Guidelines Aimed at Reducing the Risks of User Acceptance Delay in the Context of an IT Service Project Management Plan

Delays in the user acceptance of information technology (IT) service projects in Korea have occurred frequently due to various risk factors. User acceptance delays may hinder the achievement of the client’s project objectives and cause schedule delays or cost overruns. Furthermore, the client may impose a delay charge and claim for additional damages, causing serious disputes between buyer and supplier. The main causes of user acceptance delays are unclear user requirements, changes in user requirements, poor-quality development outputs, excessive functional and non-functional errors, lack of user involvement, unclear user roles and responsibilities, and unclear criteria of user acceptance test.We help foster the timely completion of user acceptance by proposing a method of identifying the risk factors in user acceptance delay and creating a project management plan to weed out the identified risks. We propose a guideline for an IT service management plan that weeds out or lowers the risk factors well in advance. To validate the guideline’s utility, we apply it to IT service projects. The results show that the guideline is effective in identifying and removing risk factors affecting delays in the user acceptance of IT service projects

Multiple Functions of Nm23-H1 Are Regulated by Oxido-Reduction System

Nucleoside diphosphate kinase (NDPK, Nm23), a housekeeping enzyme, is known to be a multifunctional protein, acting as a metastasis suppressor, transactivation activity on c-myc, and regulating endocytosis. The cellular mechanisms regulating Nm23 functions are poorly understood. In this study, we identified the modifications and interacting proteins of Nm23-H1 in response to oxidative stress. We found that Cys109 in Nm23-H1 is oxidized to various oxidation states including intra- and inter-disulfide crosslinks, glutathionylation, and sulfonic acid formation in response to H2O2 treatment both in vivo and in vitro. The cross-linking sites and modifications of oxidized Nm23-H1 were identified by peptide sequencing using UPLC-ESI-q-TOF tandem MS. Glutathionylation and oxidation of Cys109 inhibited the NDPK enzymatic activity of Nm23-H1. We also found that thioredoxin reductase 1 (TrxR1) is an interacting protein of Nm23-H1, and it binds specifically to oxidized Nm23-H1. Oxidized Nm23 is a substrate of NADPH-TrxR1-thioredoxin shuttle system, and the disulfide crosslinking is reversibly reduced and the enzymatic activity is recovered by this system. Oxidation of Cys109 in Nm23-H1 inhibited its metastatic suppressor activity as well as the enzymatic activities. The mutant, Nm23-H1 C109A, retained both the enzymatic and metastasis suppressor activities under oxidative stress. This suggests that key enzymatic and metastasis suppressor functions of Nm23-H1 are regulated by oxido-reduction of its Cys109

Stability of wheat germ oil obtained by supercritical carbon dioxide associated with lipase ethanolysis

Wheat germ oil was extracted using an environmental friendly solvent, supercritical carbon dioxide (SCCO2) at a semi-batch flow extraction process. The supercritical carbon dioxide (SC-CO2) extraction was carried out to extract oil at temperature of 40°C and pressure of 25 MPa. Ethanolysis was performed with 1,3-regiospecific lipase at different temperatures (40 to 70°C) to produce diglycerides and monoglycerides containing fatty acid ethyl esters. For determination of stability, wheat germ oil obtained by ethanolysis reactants was characterized by measuring the acid value, peroxide value, free fatty acid contents, thiocyanate method, DPPH radical scavenging effect and rancimat test. The optimized condition of 40°C shows the highest oil stability among the various conditions.Keywords: Supercritical carbon dioxide, wheat germ oil, ethanolysis, immobilized lipases, oil stabilityAfrican Journal of Biotechnology Vol. 12(22), pp. 3570-357

β-Lapachone Significantly Increases the Effect of Ionizing Radiation to Cause Mitochondrial Apoptosis via JNK Activation in Cancer Cells

β-lapachone (β-lap), has been known to cause NQO1-dependnet death in cancer cells and sensitize cancer cells to ionizing radiation (IR). We investigated the mechanisms underlying the radiosensitization caused by β-lap. cells induced ROS generation, triggered ER stress and stimulated activation of ERK and JNK. Inhibition of ROS generation by NAC effectively attenuated the activation of ERK and JNK, induction of ER stress, and subsequent apoptosis. Importantly, inhibition of ERK abolished ROS generation and ER stress, whereas inhibition of JNK did not, indicating that positive feedback regulation between ERK activation and ROS generation triggers ER stress in response to combined treatment. Furthermore, prevention of ER stress completely blocked combination treatment-induced JNK activation and subsequent apoptotic cell death. In addition, combined treatment efficiently induced the mitochondrial translocation of cleaved Bax, disrupted mitochondrial membrane potential, and the nuclear translocation of AIF, all of which were efficiently blocked by a JNK inhibitor. Caspases 3, 8 and 9 were activated by combined treatment but inhibition of these caspases did not abolish apoptosis indicating caspase activation played a minor role in the induction of apoptosis. cells are treated with combination of IR and β-lap, positive feedback regulation between ERK and ROS leads to ER stress causing JNK activation and mitochondrial translocation of cleaved Bax. The resultant decrease in mitochondrial membrane leads to translocation of AIF and apoptosis

Optical switching of the Dirac point in graphene multilayer field-effect transistors functionalized with spiropyran

A facile method for achieving optical switching of the Dirac point and conductance in reduced graphene oxide multilayer FETs that are non-covalently functionalized with a photoresponsive spiropyran derivative is presented. The photoresponsive transition from spiropyran to merocyanine induces the reversible optical switching in graphene based FETs.close6

Age-dependent resistance of a perennial herb, Aristolochia contorta against specialist and generalist leaf-chewing herbivores

Plants need to balance investments in growth and defense throughout their life to increase their fitness. To optimize fitness, levels of defense against herbivores in perennial plants may vary according to plant age and season. However, secondary plant metabolites often have a detrimental effect on generalist herbivores, while many specialists have developed resistance to them. Therefore, varying levels of defensive secondary metabolites depending on plant age and season may have different effects on the performance of specialist and generalist herbivores colonizing the same host plants. In this study, we analyzed concentrations of defensive secondary metabolites (aristolochic acids) and the nutritional value (C/N ratios) of 1st-, 2nd- and 3rd-year Aristolochia contorta in July (the middle of growing season) and September (the end of growing season). We further assessed their effects on the performances of the specialist herbivore Sericinus montela (Lepidoptera: Papilionidae) and the generalist herbivore Spodoptera exigua (Lepidoptera: Noctuidae). Leaves of 1st-year A. contorta contained significantly higher concentrations of aristolochic acids than those of older plants, with concentrations tending to decrease over the first-year season. Therefore, when first year leaves were fed in July, all larvae of S. exigua died and S. montela showed the lowest growth rate compared to older leaves fed in July. However, the nutritional quality of A. contorta leaves was lower in September than July irrespective of plant age, which was reflected in lower larval performance of both herbivores in September. These results suggest that A. contorta invests in the chemical defenses of leaves especially at a young age, while the low nutritional value of leaves seems to limit the performance of leaf-chewing herbivores at the end of the season, regardless of plant age