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The Poly-pill Replaces Poly-pharmacy Noon-time educational conferences at hospitals are sponsored by drug companies--they pay for the lunch and the speaker--a small price for a doctor's mind. I learned about the "proper care" of a person with type-2 diabetes at one of these weekly promotional events. By the end of an hour-long presentation most of the physicians in attendance were thoroughly convinced that the optimal way to treat someone with diabetes was to prescribe 20 different kinds of medications. A feeling of importance was given to this multidrug approach by introducing a new and high-tech-sounding term to describe this manner of practice: poly-pharmacology. Yes, a "competent" physician was going to be putting his sick patients on a regime of poly-pharmacy. The polypill is simply a more convenient way to practice poly-pharmacology--rather than taking pills from many bottles each day, one pill contains all the separate medications. However, widespread use of the polypill is unlikely because it would mean a serious loss of profits for the drug industries. As Dr. Wald puts it, "Pharmaceutical companies need to make money and the concept of the polypill for some will erode their existing market."2 The Poly-pharmacology for the "Well-treated" Patient Pills prescribed for these common dietary-caused conditions--one patient will typically be taking many of these: Blood pressure: ACE inhibitor Zestril beta blocker Tenormin calcium channel blocker Cardizem ; Blood sugar: sulfonylurea Glucotrol metformin Glucophage Pioglitazone Actos ; Cholesterol: atorvastatin Lipitor ezetimibe Zetia ; Uric acid: allopurinol Zyloprim ; Homocysteine: folic acid Foltx ; Triglycerides: gemfibrozil Lopid ; Hypercoagulability: clopidogrel Plavix ; aspirin is too inexpensive ; Indigestion: esomeprazole Nexium ; Anxiety: alprazolam Xanax ; Insomnia: zolpidem Ambien ; Body fat: orlistat Xenical ; Headaches: propoxyphene Darvocet ; Body aches: ibuprofen Motrin ; Constipation: an osmotic agent MiraLax ; Diarrhea: a narcotic agent Lomotil ; Body odor: deodorants and perfumes to disguise the animal food-derived odors and phentermine. 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It found no difference in healing rates after four weeks, but after eight weeks, nexium eked out a victory - a 90% healing rate versus 87 and propecia. Polyps: past, present, and future. Allergy 1999; 54: 7-11. Mygind N, Lildholdt T. Nasal polyps treatment: medical management. Allergy Asthma Proc 1996; 17: 275-82. Lanza DE, Kennedy DW. Current concepts in the surgical management of nasal polyposis. J Allergy Clin Immunol 1992; 90: 543-5. Herrod HG. Management of the patient with IgG subclass deficiency and or selective antibody.
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Ian Heslop is the assistant director of pharmacy clinical services at The Townsville Hospital, Townsville, North Queensland, Australia. Correspondence to Ian Heslop, Pharmacy Department, The Townsville Hospital, 100 Angus Smith Drive, Douglas, Townsville Q4814 Australia e-mail Ian Heslop health.qld.gov.au and testosterone.

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How gefitinib differentially inhibited the growth of MCF-7 F cells, we found that phosphorylated EGFR Y1173 is barely detectable in MCF-7 cells Fig. 4B ; . In contrast, MCF-7 F cells showed much higher phosphorylation of EGFR detected by anti-phospho-EGFR Y1173 Fig. 4B ; and anti-phosphoEGFRY1068 data not shown ; . Gefitinib decreased phosphorylation of EGFR in MCF-7 F cells. MAPK44 42 and Akt are the two important downstream factors for EGFR signal transduction pathway 21, 22 ; . Although total protein levels of MAPK44 42 and Akt were much lower, phosphorylation of both MAPK44 42 and Akt were clearly increased in MCF-7 F cells Fig. 4B ; , suggesting that the growth and survival of MCF-7 F cells might be predominantly dependent on MAPK 44 42 and Akt pathways. Gefitinib inhibited phosphorylation of MAPK44 42 in both MCF-7 and MCF-7 F cells Fig. 4B ; . However, gefitinib inhibited phosphorylation of Akt in a concentration-dependent manner only in MCF-7 F cells. U0126, an inhibitor of MEK the upstream activator of MAPK44 42 ; , inhibited cell growth in a concentration-dependent manner in both MCF-7 and MCF-7 F cells but the inhibitory effect of U0126 at concentrations from 0.625 to 5 M was significantly more apparent in MCF-7 F cells than parental MCF-7 cells Fig. 4C ; . Similarly, MCF-7 F cells were more sensitive to Ly294002, an inhibitor of PI3K one of the and phentermine.