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Why is this medication prescribed?

Beclomethasone nasal shed is acclimatized to soften symptoms of sneezing, runny, conventional, or itchy nose (rhinitis) caused aside hay fever, other allergies, or vasomotor (nonallergic) rhinitis. It is also cast-off to ward nasal polyps (bump of the lining of the nose) after nasal polyp shifting surgery. Beclomethasone nasal spray should not be reach-me-down to treat symptoms (e.g., sneezing, stuffy, runny, itchy nose) caused before the common cold. Beclomethasone nasal display is in a class of medications called corticosteroids. It works by blocking the release of determined natural substances that cause allergy symptoms.

Beclomethasone comes as a postponing (watery) to atomizer in the nose. It is normally sprayed in each nostril twice a day. Bolster the directions on your prescription categorize carefully, and ask your doctor or druggist to spell out any part you do not understand. Make use of beclomethasone faultlessly as directed. Do not utilize more or less of it or utilize consume it more over than prescribed by your doctor.

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A decrease in oxygen concentration in the blood causes a reaction in the interstitial cells of the kidneys that synthesize erythropoietin. The process occurring in interstitial cells concerns the work of many genes. The main regulation of this process is carried out by factor-1 (HIF-1), which is a heterodimeric protein consisting of two subunits (HIF-1alpha and HIF-1beta). If the oxygen concentration in the blood is within normal limits, proline residues (the heterocyclic amino acid of the freely existing HIF-1 molecule) are hydroxylated under the influence of the regulatory enzyme PHD2 (molecular oxygen sensor). Due to hydroxylation, the HIF-1 subunit acquires the ability to bind to proteincom VHL, providing tumor prevention.

Erythremia was detected in 30% of patients with constitutive activation of the STAT3 gene.

The VHL protein forms a complex with a number of E3 ubiquitin ligase proteins, which, after forming covalent bonds with other proteins, are sent to the proteasome and destroyed there. During hypoxia, hydroxylation of the HIF-1 molecule does not occur; the subunits of this protein combine and form the heterodimeric HIF-1 protein, which travels from the cytoplasm to the nucleus. Once in the nucleus, the protein binds to special DNA sequences in the promoter regions of genes (the conversion of genes into protein or RNA is induced by hypoxia). As a result of these transformations, erythropoietin is released into the bloodstream by the interstitial cells of the kidneys.

By myelopoiesis precursor cells, the genetic program embedded in them is carried out as a result of the stimulating effect of cytokines (these small peptide control (signal) molecules bind to the corresponding receptors on the surface of the precursor cells).

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When erythropoietin binds to the erythropoietin receptor EPO-R, dimerization of this receptor occurs, which activates Jak2, a kinase associated with the intracellular domains of EPO-R. Jak2 kinase is responsible for signal transmission from erythropoietin, thrombopoietin and G-CSF (granulocyte colony-stimulating factor). Due to the activation of Jak2-kinase, phospholation of a number of cytoplasmic target proteins occurs, which includes adapter proteins of the STAT family. Also, with erythremia, in some cases, a reduced level of expression of the thrombopoietin receptor MPL is detected, which is compensatory in nature. The reduction in MPL expression is secondary and is caused by a genetic defect responsible for the development of polycythemia vera.