G9 seems to be a risk factor for the development of AS. This protective effect of variant promoter alleles could be related to differences in IL- 10 production, which may be clinically relevant.

musculoskeletal diseasesAdultMalechemical and pharmacologic phenomenaRheumatologyimmune system diseasesparasitic diseasesmedicineHumansGenetic Predisposition to DiseaseSpondylitis AnkylosingAnkylosing spondylitisPolymorphism Geneticbusiness.industryIL10 microsatellite polymorphisms ankylosing spondylitisInterleukinhemic and immune systemsJoint boneMiddle Agedmedicine.diseaseInterleukin-10Interleukin 10ImmunologyMicrosatelliteFemalebusinessAnkylosing spondylitis; Interleukin-10; Microsatellite polymorphismsMicrosatellite RepeatsJoint Bone Spine
researchProduct

Interaction of allopurinol with phenprocoumon in man.

1977

Conditions in two patients on long-term phenprocoumon (Marcumar®) treatment are reported who had signs of phenprocoumon overdosage when given simultaneously allopurinol. The determination of phenprocoumon plasma concentrations in one patient showed that phenprocoumon accumulates for several weeks during treatment with allopurinol. Signs of phenprocoumon overdosage thus can appear long time after starting allopurinol treatment.

musculoskeletal diseasesAdultMalecongenital hereditary and neonatal diseases and abnormalitiesAllopurinolMyocardial InfarctionAllopurinolPharmacologyPhenprocoumonDrug DiscoveryMedicineHumansDrug InteractionsBlood CoagulationGenetics (clinical)integumentary systembusiness.industrynutritional and metabolic diseasesGeneral Medicine4-HydroxycoumarinsDrug interactionMiddle AgedPlasma concentrationPhenprocoumonMolecular MedicineBlood Coagulation TestsbusinessMathematicsmedicine.drugKlinische Wochenschrift
researchProduct