No description available.

No description available.

No description available.

No description available.

No description available.

Effect of surface treatments on Strength and durability of aluminum 6061-Henkel Hysol EA 9891RP (room temperature curing epoxy) bond was studied using single lap shear, flatwise tensile and wedge crack test. The interfacial strength (IFSS) and % cohesive fracture varied with composite adhesive thickness and 0.03-0.04 mm that maximized the interfacial fracture was chosen to compare surface treatments. The effect of treatments on IFSS and tensile strength increased in the following order: PAA+BR127 (RT) < UT+BR127 (120oC) < Alodine < Alodine+EC3901(RT) < Alodine+BR127 (RT) < PAA < UT < UT+BR127 (RT) < Alodine+EC3901 (90oC) < PAA+EC3901(RT) < PAA+EC3901(90oC) < PAA+BR127 (120oC) < UT+EC3901(90oC) < UT+EC3901(RT) < Alodine+BR127 (120oC). The environmental durability decreased in the following order Alodine+EC3901 (90oC) < Alodine+BR127 (120oC) < PAA+BR127 (120oC) < PAA+EC3901 (90oC) < UT < UT+EC3901 (90oC) < UT+EC3901 (RT) < PAA+EC3901 (RT). PAA and Alodine, combined with BR127 (120 oC) and EC3901 (90oC) are the optimal surface treatments / October 2016

Thesis (M.D.)--Boston University

Thesis (Ph.D.)--Boston University / PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you. / Cancer, the second most common cause of death in the United States, is a collection of diseases caused by uncontrolled cell growth and metastasis. The main treatment for cancer is chemotherapy, which generally kills fast growing cells nonspecifically and has many side effects. A different type of cancer treatment, called targeted therapy, aims to avoid general toxicity by using drugs that block the activity of specific gene products, usually encoded by oncogenes, which have been shown to drive tumor growth. To date, targeted therapies, alone or in combination with chemotherapies, have mainly been successful in rare subsets of patients with tumors addicted to single oncogenes. This has created a rationale to mainly treat patients with an oncogene-addiction (such as those carrying mutated or overexpressed kinases) with targeted therapies like erlotinib and trastuzumab, which inhibit human epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2/ErbB2), respectively. Here, evidence is provided that targeted therapies are also effective in tumors that are dependent on multiple growth factors - a phenomenon that is called combinatorial ligand addiction. Specifically, it is shown that ligands that bind the EGFR family and the hepatocyte growth factor receptor (HGFR/MET) can activate protein kinase B (PKB/ AKT) across a broad set of cancer cell lines, suggesting that ligand signaling is redundant and widespread. It is also shown that ErbB ligands have distinct signaling dynamics and strengths, which provides a rationale for investigating each component of the ErbB signaling network. Using a systematic approach, we found that ErbB3 is an imp01tant therapeutic target even though it is not overexpressed and lacks kinase activity. Furthermore, it is shown that cell lines with and without known oncogene-addiction express autocrine ligands and have improved growth inhibition with drug combinations that include autocrine ligand-blocking antibodies. This research demonstrates that combinatorial ligand addiction creates a new rationale for therapeutic combinations to improve efficacy and prevent resistance in cancer cells that are treated with current targeted drugs. / 2031-01-01

No description available.

No description available.