Cytokines induce effector T-helper cells during invasive aspergillosis; what we have learned about T-helper cells?

Invasive aspergillosis caused by Aspergillus species (Aspergillus fumigatus, A. flavus and A. terreus) is life-threatening infections in immunocompromised patients. Understanding the innate and adaptive immune response particularly T-helper cells (TH-cells) against these Aspergillus species and how the different sub-set of TH-cells are regulated by differentiating cytokines at primary target organ site like lung, kidney and brain is of great significance to human health. This review focuses on presentation of Aspergillus through Antigen presenting cells (APCs) to the naive CD4+ T-cells in the host. The production of differentiating/effector cytokines that activate following TH-cells e.g., TH1, TH2, TH9 and TH17 has been reported in association or alone in allergic or invasive aspergillosis. Chemokines (CXCL1, CXCL2, CCL1 and CCL20) and their receptors associated to these TH-cells have also been observed in invasive aspergillosis. Thus, further study of these TH-cells in invasive aspergillosis and other elements of adaptive immune response with Aspergillus species are required in order to have a better understanding of host response for safer and effective therapeutic outcome

Design and Development of Site Specific Grape Vineyard Fertilizer Applicator Prototype

402-407The current fertiliser application methods for grape vines are labour intensive and lead to overuse of fertiliser. Frequent rain and vineyard orchard wash over often pollute water sources. Therefore, the right amount and placement of fertiliser can not only improve crop growth but also reduce the risk of chemicals to human health and the environment. To overcome the above problems a site specific fertiliser applicator for grape vineyard with mechanical sensing system was developed. The sensing system was designed to apply fertiliser to the root zone of the plant canopy. An experimental unit was developed to optimise design and operation parameters for fertiliser production per plant. The urea's physical and engineering qualities were determined for metering mechanism design. The average value of bulk density, angle of repose, urea grain diameter, grain weight in single flute measured were 0.759 ± 0.011 gcm−3, 26.22 ± 1.18°, 3.38 ± 0.23 mm, 1.46 ± 0.04 g, respectively. The coefficient of static friction with plywood, galvanised iron and mild steel with painted surface were observed 0.3177 ± 0.0092, 0.2868 ± 0.0077, and 0.3177 ± 0.0092, respectively. For fertiliser given per plant, the effect of exposure length was p < 0.001. The sensor device opens the delivery tube for fertiliser in 0.9–0.95s

Partial Inhibition of Estrogen-Induced Mammary Carcinogenesis in Rats by Tamoxifen: Balance between Oxidant Stress and Estrogen Responsiveness

Epidemiological and experimental evidences strongly support the role of estrogens in breast tumor development. Both estrogen receptor (ER)-dependent and ER-independent mechanisms are implicated in estrogen-induced breast carcinogenesis. Tamoxifen, a selective estrogen receptor modulator is widely used as chemoprotectant in human breast cancer. It binds to ERs and interferes with normal binding of estrogen to ERs. In the present study, we examined the effect of long-term tamoxifen treatment in the prevention of estrogen-induced breast cancer. Female ACI rats were treated with 17β-estradiol (E2), tamoxifen or with a combination of E2 and tamoxifen for eight months. Tissue levels of oxidative stress markers 8-iso-Prostane F2α (8-isoPGF2α), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase, and oxidative DNA damage marker 8-hydroxydeoxyguanosine (8-OHdG) were quantified in the mammary tissues of all the treatment groups and compared with age-matched controls. Levels of tamoxifen metabolizing enzymes cytochrome P450s as well as estrogen responsive genes were also quantified. At necropsy, breast tumors were detected in 44% of rats co-treated with tamoxifen+E2. No tumors were detected in the sham or tamoxifen only treatment groups whereas in the E2 only treatment group, the tumor incidence was 82%. Co-treatment with tamoxifen decreased GPx and catalase levels; did not completely inhibit E2-mediated oxidative DNA damage and estrogen-responsive genes monoamine oxygenase B1 (MaoB1) and cell death inducing DFF45 like effector C (Cidec) but differentially affected the levels of tamoxifen metabolizing enzymes. In summary, our studies suggest that although tamoxifen treatment inhibits estrogen-induced breast tumor development and increases the latency of tumor development, it does not completely abrogate breast tumor development in a rat model of estrogen-induced breast cancer. The inability of tamoxifen to completely inhibit E2-induced breast carcinogenesis may be because of increased estrogen-mediated oxidant burden

Predicting biodiversity richness in rapidly changing landscapes: climate, low human pressure or protection as salvation?

Rates of biodiversity loss in Southeast Asia are among the highest in the world, and the Indo-Burma and South-Central China Biodiversity Hotspots rank among the world’s most threatened. Developing robust multi-species conservation models is critical for stemming biodiversity loss both here and globally. We used a large and geographically extensive remote-camera survey and multi-scale, multivariate optimization species distribution modelling to investigate the factors driving biodiversity across these two adjoining biodiversity hotspots. Four major findings emerged from the work. (i) We identified clear spatial patterns of species richness, with two main biodiverse centres in the Thai-Malay Peninsula and in the mountainous region of Southwest China. (ii) Carnivores in particular, and large ungulates to a lesser degree, were the strongest indicators of species richness. (iii) Climate had the largest effect on biodiversity, followed by protected status and human footprint. (iv) Gap analysis between the biodiversity model and the current system of protected areas revealed that the majority of areas supporting the highest predicted biodiversity are not protected. Our results highlighted several key locations that should be prioritized for expanding the protected area network to maximize conservation effectiveness. We demonstrated the importance of switching from single-species to multi-species approaches to highlight areas of high priority for biodiversity conservation. In addition, since these areas mostly occur over multiple countries, we also advocate for a paradigmatic focus on transboundary conservation planning.The majority of the team, as well as the data, were part of the core WildCRU effort supported principally by a Robertson Foundation grant to DWM