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Gangrene did not progress further. She was advised to avoid NSAIDs, particularly etodolac and ibuprofen, in the future, and was transferred to another hospital under the care of a vascular surgeon who carried out distal amputation of all the involved fingers and toes. Following successful surgery, she was discharged. However, six weeks later, she developed an infection in one of her amputated hands and died due to severe sepsis.
1. Rajkumar SV, Dispenzieri A, Fonseca R, et al. Thalidomide for previously untreated indolent or smoldering multiple myeloma. Leukemia 2002; 15: 1274 Weber DM, Gavino M, Delasalle K, et al. Thalidomide alone or with dexamethasone for multiple myeloma. Blood 1999; 94: 604A Abstract ; . 3. Dimopoulos MA, Zervas K, Kouvatseas G, et al. Thalidomide and dexamethasone combination for refractory multiple myeloma. Ann Oncol 2001 ; 12: 991 5. Weber DM, Rankin K, Gavino M, Delasalle K, Alexanian R. Thalidomide alone or with dexamethasone for previously untreated multiple myeloma. J Clin Oncol 2003; 21: 16 Gallo O, Franchi A, Magnelli L, et al. Cyclooxygenase2 pathway correlates with VEGF expression in head and neck cancer. Implications for tumor angiogenesis and metastasis. Neoplasia 2001 ; 3: 53 61. Masferrer JL, Leahy KM, Koki AT, et al. Antiangiogenic and antitumor activities of cyclooxygenase-2 inhibitors. Cancer Res 2000; 60: 1306 Leahy KM, Koki AT, Masferrer JL. Role of cyclooxygenases in angiogenesis. Curr Med Chem 2000; 7: 1163 Fosslien E. Molecular pathology of cyclooxygenase2 in neoplasia. Ann Clin Lab Sci 2000; 30: 3 Podar K, Tai YT, Davies FE, et al. Vascular endothelial growth factor triggers signaling cascades mediating multiple myeloma cell growth and migration. Blood 2001 ; 98: 428 35. Hida T, Kozaki K, Muramatsu H, et al. Cyclooxygenase-2 inhibitor induces apoptosis and enhances cytotoxicity of various anticancer agents in non-small cell lung cancer cell lines. Clin Cancer Res 2000; 6: 2006 Liu XH, Yao S, Kirschenbaum A, Levine AC. NS398, a selective cyclooxygenase-2 inhibitor, induces apoptosis and down-regulates bcl-2 expression in LNCaP cells. Cancer Res 1998; 58: 4245 Sawaoka H, Tsuji S, Tsujii M, et al. Cyclooxygenase inhibitors suppress angiogenesis and reduce tumor growth in vivo. Lab Invest 1999; 79: 1469 Tsujii M, Kawano S, Tsuji S, Sawaoka H, Hori M, DuBois RN. Cyclooxygenase regulates angiogenesis induced by colon cancer cells. Cell 1998; 93: 705 Erratum in: Cell 1998; 94: following 271. 14. Uefuji K, Ichikura T, Mochizuki H. Cyclooxygenase-2 expression is related to prostaglandin biosynthesis and angiogenesis in human gastric cancer. Clin Cancer Res 2000; 6: 135 Wun T, McKnight H, Tuscano JM. Increased cyclooxygenase-2 COX-2 ; : apotentialrole in thepathogenesis of lymphoma. Leuk Res 2004; 28: 179 Jendrossek V, Handrick R, Belka C. Celecoxib activates a novel mitochondrial apoptosis signaling pathway. FASEB J 2003; 17: 1547 Steinbach G, Lynch PM, Phillips RK, et al. The effect of celecoxib, a cyclooxygenase-2 inhibitor, in familial adenomatous polyposis. N Engl J Med 2000; 342: 1946 Pruthi RS, Derksen JE, Moore D. A pilot study of use of the cyclooxygenase-2 inhibitor celecoxib in recurrent prostate cancer after definitive radiation therapy or radical prostatectomy. BJU Int 2004; 93: 275 Brown JR, DuBois RN. Cyclooxygenase as a target in lung cancer. Clin Cancer Res 2004; 10: 4266 Altorki NK, Keresztes RS, Port JL, et al. Celecoxib, a selective cyclo-oxygenase-2 inhibitor, enhances the response to preoperative paclitaxel and carboplatin in early-stage non-small-cell lung cancer. J Clin Oncol 2003; 21: 2645 Kara IO, Sahin B. COX-2 inhibitory treatment in chronic lymphocytic leukemia: a preliminary clinical study. Leuk Lymphoma 2004; 45: 1495 Lilly MB, Drapiza L, Sheth M, Zemskova M, Bashkirova S, MorrisJ. Expression of cyclooxygenase2 COX-2 ; in human leukemias and hematopoietic cells. Blood 2004; 104: 4336 Abstract ; . 23. Waskewich C, Blumenthal RD, Li H, Stein R, Goldenberg DM, Burton J. Celecoxib exhibits the greatest potency amongst cyclooxygenase COX ; inhibitors for growth inhibition of COX-2-negative hematopoietic and epithelial cell lines. Cancer Res 2002; 62: 2029 Burton JD, Blumenthal RD, Waskewich C, Goldenberg DM. Growth inhibition of hematologic cancer cell lines by celecoxib: both Cox-2-dependent and -independent effects. Blood 2000; 99: 1318 Abstract ; . 25. Zhang M, Abe Y, Matsushima T, Nishimura J, Nawata H, Muta K. Selective cyclooxygenase 2 inhibitor NS-398 induces apoptosis in myeloma cells via a Bcl-2 independent pathway. Leuk Lymphoma 2005; 46: 425 Ladetto M, Vallet S, Trojan A, et al. Cyclooxygenase2 COX-2 ; is frequently expressed in multiple myeloma and is an independent predictor of poor outcome. Blood 2005; 105: 4784 CostesV, Portier M, Lu ZY, Rossi JF, Bataille R, Klein B. Interleukin-1 in multiple myeloma: producer cells and their role in the control of IL-6 production. Br J Haematol 1998; 103: 1152 Hinson RM, Williams JA, Shacter E. Elevated interleukin 6 is induced by prostaglandin E2 in a murine model of inflammation: possible role of cyclooxygenase-2. Proc Natl Acad Sci U S A1996; 93: 4885 90. Shishodia S, Koul D, Aggarwal BB. Cyclooxygenase COX ; -2 inhibitor celecoxib abrogates TNF-induced NF-n B activation through inhibition of activation of I n kinase and Akt in human non-small cell lung carcinoma: correlation with suppression of COX-2 synthesis. J Immunol 2004; 173: 2011 Derksen PW, Tjin E, Meijer HP, et al. Illegitimate WNT signaling promotes proliferation of multiple myeloma cells. Proc Natl Acad Sci U S A 2004; 101: 6122 Lu D, ZhaoY, Tawatao R, et al. Activation of the Wnt signaling pathway in chronic lymphocytic leukemia. Proc Natl Acad Sci U S A 2004; 101: 3118 Nakamura S, Kobayashi M, Shibata K, et al. Etodolac induces apoptosis and inhibits cell adhesion to bone marrow stromal cells in human myeloma cells. Blood 2004; 104: 4836 Abstract ; . 33. Wallace AD, Wheeler TT, Young DA. Inducibility of E4BP4 suggests a novel mechanism of negative gene regulation by glucocorticoids. Biochem Biophys Res Commun 1997; 232: 403 Morisset S, Patry C, Lora M, de Brum-Fernandes AJ. Regulation of cyclooxygenase-2 expression in bovine chondrocytes in culture by interleukin 1a, tumor necrosis factor-a, glucocorticoids, and 17h-estradiol. J Rheumatol 1998; 25: 1146 Subbarayan V, Sabichi AL, Llansa N, Lippman SM, Menter DG. Differential expression of cyclooxygenase-2 and its regulation by tumor necrosis factor-a in normal and malignant prostate cells. Cancer Res 2001 ; 61: 2720 6. Fujita J, Mestre JR, Zeldis JB, Subbaramaiah K, Dannenberg AJ. Thalidomide and its analogues inhibit lipopolysaccharide-mediated induction of cyclooxygenase-2. Clin Cancer Res 2001; 7: 3349 D'Amato RJ, Loughnan MS, Flynn E, Folkman J. Thalidomide is an inhibitor of angiogenesis. Proc Natl Acad Sci U S A 1994; 91: 4082 Kenyon BM, Browne F, D' mato RJ. Effects of thaA lidomide and related metabolites in a mouse corneal model of neovascularization. Exp Eye Res 1997; 64: 971 HM, Panigrahy D, Yuan J, D' mato RJ. ComA bination oral antiangiogenic therapy with thalidomide and sulindac inhibits tumour growth in rabbits. Br J Cancer 1999; 79: 114 Hada M, Mizutari K. A case report of metastatic pancreatic cancer that responded remarkably to the combination of thalidomide, celecoxib and irinotecan. GanTo Kagaku Ryoho 2004; 31: 1407 Hada M. Report of two cases with pleural effusion and ascites that responded dramatically to the combination of thalidomide, celecoxib, irinotecan, and CDDP infused in thoracic and abdominal cavities. Gan To Kagaku Ryoho 2004; 31: 613 Teo SK, Sabourin PJ, O'Brien K, Kook KA, Thomas SD. Metabolism of thalidomide in human microsomes, cloned human cytochrome P-450 isozymes, and Hansen's disease patients. J Biochem Mol Toxicol 2000; 14: 140 Fine HA, Figg WD, Jaeckle K, et al. Phase II trial of the antiangiogenic agent thalidomide in patients with recurrent high-grade gliomas. J Clin Oncol 2000; 18: 708 Mileshkin L, Biagi JJ, Mitchell P, et al. Multicenter.
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At the meeting on 14 November, the president did most of the talking. He noted the weak state of US defenses and pointed out that Germany had a reported air strength almost double the combined Anglo-French total. He pointed out that the United States needed to enlarge its airplane production capacity greatly to counter the mounting security threat to the United States posed by the Germans. Roosevelt intended these planes not only for the Air Corps but for the French and British as well. The president hoped that making an increased US manufacturing capacity available to the French and British would enable them to procure enough aircraft either to forestall an attack by Hitler or to help them defeat him if war came.41 The president sought an AAC of 20, 000 planes with a production capacity of 2, 000 planes a month. He knew, however, that such a program would not pass Congress. Therefore, he asked the War Department to develop a plan for building 10, 000 aircraft and for constructing new plant capacity for an additional 10, 000 aircraft a year. Although his meeting concentrated on airplanes, it supplied the spark for all subsequent Army and Air Corps prewar matriel and manpower expansion--the War Department sought not only new planes but funds to provide a balanced, combat-ready Army.42 This plan served as the blueprint for further expansion of an Air Corps that, in the autumn of 1938, had only 1, 600 aircraft on hand. Plants working on aircraft contracts for the Air Corps could produce only 88.2 planes a month.43 Even six months later, June 1939, the AAC still had only 13 operational B-17s and 22, 287 personnel--only twice the strength of the Cavalry.44 Roosevelt rejected the initial expansion plan presented to him by the Army and the Air Corps. He had asked for 0 million in Air Corps planes, but the Army and the Air Corps had requested an additional 0 million for Army matriel and 0 million for Navy aircraft plus unstated amounts for air bases and air training. The president, who was not at all sure Congress would approve the additional 0 million in the first place, redistributed the funds, giving 0 million of the 0 million to the Army matriel branches, earmarking 0 million for air bases and other nonaircraft items, and leaving 0 million for procurement of 3, 000 combat aircraft.
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Cam, however, has a much longer elimination half-life 30 to 70 h ; than other NSAIDs, and plasma half-life has been previously correlated with GI toxicity 27 ; . The second grouping of NSAIDs consists of preferential COX-2 inhibitors. In Fig. 3, we have classified these as compounds with between 5- and 50-fold selectivity for COX-2 over COX-1. Possibly more importantly, Fig. 4 implies that the selectivity of these compounds could be usefully exploited. For example, the concentrations of etodolac and meloxicam sufficient to inhibit COX-2 by 80% produce only 25% inhibition of COX-1. Despite the sparse epidemiological data, controlled trials [e.g., for meloxicam 28, 29 ; ] show that these preferential compounds have an improved GI toxicity profile. It must be remembered, however, that increasing the dosage of these agents could readily increase GI toxicity due to inhibition of COX-1 because all of the compounds in this group are capable of inhibiting this isoform of COX Fig. 1.
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Chapter 3 Raw Material Mixed Ca, Al, Mg, Fe silicate and sulphide Carbon Granular or powder Crystals Powder Powder Powder Powder Form Description aluminium oxide, modifying oxides, refining agents, flux and colouring species. Reducing agent Source Comments adjusted to glass raw material and exemestane.
Diagnosis is made by the demonstration of typical morphological changes in bone-marrow smears, including severe erythroid hypoplasia with giant and dystrophic proerythroblast 58 ; , and the detection of parvovirus DNA in blood or bone marrow using a PCR assay. Testing for parvovirus Immunoglobulin Ig ; G and IgM antibodies is not useful, as these antibody responses are usually absent or transient. 59.
Continued ; 1078, 1084 2005 ; stating that a Revisor's Note cannot override the plain language of a statute ; . This newly-gained readiness o bviates the n eed to spec ially assign judge s to fill vacant seats for the court to hear and decide cases in banc. Before the revision, if seven judges of the 13 member court were absent, the court could not have acted in banc for lack of a majority unless judges were specially assigned to fill temporarily the vacant seats, the post-revision interpretation a llows a fo ur-mem ber majority of the 6 filled se ats to decide a case in banc. 14 and exenatide
B-Lactams are considered an important part of the medical treatment of patients with bacterial endocarditis since Gram-positive cocci are the aetiological agents in the vast majority of cases with this infection. Combination therapy of b-lactam with an aminoglycoside has been tested both in vitro and in clinical studies, but results, especially from clinical studies, are often contradictory. The combination of an aminoglycoside with a b-lactam has been shown to exhibit partial or full synergy against a variety of isolates in some laboratory studies.14 However, the potential increase in the effectiveness of an antimicrobial regimen after the addition of an aminoglycoside should be weighed against the increased toxicity that may be conferred by the aminoglycoside. Consequently, the need for the addition of an aminoglycoside in the treatment of patients with certain types of bacterial endocarditis has been questioned.5, 6 In addition, the continuous changes of the susceptibilities of pathogens to antibiotics make the decision regarding the appropriate medical therapy for bacterial endocarditis more complex.79 We sought to further examine the role of aminoglycosides as combination therapy with a b-lactam in the treatment of patients with bacterial endocarditis. Although there have been few reviews in the literature about this issue, they are mostly narrative.1012 Thus, we systematically reviewed the available clinical data from studies that compared b-lactam monotherapy with the b-lactam aminoglycoside combination therapy in terms of effectiveness and toxicity.
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Campbell 2007 ; pharmacokinetics of etodolac in the horse following oral and intravenous administration journal of veterinary pharmacology and therapeutics 30 1 ; , 43– 48 doi: 1 1111 j 65-288 200 0081 x prev article next article abstract pharmacokinetics of etodolac in the horse following oral and intravenous administration l and exjade.
L'Oral has always given priority to recruiting young graduates with a view to building long-term careers. 63% of the trainee managers recruited worldwide in 2005 are under thirty * . The group thus surrounds itself with a veritable seedbed of talented individuals whom it entrusts with responsibilities from an early stage. L'Oral ranks second behind the Swiss bank UBS ; in Hewitt's "Top Companies for Leaders in Europe" listing. The aim of the survey, which involved 101 companies in nine European countries, is to identify the company that does the best job of developing talent. It reveals a close link between a company's financial performance and its ability to identify, promote and develop talented individuals.
Results superior than backpropagation. Yao and Liu 1997 ; had presented a new evolutionary system, i.e., EPNet to evolve ANN architecture and connection weights simultaneously. When tested on a number of benchmark problems such as medical diagnosis problems, credit card assessment problem, the results showed that EPNet can produce very compact ANN with good generalization ability in comparison with other algorithms and ezetimibe.
Forsyth County Government offers all full-time employees a comprehensive Cafeteria Benefits program. The Cafeteria Benefits program is arranged by Mark III Brokerage, an employee benefits firm that has worked in the public sector for over 34 years. The Cafeteria Benefits program allows you to pay for certain insurance premiums, work-related child care, and unreimbursed medical expenses before taxes are taken out of your paycheck. Paying for these benefits by this method reduces your income & FICA taxes and increases your take home pay. The Cafeteria Benefits program includes pre-tax and after-tax products listed below. Annual enrollment is the only time you may enroll in the Flexible Spending Plan, Ameritas Dental Plan or in the Kanawha Short Term Disability Plan. All employees who would like to enroll in or make a change to the Kanawha Short Term Disability Plan or Reliance Standard Term Life Plan must be seen by a Mark III Representative during an open enrollment meeting. The Plan Year is from July 1, 2007 to June 30, 2008
21. Butler C, Rollnick C, Pill R, et al. Understanding the culture of prescribing: qualitative study of general practitioners' and patients' perceptions of antibiotics for sore throats. BMJ. 1998; 317: 63742. Norris P, Simpson T, Bird K, et al. Understanding of pharmacy terms amongst three ethnic groups in New Zealand. Int J Pharm Pract. 2001; 9: 26974 and factive.
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Opps providers will continue to receive passthrough payment on items or services that qualify for pass-through payment; and non-opps providers: are not eligible for pass-through payments; will be paid under their normal payment methodologies; and should comply with all existing requirements when claims require the use of a hcpcs or cpt code.
A common misconception, according to Dr. Thomson, is that backpacks cause scoliosis. He says, "Backpacks do not cause scoliosis. Heavy backpacks can be associated with back strain but one of the most common injuries from backpacks is that the child actually trips over the backpack when it is on the ground." To read more on backpack safety and spine health Dr. Thomson suggests: "There are many websites that have good and bad information. One of the better websites is spinehealth but even this one suggests that backpacks cause scoliosis. Overall it has good suggestions and it is easy to read and faslodex.
Recruitment of regulatory T cells in ovarian carcinoma fosters immune privilege and predicts reduced survival. Nat Med. 2004; 10: 942-949 Woo EY, Chu CS, Goletz TJ, Schlienger K, Yeh H, Coukos G, Rubin SC, Kaiser LR, June CH. Regulatory CD4 + ; CD25 + ; T cells in tumors from patients with early-stage non-small cell lung cancer and late-stage ovarian cancer. Cancer Res. 2001; 61: 4766-4772 Ichihara F, Kono K, Takahashi A, Kawaida H, Sugai H, Fujii H. Increased populations of regulatory T cells in peripheral blood and tumor-infiltrating lymphocytes in patients with gastric and esophageal cancers. Clin Cancer Res. 2003; 9: 4404-4408 Sasada T, Kimura M, Yoshida Y, Kanai M, Takabayashi A. CD4 + CD25 + regulatory T cells in patients with gastrointestinal malignancies: possible involvement of regulatory T cells in disease progression. Cancer. 2003; 98: 1089-1099 Woo EY, Yeh H, Chu CS, Schlienger K, Carroll RG, Riley JL, Kaiser LR, June CH. Cutting edge: Regulatory T cells from lung cancer patients directly inhibit autologous T cell proliferation. J Immunol. 2002; 168: 4272-4276 Liyanage UK, Moore TT, Joo HG, Tanaka Y, Herrmann V, Doherty G, Drebin JA, Strasberg SM, Eberlein TJ, Goedegebuure PS, Linehan DC. Prevalence of regulatory T cells is increased in peripheral blood and tumor microenvironment of patients with pancreas or breast adenocarcinoma. J Immunol. 2002; 169: 2756-2761 Wolf AM, Wolf D, Steurer M, Gastl G, Gunsilius E, Grubeck-Loebenstein B. Increase of regulatory T cells in the peripheral blood of cancer patients. Clin Cancer Res. 2003; 9: 606-612 and etodolac.
Study reference Laine L, Cominelli F, Sloane R, Casini-Raggi V, Marin-Sorensen M, Weinstein WM. Interaction of NSAIDs and Helicobacter pylori on gastrointestinal injury and prostaglandin production: a controlled double-blind trial. Aliment Pharmacol Ther 1995; 9: 12735. Laine L, Sloane R, Ferretti M, Cominelli F. A randomized double-blind comparison of placebo, etodolac, and naproxen on gastrointestinal injury and prostaglandin production. Gastrointest Endosc 1995; 42: 42833. Lanza FL, Royer GL. NSAID-induced gastric ulceration is dose-related by weight: an endoscopic study with flurbiprofen. Am Gastroenterol 1993; 88: 6836. Lauritsen K, Rutgersson K, Bolling E, Brunner G, Eriksson S, Galmiche JP et al. Omeprazole and , ranitidine in the prevention of relapse in patients with duodenal ulcer disease. Can J Gastroenterol 1999; 13: 80613. Lei-Munhoz MS, Malavasi GM, Munhoz MLGS, Gananca HHC, Gananca FF. Comparative study with nimesulide vs potassium diclofenac in ent disease. Rev Bras Med 1990; 47: 5914. Lemmel EM, Bolten W, Vargas R, Platt PN, NissilS M, and SD. A double-blind placebo controlled study of 7.5 mg and 15 mg of meloxicam in patients with rheumatoid arthritis RA ; . Scand J Rheumatol Suppl 1994; 98: 111 Lipscomb GR, Wallis N, Armstrong G, Rees WDW. Gastrointestinal tolerability of meloxicam and piroxicam: A double-blind placebo-controlled study. Br J Clin Pharmacol 1998; 46: 1337. Lonauer G, Tisscher JR, Lim HG, Bijlsma JW. Double-blind comparison of etodolac and diclofenac in patients with rheumatoid arthritis. Curr Med Res Opin 1993; 13: 707. Lucker PW, Pawlowski C, Friederich I, Faiella F, Magni E. Double-blind, randomised, multi-centre clinical study evaluating the efficacy and tolerability of nimesulide in comparison with etodalac in patients suffering from osteoarthritis of the knee. Eur J Rheumatol Inflamm 1994; 14: 2938. Macciocchi A. Results of a Swiss phase IV study. Nimesulide in the daily practice. [German]. Ther Schweiz 1997; 13: 2705. Maeda A. Clinical efficacy of lansoprazole in treatment of gastric ulcer induced by NSAIDs. [Japanese]. Jpn Pharmacol Ther 1998; 26: 22530. Malavasi GM, Lei Munhoz MS, Caovilla HH, Munhoz ML, Freitas GF. Comparative study of nimesulide versus potassium diclofenac in acute otitis media. [Portuguese]. Rev Bra Medi 1990; 47: 3736. Manniche C, Malchow-Moller A . The influence of non-steroid anti-inflammatory drugs NSAID ; on the treatment of peptic ulceration. A prospective randomized investigation. [Danish]. Ugeskr Laeger 1987; 149: 21434. Marcon V, Cannizeuro R, Valentini M, Cressani B, Costan BF, Angonese C, et al. Sucralfate, ranitidine and no treatment in gastric ulcer management a multicenter, prospective, randomized, 24-month follow-up with a study of risk factors of relapse. Digestion 1992; 53: 728. Marques Neto JF, Samara AM. Double-blind crossover study. Cimetidine placebo in patients with rheumatoid arthritis treated with indomethacin. [Portuguese]. Folha Medica 1982; 85: 8856. Martinez RO, Casas H, Mazure PA, Leczycki H, Cosen JN, Canievsky L, et al. Gastroduodenal lesions in rheumatoid arthritis. Evaluation and treatment. [Spanish]. Acta Gastroenterol Latinoam 1988; 18: 8796. McKenna F. Efficacy of diclofenac misoprostol vs diclofenac in the treatment of ankylosing spondylitis. Drugs 1993; 45: 2430. McKenna F, Weaver A, Fiechtner JJ, Bello AE, Fort JG. COX-2 specific inhibitors in the management of osteoarthritis of the knee: a placebo-controlled, randomized, double-blind study. JCR J Clin Rheumatol 2001; 7: 1519. Medina Santillan R, Reyes GG, Mateos GE. Prevention of gastroduodenal injury induced by NSAIDs with low-dose Misoprostol. Proc West Pharmacol Soc 1999; 42: 334. Menkes CJ. Scapulo-humeral periarthritis: efficacy, safety and therapeutic benefit of etodolac 600 mg daily ; versus piroxicam 40 20 mg daily ; . Rhumatologie 1990; 42: 195200 and felbamate.
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