Search results for "COMPOUND"

showing 10 items of 35174 documents

Neridronate prevents bone loss in patients receiving androgen deprivation therapy for prostate cancer.

2004

Today, androgen deprivation therapy is a cornerstone of treatment for advanced prostate cancer, although it presents important complications such as osteoporosis. Neridronate, a relatively new bisphosphonate, is able to prevent bone loss in patients with prostate cancer during androgen ablation. Introduction: Androgen-deprivation therapy (ADT) is a cornerstone of treatment for advanced prostate cancer. This therapy has iatrogenic complications, such as osteoporosis. The aim of our study was to evaluate the efficacy of neridronate, a relatively new bisphosphonate, to prevent bone loss during androgen ablation. Materials and Methods: Forty-eight osteoporotic patients with prostate cancer, tre…

musculoskeletal diseasesMalemedicine.medical_specialtyDeoxypyridinolineTime FactorsBicalutamideAntineoplastic Agents HormonalEndocrinology Diabetes and Metabolismmedicine.medical_treatmentOsteoporosisUrologyBone and BonesAndrogen deprivation therapychemistry.chemical_compoundProstate cancerAbsorptiometry PhotonBone DensityMedicineNeridronic acidHumansOrthopedics and Sports MedicineAmino AcidsAgedCholecalciferolTriptorelin PamoateDiphosphonatesbusiness.industryProstatic NeoplasmsAndrogen AntagonistsBisphosphonatemedicine.diseaseAlkaline PhosphataseAndrogen deprivation therapy; Bisphosphonates; Neridronate; Osteoporosis; Prostate cancer; Absorptiometry Photon; Aged; Alkaline Phosphatase; Amino Acids; Androgen Antagonists; Androgens; Antineoplastic Agents Hormonal; Bone Density; Bone and Bones; Calcium; Cholecalciferol; Diphosphonates; Humans; Male; Osteoporosis; Prostatic Neoplasms; Time Factors; Triptorelin Pamoate; SurgerySurgerychemistryAndrogensOsteoporosisCalciumbusinessCholecalciferolmedicine.drugJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
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Duodenal contractile activity in dystrophic (mdx) mice: reduction of nitric oxide influence.

2003

The present study was undertaken to analyse duodenal contractility in adult dystrophic (mdx) mice. The spontaneous changes of the isometric tension and the responses of longitudinal duodenal muscle to nonadrenergic, noncholinergic (NANC) nerve stimulation and to exogenous drugs were compared between normal and mdx mice. Duodenal segments from mdx mice displayed spontaneous contractions with higher frequency than normals. N omega-nitro-L-arginine methyl ester (L-NAME) increased the frequency of contractions in normals without affecting that in mdx mice. In normals, NANC nerve stimulation elicited a transient relaxation abolished by L-NAME. In mdx mice a frank relaxation was not observed, the…

musculoskeletal diseasesMalemedicine.medical_specialtyNerve stimulationPhysiologyDuodenumInhibitory pathwayIsometric exerciseIn Vitro TechniquesInhibitory postsynaptic potentialNitric OxideSettore BIO/09 - FisiologiaNitric oxideContractilityDystrophinchemistry.chemical_compoundMiceSmooth muscleInternal medicinemedicineSpontaneous contractionAnimalsNeuroscience (all)biologyDose-Response Relationship DrugEndocrine and Autonomic SystemsIntestinal relaxationGastroenterologymusculoskeletal systemMice Inbred C57BLEndocrinologychemistrybiology.proteinMice Inbred mdxmdx miceSodium nitroprussideDystrophinGastrointestinal Motilitytissuesmedicine.drugMuscle ContractionNeurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society
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Trastuzumab-emtansine induced pleural and pericardial effusions

2021

Introduction Trastuzumab emtansine (T-DM1) is an antibody-drug conjugate which combine trastuzumab (T), a monoclonal antibody targeting the human epidermal growth factor receptor-2 (HER2), and a cytotoxic molecule derived from maytansine (DM1). Case report We report the first case of T-DM1-associated pleural and pericardial effusions three weeks after the second course of T-DM1 in a patient with breast cancer. Drug-induced pleural and pericardial effusions was implicated in the absence of other etiologies. The Naranjo Scale indicated a probable drug-induced adverse reaction. Management & outcome: The patient fully recovered after thoracentesis and discontinuation of T-DM1. The patient h…

musculoskeletal diseasesReceptor ErbB-2medicine.drug_classBreast NeoplasmsAdo-Trastuzumab EmtansineAntibodies Monoclonal HumanizedMonoclonal antibodyPericardial effusionPericardial Effusion03 medical and health scienceschemistry.chemical_compound0302 clinical medicineTrastuzumabmedicineHumansMaytansinePharmacology (medical)business.industryHuman epidermal growth factorTrastuzumabmedicine.diseaseOncologychemistryTrastuzumab emtansine030220 oncology & carcinogenesisCancer researchFemalebusiness030215 immunologymedicine.drugConjugateJournal of Oncology Pharmacy Practice
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Muscleblind, BSF and TBPH are mislocalized in the muscle sarcomere of a Drosophila myotonic dystrophy model

2012

SummaryMyotonic dystrophy type 1 (DM1) is a genetic disease caused by the pathological expansion of a CTG trinucleotide repeat in the 3' UTR of the DMPK gene. In the DMPK transcripts, the CUG expansions sequester RNA-binding proteins into nuclear foci, including transcription factors and alternative splicing regulators such as MBNL1. MBNL1 sequestration has been associated with key features of DM1. However, the basis behind a number of molecular and histological alterations in DM1 remain unclear. To help identify new pathogenic components of the disease, we carried out a genetic screen using a Drosophila model of DM1 that expresses 480 interrupted CTG repeats, i(CTG)480, and a collection of…

musculoskeletal diseasesSarcomerescongenital hereditary and neonatal diseases and abnormalitiesNeuroscience (miscellaneous)lcsh:MedicineMedicine (miscellaneous)RNA-binding proteinGenes InsectBiologyMyotonic dystrophyGeneral Biochemistry Genetics and Molecular BiologyAnimals Genetically Modifiedchemistry.chemical_compoundImmunology and Microbiology (miscellaneous)RNA interferencelcsh:PathologymedicineMBNL1AnimalsDrosophila ProteinsHumansMyotonic DystrophyGeneticsMuscleslcsh:RAlternative splicingNuclear ProteinsRNA-Binding ProteinsEpistasis Geneticmedicine.diseaseDisease Models AnimalchemistryGene Knockdown TechniquesDrosophilaFemaleRNA InterferenceTrinucleotide repeat expansionTrinucleotide Repeat ExpansionDrosophila Proteinlcsh:RB1-214Genetic screenResearch ArticleDisease Models & Mechanisms
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Chromogenic detection of nerve agent mimics

2008

The current rise in international concern over criminal terrorist attacks via chemical warfare (CW) agents has resulted in an increasing interest in the detection of these lethal chemicals. Among CW species, nerve agents are extremely dangerous and their high toxicity and ease of production underscore the need to detect these deadly chemicals via quick and reliable procedures. A number of detection systems have been developed, most of them based on enzymatic and physical methodologies. However, these usually show limitations such as low selectivity, lack of portability and a certain complexity in their use. An alternative to these classical methods that has been gaining interest in recent y…

musculoskeletal diseasesTertiary amineUNESCO::QUÍMICANerve agent mimicsElectron donorBiosensing TechniquesUNESCO::ASTRONOMÍA Y ASTROFÍSICA:QUÍMICA [UNESCO]Reductive aminationCatalysischemistry.chemical_compoundOrganophosphorus CompoundsMaterials ChemistryMoietyChemical Warfare Agentsskin and connective tissue diseasesChromogenic protocol ; Nerve agent mimics ; Internationalchemistry.chemical_classificationChromogenic protocolMolecular StructureChromogenicChemistryfungiMetals and AlloysGeneral ChemistryElectron acceptorCombinatorial chemistrySurfaces Coatings and FilmsElectronic Optical and Magnetic MaterialsDiethyl chlorophosphatebody regionsKineticsstomatognathic diseasesChromogenic CompoundsInternationalCeramics and CompositesColorimetryHypsochromic shiftAzo Compounds:ASTRONOMÍA Y ASTROFÍSICA [UNESCO]
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Enhanced prolylhydroxylase activity in the posterior annulus fibrosus of canine intervertebral discs following long-term running exercise

2010

The effect of long-term excercise on the intervertebral disc collagen concentration (hydroxyproline), collagen-synthesizing enzymes (prolyl-4-hydroxylase, PH, and galactosyl-hydroxylysyl glucosyltransferase, GGT) and hydroxypyridinium crosslinks was studied in ten female beagle dogs. The dogs were run on a treadmill for 1 year starting at the age of 15 weeks. The daily running distance was gradually increased to 40km, which distance the dogs ran for the final 15 weeks. Ten untrained dogs from the same breeding colony served as controls. The nucleus pulposus and anterior and posterior halves of the annulus fibrosus of C2-3, T10-12, L4-5 disc segments were analysed. Crosslinks were measured f…

musculoskeletal diseasesTime FactorsProcollagen-Proline DioxygenaseBeagleThoracic VertebraeHydroxyprolinechemistry.chemical_compoundDogsLumbarStress PhysiologicalPhysical Conditioning AnimalmedicineAnimalsOrthopedics and Sports MedicineTreadmillIntervertebral DiscAnnulus (mycology)Lumbar VertebraePhysical conditioningbusiness.industryIntervertebral discAnatomymusculoskeletal systemBiomechanical PhenomenaHydroxyprolinemedicine.anatomical_structurechemistryGlucosyltransferasesModels AnimalCollagen metabolismCervical VertebraePhysical EnduranceFemaleSurgeryCollagenbusinessEuropean Spine Journal
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Aberrant glycosylation of alpha-dystroglycan causes defective binding of laminin in the muscle of chicken muscular dystrophy.

2005

Dystroglycan is a central component of dystrophin-glycoprotein complex that links extracellular matrix and cytoskeleton in skeletal muscle. Although dystrophic chicken is well established as an animal model of human muscular dystrophy, the pathomechanism leading to muscular degeneration remains unknown. We show here that glycosylation and laminin-binding activity of alpha-dystroglycan (alpha-DG) are defective in dystrophic chicken. Extensive glycan structural analysis reveals that Galbeta1-3GalNAc and GalNAc residues are increased while Siaalpha2-3Gal structure is reduced in alpha-DG of dystrophic chicken. These results implicate aberrant glycosylation of alpha-DG in the pathogenesis of mus…

musculoskeletal diseasesanimal structuresGlycosylationGlycosylationBiophysicsBiochemistryChromatography AffinityExtracellular matrixchemistry.chemical_compoundStructural BiologyLamininGeneticsDystroglycanmedicineAnimalsDystroglycanMuscular dystrophyDystrophic chickenDystroglycansMuscle SkeletalMolecular BiologybiologySkeletal muscleCell BiologyMuscular Dystrophy AnimalMuscular dystrophymedicine.diseaseMolecular biologycarbohydrates (lipids)Disease Models Animalmedicine.anatomical_structurechemistrybiology.proteinPikachurinLamininPlant LectinsITGA7ChickensProtein BindingFEBS letters
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A global DNA repair mechanism involving the Cockayne syndrome B (CSB) gene product can prevent the in vivo accumulation of endogenous oxidative DNA b…

2002

The Cockayne syndrome B (CSB) gene product is involved in the repair of various types of base modifications in actively transcribed DNA sequences. To investigate its significance for the repair of endogenous oxidative DNA damage, homozygous csb(-/-)/ogg1(-/-) double knockout mice were generated. These combine the deficiency of CSB with that of OGG1, a gene coding for the mammalian repair glycosylase that initiates the base excision repair of 7,8-dihydro-8-oxoguanine (8-oxoG). Compared to ogg1(-/-) mice, csb(-/-)/ogg1(-/-) mice were found to accumulate with age severalfold higher levels of oxidited purine modifications in hepatocytes, splenocytes and kidney cells. In contrast, the basal (ste…

musculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesCancer ResearchDNA RepairTranscription GeneticDNA damageDNA repairBiologyGene productMicechemistry.chemical_compoundGeneticsAnimalsPoly-ADP-Ribose Binding ProteinsMolecular BiologyGeneDNA PrimersMice KnockoutBase SequenceHomozygoteDNA HelicasesDeoxyguanosinenutritional and metabolic diseasesBase excision repairMolecular biologyOxidative StressDNA Repair EnzymesBiochemistrychemistry8-Hydroxy-2'-DeoxyguanosineDNA glycosylaseDNADNA DamageNucleotide excision repairOncogene
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Molecular Effects of the CTG Repeats in Mutant Dystrophia Myotonica Protein Kinase Gene

2008

Myotonic Dystrophy type 1 (DM1) is a multi-system disorder characterized by muscle wasting, myotonia, cardiac conduction defects, cataracts, and neuropsychological dysfunction. DM1 is caused by expansion of a CTG repeat in the 3 untranslated region (UTR) of the Dystrophia Myotonica Protein Kinase (DMPK) gene. A body of work demonstrates that DMPK mRNAs containing abnormally expanded CUG repeats are toxic to several cell types. A core mechanism underlying symptoms of DM1 is that mutant DMPK RNA interferes with the developmentally regulated alternative splicing of defined pre-mRNAs. Expanded CUG repeats fold into ds(CUG) hairpins that sequester nuclear proteins including human Muscleblind-lik…

musculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesThree prime untranslated regionAlternative splicingBiologyMolecular biologyArticleExonchemistry.chemical_compoundCell nucleusmedicine.anatomical_structurechemistryGene expressionGeneticsmedicineGene silencingMBNL1Nuclear proteinGenetics (clinical)Current Genomics
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The effects of post-translational processing on dystroglycan synthesis and trafficking1

2003

Dystroglycan is a component of the dystrophin glycoprotein complex that is cleaved into two polypeptides by an unidentified protease. To determine the role of post-translational processing on dystroglycan synthesis and trafficking we expressed the dystroglycan precursor and mutants thereof in a heterologous system. A point mutant in the processing site, S655A, prevented proteolytic cleavage but had no effect upon the surface localisation of dystroglycan. Mutation of two N-linked glycosylation sites that flank the cleavage site inhibited proteolytic processing of the precursor. Furthermore, chemical inhibition of N- and O-linked glycosylation interfered with the processing of the precursor a…

musculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesanimal structuresCOS cellsGlycosylationbiologyLactacystinBiophysicsCell Biologymusculoskeletal systemCleavage (embryo)BiochemistryDystroglycanschemistry.chemical_compoundchemistryBiochemistryStructural BiologyGeneticsbiology.proteinDystroglycanPikachurinBinding sitetissuesMolecular BiologyFEBS Letters
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