Air pollution and children: neural and tight junction antibodies and combustion metals, the role of barrier breakdown and brain immunity in neurodegeneration.

Millions of children are exposed to concentrations of air pollutants, including fine particulate matter (PM2.5), above safety standards. In the Mexico City Metropolitan Area (MCMA) megacity, children show an early brain imbalance in oxidative stress, inflammation, innate and adaptive immune response-associated genes, and blood-brain barrier breakdown. We investigated serum and cerebrospinal fluid (CSF) antibodies to neural and tight junction proteins and environmental pollutants in 139 children ages 11.91 ± 4.2 y with high versus low air pollution exposures. We also measured metals in serum and CSF. MCMA children showed significantly higher serum actin IgG, occludin/zonulin 1 IgA, IgG, myelin oligodendrocyte glycoprotein IgG and IgM (p < 0.01), myelin basic protein IgA and IgG, S-100 IgG and IgM, and cerebellar IgG (p < 0.001). Serum IgG antibodies to formaldehyde, benzene, and bisphenol A, and concentrations of Ni and Cd were significantly higher in exposed children (p < 0.001). CSF MBP antibodies and nickel concentrations were higher in MCMA children (p = 0.03). Air pollution exposure damages epithelial and endothelial barriers and is a robust trigger of tight junction and neural antibodies. Cryptic 'self' tight junction antigens can trigger an autoimmune response potentially contributing to the neuroinflammatory and Alzheimer and Parkinson's pathology hallmarks present in megacity children. The major factor determining the impact of neural antibodies is the integrity of the blood-brain barrier. Defining the air pollution linkage of the brain/immune system interactions and damage to physical and immunological barriers with short and long term neural detrimental effects to children's brains ought to be of pressing importance for public health.

Avian-derived NS gene segments alter pathogenicity of the A/Puerto Rico/8/34 virus.

While the effect of the influenza A virus non-structural protein (NS) on cytokine production during viral infection is well known, inconsistent results have been observed with some other influenza A virus backbone studied. In this study, in order to focus on the impact of the avian NS gene segments on viral virulence, the NS genes encoded by different strains of avian influenza A viruses were incorporated into an identical [A/Puerto Rico/8/1934(H1N1), PR8] virus background to generate various NS recombinant viruses. Thus, PR8NS, PR8×[A/Hong Kong/483/97(H5N1) 483NS, PR8×[A/Ck/Korea/150/03(H9N2) 150NS, and PR8×[A/EM/Korea/W149/06(H5N1) W149NS were constructed utilizing reverse genetics. Here, we show the effects of each of these recombinant viruses upon viral pathogenesis and cytokine production during viral replication in vivo. In this regard, we found that infection of mice with the PR8×150NS recombinant virus resulted in the lowest pathogenicity (6.0×10(4)MLD50), yet elicited the highest levels of TNF-α production in bronchoalveolar lavage (BAL) fluid compared to infection with the other recombinant influenza viruses. In contrast, infection with the PR8 virus showed the highest pathogenicity (1.0×10(2)MLD50) as well as relatively high cytokine levels (IL-1α, IL-1ß, IL-17, and eotaxin) in mouse BAL fluid. In addition, the PR8 and PR8×483NS viruses induced severe and extensive inflammation in infected lungs compared with that of PR8×150 NS recombinant virus-infected mice. These results clearly demonstrate that the NS genes of diverse influenza A strains can variable impact pathogenicity, histopathology, and cytokine production in mice even when expressed in an identical genetic background.

Thermal analysis of bulk filled composite resin polymerization using various light curing modes according to the curing depth and approximation to the cavity wall.

OBJECTIVE: The purpose of this study was to investigate the polymerization temperature of a bulk filled composite resin light-activated with various light curing modes using infrared thermography according to the curing depth and approximation to the cavity wall. MATERIAL AND METHODS: Composite resin (AeliteFlo, Bisco, Schaumburg, IL, USA) was inserted into a Class II cavity prepared in the Teflon blocks and was cured with a LED light curing unit (Dr's Light, GoodDoctors Co., Seoul, Korea) using various light curing modes for 20 s. Polymerization temperature was measured with an infrared thermographic camera (Thermovision 900 SW/TE, Agema Infra-red Systems AB, Danderyd, Sweden) for 40 s at measurement spots adjacent to the cavity wall and in the middle of the cavity from the surface to a 4 mm depth. Data were analyzed according to the light curing modes with one-way ANOVA, and according to curing depth and approximation to the cavity wall with two-way ANOVA. RESULTS: The peak polymerization temperature of the composite resin was not affected by the light curing modes. According to the curing depth, the peak polymerization temperature at the depth of 1 mm to 3 mm was significantly higher than that at the depth of 4 mm, and on the surface. The peak polymerization temperature of the spots in the middle of the cavity was higher than that measured in spots adjacent to the cavity wall. CONCLUSION: In the photopolymerization of the composite resin, the temperature was higher in the middle of the cavity compared to the outer surface or at the internal walls of the prepared cavity.

Thermal analysis of bulk filled composite resin polymerization using various light curing modes according to the curing depth and approximation to the cavity wall

OBJECTIVE: The purpose of this study was to investigate the polymerization temperature of a bulk filled composite resin light-activated with various light curing modes using infrared thermography according to the curing depth and approximation to the cavity wall. MATERIAL AND METHODS: Composite resin (AeliteFlo, Bisco, Schaumburg, IL, USA) was inserted into a Class II cavity prepared in the Teflon blocks and was cured with a LED light curing unit (Dr's Light, GoodDoctors Co., Seoul, Korea) using various light curing modes for 20 s. Polymerization temperature was measured with an infrared thermographic camera (Thermovision 900 SW/TE, Agema Infra-red Systems AB, Danderyd, Sweden) for 40 s at measurement spots adjacent to the cavity wall and in the middle of the cavity from the surface to a 4 mm depth. Data were analyzed according to the light curing modes with one-way ANOVA, and according to curing depth and approximation to the cavity wall with two-way ANOVA. RESULTS: The peak polymerization temperature of the composite resin was not affected by the light curing modes. According to the curing depth, the peak polymerization temperature at the depth of 1 mm to 3 mm was significantly higher than that at the depth of 4 mm, and on the surface. The peak polymerization temperature of the spots in the middle of the cavity was higher than that measured in spots adjacent to the cavity wall. CONCLUSION: In the photopolymerization of the composite resin, the temperature was higher in the middle of the cavity compared to the outer surface or at the internal walls of the prepared cavity. .