Eating habits, obesity related behaviors, and effects of Danhak exercise in elderly Koreans

The aims of this study were to evaluate obesity-related dietary behaviors and to determine long-term exercise effects on obesity and blood lipid profiles in elderly Korean subjects. A total of 120 subjects, aged 60-75 yr, were recruited, and obesity-related dietary behaviors were determined. An exercise intervention was conducted with 35 qualified elderly females for 6 months, and body composition and blood lipids were measured 6 times at 4 week intervals. At baseline, mean BMI (kg/m2) was 24.8 for males and 23.1 for females. The females had better eating habits than the males and were more concerned with reading nutrition labels on food products (P < 0.001); they also preferred convenience foods less than the male subjects (P < 0.05). Obese individuals were more likely than overweight or normal weight individuals to misperceive their weight (P < 0.001). Those with a high BMI responded feeling more depressed (P < 0.01), lacking self-confidence (P < 0.01), and feeling isolated (P < 0.01), as well as having more difficulty doing outdoor activities (P < 0.01). After exercise, body fat (%) and WHR were significantly reduced (P < 0.05), while body weight and BMI were also decreased without statistical significance. Total cholesterol and blood HDL were significantly improved (207.1 mg/dl vs. 182.6 mg/dl, HDL: 45.6 mg/dl vs. 50.6 mg/dl, P < 0.05). Other benefits obtained from exercise were improvements in self-confidence (26.4%), movement (22.6%), stress-relief (18.9%), and depression (13.2%). In conclusion, elderly females had better eating habits and were more concerned with nutrition information and healthy diets compared to elderly males. However, misperceptions of weight and obesity-related stress tended to be very high in females who were overweight and obese, which can be a barrier to maintain normal weight. Long-term Danhak practice, a traditional Korean exercise, was effective at reducing body fat (%) and abdominal obesity, and improved lipid profiles, self-confidence, and stress

Glucocorticoid Receptor (GR)-Associated SMRT Binding to C/EBPβ TAD and Nrf2 Neh4/5: Role of SMRT Recruited to GR in GSTA2 Gene Repression

The expression of the glutathione S-transferase gene (GST), whose induction accounts for cancer chemoprevention, is regulated by activation of CCAAT/enhancer binding protein β (C/EBPβ) and NF-E2-related factor 2 (Nrf2). The present study investigated the repressing effects of activating glucocorticoid receptor (GR) on C/EBPβ- and Nrf2-mediated GSTA2 gene induction and the mechanism. Dexamethasone that activates GR inhibited constitutive and oltipraz- or tert-butylhydroquinone (t-BHQ)-inducible GSTA2 expression in H4IIE cells. Also, dexamethasone repressed GSTA2 promoter-luciferase gene activity. Dexamethasone-GR activation did not inhibit nuclear translocation of C/EBPβ or Nrf2 nor their DNA binding activities induced by oltipraz or t-BHQ. Deletion of the glucocorticoid response element (GRE) in the GSTA2 promoter abolished dexamethasone inhibition of the gene induction. Immunoprecipitation-immunoblotting, chromatin immunoprecipitation, and GST pull-down assays revealed that silencing mediator for retinoid and thyroid hormone receptors (SMRT), a corepressor recruited to steroid-GR complex for histone deacetylation, bound to TAD domain of C/EBPβ and Neh4/5 domain of Nrf2. The GSTA2 promoter-luciferase activities were decreased by SMRT but not by truncated SMRTs. The small interference RNA (siRNA) against SMRT abolished SMRT repression of the gene induction by C/EBPβ or Nrf2. The plasmid transfection and siRNA experiments directly evidenced the functional role of SMRT in GSTA2 repression. In conclusion, dexamethasone antagonizes C/EBPβ- and Nrf2-mediated GSTA2 gene induction via ligand-GR binding to the GRE, and steroid-mediated GSTA2 repression involves inactivation of C/EBPβ and Nrf2 by SMRT recruited to steroid-GR complex

Local Toxicity of Biocides after Direct and Aerosol Exposure on the Human Skin Epidermis and Airway Tissue Models

Biocides are commonly used as spray- or trigger-type formulations, thus dermal and respiratory exposure to biocide aerosol is unavoidable. However, little is known about the impact of aerosolization on the local toxicity of biocides on the skin or the airway. We compared the local toxicity of biocides after direct or aerosol exposure on reconstructed human skin epidermis and upper airway models. Three biocides, 1,2-benzisothiazol-3(2H)-one (BIT), 2-phenoxyethanol (PE), and 2-phenylphenol (OPP), most widely used in the market were selected. When the biocide was treated in aerosols, toxicity to the skin epidermis and upper airway tissue became significantly attenuated compared with the direct application as determined by the higher tissue viabilities. This was further confirmed in histological examination, wherein the tissue damages were less pronounced. LC-MS/MS and GC/MS analysis revealed that concentrations of biocides decreased during aerosolization. Importantly, the toxicity of biocides treated in 3 μm (median mass aerodynamic diameter (MMAD)) aerosols was stronger than that of 5 μm aerosol, suggesting that the aerosol particle size may affect biocide toxicity. Collectively, we demonstrated that aerosolization could affect the local toxicity of biocides on the skin epidermis and the upper airway

Rapid and Direct Detection of Apolipoprotein E Genotypes Using Whole Blood from Humans

Polymerase chain reaction (PCR) is a powerful molecular biological tool in the field of toxicity testing and diagnostics. The use of PCR for large-scale genetic testing requires an effective method of sample processing. Unfortunately, isolation of PCR-quality DNA is time-consuming. PCR performed directly on whole blood is preferred because of time efficiency, cost of the procedure, and possible automation for large-scale toxicity evaluation and diagnosis. The apolipoprotein E (APOE) gene contains two single-nucleotide polymorphisms (SNP) located at codons 112 and 158, producing three APOE protein isoforms known to be associated with the risks of developing cardiovascular disease and susceptibility to Alzheimer`s disease. In the present study, an attempt was made to use the AnyDirect solution for APOE genotyping by PCR using whole blood directly without DNA purification. Results for two PCR methods, (1) conventional PCR using purified DNA and conventional buffer and (2) direct PCR using whole blood and AnyDirect solution, were compared in four different PCR-based APOE genotyping methods including PCR restriction-fragment-length polymorphism (PCR-RFLP), allele-specific PCR, SNaPshot mini-sequencing, and multiplex tetra-primer amplification refractory mutation system (T-ARMS) PCR. There was complete concordance in the APOE genotypes between conventional PCR and direct PCR, in all four different PCR-based APOE genotyping methods. Data demonstrated that the four different PCR-based APOE genotyping methods are able to determine the APOE genotypes successfully using whole blood directly with the use of AnyDirect solution. The direct multiplex T-ARMS PCR using whole blood may be the most rapid, simple, and inexpensive method for detecting APOE genotypes among four different APOE genotyping methods.TSAI MY, 1993, CLIN CHEM, V39, P2121CARTIER R, 1992, ELECTROPHORESIS, V13, P252HIXSON JE, 1990, J LIPID RES, V31, P545EMI M, 1988, GENOMICS, V3, P373MAHLEY RW, 1988, SCIENCE, V240, P622Molloy DW, 2007, J TOXICOL ENV HEAL A, V70, P2011, DOI 10.1080/15287390701551142Park HD, 2007, CLIN CHEM LAB MED, V45, P346, DOI 10.1515/CCLM.2007.075Yang YG, 2007, CLIN CHIM ACTA, V380, P112, DOI 10.1016/j.cca.2007.01.019Yang YG, 2007, J BIOCHEM MOL BIOL, V40, P444Yang YG, 2007, J BIOTECHNOL, V131, P106, DOI 10.1016/j.jbiotec.2007.06.001Yang YG, 2007, J MICROBIOL BIOTECHN, V17, P1616Medina S, 2009, J TOXICOL ENV HEAL A, V72, P1075, DOI 10.1080/15287390903084561Cui ZH, 2009, J TOXICOL ENV HEAL A, V72, P782, DOI 10.1080/15287390902841680Xiao TL, 2009, J TOXICOL ENV HEAL A, V72, P577, DOI 10.1080/15287390802706371ROSES AD, 1994, LANCET, V343, P1564Srinivasan JR, 1998, RAPID COMMUN MASS SP, V12, P1045Donohoe GG, 1999, CLIN CHEM, V45, P143LEE MK, 2001, KOREAN J CLIN PATHOL, V21, P154Papp AC, 2003, BIOTECHNIQUES, V34, P1068Ben-Avi L, 2004, J ALZHEIMERS DIS, V6, P497Choi DW, 2004, J TOXICOL ENV HEAL A, V67, P2061, DOI 10.1080/15287390490514895HAAS H, 1994, ELECTROPHORESIS, V15, P153HACKLER R, 1994, J LIPID RES, V35, P153DAS HK, 1985, J BIOL CHEM, V260, P6240MENZEL HJ, 1983, ARTERIOSCLEROSIS, V3, P310BRESLOW JL, 1982, J LIPID RES, V23, P1224UTERMANN G, 1980, AM J HUM GENET, V32, P339