Assessing the Relevancy of National Culture in Predicting the Efficacy of Constraints in the Information Systems Consulting Domain

Opportunism is present in professional services and, as a result, organizations adopt mechanisms to constrain it. Despite the work on constraining opportunistic consultants, researchers have generally ignored the potential impact of national culture on the efficacy of constraint mechanisms. Using the theory of relationship constraints (TRC), this study examines the effectiveness of different constraint mechanisms for information systems (IS) consultants in the United States and China based on different levels of information asymmetry, tacit and explicit knowledge. While we found support in both cultures for the salience of these dimensions, we also found important distinctions for the effectiveness of different constraints between the cultures. Legal constraints are more effective in China while social constraints are more effective in the United States. While TRC is relevant in both cultures, national culture moderates the effectiveness of various constraint mechanisms and highlights the need for additional study

THE VALUE OF CHIEF DATA OFFICER PRESENCE ON FIRM PERFORMANCE

In the era of big data, there are more and more organizations trying to establish a new breed of executive, Chief Data Officer (CDO), to identify new business opportunity from data assets and optimize corporate revenue. However, the relationship between CDO presence and firm’s financial performance has not been rigorously studied and validated in literature. Based on upper echelon theory and strategic change perspectives, we examined the impact of pre-performance on the CDO appointment, as well as the CDO presence on post-performance. We collected a multi-industry dataset of 68 firms with a CDO position. The results show that the return on assets (ROA) is positively related to CDO appointment, while, market to book ratio (M/B) is negatively related to CDO appointment. In addition, we found that firms with CDO have superior financial performance than their peers who do not. This study provides an initial step towards understanding the empirical linkages between CDO presence and firm performance

Immediate Versus Delayed Topotecan after First-line Therapy in Small Cell Lung Cancer

Background and objective How to prolong progression free survival (PFS) and overall survival (OS) of patients with small cell lung cancer (SCLC) has been one of the hottest issues. We retrospectively reviewed our data to compare the survival of immediate with delayed topotecan after first-line therapy in SCLC. Methods In our retrospective study, 53 patients with SCLC were divided into two groups as follow: patients receiving topotecan-containing regimen as maintenance/consolidation (maintenance/consolidation chemotherapy group) and salvage chemotherapy (salvage chemotherapy group). The Log-rank test was used to assess the difference in OS between two groups. Cox regression model was used for the multivariable analysis of independent prognostic factors. Results Twenty-nine patients received topotecan as maintenance/consolidation treatment, whereas 24 patients salvage chemotherapy. The response rates were 51.7% and 41.7%, respectively. The median survival time were 20 months and 27 months respectively (P=0.89). Multivariate Cox regression analyses identified sex and stage as independent prognostic factors. Conclusion Efficacy of first-line therapy was improved by topotecan maintenance/consolidation treatment, which did not result in any significant survival benefits in SCLC

On the validity of the local Fourier analysis

Local Fourier analysis (LFA) is a useful tool in predicting the convergence factors of geometric multigrid methods (GMG). As is well known, on rectangular domains with periodic boundary conditions this analysis gives the exact convergence factors of such methods. In this work, using the Fourier method, we extend these results by proving that such analysis yields the exact convergence factors for a wider class of problems

LncRNA MIR4435-2HG predicts poor prognosis in patients with colorectal cancer

Background LncRNA MIR4435-2HG is observed in a variety of cancers, while its role in colorectal cancer is unknown. We aimed to demonstrate the relationship between MIR4435-2HG and colorectal cancer based on The Cancer Genome Atlas (TCGA) database. Materials and Methods Patients with colorectal cancer were collected from TCGA. We compared the expression of MIR4435-2HG in colorectal cancer and normal tissues with Wilcoxon rank sum test, and logistic regression was used to evaluate the relationship between MIR4435-2HG and clinicopathological characters. Moreover, Kaplan–Meier and Cox regression was performed to evaluate the correlation between MIR4435-2HG and survival rate. Gene set enrichment analysis (GSEA) was also conducted to annotate biological function of MIR4435-2HG. Results MIR4435-2HG level was elevated in colorectal cancer tissues. Increased level of MIR4435-2HG was significantly correlated with TNM stage (OR = 1.66 for T1/T2 vs. T3/T4; OR = 1.68 for N0 vs. N1/N2), stage (OR = 1.66 for stage 1/2 vs. stage 3/4), and carcinoembryonic antigen level before treatment (OR = 1.70 for <5 vs. ≥5) (all P-value <0.05). High MIR4435-2HG expression had a poorer progression-free survival (p = 0.048), and overall survival (OS) (P = 0.028), which were validated in the GSE92921 and GSE29621 datasets. MIR4435-2HG expression (P = 0.040, HR = 1.955 (95% CI [1.031–3.710])) was independently correlated with OS. GSEA demonstrated that the P38/MAPK pathway, the VEGF pathway, the cell adhesion molecules cams, the NOD-like receptor signaling pathway, the cell surface interactions at the vascular wall, and integrin cell surface interactions were differentially enriched in MIR4435-2HG high expression phenotype. Conclusions Increased MIR4435-2HG might be a potential biomarker for the diagnosis and prognosis of colorectal cancer. Moreover, MIR4435-2HG might participate in the development of colorectal cancer via the P38/MAPK and VEGF pathway

Ripk3 signaling regulates HSCs during stress and represses radiation-induced leukemia in mice

Receptor-interacting protein kinase 3 (Ripk3) is one of the critical mediators of inflammatory cytokine-stimulated signaling. Here we show that Ripk3 signaling selectively regulates both the number and the function of hematopoietic stem cells (HSCs) during stress conditions. Ripk3 signaling is not required for normal homeostatic hematopoiesis. However, in response to serial transplantation, inactivation of Ripk3 signaling prevents stress-induced HSC exhaustion and functional HSC attenuation, while in response to fractionated low doses of ionizing radiation (IR), inactivation of Ripk3 signaling accelerates leukemia/lymphoma development. In both situations, Ripk3 signaling is primarily stimulated by tumor necrosis factor-α. Activated Ripk3 signaling promotes the elimination of HSCs during serial transplantation and pre-leukemia stem cells (pre-LSCs) during fractionated IR by inducing Mlkl-dependent necroptosis. Activated Ripk3 signaling also attenuates HSC functioning and represses a pre-LSC-to-LSC transformation by promoting Mlkl-independent senescence. Furthermore, we demonstrate that Ripk3 signaling induces senescence in HSCs and pre-LSCs by attenuating ISR-mediated mitochondrial quality control

Small Molecule Inhibitors of 15-PGDH Exploit a Physiologic Induced-Fit Closing System

15-prostaglandin dehydrogenase (15-PGDH) is a negative regulator of tissue stem cells that acts via enzymatic activity of oxidizing and degrading PGE2, and related eicosanoids, that support stem cells during tissue repair. Indeed, inhibiting 15-PGDH markedly accelerates tissue repair in multiple organs. Here we have used cryo-electron microscopy to solve the solution structure of native 15-PGDH and of 15-PGDH individually complexed with two distinct chemical inhibitors. These structures identify key 15-PGDH residues that mediate binding to both classes of inhibitors. Moreover, we identify a dynamic 15-PGDH lid domain that closes around the inhibitors, and that is likely fundamental to the physiologic 15-PGDH enzymatic mechanism. We furthermore identify two key residues, F185 and Y217, that act as hinges to regulate lid closing, and which both inhibitors exploit to capture the lid in the closed conformation, thus explaining their sub-nanomolar binding affinities. These findings provide the basis for further development of 15-PGDH targeted drugs as therapeutics for regenerative medicine