Utilization of a waste glycerol fraction using and reusing immobilized Gluconobacter oxydans ATCC 621 cell extract

Background: Depletion of petroleum resources has enforced the search for alternative sources of renewable energy. Introduction of biofuels into the market was expected to become a solution to this disadvantageous situation. Attempts to cover fuel demand have, however, caused another severe problem­the waste glycerol generated during biodiesel production at a concentration of approximately 10% w/w. This, in turn, prompted a global search for effective methods of valorization of the waste fraction of glycerol. Results: Utilization of the waste fraction at 48 h with an initial glycerol concentration of 30 g·L-1 and proceeding with 62% efficiency enabled the production of 9 g·L-1 dihydroxyacetone at 50% substrate consumption. The re-use of the immobilized biocatalyst resulted in a similar concentration of dihydroxyacetone (8.7 g·L-1) in two-fold shorter time, with an efficiency of 85% and lower substrate consumption (35%). Conclusions: The method proposed in this work is based on the conversion of waste glycerol to dihydroxyacetone in a reaction catalyzed by immobilized Gluconobacter oxydans cell extract with glycerol dehydrogenase activity, and it could be an effective way to convert waste glycerol into a valuable product.

Whole cell & culture filtrate proteins from prevalent genotypes of Mycobacterium tuberculosis provoke better antibody & T cell response than laboratory strain H37Rv.

Background & objectives: The immune responses to different antigens of Mycobacterium tuberculosis H37Rv vary from patient to patient with tuberculosis (TB). Therefore, significant difference might be documented between the H37Rv with long histories of passages and recent clinical isolates of M. tuberculosis. In the present study, immune response of TB patients and healthy controls against 39 clinical M. tuberculosis isolates was correlated with laboratory strain H37Rv. Methods: The antibody response was studied coating whole cell extracts and culture filtrate proteins of M. tuberculosis isolates and laboratory strain H37Rv by enzyme linked immunosorbent assay (ELISA). Lymphoproliferation was studied by incorporation of tritiated thymidine and cytokines (IFN-γ and IL-4) by using commercially available kits. Results: Sero-reactivity to whole cell extract (WCE) of 11 clinical isolates was higher with pooled serum and individual's serum from tuberculosis patients showed significant reactivity (P<0.05) to ten of these isolates using ELISA. Of the WCE of 39 clinical isolates, 10 were found to be potent inducer of lymphoproliferation as well as cytokine secretion (P<0.05) in peripheral blood mononuclear cells from PPD+ healthy controls. Six culture filtrate proteins (CFPs) from these selected clinical isolates were also better inducers of antibody and T-cell response. Interpretation & conclusion: Overall, our results revealed that the clinical isolates belonging to prevalent genotypes; CAS1_Del (ST-26), East African-Indian (ST-11) and Beijing family (ST-1) induced better antibody and T cell responses compared to H37Rv laboratory strain. Further studies need to be done to purify and identify the dominant protein (s) using whole cell extract and culture filtrates from these immunologically relevant clinical M. tuberculosis isolates, which will be worthwhile to find out pathogenic factors, potential diagnostic markers and protective molecules for tuberculosis.

Effects of Adipose-derived Stromal Cells and of their Extract on Wound Healing in a Mouse Model

In this study, the authors investigated the effects of adipose-derived stromal cells (ADSCs) and of their extract on wound healing. After creating wound healing splint model on the backs of mice, ADSCs and their extract were applied. Wound healing rates were calculated at 3, 5, 7, 10, and 14 days after the wounding, and tissues were harvested at 7 and 14 days for histological analysis. Wound healing rates were significantly higher at 7, 10, and 14 days in the cell group than in the control, but in the cell extract group wound healing rates were significantly decreased (P<0.05). Histological scores and capillary densities in the cell group were significantly higher at 2 weeks (P<0.05). In the cell group, thick inflammatory cell infiltration and many capillaries were observed at 1 week, and thick epithelium and numerous large capillaries were observed at 2 weeks. The present study suggests that ADSCs accelerate wound healing as known, and the effects of ADSCs on wound healing may be due to replacing insufficient cells by differentiation of ADSCs in the wound and secreting growth factors by differentiated cells, and not due to the effect of factors within ADSCs.