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Made available in DSpace on 2022-04-28T19:42:00Z (GMT). No. of bitstreams: 0 Previous issue date: 2021-07-01 Universidade Estadual do Sudoeste da Bahia Idea Wild Fundação Grupo Boticário de Proteção à Natureza Fundação de Amparo à Pesquisa do Estado da Bahia National Geographic Society The Brazilian Atlantic Forest of Southern Bahia is a megadiverse region given its remarkable number of species and endemism. Despite being a priority region for biodiversity conservation, the role of protected and unprotected forest remnants for long-term species conservation is unknown. Here, we unveil the main patterns of occurrence and distribution of medium- and large-sized mammals in remnants of the Atlantic Forest of Southern Bahia, to generate subsidies for applied conservation strategies. We recorded mammals using camera-traps, active search, and/or line-transect surveys and complemented our species list with literature data. We thus obtained information on richness attributes, relative abundance, and biomass of mammal species per forest remnant, compared assemblages in protected and unprotected areas, and finally investigated both species-area and biomass-area relationships. From 72 forest remnants assessed, we recorded 45 mammal species, including 19 threatened locally. Protected areas were richer in species, especially concerning threatened ones, and concentrated most of the mammal biomass, which presented consistently low values for most areas. The positive and significant species-area and biomass-area relationships further corroborate these patterns since protected areas are larger in size. Despite the historic anthropogenic pressures, we conclude that Southern Bahia still harbors an expressive mammal diversity, with protected areas being critical to maintain most of the species' richness and biomass across the entire region. Nevertheless, small unprotected remnants (

Epidemiologic studies have reported that Asian sand dust (ASD) particles can affect respiratory health; however, the mechanisms remain unclear. We investigated the effects of ASD on airway epithelial cells and immune cells, and their contributing factors to the effects. Human airway epithelial cells were exposed to ASD collected on 1-3 May (ASD1) and on 12-14 May (ASD2) 2011 in Japan and heat-treated ASD1 for excluding heat-sensitive substances (H-ASD) at a concentration of 0, 3, 30 or 90 µg ml(-1) for 4 or 24 h. Furthermore, bone marrow-derived dendritic cells (BMDC) from atopic prone mice were differentiated by culture with granulocyte-macrophage colony-stimulating factor (GM-CSF) then these BMDC were exposed to the ASD for 24 h. Also splenocytes as mixture of immune cells were exposed to the ASD for 72 h. All ASD dose dependently reduced viability of airway epithelial cells. Non-heated ASD showed a dose-dependent increase in the protein release of interleukin (IL)-6 and IL-8. The raises induced by ASD1 were higher than those by ASD2. ASD1 and ASD2 also elevated ICAM-1 at the levels of mRNA, cell surface protein and soluble protein in culture medium. In contrast, H-ASD did not change most of these biomarkers. Non-heated ASD showed enhancement in the protein expression of DEC205 on BMDC and in the proliferation of splenocytes, whereas H-ASD did not. These results suggest that ASD affect airway epithelial cells and immune cells such as BMDC and splenocytes. Moreover, the difference in ASD events and components adhered to ASD can contribute to the health effects.

Although epidemiological studies have demonstrated that cedar pollen influences respiratory health, effective method for inactivating cedar pollen has not been established. Streamer discharge is a type of plasma discharge in which high-speed electrons collide with oxygen and nitrogen molecules. It reportedly has the ability to eliminate bacteria, mould, chemical substances and allergens. The present study investigated the influence of pollen on BEAS-2B cell line, derived from human airway epithelial cells, as well as the efficiency of streamer discharge on pollen-induced health effects. Airway epithelial cells were exposed to non-treated pollen and streamer-discharged pollen at doses of 100 and 1000 μg/mL for 6 or 24 h. Non-treated pollen at a dose of 1000 μg/mL significantly decreased cell viability and induced both mRNA and protein expression of interleukin-6, whereas streamer-discharged pollen showed the attenuated changes as compared with non-treated pollen. Further, scanning electron micrographs showed that streamer discharge caused the fine structural changes of pollen. These results provide the first experimental evidence that pollen at a high dose affects cell viability and inflammatory responses, and streamer discharge technology attenuates their influences by decomposing pollen.

Various metals produced from human activity are ubiquitously detected in ambient air. The metals may lead to induction and/or exacerbation of respiratory diseases, but the significant metals and factors contributing to such diseases have not been identified. To compare the effects of each metal and different oxidation states of metals on human airway, we examined the viability and production of interleukin (IL)-6 and IL-8 using BEAS-2B cell line, derived from human airway epithelial cells. Airway epithelial cells were exposed to Mn2+, V4+, V5+, Cr3+, Cr6+, Zn2+, Ni2+, and Pb2+ at a concentration of 0.5, 5, 50, or 500 μmol/L for 24 hours. Mn and V decreased the cell viability in a concentration-dependent manner, and V5+ tended to have a greater effect than V4+. The Cr decreased the cell viability, and (Cr+6) at concentrations of 50 and 500 μmol/L was more toxic than (Cr+3). Zn at a concentration of 500 μmol/L greatly decreased the cell viability, whereas Ni at the same concentration increased it. Pb produced fewer changes. Mn and Ni at a concentration of 500 μmol/L induced the significant production of IL-6 and IL-8. However, most of the metals including (V+4, V+5), (Cr+3, Cr+6), Zn, and Pb inhibited the production of both IL-6 and IL-8. The present results indicate that various heavy metals have different effects on toxicity and the proinflammatory responses of airway epithelial cells, and those influences also depend on the oxidation states of the metals.

Epidemiologic studies have reported that Asian sand dust (ASD) particles can affect respiratory health; however, the mechanisms remain unclear. We investigated the effects of ASD on airway epithelial cells and immune cells, and their contributing factors to the effects. Human airway epithelial cells were exposed to ASD collected on 1-3 May (ASD1) and on 12-14 May (ASD2) 2011 in Japan and heat-treated ASD1 for excluding heat-sensitive substances (H-ASD) at a concentration of 0, 3, 30 or 90 µg ml(-1) for 4 or 24 h. Furthermore, bone marrow-derived dendritic cells (BMDC) from atopic prone mice were differentiated by culture with granulocyte-macrophage colony-stimulating factor (GM-CSF) then these BMDC were exposed to the ASD for 24 h. Also splenocytes as mixture of immune cells were exposed to the ASD for 72 h. All ASD dose dependently reduced viability of airway epithelial cells. Non-heated ASD showed a dose-dependent increase in the protein release of interleukin (IL)-6 and IL-8. The raises induced by ASD1 were higher than those by ASD2. ASD1 and ASD2 also elevated ICAM-1 at the levels of mRNA, cell surface protein and soluble protein in culture medium. In contrast, H-ASD did not change most of these biomarkers. Non-heated ASD showed enhancement in the protein expression of DEC205 on BMDC and in the proliferation of splenocytes, whereas H-ASD did not. These results suggest that ASD affect airway epithelial cells and immune cells such as BMDC and splenocytes. Moreover, the difference in ASD events and components adhered to ASD can contribute to the health effects.