Clinical recruitment

The Changing Role of Clinical Research Associates Patient Recruitment Reduced Time to Database Lock Management of Geographically Diverse Studies... 

The rate of recruitment is one of the most frequent factors limiting the speed of clinical evaluations. Particularly in some areas, such as oncology, finding... 

Decision analytic models, or simulation models of clinical decision analysis, usually involve the creation of a treatment decision/outcome tree based on a synthesis of expert opinion, sometimes using validated methods of canvassing opinion such as recruiting a Delphi panel (Hatziandreu et al, 1994 Einarson et al, 1995). The decision tree... 

The number of study sites to be used for a clinical trial depends on the characteristics and number of subjects that need to be recruited. Often, a sufficient number of participants cannot be enrolled from a single site, especially if the study inclusion criteria are restrictive and the timeframe for recruitment is limited. In order to complete the study within a reasonable period of time, an inclusion of multiple research centers is often necessary (Chow and Liu, 1998). The selection of study sites depends on several factors including ... 

SPILKER B, CRAMER J A (1992) Patient recruitment in clinical trials. New York, Raven Press. 

The excessive electrical discharges can spread to other neurons, either adjacent ones or distant ones connected by fiber tracts. The seizure thus spreads to other areas of the brain, recruiting them into the uncontrolled firing pattern. The neurons involved may not be abnormal themselves, but are diverted from their normal functioning to participate in the wildly excessive discharges. The degree of spread and the location of brain areas involved determine the clinical manifestations of the seizure. 

The gold-standard assay used for all chemokine receptor inhibitors that reach clinical-phase trials is the chemotaxis functional assay. This assay relies on the ability of chemokines to recruit cells expressing their respective receptor to areas of inflammation. In vitro, this assay was first described in detail by Taub et al. (16) for 24/48-well plates currently, this can be achieved by using 96-well plates. Cells are incubated in the upper chamber with an antagonist for a particular receptor (at different concentrations or with buffer) and challenged to migrate to the lower chamber, which has the relevant chemokine. After 2 to 4 hours of incubation at 37°C, the upper chamber inlet is removed and the cells in the lower chamber quantified by fluorescence with, for example, Calcein AM (Invitrogen, Carlsbad, CA). 

The African-American Heart Failure Trial showed that a large number of African Americans can be recruited in sufficient numbers with enough power to show efficacy in a clinical trial. In psychiatry the large START) study of depression was made up of 24% minorities (Trivedi etal, 2006). The recently completed Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) was able to recruit enough African Americans to make up about one third of its participants (Stroup et al, 2006). 

Why are side effects important Imagine that you have been recruited for a clinical trial of an antidepressant medication. As part of the required informed-consent procedure, you are told that you may be given a placebo instead of the active medication, but because this is a double-blind trial, you will not be told which you are getting until the study is over. You are told that... 

It turns out that there is another reason for including a second medication in a clinical trial. You may remember that there is not much difference in effectiveness between one drug and another in the treatment of depression (see Chapter i). So trying to show that the new drug works better is not likely to pay off, and given how expensive clinical trials are and how difficult it can be to recruit subjects for them, a drug company would not want to include an additional arm unless it paid off. So why include it ... 

The most common criticism of our meta-analysis is the claim that the clinical trials we analysed were flawed, and that better results would have been found if the studies had been designed better. The trials were too short to show the real effect of antidepressants, the critics said. The people recruited to participate in them were not depressed enough, or they were too depressed. In any case, they were not representative of the patients who are generally seen in clinical practice. 

Most clinical trials, including the ones my colleagues and I analysed, are conducted on volunteers, many of whom are recruited for the trial by advertisements. Perhaps these depressed people are not as responsive to antidepressants as the patients seen in clinical practice. The STAR D trial that I described earlier was designed specifically to evaluate the effect of antidepressants on the kinds of patients who are typically seen in clinical practice. None of the patients in this trial were recruited by advertising. Instead, they were all patients who sought treatment for depression in family practice or psychiatric out-patient treatment facilities. Also, the usual exclusion criteria were relaxed, so that a broader range of patients was evaluated. The trial did exclude patients who had already tried antidepressants but had not responded to them, although this exclusion should result in better response rates, not worse ones. 

Elevated ET-1 in SCA patients, even in the steady state, may play an important role in the dehydration of sickle erythrocytes and the resulting enhanced intra-erythrocytic HbS polymerization. Indeed, it has been shown that ET-1 activates Ca2+- gated K+ channels in mouse erythrocytes [34]. ET-1, as a pro-inflammatory agonist, has been shown to induce the production of inflammatory cytokines by monocytes. One of the cytokines, namely TNFa enhances the adherence of sickle erythrocytes to vascular endothelium [35]. In addition, endothehns upregulate the expression of endothelial adhesion molecules such as ICAM-l, VCAM-1 and E-se-lectin, which participate in the recruitment of white cells to the site of inflammation. The overall conclusions that can be drawn from these data is that ET-1 plays a critical role in the vasospasm and inflammation that result in VOC. The major effect of HU in ameliorating the clinical symptoms of SCA likely results from its ability to inhibit the chronically activated ET-1 expression in SCA patients. 

---