2016

Leading exosome biotechnology laboratory. Specializes in the production of perinatal MSC-derived exosome products for cosmetic treatment. Request a lab tour.

Leading exosome biotechnology laboratory. Specializes in the production of perinatal MSC-derived exosome products for cosmetic treatment. Request a lab tour.

Leading exosome biotechnology laboratory. Specializes in the production of perinatal MSC-derived exosome products for cosmetic treatment. Request a lab tour.

Leading exosome biotechnology laboratory. Specializes in the production of perinatal MSC-derived exosome products for cosmetic treatment. Request a lab tour.

Leading exosome biotechnology laboratory. Specializes in the production of perinatal MSC-derived exosome products for cosmetic treatment. Request a lab tour.

Leading exosome biotechnology laboratory. Specializes in the production of perinatal MSC-derived exosome products for cosmetic treatment. Request a lab tour.

Leading exosome biotechnology laboratory. Specializes in the production of perinatal MSC-derived exosome products for cosmetic treatment. Request a lab tour.

Leading exosome biotechnology laboratory. Specializes in the production of perinatal MSC-derived exosome products for cosmetic treatment. Request a lab tour.

Leading exosome biotechnology laboratory. Specializes in the production of perinatal MSC-derived exosome products for cosmetic treatment. Request a lab tour.

Leading exosome biotechnology laboratory. Specializes in the production of perinatal MSC-derived exosome products for cosmetic treatment. Request a lab tour.

Leading exosome biotechnology laboratory. Specializes in the production of perinatal MSC-derived exosome products for cosmetic treatment. Request a lab tour.

Leading exosome biotechnology laboratory. Specializes in the production of perinatal MSC-derived exosome products for cosmetic treatment. Request a lab tour.

Leading exosome biotechnology laboratory. Specializes in the production of perinatal MSC-derived exosome products for cosmetic treatment. Request a lab tour.

Leading exosome biotechnology laboratory. Specializes in the production of perinatal MSC-derived exosome products for cosmetic treatment. Request a lab tour.

Leading exosome biotechnology laboratory. Specializes in the production of perinatal MSC-derived exosome products for cosmetic treatment. Request a lab tour.

The previous page is sending you to http://www.medipjournals.com/index.php/ijbcp/article/download/2162/2012. If you do not want to visit that page, you can return to the previous page.

Ralstonia solanacearum causes bacterial wilt disease, leading to severe crop losses. Xylem sap from R. solanacearum-infected tomato is enriched in the disaccharide trehalose. Water-stressed plants also accumulate trehalose, which increases drought tolerance via abscisic acid (ABA) signaling. Because R. solanacearum-infected plants suffer reduced water flow, we hypothesized that bacterial wilt physiologically mimics drought stress, which trehalose could mitigate. We found that R. solanacearum-infected plants differentially expressed drought-associated genes, including those involved in ABA and trehalose metabolism, and had more ABA in xylem sap. Consistent with this, treating tomato roots with ABA reduced both stomatal conductance and stem colonization by R. solanacearum. Treating roots with trehalose increased xylem sap ABA and reduced plant water use by lowering stomatal conductance and temporarily improving water use efficiency. Trehalose treatment also upregulated expression of salicylic acid (SA)-dependent tomato defense genes; increased xylem sap levels of SA and other antimicrobial compounds; and increased bacterial wilt resistance of SA-insensitive NahG tomato plants. Additionally, trehalose treatment increased xylem concentrations of jasmonic acid and related oxylipins. Finally, trehalose-treated plants were substantially more resistant to bacterial wilt disease. Together, these data show that exogenous trehalose reduced both water stress and bacterial wilt disease and triggered systemic disease resistance, possibly through a Damage Associated Molecular Pattern (DAMP) response pathway. This suite of responses revealed unexpected linkages between plant responses to biotic and abiotic stress and suggested that R. solanacearum-infected plants increase trehalose to improve water use efficiency and increase wilt disease resistance. The pathogen may degrade trehalose to counter these efforts. Together, these results suggest that treating tomatoes with exogenous trehalose could be a practical strategy for bacterial wilt management.

Burkhard Ludewig DVM is Head of the Medical Research Centre of the Kantonsspital St Gallen, Switzerland (Figure 1). His investigative work in cardio immuno

Background Cancer metastasis is the main cause leading to disease recurrence and high mortality in cancer patients. Therefore, inhibiting metastasis process or killing metastatic cancer cells by inducing apoptosis is of clinical importance in improving cancer patient survival. Previous studies revealed that fucoidan, a fucose-rich polysaccharide isolated from marine brown alga, is a promising natural product with significant anti-cancer activity. However, little is known about the role of endoplasmic reticulum (ER) stress in fucoidan-induced cell apoptosis. Principal Findings We reported that fucoidan treatment inhibits cell growth and induces apoptosis in cancer cells. Fucoidan treatments resulted in down-regulation of the glucose regulated protein 78 (GRP78) in the metastatic MDA-MB-231 breast cancer cells, and of the ER protein 29 (ERp29) in the metastatic HCT116 colon cancer cells. However, fucoidan treatment promoted ER Ca2+-dependent calmodulin-dependent kinase II (CaMKII) phosphorylation, Bcl-associated X protein (Bax) and caspase 12 expression in MDA-MB-231 cells, but not in HCT116 cells. In both types of cancer cells, fucoidan activated the phosphorylation of eukaryotic initiation factor 2 alpha (p-eIF2α)\CCAAT/enhancer binding protein homologous protein (CHOP) pro-apoptotic cascade and inhibited the phosphorylation of inositol-requiring kinase 1 (p-IRE-1)\X-box binding proteins 1 splicing (XBP-1s) pro-survival cascade. Furthermore, CHOP knockdown prevented DNA damage and cell death induced by fucoidan. Conclusion/Significance Fucoidan exerts its anti-tumor function by modulating ER stress cascades. Contribution of ER stress to the fucoidan-induced cell apoptosis augments our understanding of the molecular mechanisms underlying its anti-tumour activity and provides evidence for the therapeutic application of fucoidan in cancer.

Cardiovascular diseases, including heart attacks and strokes, continue to be the leading causes of deaths resulting in more than 17 million deaths each year worldwide. Cardiovascular disease (CVD) man...