The Fit between Client IT Capability and Vendor Competence and Its Impact on Outsourcing Success

This study investigates the impact of client firm’s IT capability, vendor firm’s competence and their fit on the outsourcing success. In theory building, by concretizing the concepts of IT capability and competence based on the resource-based view, the importance of fit between the client’s IT capability and the vendor’s competence is emphasized. We then hypothesize that both factors are stronger together than the individual impact of either the client’s IT capability or the vendor’s competence. For validation, 267 client-vendor-matched-pair data were collected. To avoid potential imbalance caused by the bilateral perspective, an exploratory approach, all-possible-subsets-regression method was adopted. The results reveal that the vendor’s competence is the most significant factor in outsourcing success, but interestingly, the fit between vendor competence and the client’s IT capability is the second most important. The client’s IT capability also has a positive impact on outsourcing success but with the smallest explanation power

pH-responsive aqueous/LC interfaces using SGLCP-b-polyacrylic acid block copolymers

Block copolymers that combine a side-group liquid crystalline polymer (SGLCP) block and a pH-responsivehydrophilic block, poly(acrylic acid) (PAA), are shown to confer pH-dependent anchoring of the director orientation at the aqueous/LC interface. The SGLCP block, poly(4-cyanobiphenyl-4-oxyundecylacrylate), was chosen based on its ability to influence the director field of the 5CB (4-cyano-4'-pentylbiphenyl). At low pH the PAA block collapses and the inherent, planar alignment tendency of 5CB at a water interface prevails. As pH increases, the polyelectrolyte block becomes increasingly charged and expands, producing a change to homeotropic anchoring. The change in anchoring occurs as quickly as the buffer can be changed (within ~2 s) and is reversible, with a response that is repeatable over as many cycles as were tested (approximately 20 cycles). The polymer-mediated anchoring persists for 6 days, indicating that the SGLCP block secures the self-assembled layer on the 5CB, even under conditions that cause repulsive interactions among the PAA blocks. Thus, SGLCP blocks can translate conformational changes of a responsive hydrophilic block into rapid, reversible changes in the director fiel

Alcohol induces cell proliferation via hypermethylation of ADHFE1 in colorectal cancer cells

BACKGROUND: The hypermethylation of Alcohol dehydrogenase iron containing 1 (ADHFE1) was recently reported to be associated with colorectal cancer (CRC) differentiation. However, the effect of alcohol on ADHFE1 hypermethylation in CRC is still unclear. METHODS: The methylation status and expression levels of ADHFE1 were investigated in primary tumor tissues and adjacent normal tissues of 73 patients with CRC, one normal colon cell line, and 4 CRC cell lines (HT-29, SW480, DLD-1, and LoVo) by quantitative methylation-specific polymerase chain reaction (QMSP) and real-time reverse transcription polymerase chain reaction (real time PCR), respectively. The effect of alcohol on the methylation status of ADHFE1 was analyzed in HT-29, SW480, DLD-1, and CCD18Co cells using QMSP, real-time PCR, immunoblot, and cell proliferation assay. RESULTS: ADHFE1 was hypermethylated in 69 of 73 CRC tissues (95%) compared to adjacent normal tissues (p < 0.05). The mRNA expression of ADHFE1 was significantly reduced in CRC compared to adjacent normal tissues (p < 0.05) and its expression was decreased in the alcohol consumption group (p < 0.05). ADHFE1 was hypermethylated and its expression was decreased in 4 CRC cell lines compared with normal colon cell line. Alcohol induced hypermethylation of ADHFE1, decreased its expression, and stimulated cell proliferation of HT-29, SW480, and DLD-1cells. CONCLUSION: These results demonstrate that the promoter hypermethylation of ADHFE1 is frequently present in CRC and alcohol induces methylation-mediated down expression of ADHFE1 and proliferation of CRC cells

Proteomic and biochemical analyses reveal the activation of unfolded protein response, ERK-1/2 and ribosomal protein S6 signaling in experimental autoimmune myocarditis rat model

<p>Abstract</p> <p>Background</p> <p>To investigate the molecular and cellular pathogenesis underlying myocarditis, we used an experimental autoimmune myocarditis (EAM)-induced heart failure rat model that represents T cell mediated postinflammatory heart disorders.</p> <p>Results</p> <p>By performing unbiased 2-dimensional electrophoresis of protein extracts from control rat heart tissues and EAM rat heart tissues, followed by nano-HPLC-ESI-QIT-MS, 67 proteins were identified from 71 spots that exhibited significantly altered expression levels. The majority of up-regulated proteins were confidently associated with unfolded protein responses (UPR), while the majority of down-regulated proteins were involved with the generation of precursor metabolites and energy metabolism in mitochondria. Although there was no difference in AKT signaling between EAM rat heart tissues and control rat heart tissues, the amounts and activities of extracellular signal-regulated kinase (ERK)-1/2 and ribosomal protein S6 (rpS6) were significantly increased. By comparing our data with the previously reported myocardial proteome of the Coxsackie viruses of group B (CVB)-mediated myocarditis model, we found that UPR-related proteins were commonly up-regulated in two murine myocarditis models. Even though only two out of 29 down-regulated proteins in EAM rat heart tissues were also dysregulated in CVB-infected rat heart tissues, other proteins known to be involved with the generation of precursor metabolites and energy metabolism in mitochondria were also dysregulated in CVB-mediated myocarditis rat heart tissues, suggesting that impairment of mitochondrial functions may be a common underlying mechanism of the two murine myocarditis models.</p> <p>Conclusions</p> <p>UPR, ERK-1/2 and S6RP signaling were activated in both EAM- and CVB-induced myocarditis murine models. Thus, the conserved components of signaling pathways in two murine models of acute myocarditis could be targets for developing new therapeutic drugs or methods aimed at treating enigmatic myocarditis.</p

Dual Therapy with Cidofovir and Mirtazapine for Progressive Multifocal Leukoencephalopathy in a Sarcoidosis Patient

Background: Progressive multifocal leukoencephalopathy (PML) is a demyelinating central nervous system disease caused by JC virus (JCV) reactivation in immunocompromised patients. The disease course of PML is often progressive, fatal and at present, there are few reports on successful treatment outcomes. Case Report: A 45-year-old man with systemic sarcoidosis presented with rapidly progressive dementia and right hemiparesis. The patient was diagnosed with PML as confirmed via brain biopsy and JCV PCR. With a combination treatment of cidofovir and mirtazapine, there was significant improvement of neurological symptoms without measurable functional deficit. Conclusion: This case suggests that dual therapy with cidofovir and mirtazapine might be an effective treatment option in PML patients with sarcoidosis