Prevalence of obesity in 4-18-year-old population in the Basque Country, Spain.

The objective of the study was to estimate the prevalence of overweight and obesity in children and adolescents in the Basque Country, Spain. It consisted of an analysis of baseline data of the Nutrition Survey, a cross-sectional study, carried out in 2004-2005. The study population comprised child and adolescent living in the Basque Country. The analysis was carried out in a representative random sample of 1178 people aged 4-18 years. Anthropometric examinations were undertaken by trained observers using standardized methods and included measurements of weight and height. Subjects were classified into different body mass index categories, according to the International Obesity Task Force guidelines. A 5.4% of the population studied was obese; 6% of males and 4.7% of females, the highest in the 11-14 age group in boys (7.2%) and in the 4-6 age group in girls (12.5%). Overweight (22.9%) was slightly higher in girls. The highest prevalence of excess weight (overweight+obesity) was observed in girls aged 4-6 years (38.4%), decreasing with age. Subjects in the 15-18 age group rated 16.6%. Boys evidenced a higher excess weight rate in the 11-14 (32.9%) and 7-10 (32%) age groups; the lowest rate was found in the 4-6 age group. Prevalence of obesity was higher in the less privileged socio-economic strata (6.9% vs. 5.2%), for both boys and girls. However, this trend was observed only in girls for overweight (25.9% vs. 21.8%). This study shows a high prevalence of obesity and overweight in the studied population and similar to other European countries and regions.

Tumor-dependent activation of rodent hepatic stellate cells during experimental melanoma metastasis.

In this work we report the presence of intrametastatic smooth-muscle iso-alpha-actin (SMA)-expressing cells which appeared from the early stages of the hepatic metastasis process of intrasplenically injected B16 melanoma (B16M) cells. They formed a network of stromal cells among B16M cells, a very low percentage of them expressing desmin. In contrast, those parts of liver tissue unaffected by metastasis had perisinusoidal desmin-expressing quiescent hepatic stellate cells (qHSC) which did not express SMA. Exposure of freshly isolated rat quiescent hepatic stellate cells (qHSC) to B16M cell-conditioned medium (B16M-CM) leads to a progressive increase (P < .01) in the number of SMA-expressing cells, which was accompanied by a parallel reduction in the number of desmin-expressing cells. In addition, B16M-CM also contained chemotactic factor(s) which significantly (P < .01) increased (50%) in vitro qHSC migration and stimulated both [3H]thymidine and [3H]glucosamine uptake in qHSC. Moreover, B16M-CM also significantly (P < .01) enhanced qHSC secretion of matrix metalloproteinase-2 (MMP-2), and unknown chemotactic factor(s) enhancing in vitro migration of B16M cells. The results suggest that B16 melanoma releases qHSC-activating factors, which induce the appearance of metastasis-infiltrating myofibroblasts by a paracrine mechanism. Such cells showed cytoskeletal alterations which are associated with enhanced proliferation, glycosaminoglycan synthesis, MMP-2 secretion, and tumor-chemotactic factor production. Thus, tumor-activated qHSC may play an important role in melanoma cell motility and invasion during hepatic metastasis progression.

Interleukin 1-dependent and -independent mouse melanoma metastases.

BACKGROUND: The adhesion of cancer cells to the endothelial lining of blood vessels, which is important for metastasis, is promoted by the action of interleukin 1 (IL-1) and other cytokines. PURPOSE: IL-1-producing melanoma cells were used to induce metastases in mice to test whether melanoma metastasis--wherever it occurs--depends on the action of IL-1. METHODS: We used the following experimental designs in this study: 1) Male C57BL/6J mice were inoculated in the left cardiac ventricle with 5 x 10(4) murine B16 melanoma cells, and no treatment was given (control animals). 2) Mice received an intraperitoneal injection of either saline (control animals) or recombinant human IL-1 receptor antagonist (rHuIL-1Ra) 2 hours before the injection of cancer cells; thereafter, they received an additional injection of saline or rHuIL-1Ra daily for 20 days. 3) Mice received an intravenous injection of either saline or rHuIL-1Ra; 15 minutes later, mice that received saline were given either a second injection of saline (control animals) or an injection of bacterial lipopolysaccharide (LPS) to stimulate host IL-1 production and endothelial cell activation. The mice that received rHuIL-1Ra were also given an injection of LPS at this time. Six hours later, all mice were inoculated with cancer cells, followed by no further treatment. In all experiments, the mice were killed 20 days after the injection of cancer cells, and metastases were counted in multiple organs and bones. Metastasis incidence values (relating to the frequency that a given site was positive for metastasis) and metastasis development index values (relating to the extent of metastasis at a given site) were calculated. A hierarchical cluster analysis was performed to determine whether groups of organs exhibited characteristic changes in their metastasis development index values in response to the three treatments given (i.e., rHuIL-1Ra, LPS, or rHuIL-1Ra plus LPS). Reported P values are two-sided. RESULTS AND CONCLUSIONS: Treatment with rHuIL-1Ra alone significantly (P<.05) reduced the occurrence of metastasis in the bone marrow, spleen, liver, lung, pancreas, skeletal muscle, adrenal gland, and heart, indicating that host- and/or melanoma-derived IL-1 promoted metastasis in these organs; treatment with rHuIL-1Ra had no effect on metastasis in the kidney, testis, brain, skin, and gastrointestinal tract, suggesting that metastasis in these latter organs was IL-1 independent. Treatment with LPS alone significantly (P<.05) enhanced metastasis in the same organs for which rHuIL-1Ra treatment reduced metastasis, except for the heart and the adrenal gland. Treatment with rHuIL-1Ra 15 minutes before LPS treatment abrogated the LPS-mediated enhancement of metastasis. Two independent organ groups for which IL-1 promoted melanoma metastasis were identified in the cluster analysis.