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60% for patients with good-risk cytogenetics, 30% for intermediate-risk cytogenetics, and 12% for poor-risk cytogenetics in patients receiving high dose cytarabine consolidation; these outcomes are similar to those on the high dose treatment arm in the SWOG trial.25 Choices for consolidation strategies currently are: 1 ; multiple cycles of high dose cytarabine, 2 ; one or more cycles of high dose cytarabine followed by autologous HCT or 3 ; allogeneic stem cell transplantation from sibling or unrelated donors. The decisions regarding autologous and allogeneic HSCT are strongly influenced by the 1 ; expected relapse rate with standard chemotherapy, 2 ; the additional morbidity and mortality associated with the transplant procedure, which in turn are strongly influenced by patient-specific comorbidity, and 3 ; salvage options. A recent comparison of autologous versus allogeneic HSCT was a combined EORTC GIMEMA trial for patients less than age 46 with results stratified by cytogenetic risks: good [t 8; 21 ; or inv 16 ; ]; normal, and poor all other abnormalities ; . In the good risk group disease-free survival was 66% for autologous HSCT and 62% for allogeneic HSCT, with 6% treatment related mortality TRM ; for autologous HSCT and 17% for allogeneic HSCT. The autologous results are comparable to the CALGB data on multiple cycles of high dose cytarabine both for relapse-free survival and mortality.26 The NCCN AML panel members did not reach a consensus on a single preferred post-remission strategy for patients with better-risk cytogenetics. Either multiple cycles of dose-intensive consolidation Category 1 ; or one cycle of dose-intensive high dose cytarabine ; consolidation followed by autologous transplantation category 2B ; can produce good survival rates 60-65% ; in this group. Factors such as patient age, comorbid conditions, and features of the disease at diagnosis, including elevated leukocyte counts 50, 000 mcL ; or number of cycles of induction to achieve remission, should play a role in choosing a consolidation strategy, as should issues regarding fertility MS-9.
28. Kim, S., Chatelut, C., Kim, J. C., Howell, S. B., Cates, C., Kormanik, P. A., and Chamberlain, M. C. Extended CSF cytarabine exposure following intrathecal administration of DTC 101. J. Clin. Oncol., 11: 2186 2193, Cella, D. F., Tulsky, D. S., Gray, G., Sarafian, B., Linn, E., and Donomi, A. The functional assessment of cancer therapy scale: development and validation of the general measure. J. Clin. Oncol., 11: 570 579, Balm, M., and Hammack, J. Leptomeningeal carcinomatosis: presenting features and prognostic factors. Arch. Neurol., 53: 626 632, Fizazi, K., Asselain, B., Vincent-Salomon, A., Jouve, M., Dieras, V., Palangie, T., Beuzeboc, P., Dorval, T., and Pouillart, P. Meningeal carcinomatosis in patients with breast carcinoma. Clinical features, prognostic factors, and results of a high-dose intrathecal methotrexate regimen. Cancer Phila. ; , 77: 13151323, 1996. Jayson, G. E., Howell, A., Harris, M., Morgenstern, G., Chang, J., and Ryder, W. D. Carcinomatous meningitis in patients with breast cancer. An aggressive disease variant. Cancer Phila. ; , 74: 31353141, 1994. Grossman, S. A., Finkelstein, D. M., Ruckdeschel, J. C., Trump, D. L., Moynihan, T., and Ettinger, D. S. Randomized prospective comparison of intraventricular methotrexate and thiotepa in patients with previously untreated neoplastic meningitis. J. Clin. Oncol., 11: 561569, 1993. Boogerd, W., Hart, A. A. M., van der Sande, J. J., and Engelsman, E. Meningeal carcinomatosis in breast cancer. Prognostic factors and influence of treatment. Cancer Phila. ; , 67: 16851695, 1991. Chamberlain, M. C., and Kormanik, P. A. Prognostic significance of coexistent bulky metastatic central nervous system disease in patients with leptomeningeal metastases. Arch. Neurol., 54: 1364 1368, Grant, R., Naylor, B., Greenberg, H. S., and Junck, L. Clinical outcome in aggressively treated meningeal carcinomatosis. Arch. Neurol., 51: 457 461, Bokstein, F., Lossos, A., and Siegal, T. Leptomeningeal metastases from solid tumors. A comparison of two prospective series treated with and without intra-cerebrospinal fluid chemotherapy. Cancer Phila. ; , 82: 1756 1763, Bigner, D. D., Brown, M., Coleman, R. E., Friedman, A. H., Friedman, H. S., McLendon, R. E., Bigner, S. H., Zhao, X-G., Wilkstrand, C. J., Pegram, C. N., Kerby, T., and Zalutsky, M. R. Phase I studies of treatment of malignant gliomas and neoplastic meningitis with 131 I-radiolabeled monoclonal antibodies anti-tenascin 81C6 and antichondroitin proteoglycan sulfate Mel-14 F ab ; 2: a preliminary report. J. Neuro-Oncol., 24: 109 122, Berg, S. L., Balis, F. M., Zimm, S., Murphy, R. F., Holcenberg, J., Sato, J., Reaman, G., Steinhertz, P., Gillespie, A., and Doherty, K. Phase I II trial and pharmacokinetics of intrathecal diaziquone in refractory meningeal malignancies. J. Clin. Oncol., 10: 143148, 1992. Adamson, P., Balis, F. M., Arndt, C. A., Holcenberg, J. S., Narang, P. K., Murphy, R. F., Gillespie, A. J., and Poplack, D. G. Intrathecal 6-mercaptopurine: preclinical pharmacology, Phase I II trial, and pharmacokinetic study. Cancer Res., 51: 6079 6083, Phillips, P. C. Methotrexate toxicity. In: D. A. Rottenberg ed. ; , Neurological Complications of Cancer Treatment, pp. 115134. Boston: Butterworth-Heineman, 1991. 42. Geiser, C. F., Bishop, Y., Jaffe, N., Furman, L., Traggis, D., and Frei, E., III. Adverse effects of intrathecal methotrexate in children with acute leukemia in remission. Blood, 45: 189 195, Resar, L. M., Phillips, P. C., Kastan, M. B., Leventhal, B. G., Bowman, P. W., and Civin, C. I. Acute neurotoxicity after intrathecal 1 D-arabinofuranosylcytosine in two adolescents with acute lymphoblastic leukemia of B-cell type. Cancer Phila. ; , 71: 117123, 1993. Baker, W. J., Royer, G. L., and Weiss, R. B. Cytarabine and neurological toxicity. J. Clin. Oncol., 4: 679 693, Boogerd, W., Moffie, D., and Smets, L. A. Early blindness and coma during intrathecal chemotherapy for meningeal carcinomatosis. Cancer Phila. ; , 65: 452 457.

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The weighted average costs-per-prescription for each product separately and for the entire data set are related parameters. The model calculates the weighted average cost-per-prescription for each product by dividing the total AWP $ ; for each strength of the prduct by the number of prescriptions. Cytarabine is given by a slow injection into a vein or under the skin. Occasionally it may be injected directly into the fluid around the spine. Cytarabine must only be given by a doctor or nurse. Your doctor will decide what dose, how often and how long you will receive it. This depends on your condition and other factors, such as your weight, age, blood tests and whether or not other medicines are being given at the same time. Cytarabine Injection may be given alone or in combination with other drugs.
In 2001, the Dr. Ricardo Jorge National Health Institute published the results of a project which, among other indications, gave information about the functional capability of the elderly. These results indicate that 8.3% of these individuals claim to be seriously incapacitated, with an estimated 12% of individuals who claim that they need help to be able to perform daily routine activities. According to this study, a large majority of these 92.5% ; are helped on an almost daily basis22. These results are important, as very little is known about functional capability among the different age groups in Portugal. At a time when the first steps are being taken in providing permanent care services, these figures are of great relevance in supporting any decision making. Adams J, Collaco-Moraes Y and de Belleroche J 1996 ; Cyclooxygenase-2 induction in cerebral cortex: An intracellular response to synaptic excitation. J Neurochem 66: 6 13. Akaike A, Kaneko S, Tamura Y, Nakata N, Shiomi H, Ushikubi F and Narumiya S 1994 ; Prostaglandin E2 protects cultured cortical neurons against N-methyl-Daspartate receptor-mediated glutamate cytotoxicity. Brain Res 663: 237243. Allgaier C and Meder W 1995 ; Cultured chick sympathetic neurons: Prostanoid EP1 receptor-mediated facilitation of noradrenaline release. Naunyn-Schmiedeberg's Arch Pharmacol 352: 447 450. Bhattacharyya DK, Lecomte M, Dunn J, Morgans DJ and Smith WL 1995 ; Selective inhibition of prostaglandin endoperoxide synthase-1 cyclooxygenase-1 ; by valeryl salicylic acid. Arch Biochem Biophys 317: 19 24. Breder CD, Dewitt D and Kraig RP 1995 ; Characterization of inducible cyclooxygenase in rat brain. J Comp Neurol 355: 296 315. Breder CD, Smith WL, Raz A, Masferrer J, Seibert K, Needleman P and Saper CB 1992 ; Distribution and characterization of cyclooxygenase immunoreactivity in the ovine brain. J Comp Neurol 322: 409 438. Cazevieille C, Muller A, Meynier F, Dutrait N and Bonne C 1994 ; Protection by prostaglandins from glutamate toxicity in cortical neurons. Neurochem Int 24: 395398. Cole DJ, Patel PM, Reynolds L, Drummond JC and Marcantonio S 1993 ; Temporary focal cerebral ischemia in spontaneously hypertensive rats: The effect of ibuprofen on infarct volume. J Pharmacol Exp Ther 266: 17131717. Collaco-Moraes Y, Aspey B, Harrison M and de Belleroche J 1996 ; Cyclooxygenase-2 messenger RNA induction in focal cerebral ischemia. J Cereb Blood Flow Metab 16: 1366 1372. Copeland RA, Williams JM, Giannaras J, Nurnberg S, Covington M, Pinto D, Pick S and Trzaskos JM 1994 ; Mechanism of selective inhibition of the inducible isoform of prostaglandin G H synthase. Proc Natl Acad Sci USA 91: 1120211206. Cullingford TE, Bhakoo K, Peuchen S, Dolphin CT, Patel R and Clark JB 1998 ; Distribution of mRNAs encoding the peroxisome proliferator-activated receptor alpha, beta, and gamma and the retinoid X receptor alpha, beta, and gamma in rat central nervous system. J Neurochem 70: 1366 1375. DeWitt DL, Meade EA and Smith WL 1993 ; PGH synthase isoenzyme selectivity: The potential for safer nonsteroidal antiinflammatory drugs. J Med 95: 40S 44S. Dugan LL, Sensi SL, Canzoniero LM, Handran SD, Rothman SM, Lin TS, Goldberg MP and Choi DW 1995 ; Mitochondrial production of reactive oxygen species in cortical neurons following exposure to N-methyl-D-aspartate. J Neurosci 15: 6377 6388. Dumuis A, Sebben M, Haynes L, Pin JP and Bockaert J 1988 ; NMDA receptors activate the arachidonic acid cascade system in striatal neurons. Nature Lond ; 336: 68 70. Futaki N, Takahashi S, Yokoyama M, Arai I, Higuchi S and Otomo S 1994 ; NS-398, a new anti-inflammatory agent, selectively inhibits prostaglandin G H synthase cyclooxygenase COX-2 ; activity in vitro. Prostaglandins 47: 5559. Greig GM, Francis DA, Falgueyret JP, Ouellet M, Percival MD, Roy P, Bayly C, Mancini JA and O'Neill GP 1997 ; The interaction of arginine 106 of human prostaglandin G H synthase-2 with inhibitors is not a universal component of inhibition mediated by nonsteroidal anti-inflammatory drugs. Mol Pharmacol 52: 829 838. Hewett SJ 1999 ; Interferon-gamma reduces cyclooxygenase-2-mediated prostaglandin E2 production from primary mouse astrocytes independent of nitric oxide formation. J Neuroimmunol 94: 134 143. Hla T, Bishop-Bailey D, Liu CH, Schaefers HJ and Trifan OC 1999 ; Cyclooxygenase-1 and -2 isoenzymes. Int J Biochem Cell Biol 31: 551557. Iadecola C, Forster C, Nogawa S, Clark HB and Ross ME 1999 ; Cyclooxygenase-2 immunoreactivity in the human brain following cerebral ischemia. Acta Neuropathol Berl ; 98: 9 14. Kainu T, Wikstrom AC, Gustafsson JA and Pelto-Huikko M 1994 ; Localization of the peroxisome proliferator-activated receptor in the brain. Neuroreport 5: 2481 2485. Keller M, Jackisch R, Seregi A and Hertting G 1985 ; Comparison of the prostanoid forming capacity of neuronal and astroglial cells in primary cultures. Neurochem Int 7: 655 665. Kimura H, Okamoto K and Sakai Y 1985 ; Modulatory effects of prostaglandin D2, E2 and F2 alpha on the postsynaptic actions of inhibitory and excitatory amino acids in cerebellar Purkinje cell dendrites in vitro. Brain Res 330: 235244. Kliewer SA, Lenhard JM, Willson TM, Patel I, Morris DC and Lehmann JM 1995 ; A prostaglandin J2 metabolite binds peroxisome proliferator-activated receptor gamma and promotes adipocyte differentiation. Cell 83: 813 819. Kliewer SA, Sundseth SS, Jones SA, Brown PJ, Wisely GB, Koble CS, Devchand P, Wahli W, Willson TM, Lenhard JM and Lehmann JM 1997 ; Fatty acids and eicosanoids regulate gene expression through direct interactions with peroxisome proliferator-activated receptors alpha and gamma. Proc Natl Acad Sci USA 94: 4318 4323. Koh JY and Choi DW 1987 ; Quantitative determination of glutamate mediated cortical neuronal injury in cell culture by lactate dehydrogenase efflux assay. J Neurosci Methods 20: 8390. Krey G, Braissant O, L'Horset F, Kalkhoven E, Perroud M, Parker MG and Wahli W 1997 ; Fatty acids, eicosanoids, and hypolipidemic agents identified as ligands of peroxisome proliferator-activated receptors by coactivator-dependent receptor ligand assay. Mol Endocrinol 11: 779 791 and cytomel.

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The advantages of liposomal cytarabine are that the drug needs to be administered only every 2 weeks, and, in principle, by maintaining a prolonged cytotoxic concentration of cytarabine, slowly dividing cells are more likely to be exposed to the drug while in s phase.
Toxicity was assessed at the weekly visits and recorded according to the WHO toxicity criteria [16]. Complete blood cell count and chemistry were performed once a week in all patients, and every other day in cases of grade 4 hematological toxicity. Bi-dimensional echocardiography was performed on completion of treatment. Clinical tumor response was assessed within 2 weeks from the end of chemotherapy, and classified according to standard WHO criteria [16]. Clinical examination, mammography and breast ultrasonography were performed to assess the regression of the tumor in both breast and axilla. In addition, chest X-ray, abdomen ultrasonography and serum tumor markers CEA, CA-15.3 ; were also performed in order to exclude the presence of distant metastases. For the pathologic analysis of response, the amount of residual epithelial neoplastic cells in the tumor mass, the mitotic index in malignant epithelial cells and the location of malignant component invasive versus intraductal ; were taken into account [17]. Response in the breast was scored as follows: class I absence of residual malignant epithelial cells class II persistence of only in situ residual malignant component class III only focal invasive tumor residuals, with substantial histological modifications of the tumor tissue related to chemotherapy and class IV no substantial modifications in the tumor mass related to chemotherapy ; . Patients showing a class I or II response in the breast, together with absence of axillary involvement, were considered as pathological complete responders and cytoxan.
The risk associated with depression was greatest among patients with frequent premature ventricular complexes. Socioeconomic factors are also important; sudden cardiac death after myocardial infarction increases 3-fold in men with low levels of education and complex ventricular ectopy compared with better educated men who have the same arrhythmias. History can provide clues to the high-risk patient. For example, in patients with ventricular tachycardia after myocardial infarction, on the basis of clinical history, the following 4 variables identify patients at increased risk of sudden cardiac death: 1 ; syncope at the time of the first documented episode of arrhythmia, 2 ; NYHA class III or IV, 3 ; ventricular tachycardia fibrillation occurring early after myocardial infarction 3 days to 2 months ; , and 4 ; history of previous myocardial infarctions.21 In some patients, family history can be important.22 Left ventricular dysfunction is a major independent predictor of total and sudden cardiac mortality in patients with ischemic and nonischemic cardiomyopathy.23 For example, in survivors of cardiac arrest who have a left ventricular ejection fraction 30%, the risk of sudden cardiac death exceeds 30% over 1 to 3 years if the patients do not have inducible ventricular tachycardia, whereas it ranges between 15% and 50% in those who have inducible ventricular tachyarrhythmias despite therapy with drugs that suppress the inducible arrhythmias or with empirical amiodarone.24, 25 Whether an ICD will reduce total mortality in patients with severe left ventricular dysfunction alone is the subject of several prospective trials, including the Multicenter Automatic Defibrillator Implantation Trial MADIT II ; and the Sudden Cardiac Death in Heart Failure Trial SCD-HeFT ; .26 These patients have competing causes of death, and unless death is caused primarily by a ventricular tachyarrhythmia that can be terminated by prompt defibrillation, the ICD may not have an important impact. Although prompt defibrillation generally restores sinus rhythm with a very high success rate, it may not be as successful in patients with very advanced ventricular dysfunction. Certain ECG abnormalities can help identify patients at increased risk for sudden cardiac death. These include the presence of AV block or intraventricular conduction defects and QT prolongation, an increase in resting heart rate to 90 bpm, and increased QT dispersion in survivors of out-ofhospital cardiac arrest. A recent study failed to support the usefulness of QT dispersion in predicting risk in patients after myocardial infarction.27 The presence of complex ventricular arrhythmias, such as nonsustained ventricular tachycardia, is also a marker1 Figure 5.

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Poisoning by primarily systemic agents 963.0 Antiallergic and antiemetic drugs Antihistamines Chlorpheniramine Diphenhydramine Diphenylpyraline Thonzylamine Tripelennamine phenothiazine-based tranquilizers 969.1 ; Antineoplastic and immunosuppressive drugs Azathioprine Busulfan Chlorambucil Cyclophosphamide Cytarabine Fluorouracil Mercaptopurine thio-TEPA antineoplastic antibiotics 960.7 ; Acidifying agents Alkalizing agents Enzymes, not elsewhere classified Penicillinase Vitamins, not elsewhere classified Vitamin A Vitamin D nicotinic acid 972.2 ; vitamin K 964.3 ; Other specified systemic agents Heavy metal antagonists Unspecified systemic agent and dacarbazine.

55 Andrews RG, Singer JW, Bernstein ID. Precursors of colony-forming cells in humans can be distinguished from colony-forming cells by expression of the CD33 and CD34 antigens and light scatter properties. J Exp Med 1989; 169: 1721-1731. Radich J, Sievers EL. New developments in the treatment of acute myeloid leukemia. Oncology Huntingt ; 2000; 14: 125-131. Ruffner KL, Matthews DC. Current uses of monoclonal antibodies in the treatment of acute leukemia. Semin Oncol 2000; 27: 531-539. Scheinberg DA, Tanimoto M, McKenzie S et al. Monoclonal antibody M195: a diagnostic marker for acute myelogenous leukemia. Leukemia 1989; 3: 440-445. Feldman E, Kalaycio M, Schulman P et al. Humanized monoclonal anti-CD33 antibody HuM195 in the treatment of relapsed refractory acute myelogenous leukemia AML ; : preliminary report of a phase II study. Proc Soc Clin Oncol 1999; 18: 4a. Jurcic JG, DeBlasio A, Dumont L et al. Molecular remission induction with retinoic acid and anti-CD33 monoclonal antibody HuM195 in acute promyelocytic leukemia. Clin Cancer Res 2000; 6: 372-380. Sievers EL, Appelbaum FR, Spielberger RT et al. Selective ablation of acute myeloid leukemia using antibody-targeted chemotherapy: a phase I study of an anti-CD33 calicheamicin immunoconjugate. Blood 1999; 93: 3678-3684. Sievers EL, Larson RA, Estey E et al. Efficacy and safety of CMA-676 in patients with AML in first relapse. Blood 1999; 94: 696a. Zein N, Sinha AM, McGahren WJ et al. Calicheamicin gamma 1I: an antitumor antibiotic that cleaves doublestranded DNA site specifically. Science 1988; 240: 1198-1201. Sievers EL, Larson RA, Estey E et al. Comparison of the efficacy and safety of gemtuzumab ozogamicin CMA-676 ; in patients 60 and 60 years of age with AML in first relapse. Proc Soc Clin Oncol 2000; 19: 8a. Earle C, Menzin J, Lang K et al. Short-term outcomes after treatment for relapsed AML: a comparison of recent CMA676 clinical trial data and historical control data. Proc Soc Clin Oncol 2000; 19: 1775a. Sievers EL, Larson RA, Estey E et al. Prolonged disease-free survival in patients with acute myeloid leukemia in first relapse treated with gemtuzumab ozogamicin Mylotarg, CMA-676 ; followed by hematopoietic stem cell transplantation. Blood 2000; 96: 320a. Sievers EL. Clinical studies of new "biologic" approaches to therapy of acute myeloid leukemia with monoclonal antibodies and immunoconjugates. Curr Opin Oncol 2000; 12: 30-35. Leopold LH, Berger MS, Cheng SC et al. Comparative efficacy and safety of gemtuzumab ozogamicin monotherapy and high dose cytarabine combination therapy in the treatment of patients with AML. Blood 2000; 96: 504a. Clift RA, Buckner CD, Appelbaum FR et al. Allogeneic marrow transplantation in patients with acute myeloid leukemia in.

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Not Approved if: Patient does not meet the above stated criteria Patient has any contraindications the use of azacitidine. Special Considerations: Azacitidne is the first agent approved for the treatment of MDS. It offers promising activity with partial and complete responses in some patients, although the results of comparative studies with other agents, such as cytarabine and decitabine, are necessary to determine its place in therapy and daclizumab. Iannuzzi A, Licenziati MR, Acampora C, et al.: Carotid artery stiffness in obese children with the metabolic syndrome. J Cardiol 97: 528531, 2006. Cytarabine is used to treat blood cancers acute non-lymphocytic leukemia, acute lymphocytic leukemia and chronic myelocytic leukemia and dactinomycin. The scientists combined imatinib 600 mg per day with cytarabine ara-c ; and idarubicin.
Activation of the PTEN mTOR STAT3 pathway in breast cancer stem-like cells is required for viability and maintenance. Proc Natl Acad Sci U S A. 2007 Oct 9; 104 41 ; : 16158-63. Epub 2007 Oct 2. Zhou J, Wulfkuhle J, Zhang H, Gu P, Yang Y, Deng J, Margolick JB, Liotta LA, Petricoin E 3rd, Zhang Y. : ncbi.nlm.nih.gov sites entrez?Db pubmed&Cmd ShowDetail View&TermToSearch 17911267&ordinalpos 2&itool EntrezSystem2.PEnt rez.Pubmed.Pubmed ResultsPanel.Pubmed RVDocSum Nutrition-induced ketosis alters metabolic and signaling gene networks in liver of periparturient dairy cows. Physiol Genomics. 2007 Oct 9; [Epub ahead of print] Loor JJ, Everts RE, Bionaz M, Dann HM, Morin DE, Oliveira R, Rodriguez-Zas SL, Drackley JK, Lewin HA. : ncbi.nlm.nih.gov sites entrez?Db pubmed&Cmd ShowDetail View&TermToSearch 17925483&ordinalpos 1&itool EntrezSystem2.PEnt rez.Pubmed.Pubmed ResultsPanel.Pubmed RVDocSum Identification of the protein targets of the reactive metabolite of teucrin a in vivo in the rat. Chem Res Toxicol, Oct 2007; 20 10 ; : 1393-408. A Druckova, RL Mernaugh, AJ Ham, and LJ Marnett. : highwire anford cgi medline pmid; 17892266?maxtoshow & HITS &hits &RESULTFORMAT &fulltext ingenuity + pathway + analysis&a ndorexactfulltext and&searchid 1&FIRSTINDEX 0&fdate 9 1 2007&res ourcetype HWCIT Candidate Genes That Determine Response to Salt in the Stroke-Prone Spontaneously Hypertensive Rat. Congenic Analysis. Hypertension. 2007 Oct 15; [Epub ahead of print] Graham D, McBride MW, Gaasenbeek M, Gilday K, Beattie E, Miller WH, McClure JD, Polke JM, Montezano A, Touyz RM, Dominiczak AF. : ncbi.nlm.nih.gov sites entrez?Db pubmed&Cmd ShowDetail View&TermToSearch 17938382&ordinalpos 1&itool EntrezSystem2.PEnt rez.Pubmed.Pubmed ResultsPanel.Pubmed RVDocSum PADGE: analysis of heterogeneous patterns of differential gene expression. Physiol Genomics. 2007 Oct 9; [Epub ahead of print] Li L, Chaudhuri A, Chant J, Tang Z. : ncbi.nlm.nih.gov sites entrez?Db pubmed&Cmd ShowDetail View&TermToSearch 17925482&ordinalpos 1&itool EntrezSystem2.PEnt rez.Pubmed.Pubmed ResultsPanel.Pubmed RVDocSum Genomic expression pathways associated with brain injury after cardiopulmonary bypass. J Thorac Cardiovasc Surg. 2007 Oct; 134 4 ; : 9961005. Ramlawi B, Otu H, Rudolph JL, Mieno S, Kohane IS, Can H, Libermann TA, Marcantonio ER, Bianchi C, Sellke FW. : ncbi.nlm.nih.gov sites entrez?Db pubmed&Cmd ShowDetail View&TermToSearch 17903520&ordinalpos 1&itool EntrezSystem2.PEnt rez.Pubmed.Pubmed ResultsPanel.Pubmed RVDocSum and dalteparin.

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Figure 4. Combination of cytarabine and SU11248 on apoptosis. MV4-11 cells cultured in the presence of SU11248, cytarabine, or both were analyzed for PARP cleavage by Western blot after 24 hours of exposure to agents. Representative results from 1 of 3 experiments are displayed. Increasing doses of either single agent increased the amount of cleaved PARP detected. The combination of agents produced a dramatic increase in the cleavage product with almost no full-length PARP detected and cytarabine.
Comparison of nitrogen mustard, cytarabine and dacarbazine as pleural sclerosing agents in rabbits. E. Marchi, F.S. Vargas, L.R. Teixeira, D.J. Fagundes, L.M.M.F. Silva, A.O. Carmo, R.W. Light. ERS Journals Ltd 1997. ABSTRACT: We have previously shown that the intrapleural injection of mitozantrone but not bleomycin resulted in pleural fibrosis. Mechlorethamine hydrochloride nitrogen mustard ; was used extensively in the past to control malignant effusions, with relatively good success. The objective of this study was to determine if the intrapleural injection of nitrogen mustard would produce pleural sclerosis in our experimental model in rabbits. We therefore evaluated sclerosing capabilities of nitrogen mustard as well as those of cytarabine and dacarbazine. Nitrogen mustard 0.4 and 0.8 mgkg-1 ; , cytarabine 3, 6 and 20 mgkg-1 ; and dacarbazine 4, 8 and 20 mgkg-1 ; were instilled intrapleurally into anaesthetized rabbits. Twenty eight days after the instillation, the animals were killed, and the pleural spaces were assessed grossly for evidence of pleurodesis and microscopically for evidence of fibrosis and inflammation. The intrapleural injection of 0.8 mgkg-1 nitrogen mustard was effective in creating pleural fibrosis, either grossly or microscopically. The mean degree scale 04 ; of gross pleurodesis in the rabbits that received 0.8 mgkg-1 nitrogen mustard was 3.21.0 and the mean degree of microscopic pleural fibrosis was 3.50.8. The intrapleural injection of 0.4 mgkg-1 nitrogen mustard and the different doses of cytarabine 3, 6 and 20 mgkg-1 ; and dacarbazine 4, 8 and 20 mgkg-1 ; were ineffective in producing pleurodesis. From this study, we conclude that the intrapleural injection of 0.8 mgkg-1 of nitrogen mustard produces clinically significant pleurodesis in rabbits. Consideration should be given to future clinical studies utilizing 0.60.8 mgkg-1 nitrogen mustard intrapleurally for the treatment of malignant pleural effusion. Eur Respir J 1997; 10: 598602 and damiana.

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