Home About us Contact
|
Home About us Contact | ||
|
|
||
Viable Cell Number (viable + cell_number)
Selected AbstractsSimultaneous saccharification and fermentation of sludge-containing cassava mash for batch and repeated batch production of bioethanol by Saccharomyces cerevisiae CHFY0321JOURNAL OF CHEMICAL TECHNOLOGY & BIOTECHNOLOGY, Issue 4 2009Gi-Wook Choi Abstract BACKGROUND: The aim of this study was to examine the repeated batch production of bioethanol from sludge-containing cassava mash as starchy substrate by flocculating yeast to improve volumetric bioethanol productivity and to simplify the process of a pre-culture system. RESULTS: For the repeated batch production of bioethanol using cassava mash, the optimal recycling volume ratio was found to be 5%. The repeated batch fermentation was completed within 36 h, while the batch fermentation was completed after 42 h. Volumetric productivity, final ethanol concentration, and ethanol yield were attained to 2.15 g L,1 h,1, 83.64 g L,1, and 85.15%, respectively. Although cell accumulation in the repeated batch process is difficult due to the cassava mash, the repeated batch process using Saccharomyces cerevisiae CHFY0321 could exhibited 10-fold higher initial viable cell number (1.7 × 107 CFU mL,1) than that of the batch process. CONCLUSION: The liquefied cassava powder was directly used for the repeated batch process without removal of sludge. Repeated batch bioethanol production by simultaneous saccharification and fermentation using self-flocculating yeast could reduce process costs and accelerate commercial applications. This result was probably due in part to the effect of the initial viable cell density. Copyright © 2008 Society of Chemical Industry [source] Protective effect of vitamin E on ultraviolet B light,induced damage in keratinocytesMOLECULAR CARCINOGENESIS, Issue 3 2002Samar Maalouf Abstract Ultraviolet (UV) B radiation is the most common environmental factor in the pathogenesis of skin cancer. Exposure of human skin to UVB radiation leads to the depletion of cutaneous antioxidants, the activation of nuclear factor kappa B (NF-,B), and programmed cell death (apoptosis). Although antioxidant supplementation has been shown to prevent UVB-induced photooxidative damage, its effect on components of cell signaling pathways leading to gene expression has not been clearly established. In the present study, the effect of the antioxidant vitamin, ,-tocopherol (,-T), and its acetate analog, ,-tocopherol acetate (,-TAc), on UVB-induced damage in primary and neoplastic mouse keratinocytes was investigated. The ability of both vitamins to modulate UVB-induced apoptosis and activation of the transcription factor NF-,B were studied. Treatment of normal and neoplastic mouse epidermal keratinocytes (308 cells) with 30,60 mJ/cm2 UVB markedly decreased viable cell number and was accompanied by DNA fragmentation. When both vitamins were applied to cells at times before and after UVB radiation, a significant increase in the percentage of viable cells and concomitant decrease in the number of apoptotic cells was noted, with vitamin pretreatment providing a better protection than posttreatment. Simultaneous posttreatment of irradiated cells with ,-TAc abolished the cytotoxic effects of UVB and restored cell viability to control levels. In addition, simultaneous posttreatment of irradiated cells with ,-T reduced the number of apoptotic cells by half, indicating a synergistic effect of two such treatments compared with any single one. Flow cytometry analysis indicated that vitamin treatment suppressed both an increase in pre-G0 cells and a decrease in cycling cells by UVB exposure. In addition, NF-,B activation was detected 2 h after UV exposure and was maintained for up to 8 h. Pretreatment with vitamins significantly inhibited NF-,B activation at 4 and 8 h. These results indicate that vitamin E and its acetate analog can modulate the cellular response to UVB partly through their action on NF-,B activation. Thus, these antioxidant vitamins are potential drugs for the protection from or the reduction of UVB-associated epidermal damage. © 2002 Wiley-Liss, Inc. [source] Time-course Expression of DNA Repair-related Genes in Hepatocytes of Zebrafish (Danio rerio) After UV-B ExposurePHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 1 2009Juliana Z. Sandrini The objective of this study was to evaluate the time-course effects of UV-B exposure on expression of genes involved in the DNA repair system of zebrafish (Danio rerio) hepatocytes, a highly competent species in terms of damage repair induced by UV radiation. For gene expression analysis (RT-PCR), cells were exposed to 23.3 mJ cm,2 UV-B, which was the dose that affected viable cell number (reduction of 30% when compared with the control group) and produced no visual alteration on cell morphology. The early response observed (6 h) showed induction in the expression of the CDKI gene (cyclin-dependent kinase inhibitor) and genes related to DNA damage repair (mainly XPC and DDB2), while the late response observed (24 h) was more related to up-regulation of p53 and genes involved in cell cycle arrest (gadd45a, cyclinG1). In all times analyzed, the anti-apoptotic gene Bcl-2 was down-regulated. Another interesting result observed was the up-regulation of the Apex- 1 gene after UV-B exposure, which could indicate the induction of oxidative lesions in the DNA molecule. In conclusion, these results demonstrate an activation of the DNA repair system in hepatocytes of zebrafish exposed to UV-B radiation, mainly involving the participation of p53. [source] Protective Effect of Viral Homologues of bcl-2 on Hybridoma Cells under Apoptosis-Inducing ConditionsBIOTECHNOLOGY PROGRESS, Issue 1 2003Joaquim Vives Targets for metabolic engineering have been identified in a hybridoma cell line to make it more robust in culture toward potential limitations inducing apoptosis. The cells were genetically modified with plasmids harboring endogenous bcl-2 gene and also with viral Bcl-2 homologues, particularly ksbcl-2 and bhrf-1 genes. When cells were exposed to apoptosis-inducing conditions (i.e., glutamine-free medium), the control cells exhibited a decrease in viable cell number within the first 12 h, whereas, for the bcl-2 and ksbcl-2 transfected cell cultures, the viable cell number did not exhibit any clear decrease until after 60 h. Furthermore, hybridoma cells expressing the viral homologue bhrf-1 were even more resistant to cell death, showing a decrease in viability of only 50% at 72 h of culture in glutamine-deprived medium, substantially lower than the 90% viability decrease observed for the control culture. In addition, and most relevant for further bioprocess applications, the cells genetically modified could be brought back to growth conditions even after being exposed to glutamine-deprived conditions during a significant time window, up to 72 h. [source] Galectin-1 supports the survival of CD45RA(,) primary myeloma cells in vitroBRITISH JOURNAL OF HAEMATOLOGY, Issue 5 2008Saeid Abroun Summary The survival and proliferation of human myeloma cells are considered to be heavily dependent on the microenvironment of bone marrow (BM). This study confirmed that galectin-1 (Gal-1) and SDF-1, were produced by bone marrow mononuclear cells of myeloma patients. The addition of Gal-1 and SDF-1, to a serum-free synthetic medium, maintained the viability of primary myeloma cells for 2 weeks similar to that before culture. While Gal-1 reduced the viable cell number in CD45RA(+) B cell lines, it maintained the viability of CD45(,) U266 and CD45RA(,)RO(+) ILKM3 myeloma cell lines in the synthetic medium. This was confirmed with the transfection of the PTPRC (CD45) RA, -RB, or -RO gene into CD45(,) U266 cells. The combination of Gal-1 and SDF-1, significantly induced phosphorylation of Akt and IkB, while the phosphorylation of ERK1/2 was significantly reduced in CD45RA(+) U266 and Raji cells but not CD45(,) or CD45RA(,) U266 cells. Furthermore, we confirmed that Gal-1 bound to CD45RA in CD45RA(+) Raji cells, and also physically interacted with ,1-integrin by immunoprecipitation followed by Western blotting and confocal microscopy. The results suggest that Gal-1 has two different actions depending on its binding partner, and supports the survival of CD45RA(,) myeloma cells. [source] | |||||||||||||