Background: Tandem walking testing is used clinically to assess balance in the office setting but is difficult to quantify. Swaystar is a belt mounted device which we use to quantify sway amplitude and velocity during walking and, using this device, we have shown that there is increased sway during tandem walking brought on by the ingestion of small doses of alcohol. During this study, we observed that at least one of our subjects showed decreased sway under the influence of alcohol, and they did so by electing to perform the required task at an increased rate of speed. This apparently paradoxical observation is consistent with some of our patients who sometimes report anecdotally that they are more secure when walking faster or when skiing down the steeper slopes at the local mountain. It has also been reported by Geurts that stability increases with increased speed, and an astute chance observation by Brandt, whose dog serendipitously suffered an acute vestibulopathy, showed him that his dog was not able to walk in a straight line, but was able to run straight. Objectives: Based on our initial experiment and the anecdotal observations of ourselves and others, we postulated that healthy young subjects would be able to decrease sway by increasing the rate of walking speed, thus developing a different strategy. Furthermore, we hypothesized that we could disrupt the performance of these subjects and increase their sway by interfering with their normal cadence while performing tandem walking. This could be accomplished by having subjects walk at an unnaturally slow speed, or in time with an assessor-set metronome another unnatural cadence ; . Methods: Twenty young healthy subjects were asked to perform tandem walking while wearing Swaystar, which measures sway amplitude and sway velocity in the pitch and roll planes. Tasks included tandem walking with five different protocols, with order of performance randomized from subject to subject. Results: In a group of healthy subjects, performance during tandem walking measured by sway amplitude in the pitch and roll planes ; deteriorated as the task speed slowed, and also deteriorated as preferred cadence was disrupted. In addition, there is a gradation of difficulty across the speeds. Conclusion: The increasingly poor performance we saw evidenced by an increase in sway in the pitch and roll planes ; is related to decrease in speed at which the subject is required to perform tandem walking. We postulate that any significant variation of the slope of this relationship from the normal is indicative of pathology. Most people have a reasonably effective strategy for balance maintenance. The concept of compensating for a vestibular lesion entails an attempt to re-create the normal patterns of walking, and a patient with active or uncompensated disease will see a precipitous decline far beyond normal, in their ability to perform tandem walking under conditions where the normal cadence is disrupted, or where they are forced to perform the task at an unnaturally slow speed. O171 Genetic Causes of Episodic Vertigo and Imbalance.
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The focus of the NICE conference was on the implementation of guidance. NICE is changing the way it presents its guidance, particularly to general practitioners and patients, so as to make it clearer and easier to implement. One topic of discussion was how far primary care trusts and other organisations should be measured on the extent to which they have implemented NICE guidelines. From April next year, the Commission for Health Care Audit and Inspection CHAI ; will take over responsibility for inspecting NHS bodies from the Commission for Health Improvement. The chairmandesignate of CHAI, Professor Sir Ian Kennedy, sounded equivocal on whether compliance with guidance should be measured by CHAI or by NICE itself. However.
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329. PYRIDINE ACETIC ACIDS: POTENT, ORALLY ACTIVE AND HIGHLY SELECTIVE ALDOSE REDUCTASE INHIBITORS ARIS ; . Leo S. Geraci 1, David E. Gunn 2, Al Sabetta 1, Diane Sawicki 1, Susan Cannan 1, Anne Carrington 1, Janet Sredy 3, Thomas DiCioccio 1, Michael C. Van Zandt 1, Alberto Podjarny 4, and Ossama El-Kabbani 5. 1 ; Chemistry, The Institute For Diabetes Discovery, 23 Business Park Drive, Branford, CT 06405, Fax: 203-315-4002, leo.geraci ipd-discovery , 2 ; Bayer Corporation, 3 ; ADSERVIO, 4 ; IGBMC, UPR de Biologie Structurale, 5 ; Montash University, Victorian College of Pharmacy Hyperglycemia is a major contributor to diabetic complications such as neuropathy, retinopathy, nephropathy and cardiovascular disease. Aldose reductase ALR2 ; , present in the tissues where complications arise, is the first enzyme in the polyol pathway and reduces some of the excess glucose to sorbitol using NADPH as a cofactor. The accumulation of intracellular sorbitol and the osmotic stress induced is implicated in the progression of diabetic complications. Other factors contributing to complications related to glucose flux through the polyol pathway include reductive stress high ratio of NADH NAD + ; , non-enzymatic glycation and the impairment of anti-oxidant defense. Therefore, an aldose reductase inhibitor developed as a treatment should slow the progress of diabetic complications. Selectivity of ARIs relative to aldehyde reductase ARL1 ; , a detoxifying enzyme with 65% sequence homology to aldose reductase, is also important. A novel series of substituted pyridine acetic acids was discovered and developed as part of our aldose reductase inhibitor program. Numerous compounds exhibited low inhibitory and verapamil.
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|RANK DRUG NAME ROUTE 1. 2. 3. NEXIUM PEG-INTRON REBETOL GLEEVEC PROTOPIC GEODON LANTUS STARLIX LUMIGAN COLAZAL REMINYL ULTRACET VALCYTE FORADIL TRAVATAN CETROTIDE VISICOL AXERT NOVOLOG OVIDREL PO SQ PO Although the number of new drug approvals has slowed in recent years, the impact of a specific few blockbuster drugs still resonates in 2001 PMPY costs. As shown in Figure 3 and Table 8, the effect of drugs introduced in 1992 and in 1993 ebbed after 1997, whereas products entering the market in 1994 and thereafter continue to represent an ever-increasing proportion of total drug spend. This pattern seems to reflect a five- to seven-year product life cycle during which products come to market, continually gain market share and then lose momentum. Only two significant products, Effexor and Serevent entered the market in 1994. While they gained in their collective , contribution over time, they accounted for only 3.9 percent of 2001 costs. In contrast, led by Prevacid Glucophage Prempro and Ultram drugs introduced in 1995 accounted for the , highest percentage of 2001 cost at 9.1 percent. However, since Glucophage went generic in early 2002, a precipitous decline probably will be seen in the contribution of 1995 new drugs to 2002 PMPY costs.|
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Ing us to question the likelihood of causation in these cases. My assessment is that the Bayesian approach is a real contribution to the evaluation of adverse drug reactions, and Paradiso-Hardy and colleagues should be congratulated for its use in their article.1 The reason that we do not use this method routinely in clinical practice is probably because it takes too much time and effort to be specific, clear and coherent. Reading a detailed analysis of a single case will make this point clear. For instance, in a case of acute renal failure possibly caused by gentamycin that I analyzed6 I had to think about the expected timing of acute renal failure if caused by gentamycin. I also had to express these expectations in quantified terms 1% on day 7, 3% on day 8, etc ; . But this was only one of many features I needed to identify and quantify: the other potential causes, their expected timing, the relevance of the urianalysis findings, the expected duration of the renal failure, the importance of pathologic data and so on. I needed to clarify and quantify all of these features before I could put the whole case together to arrive at a posterior probability for causation. This process took weeks rather the few minutes it might take an expert to arrive at a global assessment in this kind of case. The development of spreadsheet programs7, 8 and computerized expert systems9 will help, but we still have some way to go to make this approach generally applicable. But, in my opinion, the sooner the better.
15. Chang D. Influence of malignancy on the pharmacokinetics of vancomycin in infants and children. Pediatric Infect Dis J, 1995; 14 8 ; 667-73. 16. Lopez-Samblas, AM, Torres CL, Wang H., et al: Effectiveness of a gentamicin dosing protocol based on postconceptual age. Ann. Pharmacother. 1992; 26: 534-38. Ho KK, Bryson SM, Thiessen JJ, Greenberg ML, Einarson TR, Leson CL. The effects of age and chemotherapy on gentamicin pharmacokinetic and dosing in pediatric patients. Pharmacotherapy. 1995; 15 6 ; : 754-64. 18. Ramsey BW, Donkin HL, Eisenber JD., et al. Efficacy of aerosolized tobramycin in patients with cystic fibrosis. N Engl J Med. 1993; 328 : 1740-1746. 19. Hayani KC, Hatzopoulos FK; Frank AL, Thummala MR, Hantsch MJ; Schatz BM, John EG, Vidyasaqar D. Pharmacokinetics of once daily dosing of gentamicin in neonates. J Pediatr. 1997; 131: 76-80. Elhanan K, Siplovich L, Raz R. Gentamicin once-daily versus twice-daily in children. J Antimicrob Chemother. 1995; 35: 327-332. Levison ME. Pharmacodynamics of antimicrobial agents. Bactericidal and postantibiotic effects. Infect Dis Clin North Am. 1995; 9: 483-95. Craig WA. Pharmacokinetic pharmacodynamic parameters: Rationale for antibacterial dosing of mice and men. Clin Infect Dis. 1998; 26: 1-12. Craig WA, Andes D. Pharmacokinetic and pharmacodynamics of antibiotics in otitis media. Pediatr Infect Dis J. 1996; 15: 944-8.
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Leg ulcer assessment should include a general patient assessment, including any relevant psychosocial aspects an assessment of the limbs an assessment of the wound wounds. Assessment and clinical investigations should be undertaken by a health professional trained in leg ulcer management. RCN, 1998 ; . All staff who regularly undertake the assessment and management of leg ulcers are expected to attend the 4 day leg ulcer management course, provided by the Trust. Assessment enables the identification of possible causes of the ulceration, any factors affecting or delaying healing and appropriate management strategies. General assessment A full medical history should be recorded - past history plus current problems. RCN, 1998 ; . Medication Weight Nutrition Wipke-Tevis & Stotts, 1998 ; Mobility Sleep pattern Ability to self care Brody, 1990 Social history Lifestyle Cullum & Roe, 1995; Dealey, 1999; Herbert, 1997; Morison et.al., 1994; Morison et.al., 1997 ; Indicators of venous or arterial disease Some of the clinical signs and symptoms which may be indicative of venous or arterial disease are listed in Table1 Venous Previous leg ulcers attack Deep vein thrombosis actual suspected Phlebitis Family history of venous disease Leg fracture Injury to leg Varicose veins Chest pain Pulmonary Embolism Haemoptysis Swollen leg following pregnancy Arterial Cerebrovascular accident Transient ischaemic Peripheral Vascular Disease Angina Family history of cardiovascular disease Heavy smoker Diabetes Hypertension Intermittent claudication Rheumatoid Arthritis vasculitis Ischaemic rest pain Previous arterial surgery RCN, 1998 ; Table 1.
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Perspective: partial health service hospital ; . 438 patients included, complete data for 389. Costs based on four costing methods reported. Method 2 reported here: includes bottom-up resource use and staff costs; units of resource use reported; exclusions not reported. Expressed in US$ year not specified ; . Perspective: partial health service hospital ; . Sample of patients included not clear ; . Based on hospital costs and charges: includes procedure costs bottom-up staff, overheads, depreciation, interest and maintenance costs allocated by `input-output coefficients'; excludes costs before 1st intervention, rehabilitation costs, unspecified `medical treatments'. Expressed in 1987 Dutch guilders Fl ; 1 DFl 0.49 US$ ; . Perspective: partial health service hospital ; , sample of patients included. Based on hospital charges; includes hospital and clinician fees; excludes outpatient fees. Year 1980 81; source of costs not reported US.
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The data are summarized in Table 1. Stock vials and all syringes assayed contained greater concentrations of atropine sulfate than stated on the label, but all were within 5% of the nominally stated concentration, consistent with USP standards. A 1%2% decrease in atropine sulfate concentration was noted after 24 h of storage. The decreased concentration of atropine sulfate noted at 24 h differed significantly from the standard Time 0 ; atropine sulfate concentrations P 0.05 ; . No further decrease in atropine sulfate concentration was detected beyond 24 h.