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  • ISSN: 2379-089X
    Volume 3, Issue 2
    Short Note
    Christopher Richter*
    The emergence of target - specific oral anticoagulants (TSOACs) has undoubtedly improved the medical outcomes and quality of life in many patients. However, experience in this class of medication is still in a state of infancy in comparison to our experience with warfarin and parenteral anticoagulants. Drug - drug interactions and drug -diagnosis contraindications are among the concerns of many clinicians as these agents are used more and more to anticoagulate patients. Drug interactions specifically warrant an urgent focus to better understand and predict significant changes in bleeding risk when using TSOACs.
    Research Article
    von Manstein V and Groner B*
    We investigated and compared the effects of the tyrosine kinase inhibitor canertinib and the down regulation of the transcription factor Stat3 on signaling pathways and the cellular phenotypes of Tu-2449 glioma and MDA-MB-468 breast cancer cells. Tu-2449 are glioma cells in which the v-Src and Bmx tyrosine kinases, and the downstream effectors Akt and Stat3, are persistently activated. MDA-MB-468 are triple negative breast cancer cells in which the EGFR functions as Oncogenic driver and the downstream effectors, the Mek and Erk kinases, Akt and Stat3 are persistently activated. Canertinib is an anti - cancer drug which inhibited the activation of Bmx and Stat3, but not of v-Src in Tu-2449 cells. A single dose of 5 μM canertinib caused a transient G1 arrest, whereas prolonged administration of Canertinib proved cytotoxic. The down regulation of Stat3 by specific shRNA did not affect cell viability and normal cell cycle progression in vitro, but single cell infiltration and tumor growth were inhibited in vivo. The cytotoxic effects of canertinib in Tu-2449 cells are not solely mediated by Stat3 inhibition, but probably require the simultaneous inhibition of the Bmx and Akt kinases. Canertinib treatment of MDA-MB-468 breast cancer cells caused inhibition of the EGFR, Erk1/2 and Mek1/2 kinases and the downstream effectors Stat3 and Akt. In contrast to the glioma cells, the down regulation of Stat3 was sufficient to kill MDA-MB-468 cells.
    Short Communication
    Joseph JM, Kutumbarao NHV, Kesherwani M, Chandrasekaran R, and Velmurugan D*
    Computational approaches were used to evaluate and compare binding affinity of different inhibitors upon mutations in aldose reductase (AR) - inhibitor bound co-crystallized complexes. Mainly, co-crystallized wild type and mutated AR with zopolrestat and IDD393 have been used to compute structure based binding free energies. Initially, molecular docking approach based binding free energy calculation was performed for these wild and mutated AR2 complexes. Further, detailed comparative analysis of AR with IDD393 inhibitor using molecular dynamics simulation was also performed and binding free energy using MMGBSA approach was calculated. The decomposed energy of active site in mutated AR-inhibitor complexes were compared with experimental binding affinity and it substantiates the changes in the affinity upon mutation. Thus, a mutational effect on the decomposition of energy was evaluated using docking as well as molecular simulation based approaches and the affinity lost or gained with respect to the mutation is reported. This data can be used to substantiate that the biological activity is a function of its individual energy contributions from the related active site residues. The stream lining of this method can be used in future as a tool to get an alternate computing method for analysis of mutational effects in structure based drug design.
    Mohamed Roshdy Abd Elhamid Saif Eddine*
    Drug Receptor Chromatography is one of affinity Chromatography and new drug design methodology for identifying novel drug compounds from small building fragments into novel drug through affinity to specific receptor.
    Case Report
    Zeljka Aleksic*, Aleksandar Aleksic, Vladimir Mitov, Aleksandar Jolic, and Saska Manic
    Amiodarone (AMD) is a potent antiarrhythmic iodine rich agent, which may induce clinical and subclinical thyroid dysfunction (TD). We describe a male patient with the rare phenomenon of amiodarone-induced thyrotoxicosis (AIT) after subclinical hypothyroidism on AMD therapy, which was recovered after AMD with drawl alone. Normal thyroid grey scale echosonography, absent pertechnetate and MIBI uptake, along with suppressed serum TSH and elevated serum free T4 and free T3 were diagnostic criteria for the AIT type 2 and the treatment choice.
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