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The article presents a study which discusses the application of a regional Community Multi-scale Air Quality (CMAQ) modelling system at a hemispheric scale to investigate the atmospheric circulation of an air pollutant such as mercury. It relates that aircraft and ground measurements were performed to determine total gaseous mercury (TGM) concentration in the atmosphere. It mentions that the study also make used of two simulation methods.

Background Over 40% of chronic stable asthma patients have evidence of respiratory Mycoplasma pneumoniae (Mp) infection as detected by PCR, but not by serology and culture, suggesting that a low-level Mp is involved in chronic asthma. However, the role of such a low-level Mp infection in the regulation of allergic inflammation remains unknown. Objective To determine the impact of a low-level Mp infection in mice with established airway allergic inflammation on allergic responses such as eosinophilia and chemokine eotaxin-2, and the underlying mechanisms [i.e. the prostaglandin E2 (PGE2) pathway] since PGE2 inhalation before an allergen challenge suppressed the eosinophil infiltration in human airways. Methods BALB/c mouse models of ovalbumin (OVA)-induced allergic asthma with an ensuing low- or high-dose Mp were used to assess IL-4 expression, bronchoalveolar lavage (BAL) eosinophil, eotaxin-2 and PGE2 levels, and lung mRNA levels of microsomal prostaglandin E synthase-1 (mPGES-1). Primary alveolar macrophages (pAMs) from naïve BALB/c mice were cultured to determine whether Mp-induced PGE2 or exogenous PGE2 down-regulates IL-4/IL-13-induced eotaxin-2. Results Low-dose Mp in allergic mice significantly enhanced IL-4 and eotaxin-2, and moderately promoted lung eosinophilia, whereas high-dose Mp significantly reduced lung eosinophilia and tended to decrease IL-4 and eotaxin-2. Moreover, in both OVA-naïve and allergic mice, lung mPGES-1 mRNA and BAL PGE2 levels were elevated in mice infected with high-dose, but not low-dose Mp. In pAMs, IL-4/IL-13 significantly increased eotaxin-2, which was reduced by Mp infection accompanied by dose-dependent PGE2 induction. Exogenous PGE2 inhibited IL-4/IL-13-induced eotaxin-2 in a dose-dependent manner. Conclusions This study highlights a novel concept on how different bacterial loads in the lung modify the established allergic airway inflammation and thus interact with an allergen to further induce Th2 responses. That is, unlike high-level Mp, low-level Mp fails to effectively induce PGE2 to down-regulate allergic responses (e.g. eotaxin-2), thus maintaining or even worsening allergic inflammation in asthmatic airways. [ABSTRACT FROM AUTHOR]

East Asia contributes nearly 50% of the global anthropogenic mercury emissions into the atmosphere. Recently, there are concerns for the long-range transport of mercury from East Asia to North America, which may lead to enhanced dry and wet depositions in North America. In this study, we performed four monthly simulations (January , April, July and October in 2005) using CMAQ-Hg v4.6 in an East Asian model domain. Coupled with a mass balance analysis and a number of emission inventory scenarios, the chemical transport of atmospheric mercury, the seasonal mercury transport budgets and mercury emission outflow from the East Asian region were investigated. The total annual mercury deposition in the region for the modeling year is estimated to be 821 Mg, with 396 Mg contributed by wet deposition and 425 Mg contributed by dry deposition. Regional mercury transport budgets show strong seasonal variability, with a net removal of RGM (7∼5 Mg mo-1) and PHg (13∼21 Mg mo-1), and a net export of GEM (60∼130 Mg mo-1) from the study domain. The annual outflow caused by the East Asian emission is estimated to be in the range of 1369∼1671 Mg yr-1, primarily in the form of GEM. This represents about 75% of the total mercury emissions (anthropogenic and natural) in the region. The emission outflow from this source region would contribute to 20∼30% of mercury deposition in areas remote from anthropogenic emission sources. [ABSTRACT FROM AUTHOR]

Speciated samples of PM2.5 were collected at the Hamshire and Orange sites in Golden Triangle of Texas by US EPA (Environmental Protection Agency) from July of 2003 to August of 2005. A total of 269 samples for the Hamshire site and 293 samples for the Orange site with 52 species were measured; however, 22 species were excluded because of too many below-detectionlimit data. Among the 22 species excluded, 20 species are common to both sites. Due to the laboratory change about November 1st of 2004 and possible analytical artifacts, phosphorous was excluded as well. The two data sets were analyzed by positive matrix factorization (PMF) to infer the sources of PM observed at the two sites. The analysis identified nine common source-related factors: sulfaterich secondary aerosol, cement/carbon-rich, wood smoke, motor vehicle/road dust, metal processing, nitrate-rich secondary aerosol, soil, sea salt, and chloride depleted marine aerosol. Sulfate and nitrate mainly exist as ammonium salts. The sulfate-rich secondary aerosol accounts for 42% and 43% of the PM mass concentrations at the Hamshire and the Orange sites, respectively. The factor containing highest concentrations of Cl and Na was attributed to sea salt due to the proximity of the monitoring sites to the Gulf of Mexico. The chloride depleted marine aerosol was related to the sea salt aerosol but was identified separately due to the chlorine replacement reactions. Basically, the factors of sulfate, motor vehicle/road dust, nitrate, soil, sea salt, and chloride depleted marine aerosol at the two sites showed similar chemical composition profiles and seasonal variation reflecting these six factors were likely to be Golden Triangle regionally related sources. Cement/carbon-rich, wood smoke, and metal processing factor were likely to be the local sources. [ABSTRACT FROM AUTHOR]

Background: Although airway angiogenesis and edema have been proposed to contribute to the airway remodeling process in patients with asthma, there are few studies looking at these structural components in the airway tissue of asthma patients. Mycoplasma infection may be associated with chronic asthma and has been shown to induce angiogenesis and edema in a murine model.Participants and Measurements: We evaluated blood vessels and edema by immunohistochemistry in endobronchial biopsy samples from 10 normal control subjects and 15 patients with mild-to-moderate asthma before and after a 6-week treatment with clarithromycin (n = 8) or placebo (n = 7). Type IV collagen and alpha(2)-macroglobulin were used to identify blood vessels and edema in the tissue, respectively. Mycoplasma pneumoniae was evaluated by polymerase chain reaction.Setting: National Jewish Medical and Research Center.Results: At baseline, the vascularity, the number of blood vessels, and the edematous area in the airway tissue were not significantly different between asthmatic patients and normal control subjects. However, asthmatic patients demonstrated increased blood vessel size compared with normal control subjects (p = 0.03). After clarithromycin treatment in asthmatic patients, the number of blood vessels was increased (p = 0.02), while edema decreased (p = 0.049). Asthmatic patients who tested positive for M pneumoniae showed a significant increase in vascularity than asthmatic patients who tested negative for M pneumoniae (p = 0.02).Conclusion: Our data suggest that angiogenesis and edema may not be significant features of airway remodeling in patients with chronic, mild-to-moderate asthma. Clarithromycin treatment in asthmatic patients could reduce the edematous area as identified by alpha(2)-macroglobulin staining, which may lead to airway tissue shrinkage and cause an artificial increase in the number of blood vessels. [ABSTRACT FROM AUTHOR]

T lymphocytes and eosinophils are probably involved in the pathogenesis of allergic bronchopulmonary aspergillosis (ABPA), a disease characterized by pulmonary eosinophilia and high serum and lavage IgE levels. We recently developed a murine model of ABPA. To investigate the mechanisms of T lymphocyte and eosinophil recruitment to the lung in this disease, we examined the expression of ICAM-1 in the lung tissue of mouse challenged with Aspergillus fumigatus (Af) antigen, C57B1/6 mice were intranasally exposed to Af (Af group) or saline (control group) three times a week for 1, 2 or 3 weeks. On days 4, 7,14 and 21, mice were killed and lung tissue was fixed in acetone and embedded in glycol methacrylate. Serial 2-µm sections were stained with chromotrope 2R and MoAbs against ICAM-1, CD11a/CD18 (LFA-1) and CD3. Af-challenged mice presented significant increases in eosinophil, T lymphocyte and LFA-1-positive cell count and up-regulated expression of ICAM-1 in the lung tissue at all the time points examined. ICAM-1 expression intensity correlated with the number of T lymphocytes (r = 0.59, P < 0.01), LFA-1- positive cells (r = 0.68, P < 0.001), but not of eosinophils (r = -0.24, P > 0.05). These findings suggest that up-regulation of ICAM-1 expression is involved in the inflammatory process of this murine model of ABPA, and that this up-regulation may be more relevant to the T lymphocyte accumulation in the lung. [ABSTRACT FROM AUTHOR]

Coherent A1(LO) phonon and its coupling with photoexcited plasmon in wurtzite InN were generated and detected with time-resolved second-harmonic generation. The experimental results directly reveal that the plasma damping time constant is about 60∼120 fs, which depends on the photoexcited plasma density in InN. The frequency of the upper-branch A1(LO) phonon-plasmon coupling mode shifts as a function of the photoexcited plasma density. This frequency shift can be fitted consistently with different InN films by solving the InN dielectric response function and leads to the determination of the electron effective mass m∥*=(0.033±0.003)me, parallel to the c axis of wurtzite InN. [ABSTRACT FROM AUTHOR]