Search results for "RECEPTOR"

showing 10 items of 6990 documents

Regulation by oestrogens of tachykinin NK3 receptor expression in the rat uterus.

1997

The expression of the tachykinin NK3 receptor and its regulation by ovarian steroids were analyzed by reverse transcription-polymerase chain reaction (RT-PCR) in uteri from ovariectomized rats. A single transcript corresponding to the 325-bp product expected for the tachykinin NK3 receptor was detected in uteri from olive oil-treated (control) ovariectomized rats. The level of tachykinin NK3 receptor mRNA in progesterone-treated animals was similar to that observed in uteri from control ones. Tachykinin NK3 receptor mRNA levels were significantly smaller in uteri from oestrogen-treated ovariectomized rats, with approximately a 32-fold decrease. These findings suggest that oestrogen, but not…

medicine.medical_specialtyanimal structuresNk3 receptorDNA Complementarymedicine.drug_classOvariectomyUterusBiologydigestive systemcomplex mixturesPolymerase Chain ReactionInternal medicineGene expressionmedicineAnimalsRNA MessengerRats WistarProgesteronePharmacologyElectrophoresis Agar GelMessenger RNAurogenital systemmusculoskeletal neural and ocular physiologyUterusEstrogensReceptors Neurokinin-3RatsEndocrinologymedicine.anatomical_structureGene Expression RegulationEstrogenIn uteroRat uterusOvariectomized ratFemaleEuropean journal of pharmacology
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Vitellogenesis inhibition in Oncopeltus fasciatus females (Heteroptera: Lygaeidae) exposed to cadmium

2005

Abstract Newly moulted females of the insect Oncopeltus fasciatus were exposed to cadmium (Cd) dissolved in the drinking water (50–400 mg l −1 Cd) for 5 days. Cd exposure delayed ovarian maturation and inhibited egg production. Exposure to Cd, moreover, decreased hemolymph levels of the two major vitellogenin polypeptides of O. fasciatus , VG1 and VG2, in a concentration-dependent way, probably by a reduction in their synthesis. The ovarian levels of VG1 and VG2 were also decreased in Cd-exposed females. It was next investigated whether Cd effects might be a consequence of the endocrine disruption of vitellogenin synthesis, which is controlled by juvenile hormone (JH). JH replacement therap…

medicine.medical_specialtyanimal structuresPhysiologyFat Bodychemistry.chemical_elementHeteropteraVitellogeninsVitellogeninHemolymphInternal medicineHemolymphmedicineAnimalsEndocrine systemReceptorCadmiumDose-Response Relationship DrugbiologyReproductionOvaryVitellogenesisFeeding BehaviorJuvenile HormonesEndocrinologychemistryInsect ScienceJuvenile hormonebiology.proteinFemaleVitellogenesisFood DeprivationVitellogeninsCadmiumJournal of Insect Physiology
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Abnormal development of pacinian corpuscles in double trkB;trkC knockout mice.

2006

Pacinian corpuscles depend on either Aalpha or Abeta nerve fibers of the large- and intermediate-sized sensory neurons for the development and maintenance of the structural integrity. These neurons express TrkB and TrkC, two members of the family of signal transducing neurotrophin receptors, and mice lacking TrkB and TrkC lost specific neurons and the sensory corpuscles connected to them. The impact of single or double targeted mutations in trkB and trkC genes in the development of Pacinian corpuscles was investigated in 25-day-old mice using immunohistochemistry and ultrastructural techniques. Single mutations on trkB or trkC genes were without effect on the structure and S100 protein expr…

medicine.medical_specialtyanimal structuresTropomyosin receptor kinase BBiologyTropomyosin receptor kinase CS100 proteinMiceMicroscopy Electron TransmissionInternal medicinemedicineLow-affinity nerve growth factor receptorAnimalsReceptor trkBReceptor trkCReceptorMice Knockoutmusculoskeletal neural and ocular physiologyGeneral NeuroscienceImmunohistochemistryCell biologyMice Inbred C57BLEndocrinologynervous systemAnimals NewbornTrk receptorembryonic structuresKnockout mousebiology.proteinPacinian CorpusclesNeurotrophinNeuroscience letters
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Investigational agents for Crohn's disease.

2010

IMPORTANCE OF THE FIELD: Increased understanding of the biological mechanisms of Crohn's disease has opened the door to a large number of new molecules; some of these are approved for clinical use, while others remain under evaluation. In this review, we examine the clinical efficacy of all the new drugs that have been evaluated in controlled trials in the last 12 years. AREAS COVERED IN THIS REVIEW: Anti-TNF therapy has been reviewed briefly, given the many comprehensive reviews on this topic; attention is focused mainly on the other biological therapies. In assessing the clinical efficacy of these molecules, we consider only the remission rate, as this is considered the most meaningful en…

medicine.medical_specialtybiological therapy. Crohn' s disease. Integrins.Probiotics.Small molecules.DiseaseAdaptive ImmunityReceptors Tumor Necrosis FactorCrohn DiseaseGastrointestinal AgentsmedicineHumansImmunologic FactorsPharmacology (medical)Clinical efficacyIntensive care medicineRandomized Controlled Trials as TopicPharmacologyMitogen-Activated Protein Kinase KinasesBiological therapiesCrohn's diseaseEverolimusEnd pointINVESTIGATIONAL AGENTSbusiness.industryRemission InductionAntibodies MonoclonalGeneral MedicineDrugs Investigationalmedicine.diseaseImmunity InnateImmunologyCytokinesRemission rateImmunotherapybusinessCell Adhesion Moleculesmedicine.drugExpert opinion on investigational drugs
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Identification of a discrete neuronal circuit that relays insulin signaling into the brain to regulate glucose homeostasis

2021

Abstract26RFa (QRFP) is a biologically active peptide that regulates glucose homeostasis by acting as an incretin and by increasing insulin sensitivity at the periphery. 26RFa is also produced by a neuronal population localized in the hypothalamus. In the present study, we have investigated whether the 26RFa neurons may be involved in the hypothalamic regulation of glucose homeostasis. Our data indicate that 26RFa, i.c.v. injected, induces a robust antihyperglycemic effect associated with an increase of insulin production by the pancreatic islets. In addition, we found that insulin strongly stimulates 26RFa expression and secretion by the hypothalamus. RNAscope experiments revealed that neu…

medicine.medical_specialtybiologyChemistryInsulinmedicine.medical_treatmentQRFPIncretinCarbohydrate metabolismInsulin receptorEndocrinologyHypothalamusInternal medicinemedicinebiology.proteinGlucose homeostasisHormone
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Myocardial blood flow and adenosine A2Areceptor density in endurance athletes and untrained men

2008

Previous human studies have shown divergent results concerning the effects of exercise training on myocardial blood flow (MBF) at rest or during adenosine-induced hyperaemia in humans. We studied whether these responses are related to alterations in adenosine A2A receptor (A2AR) density in the left-ventricular (LV) myocardium, size and work output of the athlete's heart, or to fitness level. MBF at baseline and during intravenous adenosine infusion, and A2AR density at baseline were measured using positron emission tomography, and by a novel A2AR tracer in 10 healthy male endurance athletes (ET) and 10 healthy untrained (UT) men. Structural LV parameters were measured with echocardiography.…

medicine.medical_specialtybiologyHuman studiesPhysiologyAthletesbusiness.industryAdenosine A2A receptorBlood flowbiology.organism_classificationAdenosineHyperaemiaEndocrinologyInternal medicinemedicinemedicine.symptombusinessPerfusioncirculatory and respiratory physiologymedicine.drugThe Journal of Physiology
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Receptor Recognition Sites of Cytokines Are Organized as Exchangeable Modules

1999

Interleukin-6 (IL-6) and ciliary neurotrophic factor (CNTF) are "4-helical bundle" cytokines of the IL-6 type family of neuropoietic and hematopoietic cytokines. IL-6 signals by induction of a gp130 homodimer (e.g. IL-6), whereas CNTF and leukemia inhibitory factor (LIF) signal via a heterodimer of gp130 and LIF receptor (LIFR). Despite binding to the same receptor component (gp130) and a similar protein structure, IL-6 and CNTF share only 6% sequence identity. Using molecular modeling we defined a putative LIFR binding epitope on CNTF that consists of three distinct regions (C-terminal A-helix/N-terminal AB loop, BC loop, C-terminal CD-loop/N-terminal D-helix). A corresponding gp130-bindin…

medicine.medical_specialtybiologyLeukemia inhibitory factor receptorCell BiologyCiliary neurotrophic factorGlycoprotein 130BiochemistryEpitopeCell biologyEndocrinologyInternal medicineLeukemia inhibitory factor receptor bindingmedicinebiology.proteinLeukemia Inhibitory Factor Receptor alpha SubunitBinding siteMolecular BiologyLeukemia inhibitory factorJournal of Biological Chemistry
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MAGNESIUM METABOLISM IN INSULIN RESISTANCE, METABOLIC SYNDROME, AND TYPE 2 DIABETES MELLITUS

2007

Magnesium plays a key role in regulating insulin action, insulin-mediated glucose uptake, and vascular tone. Intracellular magnesium depletion may result in a defective tyrosine—kinase activity at the insulin receptor level, in a postreceptorial impairment in insulin action, and clinically in a worsening of insulin resistance. Intra- and extracellular alterations of magnesium metabolism have been identified in clinical states characterized by insulin resistance, such as metabolic syndrome, hypertension, altered glucose tolerance, type 2 diabetes, and aging. Several studies, from our and other’s groups, have confi rmed the clinical relevance of alterations of magnesium homeostasis in these c…

medicine.medical_specialtybiologyMagnesiumbusiness.industryInsulinmedicine.medical_treatmentGlucose uptakeType 2 Diabetes Mellituschemistry.chemical_elementType 2 diabetesmedicine.diseaseInsulin receptorEndocrinologyInsulin resistancechemistryInternal medicinemedicinebiology.proteinMetabolic syndromebusiness
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Complete blockade of the vasorelaxant effects of angiotensin-(1-7) and bradykinin in murine microvessels by antagonists of the receptor Mas

2013

Key points • Two distinct angiotensin-(1–7) [Ang-(1–7)] receptor blockers, A779 and d-Pro-Ang-(1–7), can completely prevent Ang-(1–7)-induced vasorelaxation. • Genetic deficiency of Mas completely prevents vascular responses to Ang-(1–7). • Genetic deficiency of Mas completely prevents vascular responses to other NO-dependent vasorelaxants (bradykinin). • Mas plays a key role in NO-mediated vasodilatation by modulating vasorelaxant-mediated phosphorylation of endothelial nitric oxide synthase in endothelial cells. Abstract  The heptapeptide angiotensin-(1–7) is a biologically active metabolite of angiotensin II, the predominant peptide of the renin–angiotensin system. Recently, we have show…

medicine.medical_specialtybiologyPhysiologyBradykininVasodilationAngiotensin IIUmbilical veinNitric oxideNitric oxide synthasechemistry.chemical_compoundEndocrinologychemistryInternal medicinemedicinebiology.proteinBradykinin receptorMyographThe Journal of Physiology
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PP.42.06

2015

medicine.medical_specialtybiologyPhysiologybusiness.industryPlasma renin activityFokIEndocrinologyInternal medicineInternal Medicinemedicinebiology.proteinCardiology and Cardiovascular MedicineVitamin d receptor genebusinessJournal of Hypertension
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