Pharmacology Biology

Question: Describe about the Pharmacology for Biology? Answer: Adrenergic receptors- it is a type of adrenoceptors and comes under the class of G-protein coupled receptors. These receptors are the targets of catecholamines, specifically, adrenaline and noradrenaline. Adrenaline reacts with alpha and beta adrenoceptors and resulting in vasoconstriction and vasodilation (Malawska Kulig, 2007). In the presence of low levels of circulating epinephrine, the stimulation of beta-adrenoceptors dominates, produces vasodilation and subsequently decreases the resistance associated with peripheral vessels. CD86- it is a ligand for two dissimilar proteins, these are: CD28 and CTLA-4, which are present on the cell surface of T cell (Eskandari-Nasab, Moghadampour, Najibi Hadadi-Fishani, 2014). It is basically a protein that expressed on APC and provides costimulatory signals required for the activation of T cells and their survival. TCR- It is also known as T cell receptors. These receptors are found on T lymphocyte surface and are responsible for determining antigens that are coupled with major histocompatibility complex molecules (Rivera Reyes, 2006). CD28- it is a receptor for CD86 and CD80 proteins. When these are activated by TCR ligands, the expression of CD80 is up-regulated in APCs. CD28 is basically protein in nature and is expressed on the surface of the T cells, which provides co-stimulatory signals needed for the activation of T cells and their survival (Khandaker, Zammit, Lewis Jones, 2014). The stimulation of T cells through CD28 along with TCR can give a strong signal for interleukins production, particularly: IL-6. 3IgH enhancer (also known as 3IgHRR or 3 enhancer)- this is considered as lymphoid specific transcription enhancer substance. This enhancer can be flanked by 350 base pairs invert repeat and produces a structure of transposable element. Odds ratio-it is said to be a measure of relationship between an exposure and a result. The odds ratio presents the odds, which means a result will come after a particular exposure, and this result is compared with the odds of the result taking place in the absence of the same exposure (Brockhaus, Bender Skipka, 2014). Atopic vs. non-atopic- Atopic Non-atopic Tendency toward growing certain type of hypersensitivity reactions Not affected with atopy; commonly the constriction and inflammation are not because of an allergen exposure (Pekkanen, Lampi, Genuneit, Hartikainen Jrvelin, 2012) May contain hereditary component CD40- It is a constimulatory receptor protein, generally found on the APCs and is needed for the activation of APCs. The attachment of CD154 on the T helper cells to CD40 activates APCs and provokes various downstream effects. 2. Antibodies can have in vivo effects. These effects can also be applied in an experimental sense to identify the significance of particular molecular inside the system. Such as: antibodies to the nerve growth factor shows that the factors associated with nerve growth had to be exist for sensory and sympathetic nervous system to grow. Antibodies to epidermal growth factor receptor have effects on some type of tumour development. 3. Direct effect- Dopamine directly interacts with T cells. This leads to beta 1 integrins activation and later T cell adhesion to an extra cellular matrix component. The adhesion is integrin mediated. Indirect effect- Antigen activated immune system controls the activity of central nervous system through cytokine release and this can bind to the receptors on vagus nerve and then CNS commutes back to immune system by SNS activation to release norepinephrine (Kin, 2006). 4. It can be hypothesized that individual with this type of mutation may develop Cushings syndrome (ZHOU CIDLOWSKI, 2005). This disease is related with prolonged contact to high cortisol hormone levels (Okumura et al., 2012). Individual with this mutation may also develop systemic lupus erythematosus, which is typically an autoimmune disease. Some gene associated risk factors can be shared across various type of diseased state, for example: SLE, with alleles in major histocompatibility locus. This picture demonstrates that the individual with this mutation have developed SLE and are predisposed to develop other autoimmune disorders. 5. The most challenging part of this could be the detection of proper polymorphism in such type of incidences (SLE) which can further guide to develop personalized medicines. This may also become important pharmacogenomic targets for medicinal therapy. References Brockhaus, A., Bender, R., Skipka, G. (2014). The Peto odds ratio viewed as a new effect measure.Statist. Med.,33(28), 4861-4874. doi:10.1002/sim.6301 Eskandari-Nasab, E., Moghadampour, M., Najibi, H., Hadadi-Fishani, M. (2014). Investigation of CTLA-4 and CD86 gene polymorphisms in Iranian patients with brucellosis infection.Microbiol Immunol,58(2), 135-141. doi:10.1111/1348-0421.12119 Khandaker, G., Zammit, S., Lewis, G., Jones, P. (2014). Poster #M118 A POPULATION-BASED LONGITUDINAL STUDY OF ATOPIC DISORDERS AND INFLAMMATORY MARKERS IN CHILDHOOD BEFORE PSYCHOTIC EXPERIENCES IN ADOLESCENCE.Schizophrenia Research,153, S232. doi:10.1016/s0920-9964(14)70668-1 Kin, N. (2006). It takes nerve to tell T and B cells what to do.Journal Of Leukocyte Biology,79(6), 1093-1104. doi:10.1189/jlb.1105625 Malawska, B., Kulig, K. (2007). New Development in 1-Adrenergic Receptors Antagonists.Cheminform,38(46). doi:10.1002/chin.200746230 Okumura, F., Sakuma, H., Nakazawa, T., Hayashi, K., Naitoh, I., Miyabe, K. et al. (2012). Analysis of VH gene rearrangement and somatic hypermutation in type 1 autoimmune pancreatitis.Pathology International,62(5), 318-323. doi:10.1111/j.1440-1827.2012.02788.x Pekkanen, J., Lampi, J., Genuneit, J., Hartikainen, A., Jrvelin, M. (2012). Analyzing atopic and non-atopic asthma.Eur J Epidemiol,27(4), 281-286. doi:10.1007/s10654-012-9649-y Rivera Reyes, B. (2006).Regulation of the TCR signaling pathway. ZHOU, J., CIDLOWSKI, J. (2005). The human glucocorticoid receptor: One gene, multiple proteins and diverse responses.Steroids,70(5-7), 407-417. doi:10.1016/j.steroids.2005.02.006