Search results for "lcsh:Pathology"

showing 4 items of 44 documents

The Role of Adipose Tissue and Adipokines in Obesity-Related Inflammatory Diseases

2010

Obesity is an energy-rich condition associated with overnutrition, which impairs systemic metabolic homeostasis and elicits stress. It also activates an inflammatory process in metabolically active sites, such as white adipose tissue, liver, and immune cells. As consequence, increased circulating levels of proinflammatory cytokines, hormone-like molecules, and other inflammatory markers are induced. This determines a chronic active inflammatory condition, associated with the development of the obesity-related inflammatory diseases. This paper describes the role of adipose tissue and the biological effects of many adipokines in these diseases.

medicine.medical_specialtyAgingImmunologyAdipose tissueAdipokineInflammationWhite adipose tissueReview ArticleProinflammatory cytokineOvernutritionImmune systemOvernutritionAdipokinesInternal medicinemedicinelcsh:PathologyHumansObesityInflammationSettore MED/04 - Patologia GeneraleChronic Activebusiness.industryobesity adipokines obesity related inflammatory diseasesCell Biologymedicine.diseaseEndocrinologyAdipose TissueImmunologymedicine.symptombusinesslcsh:RB1-214
researchProduct

Sequential release of TNFα and phospholipase A2 in a rat model of LPS-induced pleurisy

1997

The levels of extracellular phospholipase A2(sPLA2) and TNFα, and cell accumulation were measured in the pleural washings obtained at different times following the induction ofEscherichia colilipopolysaccharide (LPS, 100 μg/cavity) pleurisy in rats. TNFα peaked at 2 hours (3036 ± 160.3 units/ml) and decreased thereafter. Conversely, levels of sPLA2peaked at 48 hours (1.97 ± 0.64 ng/ml) and were increased further (14.02 ± 4.16 ng/ml) by pretreatment with anti-TNFα antibody. Cell accumulation was not affected by antibody pretreatment. These data indicate that the sPLA2enzyme is involved in LPS-induced pleurisy. The enzyme seems not to be stimulated by TNFα which may be involved in the downreg…

medicine.medical_specialtyLipopolysaccharideImmunologypleurisyInflammationchemistry.chemical_compoundPhospholipase A2Downregulation and upregulationInternal medicinemedicineExtracellularlcsh:Pathologyratchemistry.chemical_classificationbiologybusiness.industrylipopolysaccharideCell Biologymedicine.diseaseEndocrinologyEnzymechemistryPleurisyImmunologybiology.proteinTumor necrosis factor alphaphospholipase A2medicine.symptombusinessResearch Articlelcsh:RB1-214Mediators of Inflammation
researchProduct

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
researchProduct

Expression of p63, p53 and ki-67 in patients with cervical intraepithelial neoplasia

2017

Objective: Cervical intraepithelial neoplasia (CIN) is a dysplastic process in cervical squamous epithelium and carries a risk of progression to cervical cancer. The aim of this study was to compare expression of three biomarkers named p53, p63 and Ki-67 in patients with various grades of cervical intraepithelial neoplasia and in a control group. Material and Method: 58 patients were enrolled in the study. Each patient underwent a colposcopy-guided biopsy of the cervix. Immunostaining for markers (p53, p63 and Ki-67) was performed on tissue samples of normal cases (n=10), CIN I (n=20), CIN II (n=14), and CIN III (n=14). Results: Our study showed a significant increase of the expression of t…

p530301 basic medicineUterine Cervical Neoplasmsurologic and male genital diseasesGastroenterology0302 clinical medicineYoung adultCervical cancerp63medicine.diagnostic_testbiologyvirus diseasesMiddle AgedImmunohistochemistryfemale genital diseases and pregnancy complicationsKoilocytesurgical procedures operativemedicine.anatomical_structure030220 oncology & carcinogenesisKi-67Disease ProgressionKi-67ImmunohistochemistryFemalelcsh:RB1-214Adultmedicine.medical_specialtyAdolescentCervical intraepithelial neoplasiaPathology and Forensic MedicineYoung Adult03 medical and health sciencesInternal medicineBiopsyBiomarkers Tumorlcsh:PathologymedicineHumansneoplasmsCervixCervical intraepithelial neoplasiabusiness.industryMembrane ProteinsUterine Cervical Dysplasiamedicine.diseaseKi-67 Antigen030104 developmental biologybiology.proteinTumor Suppressor Protein p53businessTurkish Journal of Pathology
researchProduct