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Kidscreen-27 was developed as part of a cross-cultural European Union-funded project to standardise the measurement of children’s health-related quality of life. Yet, research has reported mixed evidence for the hypothesised 5-factor model, and no confirmatory factor analysis (CFA) has been conducted on the instrument with children of low socio-economic status (SES) across Ireland (Northern and Republic).
MethodThe data for this study were collected as part of a clustered randomised controlled trial. A total of 663 (347 male, 315 female) 8–9-year-old children (M = 8.74, SD = .50) of low SES took part. A 5- and modified 7-factor CFA models were specified using the maximum likelihood estimation. A nested Chi-square difference test was conducted to compare the fit of the models. Internal consistency and floor and ceiling effects were also examined.
ResultsCFA found that the hypothesised 5-factor model was an unacceptable fit. However, the modified 7-factor model was supported. A nested Chi-square difference test confirmed that the fit of the 7-factor model was significantly better than that of the 5-factor model. Internal consistency was unacceptable for just one scale. Ceiling effects were present in all but one of the factors.
ConclusionsFuture research should apply the 7-factor model with children of low socio-economic status. Such efforts would help monitor the health status of the population.
相似文献![点击此处可从《Australian and New Zealand journal of public health》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Background
Insulinomas are the most common type of neuroendocrine (NE) pancreatic islet tumors. Patients with insulinomas may develop complications associated with hyperinsulinemia. To increase the treatment options for insulinoma patients, we have tested a conditionally replicating adenovirus that has been engineered in such a way that it can specifically express therapeutic genes in NE tumors.Methods
We used a promoter-specific adenoviral vector delivery system that is regulated by an INSM1 (insulinoma-associated-1) promoter, which is silent in normal adult tissues but active in developing NE cells and tumors. Through a series of modifications, using an insulator (HS4) and neuron-restrictive silencer elements (NRSEs), an oncolytic adenoviral vector was generated that retains tumor specificity and drives the expression of a mutated adenovirus E1A gene (Δ24E1A) and the herpes simplex virus thymidine kinase (HSV-tk) gene. The efficacy of this vector was tested in insulinoma-derived MIN, RIN, βTC-1 and pancreatic (Panc-1) cells using in vitro cell survival and in vivo tumor growth assays.Results
Using in vitro insulinoma-derived cell lines and an in vivo subcutaneous mouse tumor model we found that the INSM1 promoter-driven viruses were able to replicate specifically in INSM1-positive cells. INSM1-specific HSV-tk expression in combination with ganciclovir treatment resulted in dose-dependent tumor cell killing, leaving INSM1-negative cells unharmed. When we combined the INSM1-promoter driven HSV-tk with Δ24E1A and INSM1p-HSV-tk (K5) viruses, we found that the co-infected insulinoma-derived cells expressed higher levels of HSV-tk and exhibited more efficient tumor suppression than cells infected with INSM1p-HSV-tk virus alone.Conclusions
INSM1 promoter-driven conditionally replicating adenoviruses may serve as a new tool for the treatment of insulinoma and may provide clinicians with additional options to combat this disease.![点击此处可从《American journal of industrial medicine》网站下载免费的PDF全文](/ch/ext_images/free.gif)