Construct validity of a figure rating scale for Brazilian adolescents

<p>Abstract</p> <p>Background</p> <p>Figure rating scales were developed as a tool to determine body dissatisfaction in women, men, and children. However, it lacks in the literature the validation of the scale for body silhouettes previously adapted. We aimed to obtain evidence for construct validity of a figure rating scale for Brazilian adolescents.</p> <p>Methods</p> <p>The study was carried out with adolescent students attending three public schools in an urban region of the municipality of Florianopolis in the State of Santa Catarina (SC). The sample comprised 232 10-19-year-old students, 106 of whom are boys and 126 girls, from the 5th "series" (i.e. year) of Primary School to the 3rd year of Secondary School. Data-gathering involved the application of an instrument containing 8 body figure drawings representing a range of children's and adolescents' body shapes, ranging from very slim (contour 1) to obese (contour 8). Weights and heights were also collected, and body mass index (BMI) was calculated later. BMI was analyzed as a continuous variable, using z-scores, and as a dichotomous categorical variable, representing a diagnosis of nutritional status (normal and overweight including obesity).</p> <p>Results</p> <p>Results showed that both males and females with larger BMI z-scores chose larger body contours. Girls with higher BMI z-scores also show higher values of body image dissatisfaction.</p> <p>Conclusion</p> <p>We provided the first evidence of validity for a figure rating scale for Brazilian adolescents.</p

A study of Docetaxel-induced effects in MCF-7 cells by means of Raman microspectroscopy

Chemotherapies feature a low success rate of about 25%, and therefore, the choice of the most effective cytostatic drug for the individual patient and monitoring the efficiency of an ongoing chemotherapy are important steps towards personalized therapy. Thereby, an objective method able to differentiate between treated and untreated cancer cells would be essential. In this study, we provide molecular insights into Docetaxel-induced effects in MCF-7 cells, as a model system for adenocarcinoma, by means of Raman microspectroscopy combined with powerful chemometric methods. The analysis of the Raman data is divided into two steps. In the first part, the morphology of cell organelles, e.g. the cell nucleus has been visualized by analysing the Raman spectra with k-means cluster analysis and artificial neural networks and compared to the histopathologic gold standard method hematoxylin and eosin staining. This comparison showed that Raman microscopy is capable of displaying the cell morphology; however, this is in contrast to hematoxylin and eosin staining label free and can therefore be applied potentially in vivo. Because Docetaxel is a drug acting within the cell nucleus, Raman spectra originating from the cell nucleus region were further investigated in a next step. Thereby we were able to differentiate treated from untreated MCF-7 cells and to quantify the cell–drug response by utilizing linear discriminant analysis models

Stress Response of Human Cell Lines to Ultraviolet B Irradiation

Increased expression of a specific set of genes as a consequence of extracellular stress is typically observed in all organisms. Heat shock proteins (hsps) are a set of evolutionarily conserved proteins, some constitutively expressed and others induced in response to physiological and environmental stresses(1). However,changes in expression of many stress-inducible genes often occur under conditions that are ultimately lethal to the cell. UVB has been reported to initiate a variety of hsp expression in mouse keratinocytes (2), as well as the induction of hsp72 in cultured human fibroblasts (3) and keratinocytes (4). This stress response may be extremely important in the protection of human skin from UV-induced injury. The ability of UVB to induce the expression of hsps in human skin cell is important because these proteins are critical for the survival of cells exposed to a variety of environmental stresses. In particular, a suboptimal stress response in skin cells may predispose skin to melanoma development and photoageing. Nevertheless, heat shock protein function offers a potential therapeutic target for modulation of UV-irradiation skin carcinogenesis and ageing.Reactive oxygen species (ROS) have been implicated in UVB induced damage to skin. The endogenous antioxidant capacity of skin, including nonenzymatic low molecular weight antioxidants and enzymes, may be a major determinant in its response to UVB oxidative mediated damage. Antioxidants may also modulate the expression of genes whose products are involved in carcinogenesis, ageing and inflammation (5). NF-KB may be a central target for oxidants in the UV response but signaling pathways involved in the antioxidant protection against UVB irradiation are not well understood. Large-scale gene expression analysis with eDNA arrays, provide the opportunity to observe the broad effects of UVB-irradiation and antioxidants on signaling pathways. The results presented here address the hypothesis that antioxidants may ameliorate UV-induced skin damage through the concerted modulation of gene expression

Ferritin functions as a proinflammatory cytokine via iron-independent protein kinase C zeta/nuclear factor kappaB-regulated signaling in rat hepatic stellate cells.

Circulating ferritin levels reflect body iron stores and are elevated with inflammation in chronic liver injury. H-ferritin exhibits a number of extrahepatic immunomodulatory properties, although its role in hepatic inflammation and fibrogenesis is unknown. Hepatic stellate cells respond to liver injury through production of proinflammatory mediators that drive fibrogenesis. A specific receptor for ferritin has been demonstrated on activated hepatic stellate cells, although its identity and its role in stellate cell activation is unclear. We propose that ferritin acts as a cytokine regulating proinflammatory function via nuclear factor kappaB (NF-kappaB)-regulated signaling in hepatic stellate cell biology. Hepatic stellate cells were treated with tissue ferritin and iron-free apoferritin, recombinant H-ferritins and L-ferritins, to assess the role of ferritin versus ferritin-bound iron in the production of proinflammatory mediators of fibrogenesis, and to determine whether signaling pathways act via a proposed H-ferritin endocytosis receptor, T cell immunoglobulin-domain and mucin-domain 2 (Tim-2). This study demonstrated that ferritin activates an iron-independent signaling cascade, involving Tim-2 independent phosphoinositide 3 (PI3)-kinase phosphorylation, protein kinase C zeta (PKCzeta) and p44/p42-mitogen-activated protein kinase, resulting in p50/p65-NF-kappaB activation and markedly enhanced expression of hepatic proinflammatory mediators interleukin-1beta (IL-1beta), inducible nitric oxide synthase (iNOS), regulated on activation normal T cell expressed and secreted (RANTES), inhibitor of kappa Balpha (IkappaBalpha), and intercellular adhesion molecule 1 (ICAM1). Conclusions:This study has defined the role of ferritin as a proinflammatory mediator of hepatic stellate cell biology acting through the NF-kappaB signaling pathway, and suggests a potential role in the inflammatory processes associated with hepatic fibrogenesis