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Anticancer Res. 2002 May-Jun;22(3):1673-9.
Alpha1-adrenoceptor antagonists radiosensitize prostate cancer cells via apoptosis induction.

Cuellar DC, Rhee J, Kyprianou N.

Division of Urology, The University of Maryland School of Medicine, Baltimore, USA.

BACKGROUND: Androgen-independent prostate cancer cells can undergo apoptosis in response to non-androgen ablative means such as ionizing radiation. Recent evidence documented the ability of alpha-adrenoceptor antagonists, a widely used medical therapy for the treatment of benign prostatic hypertrophy (BPH), to induce apoptosis in benign and malignant prostate cells. In this study, we evaluated the potential additive/synergistic apoptotic effect of alpha1-adrenoceptor antagonists with ionizing radiation against human prostate cancer cells in vitro. MATERIALS AND METHODS: Androgen-independent human prostate cancer cells (PC-3) were treated with two alpha1-adrenoceptor antagonists, doxazosin and terazosin, for various periods of time prior to and after exposure to ionizing radiation. Apoptosis induction, cell viability and clonogenic assays were then performed to determine loss of clonogenic survival Hoechst staining was performed to detect the apoptotic morphology in prostate cancer cells and the temporal protein expression of the apoptosis regulators bax and caspase-3, was determined using Western blot analysis. RESULTS: No significant difference in cell death of PC-3 cells was detected when either doxazosin or terazosin was combined with ionizing radiation. Terazosin treatment however, 24 hours prior to, or 24 hours post-irradiation resulted in a significant enhancement of radiation-induced loss of clonogenic survival compared to radiation alone (p<0.05). Furthermore, there was a further significant increase in apoptosis induction when cells were pre-treated with terazosin (15%), compared to treatment with radiation alone (6%). Western blot analysis revealed a significant increase in bax protein expression (but not caspase-3) in response to radiation, with no additional effect with the combination treatment (terazosin and ionizing irradiation) compared to radiation alone. CONCLUSION: This is the first study to document the ability of alpha1-adrenoceptor antagonists to enhance the apoptotic effect of ionizing radiation against human prostate cancer cells. As this alpha1-adrenoceptor-mediated elevation of the apoptotic threshold involves neither bax deregulation nor caspase-3 activation, a differential mechanism might be underlying this radiosensitizing effect. The present findings may have important clinical relevance in identifying a more effective therapeutic approach for androgen-independent prostate cancer based on the combined apoptotic effects of quinazoline-based alpha1-adrenoceptor-antagonsists and radiotherapy.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12168853&dopt=Abstract

Platelets. 2002 Aug-Sep;13(5-6):267-71.
Differential actions of naftopidil, doxazosin and nifedipine on platelet thromboxane generation and platelet-derived growth factor efflux in vitro.

Alarayyed NA, Prichard BN, Betteridge DJ, Smith CC.

Centre for Clinical Pharmacology, Department of Medicine, The Rayne Institute, Royal Free and University College Medical School, London, UK.

We examined the effects of the alpha(1)-adrenoreceptor blockers naftopidil and doxazosin and the Ca(2+) antagonist nifedipine on platelet function with reference to stimulus-induced thromboxane (TxB(2)) generation and platelet-derived growth factor (PDGF) efflux. Collagen (5 micro g/ml) caused a 12.5-fold increase in TxB(2) generation, from a basal level of 7.69 +/- 1.28 ng/10(8) platelets to 96.34 +/- 13.37 ng/10(8) platelets (P<0.001). Adrenaline (16 micro M) increased TxB(2) production 3-fold from 2.44 +/- 0.61 to 8.02 +/- 1.08 ng/10(8) platelets (P<0.01). Adrenaline-induced TxB(2) generation was inhibited 42.5 +/- 10.3% (P<0.05) and 81.8 +/- 7.5% (P<0.05) by 10 and 40micro M naftopidil, respectively. Collagen-stimulated TxB(2) generation was inhibited 59.5 +/- 9.2% (P<0.01) by 40 micro M naftopidil and 53.7 +/- 11.3% (P<0.01) by 28 micro M nifedipine. Doxazosin (7.5 and 30 micro M) did not influence adrenaline- or collagen-induced TxB(2) synthesis. Collagen increased PDGF efflux from 1.17 +/- 0.39 to 4.25 +/- 0.51 ng/10(8) platelets (P<0.01), whilst adrenaline raised concentrations from 1.08 +/- 0.19 to 5.37 + 1.02 ng/10(8) platelets (P<0.01). Naftopidil had no effect on collagen-induced PDGF release. Adrenaline-stimulated PDGF efflux was, however, inhibited 82.9 +/- 13.7% (P<0.001) and 125.7 +/- 16.3% (P<0.001) by 10 and 40 micro M naftopidil, respectively. Doxazosin (30 micro M) inhibited adrenaline-induced PDGF release by 70.3 +/- 31.5% (P<0.05), whilst nifedipine (28 micro M) had no effect on collagen-stimulated release. We conclude that naftopidil, like nifedipine, may block stimulated TxB(2) generation via inhibition of phospholipase A(2), the Ca(2+)-dependent, rate-limiting enzyme in thromboxane synthesis. Although adrenaline-induced PDGF release was inhibited by naftopidil and doxazosin, collagen-induced release was unaffected by either alpha(1)-adrenoreceptor blocker or nifedipine, indicating that platelet alpha-granular release is not dependent on Ca(2+) mobilisation or thromboxane generation. Thus, the effects of these drugs on PDGF release may be mediated through alternative cellular signalling mechanisms.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12189011&dopt=Abstract

stanford.edu

OBJECTIVES: To present a methodology for identifying specific medications for which pill splitting is clinically appropriate and cost saving, to present data from a commercial managed care population on current pill-splitting practices, and to estimate additional cost savings from extended use of this strategy. STUDY DESIGN: Retrospective pharmacy claims analysis. METHODS: Pharmacy claims data from a commercial managed care health plan covering 19,000 lives and national drug data were used to compile a list of frequently prescribed medications. Excluding medications in which packaging, formulation, and potential adverse pharmacologic outcomes prohibited splitting, we performed a cost analysis of medications amenable to splitting. RESULTS: Eleven medications amenable to pill splitting were identified based on potential cost savings and clinical appropriateness: clonazepam, doxazosin, atorvastatin, pravastatin, citalopram, sertraline, paroxetine, lisinopril, nefazadone, olanzapine, and sildenafil. For these medications, pill splitting is currently infrequent, accounting for annual savings of $6200 (or $0.03 per member per month), just 2% of the potential $259,500 (or $1.14 per member per month) that more comprehensive pill-splitting practices could save annually. CONCLUSIONS: Pill splitting can be a cost-saving practice when implemented judiciously using drug- and patient-specific criteria aimed at clinical safety, although this strategy is used infrequently.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12212758&dopt=Abstract

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