Polycyclic Aromatic Hydrocarbons (PAHs) in Road Dust Collected from Myanmar, Japan, Taiwan, and Vietnam.

In this study, we determined the concentrations of polycyclic aromatic hydrocarbons (PAHs) in road dust from Myanmar, Japan, Taiwan, and Vietnam. PAHs were detected in urban and rural areas of Myanmar at mean concentrations of 630 ng/g dry weight and 200 ng/g dry weight, respectively. PAHs were also detected in road dust from Vietnam (mean 1700 ng/g) and Taiwan (2400 ng/g). PAH diagnostic ratios suggested that fossil fuel vehicular exhaust and biomass combustion are major sources of PAHs in road dust in Myanmar. Road dust samples from Japan, Taiwan, and Vietnam had similar PAH diagnostic ratios, implying that PAH sources are similar. We assessed the human health risks posed by PAHs in road dust using carcinogenic equivalents (CEQs) and incremental lifetime cancer risk (ILCR). Mean CEQs were decreased in the order Taiwan (173 ng/g) > Vietnam (162 ng/g for Hanoi) > Myanmar (42 and 31 ng/g for Yangon and Pathein, respectively) > Japan (30 ng/g for Kumamoto). Benz[a]pyrene, fluoranthene, and benzo[b]fluoranthene, the predominant PAHs, contributed > 70% of total CEQs. High ILCR values were found for Taiwan (5.9 × 10-4 and 9.9 × 10-4 for children and adults, respectively) and Vietnam (6.5 × 10-4 and 9.2 × 10-4 for children and adults, respectively, in Hanoi), indicating that PAHs in road dust pose cancer risks to the inhabitants of Taiwan and Hanoi. To our knowledge, this is the first report to identify PAH pollution in the environment and to evaluate the human health risks of these PAHs in Myanmar.

Dimorphisms of the proteasome subunit beta type 8 gene (PSMB8) of ectothermic tetrapods originated in multiple independent evolutionary events.

The proteasome subunit beta type 8 gene (PSMB8) encodes one of the beta subunits of the immunoproteasome responsible for the generation of peptides presented by major histocompatibility complex class I molecules. Dimorphic alleles of the PSMB8 gene, termed A and F types, based on the deduced 31st amino acid residue of the mature protein have been reported from various vertebrates. Phylogenetic analysis revealed the presence of dichotomous ancient lineages, one comprising the F-type PSMB8 of basal ray-finned fishes, and the other comprising the A-type PSMB8 of these animals and both the F- and A-type PSMB8 of Xenopus and acanthopterygians, indicating that evolutionary history of the PSMB8 dimorphism was not straightforward. We analyzed the PSMB8 gene of five reptile and one amphibian species and found both the A and F types from all six. Phylogenetic analysis indicated that the PSMB8 F type was apparently regenerated from the PSMB8 A type at least five times independently during tetrapod evolution. Genomic typing of wild individuals of geckos and newts indicated that the frequencies of the A- and F-type alleles are not highly biased in these species. Phylogenetic analysis of each exon of the reptile PSMB8 gene suggested interallelic sequence homogenization as a possible evolutionary mechanism for the apparent recurrent regeneration of PSMB8 dimorphism in tetrapods. An extremely strong balancing selection acting on PSMB8 dimorphism was implicated in an unprecedented pattern of allele evolution.

Replication of a Dog-Origin H6N1 Influenza Virus in Cell Culture and Mice.

The world's first natural avian-origin H6N1 influenza A virus infection case in dogs was confirmed in Taiwan in 2014. The H6N1 virus in chickens has been endemic in Taiwan since 1972. Whether the dog H6N1 virus has interspecies transmission potential is the key issue we aim to understand. Following one virus passage in embryonated eggs and two further passages in MDCK cells, we obtained two virus derivatives, E01EE (PB1 739E and PB2 627E) and E01GK (PB1 739G and PB2 627K), respectively. The pathogenicity of E01EE and E01GK was investigated using plaque assay, growth dynamic analysis and cell viability quantification in cells from different animal species. The impact of amino acid mutation on PB1 739 and PB2 627 on viral ribonucleoprotein (RNP) activity was also analyzed. Further mouse infection experiments were performed. The results showed that both E01EE and E01GK decreased cell relative viability of canine MDCK cells, human A549 cells and chicken DF1 cells. E01Gk caused greater cellular harm in MDCK and A549 cells and had significantly higher virus titers in all of the cells compared to E01EE. The PB2 627K but not PB1 739G was the critical mutation that influenced the viral RNP activity. Both E01EE and E01GK caused mice pneumonia and considerable virus shedding, especially E01GK. This report verifies PB2 E627K mutation in virulence and spotlights the potential for the dog H6N1 virus to extend interspecies transmission.

System identification: DNA computing approach.

A DNA computing algorithm (DNACA) with an electron-ion interaction potential (EIIP) decoding scheme is proposed to identify a class of transfer functions. The DNACA includes enzyme and virus operators which provide a highly modular, flexible, and accurate self-organizing structure environment. Simulation study based on De Jong's test functions show its superior performance when compared with the improved and standard genetic algorithms (GAs).

Serum vascular adhesion protein-1 is increased in acute and chronic hyperglycemia.

BACKGROUND: The relationship between serum vascular adhesion protein-1 (VAP-1) and plasma glucose in normal and drug-naïve type 2 diabetes subjects is unclear. We examined if serum VAP-1 changed acutely to oral glucose loading and analyzed the relationship between serum VAP-1, fasting plasma glucose (FPG), hemoglobin A1c, and type 2 diabetes. METHODS: Adults without history of diabetes were included. Subjects taking anti-diabetic drugs were excluded. Serum VAP-1 was analyzed by time-resolved immunofluorometric assay. RESULTS: We recruited 333 subjects (186 females and 147 males), aged 56.1 +/- 11.6 y. After glucose challenge, serum VAP-1 rose significantly at 30 min (p < 0.0001) and lasted until 2 h (p < 0.0001). The change of serum VAP-1 between fasting and 30-min postload correlated inversely to the change of plasma insulin (r = -0.21, p = 0.049). Fasting serum VAP-1 was associated with FPG in those with FPG > or = 5.55 mmol/l (p = 0.025) but not in those with FPG < 5.55 mmol/l (p = NS). Fasting serum VAP-1 were higher in diabetic subjects (p = 0.04) and correlated positively to hemoglobin A1c (r = 0.18, p = 0.002) after adjusting for age, gender, and waist circumference. CONCLUSIONS: Serum VAP-1 is increased in both acute and chronic hyperglycemia. Whether serum VAP-1 is a good biomarker for hyperglycemia-associated complications merits further investigation.