Future Directions and Unanswered Questions

in Pyridoxal Phosphate and Derivatives (D. Dolphin, R. Poulson and O. Avramovic, eds.) John Wiley Sons, New York.(1986) p. 253. 

Yutani, K. Ogasahara, T. Tsujita, K. Kanemoto, M. Matsumoto, S. Tanaka, T. Miyashita, A. Matsushiro, Y. Sugino, E.W. Miles, J. BioL Chem., 262, 13429 (1987). 

in Biochemical and Medical Aspects of Tryptophan Metabolism (O. Hayaishi, Y. Ishimura and R. Kido, eds.) Elsevier/North-Holand Biomedical Press, Amsterdam (1980) p. 137. 

Kayastha, E.W. Miles, in Enzymes Dependent on Pyridoxal Phosphate and Other Carbonyl Compounds 

Kayastha, in Enzymes Dependent on Pyridoxal Phosphate and Other 

The global interest in the role of inflammation in the pathogenesis of atherosclerosis has led to a considerable research effort to understand the role of inflammatory mediators in the disease. Although it seems clear that chemokines play a fundamental role in both the formation of early fatty streak lesions and the subsequent development into more complex lesions, a considerable amount of research is still required before the manipulation of chemokine-chemokine receptor interactions can be considered a viable treatment option in coronary artery disease. 

Research in our laboratory is funded by the British Heart Foundation. 

Hundhausen, C., Mentlein, R., Schulte, A., Berkhout, T. A., Broadway, N., Hartmann, D., Sedlacek, R., Dietrich, S., Muetze, B., Schuster, B., Kallen, K. J., Saftig, P., Rose-John, S., and Ludwig, A. (2004). The transmembrane CXC-chemokine ligand 16 is induced by IFN-gamma and TNF-alpha and shed by the activity of the disintegrin-like metalloproteinase ADAM 10. J. Immunol. 172, 6362-6372. 

Abi-Younes, S., Sauty, A., Mach, F., Sukhova, G. K., Libby, P., and Luster, A. D. (2000). The stromal cell-derived factor-1 chemokine is a potent platelet agonist highly expressed in atherosclerotic plaques. Circ. Res. 86, 131-138. 

Aiello, R. J., Bourassa, P. A., Lindsey, S., Weng, W., Natoli, E., Rollins, B. J., and Milos, P. M. (1999). Monocyte chemoattractant protein-1 accelerates atherosclerosis in apolipoprotein E-deficient mice. Arterioscler Thromb. Vase. Biol. 19, 1518-1525. 

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Custodio A, de Castro J. Strategies for maintenance therapy in advanced non-small cell lung cancer current status, unanswered questions and future directions. Grit Rev Oncol Hematol 2012 82(3) 338-60. 

On the basis of our current knowledge, it is conceivable that K+ channels are viable diagnostic biomarkers and therapeutic targets for human cancers. Nonetheless, it should be emphasized that there is still a long way to go towards obtaining solid proof for this hypothesis. There are many unanswered questions and unsolved problems, and answering these questions will shape the future directions of the research field. Not until the key issues will have been resolved, will the clinical implications of K+ channels in cancer therapy be a reality. 

Interfaees, disloeations, and nanoeomposites Mixed hydroxides and hydroxyearbonates from surface adsorbates to nanoparticles to bulk phases FUTURE DIRECTIONS AND UNANSWERED QUESTIONS ACmOWLEDGMENTS REFERENCES... 

MECHANISM OF ACTION of Af, immunotherapy Immunization with Af and passive administration of anti-A/S antibodies have both shown profound efficacy by many criteria in APP transgenic mice. What these results leave unanswered, however, is precisely how the antibodies are achieving their effect. Do they stimulate microglial phagocytosis of existing plaques (121), or do they achieve clearance by sequestering free Af in plasma, CSF, and brain extracellular fluid (122,151). Experiments from maty laboratories continue to attempt to address this question, as it may provide insight into the nature of Af peptide accumulation and toxicity and help direct future therapeutic approaches. 

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