Parental mediation is a type of behavior that could protect children against the negative uses and effects of smartphones. Based on protection motivation theory, this research (a) predicted parental mediation based on parents' threat and efficacy perceptions and (b) predicted threat and efficacy perceptions based on parenting styles and parents' addiction to smartphone use. An online survey of 448 parents of fourth to sixth graders was conducted. Results showed that both restrictive and active parental mediation were predicted by perceived severity, response efficacy, and self-efficacy. With regard to parenting styles, (a) authoritative parenting was positively related to perceived severity as well as response- and self-efficacy, whereas (b) permissive parenting was negatively related to self-efficacy. In addition, parents' addiction was a negative predictor of perceived severity, but a positive predictor of perceived susceptibility.

We conducted a prospective study to assess the prevalence and clinical characteristics of anemia and to define the risk factors for anemia in older Koreans. From October 2002 to November 2002, 1,254 subjects over the age of 60 years were selected from a crosssectional study. All subjects underwent a complete medical history taking and laboratory testing, which included; a complete blood cell count, reticulocyte, liver and renal function tests, lipid profiles, and iron profiles. The median age was 70 years old (range, 60-95 years). The mean levels of hemoglobin (mean ± SD) were 14.5 ± 1.4 g/dL in men and 13.0 ± 1.1 g/dL in women, and the overall prevalence of anemia was 13.6% (171/1,254): 9.9% (27/273) in men and 14.7% (144/981) in women. We found that the prevalence of anemia differed significantly between those of age 60-69 and 70-79 years (P < 0.0001), those of age 60-69 and ‡80 (P < 0.0001), and those of age 70-79 and ‡80 (P = 0.0474). Hemoglobin levels were significantly lower in subjects ‡80 years old. By logistic regression testing, female sex, old age, lower albumin level, higher creatinine level, and lower body mass index were identified as independent risk factors of anemia in elderly Koreans. In conclusion, the overall prevalence of anemia in our study group was 13.6% (171/1,254), and this increased with age. Am.

Patients with advanced or metastatic gastric cancer with concomitant HP infection had a better response to chemotherapy and had an improved overall prognosis compared with patients without HP infection. Further studies are warranted to confirm these findings.

PPAR-gamma has been known to induce suppression, differentiation and reversal of malignant changes in colon cancer in vitro. However, there are several reports that PPAR-gamma ligands enhance colon polyp development in APCmin mice in vivo. These contradictory results have not yet been thoroughly explained. To explain the contradictory results, we analyzed the effects of different concentrations of the PPAR-gamma agonist, 15-deoxy-D12, 14-prostaglandin (15-d Delta PGJ2) and pioglitazone, on APC gene-mutated colon cancer cell lines (HT-29). We measured cell growth and suppression by cell count and MTT assay and analyzed the expression of beta-catenin and c-Myc protein by Western blot. In addition, we inoculated HT-29 cells into APCmin mice to compare tumor size. High concentrations (10-100 microM/L 15-d Delta PGJ2 and pioglitazone) of PPAR-gamma ligand suppressed growth, while low concentrations (0.01-1 microM/L 15-d Delta PGJ2 and pioglitazone) of PPAR-gamma ligand promoted growth. In particular, the effects of 0.1 microM/L 15-d Delta PGJ2 and pioglitazone on cell growth were statistically significant (P = 0.003, P = 0.001, respectively). Tumor growth was associated with an increase in beta-catenin and c-Myc expression. The growth of xenograft tumors was greater in PPAR-gamma ligand-treated mice than in control mice (control vs day 14: P = 0.024, control vs day 28: P = 0.007). The expression of beta-catenin and c-Myc protein were also elevated in PPAR-gamma-treated mouse tissues. PPAR-gamma ligand can promote the growth of APC-mutated HT-29 colon cancer cells in vitro and in vivo. In addition, the tumor promoting effect seems to be associated with an increase in beta-catenin and c-Myc expression. We think that well-controlled clinical trials should be conducted to confirm our results and to verify clinical applications.

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