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You may not be able to take fenofibrate, or you may require a dosage adjustment or special monitoring during treatment if you have any of the conditions listed above. Fenofibrate led to a large reduction in the need for laser surgery for diabetic retinopathy and a reduction in kidney-related complications. A Description of the Core of Treatment This can be divided into the stages described later The outcome of treatment is good: as many as 70% of alcohol-dependent persons with stable psychosocial functioning remain abstinent a year after treatment C. Intervention involves asking questions regarding alcohol problems, evaluating state markers of heavy drinking and the judicious use of screening questionnaire D. Detoxification for depressants involves a good physical examination, reassurance and the judicious use of benzodiazepines A. B. Dissolution studies revealed that formulations with 20-40 wt. % lidocaine were in the eutectic region while those with 70-80 wt. % drug contained amorphous excipient. The dissolution rates measured in these regions were among the highest. Drug-PEG solid dispersions were prepared by PGSS as well. Kerc et al. 1999 ; have increased the dissolution rate of three poorly water soluble APIs: nifedipine, felodipine and fenofibrate by using PGSS process. The authors have studied the effect of pre-expansion conditions; pressure was varied in the range of 100-200 bar, operating temperature between 65 and 185 C, according to the melting point of the processed drug. Jung et al. 1999 ; prepared solid dispersions of the antifungal agent, itraconazole and various polymers by spray-drying method. Two pH-dependent AEA and Eudragit E100 ; and four pH-independent polymers Poloxamer 188, PEG 20000, PVP, HPMC ; were compared. Dissolution tests in simulated gastric juice revealed that PEG 20000 was the best pH-independent solubilizer agent.

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Insulin secretion study For insulin secretion studies, cells were plated on 24-multiwell plates 1x105 cells per well ; . On the day of the experiment, the culture medium was completely aspirated and replaced with fresh medium containing fenofibrate, fenofibric acid or 15-deoxy-12, 14PGJ2. The direct effect of fenofibrate 10 and tricor.

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DMD #15230 Lau YY, Huang Y, Frassetto L and Benet LZ 2007 ; Effect of OATP1B transporter inhibition on the pharmacokinetics of atorvastatin in healthy volunteers. Clin Pharmacol Ther 81: 194204. Law M and Rudnicka AR 2006 ; Statin safety: a systematic review. J Cardiol 97: 52C-60C. Le Couteur DG, Martin PF, Pond SM, Bracs P, Black A, Hayes R, Woolf TF and Stern R 1996 ; Metabolism and excretion of 14C atorvastatin in patients with T-tube drainage Abstract ; . Proc Aust Soc Clin Exp Pharmacol Toxicol 3: 153. Lennernas H 2003 ; Clinical pharmacokinetics of atorvastatin. Clin Pharmacokinet 42: 11411160. Li C, Subramanian R, Yu S and Prueksaritanont T 2006 ; Acyl-coenzyme A formation of simvastatin in mouse liver preparations. Drug Metab Dispos 34: 102-110. Martin PD, Dane AL, Schneck DW and Warwick MJ 2003 ; An open-label, randomized, threeway crossover trial of the effects of coadministration of rosuvastatin and fenofibrate on the pharmacokinetic properties of rosuvastatin and fenofibric acid in healthy male volunteers. Clin Ther 25: 459-471. Mathew P, Cuddy T, Tracewell WG and Salazar D 2004 ; An open-label study on the pharmacokinetics PK ; of pitavastatin NK-104 ; when administered concomitantly with fenofibrate or gemfibrozil in healthy volunteers Abstract PI-115 ; . Clin Pharmacol Ther 75: P33. Miller DB and Spence JD 1998 ; Clinical pharmacokinetics of fibric acid derivatives fibrates ; . Clin Pharmacokinet 34: 155-162.
Statins and fibrates protect against the development of peripheral neuropathy in type 2 diabetes, an Australian epidemiological study conducted over eight years has shown. The findings were presented last month at the annual meeting of the American Diabetes Association in Chicago. A sample of 1, 294 people with diabetes was recruited to the Freemantle Diabetes Study between 1993 and 1996.A longitudinal sub-study of 531 people who had attended six comprehensive annual health assessments by November 2001 was also completed. At study entry, participants were about 64 years old, with diabetes diagnosed four years previously: 30.9 per cent had neuropathy. Fibrates and statins were used by 3.5 per cent and 6.8 per cent of participants, respectively. During the five years of follow-up of the longitudinal study, use of fibrates primarily gemfibrozil and fenofibrate ; increased to 10.4 per cent and statins mainly atorvastatin, simvastatin and pravastatin ; to 36.5 per cent. The investigators found that, after controlling for confounding variables, including changes to HbA1c levels, the time to development of newly diagnosed peripheral neuropathy in the longitudinal sub-group indicated that fibrates reduced neuropathy risk by 48 per cent and statins by 35 per cent. Presenting the findings, Timothy M. Davis, professor of medicine, University of Western Australia, said: "In our analysis, the beneficial effects of the drugs were independent of each other and they may work through different mechanisms." He added: "It is just a hypothesis, but taking both drugs may yield greater benefit than taking either drug alone and flavoxate.
The doctor put me on blood pressure medication. Comment on : Boden et al . 2007 ; Combined Use of Rosiglitazone and Fenoffibrate in Patients with Type 2 Diabetes : Prevention of Fluid Retention : Diabetes 56 : 248 - 255 J . Karalliedde e3 - e3 Genetic Influences of Adiponectin on Insulin Resistance , Type 2 Diabetes , and Cardiovascular Disease Claudia Menzaghi 1198 - 1209 Loss of Stearoyl - CoA Desaturase - 1 Improves Insulin Sensitivity in Lean Mice but Worsens Diabetes in Leptin - Deficient Obese Mice Jessica B . Flowers 1228 - 1239 Systemic Expression of Heme Oxygenase - 1 Ameliorates Type 1 Diabetes in NOD Mice Chien - Ming Hu 1240 - 1247 Cell - Permeable Pentapeptide V5 Inhibits Apoptosis and Enhances Insulin Secretion , Allowing Experimental Single - Donor Islet Transplantation in Mice Jorge D . Rivas - Carrillo 1259 - 1267 Lineage Tracing Evidence for In Vitro Dedifferentiation but Rare Proliferation of Mouse Pancreatic - Cells and urispas. CARDIAC AUTONOMIC REGULATION DURING SLEEP IN SUBJECTS WITH REM SLEEP BEHAVIOUR DISORDERS Lanfranchi P, 1, 2, 3 Fradette L, 1, 2 Rompre S, 2 Colombo R, 4 MassicotteMarquez J, 2 Fantini L, 5 Montplaisir J2 1 ; Centre de recherche, Hopital du Sacre-Coeur de Montreal, Montreal, QC, Canada, 2 ; Centre d'etude du sommeil et des rythmes biologiques, Hopital du Sacre-Coeur de Montreal, Montreal, QC, Canada, 3 ; Departement de medecine, Hopital du Sacre-Coeur de Montreal, Montreal, QC, Canada, 4 ; Service of Bioengineering, Salvatore Maugeri Foundation, Veruno, Italy, 5 ; Sleep Disorders Center Departement of Neurology, Universita Vita-Salute San Raffaele, Milan, Italy Introduction : REM behaviour sleep disorders RBD ; is a parasomnia characterized by abnormal motor activity associated with dream mentation. Previous studies showed a reduced heart rate response to motor activity during NREM and REM sleep, suggesting an autonomic nervous system dysfunction in patients with idiopathic RBD. The current study aimed to assess the cardiac autonomic changes from stage 2 NREM NREM ; to REM sleep by spectral analysis of heart rate variability in subjects with idiopathic RBD compared controls. Methods : Eight subjects with idiopathic RBD 2 females, age 637 years ; and 8 sex and age matched controls were studied. One night polysomnography was used to assess R-R variability during NREM and REM sleep. Time domain variables mean RR, standard deviation of RR, sdRR ; and frequency domain variables low frequency and high frequency components in normalized units, LFn and HFn; LF HF ratio ; were obtained from 5-minute ECG segments selected during NREM and REM sleep, while in stable conditions stable breathing pattern, no microarousals or leg movements ; . Values obtained where then averaged for each stage and analysed by 2x2 ANOVA with group RBD and controls ; as factor and state NREM and REM ; as repeated measures. Results : RR interval decreased from NREM to REM in both groups state effect p 0.02, no group by state interaction ; . No changes were observed in sdRR. LFn increased significantly ~11% ; in controls but not in RBD ~1% ; State effect p 0.01, interaction p 0.1 ; . HFn decreased. Disclaimer: the following is provided for information. It is not meant as medical advice. Please consult with your physician with any questions regarding this information. Note: numbers in brackets indicate the message number on the Parkinsn listserv, names and email addresses are attached to the messages. Messages searched are from 151 Jan 13 94 to 9341 Mar 7 96 and flunarizine.

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Rheumatology diagnostic criteria [19]. At the time of the study, most patients were not on a regular treatment of the disease, and none of them received losartan, thiazidic drugs or fenofibrate. We also invited to participate in the study healthy first-degree relatives parents, siblings or their offspring ; of the patients and 120 healthy controls with no personal or familial history of hyperuricaemia or gout. All patients, relatives and healthy controls were of the same predominant genetic background Mexican mestizos ; . The protocol of this research was approved by the Institutional Review Board of our institution and all participants received information about the study, agreed and signed an informed consent. Demographic, medical history, therapeutic and clinical data were obtained from all individuals. Blood chemistry, lipid profile, creatinine clearance CrCl ; adjusted to 1.73 m2 body surface and urinary uric acid excretion in 24 h urine sampling adjusted 1.73 m2 ; were examined by standard methods. Hyperuricaemia was defined as the level of serum uric acid 7 mg dl [417 M l] in males and 6 mg dl [357 M l] in females. Adjusted urate clearance UCl ; and uric acid excretion fraction FEUA ; were calculated. Patients with FEUA 6.5 were classified as underexcretors [20]. The diagnosis of metabolic syndrome was based on the criteria and definitions provided by the National Cholesterol Education Program Expert Panel Adult Treatment Panel III, ATP III ; criteria [21]. Chronic renal failure was considered in patients with CrCl 50 ml min and flupenthixol.

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HOW SENSITIVE IS FAAH TO `CANNABINOID RECEPTOR' LIGANDS? Stephen P.H. Alexander School of Biomedical Sciences, University of Nottingham Medical School, Nottingham NG7 2UH, ENGLAND The fatty acid ethanolamine FAE ; family includes anandamide, N-palmitoyl ethanolamine PEA ; and N-oleoylethanolamine OEA ; . Members of the FAE family are agonists at multiple 7-transmembrane receptors CB1, CB2, GPR55, GPR119 ; , and show agonist activity at transmitter-gated channels TRPV1 ; , as well as multiple nuclear receptors, in particular, the peroxisome poliferator-activated receptors PPAR ; . Given that FAEs appear to be hydrolysed principally through the action of the enzyme fatty acid amide hydrolase FAAH ; , I have investigated whether ligands active at these receptors may also regulate FAAH activity in preparations from rat liver. A microtitre plate-based spectrofluorometric assay for FAAH activity was employed, which assesses degradation of oleamide, capturing the evolved ammonia as an OPA derivative. Ligands were assessed for inhibitory activity at 100 M, alongside the `standard' inhibitor URB597 10 M ; , which completely abrograted FAAH activity. Investigating structure-activity relationships for FAEs indicated a rank order of anandamide N-stearoylethanolamine, OEA N-elaidoylethanolamine, Nstearoylethanolamine, PEA. The synthetic analogue N-benzoylethanolamine was ineffective. Of the CB1 CB2 receptor ligands, only THC 64 % control ; and HU-210 84 % ; evoked significant inhibitions of FAAH activity, while THCV, WIN55212-2, rimonabant, SR144528, AM630 and CBD were ineffective. As expected, the TRPV1 agonist NADA inhibited FAAH activity 54 % ; , as did olvanil 70 % ; , while piperine, PPAHV, isovelleral and capsaicin were without effect. Amongst the PPAR agonists, clofibrate and WY14643 evoked modest inhibitions 70 and 79 %, respectively ; , while gemfibrozil and fenofibrate were inactive. Agonists at PPAR bezafibrate and GW0742 ; were ineffective, as was rosiglitazone PPAR agonist ; . Of the PPAR antagonists, GW6471 ; was inactive, while GW9662 ; evoked a small inhibition 70 % ; . Taken together, these results indicate relatively modest effects of representative compounds active at `cannabinoid receptors'. Whether these agents accumulate sufficiently in intact cell preparations or in vivo to allow significant inhibition of FAAH activity and the consequent accumulation of endocannabinoids remains to be determined and fluvoxamine.
Pce, others ; fenofibrate tricor ; fluconazole diflucan ; gemfibrozil lopid ; itraconazole sporanox ; ketoconazole nizoral ; nefazodone serzone ; nicotinic acid or niacin niaspan ; protease inhibitors a type of drug for hiv ; such as agenerase, crixivan, fortovase, invirase, norvir, and viracept verapamil calan ; if you are taking generic mevacor - lovastatin with any of these drugs, or with large quantities of grapefruit juice ; , alert your doctor immediately at the first sign of muscle pain, tenderness, or weakness, especially if accompanied by fever or general body discomfort. This medication should not be taken by anyone who: has severe liver disease, kidney disease, or gallbladder disease is allergic to fenofibrate or any other of the fibrate class e, g and luvox.

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Before taking this medication, tell your doctor or pharmacist if you: are of asian background chinese, filipino, japanese, korean, vietnamese, or asian-indian origin ; are over the age of 70 are pregnant or intend to become pregnant are breast-feeding or intend to breast-feed are taking other medications, including prescription, non-prescription, and natural health products, as drug interactions are possible are taking other cholesterol-lowering medications such as fibrates gemfibrozil, fennofibrate ; or niacin have a family history of muscular disorders have thyroid problems have kidney or liver problems have diabetes have undergone surgery or other tissue injury have had any past problems with the muscles pain, tenderness ; , after using a statin drink three or more alcoholic drinks daily do excessive physical exercise report any unexplained muscle pain, tenderness, weakness or cramps, or any brown or discoloured urine to your doctor immediately, particularly if you are also experiencing malaise a general feeling of being unwell ; or fever. Shares held in trust by trustees. The company has been consolidated as subsidiary of the Company or their respective immediate holding company as the Company or the immediate holding company exercises control over the Board of Directors of these companies. Audited by Dalian Huanyu Certified Public Accountants, an independent member firm of Baker Tilly International. The Company has filed application for strike-off with Accounting and Corporate Regulatory Authority in Singapore. Acquisition of subsidiaries During the financial year, the Company acquired new and additional equity interest in the following subsidiaries: Date of transfer 1 April 2006 1 April 2006 d ; Subsidiaries Accel Frontline Limited BHR-Frontline Technologies Dalian ; Co., Ltd Interest acquired % 4 80 Consideration $ 1, 897, 373 Attributable net assets $ 774, 389 1 and geodon.

By the generation of mice lacking functional PPARa Lee et al., 1995 ; . PPARanull mice were viable and normal in appearance but did not display any evidence of characteristic morphological or biochemical changes when treated with efficacious peroxisome proliferators such as clotibrate and Wy14, 643. Subsequent studies revealed that PPARa-null mice have increased basal plasma levels of cholesterol and become obese with age Peters et al., 1997; Costet et al., 1998 ; . These data provided strong evidence that PPARa mediates the hypolipidemic effects of fibrates and other peroxisome proliferators. The hypolipidemic fibrates - including gemfibrozil, fenofibrate, and bezafibrate - are a class of drugs widely prescribed in western countries for reducing triglyceride levels, a risk factor for cardiovascular disease. Fibrates have the added benefit of raising levels of high-density lipoprotein HDL ; , or "good, " cholesterol and reducing levels of low-density lipoprotein LDL ; , or "bad, " cholesterol in certain subpopulations of dyslipidemic individuals. The tibrates originally were developed as cardiovascular drugs through optimization of their in vivo activity in rodent models of hyperlipidemia prior to the discovery of the PPARs. Although these drugs activate PPARa in vitro, they do so only at concentrations in the high micromolar range, which may explain why large doses i.e., 200-1200 mg day ; are required for clinical activity. Moreover, the fibrates in clinical use are only weakly selective for PPARa over the other two PPAR subtypes Brown et al., 1999 ; . A search for more-potent fibrates by scientists at Burroughs Wellcome led to synthesis of a series of urea-substituted ureido ; fibrate analogs that were active at greater than lOO-fold lower doses in rodent models of hyperlipidemia Hawke et al., 1997 ; . In our hands, these same compounds were very potent in cell-based PPARa activation assays, activating the receptor with half-maximal effective concentrations in the low nanomolar range Kliewer et al., 1997; Brown et al., 1999 ; . The strong correlation between the in vivo and in vitro potencies of these compounds provided additional evidence that PPARa is the molecular target for the hypolipidemic effects of fibrates Brown et al., 1999 ; . The lack of potency of the fibrates in clinical use had raised the question whether they exerted their effects on PPARa activity by binding directly to the receptor or by an indirect mechanism. The discovery of potent PPARa activators provided us with the reagents necessary to address this question. Standard binding assays performed with a tritiated derivative of the potent ureido fibrate GW 233 1 Figure 2 ; showed that this compound bound directly to recombinant PPARa LBD with a Kd of - Kliewer et al., 1997 ; . In competition binding assays, a series of established hypolipidemic agents and peroxisome proliferators efticiently displaced [3H]GW 233 1 from the PPARa LBD. These data provide strong evidence that the fibrates and other hypolipidemic agents mediate their therapeutic.
T's tough to lose weight--and just as difficult to keep it off. Nine out of 10 people regain lost weight, but that means 10 percent successfully keep it off. How do they do it? These 10 habits may be the key. 1 They don't go it alone. They build networks of friends, neighbors and co-workers that sustain them for day-to-day living and for weight maintenance. For example, they form walking groups that help them stick to their exercise programs. 2 They eat smart. To slim down--and stay slim--weight-loss victors also remain vigilant about nutrition, counting calories in addition to fat grams. They practice variety, balance and moderation. They cook with little or no fat and eat plenty of fruits, vegetables, whole grains.
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Rubinstein E, Keller N. Spiramycin renaissance. J Antimicrob Chemother 1998; 42: 572-6. Smith CR. The spiramycin paradox. J Antimicrob Chemother 1988; 22 Suppl B ; : 141-4. Harf R, Panteix G, Desnottes JF, Diallo N, Leclercq M. Spiramycin uptake by alveolar macrophages. J Antimicrob Chemother 1988; 22 Suppl B ; : 135-40. Kitzis M, Desnottes JF, Brunel D, Giudicelli A, Jacotot F, Andreassian B. Spiramycin concentrations in lung tissue. J Antimicrob Chemother 1988; 22 Suppl B ; : 123-6. Amsden GW. Advanced-generation macrolides: tissue-directed antibiotics. Int J Antimicrob Agents 2001; 18 Suppl 1 ; : S11-5. Shang GD, Dai JL, Wang YG. Construction and physiological studies on a stable bioengineered strain of shengjimycin. J Antibiot Tokyo ; 2001; 54: 66-73. Shi XG, Zhong DF, Sun YZ, Zhang YF. Metabolites of a novel antibiotic bitespiramycin in rat urine and bile. Chin Chem Lett 2004: 15: 431-4. Zhong DF, Shi XG, Sun L, Chen XY. Determination of three major components of bitespiramycin and their major active metabolites in rat plasma by liquid chromatography-ion trap mass spectrometry. J Chromatogr B 2003; 791: 45-53. Shi XG, Zhong DF, Sun L. Pharmacokinetics of a novel antibiotic bitespiramycin in rats. Asian J Drug Metab Pharmacokinet 2003; 3: 134-7. Osono T, Umezawa H. Pharmacokinetics of macrolides, lincosamides and streptogramins. J Antimicrob Chemother 1985; 16 Suppl A ; : 151-66. Hardy DJ, Hensey DM, Beyer JM, Vojtko C, McDonald EJ, Fernandes P. Comparative in vitro activities of new 14-, 15-, and 16-membered macrolides. Antimicrob Agents Chemother 1988; 32: 1710-9. Schoondermark-Van de Ven E, Glama J, Camps W, Vree T, Russel F, Meuwissen J, et al. Pharmacokinetics of spiramycin in the Rhesus monkey: transplacental passage and distribution in tissue in the fetus. Antimicrob Agents Chemother 1994; 38: 1922-9. Cester CC, Laurentie MP, Garcia-Villar R, Toutain PL. Spiramycin concentrations in plasma and genital-tract secretions after intravenous administration in the ewe. J Vet Pharmacol Ther 1990; 13: 7-14. Cester CC, Dubech N, Toutain PL. Effect of sexual steroid hormones on spiramycin disposition in genital tract secretions of the ewe. J Pharm Sci 1992; 81: 33-6, for example, fenofibrat3 134. There are several ways to avoid paying lift-gate delivery costs and tricor.

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Adolescents Young people aged 16 and 17 are generally presumed to have the ability to consent to their own medical treatment, including contraceptive treatment. Health professionals can provide contraceptive advice and treatment to a young person under the age of 16 without parental involvement if the young person is judged to understand the advice provided and its implications and her his physical or mental health would otherwise be likely to suffer and so provision of advice or treatment is in their best interest.80 It is considered to be good practice to follow the criteria outlined by Lord Justice Fraser in the case of Gillick versus West Norfolk and Wisbech Area Health Authority AHA ; and the Department of Health and Social Services DHSS ; when deciding whether a patient under 16 is competent to consent to treatment. These criteria known as the Fraser guidelines or `Gillick competence' ; are that: the young person will understand the professional's advice; the young person cannot be persuaded to inform their parents; the young person is likely to begin, or to continue having, sexual intercourse with or without contraceptive treatment; unless the young person receives contraceptive treatment, their physical or mental health, or both, are likely to suffer; the young person's best interests require them to receive contraceptive advice or treatment with or without parental consent. Production of delivery devices, formulation, filling and packaging of pharmaceuticals: A Use of materials, water and energy. A Disposal of solid waste. A Discharge of wastewater.

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Mission Statement Breast Cancer Action carries the voices of people affected by breast cancer to inspire and compel the changes necessary to end the breast cancer epidemic. Core Principles and Values 1. We are a membership-based organization that values the involvement of grassroots activists throughout the country and around the world to further our mission. 2. We honor each person's commitment and energy to our mission. 3. We are not afraid to examine all sides of all issues. 4. We cannot be bought. 5. We tell the truth about what we discover. 6. We serve individuals while reaching the broader population. 7. We address the significance of environmental links to human health. 8. We encourage people to participate fully in decisions relating to breast cancer. 9. We believe access to information is vital. 10. We work for structural changes toward social justice to accomplish our mission. Breast Cancer Action 55 New Montgomery Street, #323 San Francisco, CA 94105 Phone: 415 243-9301 Toll free: 877 2-STOP-BC [877 278-6722] Fax: 415 243-3996 E-mail: info bcaction Web site: bcaction Board Members Jo Ann Madigan, President Dorothy Geoghegan, Vice President Denise Wells, Treasurer Bhavna Shamasunder, Secretary Diane Carr, Kim Cox, Gail Kaufman, Ellen Lew, JoAnn Loulan, Renetia Martin, Belle Shayer emerita ; , Sylvia Sokol, Jane Sprague Zones Staff Barbara A. Brenner, Executive Director Angela Carrier, Office Coordinator Rebecca Farmer, Communications Officer Sarah Lightfoot, Development Associate Alex Momtchiloff, Development Director Pauli Ojea, Community Organizer Brenda Salgado, Program Manager Lisa Wanzor, Associate Director BCA Newsletter BCA 2005, ISSN #1088-386X, published bimonthly by BCA. Articles on detection and treatment do not constitute endorsements but are intended solely to inform. Call for permission before reprinting. To subscribe, send name and address to BCA. Requested annual donation is $50, but no one is refused for lack of funds. Editor: Rebecca Farmer Editorial Assistance: Robert Gomez Layout: Yvonne Day, Y. Day Designs Editorial Board: Barbara Brenner, Rebecca Farmer, Lauren John, Jane Sprague Zones.

27. Memisogullari R, Taysi S, Bakan E, Capoglu l. Antioxidant status and lipid peroxidation in type 11 diabetes mellitus. Cell Biochem Funct 2003; 21: 291-6. Yamada H, Yamada K, Waki M, Umegaki K. Lymphocyte and plasma vitamin C levels in type 2 diabetic patients with and without diabetes complications. Diabetes Care 2004; 27: 2491-2. Fouad T. Antioxidant, nature and chemistry. The Doctor s Lounge-net2005 : thedoctors lounge medlounge articles antioxidants antioxidants11 . 30. Desager JP, Hullhoven R, Harvengt C. Uricosuric effect of fenofibrate in healthy volunteers. J Clin Pharmacol 1980; 20: 560-4. Harvengt C, Heller F, Desager JP. Hypolipidemic and hypouricemic action of fenofibrate in various types of hyperlipoproteinemia. Artery 1980; 7: 73-82. Marais AD, Firth JC, Bateman ME. Atrovastatin: an effective lipid modifagent in familial hypercholesterolemia. Arterioscler Thromb Vasc Biol 1997; 17: 1527-31. Giral P, Bruckert E, Jacob N. Homocysteine and lipid lowering agents: a comparison between atrovastatin and fenofibrate in patients with mixed hyperlipidemia. Atherosclerosis 2001; 154: 421-37. Milionis HJ, Kakafika AI, Tsouli SG, Athyros VG, bairaktari ET, Seferiadis KI, et al. Effects of statin on uric acid homeostasis in patients with primary hyperlipidemia. Heart J 2004; 148: 635-40. Alderman M, Alyer KJV. Uric acid: role in cardiovascular disease and effects of losartan. Curr Med Res Opin 2004; 20: 369-79. Ceriello A. New insights on oxidative stress and diabetic complications may lead to a causal antioxidant therapy. Diabetes Care 2003; 26: 1589-96. Greene DA, Stevens MJ, Obrosova I, Feldman EI. Glucose induced oxidative stress and programmed cell death in diabetic neuropathy. Eur J Pharmacol 1999; 375: 217-23. Waring WS, Webb DJ, Maxwell SRJ. Uric acid as a risk factor for cardiocvascular disease. Q J Med 2000; 93: 707-13. Chamorro A, Obach V, Carver A, Revilla M, Deulofeu R. ApontPrognostic significance of uric acid serum concentration in patients with acute stroke. Stroke 2002; 33: 1048. : stroke.ahajournals cgi content full 33 4.

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