Search results for "model [particle]"

showing 10 items of 1261 documents

Remarks on GRN-type systems

2020

Systems of ordinary differential equations that appear in gene regulatory networks theory are considered. We are focused on asymptotical behavior of solutions. There are stable critical points as well as attractive periodic solutions in two-dimensional and three-dimensional systems. Instead of considering multiple parameters (10 in a two-dimensional system) we focus on typical behaviors of nullclines. Conclusions about possible attractors are made.

0301 basic medicineComputer sciencelcsh:RGeneral EngineeringGene regulatory networkattractorslcsh:MedicineType (model theory)Nullcline03 medical and health sciences030104 developmental biology0302 clinical medicineordinary differential equations030220 oncology & carcinogenesisOrdinary differential equationAttractorgenetic regulatory networksApplied mathematicslcsh:Qlcsh:ScienceFocus (optics)4open
researchProduct

The Problem of Mental Action: Predictive Control Without Sensory Sheets by Metzinger, T. (2017). In Philosophy and Predictive Processing, eds T. Metz…

2018

A growing number of studies on the acquisition of lexical tone by adult learners have revealed that factors such as language background, musical experience, cognitive abilities, and neuroanatomy all play a role in determining tone learning success. On the basis of these findings, it has been argued that the effectiveness of tone learning in adulthood depends on individual differences in these factors. However, it is not clear whether similar individual differences play an analogous role in tone learning in childhood. Indeed, relatively few studies have made comparisons between how adults and children learn lexical tones. Here, we review recent developments for tone learning in both adults a…

0301 basic medicineControl theory (sociology)General Commentarylcsh:BF1-990predictive processingSensory systemmental actioncontrol theory03 medical and health sciencesModel predictive controllcsh:Psychology030104 developmental biology0302 clinical medicineactive inferenceaction-oriented cognitionPsychologyPsychologyMental action030217 neurology & neurosurgeryGeneral PsychologyCognitive psychologyFrontiers in Psychology
researchProduct

Apoptosis induced by a HIPK2 full-length-specific siRNA is due to off-target effects rather than prevalence of HIPK2-Δe8 isoform

2017

Small interfering RNAs (siRNAs) are widely used to study gene function and extensively exploited for their potential therapeutic applications. HIPK2 is an evolutionary conserved kinase that binds and phosphorylates several proteins directly or indirectly related to apoptosis. Recently, an alternatively spliced isoform skipping 81 nucleotides of exon 8 (Hipk2-Δe8) has been described. Selective depletion of Hipk2 full-length (Hipk2-FL) with a specific siRNA that spares the Hipk2-Δe8 isoform has been shown to strongly induce apoptosis, suggesting an unpredicted dominant-negative effect of Hipk2-FL over the Δe8 isoform. From this observation, we sought to take advantage and assessed the therape…

0301 basic medicineGene isoformMaleProgrammed cell deathSmall interfering RNACell SurvivalBlotting WesternMice Nudecolorectal cancerApoptosisHIPK2BiologyProtein Serine-Threonine KinasesGene Expression Regulation Enzymologic03 medical and health sciencesExonRNA interferenceCell Line TumorAnimalsHumansViability assayoff-target effectCell Line TransformedSettore MED/04 - Patologia GeneraleKinaseReverse Transcriptase Polymerase Chain ReactionAlternative splicingalternative splicing isoformoff-target effectsExonsHCT116 CellsMolecular biologyXenograft Model Antitumor AssaysCell biologyGene Expression Regulation NeoplasticIsoenzymesAlternative Splicing030104 developmental biologyRNAi TherapeuticsOncologyalternative splicing isoformsNeoplastic Stem CellsRNA InterferenceHIPK2; alternative splicing isoforms; colorectal cancer; off-target effects; siRNA therapeutic applicationsiRNA therapeutic applicationCarrier ProteinsColorectal NeoplasmsGene DeletionResearch Paper
researchProduct

miR-22 suppresses DNA ligase III addiction in multiple myeloma

2019

Multiple myeloma (MM) is a hematologic malignancy characterized by high genomic instability. Here we provide evidence that hyper-activation of DNA ligase III (LIG3) is crucial for genomic instability and survival of MM cells. LIG3 mRNA expression in MM patients correlates with shorter survival and even increases with more advanced stage of disease. Knockdown of LIG3 impairs MM cells viability in vitro and in vivo, suggesting that neoplastic plasmacells are dependent on LIG3-driven repair. To investigate the mechanisms involved in LIG3 expression, we investigated the post-transcriptional regulation. We identified miR-22-3p as effective negative regulator of LIG3 in MM. Enforced expression of…

0301 basic medicineGenome instabilityCancer ResearchmiR-22 LIG3DNA repairDNA damageDNA repairApoptosisLIG3ArticleDNA Ligase ATP03 medical and health sciences0302 clinical medicinemicroRNABiomarkers TumorTumor Cells CulturedHumansPoly-ADP-Ribose Binding ProteinsCell ProliferationmiRNAchemistry.chemical_classificationRegulation of gene expressionGene knockdownDNA ligaseLeukemiamicroRNAChemistryHematologyPrognosisXenograft Model Antitumor AssaysGene Expression Regulation Neoplasticmultiple myelomaMicroRNAs030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchpharmacologyDNA DamageLeukemia
researchProduct

Modulating endothelial adhesion and migration impacts stem cell therapies efficacy

2020

Abstract Background Limited knowledge of stem cell therapies` mechanisms of action hampers their sustainable implementation into the clinic. Specifically, the interactions of transplanted stem cells with the host vasculature and its implications for their therapeutic efficacy are not elucidated. We tested whether adhesion receptors and chemokine receptors on stem cells can be functionally modulated, and consequently if such modulation may substantially affect therapeutically relevant stem cell interactions with the host endothelium. Methods We investigated the effects of cationic molecule polyethylenimine (PEI) treatment with or without nanoparticles on the functions of adhesion receptors a…

0301 basic medicineHomingCell- and Tissue-Based TherapyMedizinCCR4lcsh:MedicineStem cellsMiceChemokine receptor0302 clinical medicineCell MovementCells CulturedMigrationlcsh:R5-920Cell DifferentiationAdhesion; Glioma; Homing; Migration; Stem cells; StrokeGeneral MedicineGlioma3. Good healthCell biologyStrokemedicine.anatomical_structureCellular Microenvironment030220 oncology & carcinogenesisAdhesionStem celllcsh:Medicine (General)Research PaperEndotheliumBiologyMesenchymal Stem Cell TransplantationGeneral Biochemistry Genetics and Molecular BiologyCell LineImmunophenotyping03 medical and health sciencesIn vivoCell AdhesionmedicineAnimalsHumansEndotheliumMesenchymal stem celllcsh:RMesenchymal Stem CellsXenograft Model Antitumor AssaysIn vitroRatsDisease Models Animal030104 developmental biologyBiomarkersStem Cell TransplantationHoming (hematopoietic)EBioMedicine
researchProduct

Noncanonical GLI1 signaling promotes stemness features and in vivo growth in lung adenocarcinoma

2016

Aberrant Hedgehog/GLI signaling has been implicated in a diverse spectrum of human cancers, but its role in lung adenocarcinoma (LAC) is still under debate. We show that the downstream effector of the Hedgehog pathway, GLI1, is expressed in 76% of LACs, but in roughly half of these tumors, the canonical pathway activator, Smoothened, is expressed at low levels, possibly owing to epigenetic silencing. In LAC cells including the cancer stem cell compartment, we show that GLI1 is activated noncanonically by MAPK/ERK signaling. Different mechanisms can trigger the MAPK/ERK/GLI1 cascade including KRAS mutation and stimulation of NRP2 by VEGF produced by the cancer cells themselves in an autocrin…

0301 basic medicineMAPK/ERK pathwayCancer ResearchLung NeoplasmsPyridinesPyridineMitogen-Activated Protein Kinase KinaseMice SCIDMiceCarcinoma Non-Small-Cell LungRNA Small InterferingNon-Small-Cell LungMolecular Biology; Genetics; Cancer ResearchTumorbiologyintegumentary systemHedgehog signaling pathwayCell biologyNeoplastic Stem CellsFemaleRNA InterferenceOriginal ArticleHumanXenograft Model Antitumor AssayAdenocarcinomaSCIDSmall InterferingZinc Finger Protein GLI1Cell LineProto-Oncogene Proteins p21(ras)Adenocarcinoma; Animals; Carcinoma Non-Small-Cell Lung; Cell Line Tumor; Female; Humans; Lung Neoplasms; Mice; Mice SCID; Mitogen-Activated Protein Kinase Kinases; Neoplastic Stem Cells; Neuropilin-2; Proto-Oncogene Proteins p21(ras); Pyridines; Pyrimidines; RNA Interference; RNA Small Interfering; Xenograft Model Antitumor Assays; Zinc Finger Protein GLI1; Molecular Biology; Genetics; Cancer Research03 medical and health sciencesParacrine signallingGeneticSettore MED/04 - PATOLOGIA GENERALEstem cellsCancer stem cellGLI1Cell Line TumorGeneticsAnimalsHumansAutocrine signallingMolecular BiologyMitogen-Activated Protein Kinase KinasesSettore MED/06 - ONCOLOGIA MEDICAAnimalCarcinomaXenograft Model Antitumor AssaysNeuropilin-2Lung Neoplasmlung cancer030104 developmental biologyPyrimidinesPyrimidineCancer cellbiology.proteinRNANeoplastic Stem CellSmoothened
researchProduct

Autocrine CCL5 Effect Mediates Trastuzumab Resistance by ERK Pathway Activation in HER2-Positive Breast Cancer.

2020

Abstract HER2-positive breast cancer is currently managed with chemotherapy in combination with specific anti-HER2 therapies, including trastuzumab. However, a high percentage of patients with HER2-positive tumors do not respond to trastuzumab (primary resistance) or either recur (acquired resistance), mostly due to molecular alterations in the tumor that are either unknown or undetermined in clinical practice. Those alterations may cause the tumor to be refractory to treatment with trastuzumab, promoting tumor proliferation and metastasis. Using continued exposure of a HER2-positive cell line to trastuzumab, we generated a model of acquired resistance characterized by increased expression …

0301 basic medicineMAPK/ERK pathwayCancer ResearchMAP Kinase Signaling SystemReceptor ErbB-2medicine.medical_treatmentMice NudeApoptosisBreast NeoplasmsCCL5Metastasis03 medical and health sciencesMice0302 clinical medicineBreast cancerAntineoplastic Agents ImmunologicalTrastuzumabmedicineBiomarkers TumorTumor Cells CulturedGene silencingAnimalsHumansskin and connective tissue diseasesAutocrine signallingneoplasmsChemokine CCL5Neoadjuvant therapyCell Proliferationbusiness.industryGene Expression ProfilingTrastuzumabmedicine.diseaseXenograft Model Antitumor AssaysGene Expression Regulation NeoplasticAutocrine Communication030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchFemalebusinessmedicine.drugMolecular cancer therapeutics
researchProduct

A PTEN inhibitor displays preclinical activity against hepatocarcinoma cells

2016

Phosphatase and tensin homolog (PTEN) gene is considered a tumor suppressor gene. However, PTEN mutations rarely occur in hepatocellular carcinoma (HCC), whereas heterozygosity of PTEN, resulting in reduced PTEN expression, has been observed in 32–44% of HCC patients. In the present study, we investigated the effects of the small molecule PTEN inhibitor VO-OHpic in HCC cells. VO-OHpic inhibited cell viability, cell proliferation and colony formation, and induced senescence-associated β-galactosidase activity in Hep3B (low PTEN expression) and to a lesser extent in PLC/PRF/5 (high PTEN expression) cells, but not in PTEN-negative SNU475 cells. VO-OHpic synergistically inhibited cell viability…

0301 basic medicineMAPK/ERK pathwayPTENCarcinoma HepatocellularsenescenceTumor suppressor geneCell SurvivalMicePhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineReportOrganometallic CompoundsAnimalsHumansPTENTensinViability assayHCCProtein kinase BMolecular BiologyPI3K/AKT/mTOR pathwayCell ProliferationbiologyCell growthTOR Serine-Threonine KinasesAKTLiver NeoplasmsPTEN PhosphohydrolaseCell BiologySorafenibXenograft Model Antitumor Assaysdigestive system diseasesVO-OHpicGene Expression Regulation Neoplastic030104 developmental biology030220 oncology & carcinogenesisbiology.proteinCancer researchSignal TransductionDevelopmental Biology
researchProduct

Elimination of large tumors in mice by mRNA-encoded bispecific antibodies.

2016

The potential of bispecific T cell-engaging antibodies is hindered by manufacturing challenges and short serum half-life. We circumvented these limitations by treating mice with in vitro-transcribed pharmacologically optimized, nucleoside-modified mRNA encoding the antibody. We achieved sustained endogenous synthesis of the antibody, which eliminated advanced tumors as effectively as the corresponding purified bispecific antibody. Because manufacturing of pharmaceutical mRNA is fast, this approach could accelerate the clinical development of novel bispecific antibodies.

0301 basic medicineMaleBispecific antibodyT-LymphocytesImmunoblottingEndogenyEnzyme-Linked Immunosorbent AssayIn Vitro TechniquesGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesMiceMice Inbred NODCell Line TumorNeoplasmsAntibodies BispecificMedicineAnimalsHumansRNA MessengerMessenger RNAMice Inbred BALB Cbiologybusiness.industryRNAGeneral MedicineMolecular biologyImmunohistochemistryXenograft Model Antitumor AssaysTumor Burden030104 developmental biologyCell cultureDrug deliveryLuminescent Measurementsbiology.proteinImmunohistochemistryCytokinesFemaleAntibodybusinessNature medicine
researchProduct

miR-21 antagonism abrogates Th17 tumor promoting functions in multiple myeloma

2020

Multiple myeloma (MM) is tightly dependent on inflammatory bone marrow microenvironment. IL-17 producing CD4+ T cells (Th17) sustain MM cells growth and osteoclasts-dependent bone damage. In turn, Th17 differentiation relies on inflammatory stimuli. Here, we investigated the role of miR-21 in Th17-mediated MM tumor growth and bone disease. We found that early inhibition of miR-21 in naive T cells (miR-21i-T cells) impaired Th17 differentiation in vitro and abrogated Th17-mediated MM cell proliferation and osteoclasts activity. We validated these findings in NOD/SCID-g-NULL mice, intratibially injected with miR-21i-T cells and MM cells. A Pairwise RNAseq and proteome/phosphoproteome analysis…

0301 basic medicineMaleCancer ResearchBone diseaseApoptosisBone NeoplasmsNodMice SCIDBone NeoplasmT-Lymphocytes RegulatoryTh17 Cell03 medical and health sciencesMice0302 clinical medicineDownregulation and upregulationgammopathiesMice Inbred NODmedicineTumor Cells CulturedTumor MicroenvironmentBiomarkers TumorAnimalsHumansMultiple myelomaCell ProliferationChemistryCell growthAnimalApoptosiHematologymedicine.diseasePrognosisXenograft Model Antitumor AssaysIn vitroGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCase-Control StudiesCancer researchTh17 CellsBone marrowAntagonismCase-Control StudieMultiple Myeloma
researchProduct