This study was conducted to analyze the effect of male middle school students'eating school breakfast on their attitudes toward breakfast and school breakfast. In addition, the effect of school breakfast on breakfast-related eating behaviors and academic achievement was investigated. The study subjects were selected from a male middle school located in Gyeonggi-do, Republic of Korea. Breakfast was provided at the school for 7 weeks during the 2nd semester of the year 2006. Two sophomore classes were selected for the experimental study. All the students from one class (n = 34; School Breakfast Eaters) have eaten school breakfast while none of the students from the other class (n = 33; School Breakfast Non-eaters) have done so. About two weeks after the school breakfast service was terminated, questionnaires were distributed to the two classes and the responses were analyzed. The results showed that School Breakfast Eaters had more positive attitudes toward breakfast and school breakfast than School Breakfast Non-eaters. In addition, School Breakfast Eaters perceived the positive effect of eating breakfast on their school life more highly than School Breakfast Non-eaters. However there was no significant difference between the two groups in their breakfast eating behaviors in terms of breakfast skipping when the breakfast service was not available. No significant difference was found between the two groups with regards to math score variation before and after school breakfast service. In conclusion, school breakfast for 7 weeks had positive effects on male middle school students'attitudes toward breakfast and school breakfast, although the effect was not confirmed in their breakfast-related eating behaviors after the school breakfast service was terminated.
Achievement ; Breakfast ; Eating ; Feeding Behavior ; Humans ; Male ; Republic of Korea ; Surveys and Questionnaires

BACKGROUND: Leukemic cells originate from hypoxic bone marrow, which protects them from anti-cancer drugs. Although many factors that cause drug resistance in leukemic cells have been studied, the effect of hypoxia on drug-induced apoptosis is still poorly understood. METHODS: In this study, we examined the effect of hypoxia on anti-leukemic drug resistance in leukemic cell lines treated with cobalt chloride (CoCl2), a hypoxia-mimetic agent. Cellular proliferation was evaluated using the methyl thiazolyl tetrazolium (MTT) assay. Flow cytometry analysis and western blots were performed to investigate apoptosis-related proteins. RESULTS: Unlike its previously known apoptotic effect, the expression of HIF-1alpha increased the survival rate of human promyelocytic leukemia HL-60 cells when these cells were exposed to anti-leukemic drugs; these effects were mediated by heat-shock protein HSP70 and the pro-apoptotic protein Bax. CONCLUSION: These findings may provide new insights for understanding the mechanisms underlying hypoxia and for designing new therapeutic strategies for acute myeloid leukemia.
Anoxia ; Apoptosis ; Arsenicals ; Blotting, Western ; Bone Marrow ; Cell Line ; Cell Proliferation ; Cobalt ; Drug Resistance ; Flow Cytometry ; Heat-Shock Proteins ; HL-60 Cells ; Humans ; Leukemia ; Leukemia, Myeloid, Acute ; Oxides ; Proteins ; Survival Rate

Chromatin structure has a crucial role in a diversity of physiological processes, including development, differentiation and stress responses, via regulation of transcription, DNA replication and DNA damage repair. Histone deacetylase (HDAC) inhibitors regulate chromatin structure and activate the DNA damage checkpoint pathway involving Ataxia-telangiectasia mutated (ATM). Herein, we investigated the impact of histone acetylation/deacetylation modification on the ATM-mediated transcriptional modulation to provide a better understanding of the transcriptional function of ATM. The prototype HDAC inhibitor trichostain A (TSA) reprograms expression of the myeloid cell leukemia-1 (MCL1) and Gadd45alpha genes via the ATM-mediated signal pathway. Transcription of MCL1 and Gadd45alpha is enhanced following TSA treatment in ATM+ cells, but not in isogenic ATM- or kinase-dead ATM expressing cells, in the ATM-activated E2F1 or BRCA1-dependent manner, respectively. These findings suggest that ATM and its kinase activity are essential for the TSA-induced regulation of gene expression. In summary, ATM controls the transcriptional upregulation of MCL1 and Gadd45alpha through the activation of the ATM-mediated signal pathway in response to HDAC inhibition. These findings are important in helping to design combinatory treatment schedules for anticancer radio- or chemo-therapy with HDAC inhibitors.
Cell Cycle Proteins/genetics/*metabolism ; DNA Damage/*genetics ; DNA-Binding Proteins/*metabolism ; E2F1 Transcription Factor/metabolism ; Gene Expression Regulation/drug effects ; Histone Deacetylase Inhibitors/*pharmacology ; Histone Deacetylases/*metabolism ; Humans ; Hydroxamic Acids/pharmacology ; Nuclear Proteins/genetics/metabolism ; Promoter Regions, Genetic/genetics ; Protein Binding/drug effects ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins c-bcl-2/genetics/metabolism ; RNA, Messenger/genetics/metabolism ; *Transcription, Genetic/drug effects ; Tumor Suppressor Proteins/*metabolism