Related company under the common ownership and control of a corporate entity. "Label" means a display of written, printed, or graphic matter upon the immediate container of any drug or device. "Pedigree" means a document in a form, written or electronic, approved by the Board that records each distribution of any given drug, from the sale by a pharmaceutical manufacturer through acquisition and sale by any wholesaler or repackager until final sale to a pharmacy for dispensing to a patient or a Practitioner administering the drug and includes the following information: 1 ; The source of the Drug s ; , including the name and principal address of the seller; 2 ; The amount of the Drug, its dosage form and strength, the date of the purchase, the sales invoice number, container size, number of containers, expiration date s ; , and lot number s ; of the Drug; 3 ; The business name and address of each owner of the Drug, its shipping information, including the name and address of each person certifying delivery or receipt of the Drug; 4 ; Information that states the Wholesale Distributor has conducted Due Diligence of the Wholesale Distributor s ; from whom the Wholesale Distributor purchased, or may have purchased the Drug; and 5 ; A certification from the Designated Representative of the Wholesale Distributor that the information contained therein is true and accurate under penalty of perjury.
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An article appearing in the New England Journal of Medicine in August 200110 discusses the possibility of an increased incidence of cardiovascular or cerebrovascular events in patients on COX-2 specific agents. This study reviewed results of many clinical trials and raised concern about thrombotic events. However, on close analysis of all data, it must be noted that the VIGOR trial in particular did not permit patients to take their daily aspirin even if at risk for cardiovascular events ~4% of patients ; . Approximately 0.8% of trial patients versus 0.4% of control population thus sustained a thrombotic event. The CLASS trial revealed no significant difference in cardiovascular events between the group receiving celecoxib group and the control subjects taking diclofenac. One perspective is that diclofenac CLASS trial control drug ; has a weak antiplatelet effect, whereas naproxen VIGOR trial control drug ; has a very potent antiplatelet effect. By virtue of the action of the COX-2 inhibitors, they have minimal if any effect on the platelet as they do not inhibit the production of thromboxane A2. Another consideration is that rofecoxib in a dosage of.
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References 1. McBean AM, Shuling L, Gilbertson DT, Collins AJ: Differences in diabetes prevalence, incidence, and mortality among the elderly of four racial ethnic groups: whites, blacks, hispanics, and Asians. Diabetes Care 27: 23172324, 2004 National Center for Chronic Disease Prevention and Health Promotion, Diabetes.
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Counseling and psychotherapy necessary to sustain patients through the initiation and maintenance phase of treatment are the exception, not the rule, despite established benefits , 4 too many elderly persons and practitioners ; view depression in advanced age as inevitable rather than treatable.
| How does celecoxib workFig. 2. The inhibition of NE-induced PGE2 release by cells coincubated with dexamethasone, indomethacin, or celecoxib. Cells, stimulated by NE 10 were coincubated with 1-antitrypsin 200 g ml ; , dexamethasone 10 M ; , indomethacin 1 M ; , or celecoxib 1 M ; for 1 h. Mean values SE ; are shown for 4 separate determinations. A significant inhibition P 0.05 ; compared with NEstimulated cells is indicated. ajplung and clomid.
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Protease Inhibitors are designed to inhibit the function of the HIV protease enzyme. Protease acts at a different stage of the replication process than reverse transcriptase RT ; . Protease inhibitors act by preventing cleavage of HIV viral polyproteins into active proteins by blocking the enzyme's active site. Cleavage of HIV viral polyproteins into active proteins occurs during the process by which HIV normally replicates. The goal of the protease inhibitor thus is to stop the protease from helping to assemble a new virus by preventing sometimes referred to as gumming up ; protease from cutting long chains of proteins into shorter pieces that HIV needs to assemble a new virus. They interrupt the way HIV uses a healthy cell to make more viruses.
Angiotensin-converting enzyme ACE ; inhibitors for hypertension.43 Therefore, use caution when combining "nephro-effecting" drugs in patients with elevated serum creatinine levels. Bone consequences. In the orthopedic literature, NSAIDs are known to impair fracture healing.44, 45 Because of confounders such as smoking, which also is a known impedance to osteogenesis, orthopedists are uncertain if COX-2i demonstrate a similar pharmacological propensity. However, a periodontal study evaluated COX-2i, as well as constituents vital to intrabony periodontal defect repair such as enamel matrix proteins ; , and found no differences in pocket depths of patients taking COX-2i compared with control subjects.46 Other researchers find that COX-2i prevent the progression of periodontitis in human cultured gingival fibroblast and rodent alveolar bone.47, 48 These results suggest that COX2i may be bone-sparing. Pulmonic consequences. Prostaglandins provide pulmonary vascular tone in both physiological and inflammatory states. An animal study suggests that bronchiolar epithelium and the veins of hilar smooth muscle constitutively express COX-1, and smaller smooth muscle arterioles express COX-2; both isoforms promote pulmonic vasoregulation in states of homeostasis and inflammation.49 In tissues with chronic inflammation, COX-1 inhibition leads to a metabolic shift to the leukotriene pathway.50 Nonselective NSAIDs inhibit both COX-1 and COX-2 in the lungs, thus promoting excessive leukotrienes, leading to profuse airway edema from this sequential chemotaxis and cytokine release. People with a history of asthma or with nasal polyps often report a hypersensitivity to aspirin and other NSAIDs. Most patients with hypersensitivity to NSAIDs or with asthma can tolerate rofecoxib.51, 52 Patients who report having had aspirin-induced asthma now can receive rofecoxib without respiratory embarrassment.53 This analgesic choice is a safe alternative to aspirin desensitization or narcotic use. Allergic manifestations, including severe lifethreatening anaphylaxis, often are adverse drug reactions ADRs ; to sulfonamides. Celecozib is a sulfonamide derivative, and it possesses some small sulfa-allergic potential, according to a couple of reports.54, 55 Although one cohort study shows that celecoxib has 80 percent more ADRs than rofecoxib at a relative risk of 1.8, such reactions are not clinically significant.56 Another and doxycycline.
Celecoxib-PLGA Microparticle Group 181.42 184.43 62.14 0 85.5 4.5 4.7.
ATL Assay. ATL concentrations in the urine were measured by using a commercial ELISA kit Neogen, Lansing, MI ; according to the manufacturer's instructions 11, 12 ; . Urine was collected on days 0, 8, and 15 for 6 h after drug administration, and samples were extracted according to a published method 23 ; . The Ab used in this assay specifically recognizes 15 R ; -epi-LXA4 and has been characterized by others 10 ; . The identity of 15 R ; -epi-LXA4 in samples was also confirmed by using a dual pump RP-HPLC analysis 11, 23 ; . The column Waters Symmetry C18, 3 m, 2.1 150 mm ; was eluted with MeOH H2O acetic acid 65: 35: 0.01; vol vol vol ; at a flow rate of 0.2 ml min. Postrun analysis was performed with the MILLENNIUM 32 chromatography manager Waters ; . LXA4 and 15 R ; -epi-LXA4 were identified by online UV spectral analysis and comparison of their retention times with those of authentic standards LXA4 was obtained from Cascade Biochem, Reading, U.K. ; . The 15 R ; epi-LXA4-methylester kindly provided by C. N. Serhan, Harvard Medical School, Boston ; was converted to free acid by saponification as described 23 ; . Plasma Salicylate and Celdcoxib Levels. For measurement of plasma salicylate and celecoxib levels, blood samples were taken before and 6 h after the last dose of each drug. Blood samples were centrifuged at 4, 200 g for 10 min at 4C. Specimens were subsequently stored at 20C and assayed by HPLC Prostar 330, Varian ; according to a published method 24 ; . The celecoxib concentrations were determined by using a HPLC assay with fluorescence detection for human plasma as described 25 ; . Statistical Analysis. Data were analyzed by using a nonparametric and erythromycin.
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ARCHER, D. L. 1996 ; Food Control, 7, 181. BEUCHAT, L. R. 1995 ; J. Food Sci., 59, 204. FARKAS, J. 1998 ; Studies on Low-Dose Irradiation of Prepackaged Prepared Vegetables. IAEA Progress Rep., Time period covered: 1 April 1997 - 1 February 1998. Res. Contr. No. 9603 R0. FARKAS, J., ANDRSSY, ., MSZROS. L, and BNTI, D. 1995 ; Acta Microbiol. Immunol.Hung., 42, 19. FARKAS, J., SRAY, T., MOHCSI-FARKAS, Cs., HORTI, K. and ANDRSSY, . 1997 ; Adv. Food Sci. CMTL ; , 19 3 4 ; 111. LOAHARANU, P. and MURREL, D. 1994 ; Trends in Food Sci. & Technol., 5 6 ; 190. MONK, J. D., BEUCHAT, L. R. and DOYLE, M.P. 1995 ; J. Food Prot., 58, 197. SCHLECH, W.F., LAVIGNE, P. M., BORTOLUSSI, R.A., ALLEN, A. C., HALDANE, E.V., WORT, A., HIGHTOWER, A. W., JOHNSON, S. E., KING, S. H., NICHOLLS, E.S. and BROOME, C. V. 1983 ; New Engl. J. Med., 308, 203 and exelon.
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Pharmaceutical representatives: The goal of the University Health System is to foster an environment in which drug representatives provide information to medical, pharmacy, and nursing staff that will promote safe and cost-effective use of medications. Appropriate activities of the pharmaceutical industry within the System include: supporting continuing medical education and sponsoring educational activities of trainees and house officers providing medications through sampling and "special access" programs to indigent populations seen in the System disseminating information about products and therapies It is the position of the System and the Pharmacy & Therapeutics Committee that all interactions between the pharmaceutical industry and house staff and trainees should be guided by the principle of support for educational endeavors and assistance with the medical care of patients. It is acknowledged that pharmaceutical representatives should have the opportunity of discussing their products with physicians and pharmacists as long as the information is objective and based on scientific evidence. Staff should not rely on pharmaceutical representatives for formulary and subsidy information. Please refer to the UT UHS Clinical Intranet for updated medication policies. 1. Ceelcoxib Celebrex ; Per P & T, Celebrex is restricted to rheumatoid arthritis and the pathway for the Management of Osteoarthritis. Approval for the MAP Medication Assistance Program ; requires prior authorization 358-3224 ; and the completion of the GI-toxicity assessment tool. Due to a recent change in the Pfizer patient assistance operations, MAP can no longer obtain immediate approval for dispensing of Celebrex from Pharmacy. Pfizer's new program requires that all new patients use Pfizer's Connection to Care, which generally takes four to six weeks to arrive. In the interim, CareLink will NOT subsidize Celebrex. Among patients with a history of ulcer bleeding, treatment with celecoxib was as effective as treatment with diclofenac plus omeprazole, with respect to the prevention of recurrent bleeding. Renal adverse events are common in susceptible patients receiving celecoxib or diclofenac plus omeprazole. Neither regimen can completely eliminate the risk of recurrent ulcer complications in patients with high risk. N Engl J Med 2002; 347: 2104-10. ; Formulary non-steroidal anti-inflammatory agents NSAIDs ; available for substitution include ibuprofen, indomethacin, naproxen, piroxicam, and salsalate. Gastric acid secretion inhibitors that may be used in combination with traditional NSAIDs are esomeprazole preferred ; , pantoprazole, and lansoprazole. 2. Fluticasone Salmeterol AdvairTM Diskus ; Per P & T, initiation of therapy with high-dose inhaled steroids which includes AdvairTM 250 mg for a child or AdvairTM 500 mg for an adult ; is restricted to Pulmonary Services. Due to the expense of AdvairTM, CareLink requires that all patients be referred to the MAP office to enroll or determine eligibility. CareLink will subsidize only if MAP enrollment is verified or unless the patient does not qualify for MAP and fluoxetine.
Objective: to compare the effect of celecoxbi vs placebo treatment on clinical and gait variables in knee osteoarthritis oa ; patients; focusing on the efficiency of the locomotor mechanism.
Christoph Waldner1 , Bernd Grabensee1 , Karsten Schrr2 , Peter Heering1 . 1 Nephrology, Heinrich Heine University, Dsseldorf, Germany; 2 Pharmacology, Heinrich Heine University, Germany Background: Renal cyclooxygenase COX ; activity is responsible for the production of the prostaglandins PG ; E2 , I2 and thromboxane TxA2 ; . These mediators interact with distinct G protein-coupled receptors which regulate renal hemodynamics. In the present study we investigated the expression of the three PGE2 receptors EP2 , EP3 and EP4 and the receptors for PGI2 and TxA2 in rats with passive Heymann Nephritis PHN ; and their regulation by selective COX-2 inhibition with celecoxib. Methods: Four groups of Wistar rats were used n 8, each ; : group 1: healthy animals, group 2: healthy animals treated with celedoxib 5 mg kg day ; , group 3: rats with PHN, group 4: rats with PHN receiving celecoxib. Kidneys were removed 28 days after induction of PHN. The expression of cortical mRNA for the EP2 , EP3 , EP4 , IP and the TP receptor was determined by means of semiquantitative reverse transcriptase polymerase chain reaction. Cultured mesangial cells MC ; were incubated with PGE2 and their EP3 receptor mRNA expression was measured at several time points. Results: Rats with PHN group 3 ; showed an 1.8 fold increase in renal cortical EP3 receptor mRNA expression as compared to healthy control animals group 1, p 0.05 ; . In cdlecoxib treated PHN rats group 4 ; the mRNA expression of the EP3 and the EP4 receptor was significantly reduced as compared to rats without treatment group 3 ; . In healthy animals, this mRNA expression was unaffected by the application of celecoxib group 2 vs. group 1 ; . No changes were observed in the expression of the other PG-receptors. In cultured MC, exogenous PGE2 enhanced EP3 mRNA expression nearly 4-fold after 6 h incubation time. Conclusions: These data suggest a predominant role of the EP3 receptor in the transduction of PGE2 -actions in PHN. Furthermore the downregulation of the EP3 receptor appears to be mediated by inhibition of PGE2 synthesis. This suggests that PGE2 might potentiate its effects in the kidney by upregulating its own receptors and metformin and celecoxib.
And can result in inflammatory changes in the synovium similar to those of RA. These manifest as joint stiffness, loss of physical mobility, and occasionally as joint swelling or redness.3 Synovial inflammation may be present in early stages of OA, but it is more often seen in advanced stages. OA joint pain, however, does not correlate with histologic evidence of joint inflammation.4 Most patients with arthritis are treated by primary care physicians. Therapy for OA is largely palliative, aimed at increasing physical function by relieving joint pain and reducing inflammation.5 Control of systemic inflammation and prevention or slowing of disease progression are additional treatment goals in patients with RA. While no pharmacologic agents have been shown to prevent or delay the progression of structural damage in OA, disease-modifying antirheumatic drugs DMARDs ; appear to have the capacity to alter the clinical course of RA.6, 7 Because of their analgesic and anti-inflammatory effects, nonsteroidal anti-inflammatory drugs NSAIDs ; are the class of medication most commonly used to treat joint pain and stiffness in patients with OA and RA.4, 810 Nonselective NSAIDs inhibit the isozymes of cyclooxygenase COX ; , COX-1 and COX-2. See articles by Bingham and Cronstein in this supplement. ; Preclinical studies strongly suggest that inhibition of COX-2 is primarily responsible for many of the therapeutic benefits of NSAIDs, while inhibition of COX-1 can lead to toxic effects.8, 11, 12 For this reason, the American College of Rheumatology ACR ; recently recommended replacing nonselective NSAID therapy with therapy with a coxib agent, a COX-2selective inhibitor, when treating a patient with OA at increased risk of developing an NSAIDrelated toxicity.5 Patients with OA or RA increased risk of developing NSAID-related gastrointestinal GI ; toxicities include those who are older 65 years of age and above ; , have a history of a prior symptomatic or complicated ulcer, require chronic high-dose NSAID therapy, or take concomitant corticosteroid or anticoagulant therapy.4, 5, 1315 The introduction of coxibs represents one of the most rapid development programs of a pharmacologic agent in rheumatology. The first two coxibs, celecoxib and rofecoxib, were approved for use in the United States only a few years after COX-2, the inducible form of COX, was first identified16 and its pathogenic role in pain and inflammation proVOLUME 69 SUPPLEMENT I.
In an attempt to standardize clinical nursing practice, the North American Nursing Diagnosis Association NANDA ; has published a list of nursing diagnoses that have been approved through the 2002 NANDA NIC NOC International Conference. Standardization of nursing actions and common terminology is important in the provision of consistent care over time, among nurses, across shifts, and even between different health-care agencies. This text incorporates the nomenclature of Taxonomy II that has been adopted by NANDA. There are those individuals who believe that NANDA's list is incomplete. My intent is not to judge the completeness of this list but to suggest the need for clinical testing of what is available. NANDA encourages nurses to submit new diagnoses for consideration, after the nurses have conducted testing and research of the diagnoses in the clinical setting. There are three essential components in a nursing diagnosis, which comprise the PES format Gordon, 1987 ; . The "P" identifies the health problem; the "E" represents the etiology or cause ; of the problem; and the "S" describes a cluster of signs and symptoms, or what has come to be known as "defining characteristics." These three parts are combined into one statement by the use of "connecting words." The diagnosis is then written as: Problem "related to" etiology "evidenced by" signs and symptoms defining characteristics ; . The problem can be identified as the human response to actual or potential health problems as assessed by the nurse. The etiology may be represented by past experiences of the individual, genetic influences, current environmental factors, or pathophysiological changes. The defining characteristics describe what the client says and what the nurse observes that indicate the existence of a particular problem. Nursing diagnoses, then, become the basis for the care plan. This book may be used as a guide in the construction of care plans for various psychiatric clients. The concepts are presented in such a manner that they may be applied to various types of health-care settings: inpatient hospitalization, outpatient clinic, home health, partial hospitalization, and private practice, to name a few. Major divisions in the book are identified by psychiatric diagnostic categories, according to the order in which they appear in the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision DSM-IV-TR and ilosone.
The present study shows that celecoxib, but not rofecoxib or NS-398, decreases endothelial TF expression and activity. Expression of encrypted TF may account for the observation that inhibition of TF activity is less pronounced than the decrease in protein expression.13 TNF- is a potent inducer of TF expression6, 14; indeed, both TNF- and TF are expressed in atherosclerotic plaques.1, 7, 15 Therefore, we used this cytokine to mimic the inflammatory environment of the vessel wall for assessment of the effect of coxibs on TF expression. The MAP kinases JNK, p38, and ERK are involved in regulating TF expression in vascular cells in response to several stimuli.5, 6, 14 Consistent with this observation, all 3 MAP kinases were transiently activated in human aortic endothelial cells after stimulation with TNF- . TNF- induced JNK activation was reduced by celecoxib but not by rofecoxib or NS-398. This observation is consistent with recent findings that celecoxib inhibits JNK activation in cancer cells.16 Inhibition of JNK by its specific inhibitor SP600125 impaired TF expression in response to TNF- , which confirms the regulatory role of this MAP kinase in TNF- induced TF expression. We therefore conclude that the inhibitory effect of celecoxib on JNK phosphorylation mediates the reduction in TF expression. Whether JNK represents the direct intracellular target of celecoxib or whether it reduces TF expression through another mediator is unknown. Because rofecoxib and the experimental coxib NS-398 did not show any effect on TF expression or JNK activation, the effect of celecoxib on TF expression and.
Please refer to the comparison chart on pages 10 -11 for a description of prescription drug benefits provided by the hmo, pos or ppo options.
Side-effects of Celecpxib on offspring The growth of all mouse pups born from mice administered Celecosib 50, 10 and 1mg kg ; is shown in Figure 1. With any dose of Celecoxib, the growth rate of mouse pups following treatment of Celecoxib was the same as that of non-treated mouse pups. The male female ratio of offspring born from mice administered Celecoxib 50, 10, and 1 mg kg ; , and the pregnancy rate of female offspring with male offspring are shown in Table II. With any dose of Celecoxib, the male female rate of offspring and pregnancy rates were the same as the controls, and the successful pregnancy rates were 100%. The weights of a kidney from mice whose mothers were administered with Celecoxib 50 mg kg n 10 ; were 207.0 11.6 mg, and they were not different from those of offspring after no administration of Celecoxib 206.0 12.6 mg, n 597.
TNF-, IL-1 and IL-6 in the serum of Celecoxib-treated mice The concentrations of TNF-, IL-1, and IL-6 in maternal serum taken from mice 1, 4, and 10 h after the second administration of LPS are shown in Figure 3. The TNF-, IL-1, and IL-6 concentrations in maternal serum did not change significantly after administration of Celecoxib 10mg kg ; . Constriction of the ductus arteriosus in Celecoxib and Indomethacin-treated rats In this study with rats, maternal or fetal death was not recorded. The results of ductus arteriosus constriction in Celecoxibtreated near-term on the 21st day of pregnancy ; rats in this study are shown in Figure 4B and C. Sagittal cross-sections of the fetal heart showed markedly increased constriction of the fetal ductus arteriosus after administration of either Celecoxib or Indomethacin compared with the fetus without medication Figure 4D ; . The fetal ductus arteriosus was con.
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7. Ray WA, Stein CM, Daugherty JR, Hall K, Arbogast PG, Griffin MR. COX-2 selective non-steroidal anti-inflammatory drugs and risk of serious coronary heart disease. Lancet 2002; 360: 10713. Konstam MA, Weir MR, Reicin A, Shapiro D, Sperling RS, Barr E et al. Cardiovascular thrombotic events in controlled clinical trials of rofecoxib. Circulation 2001; 104: 22808. Chenevard R, Hurlimann D, Bechir M, Enselet F, Spieker L, Hermann M. Selective COX2 inhibition improves endothelial function in coronary artery disease. Circulation 2003; 107: 4059. Singh G, Fort JG, Triadafilopoulos G, Bello A, Stanford SB, Peapack, NJ. Benefits of using celecoxib in patients on lowdose aspirin ASA ; : data from SUCCESS 1, a 12-week, multinational trial with 13, 274 patients with osteoarthritis. ACR ARHP 65th Annual Scientific Meeting, San Francisco. 10-15 November 2001. Abstract 1032. 11. Deeks JJ, Smith LA, Bradley MD. Efficacy, tolerability and upper gastrointestinal safety of celecoxib for treatment of osteoarthritis and rheumatoid arthritis: systematic review of randomized controlled trials. BMJ 2002; 325: 61923. Metcalfe, S. Celecoxib's relative gastrointestinal safety is overstated. BMJ 2003; 326: 334. MeReC Briefing. NSAIDs and gastroprotection, COX-II selective inhibitors. 2002. Available at: npc accessed 15 January 2004 ; . 14. Lothian Prescribing Bulletin. New COX2 guidelines. Issue No. 5. October November 2003. 15. Gottlieb S. Cardioprotective effects of aspirin compromised by other NSAIDs. BMJ 2003; 327: 520. Ibuprofen, aspirin, other NSAIDs and cardioprotection. North West Medicines Information Centre Bulletin. March 2003. 17. NHS North Derbyshire, Chesterfield PCT. Effect of ibuprofen on the cardioprotection provided by aspirin. Prescribing & Clinical Effectiveness Newsletter. Volume 2: Issue 3, June 2003. 18. Curtis JP, Wang Y, Portnay EL, Masoudi FA, Havranek EP, Krumholz HM. Aspirin, ibuprofen and mortality after myocardial infarction: retrospective cohort study. BMJ 2003; 327: 13223. Wolfe F, Anderson J, Burke TA, Arguelles LM, Pettitt D. Gastroprotective therapy and risk of gastrointestinal ulcers: risk reduction by COX-2 therapy. Journal of Rheumatology 2002; 29: 46773. Hawkey CJ, Langman MJS. Non-steroidal anti-inflammatory drugs: overall risks and management. Complementary roles for COX2 inhibitors and proton pump inhibitors. Gut 2003; 52: 6008. February 2004 The Pharmaceutical Journal Vol 272 ; 221.
Plauschinat CA * , Doyle JJ, Thaker DJ. Novartis Pharmaceuticals Corporation, One Hanover Plaza, East Hanover, NJ 07936 INTRODUCTION: Blood pressure BP ; control is crucial in reducing.
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