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Precursor to testosterone, and it converts naturally to testosterone through a wellrecognized pathway. In several published studies, the efficacy of androstenedione as a prohormone is examined; one trial 14 indicated that it was effective in increasing the level of testosterone, and another 15 demonstrated that androstenedione increased the level of estrogen and slightly increased the level of testosterone. Androstenedione has two pathways to active metabolites; this may be the reason for the discrepancy in the results of the studies described. Androstenedione converts to estrone as well as testosterone. Therefore, the effect of androstenedione in increasing the level of testosterone is somewhat compromised by having two pathways to estrogen one is testosterone-estradiol; the other is a pathway directly to estrone ; . Androstenedione has been administered orally in a dosage of up to 500 mg day. Like other hormones, it would probably be ef.
Discussion. Corneal infections of fungal aetiology are very common and represent 30% to 40% of all cases of culture-positive infectious keratitis. Combating fungal keratitis is of special importance in India harbouring the largest agrarian population at risk of developing blindness due to the limited availability of antifungal drugs and the lack of response during the therapy. Certain Aspergillus species, mainly A. flavus 23, 25 ; , A. terreus 25 ; , A. fumigatus 23, 25 ; and A. niger 3 ; have long been.
19. Grussendorf-Conen EI, Jacobs S. Efficacy of imiquimod 5% cream in the treatment of recalcitrant warts in children. Pediatr Dermatol 2002; 19: 263-6. Muzio G, Massone C, Rebora A. Treatment of nongenital warts with topical imiquimod 5% cream. Eur J Dermatol 2002; 12: 347-9. Vanhooteghem O, Richert B, de la Brassinne M. Raynaud phenomenon after treatment of verruca vulgaris of the sole with intralesional injection of bleomycin. Pediatr Dermatol 2001; 18: 249-51. Hayes ME, O'Keefe EJ. Reduced dose of bleomycin in the treatment of recalcitrant warts. J Acad Dermatol 1986; 15 5 pt 1 ; 1002-6. 23. Munn SE, Higgins E, Marshall M, Clement M. A new method of intralesional bleomycin therapy in the treatment of recalcitrant warts. Br J Dermatol 1996; 135: 969-71. al Aboosi M. Treatment of plane warts by tretinoininduced irritant reaction. Int J Dermatol 1994; 33: 826-7. Gelmetti C, Cerri D, Schiuma AA, Menni S. Treatment of extensive warts with etretinate: a clinical trial in 20 children. Pediatr Dermatol 1987; 4: 254-8. Johnson SM, Roberson PK, Horn TD. Intralesional injection of mumps or Candida skin test antigens: a novel immunotherapy for warts. Arch Dermatol 2001; 137: 451-5.
The mechanisms of idiopathic pulmonary fibrosis pathogenesis, a chronic and progressive interstitial lung disease, remain elusive. The complement system, a crucial arm of the innate immune response, plays a pivotal role in several pathological disorders; however, the contribution of individual complement components to lung fibrosis has not yet been examined. Complement factor 5 C5 ; and its cleavage product C5a are critical mediators in inflammatory diseases. Thus, to evaluate the role of C5 in lung fibrosis, we compared congenic C5-sufficient and C5-deficient mice in a well-characterized murine model of bleomycin-induced pulmonary fibrosis. C5-deficient mice had an exaggerated inflammatory phenotype compared with C5-sufficient mice during acute bleomycin-induced lung injury. These findings suggest a protective and anti-inflammatory role for C5, which was linked to the regulation of matrix metalloproteinases involved in cell migration. In contrast, C5 had a detrimental effect during chronic stages of bleomycin-induced injury, indicating a profibrotic role for C5. This deleterious activity for C5 was associated with expression of the fibrogenic cytokine TGF- 1 and matrix metalloproteinase-3, an important mediator in fibroblast contraction. Altogether, our data reveal novel and opposing roles for C5 in both inflammation and tissue repair. Furthermore, these findings provide insight into the development of new therapeutic strategies for idiopathic pulmonary fibrosis patients. The Journal of Immunology, 2005, 175: 1894 diopathic pulmonary fibrosis IPF ; 3 is a chronic interstitial lung disease of unknown etiology, characterized by diffuse and progressive fibrosis, which leads to a dramatic loss of pulmonary function 1 ; . This inflammatory and fibroproliferative disorder has an incidence of 15 per 100, 000 year in the U.S., and results in death in 50 60% of the cases 2 ; . The mechanisms underlying IPF pathogenesis remain largely unknown, although etiologic factors such as viral insults, smoking, and genetic predisposition have been associated in the process 1 ; . Although several studies have implicated a variety of cytokines, chemokines, and extracellular matrix components in the development of pulmonary fibrosis 35 ; , the origin of tissue injury and the immunological components involved in the abnormal repair process observed in IPF are still unclear. Moreover, IPF patients respond poorly to the current therapeutic regimens 6 thus, a better understanding of this disorder is clearly warranted. The experimental model of bleomycin-induced pulmonary fibrosis has been used extensively to elucidate the basis of pulmonary fibrosis 7 ; . Administration of bleomycin to rodents induces an early inflammatory response, characterized by marked infiltra.
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Table 1. Monoamine concentrations in pg mg protein mean S.E.M. ; in the MPOA, SCN, ME and ARN of the rat hypothalamus at 1900 h on pro-oestrus after administration of saline or DPDPE or co-administration of DPDPE with the opioid antagonist, naloxone, at 1300 h on the same day. Area NA DHPG DA Saline n 16 ; MPOA SCN ME ARN 34.5 35.1 33.2 DPDPE n 10 ; MPOA SCN ME ARN 20.1 25.3 18.2.
See Table 4-11 on page 4-6 for supported modifiers by platform. This command retrieves the threshold level of one or more monitored parameters. Notes and boniva.
1. Ries LAG, Eisner MP, Kosary CL: SEER Cancer Statistics, 1973-1998. Bethesda, MD, National Cancer Institute, 2001. 2. Galanis E, Buckner J: Chemotherapy for high-grade gliomas. Br J Cancer, 82: 1371-1380, 2000. De Angelis LM: Brain tumors. N Engl J Med, 344: 114-123, 2001. Medical Research Council Brain Tumor Working Party: Randomized trial of procarbazine, lomustine, and vincristine in the adjuvant treatment of high-grade astrocytoma: A Medical Research Council trial. J Clin Oncol 19: 509-518, 2001. Macdonald DR, Kiebert G, Prados M, Yung A, Olson J: Benefit of TMZ compared to procarbazine in treatment of glioblastoma multiforme at first relapse: effect on neurological functioning, performance status and health-related quality of life. Cancer Invest, 23: 138-144, 2005. Stupp R, Mason WP, Van Den Bent MJ: Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. N Engl J Med, 352: 987-996, 2005. Kleihucs P, Cavenee WK: Pathology and genetics of tumors of the nervous system. Lyon: IARC Press, 2000. 8. Kleihues P, Ohgaki H: Primary and secondary glioblastomas: from concept to clinical diagnosis. Neuro-oncology, l: 44-51, 1999. 9. Burton EC, Lambom KR, Forsyth P, Scott J, O'Campo J, Uyehara-Lock J, Prados M, Berger M, Passe S, Uhm J, O'Neill BP, Jenkins RB, Aldape KD: Aberrant p53, mdm2 and proliferation differ in glioblistomas from long-term compared with typical survivors. Clin Cancer Res, 8: 180-187, 2002. Sehgal A: Molecular changes during the genesis of human gliomas. Semin Surg Oncol, 14: 3-12, 1998. Simmons ML, Lamborn KR, Takahashi M, Chen P, Israel MA, Berger MS, Godfrey T, Nigro J, Prados M, Chang S, Barker FG, Aldape K: Analysis of complex relationships between age, p53, epidermal growth factor receptor and survival in glioblastoma patients. Cancer Res, 61: 1122-1128, 2001. Von Deimling A, Louis DN, Wiestler OD: Molecular pathways in the formation of gliomas. Glia, 15: 328-338, 1995. Schroder R, Bien K, Kotl R, Meyers I, Vossing R: The relationship between Ki-67 labeling and mitotic index in gliomas and meningiomas: demonstration of the variability of the intermitotic cycle time. Acta Neuropathol, 82: 389-394, 1991. McKeever PE, Strawderman MS, Yamini B, Mikhail AA, Blaivas M: MIB-1 proliferation index predicts survival among patients with grade II astrocytoma. J Neuropathol Exp Neurol, 57: 931-936, 1998. Montine TJ, Vandersteenhoven JJ, Aguzzi A, Boyko OB, Dodge RK, Kerns BJ, Burger PC: Prognostic significance of Ki-67 proliferation index in supratentorial fibrillary astrocytic neoplasms. Neurosurgery, 34: 674-679, 1994. Torp SH, Helseth E, Dalen A, Unsgaard G: Relationships between Ki-67 labeling index, amplification of the epidermal growth factor receptor gene, and prognosis in human glioblastomas. Acta Neurochir, 117: 182-186, 1992. Wakimoto H, Aoyagi M, Nakayama T, Nagashima G, Yamamoto S, Tamaki M, Hirakawa K: Prognostic significance of Ki-67 labeling indices obtained using MIB-1 monoclonal antibody in patients with supratentorial astrocytomas. Cancer, 77: 373-380, 1996. Pigott TJ, Lowe JS, Palmer J: Statistical modelling in analysis of prognosis in glioblastoma multiforme: a study of clinical variables and Ki-67 index. Br J Neurosurg, 5: 61-66, 1991. Andreas M Stark, Arya Nabavi N: Glioblastoma multiforme report of 267 cases treated at a single institution. Surg Neurol, 63: 162-169, 2005. Burger PC, Green SB: Patient age, histological features and length of survival in patients with glioblastoma multiforme. Cancer, 59: 1617-1625; 1987. Davis FG, Freels S, Grutsch J, Barlas S, Brem S: Survival rates in patients with primary malignant brain tumor stratified by patient age and tumor histological type: an analysis based on surveillance, epidemiology, and end results SEER ; data, 1973-1991. J Neurosurg, 88: 1-10, 1998. Hall WA: Extending survival in gliomas: surgical resection or immunotherapy? Surg Neurol, 61: 145-148, 2004. Walker MD, Alexander E Jr, Hunt WE: Evaluation of BCNU and or radiotherapy in the treatment of anaplastic gliomas: A cooperative clinical trial. J Neurosurg, 49: 333-343, 1978. Kristiansen K, Hagen S, Kollevold T: Combined modality therapy of operated astrocytomas grade III and IV: Confirmation of the value of postoperative irradiation and lack of potentiation of bleomycin on survival time. A prospective multicenter trial of the Scandinavian Glioblastoma Study Group. Cancer, 47: 649-652, 1981. Walker MD, Green SB, Byar DP: Randomized comparisons of radiotherapy and nitrosoureas for the treatment of malignant glioma after surgery. N Engl J Med, 303: 1323-1329, 1980. Laperriere N, Zuraw L, Cairncross G: Radiotherapy for newly diagnosed malignant glioma in adults: a systematic review: Radiother Oncol, 64: 259-273; 2002.
22. Ortiz E. Market withdrawal of Vioxx: is it time to rethink the use of COX-2 inhibitors? J Manag Care Pharm. 2004; 10 6 ; : 551-54. 23. Curtiss FR. Cost-effective use of COX-2 drugs and NSAIDs. J Manag Care Pharm. 2002; 8 4 ; : 295-96. 24. Burton TM, Harris G. Note of caution--study raises specter of cardiovascular risk for hot arthritis pills. Vioxx and Celebrex marketers dispute the research, sought to downplay it. Wall Street Journal. August 22, 2001: A1. 25. Burton TM. Backlash is brewing among companies who believe flashy ads drive up costs. Wall Street Journal. March 13, 2001: B1. 26. Sharpe R. Several deaths show a link to Celebrex. Wall Street Journal. April 20, 1999: B6. 27. Bull SA, Conell C, Dampen DH. Relationship of clinical factors to the use of COX-2 selective NSAIDs within an arthritis population in a large HMO. J Manag Care Pharm. 2002; 8 4 ; : 252-58. 28. Chan FK, Hung LC, Suen BY, et al. Celecoxib versus diclofenac and omeprazole in reducing the risk of recurrent ulcer bleeding in patients with arthritis. N Engl J Med. 2002; 347: 2104-10. Sung JY, Lau JY, Chan FK, Graham DY, How often are endoscopic ulcers in NSAID trials diagnosed as actual ulcers by experienced endoscopists? [abstract]. Gastroenterology 2001; 120 suppl ; 1A-597. 30. Derry S, Loke YK. Risk of gastrointestinal haemorrhage with long-term use of aspirin: meta-analysis. BMJ. 2000; 321: 1183-87. Graham DY, NSAIDs, Helicobacter pylori, and Pandora's box. N Engl J Med. 2002; 347: 2162-63. Prices obtained from drugstore ; e.g., Celebrex price available at: : drugstore pharmacy prices drugprice ?ndc 00025152531 &trx 1Z5006. Accessed July 31, 2005 and bortezomib.
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A decision tree analysis model was designed by a panel of experts to perform a cost-effectiveness and a budget-impact analyses of the long-term use of LAM and ADV Time horizon: 4 years Efficacy data obtained from published results of clinical trials Base-case calculations were carried out by applying a 3% annual discount rate to the costs Perspective of the Spanish Public Health System, which incurs only in direct healthcare costs in euros 2003 ; : treatment costs, consultations, diagnostic and laboratory tests, resistance test, decompensation costs Cost-effectiveness ratios CER; cost for each unit of effectiveness produced by each of the drugs ; of LAM or ADV: - CER LAM Cost LAM 3 years ; Effectiveness response ; LAM - CER ADV Cost ADV 3 years ; Effectiveness response ; ADV Incremental cost-effectiveness ratio ICER, additional cost incurred to achieve an extra unit of effectiveness ; : - ICER ADV vs. LAM Cost ADV Cost LAM ; Effectiveness ADV Effectiveness LAM ; Assumptions - Treatment population is similar for both strategies - Adverse events profiles of both drugs are similar and therefore their possible treatment costs have not been considered - Therapeutic response and HBV drug resistance are evaluated each year and depending on the results Figure 1 ; : Patients without HBV drug resistance continue with the same therapy until Year 4 Patients with LAM resistance are switched directly to ADV Patients with ADV resistance or non-response are discontinued from treatment and no other therapeutic intervention is started due to insufficient information regarding alternative therapies.
Maria Cristina Paiva de Arajo * Turmeric, the powder from the root of Curcuma longa Linn. Zingiberaceae ; , has been widely used as a coloring and flavoring agent, and in the treatment of inflammatory conditions and other diseases. Curcumin, an important pigment of turmeric, is commonly used as a coloring agent in foods, drugs and cosmetics. This natural phenolic compound has been known since ancient times to possess a variety of pharmacological activities and therapeutic properties. Turmeric and curcumin are known to act as antioxidant, antimutagenic and anticarcinogenic agents. We investigated the role of both antioxidants, turmeric and curcumin, on the chromosomal damage induced by the oxidizing agents bleomycin and -radiation in Chinese hamster ovary CHO ; cells. The effect of curcumin on the chromosomal damage induced by thiourea, ferrous ions Fe + 2 ; , ferric ions Fe + 3 ; and hydrogen peroxide H2O2 ; was also evaluated. Cultured cells received three doses of each drug, turmeric 100, 250 and 500 g ml ; and curcumin 2.5, 5 and 10 g ml ; , one hour before they were submitted to bleomycin 10 g ml ; -radiation 2.5 Gy ; treatment, which occurred during the G1 S, S and G2 S phases of the cell cycle. The bleomycin treatment lasted 30 min. Curcumin 15 g ml ; was tested with three doses of Fe + 1.25, 2.5 and 5.0 g ml ; , Fe 1.25, 2.5 and 5.0 g ml ; or 2O2 1.7, 3.4 and 6.8 g ml ; , by simultaneous treatment. Thiourea 10, 20 and 40 g ml ; was added to cultures 15 min before the curcumin treatment. The combined treatment with curcumin plus Fe + 2, Fe H2O2 or thiourea lasted 13 h. Three hundred metaphases, one hundred in each experiment, were analyzed per treatment in order to determine the frequencies of chromosomal aberrations, and the mitotic index was obtained by counting the number of mitotic cells in 3000 cells per treatment. Turmeric was not clastogenic by itself, whereas curcumin at 10-15 g ml increased the frequency of chromosomal damage. It mainly induced chromatid breaks and gaps. Neither turmeric nor curcumin had a protective effect against the clastogenicity of bleomycin and -radiation. Instead, a potentiating effect was observed with both natural antioxidants. Turmeric enhanced -radiation-induced chromosomal damage at G2 S phase, and curcumin increased both bleomycinand -radiation-induced chromosomal damage at the S and G2 S phases of the cell cycle. These results clearly indicate and bosentan.
Biochemistry and growth of a malignant cell line. Eur. J. Cancer, 8: 561 " 25. Overgaard, K., and Overgaard, J. Investigations on the possibility of a 571, 1972. thermic tumor therapy. II. Action of combined heat-roentgen treatment on a 11. Dietzel, S. Tumor und Temperatur. In: Aktuelle Probleme bei der Anwendung transplanted mouse mammary carcinoma. Eur. J. Cancer, 8: 573-575, thermischer Verfahren in Onkologie und Strahlentherapie. Munich: Urban & 1972. Schwarzenberg, 1975. 26. Overgaard, K., and Overgaard, J. Pathologyof heat damage. In: Proceed 12. Gerner, E. W., Boone, A., Connor, W. 0., Hicks, J. A., and Boone, M. L. M. ings. International Symposium on Cancer Therapy by Hyperthermia and A transient thermotoierantsurvivalresponse produced by single thermal Radiation, pp. 115"1 WashIngton, D. C.: 1975. 27. doses in HeLa cells. Cancer Res., 36: 1035-i 040, Palzer, A. J., and Heidelberger, C. Studies on the quantitative biology of i 3. Giovanella, B. C. , Lohmann, W. A., and Heidelberger, C. Effects of elevated hyperthermia killing of HeLa cells. Cancer Res. 33: 41 5"4211973. , temperatures and drugs on the viability of Li 210 leukemia cells. Cancer 28. Pettigrew, A. T., GaIt, J. M., Ludgatem, C. M., and Smith, A. N. Clinical Res., 30: i623-163i, 1970. effects of whole-body hyperthermia in advanced malignancy. Br. Med. J., 4: 14. Giovaneila, B. C., Morgan, A. C., Stehlin, J. S., and Williams, L. J. Selective 679"682, 1974. lethal effect of supranormal temperatures on mouse sarcoma cells. Cancer 29. Roti Aoti, J. L., and Winward, A. T. The effects of hyperthermia on the Aes., 33: 2568-2578, 1973. protein to DNA ratio of isolated HeLa chromatin. Radiat. Res., in press, 15. Hahn, G. M., Braun, J., and Har-Kedar. Thermochemotherapy: synergism 1979. between hyperthermia and Adriamycin or bleomycin ; in mammalian cell 30. Stehlln, J. S., Glovanella, B. C., Ipolyl, P. D., Muenz, L. A., and Anderson. Inactivation. Proc. Nafi. Acad. Sd. U. S. A., 42: 937-940, 1975. R. F. Resultsof hyperthermicperfusionfor melanomaof the extremities. 16. HarrIs, N. Growthand survivalof mammaliancellsundercontinuous thermal Surg. Gynecol. Obst., 140: 339-348, 1975. stress. Exp. Cell Aes., 56: 382-386, 1969 Suit, H. D., and Shwayder, M. Hyperthermia: potential as antitumor agent. 17. Kim, J. H., Kim, S. H., and Hahn, E. W. Thermoenhancement of the Cancer, 34: 122"129, 1974. radiosensitivity using cultured normal and neoplastic cells. AJA Am. J. 32. Turano, C., Fenaro, A., and Starr, A. The biochemical mechanisms of Roentgenol. ; , 12: 860"864, i 974. selective heat sensitivity of cancer cells. I. Studies on lysosomes. Eur. J. 18. Larkln, J. M., Edwards, W. S., Smith, D.E., and Clark, P. J. Systemic Cancer, 6: 67"72, 1970. thermotherapy: description of a method and physiologic tolerance in clinical 33. Warocquier, A., and Scherrer, K. RNA metabolism in mammalian cells at subjects. Cancer, 40: 3155"31 1977. elevated temperature. Eur. J. Biochem., 10: 362-370, 1969. Leith, J. T., Miller, A. C., Gerner, E. W., and Boone, M. L. M. Hyperthermic 34. Westra, A., and Dewey, W. C. Variationand sensitivity heat shockduring to potentlatlon: biological aspects and applications to radiation therapy. Can the cell cycle of Chinese hamster cells in vitro. Int. J. Radlat. Biol. Aelat. cer, 39: 766"779, 1977. Stud. Phys. Chem. Med., 19: 467"477, 97i. i.
The images reported here show with great detail the atomic structure and topography of a natural 010 ; cleavWith the advent of scanning tunneling microscopy STM ; Binnig et al., 1982 ; and atomic force microscopy agesurface.The goal of this study is to determine whether AFM ; Binnig et al., 1986 ; , scientistsin a variety of dis- the surfaceis an ideal termination of the bulk structure. ciplines have been able to obtain unprecedentedinfor- We baseour results on a comparison of measuredsurface mation on the atomic-scale structure and topography of orientations and nearestneighbor distancesfrom the AFM surfaces.In the field of mineralogy, nearly all surface images with those from a surfaceprojection of the bulk AFM-STM studies to date have imaged structurally sim- structure, as deducedfrom X-ray and neutron diffraction ple minerals that cleavealong well-definedatomic planes. data in the literature. From this comparison, we note that Two very recent studies have focused on framework there is no evidence for surface reconstruction, and in silicate minerals, quartz and albite. Gratz et al. 1991 ; general terms, the correspondencebetween the surface investigatedthe development of etch pits and the move- and bulk structures is very close. The largest measured ment of atomic-scale ledges during the dissolution of differencesin nearestneighbor distanceswas 0.2-0.4 A. quarlz. Hochella et al. 1990 ; studied the surfaceof albite The measureddifferencesmay be due to a variety of reasons, as we discusslater on. both with AFM and low-energy electron difraction LEED ; . Their AFM imagesreveal the presence nanoof ExpBmNrnNr, q.L meter-sized surface pits and depressions.Both of these microscope studiesdid not achieveatomic-scaleresolution, however. Atomic force In this paper we use AFM images to determine the The NanoScope II contact mode AFM from Digital atomic-scale surface structure and topography of the 010 ; Instruments used in this experiment is based on an opplane of albite. We have chosenalbite for AFM imaging tical lever design Meyer and Amer, 1988; Alexander et for two main reasons: its general geological importance al., 1989 ; that has been described in detail in previous in the Earth's crust and the fact that its bulk structure is publications Ruger and Hansma, 1990 ; . In this study well known. In addition, the chemical and structural evo- imaging forces ranged from l0 to 100 nN using l2o-pm lution of the near-surfaceregion after alteration has been SirNo cantilevers from Digital Instruments ft 0.6 N studied with a variety of spectroscopictechniques, both m ; with integral tips. Lower forces can be used, but imfor albite Hellmann et al., 1990 ; , and other feldspars proved image quality is usually obtained on rigid crys Caseyet al., 1989 ; .Thus, this presentstudy should serve talline materials at higher forces. The AFM can operate as a basis for providing new and complementary infor- under a variety of fluids; however, the images presented mation on the surface structure and reactivitv of albite here were all taken in air using a piezotranslator with a surfaces. s c a This study utilized low albite from Amelia Court House, * To whom correspondence should be addressed. Viryinia; it was supplied by Wards Scientific EstablishINrnooucrroN and botox.
1. Barranco, S. C., and Humphrey, R. M. The Effects of Bleomycin on Survival and Cell Progression in Chinese Hamster Cells in Viiro. Cancer Res., 31: 1218 1223, Bruce, W. R., Meeker, B. E., and Valeriote, F. A. Comparison of the Sensitivity of Normal Hematopoietic and Transplanted Lymphoma Colony-forming Cells to Chemotherapeutic Agents Administered in vivo. 3. Nati. Cancer Inst., 37: 233 245, Cohen, A. M., Philips, F. S., and Sternberg, S. S. Studies of the.
Growth inhibition was measured using a proliferation assay in which the number of cells is related to the amount of protein SRB ; . Cells treated with several concentrations of bleomycin 1051010 M ; were compared with control growth of untreated cells. IC50 and IC25, the concentrations of bleomycin at which 50 and 25%, respectively, of cell growth was inhibited compared with the untreated control growth. The missing values blanks in the table ; are due to failures in cell growth and bronchial.
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Monoclonal antibodies and other reagents. We used the following monoclonal antibodies MAbs ; and reagents: 1 mg ml propidium iodide PI ; stock solution Calbiochem, La Jolla, CA ; in phosphatebuffered saline PBS annexin V-FITC PharMingen, San Diego, CA 1 mCi ml sterile [3H]methylthymidline Amersham Biosciences, Rehovot, Israel GSH Sigma, St. Louis, MO 2 , 7 -dichlorofluorescin diacetate DCFH DA ; and MitoTracker RedCMXRos mitochondrial membrane potential MTP ; tracker Molecular Probes, Eugene, OR bleomycin ASTA Medica ; and caspase-8 [z-IETD-fluoromethyl ketone fmk ; ] and caspase-9 z-LEHD-fmk ; inhibitors R&D Systems, Minneapolis, MN FasL antagonist, anti-mouse FasL MAb, clone-MFL3, and Jo2-Fas agonist PharMingen IgG control, cloneRGE53 Chemicon International, Temecula, CA caspase-8 and -9 activity assays kit BioVision, Mountain View, CA ; . Cell culture systems. We used the murine type II lung epithelial cell line ATCC, MLE-15 ; , an extensively used model 5, 6, 10, ; . Cells were maintained in hydrocortisone insulin transferrin estradiol selenium HITES ; medium Industrial Laboratories, Beit HaEmek, Israel ; that was supplemented with 2 mM Lglutamine, 10% heat-inactivated FBS Sigma, St. Louis, MO ; , and 5 mM Pen-Strep Industrial Laboratories, Beit HaEmek, Israel ; . Cultures were incubated at 37C in a humidified atmosphere with 5% CO2. MLE cells 0.5 106 ; were cultured in HITES medium, with or without 100 mU ml of bleomycin and with or without 10 mM reduced glutathione, or 30 60 M caspase inhibitors, and were assayed at 0.5, 1, 24, or 48 h. ROS levels, caspase activities, and MTP disruption were assayed at 24 h. trigger Fas-induced apoptosis, Fas was.
The patients were treated with Milwaukee great aid in correction and fusion. The and bumetanide.
1. Clinical Nurse IV, Duke Raleigh Hospital, Raleigh; 2. Program Manager, Radiation Oncology, University of Pittsburgh Hillman Cancer Center.
TREATMENT GROUP PAROXETINE PLACEBO TOTAL NUMBER OF PATIENTS : 95 100.0% 98 PATIENTS WITH ADVERSE EXPERIENCES : 73 76.8% 80 BODY SYSTEM : PREFERRED TERM N % N % N % RASH 1 1.1 0 0.0 1 0.5 RASH 2 2.1 2 SKIN BENIGN NEOPLASM 0 0.0 1 1.0 1 SKIN DISCOLORATION 0 0.0 1 1.0 1 SKIN HYPERTROPHY 1 1.1 0 0.0 1 0.5 SWEATING 1 1.1 2 Special Senses ABNORMAL VISION BLEPHARITIS EAR DISORDER OTITIS MEDIA TINNITUS Urogenital System ALBUMINURIA GLYCOSURIA HAEMATURIA URINARY INCONTINENCE URINE ABNORMALITY 5 0 1 5.3 0.0 1.1 3.2 0.0 0.0 2.1 1.1 4 0 4.1 2.0 0.0 1.0 0.0 3.1 0.0 1.0 0.0 9 2 1 and buprenorphine.
Since TGF- 1 was repeatedly shown to be a profibrotic mediator in the bleomycin induced lung injury model, we studied TGF- 1 expression after electroporation mediated hHGF gene transfer. TGF- 1 was decreased after treatment with pCikhHGF compared to treatment with the empty vector pCik Figure 7 ; , suggesting that TGF- 1 is involved in the hHGF-induced reduction of bleomycin induced lung fibrosis.
PLACENTA PREVIA SIGNS & SYMPTOMS: 1. Painless vaginal bleeding during the 2nd or 3rd trimester 2. Signs and symptoms of shock OBTAIN HISTORY OF: 1. Painless vaginal bleeding during the 2nd & 3rd trimester 2. Past C-section delivery 3. Placenta Previa in current or past deliveries 4. Time and amount of bleeding 5. Color of blood and any clots present 6. Prenatal care and buspirone.
Steven W. Johnson, Nicola B. Mercuri, " and Ft. Alan North Vellum Institute and Department of Neurology, Oregon Health Sciences University, Portland, Oregon 97201.
Solid-phase extraction-liquid chromatography-electrospray tandem mass spectrometry method. Anal. Chem., 76: 6998-7006. Rodriguez-Mozaz, S., Marco, M.-P., Lopez de Alda, M. J. and Barcelo, D. 2004c ; . Biosensors for environmental monitoring of endocrine disruptors: a review article. Anal. Bioanal. Chem., 378: 588-598. Rodriguez-Mozaz, S., Lopez de Alda, M. J., Marco, M.-P. and Barcelo, D. 2005b ; . Biosensors for environmental monitoring - A global perspective. Talanta, 65: 291-297. Rogers, H. R. 1996 ; . Sources, behaviour and fate of organic contaminants during sewage treatment and in sewage sludges. Sci. Total Environ., 185: 3-26. Rooklidge, S. J. 2004 ; . Environmental antimicrobial contamination from terraccumulation and diffuse pollution pathways. Sci. Total Environ., 325: 1-13. Rooklidge, S. J., Burns, E. R. and Bolte, J. P. 2005 ; . Modeling antimicrobial contaminant removal in slow sand filtration. Water Res, 39: 331-339. Rosenfeldt, E. J. and Linden, K. G. 2004 ; . Degradation of endocrine disrupting chemicals bisphenol A, ethinyl estradiol, and estradiol during UV photolysis and advanced oxidation processes. Environ. Sci. Technol., 38: 5476-5483. Ross, G. 2004 ; . The public health implications of polychlorinated biphenyls PCBs ; in the environment. Ecotoxicol. Environ. Safety, 59: 275-291. Routledge, E. J., Sheahan, D., Desbrow, C., Brighty, G. C., Waldock, M. and Sumpter, J. P. 1998 ; . Identification of estrogenic chemicals in STW effluent. 2. In vivo responses in trout and roach. Environ. Sci. Technol., 32: 1559-1565. Rudel, R. A., Camann, D. E., Spengler, J. D., Korn, L. R. and Brody, J. G. 2003 ; . Phthalates, alkylphenols, pesticides, polybrominated diphenyl ethers, and other endocrine-disrupting compounds in indoor air and dust. Environ. Sci. Technol., 37: 4543-4553. Rule, K. L., Comber, S. D. W., Ross, D., Thornton, A., Makropolous, C. K. and Rautiu, R. 2006 ; . Sources of priority substances entering an urban wastewater catchment - trace organic chemicals. Chemosphere, 63: 581-591. Russell, D. J. and McDuffie, B. 1983 ; . Analysis of phthalate esters in environmental samples: Separation from PCBs and pesticides using dual column liquid chromatography. Int. J. Environ. Anal. Chem., 15: 165-183. Rutishauser, B. V., Pesonen, M., Escher, B. I., Ackermann, G. E., Aerni, H.-R., Suter, M. J.F. and Eggen, R. I. L. 2004 ; . Comparative analysis of estrogenic activity in sewage treatment plant effluents involving three in vitro assays and chemical analysis of steroids. Environ. Toxicol. Chem., 23: 857-864. Sabik, H., Gagnon, C., Houde, F. O. and de Blois, C. 2004 ; . Distribution, fate, and behavior of nonylphenol ethoxylates and degradation products in the dispersion plume of a major municipal wastewater effluent. Environ. Forensics, 5: 61-70 and busulfan and bleomycin.
S Districts provide training sessions at district meetings C Usually run by experienced representatives S Outside vendors are utilized to provide new approaches C Simulations, Inc. provides selling skills workshops S Regional training provided for larger group needs S Computer-based training is utilized for self improvement C CD-ROM on Word, Excel, etc. S Intranet provides updates on home office continuing education C District managers submit names to regional directors for classes C Classes are offered on specific products and developmental areas e.g., managed care or hospital sales.
Bleomycin treatment. Male C57Bl 6J and Balb C mice supplied by Charles River, Calco, Italy ; of 3 4 age were used in this study. All animal experiments were conducted in conformance with the "Guiding Principles for Research Involving Animals and Human Beings" and was approved by the Local Ethics Committee of the University of Siena. For each strain of mice, different groups of animals were used. A group received a single intratracheal instillation of 0.1 g bleomycin Rhone-Poulenc Rorer, Milan, Italy ; in saline solution 50 l ; . Another group was instilled intratracheally with the same amount of saline. All intratracheal instillations were performed under ether anesthesia. At various times after the treatment, the animals from all groups were injected with an overdose of pentobarbital sodium and exsanguinated by cutting the abdominal aorta. The lungs were then excised and processed for conventional light microscopy and immunohistochemistry or RNase protection assay RPA ; . Morphology and immunohistochemistry. The lungs from the different groups of mice were fixed intratracheally with buffered formalin 5% ; at a constant pressure of 20 cmH2O for 4 h and then immersed in the same fixative for an additional hour. The samples and butorphanol.
We analyzed total cellular GSH to determine whether bleomycin was able to regulate GSH formation. A spectrophotometric assay for total cellular GSH showed that both 0.1 and 1.0 g ml of bleomycin caused approximately twofold increases within 18 h compared with control Fig. 1B ; . These results were comparable with the twofold increase in total cellular GSH induced by an 18-h treatment with 100 M H2O2, used as a positive control 43 ; . The enzyme -GCS controls the key regulatory step in the production of cellular GSH 6, 35, 44 ; . Northern blot analysis shows that -GCSh mRNA levels are upregulated by bleomycin in BPAEC. Figure 2A is a representative time course in which -GCSh mRNA is increased by 30 min in response to 1 g bleomycin. BSO, an agent known to induce -GCSh expression, was used as a positive control 44 ; . Our probe for -GCSh is based on rat cDNA, but the bovine size, sequence, and, therefore, complementarity to rat -GCSh are not known. The rat mRNA was included as a positive control for the position of -GCSh Fig. 2A ; . Densitometry of the representative data showed that within 30 min, bleomycin caused a 1.5-fold increase in -GCSh mRNA levels, whereas at 36 h bleomycin induced a 33.5-fold increase Fig. 2C ; . BSO exposure for 3 and 6 h induced a 2.5- and 2-fold increase in -GCSh mRNA, respectively.
Materials components ; . The design of studs cleats needs to be considered in both plan and profile view, and also with respect to both contact area and radius of curvature. Contact area relates to contact pressure and hence the risk of bruising to, and penetration of, a player's skin. Radius or sharpness of edges relates to risk of cutting the skin. In addition, there are whole sole design factors to consider including sole rigidity and edge profile. Table 1 summarises many of the potential risk factors that should be considered - the list is not exhaustive. Attention is also drawn to legislation such as the EU General Product Safety Directive 92 59 EEC ; , which applies to all products sold within the European Union. Equivalent or similar legislation may apply in other countries or regions of the world.
Phosphorus retention in soils is influenced by the form of P added. The potential impact of one P compound on the sorption of other P compounds in soils has not been widely reported. Sorption isotherms were utilized to quantify P retention by benchmark soils from Indiana, Missouri, and North Carolina when P was added as inorganic P Pi ; or organic P b-D-glucose-6-phosphate, G6P; adenosine 59-triphosphate, ATP; and myoinositol hexaphosphate, IP6 ; and to determine whether soil P sorption by these organic P compounds and Pi was competitive. Isotherm supernatants were analyzed for pH and total P using standard protocols, while Pi and organic P compounds were assayed using ion chromatography. Under the controlled conditions of this study, the affinity of all soils for P sources followed the order IP6 . G6P . ATP . Pi. Each organic P source had a different potential to desorb Pi from soils, and the order of greatest to least Pi desorption was G6P . ATP . IP6. Glucose-6-phosphate and ATP competed more directly with Pi for sorption sites than IP6 at greater rates of P addition, but at the lesser rates of P addition, IP6 actually desorbed more Pi. Inositol hexaphosphate was strongly sorbed by all three soils and was relatively unaffected by the presence of other P sources. Decreased total P sorption due to desorption of Pi can be caused by relatively small additions of organic P, which may help explain vertical P movement in manured soils. Sorption isotherms performed using Pi alone did not accurately predict total P sorption in soils.
Among all trials the results of the meta-analysis should be regarded with some caution. In particular, the authors point to the markedly discordant results obtained in the GESCIA Dovall et al. 1994 ; and STATCHF Singh et al. 1995 ; trials, which enrolled patients with a similar underlying, risk for arrhythmic death. Therefore the benefit from amiodarone remains to be firmly established. However it is one of the few drug options that does not seem to have any proarrhythmic potential and it does not increase the risk of SCD. This makes it an appropriate choice for patients at high risk of arrhythmic death.
Nerves. Exercise is a pretty good one. The cold pressor test is another one. It remains to be seen whether single nucleotide type polymorphisms at the CGA locus really do predict the response to cold pressor tests. We actually just finished resequencing the CGA locus within the last, about 2 months, and as soon as we found these polymorphisms we've set them up as single nucleotide polymorphism or SNIP assays, and now we're running them on our larger cohort. Actually now we work largely with twins. We've got about 140 twin pairs we've studied, and we're busily testing all these polymorphisms in the twins to see if they do, in fact, predict the cold stress response. DR. KOPIN: The other issues is whether or not the same proteins are present in the sympathetic nerves as they are in the adrenal medulla. Have you done any histological studies to look for this? DR. O'CONNOR: It looks to us as they're the same ones, and we have not. We've done a little study in human beings, a good source of post ganglionic sympathetic nerves in humans is the vas deferens. A good source of post ganglionic sympathetic nerves in rodents is also the vas deferens. In a larger animal it would be the sperlip nerve in the cow, and with the now-retired Dick Klein, who spent a lot of time purifying so-called large dense core vesicles and post ganglionic sympathetic nerves -- post ganglionic sympathetics at the large core and small core vesicles. The large core vesicles are supplied with peptides. The small core vesicles are electron-dense but seem to have no peptides, just the catecholamines. Then the large core vesicles, it would appear there is authentic chromogranin A with the same molecular mass and the same immunoreactivity as the form found in the adrenal medulla, so I think the protein is there. DR. KOPIN: Just let me get clear what you just said. Did you say that the large granules in the sympathetic nerves do not have catecholamines? DR. O'CONNOR: No, that the large dense core vesicles are supplying both catecholamines and peptides, and the catecholamine to peptide ratio is about the same as it is the adrenal medullary granules. Peculiarly, the small dense core vesicles seem not to have the peptides, seem only to have the catecholamines. One school of thought is that these are formed by membrane retrieval from the large dense core vesicles after exocytosis with subsequent endocytosis. They've got the right transmitters. They've got the right transporters in terms of VMAT and the proton translating ATPA's to really accumulate catecholamines from the situs, but they've lost their peptides by virtue of exocytosis. If we go the large dense core vesicles we do find chromogranin A, and interestingly enough there are nicotinic receptors found all the way up to the termini of post ganglionic sympathetic axons, which you could study and boniva.
WM, Pastore L, Houghton DC. Fatal pulmonary bleomycin toxicity in cisplatinum-induced acute renal failure. Cancer 11eat Rep 1980; 64: 921-24 Catane R, Schwade JG, Turrisi AT, Webber BL, Muggia FM. Pulmonary toxicity after radiation and bleomycin: a review. IntJ Radiat Oncol Biol Phys 1979; 5: 1513-18 Goldiner PL, Carlon CC, Cvitkovic E, Schweizer 0, Howland WS. Factors influencing postoperative morbidity and mortality in patients treated with bleomycin. Br Med J 1978; 1: 1664-67 Sostman HD, Matthay BA, Putman CE. Cytotoxic drug-induced.
Placebo in overweight noninsulin-dependent diabetics after 12 weeks40 in clinical trials lasting 12-52 weeks, sibutramine appears to have a neutral effect on both blood glucose and the lipid profile, though it can increase blood pressure as discussed below.
5. Klesges RC et al. Varenicline for smoking cessation: definite promise, but no panacea. JAMA 2006; 296: 94-5. Cahill K et al. Nicotine receptor partial agonists for smoking cessation. Cochrane Database of Systematic Reviews - Issue 1 January 2007. R ; 7. British medical Association and Royal Pharmaceutical Society of Great Britain. British National Formulary No. 52. Section 4.10. September 2006. 8. National Institute for Health and Clinical Excellence. Guidance on the use of nicotine replacement therapy NRT ; and bupropion for smoking cessation. March 2002. G.
Among the 3, 726 students who reported at least one gambling activity during the last school year, the majority are non-problem gamblers 80.7% ; score of 0 on the CPGI ; , while 13.2% are at-risk for developing a gambling problem, and 6.2% have a moderate or severe gambling problem. The patterns of gambling severity differ according to the major demographic variables except for living arrangement. In this case, the prevalence of non-problematic and problematic gambling does not differ between students living on campus and those living off campus with or without their family.
To study the efficacy of intralesional bleomycin as a sclerosing agent for peripheral cystic hygromas, 15 patients were treated. Intralesional injection of bleomycin into the lymphangiomas was given at a does not exceeding 0.5 mg per kg of body weight, at intervals of 2 weeks. The regression response of the swelling was graded as excellent total disappearance ; , good 50% reduction ; , and poor 50% decrease ; . Reduction in the size of the mass was usually seen by 2 weeks to 6 months and the number of injections for each patient varied from 1-5. A significant reduction was seen in 86.7% 13 patients ; and 53.3% 8 cases ; of them showed complete disappearance. Eleven of the 12 cystic lesions showed excellent to good response. No significant complications were noted. The average follow-up period was 28 months 23-37 months.
Unresectable head and neck cancers, local-regional control by radiotherapy alone is accomplished in 30% of cases, yet many of these patients suffer recurrence outside the irradiated port 1 ; . For these reasons, increased attention is being paid to the combined use of radiotherapy and chemotherapy 2 ; . A variety of approaches have been investigated, including alternating chemotherapy and radiotherapy and concomitant treatment. In some cases, the results have been encouraging, with trends toward decreased rates of distant failure, increased local control, and increased organ preservation rates 35 ; . At the same time, combined treatments are frequently associated with increased normal tissue toxicities, and there is considerable room for improvement of the combined treatment strategies. Most agents have been chosen for combination with radiotherapy based on their known clinical activity in particular disease sites. For example, agents such as cisplatin 6, 7 ; , 5-fluorouracil 8, 9 ; , bleomycin 10 ; , methotrexate 11 ; , and mitomycin C 12 ; , which have been shown previously to have activity in the treatment of head and neck cancer on their own, have more recently been used in combination with radiotherapy. Alternatively, agents that might serve to overcome resistance mechanisms associated with radiotherapy could be chosen. Our group and others previously explored the use of nucleoside analogues such as fludarabine phosphate in combination with radiation 13, 14 ; . The rationale for such a choice was that fludarabine is an inhibitor of DNA replication and a DNA chain terminator 1518 ; and thus might poison DNA repair in radioresistant tumor cells and also slow tumor regrowth during a fractionated schedule. Indeed, in vitro and preclinical mouse tumor model studies demonstrated that fludarabine could offer a radioenhancement ratio of 1.24 2.14, depending on the timing of fludarabine administration relative to radiation, the dose of fludarabine, tumor type, and schedule of radiation 19 21 ; . Interestingly, whereas fludarabine enhanced radioresponse when given just before irradiation which would be expected for a repair inhibitor ; , the greatest tumor radioresponse was observed when fludarabine was administered at least 24 h before radiation. Subsequent mechanistic studies demonstrated that radioenhancement was associated with fludarabine-induced apoptosis and preferential cell loss of cells in S-phase through an apoptotic pathway, delayed cell cycle progression, and subsequent parasynchronization of tumor cells into the radiosensitive G2-M phases of the cell cycle 22 ; . In addition, on an optimized schedule, fludarabine did not significantly modify the radioresponse of a number of normal tissues 20, 21, 23 ; . Thus, it appeared that nucleoside analogues could improve the therapeutic ratio of radiotherapy when used on an optimized schedule. A clinical Phase I trial is presently under way exploring this combination in patients with locally advanced head and neck cancer. Because fludarabine has shown little single-agent activity in solid tumors at the schedules used 24 ; , other nucleoside analogues with similar mechanisms of action may have more favorable characteristics for use in solid tumors. One such possibility is gemcitabine, 5 a.
Cancer res, 1982 apr, 42 4 ; , 1399 - 404 comparison of the sequences at specific sites on dna cleaved by the antitumor antibiotics talisomycin and bleomycin ; mirabelli ck et al; we have investigated the site-specific cleavage of dna by the antitumor antibiotics talisomycin and bleomycin by using 5'- or 3'-terminal 32p-labeled restriction fragments of pbr 322 dna.
Diminished class II expression in these cells has been associated with abnormal posttranslational modification of class II proteins involving aberrant terminal glycosylation 5, 7, 55 ; and with abnormal intracellular trafficking characterized by an accumulation of class II in an endoplasmic reticulum compartment 5, 7 ; . In our study, the observed delay in cell surface expression of some class II proteins in IFN induced ThM cannot be attributed to the absence of an invariant chain, since cells contained both invariant chain mRNA and protein 2 days after IFN- induction Figs. 3 and 6, l and m ; . Professional APCs contain an Ag-processing compartment, designated MIIC, that is characterized by its contents of class II proteins, DM, and lysosomal and late endosomal markers. MIICs in a B lymphoblastoid cell are depicted clearly in Figure 7; DR, DQ, and DM colocalize extensively in discrete intracellular compart.
To examine differences in baseline characteristics between groups, we used 2 analysis for binary variables and the Kruskal-Wallis test for continuous variables. A Cox proportional hazards model was constructed by standard statistical tests on proportionality to compare 2-year adherence between the cohorts, while adjusting for potential confounders. Time to discontinuation was defined as the dependent variable. The.
6207 The extractability of NCA and MCA into ethyl acetate along with the inhibition of release by NDGA, DEC, and AA-861 suggests that the activity is composed of lipoxygenase product. The NCA and MCA was inhibited by LTB4 receptor antagonist. Although, the release of LTB4 from HLF in response to bleomycin was not significant compared with control, the concentration of LTB4 reached the chemotactic range of neutrophils and monocytes. Thus, LTB4 may be one of the important chemoattractants for neutrophils and monocytes released from fibroblasts constitutively. Although bleomycin stimulated the release of many cytokines from lung fibroblasts, it did not augment the release of LTB4 by RIA. Because NCA and MCA were inhibited by LTB4 receptor antagonist, and because the column chromatographic profiles showed the increase in lowest m.w., we expected the augmented release of LTB4 from HLF. However, the release of LTB4 was not significant. The exact mechanisms for bleomycin to stimulate fibroblasts resulting in the release of cytokines are uncertain, and the mechanism of activation or synthesis of 5-lipoxygenase in fibroblasts is also unclear. We speculate that the stimulatory potential of bleomycin is not enough for the activation or synthesis of 5-lipoxygenase in fibroblasts compared with other stimulus, which induced LTB4 release from fibroblasts. However, it might be possible that bleomycin induced the release of 12- or 15-hydroxyeicosa tetraenoic acid, which were NCA and MCA, instead of LTB4, and this may explain the augmentation of the lowest chemotactic peaks. In conclusion, bleomycin stimulated HLF to release NCA and MCA. The released activities were chemotactic by checkerboard analysis. The released NCA and MCA by bleomycin were IL-8, GCSF, MCP-1, GM-CSF, TGF- , and LTB4. These results suggest that lung fibroblasts may play a role in the inflammatory cell recruitment by releasing chemotactic activity in response to bleomycin.
With the combination of actinomycin D, chlorambucil, and methotrexate.3 Subse quent studies confirmed a response rate of 50 percent to 70 percent, which included complete remissions of 10 percent to 20 percent.4 These early studies were signif icant not only for their response rates, but because about one half of the patients who achieved complete remissions were per manently cured. Death was inevitable in patients attaining less than a complete re mission and in the other half of those who attained complete remission but relapsed. If a complete responder was destined to relapse, he did so within two years of the initiation of chemotherapy. For this rea son, a two-year disease-free status was le gitimately considered a cure. Later in the 1960s, vinblastine was shown to be an active anticancer agent.5 In the 1970s, bleomycin was shown to have activity in germinal neoplasms.6 Samuels et al were the first to successfully combine vinblastine and bleomycin; this apparently synergistic two-drug regimen was a major advance. Initial studies VB I ; with vinblastine plus bleomycin utilized dosages of 0.4 to 0.6 mg kg of vinblastine plus 15 mg M2 twice weekly of bleomycin and produced 33 percent complete remis sions with a relapse rate of 23 percent.7 In 1973, Samuels et al employed continuous infusions of bleomycin; this VB-III pro gram produced a 57 percent complete re mission rate, with 45 percent of patients currently free of disease.8 The next major advance was the dis covery of the activity of cis-diamminedi chloroplatinum in germinal neoplasms . This agent appeared to be the most active single agent. The drug has the interesting property of being relatively nonmyelosup pressive, making it an ideal agent to add to combination chemotherapy regimens.
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