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Review: A study looked at why GP numbers in Canada were declining. The causes in order of importance were: a longer postgraduate training period being required, restriction on foreign trained doctors, rising rates of retirement, reduced medical school enrolments, emigration to the US and the greater ratio of female graduates. Comment: The longer period of GP training had the effect of greatly reducing the likelihood that new medical graduates would ever have a taste of general practice. The need to ask the same questions in NZ is even more pressing that it is in Canada.
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The supervising physician has experience and or expertise in the same area of medicine as the certified Nurse Practitioner. State law ; There are written clinical protocols that were developed by the supervising physician and nurse practitioner, they are dated and signed, are reviewed and updated at least biennially and are available at the site. State law ; The physician supervisor or covering physician is available 24 hours per day, 7 days per week. By phone is okay ; . State law ; The Nurse Practitioner has a supervising Primary Care Physician who provides or arranges for inpatient care of the Nurse Practitioner's patients.
To the Editor: Dr. Leventhal's review of fibromyalgia treatment 1 ; fails to indicate that long-term studies have not shown useful benefit from fibromyalgia treatment. Somewhat surprisingly, he omits from his review our multicenter, 7-year study on fibromyalgia outcomes among 538 patients who were seen in the clinics of fibromyalgia experts and who were exposed to many of the treatments labeled as effective in Leventhal's review 2 ; . It appears useful to repeat our study conclusions: "Patients with established fibromyalgia, seen in rheumatology centers in which there was a special interest in the disease, and who were not followed up for as long as 7 years, had markedly abnormal scores for pain, functional disability, fatigue, sleep disturbance, and psychological status, and these values did not change substantially over time." In knowing what works, it is important to understand what is meant by "working." Dr. Leventhal does not define terms that he uses, such as "benefit, " "improvement, " "effective, " and "effectiveness." Except for an occasional perfunctory use of the word "clinically, " he does not distinguish between statistical and clinical significance. Having worked in fibromyalgia research for many years 2, 3 ; , I suggest that an effective treatment must produce a sustained improvement of at least 20%. It is fundamentally wrong to extrapolate short-term data to long-term outcomes. In his discussion of causes and mechanisms of fibromyalgia, Dr. Leventhal ignores a huge body of literature linking psychological abnormality and psychosocial distress to the production and maintenance of fibromyalgia symptoms. To do this is to terribly distort the reality of fibromyalgia. If treatments do not work in a sustained and useful way, they should not be used 4 ; . Physicians, with their treatments and beliefs, can be responsible for creating and sustaining illness, as in the case of the growing fibromyalgia epidemic 5 ; . Frederick Wolfe, MD Arthritis Research Center Foundation Wichita, KS 67214 and
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Literature studies confirm that on average, smokers weigh 3 to 4 less than non-smokers and ex-smokers. The difference increases with age, and the effect of smoking on weight appears to be more obvious among women than among men. However, in the course of time the difference in body weight between smokers and nonsmokers may reverse. For example, smokers in Finland now weigh more than non-smokers. The explanation is that many people have given up smoking, and those who have not are also the ones who are less physically active and eat less healthy food. The studies that were consulted primarily focused on the difference in kilos rather than differences in the Body Mass Index BMI ; , even though the latter may in fact be more revealing. Nor did the researchers specifically look for studies about the distribution of bodily fat. There are clear signs, however, that an unhealthy distribution of fat in the body is more common among smokers than among non-smokers.
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Table 4. Determination of triprolidine-HCl from pharmaceutical preparations and premphase.
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The AmpliChip CYP450 Test is powered by Affymetrix technology. It provides comprehensive coverage of gene variations including deletions and duplications for the 2D6 and 2C19 genes, which play a role in the metabolism of about 25% of all prescription drugs. It is intended to be an aid for physicians in individualizing treatment doses for patients on therapeutics metabolised through these genes and provera.
67. Fiedler, B., Lohmann, S. M., Smolenski, A., Linnemuller, S., Pieske, B., Schroder, F., Molkentin, J. D., Drexler, H., and Wollert, K. C. 2002 ; Proc Natl Acad Sci U S A 99, 11363-11368 68. Zahabi, A., Picard, S., Fortin, N., Reudelhuber, T. L., and Deschepper, C. F. 2003 ; J Biol Chem 278, 47694-47699 69. Hassan, M. A., and Ketat, A. F. 2005 ; BMC Pharmacol 5, 10 70. Takimoto, E., Champion, H. C., Li, M., Belardi, D., Ren, S., Rodriguez, E. R., Bedja, D., Gabrielson, K. L., Wang, Y., and Kass, D. A. 2005 ; Nat Med 11, 214-222.
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Intraabdominal and subcutaneous fat magnetic resonance imaging ; A series of T1-weighted trans-axial scans for the measurement of intraabdominal and subcutaneous fat were acquired from a region extending from 8 cm above to 8 cm below the 4th and 5th lumbar interspace 16 slices; field of view: 375 500 mm2; slice thickness: 10 mm; breath-hold repetition time: 138.9 ms; echo time: 4.1 ms ; . Intraabdominal and subcutaneous fat areas were measured by using an image analysis program ALICE, version 3.0; Parexel, Waltham, MA ; . A histogram of pixel intensity in the intraabdominal region was displayed, and the intensity corresponding to the nadir between the lean and fat peaks was used as a cutoff. Intraabdominal adipose tissue was defined as the area of pixels in the intraabdominal region above this cutoff. For calculation of subcutaneous adipose tissue area, a region of interest was first manually drawn at the demarcation of subcutaneous adipose tissue and intraabdominal adipose tissue as previously described 29 ; . The reproducibility of repeated measurements of subcutaneous and intraabdominal fat volumes as determined on 2 separate occasions in our laboratory is 3% and 5% 30 ; . Ambulatory blood pressure monitoring Noninvasive 24-h blood pressure monitoring was performed on a normal weekday by using an automatic ambulatory blood pressure monitoring device Diasys Integra; Novacor SA, Rueil-Malmaison, France ; . The monitor was set to record blood pressure and heart rate every 15 min during the day and every 30 min during the night. Day and night were defined from awake and sleeping periods in each patient's diary. Other measurements Percentage body fat was determined by using bioelectrical impedance analysis BioElectrical Impedance Analyzer System model #BIA-101A; RJL Systems, Detroit ; 31 ; . To calculate the waist-to-hip ratio, waist circumference was measured midway between the spina iliaca superior and the lower rib margin, and hip circumference was measured at the level of the greater trochanters 32 ; . Serum free fatty acids and fatty acid composition of serum phospholipids Serum free fatty acids were measured by using a fluorometric method 33 ; . The fatty acid methyl ester composition of serum phospholipids was determined with gas chromatography after a thin-layer chromatography separation of phospholipids from serum fat extract 34 ; and interesterification to methyl esters 35 ; . The HP 6980 gas chromatograph Hewlett-Packard, Avondale, PA ; was equipped with a 25-m silica column NB 351; HNU-Nordion Ltd, Helsinki ; and a split injection system. Hydrogen was used as carrier gas. The interassay precision varied from 2% to 10%, depending on the peak size. Other analytic procedures Plasma glucose concentrations were measured in duplicate with the glucose oxidase method by using a Beckman Glucose Analyzer II Beckman Instruments, Fullerton, CA; 36 ; . Serum free insulin concentrations were measured by radioimmunoassay Phadeseph Insulin RIA; Pharmacia & Upjohn Diagnostics, Uppsala, Sweden ; after precipitation with polyethylene glycol.
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Must be adjusted for reductions in energy expenditure EE ; due to reduced body weight as the diet progresses 1719 ; . The lowering of resting EE REE ; , and thus total EE TEE ; , is chiefly due to diet-related loss of cell mass in metabolically active tissues 20 ; . In addition, the energy cost of physical activity is directly proportional to body mass, and the total energy expended in walking, running, climbing stairs, and other weight-related activities therefore declines with weight loss 21 ; . The specific metabolic rate of cells ie, EE unit of mass ; may also vary with energy supply, and thus metabolic adaptations may further reduce the rate and amount of weight loss beyond that accounted for solely by changes in body mass. Two mechanisms are possible contributors to a reduction in the specific metabolic rate. One is an increased efficiency net chemical or physical work done per kcal expended ; and the other is a reduction in the level of work total chemical or physical work performed ; . Thus, the magnitude of "predicted" weight loss with a specified energy deficit cannot be calculated as in the simple clinical model; indeed, reliable weight-loss predictions are much more complex 1719 ; . Accordingly, we present an approach for estimating both the adherence to a prescribed reduction in baseline EI and the related weight loss in accordance with LCD treatment. Given a fixed reduction in caloric intake at baseline, the magnitude of negative energy balance will decline nonlinearly over time, and the compliant subject will eventually reach equilibrium at a new, lower body weight 1719 ; . More detailed examinations of weight-loss kinetics are reported by Kozusko 17 ; , Antonetti 18 ; , and Alpert 19 ; . A critical assumption in the modeling of EE is that subjects with reduced obesity RO ; are in energy equilibrium and thus are no longer losing weight. Even small changes in energy balance can have large relative effects on EE. Two factors must be considered in presenting our model of energy balanceweight loss. First, we assume that fractional energy absorption [ FEA ; ie, % of gross EI available after adjustment for fecal energy losses] is the same in the new steady state as it was at baseline before weight loss. An adaptive increase in FEA, or energy digestibility 22 ; , would be one factor contributing to the less-than-predicted weight loss with LCDs. Second, we assume that EE in the weight-reduced state is comparable to that in never-obese subjects of equivalent sex, age, body weight, and activity level. If major adaptations in EE occur with long-term weight loss, the actual magnitude of induced negative energy balance will be less than "expected" on the basis of the prescribed energy deficit. Expected values are usually derived from healthy, weight-stable, never-obese control subjects. Alternatively, the metabolic adaptation hypothesis predicts that RO subjects maintain the same body mass as do comparable never-obese subjects who have a substantially lower EI 23 ; . According to this theory, the RO subjects would maintain a higher body mass than never-obese subjects who have the same EI 2326 ; . An adaptive lowering of TEE greater than that expected for the body mass change would be another explanation for the relatively small weight loss observed with LCDs. Calculations predicting the weight loss expected for a given reduction in EI assume that subjects are fully compliant with the prescribed energy deficit. Lack of adherence--ie, not maintaining the prescribed EI--is another explanation for the small maximal weight loss observed with LCDs. The interplay of these 3, because p3riactin drug!
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Soumerai, Stephen B. "Benefits And Risks Of Increasing Restrictions On Access To Costly Drugs In Medicaid." Health Affairs, 23, no. 1 2004 ; : 135-146. Steiger, William, U.S. Department of Health and Human Services. Correspondence to the Honorable J.W. Lee, M.D., Director-General, World Health Organization. 30 Oct. 2003. Stiglitz, Joseph. "Give Prizes not Patents." New Scientist 23 December 2006. Stiglitz, Joseph. "Scrooge and Intellectual Property Rights: A Medical Prize Fund Could Improve the Financing of Drug Innovations." British Medical Journal vol. 333: 1279-80. Trouiller, P., P. Olliaro, E. Torreele, J. Orbinski, R. Laing, R. Ford. "Drug Development for Neglected Diseases: a Deficient Market and a Public-Health Policy Failure." The Lancet vol. 359, iss. 9324: 2188-2194. TVnz, "Deal reached over cancer drug, " 19 Dec. 2005. Tvnz.co.nz. Accessed 19 Dec. 2005. Veeken, Hans, Bernard Pcoul. "Drugs for 'Neglected Diseases': a Bitter Pill." Tropical Medicine & International Health vol. 5 ; : 309311. Marlynn Wei. Should Prizes Replace Patents? A Critique of the Medical Innovation Prize Act of 2005. Boston University Journal of Science and Technology Law working paper ; . 2007. Weisbrod, Burton A. "Solving the Drug Dilemma." The Washington Post 22 Aug. 2003. Wittes, Robert E. "Cancer Weapons, Out of Reach." Washington Post 15 Jun. 2004. Woolley, Scott. "Prizes Not Patents." Forbes Magazine May 2006. Wright, Brian. "The Economics of Investment Incentives: Patents, Prizes, and Research Contracts." The American Economic Review vol. 73: 691-707. Yamey, G., and E. Torreele. "The World's Most Neglected Diseases: Ignored by the Pharmaceutical Industry and by Public-private Partnerships." BMJ vol. 27, iss. 325 7357 ; : 176-7.
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