Search results for "ANEM"

showing 10 items of 405 documents

Non-immune hydrops fetalis: Two case reports

2021

BACKGROUND Fetal hydrops is a serious condition difficult to manage, often with a poor prognosis, and it is characterized by the collection of fluid in the extravascular compartments. Before 1968, the most frequent cause was the maternal-fetal Rh incompatibility. Today, 90% of the cases are non-immune hydrops fetalis. Multiple fetal anatomic and functional disorders can cause non-immune hydrops fetalis and the pathogenesis is incompletely understood. Etiology varies from viral infections to heart disease, chromosomal abnormalities, hematological and autoimmune causes. CASE SUMMARY A 38-year-old pregnant woman has neck lymphoadenomegaly, fever, cough, tonsillar plaques at 14 wk of amenorrhea…

Fetusmedicine.medical_specialtyAmniotic fluidHeart diseaseObstetricsbusiness.industryAnemiaFetal transfusionFetal anemiaGeneral Medicinemedicine.diseaseHydrops fetalisPreterm cesarean sectionBlood chemistryInfectious disease (medical specialty)Hydrops fetalisCase reportmedicineEtiologybusinessCordocentesisWorld Journal of Clinical Cases
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Impact of Safety-Related Dose Reductions or Discontinuations on Sustained Virologic Response in HCV-Infected Patients: Results from the GUARD-C Cohor…

2015

Background: Despite the introduction of direct-acting antiviral agents for chronic hepatitis C virus (HCV) infection, peginterferon alfa/ribavirin remains relevant in many resource-constrained settings. The non-randomized GUARD-C cohort investigated baseline predictors of safety-related dose reductions or discontinuations (sr-RD) and their impact on sustained virologic response (SVR) in patients receiving peginterferon alfa/ribavirin in routine practice. Methods: A total of 3181 HCV-mono-infected treatment-naive patients were assigned to 24 or 48 weeks of peginterferon alfa/ribavirin by their physician. Patients were categorized by time-to-first sr-RD (Week 4/12). Detailed analyses of the i…

Genetics and Molecular Biology (all)MaleChronic HepatitisHepacivirusRibavirin/adverse effectsAsthenia/chemically inducedHepacivirusPolyethylene GlycolBiochemistryPolyethylene GlycolsBody Mass IndexChronic Liver Disease0302 clinical medicineNeutropenia/chemically inducedInterferon-alpha/adverse effectsMedicineChroniclcsh:ScienceLiver Diseasesvirus diseasesAntiviral Agents/adverse effectsCohortScience & Technology - Other Topics030211 gastroenterology & hepatologyDrug Therapy CombinationCohort studyHumanmedicine.medical_specialtyAlpha interferonGastroenterology and HepatologyAntiviral AgentsMicrobiologyDose-Response Relationship03 medical and health sciencesPharmacotherapyHepatitis C Chronic/drug therapyDose Prediction MethodsDrug TherapyAnemia/chemically inducedHumansHemoglobinAgedMedicine and health sciencesBiochemistry Genetics and Molecular Biology (all)HepaciviruScience & TechnologyDose-Response Relationship DrugFlaviviruseslcsh:ROrganismsBiology and Life SciencesProteinsmedicine.diseasedigestive system diseaseschemistryAgricultural and Biological Sciences (all)Withholding TreatmentAstheniaImmunologyProportional Hazards Modellcsh:QHuman medicineRNA virusesPhysiologylcsh:MedicinePeginterferon-alfaPolyethylene Glycols/adverse effectsAdult; Aged; Anemia; Antiviral Agents; Asthenia; Cohort Studies; Dose-Response Relationship Drug; Drug Therapy Combination; Female; Hepacivirus; Hepatitis C Chronic; Host-Pathogen Interactions; Humans; Interferon-alpha; Male; Middle Aged; Neutropenia; Outcome Assessment (Health Care); Polyethylene Glycols; Proportional Hazards Models; RNA Viral; Recombinant Proteins; Ribavirin; Withholding Treatment; Agricultural and Biological Sciences (all); Biochemistry Genetics and Molecular Biology (all); Medicine (all)Cohort Studieschemistry.chemical_compoundOutcome Assessment Health CareMedicine and Health Sciences030212 general & internal medicineViralPathology and laboratory medicineMultidisciplinarybiologyHepatitis C virusPharmaceuticsMedicine (all)AnemiaHepatitis CHematologyRecombinant ProteinOutcome Assessment (Health Care)/methodsMiddle AgedMedical microbiologyHepatitis CRecombinant ProteinsHost-Pathogen InteractionMultidisciplinary SciencesPhysiological ParametersResearch DesignCombinationHost-Pathogen InteractionsVirusesRNA ViralFemaleDrugPathogensHost-Pathogen Interactions/drug effectsResearch ArticleAdultNeutropeniaClinical Research DesignResearch and Analysis MethodsOutcome Assessment (Health Care)Internal medicineRibavirinRecombinant Proteins/adverse effectsRNA Viral/bloodAdult; Aged; Anemia; Antiviral Agents; Asthenia; Cohort Studies; Dose-Response Relationship Drug; Drug Therapy Combination; Female; Hepacivirus; Hepatitis C Chronic; Host-Pathogen Interactions; Humans; Interferon-alpha; Male; Middle Aged; Neutropenia; Outcome Assessment (Health Care); Polyethylene Glycols; Proportional Hazards Models; RNA Viral; Recombinant Proteins; Ribavirin; Withholding TreatmentAdult; Aged; Anemia; Antiviral Agents; Asthenia; Cohort Studies; Dose-Response Relationship Drug; Drug Therapy Combination; Female; Hepacivirus; Hepatitis C Chronic; Host-Pathogen Interactions; Humans; Interferon-alpha; Male; Middle Aged; Neutropenia; Outcome Assessment (Health Care); Polyethylene Glycols; Proportional Hazards Models; RNA Viral; Recombinant Proteins; Ribavirin; Withholding Treatment; Medicine (all); Biochemistry Genetics and Molecular Biology (all); Agricultural and Biological Sciences (all)Proportional Hazards ModelsAntiviral Agentbusiness.industryRibavirinBody WeightHepacivirus/drug effectsViral pathogensInterferon-alphaHepatitis C Chronicbiology.organism_classificationHepatitis virusesMicrobial pathogensRNAAdverse EventsCohort StudiebusinessPloS one
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Thalassemia (Microkarterocytosis) and Drepanocytosis their Forms and Genetics

1952

SummaryThalassemia, that I propose to call Microkarterocytosis, can be divided into three forms to be distinguished under the names of minima (healthy carriers), minor (Rietti and Greppi's disease), major (Cooley disease).It can be inferred that Thalassemia is a mutation developped in a mediterranean superior paleolitic race that showed also the character high cheek bones.In my researches of 1941-42 I for first showed that thalassemia is a dominant hereditary character with homozigotic letal effect (heterozigotes the healthy carriers, homozigotes Cooley' patients).Heterozigotes throug an increased expression of the morbid gene develop Rietti and Greppi disease, as I inferred in 1949.The res…

GeneticsHereditybusiness.industryAnemiaThalassemiabeta-ThalassemiaAnemia Sickle CellGeneral MedicineDiseasemedicine.diseaseSickle cell anemiaSickle Cell TraitRace (biology)Cheek bonesHumansThalassemiaMedicineAnemia sickle-cellbusinessActa geneticae medicae et gemellologiae
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Fanconi anemia (FA) and crosslinker sensitivity: Re-appraising the origins of FA definition

2015

The commonly accepted definition of Fanconi anemia (FA) relying on DNA repair deficiency is submitted to a critical review starting from the early reports pointing to mitomycin C bioactivation and to the toxicity mechanisms of diepoxybutane and a group of nitrogen mustards causing DNA crosslinks in FA cells. A critical analysis of the literature prompts revisiting the FA phenotype and crosslinker sensitivity in terms of an oxidative stress (OS) background, redox-related anomalies of FA (FANC) proteins, and mitochondrial dysfunction. This re-appraisal of FA basic defect might lead to innovative approaches both in elucidating FA phenotypes and in clinical management.

Geneticsbusiness.industryDNA repairDNA damageMitomycin CDiepoxybutaneHematologymedicine.diseasemedicine.disease_causeFANC proteinschemistry.chemical_compoundOncologychemistryFanconi anemiaChromosome instabilityPediatrics Perinatology and Child HealthmedicineCancer researchbusinessOxidative stressPediatric Blood & Cancer
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Hypoxia and anemia: effects on tumor biology and treatment resistance

2004

In locally advanced solid tumors, oxygen (O2) delivery is frequently reduced or even abolished. This is due to abnormalities of the tumor microvasculature, adverse diffusion geometries, and tumor-associated and/or therapy-induced anemia. Up to 50-60% of locally advanced solid tumors may exhibit hypoxic and/or anoxic tissue areas that are heterogeneously distributed within the tumor mass. In approximately 30% of pretreatment patients, a decreased O2 transport capacity of the blood as a result of tumor-associated anemia can greatly contribute to the development of tumor hypoxia. While normal tissues can compensate for this O2 deficiency status by a rise in blood flow rate, locally advanced tu…

Genome instabilityAnemiaClinical BiochemistryDrug resistanceBiologyRadiation ToleranceNeoplasmsmedicineHumansHypoxiaRegulation of gene expressionTumor hypoxiaBiochemistry (medical)NF-kappa BNuclear ProteinsAnemiaHematologyHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitPrognosismedicine.diseaseNeoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation NeoplasticOxygenHypoxia-inducible factorsDrug Resistance NeoplasmTumor progressionImmunologyDisease ProgressionCancer researchHypoxia-Inducible Factor 1medicine.symptomCell DivisionTranscription FactorsTransfusion Clinique et Biologique
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Tumor Hypoxia and Malignant Progression

2004

Publisher Summary This chapter discusses tumor hypoxia and malignant progression. Hypoxic (or anoxic) areas arise as a result of an imbalance between the supply and the consumption of oxygen. Whereas in normal tissues or organs the O2 supply matches the metabolic requirements, in locally advanced solid tumors the O2 consumption rate of neoplastic as well as stromal cells may outweigh an insufficient oxygen supply and result in the development of tissue areas with very low O2 levels. Major pathogenetic mechanisms involved in the emergence of hypoxia in solid tumors are (a) severe structural and functional abnormalities of the tumor microvessels (b) a deterioration of the diffusion geometry, …

Genome instabilityStromal cellTumor hypoxiaAnemiaHypoxia (medical)Biologymedicine.diseasePathogenesisImmunologymedicineCancer researchImmunohistochemistrymedicine.symptomTranscription factor
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Low Hemoglobin Levels and the Onset of Cognitive Impairment in Older People: The PRO.V.A. Study

2016

Low hemoglobin (Hb) levels are attracting interest as a risk factor for cognitive impairment, but with contrasting evidence emerging from the current literature. The aim of our work was to investigate the relationship between baseline serum Hb levels and the incidence of cognitive impairment in older people over a follow-up of 4.4 years. Our study considered a sample of 1227 elderly subjects cognitively intact at baseline, enrolled under the Progetto Veneto Anziani (Pro.V.A.) among 3099 screened subjects. For all participants, we measured serum Hb levels on blood samples; incident cognitive impairment was defined as a Mini Mental State Examination (MMSE) score <24 and confirmed by geriat…

GerontologyMalesex differencesAgingmedicine.medical_specialtyAnemiaelderlyNOhemoglobin concentration03 medical and health sciencesHemoglobins0302 clinical medicineInternal medicinemedicineDementiaHumansCognitive Dysfunction030212 general & internal medicineHemoglobinRisk factorCognitive impairmentAgedcognitive impairmentAged 80 and overSex CharacteristicsMini–Mental State Examinationmedicine.diagnostic_testbusiness.industryIncidence (epidemiology)Incidencemedicine.diseaseanemiaConfidence intervalanemia; cognitive impairment; dementia; elderly; hemoglobin concentration; sex differencesFemaleGeriatrics and Gerontologybusiness030217 neurology & neurosurgerySex characteristicsFollow-Up Studiesdementia
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Primary Plasma Cell Leukemia Associated with Adult Fanconi Syndrome

2006

Abstract Primary plasma cell leukemia (PCL) is a rare variant of multiple myeloma that occurs de novo in patients without a history of plasma cell disorder. We describe a case of λ PCL that showed a prolonged survival of 2 years and 6 months associated with a generalized dysfunction of the proximal renal tubule. On presentation, the patient had anemia (hemoglobin level, 11 g/dL), thrombocytopenia (platelet count, 102,000/μL), and renal insufficiency (creatinine level, 2.75 mg/dL; creatinine clearance, 19 mL per minute; urea, 71 mg/dL). In addition to the common clinical picture, our case showed proteinuria (30 mg/dL), glycosuria (150 mg/dL) with normal glycemia, low uric acid concentration …

GlycosuriaPlasma cell leukemiaAdhesion molecules λ light-chain disease Multiple myelomamedicine.medical_specialtyCreatininebusiness.industryAnemiaFanconi syndromeRenal functionGeneral MedicineSettore MED/08 - Anatomia Patologicamedicine.diseasechemistry.chemical_compoundEndocrinologychemistryInternal medicinemedicineUric acidmedicine.symptombusinessMultiple myeloma
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Cytomegalovirus inhibits the engraftment of donor bone marrow cells by downregulation of hemopoietin gene expression in recipient stroma

1998

ABSTRACT Cytomegalovirus (CMV) disease after bone marrow (BM) transplantation is often associated with BM graft failure. There are two possible reasons for such a correlation. First, a poor hematopoietic reconstitution of unrelated etiology could promote the progression of CMV infection by the lack of immune control. Alternatively, CMV infection could interfere with the engraftment of donor BM cells in recipient BM stroma. Evidence for a causative role of CMV in BM aplasia came from studies in long-term BM cultures and from the murine in vivo model of CMV-induced aplastic anemia. A deficiency in the expression of essential stromal hemopoietins, such as stem cell factor (SCF), has indicated …

Graft RejectionMaleStromal cellImmunologyPopulationCytomegalovirusDown-RegulationViral Pathogenesis and ImmunityStem cell factorBiologyHematopoietic Cell Growth FactorsMicrobiologyMiceVirologymedicineAnimalsAplastic anemiaeducationBone Marrow Transplantationeducation.field_of_studyMice Inbred BALB CHematopoietic Cell Growth Factorsmedicine.diseaseTransplantationHaematopoiesisTransplantation Isogeneicmedicine.anatomical_structureInsect ScienceImmunologyCytomegalovirus InfectionsFemaleBone marrowStromal Cells
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Fanconi's anaemia cells have normal steady-state levels and repair of oxidative DNA base modifications sensitive to Fpg protein

1998

Abstract Cells from Fanconi's anaemia (FA) patients are abnormally sensitive to oxygen. However, a distinct genetic defect in either the cellular defence against reactive oxygen species (ROS) or in their metabolic generation has not been identified to date. Recently, the gene for the human 8-hydroxyguanine (8-oxoG) glycosylase, which removes this oxidative base modification from the genome, has been localized on chromosome 3p25, i.e., in the same region as the FA complementation group D (FAD) gene. We therefore studied the removal of photosensitization-induced 8-oxoG residues from the DNA of FA cells, using Fpg protein, the bacterial 8-oxoG glycosylase, to quantify the lesions by alkaline e…

GuanineDNA RepairLightDNA repairBiologyToxicologymedicine.disease_causechemistry.chemical_compoundFanconi anemiaGeneticsmedicineHumansN-Glycosyl HydrolasesMolecular BiologyGeneCells CulturedPhotosensitizing AgentsDNAmedicine.diseaseMolecular biologyNuclear DNAComplementationOxidative StressFanconi AnemiaDNA-Formamidopyrimidine GlycosylaseBiochemistrychemistryDNA glycosylaseCell DivisionOxidative stressDNAMutation Research/DNA Repair
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