Search results for "Muscle hypertrophy"

showing 10 items of 152 documents

Morphometric analysis of the parotid gland affected by alcoholic sialosis

2008

Background:  In alcoholic parotid sialosis, the gland is frequently enlarged due to ductal and/or acinar hypertrophy, ductal hyperplasy and stromal fat infiltration. The aim of this study was to determine acinar and ductal dimensions, the number of striated ducts and the proportion of fat tissue in patients with and without alcoholic parotid sialosis. Methods:  Twelve parotid biopsy samples from patients with hepatic alcoholic cirrhosis and those from seven controls were used. A morphometrical study with a digital image analyser attached to an optical microscope was carried out. Direct and indirect indicators from acinar and ductal dimensions were recorded. The number of striated ducts and …

Cancer ResearchAlcoholic liver diseasePathologymedicine.medical_specialtyStromal cellmedicine.diagnostic_testbusiness.industryAdipose tissuemedicine.diseaseSialadenitisPathology and Forensic MedicineMuscle hypertrophyParotid glandmedicine.anatomical_structurestomatognathic systemOtorhinolaryngologyMorphometric analysisBiopsymedicinePeriodonticsOral SurgerybusinessJournal of Oral Pathology & Medicine
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miR-133a Enhances the Protective Capacity of Cardiac Progenitors Cells after Myocardial Infarction

2014

Summary miR-133a and miR-1 are known as muscle-specific microRNAs that are involved in cardiac development and pathophysiology. We have shown that both miR-1 and miR-133a are early and progressively upregulated during in vitro cardiac differentiation of adult cardiac progenitor cells (CPCs), but only miR-133a expression was enhanced under in vitro oxidative stress. miR-1 was demonstrated to favor differentiation of CPCs, whereas miR-133a overexpression protected CPCs against cell death, targeting, among others, the proapoptotic genes Bim and Bmf. miR-133a-CPCs clearly improved cardiac function in a rat myocardial infarction model by reducing fibrosis and hypertrophy and increasing vasculari…

Cardiac function curveProgrammed cell deathMyocardial InfarctionGene ExpressionCardiomegalyBiologyBiochemistryArticleMuscle hypertrophyParacrine signallingDownregulation and upregulationmiR-133a; Cardiac Progenitors Cells; Myocardial InfarctionFibrosisREGENERATIONmicroRNAGeneticsmedicineMyocyteAnimalsRNA MessengerOXIDATIVE STRESSlcsh:QH301-705.5ENGINEERED HEART-TISSUElcsh:R5-920Gene Expression ProfilingMICRORNAComputational BiologyCell BiologyMUSCLEmedicine.disease3. Good healthCell biologyRatsAPOPTOSISHYPERTROPHYMicroRNAsDIFFERENTIATIONlcsh:Biology (General)ImmunologyGROWTHRNA Interferencelcsh:Medicine (General)EMBRYONIC STEM-CELLSMyoblasts CardiacDevelopmental BiologyStem Cell Reports
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Inhibition of class I histone deacetylase with an apicidin derivative prevents cardiac hypertrophy and failure

2008

AIMS: Recent studies have demonstrated the importance of chromatin remodelling via histone acetylation/deacetylation for the control of cardiac gene expression. Specific histone deacetylases (HDACs) can, in fact, play a positive or negative role in determining cardiac myocyte (CM) size. Here, we report on the effect on hypertrophy development of three inhibitors (HDACi) of class I HDACs. METHODS AND RESULTS: The compounds were first analysed in vitro by scoring hypertrophy, expression of foetal genes, and apoptosis of neonatal rat CMs stimulated with phenylephrine, an alpha1-adrenergic agonist. This initial screening indicated that a truncated derivative of apicidin with class I HDAC specif…

Cardiac function curvemedicine.medical_specialtyHypertrophy Heart failurePhysiologymedicine.drug_classBiologyPeptides CyclicHistone DeacetylasesCell LineMuscle hypertrophychemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineAnimalsHumansMyocytes CardiacEnzyme InhibitorsRats WistarCells CulturedHeart FailurePressure overloadHistone deacetylase inhibitorHypertrophic cardiomyopathyHypertrophymedicine.diseaseRatsHistone Deacetylase InhibitorsDisease Models AnimalEndocrinologychemistryEchocardiographyHeart failureHypertrophy Left VentricularHistone deacetylaseCardiology and Cardiovascular MedicineApicidinCardiovascular Research
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Deleting Full Length Titin Versus the Titin M-Band Region Leads to Differential Mechanosignaling and Cardiac Phenotypes

2019

Background: Titin is a giant elastic protein that spans the half-sarcomere from Z-disk to M-band. It acts as a molecular spring and mechanosensor and has been linked to striated muscle disease. The pathways that govern titin-dependent cardiac growth and contribute to disease are diverse and difficult to dissect. Methods: To study titin deficiency versus dysfunction, the authors generated and compared striated muscle specific knockouts (KOs) with progressive postnatal loss of the complete titin protein by removing exon 2 (E2-KO) or an M-band truncation that eliminates proper sarcomeric integration, but retains all other functional domains (M-band exon 1/2 [M1/2]-KO). The authors evaluated c…

Cardiomyopathy DilatedMaleSarcomeresanimal structuresVentricular Dysfunction Rightmacromolecular substances030204 cardiovascular system & hematologyMechanotransduction CellularVentricular Function LeftArticleMuscle hypertrophyVentricular Dysfunction Left03 medical and health sciences0302 clinical medicinePhysiology (medical)AnimalsMedicineMyocytes CardiacMuscle Skeletal030304 developmental biologyMice Knockout0303 health sciencesbiologybusiness.industryMolecular springmusculoskeletal systemPhenotypeCell biologyMuscular AtrophyPhenotypeMuscle diseasecardiovascular systemVentricular Function Rightbiology.proteinTitinCardiology and Cardiovascular MedicinebusinessProtein KinasesGene DeletionDifferential (mathematics)Circulation
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Therapeutic Modulation of Urinary Bladder Function: Multiple Targets at Multiple Levels

2015

Storage dysfunction of the urinary bladder, specifically overactive bladder syndrome, is a condition that occurs frequently in the general population. Historically, pathophysiological and treatment concepts related to overactive bladder have focused on smooth muscle cells. Although these are the central effector, numerous anatomic structures are involved in their regulation, including the urothelium, afferent and efferent nerves, and the central nervous system. Each of these structures involves receptors for—and the urothelium itself also releases—many mediators. Moreover, hypoperfusion, hypertrophy, and fibrosis can affect bladder function. Established treatments such as muscarinic antago…

Central Nervous Systemmedicine.medical_specialtyUrinary BladderPopulationCentral nervous systemMuscarinic Antagonistsurologic and male genital diseasesToxicologyBioinformaticsMuscle hypertrophyNeurons EfferentFibrosisInternal medicinemedicineAnimalsHumansNeurons AfferentUrotheliumeducationPharmacologyeducation.field_of_studyUrinary bladderbusiness.industryUrinary Bladder DiseasesMuscle SmoothAdrenergic beta-AgonistsHyperplasiamedicine.diseasefemale genital diseases and pregnancy complicationsUrodynamicsTreatment OutcomeEndocrinologymedicine.anatomical_structureOveractive bladderAdrenergic alpha-1 Receptor AntagonistsUrological AgentsUrotheliumbusinessSignal TransductionAnnual Review of Pharmacology and Toxicology
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Function And Morphology Of The Urinary Bladder After Denervation

2021

Öz bulunamadı.

Denervationmedicine.medical_specialtyContraction (grammar)Urinary bladderMorphology (linguistics)Physiologybusiness.industryUrinary BladderUrologyDenervationMuscle hypertrophymedicine.anatomical_structurePhysiology (medical)medicinebusiness
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MODULATION OF BLADDER α1-ADRENERGIC RECEPTOR SUBTYPE EXPRESSION BY BLADDER OUTLET OBSTRUCTION

2002

Purpose: α1-Adrenergic receptor (α1AR) antagonists are effective for relieving obstructive and irritative symptoms in patients with bladder outlet obstruction. While the α1aAR is responsible for prostate smooth muscle relaxation and outlet obstruction relief, to our knowledge the mechanisms underlying the relief of irritative symptoms remain to be determined. Therefore, we investigated mechanisms by which bladder α1AR subtypes may be involved in this process.Materials and Methods: We studied 42 rats, including 6 unoperated controls, 17 sham operated controls and 19 obstructed animals. Animals were characterized for baseline voiding pattern, followed by surgical intervention or sham surgery …

Detrusor musclemedicine.medical_specialtyUrinary bladderbusiness.industryUrologyUrinary bladder neck obstructionSham surgeryUrologyurologic and male genital diseasesmedicine.diseaseMuscle hypertrophySurgeryNeck of urinary bladderBladder outlet obstructionmedicine.anatomical_structureProstatemedicinebusinessJournal of Urology
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Alcohol consumption and hormonal alterations related to muscle hypertrophy: a review

2014

Detrimental effects of acute and chronic alcohol (ethanol) consumption on human physiology are well documented in the literature. These adversely influence neural, metabolic, cardiovascular, and thermoregulatory functions. However, the side effects of ethanol consumption on hormonal fluctuations and subsequent related skeletal muscle alterations have received less attention and as such are not entirely understood. The focus of this review is to identify the side effects of ethanol consumption on the major hormones related to muscle metabolism and clarify how the hormonal profiles are altered by such consumption.

Endocrinology Diabetes and MetabolismMedicine (miscellaneous)PhysiologyAlcoholReviewClinical nutritionBioinformaticsMuscle hypertrophychemistry.chemical_compoundMedicineQMNutrition and DieteticsEthanolbusiness.industrySkeletal muscleHormonesmedicine.anatomical_structurechemistryMuscle hypertrophyAlcoholProtein synthesisbusinessGVAlcohol consumptionThermoregulatory functionsHormoneNutrition & Metabolism
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Molecular signaling in muscle is affected by the specificity of resistance exercise protocol

2010

Mammalian target of rapamycin and mitogen-activated protein kinase (MAPK) signaling pathways have been highlighted as important for muscle adaptations and thus, they may distinguish adaptations to different exercises. Typically, resistance exercise designed for muscle hypertrophy has moderate intensity (60-80% of one repetition maximum, 1 RM) while one prioritizing maximal strength with minor hypertrophy has a higher intensity (≥90% of 1 RM). Eight untrained men (28.4 ± 3.7 years) conducted two different bilateral leg press exercise protocols: hypertrophic (5 × 10 RM) and pure maximal strength (15 × 1 RM) in a counterbalanced, cross-over design with 1 week between exercises. Vastus laterali…

MAPK/ERK pathwaymedicine.medical_specialtyVastus lateralis muscleSkeletal musclePhysical Therapy Sports Therapy and RehabilitationP70-S6 Kinase 1BiologyMuscle hypertrophymedicine.anatomical_structureEndocrinologyInternal medicineOne-repetition maximummedicinePhosphorylationOrthopedics and Sports MedicineLeg pressScandinavian Journal of Medicine & Science in Sports
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Radiotherapy before or during androgen-deprivation therapy does not blunt the exercise-induced body composition protective effects in prostate cancer…

2021

Background Androgen deprivation therapy (ADT) contributes to lean mass loss and adiposity increases in prostate cancer patients. Radiotherapy during ADT might act synergistically and further worsen body composition. Previous investigations have shown that resistance training is an effective method of preserving body composition during ADT, however, most have not accounted for direct or indirect effects of other therapies, such as radiotherapy. Therefore, the purpose of this study was to examine training adaptations of the tissue composition in patients receiving radiation therapy (RT) prior or during ADT. Methods Analyses were performed by combining data from two previous trials for a total…

Male0301 basic medicineAgingmedicine.medical_treatmentBiochemistryMuscle hypertrophylaw.inventionAndrogen deprivation therapyProstate cancer0302 clinical medicineEndocrinologyRandomized controlled triallawRandomized Controlled Trials as Topicadipositykuntoliikuntamuscle massAndrogensBody Compositionhypertrophyliikuntahoitomedicine.medical_specialtyUrology03 medical and health sciencesAtrophyatrophyGeneticsmedicineHumansAerobic exerciseMuscle StrengthMolecular BiologyatrofiaAgedkehonkoostumussyöpähoidotbusiness.industryProstatic NeoplasmsAndrogen AntagonistsCell Biologymedicine.diseaseRadiation therapysädehoito030104 developmental biologyresistance exerciselihasmassaLean body massbusinesslihassurkastumasairaudet030217 neurology & neurosurgery
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