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Adherence and persistence associated with the pharmacologic treatment of osteoporosis in a managed care setting.: South Med J, Vol. 99, No. 6. (June 2006), pp. 570-575.BACKGR OUND: The effectiveness of chronic therapies can be compromised by poor adherence and persistence. MATERIALS AND METHODS: Investigators identified a continuously benefit-eligib le cohort of women from a large, geographically diverse, national managed care plan who were newly diagnosed and treated for osteoporosis with alendronate, risedronate, or raloxifene. Drug utilization parameters were evaluated over a 12-month follow-up period for the study population. Adherence was assessed using a medication possession ratio calculated as total days of therapy for medication dispensed/365 days of study follow-up. Persistence was defined as continuous therapy on the same drug for each month over the entire study period. Adherence and persistence were also evaluated for all three study agents in women > or = 65 years of age. RESULTS: In the study cohort (N = 10,566), 12-month adherence/ persistence rates were alendronate 61%/21%, risedronate 58%/19%, and raloxifene 54%/16%. Rates in women > or = 65 years were similar to those in the entire study cohort. Weekly bisphosphonate users had slightly higher 12-month adherence (63% versus 54%, P < 0.05) and persistence (22% versus 19%, P = NS) rates than did daily users, independent of agent. CONCLUSION: Chronic oral-dosed osteoporosis therapies are associated with poor adherence and persistence, regardless of age or dosing regimen. Drug therapies and patient management approaches associated with improved adherence and persistence could improve the likelihood of achieving the therapeutic benefits observed in rigorously controlled clinical trials.

Source: South Med J, Vol. 99, No. 6. (June 2006), pp. 570-575.
Breast cancer management: quality-of-lif e and cost considerations .: Pharmacoeconom ics, Vol. 21, No. 6. (2003), pp. 383-396.The purpose of this article was to provide a literature-bas ed extensive overview of the quality-of-lif e and cost issues posed by the management of breast cancer. Incidence and mortality rates vary widely in different countries. Breast cancer accounts approximately for one-fifth of all deaths in women aged 40-50 years. The 1994-1998 incidence rate in the US population was on average 114.3 per 100 000 women. Treatment options include surgery, radiotherapy and drug therapy (cytotoxic and endocrine drugs). All treatment options affect patients' health-related quality of life (HR-QOL) in various ways. The use of cytotoxic agents has a particularly large HR-QOL impact. HR-QOL questionnaires are complex tools, not routinely used in breast cancer trials.Worldwi de, around 10 million individuals develop cancer each year; this figure is expected to increase to 15 million in 2020. For all cancers, the total economic burden of this disease worldwide was projected by the authors to be in the range of $US 300-400 billion in 2001 (about $US 100-140 billion as direct costs and the remainder as indirect costs [morbidity and mortality]). According to the National Institute of Health (NIH), the total cost of cancer was estimated at $US 156.7 billion in 2001 in US ($US 56.4 billion as direct costs, $US 15.6 as indirect morbidity costs, and $US 84.7 billion as indirect mortality costs). Based on limited information, in the US, breast cancer can be projected to account for about one-fifth/one- fourth of the total cost of cancer. Breast cancer treatment costs are higher in the US than in other developed countries. Both direct and indirect costs are dependent on disease stage. The per-patient costs for initial care in 1992 were estimated at $US 10 813, for continuing care at $US 1084 and for terminal care at $US 17 886. Stage-specific costs provide information for cost-effective ness analyses of cancer-control initiatives, such as screening programmes. Economic studies on breast cancer are heterogeneous, and the cost estimates made are not easily generalisable. The cost of treatment for breast cancer in developing countries is < or =5% of that in developed regions.

Source: Pharmacoeconomics, Vol. 21, No. 6. (2003), pp. 383-396.
Raloxifene examined for breast cancer prevention.: Am J Health Syst Pharm, Vol. 64, No. 17. (1 September 2007)

Source: Am J Health Syst Pharm, Vol. 64, No. 17. (1 September 2007)
Safety and efficacy of antiestrogens for prevention of breast cancer.: Am J Health Syst Pharm, Vol. 57, No. 14. (15 July 2000)The rationale for clinical trials of antiestrogens for prevention of breast cancer, potential concerns with antiestrogens, and clinical trials of antiestrogens for breast cancer prevention are discussed. Extensive preclinical evidence supports clinical investigation and use of tamoxifen for preventing breast cancer. The efficacy of tamoxifen in the treatment of advanced breast cancer and as adjuvant therapy has further strengthened the rationale for use in prevention. Tamoxifen is well tolerated and, like raloxifene, has been associated with non-cancer-rel ated benefits. The major concerns with tamoxifen are an increased risk of thromboembolic events and endometrial cancer and an association with ocular disorders. Little is known about the long-term safety of raloxifene. Three randomized, double-blind, placebo-contro lled clinical trials of tamoxifen 20 mg (as the citrate) daily for the prevention of breast cancer and one post hoc analysis and a literature review examining the effect of raloxifene on breast cancer risk (as a secondary endpoint) have been published. In one of the three trials of tamoxifen, the rate of invasive breast cancer was reduced 49%; in the other two trials, no reduction in breast cancer was found. Raloxifene apparently reduced the frequency of breast cancer. On the basis of the positive tamoxifen trial, tamoxifen can be offered to women with a five-year projected risk of breast cancer of > or = 1.67%, as determined by the Gail model. Risks and benefits should be evaluated for each patient. Tamoxifen may offer some women protection against breast cancer. Raloxifene may also have a preventive role, but more study is needed.

Source: Am J Health Syst Pharm, Vol. 57, No. 14. (15 July 2000)
Chemopreventio n of breast cancer: tamoxifen, raloxifene, and beyond.: Am J Ther, Vol. 13, No. 4. (g 2006), pp. 337-348.Breast cancer is the most common cancer and the second most common cause of cancer death among women in the United States. While nonrandomized studies have reported that prophylactic mastectomy or oophorectomy can significantly reduce the risk of breast cancer, these approaches are unacceptable to the majority of women. Chemopreventio n, which is defined as the prevention of cancer by pharmacologica l agents that inhibit or reverse the process of carcinogenesis , has thus increasingly become the focus of breast cancer prevention efforts. The first-generati on selective estrogen receptor modulator (SERM) tamoxifen is the only US Food and Drug Administration - approved drug for breast cancer prevention and reduces the risk of breast cancer by as much as 50% in high-risk women. Raloxifene, a second-generat ion SERM, also has demonstrated efficacy for breast cancer prevention and is being compared with tamoxifen in a large randomized trial that has recently completed accrual. The aromatase inhibitors (AIs) decrease the incidence of contralateral breast cancer when used in the adjuvant setting and are being evaluated in ongoing primary prevention studies. In addition, a number of novel agents, including antiinflammato ry drugs and retinoid derivatives, which appear to be of promise based on preclinical and epidemiologica l data, are under investigation. Several important challenges remain, including determination of the appropriate dose and duration of treatment when used in the primary prevention setting and development of new research models using surrogate end points for breast cancer incidence and mortality to permit more rapid clinical application of promising new agents.

Source: Am J Ther, Vol. 13, No. 4. (g 2006), pp. 337-348.
Early discontinuatio n of tamoxifen: a lesson for oncologists.: Cancer, Vol. 109, No. 5. (1 March 2007), pp. 832-839.BACKGR OUND: Five years of treatment provides the optimum duration of tamoxifen therapy for the prevention of breast cancer recurrence and mortality. Durations of adjuvant tamoxifen therapy less than 5 years are associated with poorer outcomes for breast cancer patients. The purpose of the study was to assess rates of tamoxifen nonpersistence (early discontinuatio n) in women aged 35 years or older using prescription refill data from a national prescribing database. METHODS: A cohort of 2816 women commencing tamoxifen as initial hormonal therapy was identified between January 2001 and January 2004. The cumulative tamoxifen persistence rate was calculated for these women and the relation between nonpersistence and clinical and demographic variables assessed. RESULTS: Within 1 year of commencing treatment the cumulative tamoxifen nonpersistence rate was 22.1%. This is twice the rate of treatment discontinuatio n observed in other studies by this time. By the end of follow-up at 3.5 years, the cumulative nonpersistence rate had increased to 35.2%. Determinants of nonpersistence identified included age and a history of antidepressant use. CONCLUSIONS: The rate of nonpersistence with tamoxifen therapy is higher than previously reported. This study demonstrates that persistence with tamoxifen cannot be assumed and raises concerns about persistence with other oral hormonal therapies for breast cancer and oral antineoplastic s in general. Oncologists need to identify those at risk of nonpersistence and develop strategies to combat this barrier to treatment success.

Source: Cancer, Vol. 109, No. 5. (1 March 2007), pp. 832-839.
Stochastic active contour for cardiac MR image segmentation: Image Processing, 2003. ICIP 2003. Proceedings. 2003 International Conference on, Vol. 2 (2003), pp. II-1097-100 vol.3.We develop an energy based automatic image segmentation algorithm using a novel active contour scheme. The algorithm overcomes some unique challenges arising in cardiac MR images. Two features are particularly relevant. The first is that it uses region-based information captured by a stochastic model. As a result, our method is robust to assumed initial conditions and can be applied to a large range of images, particularly when the contrast is low. The second feature is the incorporation of prior knowledge on the shape of the organ to be segmented. For cardiac image segmentation, it is sufficient to assume that the shape resembles an ellipse.

Source: Image Processing, 2003. ICIP 2003. Proceedings. 2003 International Conference on, Vol. 2 (2003), pp. II-1097-100 vol.3.
AC and DC percolative conductivity of single wall carbon nanotube polymer composites: Journal of Polymer Science Part B: Polymer Physics, Vol. 43, No. 22. (2005), pp. 3273-3287.The equations needed to correctly interpret both AC and DC conductivity results of single wall carbon nanotube (SWNT) polymer composites and the scaling of these results onto a single master curve are presented. Brief discussions on the factors that determine the critical volume fraction (&phis;c) and the percolation exponent (t) are also given. The results for a series of SWNT-polyimide composites are presented and the parameters obtained from fitting these results are discussed. The critical volume fraction for electrical percolation of the present composite was about 0.0005. Results obtained from previous work on SWNT (MWNT)-polymer composites and other percolation systems and the modeling (interpretatio n) of these results are also discussed and compared. © 2005 Wiley Periodicals, Inc. J Polym Sci Part B: Polym Phys 43: 3273-3287, 2005

Source: Journal of Polymer Science Part B: Polymer Physics, Vol. 43, No. 22. (2005), pp. 3273-3287.
Regulation of Adenylyl Cyclase Isozymes on Acute and Chronic Activation of Inhibitory Receptors: Mol Pharmacol, Vol. 54, No. 2. (1 August 1998), pp. 419-426.Adenyl yl cyclase superactivatio n, a phenomenon by which chronic activation of inhibitory Gi/o-coupled receptors leads to an increase in cAMP accumulation, is believed to play an important role as a compensatory response of the cAMP signaling system in the cell. However, to date, the mechanism by which adenylyl cyclase activity is regulated by chronic exposure to inhibitory agonists and the nature of the adenylyl cyclase isozymes participating in this process remain largely unknown. Here we show, using COS-7 cells transfected with the various AC isozymes, that acute activation of the D2 dopaminergic and m4 muscarinic receptors inhibited the activity of adenylyl cyclase isozymes I, V, VI, and VIII, whereas types II, IV, and VII were stimulated and type III was not affected. Conversely, chronic receptor activation led to superactivatio n of adenylyl cyclase types I, V, VI, and VIII and to a reduction in the activities of types II, IV, and VII. The activity of AC-III also was reduced. This pattern of inhibition/sti mulation of the various adenylyl cyclase isozymes is similar to that we recently observed on acute and chronic activation of the micro-opioid receptor, suggesting that isozyme-specif ic adenylyl cyclase superactivatio n may represent a general means of cellular adaptation to the activation of inhibitory receptors and that the presence/absen ce and intensity of the adenylyl cyclase response in different brain areas (or cell types) could be explained by the expression of different adenylyl cyclase isozyme types in these areas.

Source: Mol Pharmacol, Vol. 54, No. 2. (1 August 1998), pp. 419-426.
Differential Coupling of Serotonin 5-HT1A and 5-HT1B Receptors to Activation of ERK2 and Inhibition of Adenylyl Cyclase in Transfected CHO Cells: Journal of Neurochemistry , Vol. 73, No. 1. (1999), pp. 162-168.Abstra ct: Although the subtypes of serotonin 5-HT1 receptors have distinct structure and pharmacology, it has not been clear if they also exhibit differences in coupling to cellular signals. We have sought to compare directly the coupling of 5-HT1A and 5-HT1B receptors to adenylyl cyclase and to the mitogen-activa ted protein kinase ERK2 (extracellular signal-regulat ed kinase-2). We found that 5-HT1B receptors couple better to activation of ERK2 and inhibition of adenylyl cyclase than do 5-HT1A receptors. 5-HT stimulated a maximal fourfold increase in ERK2 activity in nontransfected cells that express endogenous 5-HT1B receptors at a very low density and a maximal 13-fold increase in transfected cells expressing 230 fmol of 5-HT1B receptor/mg of membrane protein. In contrast, activation of 5-HT1A receptors stimulated only a 2.8-fold maximal activation of ERK2 in transfected cells expressing receptors at 300 fmol/mg of membrane protein but did stimulate a 12-fold increase in activity in cells expressing receptors at 3,000 fmol/mg of membrane protein. Similarly, 5-HT1A, but not 5-HT1B, receptors were found to cause significant inhibition of forskolin-stim ulated cyclic AMP accumulation only when expressed at high densities. These findings demonstrate that although both 5-HT1A and 5-HT1B receptors have been shown to couple to G proteins of the Gi class, they exhibit differences in coupling to ERK2 and adenylyl cyclase.

Source: Journal of Neurochemistry, Vol. 73, No. 1. (1999), pp. 162-168.

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