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Lozol

By A. Stan. National Defense University.

The questions to be asked in method comparison studies fall into two categories: (a) Properties of each method: How repeatable are the measurements? This may include both errors due to repeatability and errors due to patient/method interactions buy lozol 1.5mg low cost. Under properties of each method we could also include questions about variability between observers generic lozol 1.5 mg, between times lozol 1.5mg visa, between places, between position of subject, etc. Most studies standardize these, but do not consider their effects, although when they are considered, confusion may result. Altman’s (1979) criticism of the design of the study by Serfontein and Jaroszewicz (1978) provoked the response that: “For the actual study it was felt that the fact assessments were made by two different observers (one doing only the Robinson technique and the other only the Dubowitz method) would result in greater objectivity” (Serfontein and Jaroszewicz, 1979). What we need is a design and analysis which provide estimates of both error and bias. We feel that a relatively simple pragmatic approach is preferable to more complex analyses, especially when the results must be explained to non-statisticians. It is difficult to produce a method that will be appropriate for all circumstances. What follows is a brief description of the basic strategy that we favour; clearly the various possible complexities which could arise might require a modified approach, involving additional or even alternative analyses. Properties of each method: repeatability The assessment of repeatability is an important aspect of studying alternative methods of measurement. Replicated measurements are, of course, essential for an assessment of repeatability, but to judge from the medical literature the collection of replicated data is rare. Repeatability is assessed for each measurement method separately from replicated measurements on a sample of subjects. We obtain a measure of repeatability from the within- subject standard deviation of the replicates. The British Standards Institution (1979) define a coefficient of repeatability as “the value below which the difference between two single test results. Provided that the differences can be assumed to follow a Normal distribution this coefficient is 2. For the purposes of the present analysis the standard deviation alone can be used as the measure of repeatability. It is important to ensure that the within-subject repeatability is not associated with the size of the measurements, in which case the results of subsequent analyses might be misleading. The best way to look for an association between these two quantities is to plot the standard deviation against the mean. If there are two replicates x1 and x2 then this reduces to a plot of | x1 – x2| against (x1 + x2)/2. From this plot it is easy to see if there is any tendency for the amount of variation to change with the magnitude of the measurements. The correlation coefficient could be tested against the null hypothesis of r = 0 for a formal test of independence. If the within-subject repeatability is found to be independent of the size of the measurements, then a one-way analysis of variance can be performed. The residual standard deviation is an overall measure of repeatability, pooled across subjects. If, however, an association is observed, the results of an analysis of variance could be misleading. Several approaches are possible, the most appealing of which is the transformation of the data to remove the relationship. If the relationship can be removed, a one-way analysis of variance can be carried out. Repeatability can be described by calculating a 95 per cent range for the difference between two replicates.

Recent evidence from the Interheart study (31) has highlighted the adverse effects of use of any tobacco product and generic lozol 2.5mg online, importantly cheap 1.5 mg lozol fast delivery, the harm caused by even very low consumption (1–5 cigarettes a day) lozol 1.5mg with amex. The benefits of stopping smoking are evident; however, the most effective strategy to encourage smoking cessation is not clearly established. All patients should be asked about their tobacco use and, where relevant, given advice and counselling on quitting, as well as reinforcement at follow-up. There is evidence that advice and counselling on smoking cessation, delivered by health profession- als (such as physicians, nurses, psychologists, and health counsellors) are beneficial and effective (125–130). Several systematic reviews have shown that one-time advice from physicians during routine consultation results in 2% of smokers quitting for at least one year (127, 131). Similarly, nicotine replacement therapy (132, 133) can increase the rate of smoking cessation. Nico- tine may be administered as a nasal spray, skin patch or gum; no particular route of administration seems to be superior to others. In combination with the use of nicotine patches, amfebutamone may be more effective than nicotine patches alone, though not necessarily more effective than amfebutamone alone (135, 136). Nortriptyline has also been shown to improve abstinence rates at 12 months compared with a placebo. Both agents have appreciable discontinuation rates because of side- effects (135–137). Data from observational studies suggest that passive cigarette smoking produces a small increase in cardiovascular risk (138–140). Whether reducing exposure to passive cigarette smoke reduces cardiovascular risk has not been directly established. The interventions described above targeted at individuals may be less effective if they are imple- mented in populations exposed to widespread tobacco advertising, sponsorship of sporting activities by the tobacco industry, low-cost tobacco products, and inadequate government tobacco control policies. There is evidence that tobacco consumption decreases markedly as the price of tobacco products increases. Bans on advertising of tobacco products in public places and on sales of tobacco to young people are essential components of any primary prevention programme addressing noncommunicable diseases (140). The cholesterol-raising properties of saturated fats are attributed to lauric acid (12:0), myristic acid (14:0), and palmitic acid (16:0). Stearic acid (18:0) and saturated fatty acids with fewer than 12 carbon atoms are thought not to raise serum cholesterol concentrations (146, 147). The effects of different saturated fatty acids on the distribution of cholesterol over the various lipoproteins are not well known. Trans-fatty acids come from both animal and vegetable sources and are produced by partial hydro- genation of unsaturated oils. Metabolic and epidemiological studies have indicated that trans-fatty acids increase the risk of coronary heart disease (145, 152, 153). It has also been demonstrated that replacing saturated and trans-unsaturated fats with monounsaturated and polyunsaturated fats is more effective in preventing coronary heart disease events than reducing overall fat intake (145, 153, 155). Current guidelines recommend a diet that provides less than 30% of calories from dietary fat, less than 10% of calories from saturated fats, up to 10% from polyunsaturated fats, and about 15% from monounsaturated fats (86, 88, 148). Metabolic studies have shown that dietary cholesterol is a determinant of serum cholesterol concentration (156–158). Reducing dietary cholesterol by 100 mg a day appears to reduce serum cholesterol by about 1% (147). However, there is marked individual variation in the way serum cholesterol responds to dietary cholesterol (159); dietary cholesterol seems to have a relatively small effect on serum lipids, compared with dietary saturated and trans-fatty acids (88, 104, 158). Studies have demonstrated that, in controlled conditions, it is possible to modify behaviour, but in daily life the required intensity of supervision may not be practicable. The effects of advice about reducing or modifying dietary fat intake on total and cardiovascular mortality and cardiovascular morbidity in real-life settings were assessed in a systematic review of 27 studies, comprising 30 902 person–years of observation (160). The interventions included both direct provision of food and, in most trials, dietary advice to reduce intake of total fat or saturated fat or dietary cholesterol, or to shift from saturated to unsaturated fat. The pooled results indicate that reducing or modifying dietary fat reduces the incidence of combined cardiovascular events by 16% (rate ratio 0. The reduction in cardiovascu- lar mortality and morbidity was more pronounced in trials lasting at least 2 years.

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