Administering methotrexate by injection
465. Galton, D.A.G., Till, M. 1955 ; Myleran in chronic myeloid leukaemia. Lancet 1: 425-430. Gluckman, E., Devergie, A., Lokiec, F., Poirier, O., and Baumelou, A. 1981 ; Nephrotoxicity of cyclosporin A in bone-marrow transplantation.Lancet 2: 144-5. Gottlieb, J.A., Mendelson, D., Serpick, A.A. 1970 ; An evaluation of large intermittent intravenous doses of cyclophosphamide NSC-26271 ; in the treatment of metastatic malignant melanoma. Cancer Chemother Rep 54: 365-7. Grande T & Bueren J.A. 1995 ; Analysis of the hematopoiesis in mice irradiated with 500mGy of X-rays at different stages of development. Radiation Res 143: 327-333 Grem, J.L., Tutsch, K.D., Simon, K.J., Alberti, D.B., Willson, J.K., Tormey, D.C., Swaminathan, S., Trump, D.L. 1987 ; Phase I study of taxol administered as a short i.v. infusion daily for 5 days. Cancer Treat Rep 71: 11791184. Greenberg P., Bax I., Mara B., Schrier S., Alterations of granulopoiesis following chemotherapy. 1974 ; Blood 44: 375-383 Gribaldo L, Piccirillo M, Casati S, Collotta A, Mineo E, Pessina A. 1998 ; Drug sensitivity of Granulocyte-Macrophage precursors GM-CFU ; from fresh murine bone marrow and from longterm bone marrow cultures. Toxicology in vitro 12: 39-45 Gribaldo L, Bueren J, Deldar A, Okland P, Meredith C, Moneta D, Mosesso P, Parchment R, Parent-Massin D, Pessina A, San Roman J, Schoeters G. 1996 ; The use of "in vitro" systems for evaluating haematotoxicity. The report of recommendations of ECVAM workshop 14. ATLA 24: 211231. Hamburger, A.W., Zsebo, K, and Chow, F.P. 1993 ; Failure of stem cell factor to ameliorate AZTinduced anemia in immunodeficient mice. Eur J Haematol 50: 172-8. Hutton, J.J., Von Hoff, D.D., Kuhn, J., Phillips, J., Hersh, M., Clark, G. 1984 ; Phase I clinical investigation of 5'-monophosphate NSC 312887 ; , a new purine antimetabolite. Cancer Res 44: 4183-4186. Intramural Toxicology Branch. 1984 ; Report # 84-005. Bethesda, MD 20817 USA: DCT, U.S. National Cancer Institute. Kruter, F., Eisenberger, M., Sinibaldi, V. et al. 1992 ; Phase II trial of 5 day continuous intravenous infusion of 6-thioguanine in patients with recurrent and metastatic squamous cell carcinoma of the head and neck. Invest New Drugs 10: 89-91. Lewis, I.D., Rawling, T., Dyson, P.G., Haylock, D.N., Juttner, D.N., To, L.B. 1996 ; Standardization of the CFU-GM assay using hematopoietic growth factors. J Hematother 5: 625630. Lokich, J.J., Curt, G. 1985 ; A phase I and pharmacology study of continuous-infusion low-dose methotrexate administration. Cancer 56: 2391-2394.
Effects of Cofactors on the Labeling of NuoM by [3H]azido-Q--Table 1 shows the effects of 400 mM of NADH, NAD and ATP on [3H]azido-Q labeling of NuoM. NAD and ATP had essentially no effect, which is consistent with the data recently reported by Dr.Yagi's group during photoaffinity labeling of inhibitor quinone probes in complex I when isolated submitochondrial particles were used 37 ; . [3H]azido-Q labeling of NuoM subunit was not influenced by prior NADH incubation, even though NADH has been reported to stimulate the labeling of inhibitor quinone probes in mitochondrial complex I 37, 39 ; . Similar data was also.
Methotrexate vomiting
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In subsequent pre-clinical experiments conducted in 2001 and 2002, the Company studied the toxicity reduction of DAVANAT 5-FU, in accordance with FDA guidelines and recommendations, on rats acute and long-term toxicity study ; and dogs acute and long-term toxicity study ; . The purpose of this study was to measure the effect of DAVANAT 5-FU on blood structure and survival of these animals. Results indicated that DAVANAT 5-FU decreased toxicity, resulting in lower animal mortality, as well as decreased loss of blood structure components versus the results in animals that were administered 5-FU alone. These studies were presented to the FDA as part of an Investigational New Drug IND ; submission. Additional toxicity studies on rats were conducted using escalating dosages of DAVANAT, with results submitted to the FDA in an amendment to the IND in support of the Phase I clinical trials. The results of these additional toxicity studies were such that the FDA permitted the Company to commence Phase I clinical trials. Efficacy Studies Independent studies were conducted at Southern Research Institute and at Charles River Laboratories to test a potential change in the therapeutic efficacy of DAVANAT 5-FU. Results from the study demonstrated that DAVANAT could increase the efficacy of 5-FU when administered into cancercarrying animals. The studies, which were conducted with two different human colon tumors implanted into test animals, demonstrated a reduction in tumor size following administration of 5-FU alone, with a more significant decrease achieved following the administration of DAVANAT 5-FU, illustrated in Figure 5. With these results, Pro-Pharmaceuticals believes that DAVANAT may significantly decrease the toxicity of chemotherapeutics.
P.217 ANTITUMOR ACTIVITY OF MANNAN-METHOTREXATE CONJUGATE IN VITRO AND IN VIVO R. Budzynska, D. Nevozhay, M.S. Omar, A. Opolski & J. Boratynski IIET, PAS, Wroclaw, Poland Methotrexate MTX ; is widely used in the treatment of the number of oncological and hematological diseases. However, MTX also has known limitations, due to its low plasma half-life, toxicity for normal proliferating cells and resistance to the drug. This motivated scientists to look for the ways of the drug improvement. Others and we have recently published several reports about coupling MTX to different macromolecular carriers. This strategy seems to be perspective in obtaining preparations with amended antitumor properties. The aim of this work was to investigate anticancer activity of MTX coupled with mannan carrier. The obtained conjugate was pure and stable at different conditions. Three cell lines were applied for in vitro studies: A549 human non-small cell lung carcinoma ; , B16 murine melanoma ; and P388 murine leukemia ; . The in vitro cytotoxic effect of all agents was examined after 72-hour exposure of the cultured cells to varying concentrations of the tested agents and computing average 50% inhibitory concentration IC50 ; dose. The investigation was also performed in the in vivo murine leukemia model P388 ; . Mice, randomly divided in groups, were injected with 10 6 leukemia cells i.p., and 24 hours later each mouse was injected with 80 mg kg of appropriate agent. Studies revealed that mannan-MTX conjugate had from 30 to 45-fold smaller in vitro antiproliferative activity in comparison with free MTX. IC50 for A549, B16 and P388 cell lines were 1.814 0.104 microg ml, 3.187 2.355 microg ml, 0.1193 0.0573 microg ml for mannan-MTX and 0.058 0.002 microg ml, 0.068 0.021 microg ml, 0.0036 0.0006 microg ml for free MTX respectively. We have also evaluated the antitumor properties of mannan-MTX conjugate in in vivo model. Results of the experiment revealed that mannan-MTX conjugate had the advantage over the free MTX in terms of antitumor effect in vivo. Mice treated by the conjugate benefited from the statistically significant longer survival in comparison with mice treated by the free MTX p 0.001 ; and nontreated leukemia-bearing animals in control group p 0.001 ; . Median survival times were 11, 16 and 22 days for control, free MTX and conjugate treated groups respectively. Data on average weight changes during the run of the experiment allow us to conclude that mannan-MTX conjugate has somehow higher toxicity in comparison with free MTX. However, this did not result in.
Methotrexate for ectopic pregnancy and hair colouring
Justed models. For both adjusted models, the baseline covariate with the highest individual hazard ratio estimate was heart failure 1.92 in the systolic pressure model and 1.94 in the diastolic pressure model ; , indicating an almost doubled risk for the primary outcome after adjusting for blood pressure. However, the interactions of baseline heart failure with systolic pressure and systolic pressure squared were not statistically significant when added to this model. A similar observation was made for the diastolic pressure model. The bottom panel of Figure 2 shows the relative risk for reduced or increased blood pressure adjusted for differences in baseline heart failure, with a nadir estimated at 116 83 mm Hg. For diastolic pressure, adjusting for baseline heart failure alone slightly reduced the relative level of risk but did not change the shape of the curve compared with the unadjusted analysis. A J-shaped relationship with diastolic pressure was also observed for death from all causes the outcome that accounted for the highest proportion of events in the primary outcome; data not shown for MI fatal and nonfatal and to a much lesser extent for stroke fatal and nonfatal ; Figure 3 ; . The incidence ratio between MI and stroke remained remarkably constant over a wide range of blood pressure strata. However, this ratio increased with a progressive decrease in diastolic blood pressure Figure 3 ; . The preponderance of MI over stroke with progressively decreasing diastolic blood pressure suggests that the compromised coronary perfusion resulting from low diastolic blood pressure could be a factor. Interactions between diastolic pressure and the primary outcome were statistically significant only for U.S. residency, hypercholesterolemia, previous revascularization, and diabetes. Sex P 0.050 ; and smoking history P 0.080 ; were borderline significant P 0.1 ; . Analysis of hazard ratios for the primary outcome versus diastolic and methylcellulose.
Conclusion Human data on local irritation corrosion caused by DODMAC are not available. Pure DODMAC exhibits only moderate skin irritation in rabbits, while the technical grade substance containing 12% isopropanol ; demonstrated severe corrosive properties. The relevance of such data for the assessment of the skin irritant properties of pure DODMAC is questionable. However, the local corrosivity of technical grade DODMAC is crucial for the evaluation of results of toxicological testing performed in order to assess acute effects after application of DODMAC. Based on the reported data, technical grade "DODMAC" containing approximately 12% isopropanol ; is to be classified "C, corrosive" and labeled "R 34, causes burns" according to the EU legislation.
Normal values. The injection of methotrexate on days 0 and 7 resulted in a 51% decrease of femoral granuloid cell values on day 8 p 0.05 ; followed by a return to normal values between days 12-16. After that, a transient no significant reduction in the femoral granuloid compartment was seen before a new recovery took place. Administration of filgrastim, starting on day 8, prevented the drop in femoral granuloid cells found on day 20 in mice treated with MTX alone. There were not stimulating effects of the hemopoietic growth factor along the period of observation, except a transient increase of granuloid precursor cells per femur noted on day 24 in filgrastim treated mice p 0.05 ; , when compared with control values. These results suggest a decrease in the proliferation capacity of bone marrow myeloid precursors in mice pretreated with methotrexate. The effects of two doses of methotrexate treatment alone or followed by filgrastim administration on spleen granuloid precursor cells values are shown in figure 4. While methotrexate treatment alone had little or no effect on granulocytic population content, daily administration of filgrastim starting on day 8 24 h after the last dose of MTX ; , had an important stimulatory and methyldopa.
Methotrexate use in multiple sclerosis
Combination therapy of infliximab and methotrexate in RA C. Antoni & J.R. Kalden.
Acknowledgments-We thank Dr. Richard B. Kim and Dr. Diarmuid OShea Divisionof Clinical Pharmacology, Vanderbilt University Medical School ; forphenotyping some of the individuals used in this study, Dr. Jerome Lasker Mt. Sinai School of Medicine, New York, NY ; , for providing the polyclonal antibody to human CYP2C9, and Dr. Gordon Ibeanu NIEHS ; for helpful suggestions during this work and methysergide.
Acromegaly was diagnosed, in 1976, in a 16-year-old girl with secondary amenorrhoea. The mean serum GH concentration was , 400 mU l, decreasing to , 150 mU l with bromocriptine 40 mg daily `safe' GH concentrations for treated acromegaly are , 5 mU l ; External pituitary irradiation was followed, shortly after, by probable pituitary apoplexy. In 1977, the patient underwent trans-sphenoidal surgery with removal of GH-staining adenoma. Between 1978 and 1986 there was massive expansion of the tumour through the right cavernous sinus into the infratemporal fossa, with an increase in serum GH from 42 to .1000 mU l and intractable trigeminal pain, requiring craniotomy and transfrontal resection of intra-cavernous-sinus tumour. The pain improved and serum GH concentrations decreased to , 350 mU l. In 1988, the patient received stereotactic radiotherapy to an orbital extension of tumour, but the infratemporal portion could not be safely targeted. GH concentrations decreased to , 200 mU l. In 1991, a nadir GH of 70 was achieved with subcutaneous octreotide 2500 mg daily by continuous infusion. Treatment with cabergoline caused adverse psychological symptoms. Two cycles of chemotherapy Iomustine and 5-fluorouracil ; were unsuccessful.
In physiological saline. Each infusion was separated by 1-h infusions of 10% homologous serum in saline. All infusions were performed at a rate of 6.61 ml h using a perfusor pump "Perfusor W. Germany ; . Blood samples ipsilateral UOV every 20 mm and metolazone.
Caution with a significant stabilizing effect of mayo methotrexate prescribing information foundation has risk of hiv aids patients.
1. Farber S, Diamond LK, Mercer RD, et al. Temporary remissions in acute leukemia in children produced by the folic acid antagonist, 4-aminopteroyl glutamaic acid aminopterin ; . N Engl J Med 1948; 238: 787 Kersey JH. Fifty years of studies of the biology and therapy of childhood leukemia. Blood 1997; 90: 4243. Pui CH, Evans WE. Treatment of acute lymphoblastic leukemia. N Engl J Med 2006; 354: 166 Moos PJ, Raetz EA, Carlson MA, et al. Identificationof gene expression profiles that segregate patients with childhoodleukemia. Clin Cancer Res 2002; 8: 3118 Yeoh EJ, Ross ME, Shurtleff SA, et al. Classification, subtype discovery, and prediction of outcome in pediatric acute lymphoblastic leukemia by gene expression profiling. Cancer Cell 2002; 1: 133 Holleman A, Cheok MH, den Boer ML, et al. Gene expression patterns in drug resistant acute lymphoblastic leukemia cells and response to treatment. N Engl J Med 2004; 351: 533 Cario G, Stanulla M, Fine BM, et al. Distinct gene expression profiles determine molecular treatment response in childhood acute lymphoblastic leukema. Blood 2005; 105: 821 Lugthart S, Cheok MH, den Boer ML, et al. Identification of genes associated with chemotherapy cross resistance and treatment response in childhood acute lymphoblastic leukemia. Cancer Cell 2005; 7: 375 Kato GJ, Quddus FF, Shuster JJ, et al. High glucocorticoid receptor content of leukemic blasts is a favorable prognostic factor in childhood acute lymphoblastic leukemia. Blood 1993; 82: 2304 den Boer ML, Pieters R, Kazemier KM, et al. Relationship between major vault protein lung resistance protein, multidrug resistance-associated protein, P-glycoprotein expression, and drug resistance in childhood leukemia. Blood 1998; 91: 2092 Dhooge C, De Moerloose B, Laureys G, et al. P-glycoprotein is an independent prognostic factor predicting relapse in childhood acute lymphoblastic leukemia: results of a 6 year prospective study. Br J Haematol 1999; 105: 676 Sauerbrey A, Sell W, Steinbach D, et al. Expression of the BCRP gene ABCG2 MXR ABCP ; in childhood acute lymphoblastic leukemia. Br J Haematol 2002; 118: 147 Levy AS, Sather HN, Steinherz PG, et al. Reduced folate carrier and dihydrofolate reductase expression in acute lymphoblastic leukemia may predict outcome: a Children's Cancer Group study. J Pediatr Hematol Oncol 2003; 25: 688 Steinbach D, Wittig S, Cario G, et al. The multidrug resistance-associated protein 3 MRP3 ; is associated with a poor outcome in childhood ALL and may acount for the worse prognosis in male patients and T-cell immunophenotype. Blood 2003; 102: 4493 Fine BM, Kaspers GJL, Ho M, et al. A genome-wide view of the in vitro response to L-asparaginase in acute lymphoblastic leukemia. Cancer Res 2005; 65: 291 Guerin E, Entz-Werle N, Eyer D, et al. Modification of topoisomerase genes copy number in newly diagnosed childhood acute lymphoblastic leukemia. Leukemia 2003; 17: 532 Kager L, Cheok M, Yang W, et al. Folate pathway gene expression differs in subtypes of acute lymphoblastic leukemia and influences methotrexate pharmacodynamics. J Clin Invest 2005; 115: 110 Holleman A, de Boer ML, Menezes RX, et al. The expression of 70 apoptosis genes in relation to lineage, genetic subtype, cellular drug resistance, and outcome in childhood acute lymphoblastic leukemia. Blood 2005; 107: 769 Plasschaert SLA, de Bont ESJM, Boezen M, et al. Expression of multidrug resistance-associated proteins predicts prognosis in childhood and adult acute lymphoblastic leukemia. Clin Cancer Res 2005; 11: 8661 Gorlick R, Goker E, Trippett T, et al. Intrinsic and acquired resistance to methotrexate in acute leukemia. N Engl J Med 1996; 335: 1041 Shah SJ, Taub JW, Witt TL, et al. Relationship of p15 and p16 gene alterations to elevated dihydrofolate reductase in childhood acute lymphoblastic leukemia. Br J Haematol 2001 ; 113: 746 6. Flatley RM, Payton SG, Taub JW, Matherly LH. Primary acute lymphoblastic leukemia cells use a novel promoter and 5non-coding exon for the human reduced folate carrier that encodes a modified carrier translated from an upstream translational start. Clin Cancer Res 2004; 10: 5111 Liu M, GeY, Payton SG, et al. Transcriptional regulation of the human reduced folate carrier in childhood acute lymphoblastic leukemia cells. Clin Cancer Res 2006; 12: 608 SAS Institute, Inc. SAS OnlineDocR 9.1.3. Cary NC ; : SAS Institute, Inc.; 2005. 25. R Development CoreTeam. R: a language and environment for statistical computing. R Foundation for Statistical Computing, Vienna, Austria. ISBN 3-900051-07-0, URL. Available from: : R-project .2005. 26. Margolin JF, Poplack DG. Acute lymphoblastic leukemia. In: Pizza PA, Poplack DG, editors. Principles and practice of pediatric oncology. Philadelphia PA ; : J.B. Lippincott Co.; 1997. 27. Whitehead VM, Shuster JJ, Vuchich MJ, et al. Accumulation of methotrexate and methotrexate polyglutamates in lymphoblasts and treatment outcome in children with B-progenitor-cell acute lymphoblastic leukemia: a Pediatric Oncology Group study. Leukemia 2005; 19: 533 Barredo JC, Synold TW, LaverJ, et al. Differences in constitutive and post-methotrexate folylpolyglutamate synthetase activity in B-lineage and T-lineage leukemia. Blood 1994; 84: 564 Galpin AJ, Schuetz JD, Masson E, et al. Differences in folylpolyglutamate synthetase and dihydrofolate reductase expression in human B-lineage versus T-lineage leukemic lymphoblasts: mechanisms for lineage differences in methotrexate polyglutamylation and cytotoxicity. Mol Pharmacol 1997; 52: 155 Schuetz JD, Matherly LH, Westin EH, Goldman ID. Evidence for a functional defect in the translocation of the methotrexate transport carrier in a methotrexate resistant murine L1210 leukemia cell line. J Biol Chem 1988; 263: 9840 Jansen G, Mauritz R, Drori S, et al. A structurally altered human reduced folate carrier with increased folic acid transport mediates a novel mechanism of antifolate resistance. J Biol Chem 1998; 273: 30189 Sirotnak FM, Moccio DM, Kelleher LE, Goutas LJ. Relative frequency and kinetic properties of transport-defective phenotypes among methotrexate resistant L1210 clonal cell lines derived in vivo. Cancer Res 1981 ; 41: 4447 52. GuoW, Healey JH, Meyers PA, et al. Mechanisms of methotrexate resistance in osteosarcoma. Clin Can Res 1999; 5: 621 Zhang L, Taub JW, Williamson M, et al. Reduced folate carrier gene expression in childhood acute lymphoblastic leukemia: relationship to immunophenotype and ploidy. Clin Can Res 1998; 4: 2169 Payton SG, Haska CL, Flatley RM, Ge Y, Matherly LH. Effects of 5 untranslated region diversity on the posttranslational regulation of the human reduced folate carrier. Biochim Biophys Acta. In press. 36. Goldman ID, Matherly LH. The cellular pharmacology of methotrexate. PharmacolTher 1985; 28: 77 and micafungin.
Methotrexate and psoriasis and folic acid
Results are the mean f SD for four separate animal observations. Whole rat brain minus cerebellum was homogenized and subcellular fractions were prepared by the method of Whittaker 1969 ; as described under "Materials and Methods.
Tell your health care provider if you are taking any other medicines, especially any of the following: medicines that suppress the immune system, such as corticosteroids eg, prednisone ; , cancer chemotherapy eg, methotrexate ; , or cyclosporine, because effectiveness of menactra may be decreased anticoagulants eg, warfarin ; because the risk of bleeding may be increased this may not be a complete list of all interactions that may occur and midodrine.
1996b; Gray et al., 1996 ; , it was possible that the [ 125I]- BgTx binding observed on stratum radiatum interneurons could represent either receptors on the interneurons themselves or on nerve terminals forming synapses on the cell bodies of interneurons. Although the electrophysiological data already presented made this possibility appear unlikely, we localized 7 mRNA expression by in situ hybridization in hippocampus as well. Those studies demonstrated intense labeling of the cell bodies of stratum radiatum interneurons Fig. 7D ; , whereas a much lower level of hybridization was observed over the pyramidal cell layer, despite the much greater density of cell bodies Fig. 7E ; . Thus, CA1 interneurons express 7 mRNA, have high levels of [ 125I]- BgTx binding sites, and have BgT x-sensitive physiological responses to ACh. The only one of those traits shared by CA1 pyramidal cells is a relatively weak expression of 7 mRNA and methotrexate.
Shin-ichiro Miura1, 2, Masahiro Fujino1, Hiroyuki Hanzawa, Yoshihiro Kiya, Satoshi Imaizumi, Yoshino Matsuo, Sayo Tomita, Yoshinari Uehara, Sadashiva S. Karnik, Hiroaki Yanagisawa, Hiroyuki Koike, Issei Komuro , and Keijiro Saku From the Department of Cardiology, Fukuoka University School of Medicine, Fukuoka 814-0180, Japan, Research and Development Headquarters, Sankyo Company, Ltd., Tokyo 140-0005, Japan, Department of Molecular Cardiology, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, and Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan and mifeprex.
In a 24-week, randomized, placebocontrolled trial of 241 patients, Weinblatt et al.2 evaluated the efficacy of SQ adalimumab 20, 40, or 80 mg ; , given every other week, compared with placebo in patients continuing to take their longterm, stable dosage of methotrexate. Patients were 18 years of age or older with a diagnosis of RA, according to the 1987 revised criteria of the American College of Rheumatology ACR ; .3 Another criterion for inclusion in the study was previous treatment with methotrexate for a minimum of six months at a stable.
Enbrel methotrexate
Infliximab, a chimeric monoclonal antibody directed against tumor necrosis factor a, is an established treatment for crohn's disease but not ulcerative colitis and mifepristone.
Dental caries is a transmissible bacterial infection.1, 2 Infants are not born with the pathogenic organisms but acquire them from other members of the family unit. Transmission from caregiver to child is called "vertical transmission". Studies have shown that caregivers can inoculate even predentate infants.3 "Horizontal transmission" from sibling to sibling or from spouse to spouse has also been proven.2 The main etiologic agents for dental caries are mutans streptococci MS ; and Lactobacillus LB ; .4 These organisms not only tolerate an acidic environment aciduric ; , but they also produce small-chain organic acids acidogenic ; by fermenting dietary carbohydrates--including but not limited to sucrose. These acids are small enough to diffuse subsurface into the enamel and dentin in fluid-filled spaces between the mineral crystals. Once subsurface, the and methylcellulose.
Progressive MS Cyclophosphamide Progressive MS Progressive MS Methotrexate Azathioprine Progressive MS MS MS Cladribine Patients with both relapsing and progressive forms of MS Patients w. relapsing and progressive forms of MS Cyclosporine Progressive MS Progressive MS and miglitol.
Psoriasis methotrexate is indicated in the symptomatic control of severe, recalcitrant, disabling psoriasis that is not adequately responsive to other forms of therapy, but only when the diagnosis has been established, as by biopsy and or after dermatologic consultation.
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