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When examining the medical doctrines of previous empires, they reveal the influence of religion, societal attitudes, and the historical context that influenced the scholars that penned them. The advancements during the Islamic Golden age can be seen in the field of medicine, which had the Greco-Roman medical corpus as their foundation and the source of the theory of the four humors and anatomical beliefs. This paper will analyze the effect of cultural, societal, and historical influences on the medical doctrines of Muslim medieval physicians in the Golden Age and the works of the Roman physician Galen, and demonstrate how these effects result in similarities and differences in medical practice and the understanding of disease and anatomy. Due to translation efforts that were supported by religious views on the accumulation of knowledge and the efforts of the Abbasid empire, resultant acceptance of the theory of the four humors and anatomical doctrines is observed in the treatment and perception of disease, which would consist of this paper's focus on surgery, diet therapy and associations with nature. However, with further analysis of the extent of this acceptance and the findings in the Islamic medical doctrines, the differences in experimental methods, religious interpretations, and cultural attitudes shows a deviation from the Galenic tradition, with the second set of the paper's focus being human dissection, cause of disease, and experimentation. The purpose of this research is to demonstrate the impact of religion, societal attitudes, culture and the accepted paradigm on the practice of medicine and the study of anatomy, and what would cause a challenge against the legacy of Galen.
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The synergistic effects between Vorinostat and Tamoxifen observed through a phase II study on breast cancer patients resistant to hormone therapy may involve more than the modulation of ER-alpha to reverse Tamoxifen resistance in ERBC cells. RT-qPCR of genes expressed in Tamoxifen resistant cells, trefoil factor 1(TFF1) and v-myc avian myelocytomatosis viral oncogene homolog (MYC), were evaluated along with ESR1 and Diablo as a control. MYC was observed to have increased expression in the treated cells, whereas the other genes had a decrease in their expression levels after the cells were treated for 3 days with Vorinostat IC30 of 1 µM. As for targeting the AR, MCF7 Tamoxifen sensitive and resistant cells were not affected by the AR antagonists to determine an IC50. The cell viability for all MCF7 sub-clones only decreased for high concentrations of 5.56 µM - 50 µM in Bicalutamide and 16.67 µM – 50 µM of MDV1300. Furthermore, hormone depletion of MCF7 G11 Tamoxifen resistant sub-clones did not show a great response to DHT stimulation or the AR antagonists. In the RT-qPCR, the MCF7 G11 cells showed an increase in mRNA expression for ER, AR, and PR after 4 hours of treatment with estradiol. As for the DHT treatment, ER, AR, PR, and PSA had a minimal increase in the fold change, but the fold change in AR was less than in the estradiol treatment. The Mayo Clinic will investigate the possible usage of AR as a biomarker through immunohistochemistry.
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