Search results for "Mito"

showing 10 items of 2513 documents

Perturbed Glucose Metabolism: Insights into Multiple Sclerosis Pathogenesis

2014

Multiple sclerosis (MS) is a complex debilitating disease of the central nervous system perceived to result from the autoimmune effect of T cells in damaging myelin sheath. However, the exact pathogenesis of the disease remains elusive. Initial studies describing the possibility of defective pyruvate metabolism in MS were performed in 1950s. The group observed elevated blood pyruvate level in both fasting and postprandial times in MS patients with relapse. Similarly, other investigators also reported increased fasting pyruvate level in this disease. These reports hint to a possible abnormality of pyruvate metabolism in MS patients. In addition, increase in levels of Krebs cycle acids like a…

medicine.medical_specialtyMini ReviewCentral nervous systemDiseaseCarbohydrate metabolismBioinformaticsmultiple sclerosislcsh:RC346-429PathogenesisInternal medicinebrain glucose metabolismmedicineneurodegenerative diseaseslcsh:Neurology. Diseases of the nervous systemmitochondrial defectsbusiness.industryMultiple sclerosisand neurodegenerative diseasesmedicine.diseasecell-specific mechanismsReview articleCitric acid cycleMetabolic pathwaymedicine.anatomical_structureEndocrinologyNeurologyNeurology (clinical)businessNeuroscienceFrontiers in Neurology
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Mitochondrial dysfunction in cholestatic liver diseases

2011

et al.

medicine.medical_specialtyMitochondrial DNABiliary cirrhosisMitochondrial HepatopathyApoptosisReviewBiologyMitochondrionmedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyLiver diseaseCholestasisInternal medicinemedicineHumansBiología y BiomedicinaCholestasisGeneral Immunology and MicrobiologyLiver Diseasesmedicine.diseaseBile acidsCell biologyMitochondriaEndocrinologyMitochondrial biogenesisOxidative stressMitochondrial functionMitochondrial dysfunctionOxidative stressFrontiers in Bioscience (Elite edition) 4: 2233-2252 (2012)
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Low-Dose Aclacinomycin and Intermediate-Dose Cytosine Arabinoside in Relapsed and Refractory Acute Myelogenous Leukemia

1990

Nineteen patients with relapsed or refractory acute myelogenous leukemia were treated with escalating doses of aclacinomycin (ACLA 20–30 mg/m2 daily for 5 days) and intermediate-dose cytosine arabinoside (Ara-C 1 g/m2 twice daily for 4 days). Most patients had received previous therapy with high- or intermediate-dose Ara-C plus mitoxantrone (HAM, IAM) and TAD (6-thioguanine, standard-dose cytosine arabinoside, and daunorubicin). Four patients had had repeated relapses and another three were treated for primary treatment failure following induction with HAM or I AM.

medicine.medical_specialtyMitoxantroneDaunorubicinbusiness.industryLow dosemedicine.diseaseGastroenterologyMyelogenouschemistry.chemical_compoundLeukemiaRefractorychemistryInternal medicinemedicinePrimary treatmentbusinessCytosinemedicine.drug
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A Multicenter Phase I/II Trial of the Combination of Imatinib Mesylate with Mitoxantrone/Etoposide and Cytarabine in Patients with CML in Myeloid Bla…

2004

Abstract The combination of imatinib with mitoxantrone, etoposide or cytarabine were shown to be additive to highly synergistic on BCR-ABL-positive leukemias in vitro by several investigators, including our group. Therefore, we initiated a phase I/II trial for patients with myeloid blast crisis of chronic myelogenous leukemia. Patients were treated in four cohorts starting from mitoxantrone 10 mg/m2/d and etoposide 100 mg/m2/d for 2 or 3 consecutive days and start of imatinib 600 mg/d from day 15 (cohorts #1 and #2) or from day 1 (cohorts #3 and #4). Cytarabine was given at a dose of 10 mg/m2/d s.c. as maintenance treatment. Seventeen patients were included in the study: 8 pts in cohort 1, …

medicine.medical_specialtyMitoxantroneLeukopeniabusiness.industryImmunologyCell BiologyHematologymedicine.diseaseBiochemistryGastroenterologySurgeryTransplantationImatinib mesylateInternal medicinemedicineMucositisCytarabinemedicine.symptombusinessEtoposideProgressive diseasemedicine.drugBlood
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Preliminary Phase II Study Results of BBR2778 in Combination with Cyclophosphamide, Vincristine, and Prednisone in Patients with Relapsed Aggressive …

2004

Abstract Background: Pixantrone (BBR 2778) is a novel aza-anthracenedione with superior activity compared to doxorubicin and mitoxantrone in various tumor models including hematological malignancies. Pixantrone single agent therapy led to major responses in patients (pts) with aggressive lymphoma including diffuse large B-cell lymphoma (DLCL). The safety of a CHOP-like regimen with pixantrone replacing doxorubicin (CPOP) was assessed in a dose-ranging study indicating a recommended dose of 150 mg/m² for pixantrone. Method: In this phase II study the primary objective was to assess the efficacy of the CPOP regimen (cyclophosphamide 750 mg/m² d1, pixantrone 150mg/m² d1, vincristine 1.4mg/m² d…

medicine.medical_specialtyMitoxantronePixantroneAnthracyclinebusiness.industryImmunologyFollicular lymphomaAggressive lymphomaCell BiologyHematologymedicine.diseaseBiochemistryGastroenterologySurgeryNon-Hodgkin's lymphomachemistry.chemical_compoundchemistryInternal medicinemedicineMantle cell lymphomabusinessFebrile neutropeniamedicine.drugBlood
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PGC-1α: a master gene that is hard to master

2012

Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) is a transcriptional coactivator that favorably affects mitochondrial function. This concept is supported by an increasing amount of data including studies in PGC-1α gene-deleted mice, suggesting that PGC-1α is a rescue factor capable of boosting cell metabolism and promoting cell survival. However, this view has now been called into question by a recent study showing that adeno-associated virus-mediated PGC-1α overexpression causes overt cell degeneration in dopaminergic neurons. How is this to be understood, and can these seemingly conflicting findings tell us something about the role of PGC-1α in cell stress and in cont…

medicine.medical_specialtyModels NeurologicalSettore BIO/11 - Biologia MolecolareRNA-binding proteinBiologyMitochondrionSettore BIO/09 - FisiologiaMiceCellular and Molecular NeuroscienceHeat shock proteinInternal medicinemedicineAnimalsHomeostasisHumansReceptorMolecular BiologyTranscription factorHeat-Shock ProteinsMice KnockoutPharmacologyPGC-1α Mitochondria Dopaminergic neurons Transgenic animal Adenovirus Parkinson’s diseaseDopaminergic NeuronsDopaminergicRNA-Binding ProteinsParkinson DiseaseCell BiologyPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMitochondriaEndocrinologyCell metabolismNerve DegenerationTrans-ActivatorsMolecular MedicineNeuroscienceHomeostasisTranscription FactorsCellular and Molecular Life Sciences
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Mechanisms of C-reactive protein-induced blood-brain barrier disruption.

2009

Background and Purpose— Increased mortality after stroke is associated with brain edema formation and high plasma levels of the acute phase reactant C-reactive protein (CRP). The aim of this study was to examine whether CRP directly affects blood–brain barrier stability and to analyze the underlying signaling pathways. Methods— We used a cell coculture model of the blood–brain barrier and the guinea pig isolated whole brain preparation. Results— We could show that CRP at clinically relevant concentrations (10 to 20 μg/mL) causes a disruption of the blood–brain barrier in both approaches. The results of our study further demonstrate CRP-induced activation of surface Fcγ receptors CD16/32 fo…

medicine.medical_specialtyMyosin light-chain kinaseMyosin Light ChainsGuinea PigsBrain Edemamedicine.disease_causeBlood–brain barrierp38 Mitogen-Activated Protein KinasesMyosin light chain kinase activityTight JunctionsInternal medicineMyosinmedicineAnimalsPhosphorylationReceptorCells CulturedAdvanced and Specialized Nursingbusiness.industryReceptors IgGCoculture TechniquesCell biologyRatsStrokeEndocrinologymedicine.anatomical_structureC-Reactive ProteinBlood-Brain BarrierPhosphorylationNeurology (clinical)Endothelium VascularSignal transductionCardiology and Cardiovascular MedicinebusinessReactive Oxygen SpeciesOxidative stressSignal TransductionStroke
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Combination of Rehabilitative Therapy with Ultramicronized Palmitoylethanolamide for Chronic Low Back Pain: An Observational Study

2019

Abstract Introduction Chronic low back pain (LBP) caused by intervertebral disc herniation was reported in the 2010 Global Burden of Disease study to be the main reason for years lived with disability. It causes significant personal, social, and economic burdens. Many of those who suffer from LBP find conventional medical treatments to be unsatisfactory for treating their pain, so they are increasingly resorting to complementary and alternative medicine (CAM) therapies. Given that the population is aging, there is an urgent need to characterize the combinations of complementary therapies that yield the best outcomes and treatments, even for prolonged periods. This observational study aimed …

medicine.medical_specialtyPain medicinePopulationlcsh:RD78.3-87.3Quality of lifeMedicineMultitarget approachNdultidisciplinary therapir:educationComplementary and alternative medicirreeducation.field_of_studyMassagebusiness.industryBrief ReportUltramicronized palmitlethanolamideChronic low back pajnChronic painmedicine.diseaseUltramicronized palmitoylethanolamideLow back painAnesthesiology and Pain MedicineComplementary and alternative medicinelcsh:AnesthesiologyMultidisciplinary therapiesPhysical therapyChronic low back painMcKenzie methodObservational studyNeurology (clinical)medicine.symptombusinessPain and Therapy
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Genetic Deletion of JNK1 and JNK2 Aggravates the DSS-Induced Colitis in Mice

2007

The c-Jun N-terminal kinases (JNKs) are considered as novel targets for therapy of inflammatory bowel diseases (IBD). However, the relevant JNK isoforms have to be elucidated. Here, we analyze the individual contribution of the JNK1 and JNK2 isoforms in a dextran sulfate sodium (DSS) model of experimental colitis. JNK1 and JNK2 knockout mice (JNK1 ko, JNK2 ko) and their wild-type controls (WT1, WT2) received three cycles of DSS treatment, each consisting of 1.7% DSS for 5 days, followed by 5 days with water. Animals were daily evaluated by a disease activity index (DAI) comprising measurement of body weight, estimation of stool consistency, and test for occult blood/gross rectal bleeding. A…

medicine.medical_specialtyPathologyCryptApoptosisMice TransgenicInflammatory bowel diseaseGastroenterologyProinflammatory cytokineMiceCecumImmune systemInternal medicineWeight LossAnimalsMitogen-Activated Protein Kinase 9MedicineMitogen-Activated Protein Kinase 8Single-Blind MethodIntestinal MucosaColitisCrosses Geneticbusiness.industryDextran SulfateColitismedicine.diseaseMice Inbred C57BLmedicine.anatomical_structureApoptosisChronic DiseaseKnockout mouseSurgeryGastrointestinal HemorrhagebusinessJournal of Investigative Surgery
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Clear cell variant of calcifying epithelial odontogenic tumor: case report with immunohistochemical findings

2015

Calcifying epithelial odontogenic tumor (CEOT) is a rare benign odontogenic neoplasm, locally aggressive, characterized by sheets and nests of polyhedral epithelial cells exhibiting eosinophilic cytoplasm or less often clear cytoplasm. Additional features include nuclear pleomorphism without mitotic activity, concentric calcifications, and deposits of amyloid. Herein, we present an additional example of clear cell variant of CEOT occurring in a 25-year-old female. Microscopically, the tumor consisted on proliferation of epithelial cells with eosinophilic, clear vacuolated cytoplasm interspersed with focal areas of amyloid deposition. Tumor cells were immunopositive for AE1/AE3, CK14, CK19, …

medicine.medical_specialtyPathologyOral Medicine and Pathologybusiness.industryCase ReportOdontologíamedicine.disease:CIENCIAS MÉDICAS [UNESCO]Benign Odontogenic NeoplasmCiencias de la saludCalcifying epithelial odontogenic tumorstomatognathic diseasesCytoplasmEosinophilicUNESCO::CIENCIAS MÉDICASMedicineImmunohistochemistryHistopathologybusinessGeneral DentistryMitosisClear cell
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