Indoor Air Pollutant (Toluene) Reduction Based on Ultraviolet-A Irradiance and Changes in the Reactor Volume in a TiO2 Photocatalyst Reactor.

This study experimentally confirmed the effect of TiO2 photocatalysts on the removal of indoor air pollutants. In the experiment, toluene, a representative indoor air pollutant, was removed using a coating agent containing TiO2 photocatalysts. Conditions proposed by the International Organization for Standardization (ISO) were applied mutatis mutandis, and a photoreactor for an experiment was manufactured. The experiment was divided into two categories. The first experiment was conducted under ISO conditions using the TiO2 photocatalyst coating agent. In the second experiment, the amount of ultraviolet-A (UV-A) light was varied depending on the lamp's service life, and the volume of the reactor was varied depending on the number of contaminants. The results showed that the TiO2 photocatalytic coating agent reduced the effect of toluene. This reduction effect can be increased as a primary function depending on the changes in the amount of UV-A light and reactor volume. However, because toluene is decomposed in this study, additional organic pollutants such as benzene and butadiene can be produced. Because these pollutants are decomposed by the TiO2 photocatalysts, the overall reduction performance may change. Nonetheless, TiO2 photocatalysts can be used to examine the effect of indoor pollutant reduction in indoor ventilation systems and building materials.

Development of electrochemical biosensor for detection of pathogenic microorganism in Asian dust events.

We developed a single-walled carbon nanotubes (SWCNTs)-based electrochemical biosensor for the detection of Bacillus subtilis, one of the microorganisms observed in Asian dust events, which causes respiratory diseases such as asthma and pneumonia. SWCNTs plays the role of a transducer in biological antigen/antibody reaction for the electrical signal while 1-pyrenebutanoic acid succinimidyl ester (1-PBSE) and ant-B. subtilis were performed as a chemical linker and an acceptor, respectively, for the adhesion of target microorganism in the developed biosensor. The detection range (102-1010 CFU/mL) and the detection limit (102 CFU/mL) of the developed biosensor were identified while the response time was 10 min. The amount of target B. subtilis was the highest in the specificity test of the developed biosensor, compared with the other tested microorganisms (Staphylococcus aureus, Flavobacterium psychrolimnae, and Aquabacterium commune). In addition, target B. subtilis detected by the developed biosensor was observed by scanning electron microscope (SEM) analysis.

Computer use at work is associated with self-reported depressive and anxiety disorder.

BACKGROUND: With the development of technology, extensive use of computers in the workplace is prevalent and increases efficiency. However, computer users are facing new harmful working conditions with high workloads and longer hours. This study aimed to investigate the association between computer use at work and self-reported depressive and anxiety disorder (DAD) in a nationally representative sample of South Korean workers. METHODS: This cross-sectional study was based on the third Korean Working Conditions Survey (2011), and 48,850 workers were analyzed. Information about computer use and DAD was obtained from a self-administered questionnaire. We investigated the relation between computer use at work and DAD using logistic regression. RESULTS: The 12-month prevalence of DAD in computer-using workers was 1.46 %. After adjustment for socio-demographic factors, the odds ratio for DAD was higher in workers using computers more than 75 % of their workday (OR 1.69, 95 % CI 1.30-2.20) than in workers using computers less than 50 % of their shift. After stratifying by working hours, computer use for over 75 % of the work time was significantly associated with increased odds of DAD in 20-39, 41-50, 51-60, and over 60 working hours per week. After stratifying by occupation, education, and job status, computer use for more than 75 % of the work time was related with higher odds of DAD in sales and service workers, those with high school and college education, and those who were self-employed and employers. CONCLUSIONS: A high proportion of computer use at work may be associated with depressive and anxiety disorder. This finding suggests the necessity of a work guideline to help the workers suffering from high computer use at work.

Long working hours may increase risk of coronary heart disease.

OBJECTIVE: To evaluate the association between long working hours and risk of coronary heart disease (CHD) estimated by Framingham risk score (FRS) in Korean adults. METHODS: This study evaluated adult participants in Korean National Health and Nutrition Examination Survey IV (2007-2009). After inclusion and exclusion criteria were applied, the final sample size for this study model was 8,350. Subjects were asked about working hours and health status. Participants also completed physical examinations and biochemical measurement necessary for estimation of FRS. Multiple logistic regression was conducted to investigate the association between working hours and 10-year risk for CHD estimated by FRS. RESULTS: Compared to those who work 31-40 hr, significantly higher 10-year risk was estimated among subjects working longer hours. As working hours increased, odds ratio (OR) for upper 10 percent of estimated 10-year risk for CHD was increased up to 1.94. CONCLUSIONS: Long working hours are significantly related to risk of coronary heart disease.

Fucosterol isolated from Undaria pinnatifida inhibits lipopolysaccharide-induced production of nitric oxide and pro-inflammatory cytokines via the inactivation of nuclear factor-κB and p38 mitogen-activated protein kinase in RAW264.7 macrophages.

It has been reported that fucosterol has anti-diabetic, anti-oxidant, and anti-osteoporotic effects. We investigated the anti-inflammatory effects and the underlying molecular mechanism of fucosterol in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages. Fucosterol suppressed the expressions of inducible nitric oxide synthase (iNOS), tumour necrosis factor-α (TNF-α), and interleukin-6 (IL-6) by downregulating their transcriptions, and subsequently inhibited the productions of nitric oxide, TNF-α, and IL-6. In addition, fucosterol attenuated LPS-induced DNA binding and the transcriptional activity of nuclear factor-κB (NF-κB). These reductions were accompanied by parallel reductions in the phosphorylation and nuclear translocation of NF-κB. Furthermore, fucosterol attenuated the phosphorylations of mitogen-activated protein kinase kinases 3/6 (MKK3/6) and mitogen-activated protein kinase-activated protein kinase 2 (MK2), which are both involved in the p38 MAPK pathway. These results suggest that the anti-inflammatory effects of fucosterol are associated with the suppression of the NF-κB and p38 MAPK pathways.

Anti-inflammatory and anti-arthritic effects of new synthetic 3-(4-hydroxyphenyl)-4-(4-thiomethoxyphenyl)-1H-pyrrole-2,5-dione.

We previously reported that 3-(4-hydroxyphenyl)-4-(4-thiomethoxyphenyl)-1H-pyrrole-2,5-dione (1, HMP) has a strong inhibitory effect on prostaglandin E(2) (PGE(2)) production. In this study, the anti-inflammatory and anti-arthritic effects of HMP were evaluated on LPS-induced RAW 264.7 macrophages and rats with carrageenan-induced paw edema and adjuvant-induced arthritis (AIA). The attenuation of PGE(2) production by HMP was found to be caused by the inhibition of cyclooxygenase-2 (COX-2) activity, but not COX-1 activity. However, HMP did not affect COX-2 at the protein or mRNA levels, whereas it suppressed the releases and expressions of inflammatory cytokines, such as, interleukin-1ß (IL-1ß) and IL-6 in LPS-induced macrophages. Furthermore, HMP suppressed LPS-induced nitric oxide (NO) production by down regulating the protein and mRNA expressions of inducible nitric oxide synthase (iNOS). In rats with carrageenan-injected acute inflammation, oral administration of HMP (25 or 50mg/kg, po) reduced paw swelling, and PGE(2) release and myeloperoxidase (MPO) activity in tissue. Furthermore, HMP (25 or 50mg/kg, po) significantly reduced paw swelling, arthritic indices and plasma PGE(2) concentrations in rat with AIA. These results show that HMP reduces swelling in a model acute inflammation and inhibits arthritic responses in a model of chronic inflammation via the inhibition of PGE(2) production. These results suggest that HMP is a potential therapeutic agent for the treatment of arthritis and associated disorders.

4'-bromo-5,6,7-trimethoxyflavone represses lipopolysaccharide-induced iNOS and COX-2 expressions by suppressing the NF-κB signaling pathway in RAW 264.7 macrophages.

The regulations of the NO and PGE(2) productions are research topics of interest in the field of anti-inflammatory drug development. In the present study, 5,6,7-trimethoxy- and 5,6,7-trihydroxyflavones 3a-3g were synthesized from cinnamic acid derivatives. In particular, 4'-bromo-5,6,7-trimethoxyflavone (3b) most potently inhibited the productions of NO and PGE(2) in LPS-treated RAW 264.7 cells (IC(50)=14.22 ± 1.25 and 10.98 ± 6.25 µM, respectively), and these inhibitory effects were more potent than those of oroxylin A or baicalein. Consistent with these findings, 3b concentration-dependently reduced the LPS-induced expressions of iNOS and COX-2 at the protein and mRNA levels. In addition, the release of TNF-α, IL-6, and IL-1ß and the mRNA expressions of these cytokines were reduced by 3b in a concentration-dependent manner. Furthermore, 3b attenuated the LPS-induced transcriptional activities of NF-κB and this was accompanied by parallel reductions in the degradation and phosphorylation of IκB-α, and consequently by a decrease in the nuclear translocation of the p65 subunit of NF-κB. Taken together, these results suggest that suppressions of the expressions of iNOS, COX-2, TNF-α, IL-6, and IL-1ß via NF-κB inactivation are responsible for the anti-inflammatory effects of 3b.

BRN-103, a novel nicotinamide derivative, inhibits VEGF-induced angiogenesis and proliferation in human umbilical vein endothelial cells.

Anti-angiogenesis is regarded as an effective strategy for cancer treatment, and vascular endothelial growth factor (VEGF) plays a key role in the regulations of angiogenesis and vasculogenesis. In the present study, the authors synthesized five novel nicotinamide derivatives which structurally mimic the receptor tyrosine kinase inhibitor sunitinib and evaluated their anti-angiogenic effects. Transwell migration assays revealed that 2-(1-benzylpiperidin-4-yl) amino-N-(3-chlorophenyl) nicotinamide (BRN-103), among the five derivatives most potently inhibited VEGF-induced human umbilical vein endothelial cells (HUVECs). In addition, BRN-103 dose-dependently inhibited VEGF-induced migration, proliferation, and capillary-like tube formation of HUVECs and vessel sprouting from mouse aortic rings. To understand the molecular mechanisms responsible for these activities, the authors examined the effect of BRN-103 on VEGF signaling pathways in HUVECs. BRN-103 was found to suppress the VEGF-induced phosphorylation of VEGF receptor 2 (VEGR2) and the activations of AKT and eNOS. Taken together, these results suggest that BRN-103 inhibits VEGF-mediated angiogenesis signaling in human endothelial cells.