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Oped severe myelosuppression and the patient achieving CR had a median time of granulocyte and platelet recovery of 33 days range 31 to 45 ; and 55 days range 35 to 114 ; , respectively. During the induction treatment all patients experienced febrile episodes. In particular, we observed 10 episodes of fever of unknow origin FUO ; and nine episodes of documented sepsis. These were due to gram-positive germs in five cases, to gram-negative germs in three cases and to mixed fungal + bacterial ; agents in one case. Five patients developed an infectious tissue localization consisting in one patient of aspergillosis of the maxillary sinus and in four patients of lung infiltrations one by aspergillus, one by Candida + pseudomonas, two by microbiologically undefined germs ; . Of 17 patients, 16 95% ; required platelet-support therapy; of these, six patients had grade 2 hemorrhagea and one case 9 ; , affected by multiple pulmonary infiltrates, died in CR of haemothorax after recovering from the induction treatment. Concerning the non-hematologic toxicity, five cases of grade 2 mucositis and five of grade 2 hepatotoxicity were observed Table 3 ; . Post-remission therapy and follow-up of the responders are shown in Table 4. Five of the 11 patients who achieved CR were eligible for a transplantation; one patient patient 1 ; received allo-BMT on day 70 after the start of induction therapy; four patients cases 2, 3, 4, ; received auto-BMT after a median time of 105 days range 70 to 300 days ; after the start of induction therapy. Cytogenetic response at the time of BM harvest is indicated in Tables 1 and 2. Among the four autotransplanted patients, one case 2 ; received a bone marrow purged in vitro with bcr-abl antisense oligodeoxynucleotide [19]. Of the remaining 6 of 11 patients who were ineligible for BMT, five received no further treatment because of persistent pneumonia infiltrates case 6 ; , severe liver toxicity case 7 ; , persistent thrombocytopenia case 9 ; and early relapse case 8, 10 ; . The last patient enrolled in the study is receiving conventional chemotherapy and is on the waiting list for unrelated BMT. After a median follow-up of 8.5 months range 1 to 36.
Prominent in ambulatory than non-ambulatory patients, some of these reactions may be alleviatedif the patient lies down Others euphoria. dysphoria. constipation.skin rashand pruritus. Dosage and AdmInIstration: Dosage should be adjustedaccording to severityof pain and response
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1. McGeown MG. Immunosuppression for kidney transplantation. Lancet 1973; 2: 310312 McGeown MG, Kennedy JA, Loughridge WG et al. One hundred kidney transplants in the Belfast city hospital. Lancet 1977; 2: 648651 Starzl TE, Marchioro TL, Waddell WR. The reversal of rejection in human renal homografts with subsequent development of homograft tolerance. Surg Gynecol Obstet 1963; 117: 385389 American College of Surgeons NIH Organ Transplant Registry. The 12th report of the human renal transplant registry. JAMA 1975; 233: 787 Opelz G, Sengar DP, Mickey MR, Terasaki PI. Effect of blood transfusions on subsequent kidney transplants. Transplant Proc 1973; 5: 253259 Chan L, French ME, Beare J, Oliver DO, Morris PJ. Prospective trial of high-dose versus low-dose prednisolone in renal transplantation. Transplant Proc 1980; 12: 323326 Morris PJ, Chan L, French ME, Ting A. Low-dose oral prednisolone in renal transplantation. Lancet 1982; 1: 525527 Buckles JA, Mackintosh P, Burnes AD. Controlled trial of lowversus high-dose oral steroid therapy in 100 cadaveric renal transplants. Proc EDTA 1981; 18: 394399 Papadakis JT, Bewick M, Brown CM et al. Low dose steroids in renal transplantation. Lancet 1982; 1: 916917 Salaman JR, Griffin PJ, Price K. High- or low-dose steroids for immunosuppression. Transplant Proc 1983; 15: 1086 Walker RG, d'Apice AJ, Mathew TH et al. Long-term followup of a prospective trial of low-dose versus high-dose steroids in cadaveric renal transplantation. Transplant Proc 1987; 19: 2834 McGeown MG, Craig WJ. Results of renal transplantation five to twenty-six years after surgery, using azathioprine and lowdose prednisolone as sole immunosuppression. Clin Transplant 1996; 265270 13. Cave MH, Doherty CC, Douglas JF et al. Live donor renal transplantation: the experience of the Belfast Renal Unit. Ir J Med Sci 1989; 158: 267268 Morris PJ. Cyclosporine. In: WB Saunders, Morris PJ ed. Kidney Transplantation: Principles and Practice, 4th edn, Philadelphia, 1994; 179201 15. Pirsch JD, Miller J, Deierhoi MH et al. A comparison of tacrolimus FK506 ; and cyclosporine for immunosuppression after cadaveric and transplantation. Transplantation 1997; 63: 977983 The Tricontinental Mycophenolate Mofetil Renal Transplantation Study Group. A blinded, randomized clinical.
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Environment can create significant problems for the evacuation force. Interpreters may be required to assist the search squads in moving from the assembly areas and to locate evacuees who are not at home or whose addresses are incorrect. A security squad provides security to the team during movement and in the assembly area. Consideration should be given to attachment of one-to-three member Tactical PSYOP Teams, with their.
HE FUNCTIONS OF ghrelin, the newly discovered 28amino acid peptide produced by gastric neuroendocrine cells, are not yet clear 1, 2 ; . It known that ghrelin is an orexigenic peptide that acts on hypothalamic neurons that regulate energy balance 3 ; . In humans, circulating ghrelin levels vary acutely and chronically with nutritional status; levels are elevated in fasting, fall with food intake, are low in obesity, and rise with weight loss 4 8 ; . The mechanisms for these changes in ghrelin levels with nutrient intake are not yet known, but changes in other metabolic factors such as insulin may play a role 9 ; . Exogenously administered ghrelin is also a potent stimulator of pituitary GH secretion 10, 11 ; . However, the role of ghrelin in endogenous GH secretion is not yet clear. Currently available data do suggest that ghrelin may play a role in referring signals from the gastrointestinal GI ; tract on nutritional state to the hypothalamic-pituitary GH axis. Little is known about the physiology of ghrelin secretion in acromegaly. Some recent data have suggested that ghrelin levels are lowered in patients with active acromegaly 12 ; , and some, but not all, evidence indicates that circulating concentrations of GH and or IGF-I could influence ghrelin secretion 1318 ; . Increasing evidence also suggests that insulin may be an important regulator of ghrelin secretion 9 and cylert.
Confined to the A-V node and does not include the accessory pathway. 2 ; that the effect on A-V and V-A conduction over the accessory pathway following drug administration is not the same.
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There was one case of Kaposi sarcoma occurring 35 months after transplantation and presenting with multiple skin lesions and mucosal involvement of the stomach confirmed at endoscopic and histological examination. Following a drastic reduction in immunosuppression cessation of azathioprine and reduction in cyclosporine A ; , there was only partial resolution of the Kaposi sarcoma; complete recovery occurred only after two courses of chlorambucil 5 mg ; . Lymphoproliferative disease was diagnosed in one patient who received OKT3 at a dosage of 95 mg 5 months after transplantation and who presented with weight lost, fever of unknown origin and pancytopenia. There was no evidence of recent or acute EBV infection normal IgM and IgG antibody levels ; . On bone marrow examination a diffuse lymphoproliferative infiltration corresponding to lymphatic leukaemia or lymphoblastic lymphoma was present An exact diagnosis of the immunohistological identified T-cells could not be established. Despite cessation of immunosuppressive therapy and chemotherapy with bleomycin, vincristine sulphate, cyclophosphamide, cisplatin and prednisone, the lymphoblastic infiltration of bone marrow persisted. The patient died one and a half months after tumor diagnosis of a fulminant septicemia induced by agranulocytosis. At necropsy, a persistent bone marrow aplasia without T-cell proliferation, chronic pneumonia and necrotic bronchiolitis caused by an infiltrative aspergillosis were found.
AHLEMEYER, B., WEITRAUT, H. AND SCHONER, W. 1992 ; . Cultured chick-embryo heart cells respond differently to ouabain as measured by increase in their intracellular Na + concentration. Biochim. biophys. Acta 1137, 135142. AMARINO, G. P. AND FOX, M. H. 1995 ; . Intracellular Na + measurements using sodium green tetraacetate with flow cytometry. Cytometry 21, 248256. ARSLAN, P., VIRGILIO, D. F., BELTRAME, M., TSIEN, R. Y. AND POZZAN, T. 1985 ; . Cytosolic Ca2 + homeostasis in Ehrlich and Yoshida carcinomas: a new, membrane-permeant chelator of heavy metals reveals that these ascites tumour cell lines have normal cytosolic free Ca2 + . J. biol. Chem. 260, 27192727. BENDERS, A. A. G. M., LI, J., LOCK, R. A. C., BINDELS, R. J. M., WENDELAAR BONGA, S. E. AND VEERKAMP, J. H. 1994 ; . Copper toxicity in cultured human skeletal muscle cells: the involvement of Na + -ATPase and the Na + Ca2 + -exchanger. Pflgers Arch. 428, 461467. CAPPARELLI, E. V. 1992 ; . New calcium channel blockers: improved therapy? Clin. Pharmac. 11, 549552. CHERN, Y. J., CHUEH, S. H., LIN, Y. J., HO, C. M. AND KAO, L. S. 1992 ; . Presence of Na + Ca2 + exchange activity and its regulation of intracellular calcium concentration in bovine adrenal chromaffin cells. Cell Calcium 13, 99106. EDDY, F. B. AND CHANG, Y. G. 1993 ; . Effects of salinity in relation to migration and development in fish. In The Vertebrate Gas Transport Cascade; Adaptation to Enviroment and Mode of Life ed. J. Eduardo and P. W. Bicudo ; , pp. 3542. Boca Raton, FL: CRC Press. EHRENFELD, J., LACOSTE, I., GARCIA-ROMEU, F. AND HARVEY, B. 1990 ; . Interdependence of Na + and H + transport in frog skin. In Animal Nutrition and Transport Processes, vol. 2, Transport, Respiration and Excretion: Comparative and Environmental Aspects ed. J. P. Truchot and B. Lahlou ; , pp. 152170. Basel: Karger. EWART, H. S. AND KLIP, A. 1995 ; . Hormonal regulation of the Na + K -ATPase: mechanisms underlying rapid and sustained changes in pump activity. Am. J. Physiol. 269, C295C311. FLIK, G. 1997 ; . Transport and housekeeping of calcium in fish gills. In Society for Experimental Biology Symposium Bill Potts Springer in press ; . FLIK, G., KANEKO, T., GRECO, A. M., LI, J. AND FENWICK, J. C. 1997 and cytomel.
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| Cyclosporine nauseaThe striped marmoset normally thrives in an environment abundant in deciduous trees. The lush greenery provided by the trees gives the striped marmoset enough nourishment to keep it healthy during its reproductive cycle, ensuring that newborn striped marmosets will replace any older ones who die off. However, in the Torkanda region, which is known for its large number of deciduous trees, the striped marmoset population is considered endangered. Which of the following, if true, best explains the apparent discrepancy in the argument above? A ; Many species of animals that can be found in the Torkanda region, including brown bears and flying squirrels, are considered endangered. B ; The striped marmoset is thought to be endangered in several regions of South America and Africa. C ; The long-eared mongoose, which is indigenous to the Torkanda region, is a natural predator of the striped marmoset. D ; The Torkanda region is known for its harsh winters, where temperatures frequently drop well below freezing. E ; Striped marmosets have very rapid metabolism, which is aided by the nutrients found in the leaves and shoots of deciduous trees
Toxicity is increased when used in combination with cyclosporine. Anti-neoplastic agents may enhance the potential of amphotericin B for renal toxicity, bronchospasm, and hypotension. Additionally, steroids, digitalis, and thiazides may potentiate hypokalemia. Topical applications may cause punctate epithelial corneal erosions and occasionally a greenish discoloration of the cornea. The penetration of topically applied amphotericin B is less than that of topically applied natamycin through an intact corneal epithelium. 78.Natamycin Natacyn ; is the drug of choice in Fusarium keratitis. It is a predominantly a fungicidal polyene antibiotic, derived from Streptomyces natalensis that possesses in vitro activity against yeast and filamentous fungi, including Candida, Aspergillus, Cephalosporium, Fusarium, and Penicillium species. The drug binds to fungal cell membrane forming a polyen-esterol complex altering membrane permeability and depleting essential cellular constituents. Generally, therapy with Natamycin should be continued for 14-21 days or until the fungal keratitis has resolved. In many cases, it may help to reduce dosage gradually. Failure of keratitis to improve following 7-10 days of using the drug suggests resistance to the drug. Adherence of suspension to areas of epithelial ulceration or retention in fornices can occur. 79.Azoles imidazoles and triazoles ; include ketoconazole, miconazole, fluconazole, itraconazole, econazole, and clotrimazole. They inhibit ergosterol synthesis at low concentrations, and, at higher concentrations, they appear to cause direct damage to cell walls. Oral fluconazole and ketoconazole are absorbed systemically with good levels in the anterior chamber and the cornea; therefore, they should be considered in the management of deep fungal keratitis. Side effects of the drug Ketoconazole when administered systemically includes liver toxicity, impotence, decreased libido, and gynecomastia 80.Ketoconazole is an imidazole broad-spectrum antifungal agent. It inhibits synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death. The drug has a fungistatic activity. It is often used systemically in the treatment of deep fungal infections. Studies have shown intraocular penetration in keratitis due to Fusarium, Aspergillus, Curvularia, and Candida species. Isoniazid may decrease bioavailability of ketoconazole. Co-administration with rifampin decreases effects of rifampin and ketoconazole. The drug may increase effect of anticoagulants; may increase toxicity of steroids and cyclosporine cyclosporine dosage can be adjusted ; and may also decrease theophylline levels. The drug may be associated with liver toxicity and may reversibly decrease steroid serum levels. The adverse effects of the drug can be reduced with dose of 200-400 mg d. It is advisable to administer antacid, anticholinergics drugs, or H2 blockers at least 2 hours after taking ketoconazole. Other adverse effects include impotence, decreased libido, and gynecomastia 81.Fluconazole is an alternative drug to ketoconazole in the treatment of deep fungal keratitis caused by a variety of fungi. The drug has a fungistatic activity. It is a synthetic oral antifungal that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation, which prevents conversion of lanosterol to ergosterol, thereby disrupting cellular membranes. The drug blood levels may increase when used in combination with hydrochlorothiazides; and may decrease with co-administration of rifampin. Co-administration of fluconazole may decrease phenytoin concentrations; may increase concentrations of theophylline, and effects of anticoagulants may increase with fluconazole coadministration. Increases in cyclosporine concentrations may occur when administered concurrently. The drug may be nephrotoxic and dose should be adjusted in renal insufficiency. It may also cause clinical hepatitis, cholestasis, and fulminant hepatic failure and death in patients with underlying medical conditions AIDS, malignancy ; and while taking multiple concomitant medications and cytoxan.
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Using the outpatient prescription claims database of a large, national pharmaceutical benefit manager. The cohort included 765423 subjects 65 years or older, who were covered by a pharmaceutical benefit manager and filed 1 or more prescription drug claims during 1999. Main outcome measures were the proportion of subjects who filled a prescription for 1 or more drugs of concern and the proportion of subjects who filled prescriptions for 2 or more of the drugs.
| Were unaffected. The drop in cardiac output was attributed to either dilatation of the peripheral blood vessels with pooling of blood in the systemic veins and capillaries and a reduction in venous return or reduced sympathetic tone of the heart muscle with decreased contractility. It was reasoned that if the effect of hexamethonium bromide was on the tone of the pulmonary arterioles, the fall in thepul and dacarbazine.
Toxicity was acceptable, with mucositis being dose-limiting and hyperbilirubinemia prevalent as a known pharmacodynamic effect of psc 83 cyclosporine a works in similar ways to overcome the p-glycoprotein pump, thus increasing intracellular anthracycline levels, and is still being evaluated in studies.
Jusko WJ, eds. Applied pharmacokinetics. Spokane, WA: Applied Therapeutics, 1993: 6-159. Slaughter RL, Edwards DJ. Recent advances: the cytochrome P450 enzymes. Ann Pharmacother 1995; 29: 61924. Brosen K. Recent developments in hepatic drug oxidation: implications for clinical pharmacokinetics. Clin Pharmacokinet 1990; 18: 22039. Guengerich FP. Catalytic selectivity of human cytochrome P450 enzymes: relevance to drug metabolism and toxicity. Toxicol Lett 1994; 70: 1338. Nebert DW, Adesnich M, Coon MJ, et al. The P450 gene superfamily: recommended nomenclature. DNA 1987; 6: 111. Coutts RT. Polymorphism in the metabolism of drugs, including antidepressant drugs: comments on phenotyping. J Psychiatry Neurosci 1994; 19: 3044. Kunze KL, Wienkers LC, Thummel KE, Trater WF. Warfarin-fluconazole. I. Inhibition of the human cytochrome P450-dependent metabolism of warfarin by fluconazole: in vitro studies. Drug Metab Dispos 1996; 24: 41421. Black DJ, Kunze KL, Wienkers LC, et al. Warfarinfluconazole. II. A metabolically based drug interaction: in vitro studies. Drug Metab Dispos 1996; 24: 4228. Ereshefsky L, Riesenman C, Francis Lam YW. Antidepressant drug interactions and the cytochrome P450 system: the role of cytochrome P450 2D6. Clin Pharmacokinet 1995; 29 suppl 1 ; : 1019. Cooke CE, Sklar GE, Nappi JM. Possible pharmacokinetic interaction with quinidine: ciprofloxacin or metronidazole? Ann Pharmacother 1996; 30: 3646. Heimark LD, Wienkers L, Dunze K, et al. The mechanism of the interaction between amiodarone and warfarin in humans. Clin Pharmacol Ther 1992; 51: 398407. Soto J, Alsar MJ, Sacristan JA. Assessment of the time course of drugs with inhibitory effects of hepatic metabolic activity using successive salivary caffeine tests. Pharmacotherapy 1995; 15: 7814. Shinn AF. Clinical relevance of cimetidine drug interactions. Drug Saf 1992; 7: 24567. Pirttiaho HI, Sotaniemi EA, Pelkonen RO, et al. Hepatic blood flow and drug metabolism in patients on enzymeinducing anticonvulsants. Eur J Clin Pharmacol 1982; 22: 4415. Harder S, Thurmann P. Clinically important drug interactions with anticoagulants. an update. Clin Pharmacokinet 1996; 30: 41644. Grange JM, Winstanley PA, Davies PDO. Clinically significant drug interactions with antituberculosis agents. Drug Saf 1994; 11: 24251. Cupp MJ, Tracy TS. Role of the cytochrome P450 3A subfamily in drug interactions. US Pharmacist 1997: HS 921. Schein JR. Cigarette smoking and clinically significant drug interactions. Ann Pharmacother 1995; 29: 113948. Nemeroff CB, DeVane L, Pollock BG. Newer antidepressants and the cytochrome P450 system. J Psychiatry 1996; 153: 31120. Honig PK, Woosley RL, Zamani K, Conner DP, Cantilena LR. Changes in the pharmacokinetics and electrocardiographic pharmacodynamics of terfenadine with concomitant administration of erythromycin. Clin Pharmacol Ther 1992; 52: 21318. Mathews DR, McNutt B, Okerholam R, Flicker M, McBride G. Torsades de pointes occurring in association with terfenadine use. JAMA 1991; 266: 23756. Honig PK, Wortham DC, Zamani K, Conner DP, Mullin JC, Cantilena LR. Terfenadine-ketoconazole interaction: pharmacokinetic and electrocardiographic consequences. JAMA 1993; 269: 151318. Monahan BP, Ferguson CL, Killeavy ES, Lloyd BK, Troy J, Cantilena LR. Torsades de pointes occurring in association with terfenadine use. JAMA 1990; 264: 278890. Pratt CM, Ruberg S, Morganroth J, et al. Dose-response relation between terfenadine Seldane ; and the QT interval on the scalar electrocardiogram: distinguishing a drug effect from spontaneous variability. Heart J 1996; 131: 47280. Woosley RL. Cardiac actions of antihistamines. Annu Rev Pharmacol Toxicol 1996; 36: 23352. Francois I, De Nutte N. Nonulcer dyspepsia: effect of the gastrointestinal prokinetic drug cisapride. Curr Ther Res 1987; 41: 8918. Wysowski DK, Bacsanyi J. Cisapride and fatal arrhythmia. N Engl J Med 1996; 335: 2901. Inman W, Kubota K. Tachycardia during cisapride treatment. BMJ 1992; 305: 1019. Bran S, Murray W, Hirsch IB, Plamer JP. Long QT syndrome during high-dose cisapride. Arch Intern Med 1995; 155: 7658. Olsson S, Edwards IR. Tachycardia during cisapride treatment. BMJ 1992; 305: 7489. Abramowicz M, ed. Fexofenadine. Med Lett 1996; 38: 956. Kivisto KT, Neuvonen PJ, Klotz U. Inhibition of terfenadine metabolism: pharmacokinetic and pharmacodynamic consequences. Clin Pharmacokinet 1994; 27: 15. Gillum JG, Isreal DS, Polk RE. Pharmacokinetic drug interactions with antimicrobial agents. Clin Pharmacokinet 1993; 25: 45082. Cantilena LR, Sorrels S, Wiley T, Wortham D. Fluconazole alters terfenadine pharmacokinetics and electrocardiographic pharmacodynamics [abstr]. Clin Pharmacol Ther 1995; 57: 185. Harris S, Hilligoss DM, Colangelo PM, Eller M, Okerholm R. Azithromycin and terfenadine: lack of drug interaction. Clin Pharmacol Ther 1995; 58: 31015. Amsden GW. Macrolides versus azalides: a drug interaction update. Ann Pharmacother 1995; 29: 90617. van-Rosenteil NA, Adam D. Macrolide antibacterials. Drug interactions of clinical significance. Drug Saf 1995; 13: 10522. Abramowicz M, ed. Mibefradil--a new calcium-channel blocker. Med Lett 1997; 39: 1035. DeVane L. Pharmacokinetics of the newer antidepressants: clinical relevance. J Med 1994; 97 suppl 6A ; : 13S23. Shen WW. Cytochrome P450 monooxygenases and interactions of psychotropic drugs: a five-year update. Int J Psychiatry Med 1995; 25: 27790. Swims MP. Potential terfenadine-fluoxetine interaction. Ann Pharmacother 1993; 27: 14045. Marchiando RJ, Cook MD. Probable terfenadine-fluoxetineassociated cardiac toxicity. Ann Pharmacother 1995; 29: 9378. Finley PR. Selective serotonin reuptake inhibitors: pharmacologic profiles and potential therapeutic distinctions. Ann Pharmacother 1994; 28: 135969. Bristol-Myers Squibb Co. Serzone nefazodone ; package insert. Princeton, NJ; 1997. Solvay Pharmaceuticals. Luvox fluvoxamine ; package insert. Marietta, GA; 1997. Robinson DS, Roberts DL, Smith JM, et al. The safety profile of nefazodone. J Clin Psychiatry 1996; 57 suppl 2 ; : 318. Pfizer, Inc. Zoloft sertraline ; package insert. Wilkes-Barre, PA; 1997. Morton WA, Sonne SC, Verga MA. Venlafaxine: a structurally unique and novel antidepressant. Ann Pharmacother 1995; 29: 38795. Kupferschmidt HT, Riem H, Ziegler WH, Meier PJ, Krahenbuhl S. Interaction between grapefruit juice and midazolam in humans. Clin Pharmacol Ther 1995; 58: 208. Fuhr U, Dummert AL. The fate of naringin in humans: a key to grapefruit juice-drug interactions: Clin Pharmacol Ther 1995; 58: 36573. Hollander AMJ, van Rooij J, Lentjes EGWM, et al. The effect of grapefruit juice on cyclosporine and prednisone metabolism in transplant patients. Clin Pharmacol Ther 1995; 57: 31824. Spence JD. Drug interactions with grapefruit: whose responsibility is it to warn the public? Clin Pharmacol Ther 1997; 61: 395400. Edwards DJ, Bernier SM. Naringin and naringenin are not and daclizumab.
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May be more relevant models of restenosis have not been reported. Another design using a metallic backbone coated with PLLA polymer has shown promise as a drug eluting stent in preliminary experiments Fig 4B ; .63 After implantation within injured porcine coronary arteries, release of the test agent dexamethasone from the monolithic polymer matrix was documented to occur for at least 28 days. Although the dexamethasone proved ineffective in reducing neointimal proliferation in this model, the PLLA polymer did not evoke an inflammatory reaction and appeared to be an effective and cyclosporine.
1. Birkeland SA. Steroid-free immunosuppression in renal transplantation [Letter; comment]. Lancet 1996; 348: 1105. Ratcliffe PJ, Dudley CR, Higgins RM, Firth JD, Smith B, Morris PJ. Randomised controlled trial of steroid withdrawal in renal transplant recipients receiving triple immunosuppression [See comments]. Lancet 1996; 348: 643. Birkeland SA. Steroid-free immunosuppression after kidney transplantation with antithymocyte globulin induction and cyclosporine and mycophenolate mofetil maintenance therapy. Transplantation 1998; 66: 1207. Rodino MA, Shane E. Osteoporosis after organ transplantation. J Med 1998; 104: 459. Keogh A, Macdonald P, Harvison A, Richens D, Mundy J, Spratt P. Initial steroid-free versus steroid-based maintenance therapy and steroid withdrawal after heart transplantation: two views of the steroid question. J Heart Lung Transplant 1992; 11: 421 and dactinomycin.
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