Search results for "INHIBITOR"

showing 10 items of 3742 documents

Developmental effects of the protein kinase inhibitor kenpaullone on the sea urchin embryo

2017

The selection and validation of bioactive compounds require multiple approaches, including in-depth analyses of their biological activity in a whole-animal context. We exploited the sea urchin embryo in a rapid, medium-scale range screening to test the effects of the small synthetic kinase inhibitor kenpaullone. We show that sea urchin embryos specifically respond to this molecule depending on both dose and timing of administration. Phenotypic effects of kenpaullone are not immediately visible, since this molecule affects neither the fertilization nor the spatial arrangement of blastomeres at early developmental stages. Nevertheless, kenpaullone exposure from the beginning of embryogenesis …

0301 basic medicineSea urchinEmbryo NonmammalianIndolesPhysiologymedicine.drug_classHealth Toxicology and MutagenesisMesenchymeSettore BIO/11 - Biologia MolecolareContext (language use)ToxicologyBiochemistry03 medical and health sciencesbiology.animalBotanymedicineAnimalsEpithelial–mesenchymal transitionProtein Kinase InhibitorsSea urchinKinase inhibitorMolecular StructurebiologyEmbryogenesisGene Expression Regulation DevelopmentalCell BiologyGeneral MedicineBlastomereBenzazepinesProtein kinase inhibitorEmbryonic stem cellKenpaulloneCell biology030104 developmental biologymedicine.anatomical_structureEmbryonic developmentembryonic structuresParacentrotusGene expressionComparative Biochemistry and Physiology Part C: Toxicology & Pharmacology
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p53 and p53-related mediators PAI-1 and IGFBP-3 are downregulated in peripheral blood mononuclear cells of HIV-patients exposed to non-nucleoside rev…

2019

The improved effectiveness and safety of the combined antiretroviral therapy (cART) has largely diminished mortality and AIDS-defining morbidity of HIV-patients. Nevertheless, chronic age-related diseases in these individuals are more common and their underlying pathogenic mechanisms of these actions seem to involve accelerated aging and enhanced inflammation. The present study explores markers of these processes in a heterogenous Spanish HIV cohort using peripheral blood samples of HIV-patients and matched uninfected controls. We isolated periheral blood mononuclear cells (PBMCs) and i) compared the expression of a panel of 14 genes related to inflammation and senescence in PBMCs of HIV-pa…

0301 basic medicineSenescenceAdultMaleAnti-HIV Agents030106 microbiologyDown-RegulationInflammationHIV InfectionsCCL2Peripheral blood mononuclear cell03 medical and health sciencesVirologyAntiretroviral Therapy Highly ActivePlasminogen Activator Inhibitor 1medicineCXCL10HumansCellular SenescencePharmacologyInflammationbusiness.industryInterleukin-6Interleukin-18virus diseasesMiddle AgedCCL20Chemokine CXCL10030104 developmental biologyInsulin-Like Growth Factor Binding Protein 3ImmunologyLeukocytes MononuclearReverse Transcriptase InhibitorsInterleukin 18Tumor necrosis factor alphaFemalemedicine.symptomTumor Suppressor Protein p53businessAntiviral research
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Anti-PCSK9 treatment: is ultra-low low-density lipoprotein cholesterol always good?

2018

Anti-PCSK9 (proprotein convertase subtilisin kexin 9) monoclonal antibodies (Mab) are novel, potent lipid-lowering drugs. They demonstrated to improve the lipid profile in high cardiovascular risk patients. Anti-PCSK9 Mab inhibit the targeted low-density lipoprotein (LDL)-receptor degradation induced by PCSK9 protein and are able to reduce LDL cholesterol (LDL-C) levels on top of conventional lipid-lowering therapy. Though these drugs proved to be very safe in the short-term, little is known about the possible long-term effects, due to the short period of their marketing. The genetic low cholesterol syndromes (LCS) represent the natural models of the lipid-lowering anti-PCSK9 therapy, and a…

0301 basic medicineSerine Proteinase InhibitorsTime FactorsPhysiologymedicine.drug_class030204 cardiovascular system & hematologyPharmacologyMonoclonal antibodyRisk Assessment03 medical and health sciencesPCSK9 Genechemistry.chemical_compound0302 clinical medicineRisk FactorsPhysiology (medical)Diabetes mellitusmedicineAnimalsHumansDyslipidemiasmedicine.diagnostic_testbusiness.industryCholesterolPCSK9Anticholesteremic AgentsPCSK9 InhibitorsAntibodies MonoclonalCholesterol LDLmedicine.diseaseFatty LiverHypocholesterolemia030104 developmental biologyTreatment OutcomechemistryDiabetes Mellitus Type 2lipids (amino acids peptides and proteins)Proprotein Convertase 9Cardiology and Cardiovascular MedicineLipid profilebusinessCognition DisordersBiomarkersLipoproteinCardiovascular research
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Gut microbiota and cancer: How gut microbiota modulates activity, efficacy and toxicity of antitumoral therapy

2019

Gut microbiota is involved in gastrointestinal carcinogenesis. Also, it modulates the activity, efficacy and toxicity of several chemotherapy agents, such as gemcitabine, cyclophosphamide, irinotecan, cisplatin and 5-Fluorouracil, and target therapy, such as tyrosine kinase inhibitors. More recently, accumulating data suggest that the composition of gut microbiota may also affect efficacy and toxicity of cancer immunotherapy. Therefore, the manipulation of gut microbiota through antibiotics, probiotics, prebiotics or fecal transplantation has been investigating with the aim to improve efficacy and mitigate toxicity of anticancer drugs.

0301 basic medicineSettore MED/06 - Oncologia Medicamedicine.drug_class5-Fluorouracilmedicine.medical_treatmentAntibioticsAntineoplastic AgentsImmune checkpoint inhibitorGut floraPharmacologyIrinotecandigestive systemImmune checkpoint inhibitors03 medical and health sciences0302 clinical medicineCancer immunotherapyNeoplasmsmedicineAnimalsHumansCyclophosphamide5-Fluorouracil; Cisplatin; Cyclophosphamide; Gemcitabine; Immune checkpoint inhibitors; Irinotecan; Microbiota; Tyrosine kinase inhibitorsTyrosine kinase inhibitorsChemotherapybiologybusiness.industryMicrobiotaCancerHematologyFecal Microbiota Transplantationbiology.organism_classificationmedicine.diseaseGemcitabineGemcitabineGastrointestinal MicrobiomeIrinotecan030104 developmental biologyOncology030220 oncology & carcinogenesisToxicityImmunotherapyCisplatinbusinessmedicine.drugCritical Reviews in Oncology/Hematology
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Characterization of a mutant form of human apolipoprotein B (Thr26_Tyr27del) associated with familial hypobetalipoproteinemia

2016

We have previously identified a deletion mutant of human apoB [apoB (Thr26_Tyr27del)] in a subject with primary hypobetalipoproteinemia. The present study determined the effect of Thr26_Tyr27del mutation on apoB secretion using transfected McA-RH7777 cells. Transient or stable transfection of apoB-48 containing the Thr26_Tyr27del mutation showed drastically reduced secretion of the mutant as compared to wild-type apoB-48. No lipoproteins containing the mutant apoB-48 were secreted into the medium. Incubation of transfected cells in a lipid-rich medium in the presence of cycloheximide showed rapid turnover of cell-associated mutant apoB-48 as compared to that of wild-type apoB-48. Immunofluo…

0301 basic medicineSettore MED/09 - Medicina InternaTime FactorsApolipoprotein B-48 secretionApolipoprotein BMutantDNA Mutational AnalysisApolipoprotein B mutation Apolipoprotein B-48 secretion Hypobetalipoproteinemia Proteasomal degradation030204 cardiovascular system & hematologymedicine.disease_causeEndoplasmic ReticulumHypobetalipoproteinemiaschemistry.chemical_compound0302 clinical medicineProteasomal degradationProteolysiSequence DeletionMutationbiologyMedicine (all)TransfectionProteasome InhibitorPhenotypeBiochemistryApolipoprotein B-100lipids (amino acids peptides and proteins)Proteasome InhibitorsHumanHeterozygoteProteasome Endopeptidase ComplexTime FactorCycloheximideTransfectiondigestive systemCell LineDNA Mutational Analysi03 medical and health sciencesmedicineHumansSecretionGenetic Predisposition to DiseaseMolecular BiologyEndoplasmic reticulumnutritional and metabolic diseasesCell Biologymedicine.diseaseMolecular biology030104 developmental biologychemistryProteolysisbiology.proteinHypobetalipoproteinemiaApolipoprotein B mutationApolipoprotein B-48Hypobetalipoproteinemia
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PACAP38 and PAC1 receptor blockade: a new target for headache?

2018

Abstract Pituitary adenylate cyclase activating polypeptide-38 (PACAP38) is a widely distributed neuropeptide involved in neuroprotection, neurodevelopment, nociception and inflammation. Moreover, PACAP38 is a potent inducer of migraine-like attacks, but the mechanism behind this has not been fully elucidated. Migraine is a neurovascular disorder, recognized as the second most disabling disease. Nevertheless, the antibodies targeting calcitonin gene-related peptide (CGRP) or its receptor are the only prophylactic treatment developed specifically for migraine. These antibodies have displayed positive results in clinical trials, but are not effective for all patients; therefore, new pharmacol…

0301 basic medicineSide effectPAC1 receptorMigraine DisordersMigraine Disorders/drug therapylcsh:MedicinePituitary Adenylate Cyclase-Activating Polypeptide/antagonists & inhibitorsReview ArticleTriptansPharmacologyCalcitonin gene-related peptidePACAPNeuroprotectionmigraine; PAC1 receptor; PACAP; prophylactic treatment; animals; disease models animal; headache; humans; migraine disorders; pituitary adenylate cyclase-activating polypeptide; receptors pituitary adenylate cyclase-activating polypeptide type I; neurology (clinical); anesthesiology and pain medicine03 medical and health sciences0302 clinical medicineAnimalsHumansMedicineMigraine treatmentReceptorMigraineHeadache/drug therapybusiness.industrylcsh:RHeadacheGeneral Medicinemedicine.disease3. Good healthBlockadeDisease Models Animal030104 developmental biologyAnesthesiology and Pain MedicineMigrainePituitary Adenylate Cyclase-Activating PolypeptideNeurology (clinical)businessProphylactic treatment030217 neurology & neurosurgeryReceptors Pituitary Adenylate Cyclase-Activating Polypeptide Type IReceptors Pituitary Adenylate Cyclase-Activating Polypeptide Type I/antagonists & inhibitorsmedicine.drugJournal of Headache and Pain
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GSK-3 in liver diseases: Friend or foe?

2020

Liver diseases, including hepatitis due to hepatitis B or C virus infection, non-alcoholic fatty liver disease, and hepatocellular carcinoma pose major challenges for overall health due to limited curative treatment options. Thus, there is an urgent need to develop new therapeutic strategies for the treatment of these diseases. A better understanding of the signaling pathways involved in the pathogenesis of liver diseases can help to improve the efficacy of emerging therapies, mainly based on pharmacological approaches, which influence one or more specific molecules involved in key signal transduction pathways. These emerging therapies are very promising for the prevention and treatment of …

0301 basic medicineSignaling pathwaysDruggabilityDiseaseBioinformaticsNon-alcoholic fatty liver disease (NAFLD)Glycogen Synthase Kinase 303 medical and health sciences0302 clinical medicineGSK-3Glycogen synthase kinase 3 (GSK-3)AnimalsHumansMedicineHepatitis B virus (HBV)Molecular Targeted TherapyEnzyme InhibitorsHepatocellular carcinoma (HCC)Molecular BiologyHepatitisbusiness.industryLiver DiseasesFatty liverDisease ManagementHepatitis C virus (HCV)Cell BiologyHepatitis Bmedicine.disease030104 developmental biologyGene Expression RegulationMultigene Family030220 oncology & carcinogenesisHepatocellular carcinomaHost-Pathogen InteractionsDisease SusceptibilitySignal transductionbusinessBiomarkersSignal TransductionBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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PCSK9-D374Y mediated LDL-R degradation can be functionally inhibited by EGF-A and truncated EGF-A peptides: An in vitro study.

2019

Abstract Background and aims Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to low density lipoprotein receptor (LDLR) through the LDLR epidermal growth factor-like repeat A (EGF-A) domain and induces receptor internalization and degradation. PCSK9 has emerged as a novel therapeutic target for hypercholesterolemia. Clinical studies with PCSK9 inhibiting antibodies have demonstrated strong LDL-c lowering effects, but other therapeutic approaches using small molecule inhibitors for targeting PCSK9 functions may offer supplementary therapeutic options. The aim of our study was to evaluate the effect of synthetic EGF-A analogs on mutated (D374Y) PCSK9-D374Y mediated LDLR degradatio…

0301 basic medicineSmall peptidesmedia_common.quotation_subject030204 cardiovascular system & hematologyDecoy strategyPCSK903 medical and health sciences0302 clinical medicineHumansInternalizationCells Culturedmedia_commonExpression vectorEpidermal Growth FactorChemistryPCSK9PCSK9 InhibitorsTransfectionProprotein convertasePCSK9 inhibitionIn vitroCell biologyEGF-A domain030104 developmental biologyLDLRReceptors LDLLDL receptorMutationKexinlipids (amino acids peptides and proteins)Proprotein Convertase 9Cardiology and Cardiovascular MedicineAtherosclerosis
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Sorafenib plus topotecan versus placebo plus topotecan for platinum-resistant ovarian cancer (TRIAS): a multicentre, randomised, double-blind, placeb…

2018

Summary Background Antiangiogenic therapy has known activity in ovarian cancer. The investigator-initiated randomised phase 2 TRIAS trial assessed the multi-kinase inhibitor sorafenib combined with topotecan and continued as maintenance therapy for platinum-resistant or platinum-refractory ovarian cancer. Methods We did a multicentre, double-blind, placebo-controlled, randomised, phase 2 trial at 20 sites in Germany. Patients (≥18 years) with platinum-resistant ovarian cancer previously treated with two or fewer chemotherapy lines for recurrent disease were stratified (first vs later relapse) in block sizes of four and randomly assigned (1:1) using a web-generated response system to topotec…

0301 basic medicineSorafenibAdultmedicine.medical_specialtyTime FactorsPerforation (oil well)Angiogenesis InhibitorsPlatinum CompoundsNeutropeniaPlaceboGastroenterologyDrug Administration Schedule03 medical and health sciences0302 clinical medicineMaintenance therapyDouble-Blind MethodInternal medicineGermanyAntineoplastic Combined Chemotherapy ProtocolsmedicineClinical endpointHumansProgression-free survivalProtein Kinase InhibitorsAgedOvarian Neoplasmsbusiness.industryMiddle AgedSorafenibmedicine.diseaseProgression-Free Survival030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisDisease ProgressionTopotecanFemaleTopoisomerase I InhibitorsbusinessTopotecanmedicine.drugThe Lancet. Oncology
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Trial Design and Endpoints in Hepatocellular Carcinoma: AASLD Consensus Conference

2020

Proper trial design is critical for the success of clinical investigations. Hepatocellular carcinoma (HCC) is a complex disease that has several unique properties. In 2008, after the approval of sorafenib, a panel of experts proposed guidelines for trial design and endpoints in HCC that have been instrumental during the last decade and provided a framework to allow an homogeneous analysis of reported investigations. Since then, several phase III studies have been reported and novel challenges have emerged. A panel of experts conveyed by AASLD organized a Special Topic Conference on trial design and endpoints to address those emerging challenges. This review summarizes the analysis and concl…

0301 basic medicineSorafenibmedicine.medical_specialtyCarcinoma HepatocellularConsensusEndpoint DeterminationMEDLINEDisease03 medical and health sciences0302 clinical medicinemedicineHumansProgression-free survivalChemoembolization TherapeuticLiquid biopsyIntensive care medicineAdverse effectImmune Checkpoint InhibitorsProtein Kinase InhibitorsClinical Trials as TopicHepatologybusiness.industryLiver NeoplasmsLiquid Biopsymedicine.diseaseLiver TransplantationClinical trial030104 developmental biologyResearch DesignHepatocellular carcinoma030211 gastroenterology & hepatologybusinessmedicine.drugHepatology
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