Фармакологија и клинички испитувања
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Questions and Answers

Kako deluje G-protein na intracelularnite receptori?

  • Inaktivira adenil ciklaza za prekin na cAMP sintezata
  • Vozbujduva adenil ciklaza za sinteza na cAMP (correct)
  • Povreduva lecitinot za osloboduvanje na alfa subenota
  • Stimulira sintezata na regulatorot
  • Kade se locira domenot na protein kinazite na protein-tirozin kinaznite receptori?

  • Vo jedroto na kletkata
  • Vo citoplazmatskiot domen (correct)
  • Vo ekstracelularniot domen
  • Vo membranskite domeni
  • Koj od slednite funkcii e karakteristichen za duvanoksidul (NO)?

  • Podobruva aktivnosta na adenil ciklaza, namaluvaјki gi nivoite na sAMR i prouzrokuvaјki vazodilatacija
  • Podobruva aktivnosta na adenil ciklaza, zgolemuvaјki gi nivoite na cAMP i prouzrokuvaјki vazodilatacija (correct)
  • Namaluva aktivnosta na adenil ciklaza, namaluvaјki gi nivoite na cAMP i prouzrokuvaјki vazodilatacija
  • Namaluva aktivnosta na adenil ciklaza, zgolemuvaјki gi nivoite na sAMR i prouzrokuvaјki vazodilatacija
  • Study Notes

    • G-proteins bind to intracellular receptors, causing their conformational change and subsequent phosphorylation of GDP to GTP, leading to the release of an α subunit that activates adenyl cyclase for cAMP synthesis.
    • G-protein: a regulator; adenyl cyclase; lecithin; cAMP.
    • Apaf-1 protein induces apoptosis in cells.
    • Caspase activation: P53, Bcl-2, Apaf-1, and others.
    • For a non-linear drug, at constant dosing, the maximum concentration (Cmax) and half-life (T1/2) affect the elimination constant and area under the curve (AUC) disproportionately.
    • A large family of receptors with no extracellular domain includes; JAK/STAT is a tyrosine kinase receptor pathway.
    • The domain of protein tyrosine kinase receptors responsible for synthesizing protein kinases is located within the cytoplasmic domain.
    • Proteins and large insoluble molecules can be introduced into the body via _______ mechanism.
    • Agonists, antagonists, and inverse agonists are types of protein receptor drug interactions.
    • A biological model does not perfectly resemble human disease even if it has a similar genotype, pathophysiology, trigger, and therapeutic response.
    • Measuring a new compound's pharmacological activity: ligand binding assays, functional assays, toxicity, and pharmacodynamics.
    • The continuous addition of a drug dosage when receptors are saturated results in no change in the rate of drug excretion.
    • Adding an irreversible antagonist to an agonist decreases Cmax and increases Tmax, but AUC remains relatively unchanged.
    • G-protein signaling activation: Gα acts on GDP synthesis; Gαγβ binds to active G protein-coupled receptors; Gα is phosphorylated, turning GDP into GTP.
    • The deactivation of G-protein receptors: not specified in the text.
    • Nitric oxide (NO) functions: a) enhancing adenyl cyclase activity, increasing sGMP, and causing vasodilation; b) decreasing adenyl cyclase activity, decreasing sAMR, and causing vasodilation; c) decreasing adenyl cyclase activity, increasing sAMR, and causing vasodilation; d) enhancing adenyl cyclase activity, decreasing sAMR, and causing vasodilation.
    • Muscarinic receptors: a) M1; b) M2; c) M3; d) M4; e) M5; muskimol.

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    Ова прашање вклучува константата на рамнотежа при лек-рецептор интеракции, употребата на здрави пациенти во фазите на испитување и синтезата на втор гласник при реакција на инозитолтрифосфата+ фосфолипаза С.

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