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

Principal factors that determine the extension of detection range in molecular beacon aptamer/conjugated polyelectrolyte bioassays.

A strategy to extend the detection range of weakly-binding targets is reported that takes advantage of fluorescence resonance energy transfer (FRET)-based bioassays based on molecular beacon aptamers (MBAs) and cationic conjugated polyelectrolytes (CPEs). In comparison to other aptamer-target pairs, the aptamer-based adenosine triphosphate (ATP) detection assays are limited by the relatively weak binding between the two partners. In response, a series of MBAs were designed that have different stem stabilities while keeping the constant ATP-specific aptamer sequence in the loop part. The MBAs are labeled with a fluorophore and a quencher at both termini. In the absence of ATP, the hairpin MBAs can be opened by CPEs via a combination of electrostatic and hydrophobic interactions, showing a FRET-sensitized fluorophore signal. In the presence of ATP, the aptamer forms a G-quadruplex and the FRET signal decreases due to tighter contact between the fluorophore and quencher in the ATP/MBA/CPE triplex structure. The FRET-sensitized signal is inversely proportional to [ATP]. The extension of the detection range is determined by the competition between opening of the ATP/MBA G-quadruplex by CPEs and the composite influence by ATP/aptamer binding and the stem interactions. With increasing stem stability, the weak binding of ATP and its aptamer is successfully compensated to show the resistance to disruption by CPEs, resulting in a substantially broadened detection range (from millimolar up to nanomolar concentrations) and a remarkably improved limit of detection. From a general perspective, this strategy has the potential to be extended to other chemical- and biological-assays with low target binding affinity

‘Evidence of an auxin signal pathway, microRNA167-ARF8-GH3, and its response to exogenous auxin in cultured rice cells’

MicroRNA167 (miR167) was shown to cleave auxin responsive factor 8 (ARF8) mRNA in cultured rice cells. MiR167 level was found to be controlled by the presence of auxin in the growth medium. When cells grew in auxin-free medium, miR167 level decreased, resulting in an increase in the level of ARF8 mRNA. Cells growing in the normal growth medium containing auxin showed a reversed trend. It was also shown that expression of OsGH3-2, an rice IAA-conjugating enzyme, was positively regulated by ARF8. Delivery of synthesized miR167 into cells led to decrease of both ARF8 mRNA and OsGH3-2 mRNA. This study provides an evidence in which the exogeneous auxin signal is transduced to OsGH3-2 through miR167 and ARF8 in sequence. This proposed auxin signal transduction pathway, auxin-miR167-ARF8-OsGH3-2, could be, in conjunction with the other microRNA-mediated auxin signals, an important one for responding to exogeneous auxin and for determining the cellular free auxin level which guides appropriate auxin responses

Radiofrequency Ablation of Thyroid Nodules: Basic Principles and Clinical Application

Radiofrequency (RF) ablation has been gaining popularity as a minimally invasive treatment for benign thyroid nodules regardless of the extent of the solid component. RF ablation of benign nodules demonstrated volume reductions of 33–58% after one month and 51–85% after six months, while solving nodule-related clinical problems. RF ablation has recently shown positive short-term results for locoregional control as well as symptom improvement in patients with recurrent thyroid cancers. This paper reviews the basic physics, indications, patient preparation, devices, procedures, clinical results, and complications of RF ablation

Sequential whole cell conversion process for production of D-psicose and D- mannitol from D-fructose

Rare sugars, which exist only limited quantities naturally, have received considerable attention because of its various specific nutritional and biological functions. Likewise, D-psicose (D-ribo-2-hexulose or D-allulose), a C-3 epimer of D-fructose, has many uses which include reducing intra-abdominal fat accumulation, protecting pancreas beta-islets and improving insulin sensitivity. Especially, D-psicose has only 0.3% calories compared to sucrose, while it has 70% relative sweetness. Additionally, in 2012, D-psicose was approved as a food additive and designated as Generally Recognized As Safe (GRAS) by Food and Drug Administration (FDA). Despite such abundant advantages, there is no economical way of mass production of D-psicose. Recently, biological production of D-psicose from D-fructose using D-psicose 3-epimerase (DPE) has been developed. However, the conversion yield is below 30%, which causes an undesirable increase of purification cost because of the similar solubility of D-psicose and D-fructose. Thus, we addressed the problem by converting the residual fructose, after the reaction of D-psicose production, to D-mannitol, which has a low solubility. The sequential whole cell conversion reactions for D-psicose and D-mannitol allow a convenient and economic purification of both products. This work was supported by a grant from the Next-Generation BioGreen 21 Program (SSAC, grant#: PJ01106201), RDA, Korea. Reference 1) Carsten Bäumchen & Stephanie Bringer-Meyer (2007), Expression of glf Z.m. increases D-mannitol formation in whole cell biotransformation with resting cells of Corynebacterium glutamicum, Appl Microbiol Biotechnol 76(3):545–52. 2) Ortiz, M. E., Bleckwedel, J., Raya, R. R., & Mozzi, F. (2013). Biotechnological and in situ food production of polyols by lactic acid bacteria, Appl Microbiol Biotechnol 97:4713-4726 3) Park, Y., Oh, E. J., Jo, J., Jin, Y., & Seo, J. (2016). Recent advances in biological production of sugar alcohols. Curr Opin Biotechnol 37:105–113

Damage-associated molecular patterns as a mechanism of sevoflurane-induced neuroinflammation in neonatal rodents

Background General anesthesia is inevitable for pediatric patients undergoing surgery, though volatile anesthetic agents may cause neuroinflammation and neurodevelopmental impairment; however, the underlying pathophysiology remains unclear. We aimed to investigate the neuroinflammation mechanism in developing rat brains associated with sevoflurane exposure time, by identifying the specific damage-associated molecular patterns (DAMPs) pathway and evaluating the effects of non-steroidal anti-inflammatory drugs (NSAIDs) in alleviating neuroinflammation. Methods A three-step experiment was conducted to investigate neuroinflammation induced by sevoflurane. First, the exposure time required for sevoflurane to cause neuroinflammation was determined. Next, the specific pathways of DAMPs involved in neuroinflammation by sevoflurane were identified. Finally, the effects of NSAIDs on sevoflurane-induced neuroinflammation were investigated. The expression of various molecules in the rat brain were assessed using immunohistochemistry, immunofluorescence, quantitative real-time polymerase chain reaction, western blot analysis, and enzyme-linked immunosorbent assay. Results In total, 112 rats (aged 7 days) were used, of which six rats expired during the experiment (mortality rate, 5.3%). Expression of CD68, HMGB-1, galectin-3, TLR4, TLR9, and phosphorylated NF-κB was significantly increased upon 6 h of sevoflurane exposure. Conversely, transcriptional levels of TNF-α and IL-6 significantly increased and IFN-γ significantly decreased after 6 h of sevoflurane exposure. Co-administration of NSAIDs with sevoflurane anesthesia significantly attenuated TNF-α and IL-6 levels and restored IFN-γ levels. Conclusions In conclusion, 6 h of sevoflurane exposure induces neuroinflammation through the DAMPs pathway, HMGB-1, and galectin-3. Co-administration of ibuprofen reduced sevoflurane-induced neuroinflammation