Uncertainty quantification of granular computing-neural network model for prediction of pollutant longitudinal dispersion coefficient in aquatic streams.

Discharge of pollution loads into natural water systems remains a global challenge that threatens water and food supply, as well as endangering ecosystem services. Natural rehabilitation of contaminated streams is mainly influenced by the longitudinal dispersion coefficient, or the rate of longitudinal dispersion (Dx), a key parameter with large spatiotemporal fluctuations that characterizes pollution transport. The large uncertainty in estimation of Dx in streams limits the water quality assessment in natural streams and design of water quality enhancement strategies. This study develops an artificial intelligence-based predictive model, coupling granular computing and neural network models (GrC-ANN) to provide robust estimation of Dx and its uncertainty for a range of flow-geometric conditions with high spatiotemporal variability. Uncertainty analysis of Dx estimated from the proposed GrC-ANN model was performed by alteration of the training data used to tune the model. Modified bootstrap method was employed to generate different training patterns through resampling from a global database of tracer experiments in streams with 503 datapoints. Comparison between the Dx values estimated by GrC-ANN to those determined from tracer measurements shows the appropriateness and robustness of the proposed method in determining the rate of longitudinal dispersion. The GrC-ANN model with the narrowest bandwidth of estimated uncertainty (bandwidth-factor = 0.56) that brackets the highest percentage of true Dx data (i.e., 100%) is the best model to compute Dx in streams. Considering the significant inherent uncertainty reported in the previous Dx models, the GrC-ANN model developed in this study is shown to have a robust performance for evaluating pollutant mixing (Dx) in turbulent environmental flow systems.

ATG16L1 regulated IL-22 induced IFN level in Pseudomonas aeruginosa Lung Infection via cGAS signal passage.

OBJECTIVE: This study explored that the possible effects and mechanism of ATG16L1 in pseudomonas aeruginosa lung infection. METHODS: C57BL/6J mice were anesthetized with isoflurane and intratracheally (I.T.) inoculated with 5 × 106 CFU of Pseudomonas aeruginosa strain PA14. RAW264.7 macrophages were stimulated with 0.1 mg/ml of lipopolysaccharide (LPS). RAW264.7 macrophages were stimulated with 0.1 mg/ml LPS. Hematoxylin-Eosin (H&E), Immunofluorescence, sample acquisition, qPCR validation, Enzyme linked immunosorbent assay (ELISA) and immunofluorescence analysis were used this experiment. RESULTS: ATG16L1 mRNA and protein expressions in mice with pseudomonas aeruginosa lung infection were also suppressed. ATG16L1 gene reduced inflammation and INF-γ levels in vitro model. On the other hand, ATG16L1 protein presented lung injury and inflammation levels in mice of pseudomonas aeruginosa lung infection. ATG16L1 regulated cGAS/IL-22 signal passage in model of pseudomonas aeruginosa lung onfection. CONCLUSION: These findings indicate that ATG16L1 reduced IL-22 induced IFN level in pseudomonas aeruginosa lung infection via cGAS signal passage, which may provide a new therapeutic scheme for viral diseases or inflammatory diseases and its associated complications.

The JAK/STAT3 signaling pathway mediates inhibition of host cell apoptosis by Chlamydia psittaci infection.

The JAK-STAT3 signaling pathway is a key regulator of cell growth, motility, migration, invasion and apoptosis in mammalian cells. Infection with intracellular pathogens of the genus Chlamydia can inhibit host cell apoptosis, and here we asked whether the JAK-STAT3 pathway participates in chlamydial anti-apoptotic activity. We found that, compared with uninfected cells, levels of JAK1 and STAT3 mRNA as well as total and phosphorylated JAK1 and STAT3 protein, were significantly increased in C. psittaci-infected HeLa cells. Moreover, the apoptosis rate of infected cells was higher after treatment with the tyrosine kinase inhibitor AG-490 (2-cyano-3-(3, 4-dihydroxyphenyl)-N-(phenylmethyl)-2-propenamide). Immunoblotting of apoptosis-related proteins showed that C. psittaci infection reduces Bax, but increases Bcl-2, protein levels, resulting in reduced activation of caspase-3, caspase-7, caspase-9 and PARP; AG490 attenuates these effects. Together, our data suggest that the JAK/STAT3 signaling pathway facilitates the anti-apoptotic effect of C. psittaci infection by reducing the Bax/Bcl-2 apoptotic switch ratio, and by inhibiting the intracellular activation of key pro-apoptotic enzymes.

Deficiency of LIGHT signaling pathway exacerbates Chlamydia psittaci respiratory tract infection in mice.

LIGHT, a costimulatory member of the immunoglobulin superfamily (Ig SF), can greatly impact T cell activation. The role of the LIGHT signaling pathway in chlamydial infection was evaluated in mice following respiratory tract infection with Chlamydia psittaci. Compared with wild type (WT) mice, LIGHT knockout (KO) mice showed significant reduction of body weight, much lower survival rate, higher bacterial burden, prolonged infection time courses and more severe pathological changes in lung tissue. The mRNA levels of IFN-γ, TNF-α, IL-17 and IL-12 in the lung tissue of LIGHT KO mice were significantly lower than those in WT mice. While there was no obvious difference in the percentages of CD4+ and CD8+ T cells in the spleens of the two groups of mice, there was a markedly elevated percentage of CD4+ CD25+ FoxP3+ Treg cells in LIGHT KO mice. Together, these results demonstrate that the LIGHT signaling pathway is not only required for inflammatory cytokine production as part of the host response to chlamydial infection, but also influences the differentiation of CD4+ CD25+ FoxP3+ Treg cells, both of which may be essential for control of C. psittaci respiratory tract infection.

[Role of LIGHT signal pathway in Chlamydia muridarum urogenital infection in mice].

OBJECTIVE: To study the role of lymphotoxin-like inducible protein that competes with glycoprotein D for herpesvirus entry on T cells (LIGHT) in the development of protective immunity and pathology during Chlamydia Muridarum urogenital infection in mice. METHODS: C57BL/6J wild type (wt) and mice deficient in LIGHT (LIGHT KO) were inoculated intravaginally with 1 x 10(4) IFUs of live C. muridarum organisms. Half mice of each group were reinfected on day 49 after primary infection. We took mice vaginal swabs every 3 or 4 days to monitor live organism shedding. On day 80 after the primary infection, mice were sacrificed, the vaginal tract was isolated for pathology analysis. The spleen cells were collected and IL-4, IL-5, IL-17 and IFN-y were detected by ELISA in the spleen cells culture supernatant after restimulated by UV-MoPn EB. The titers of different Ab isotypes were measured in mice serum by Indirect Immunofluorescence Assay. RESULTS: The chlamydia shedding time of LIGHT KO mice was similar to wild type mice, which cleared the organisms within 28 days after primary infection, and acquired protective immunity against C. muridarum reinfection. All mice regardless of genotypes developed severe upper genital tract pathology and showed no significant difference between LIGHT KO and wild type mice. All mice developed robust anti-C. muridarum organism IgG antibody responses and the ratios of IgG2a versus IgG1 showed no significant difference between LIGHT KO and wild type mice. Splenocytes from MoPn-infected LIGHT KO and wild type mice produced high levels of IFN-gamma and IL-17, but IL-4 and IL-5 couldn't be detected. CONCLUSIONS: LIGHT signal pathway may not correlated with protection against C. muridarum urogenital tract infection and urogenital tract pathology induced by C. muridarum.