Search results for "HERA"

showing 10 items of 14928 documents

Difference in Markers of Microbial Translocation and Cell Apoptosis in HIV Monoinfected and HIV/HCV Coinfected Patients

2019

Abstract Immune activation in human immunodeficiency virus (HIV) infection is driven by microbial translocation and in HIV patients is one of the contributors to faster progression of liver disease along with increased cell apoptosis. The aim of the study was to compare microbial translocation and apoptosis markers in HIV monoinfected and HIV/hepatitis C virus (HCV) coinfected patients, depending on HIV immune status and antiretroviral treatment (ART). We analysed data for 78 HIV monoinfected and 105 HIV/HCV coinfected patients from the Rīga East University Hospital. Lipopolysaccharide (LPS), endotoxin core antibodies (EndoCAb), cytokeratin 18 (CK18) and cyto-chrome c (Cyt-c) levels were me…

0301 basic medicineNecrosismicrobial translocationScience030106 microbiologyChromosomal translocation03 medical and health sciences0302 clinical medicinePharmacotherapyImmune systemmedicine030212 general & internal medicineMultidisciplinarybiologybusiness.industrylipopolysaccharideQapoptosisvirus diseasesHepatitis Cmedicine.diseaseVirologyApoptosisbiology.proteinmedicine.symptomAntibodybusinessMicrobial translocationProceedings of the Latvian Academy of Sciences. Section B, Natural Sciences
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Two different pathogenic mechanisms, dying-back axonal neuropathy and pancreatic senescence, are present in the YG8R mouse model of Friedreich ataxia

2016

Frataxin (FXN) deficiency causes Friedreich's ataxia (FRDA), a multisystem disorder with neurological and non-neurological symptoms. FRDA pathophysiology combines developmental and degenerative processes of dorsal root ganglia (DRG), sensory nerves, dorsal columns and other central nervous structures. A dying-back mechanism has been proposed to explain the peripheral neuropathy and neuropathology. In addition, affected individuals have non-neuronal symptoms such as diabetes mellitus or glucose intolerance. To go further in the understanding of the pathogenic mechanisms of neuropathy and diabetes associated with the disease, we have investigated the humanized mouse YG8R model of FRDA. By bio…

0301 basic medicineNervous systemAgingPathologylcsh:MedicineMedicine (miscellaneous)Mice0302 clinical medicineImmunology and Microbiology (miscellaneous)Ganglia SpinalInsulin-Secreting CellsInsulin SecretionInsulinMuscle spindleDorsal root gangliaCellular SenescenceDiabetisbiologyMusclesDiabetesAnatomyMitochondria3. Good healthmedicine.anatomical_structureSistema nerviós simpàticDying-back neuropathyPeripheral nervous systemCell senescencemedicine.symptomOxidation-Reductionlcsh:RB1-214Research ArticleSenescencemedicine.medical_specialtyAtaxiaNeuroscience (miscellaneous)Friedreich’s ataxiaNeuropathologyGeneral Biochemistry Genetics and Molecular BiologyPàncreesMalalties del sistema nerviós03 medical and health sciencesPeripheral Nervous Systemlcsh:PathologymedicineAnimalsHumansPancreasIslet of Langerhanslcsh:R302Friedreich's ataxiaNervous system Diseasesmedicine.diseaseAxonsMice Inbred C57BLDisease Models Animal030104 developmental biologyPeripheral neuropathyFriedreich AtaxiaSympathetic nervous systemMutationHumanized mouseFrataxinbiology.proteinEnergy Metabolism030217 neurology & neurosurgeryDisease Models & Mechanisms
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Stem Cells and Other Emerging Agents as Innovative "Drugs" in Neurodegenerative Diseases: Benefits and Limitations.

2018

The brain has a limited process of repair/regeneration linked to the restricted and localized activity of neuronal stem cells. Consequently, it shows a reduced capacity to counteract the age-related loss of neural and glial cells and to repair the consequent injuries/lesions of nervous system. This progressively determines nervous dysfunction and onset/progression of neurodegenerative diseases, which represent a serious social (and economic) problem of our populations. Thus, the research of efficient treatments is encouraged. Stem cell therapy might represent a solution. Today, it, indeed, represents the object of intensive research with the hope of using it, in a near future, as effective …

0301 basic medicineNervous systemAgingPathologymedicine.medical_specialtyself‐repair/regenerative processmedicine.medical_treatmentbrainneurodegenerative pathologiestem cell therapyinnovative intervention measures03 medical and health sciences0302 clinical medicineIntervention (counseling)medicineSettore MED/05 - Patologia ClinicaAnimalsHumansbrain self‐repair/regenerative process innovative intervention measuresbusiness.industryRegeneration (biology)Stem CellsNeurodegenerative DiseasesStem-cell therapyneuronal stem cell030104 developmental biologymedicine.anatomical_structureTreatment Outcomeself-repair/regenerative proceGeriatrics and GerontologyStem cellbusinessNeuroscience030217 neurology & neurosurgeryinnovative intervention measureStem Cell TransplantationRejuvenation research
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The Role of SVZ Stem Cells in Glioblastoma

2019

As most common primary brain cancer, glioblastoma is also the most aggressive and malignant form of cancer in the adult central nervous system. Glioblastomas are genetic and transcriptional heterogeneous tumors, which in spite of intensive research are poorly understood. Over the years conventional therapies failed to affect a cure, resulting in low survival rates of affected patients. To improve the clinical outcome, an important approach is to identify the cells of origin. One potential source for these are neural stem cells (NSCs) located in the subventricular zone, which is one of two niches in the adult nervous system where NSCs with the capacity of self-renewal and proliferation resid…

0301 basic medicineNervous systemCancer ResearchSubventricular zoneReviewBiologylcsh:RC254-282brain tumor stem cells03 medical and health sciences0302 clinical medicineCancer stem cellmedicineProgenitor cellneural stem cellstherapyNeurogenesisglioblastomasubventricular zoneCancerlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseNeural stem cellnervous system diseasesneurogenesis030104 developmental biologymedicine.anatomical_structurenervous systemOncology030220 oncology & carcinogenesisCancer researchStem cellCancers
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Homeostatic interplay between electrical activity and neuronal apoptosis in the developing neocortex

2017

An intriguing feature of nervous system development in most animal species is that the initial number of generated neurons is higher than the number of neurons incorporated into mature circuits. A substantial portion of neurons is indeed eliminated via apoptosis during a short time window - in rodents the first two postnatal weeks. While it is well established that neurotrophic factors play a central role in controlling neuronal survival and apoptosis in the peripheral nervous system (PNS), the situation is less clear in the central nervous system (CNS). In postnatal rodent neocortex, the peak of apoptosis coincides with the occurrence of spontaneous, synchronous activity patterns. In this …

0301 basic medicineNervous systemCentral nervous systemApoptosisNeocortexBiologyMembrane Potentials03 medical and health sciences0302 clinical medicineNeurotrophic factorsmedicineAnimalsHumansNeuronsNeocortexGeneral Neuroscience030104 developmental biologymedicine.anatomical_structurenervous systemApoptosisCerebral cortexPeripheral nervous systemSynapsesCalciumNeuroscience030217 neurology & neurosurgeryHomeostasisNeuroscience
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Profilin 1 delivery tunes cytoskeletal dynamics toward CNS axon regeneration

2020

After trauma, regeneration of adult CNS axons is abortive, causing devastating neurologic deficits. Despite progress in rehabilitative care, there is no effective treatment that stimulates axonal growth following injury. Using models with different regenerative capacities, followed by gain- and loss-of-function analysis, we identified profilin 1 (Pfn1) as a coordinator of actin and microtubules (MTs), powering axonal growth and regeneration. In growth cones, Pfn1 increased actin retrograde flow, MT growth speed, and invasion of filopodia by MTs, orchestrating cytoskeletal dynamics toward axonal growth. In vitro, active Pfn1 promoted MT growth in a formin-dependent manner, whereas localizati…

0301 basic medicineNervous systemGrowth ConesNeuromuscular Junctionmacromolecular substancesGlial scar03 medical and health sciencesMiceProfilins0302 clinical medicineTransduction GeneticmedicineAnimalsAxonGrowth coneCytoskeletonSpinal Cord InjuriesMice KnockoutbiologyRegeneration (biology)General MedicineGenetic TherapyDependovirusSciatic NerveCell biologyNerve Regeneration030104 developmental biologymedicine.anatomical_structurenervous system030220 oncology & carcinogenesisForminsbiology.proteinSciatic nerveFilopodiaResearch Article
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Role of RAS mutation status as a prognostic factor for patients with advanced colorectal cancer treated with first-line chemotherapy based on fluorop…

2016

The role of Kirsten rat sarcoma viral oncogene homolog (KRAS) and neuroblastoma RAS viral oncogene homolog (NRAS) mutations as negative predictors for anti-epidermal growth factor receptor (EGFR) therapies in metastatic colorectal cancer (CRC) has been firmly established. However, whether the RAS mutation status plays a role as a biomarker for anti-vascular endothelial growth factor (VEGF) treatment remains controversial. Data from 93 CRC patients who received first-line cytotoxic chemotherapy with fluoropyrimidines and oxaliplatin, with or without bevacizumab, were analyzed. We investigated the association between the RAS mutation status and clinical outcomes in terms of response rate, pro…

0301 basic medicineNeuroblastoma RAS viral oncogene homologOncologyCancer Researchmedicine.medical_specialtyBevacizumabColorectal cancermedicine.medical_treatmentmedicine.disease_cause03 medical and health sciences0302 clinical medicineInternal medicinemedicineChemotherapyOncogenebusiness.industryCancerArticlesmedicine.diseaseOxaliplatin030104 developmental biologyOncology030220 oncology & carcinogenesisKRASbusinessmedicine.drugMolecular and Clinical Oncology
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How to Deal with Second Line Dilemma in Metastatic Colorectal Cancer? A Systematic Review and Meta-Analysis

2019

Monoclonal antibodies targeting epidermal growth factor receptor (EGFR) or vascular endothelial growth factor (VEGF) have demonstrated efficacy with chemotherapy (CT) as second line treatment for metastatic colorectal cancer (mCRC). The right sequence of the treatments in all RAS (KRAS/NRAS) wild type (wt) patients has not precisely defined. We evaluated the impact of aforementioned targeted therapies in second line setting, analyzing efficacy and safety data from phase III clinical trials. We performed both direct and indirect comparisons between anti-EGFR and anti-VEGF. Outcomes included disease control rate (DCR), objective response rate (ORR), progression-free survival (PFS), overall su…

0301 basic medicineNeuroblastoma RAS viral oncogene homologOncologyCancer Researchmedicine.medical_specialtytargeted agentsColorectal cancermedicine.medical_treatmentEGFRPopulationPhases of clinical researchcolorectal cancerReviewmedicine.disease_causelcsh:RC254-282meta-analysi03 medical and health sciences0302 clinical medicineInternal medicinemedicineEpidermal growth factor receptoreducationChemotherapyeducation.field_of_studybiologybusiness.industrysequencemedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensVEGFmeta-analysis030104 developmental biologyOncology030220 oncology & carcinogenesisMeta-analysisbiology.proteinKRASsecond linebusinessCancers
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Impact of BRAF and RAS mutations on first-line efficacy of FOLFIRI plus cetuximab versus FOLFIRI plus bevacizumab: analysis of the FIRE-3 (AIO KRK-03…

2017

Abstract Background RAS and BRAF mutations have been identified as negative prognostic factors in metastatic colorectal cancer. Efficacy of 5-fluorouracil, leucovorin, irinotecan (FOLFIRI) plus bevacizumab in patients with RAS-mutant tumours needs to be further evaluated. Whether to treat patients with BRAF-mutant tumours with either bevacizumab or anti-epidermal growth factor receptor (EGFR) antibodies remains unclear. Methods Patients treated within the FIRE-3 trial were retrospectively tested for BRAF and RAS mutations using formalin fixated paraffin embedded (FFPE) tumour material applying pyrosequencing for KRAS and NRAS exon 2, 3 and 4 mutations as far as for BRAF mutations. Survival …

0301 basic medicineNeuroblastoma RAS viral oncogene homologOncologyMaleProto-Oncogene Proteins B-rafCancer Researchmedicine.medical_specialtyBevacizumabColorectal cancerLeucovorinCetuximabmedicine.disease_causeProto-Oncogene Proteins p21(ras)03 medical and health sciences0302 clinical medicineInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansneoplasmsSurvival analysisAgedRetrospective StudiesCetuximabbusiness.industryLiver NeoplasmsExonsMiddle Agedmedicine.diseasedigestive system diseasesIrinotecanBevacizumab030104 developmental biologyTreatment OutcomeOncology030220 oncology & carcinogenesisMutationFOLFIRICamptothecinFemaleKRASFluorouracilbusinessColorectal Neoplasmsmedicine.drugEuropean journal of cancer (Oxford, England : 1990)
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Does bevacizumab impact anti-EGFR therapy efficacy in metastatic colorectal cancer?

2016

IF 5.008; International audience; Anti-EGFR therapy and antiangiogenic therapies are used alone or in combination with chemotherapies to improve survival in metastatic colorectal cancer. However, it is unknown whether pretreatment with antiangiogenic therapy could impact on the efficacy of anti-EGFR therapy. We selected one hundred and twenty eight patients diagnosed with advanced colorectal cancer with a KRAS and NRAS unmutated tumor. These patients were treated with cetuximab or panitumumab alone or with chemotherapy as second or third-line. Univariate and multivariate Cox model analysis were performed to estimate the effect of a previous bevacizumab regimen on progression free survival a…

0301 basic medicineNeuroblastoma RAS viral oncogene homologOncologyMaleVascular Endothelial Growth Factor AColorectal cancerCetuximabAngiogenesis Inhibitorsmedicine.disease_causeTrialGTP PhosphohydrolasesRas mutations[ SDV.CAN ] Life Sciences [q-bio]/Cancer0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsDrug InteractionsAged 80 and overCetuximabPanitumumabAntibodies MonoclonalMiddle Aged3. Good healthErbB ReceptorsOncology030220 oncology & carcinogenesisFemaleKRASColorectal Neoplasms1st-Line treatmentmedicine.drugResearch PaperAdultSTAT3 Transcription Factormedicine.medical_specialtyBevacizumabAntineoplastic Agents[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologybevacizumabIrinotecanDisease-Free SurvivalTumor angiogenesisProto-Oncogene Proteins p21(ras)03 medical and health sciencesVEGFRInternal medicineCell Line TumormedicinePanitumumabHumansEndothelial growth-FactorChemotherapyProgression-free survivalAgedbusiness.industry[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMembrane Proteinsmetastatic colon cancerStat-3medicine.diseaseVascular Endothelial Growth Factor Receptor-2IrinotecanRandomized phase-III030104 developmental biologyanti-EGFR therapyFactor receptorCaco-2 Cellsbusiness
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