Examining Leader-Member Exchange as a Moderator of the Relationship between Emotional Intelligence and Creativity of Software Developers

This paper investigates how leader-member exchange (LMX) and emotional intelligence (EI) are associated with employees??? creativity in high-tech firms. We develop a model that considers LMX and EI as predictors of creativity with LMX as a boundary condition for the relationship between EI and creativity. Results reveal that LMX is a strong predictor of creativity. However, EI does not directly affect creativity. More interestingly, the interaction between EI and LMX negatively influences creativity such that EI is detrimental for creativity only when LMX is high. Thus, the role of LMX for employees??? creativity may be paradoxical. Further, the positive role of EI reported in current literature may be overly simplistic, and its role may be contingent on the quality of LMX and the other context.ope

Measurement of hepatitis B virus DNA in fresh versus processed dentin from chronically infected patients

Background Demineralized dentin matrix (DDM) is commonly used as a bone-graft substitute. This study measured and compared human hepatitis B viruses (HBV) DNA in fresh dentin to that of dentin processed into DDM extracted during dental treatment from HBV-infected patients. The hypothesis was that the processing procedure for DDM would inactivate or eliminate HBV in the dentin matrix obtained from infected patients. Methods Dentin from eighteen HBV-infected patients was collected and each dentin specimen was divided into two fragments. One fragment was used before processing as fresh dentin (control group) and the other was processed into DDM (experimental group). DNA was extracted and purified from each fresh and processed dentin specimen and the HBV DNA copy number quantitated by real time polymerase chain reaction. The HBV DNA copy number in the fresh dentin specimens were compared relative to serologic test results. The second parameter was to evaluate the effectiveness of the processing procedure (defatting, demineralization, freeze-drying, and sterilization) to inactivate or eliminate HBV by comparing the DNA copy number in the processed DDM with that in the matched fresh dentin specimens. All results were analyzed using Mann–Whitney U test to compare numerical measurements between groups and differences were considered statistically significant at P-values less than 0.05. Results The presence of HBV DNA was detected in 55.56% (10/18) of the fresh dentin specimens. For the ten HBV DNA-positive fresh dentin specimens, HBV DNA was detected in two (20%) of the matched processed dentin specimens. The copy number of HBV DNA in the two positive processed dentin specimens was 1.79 and 4.03, which were statistically lower than that of the fresh dentin specimens (P = 0.0167). Conclusions The results from this study suggested that fresh dentin may be a carrier of HBV and that the procedure used to generate DDM extensively reduced the levels of HBV DNA. Further studies are needed to evaluate the infectivity of HBV in processed dentin.This research was supported by a grant from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI) funded by the Ministry of Health & Welfare, Republic of Korea (Grant Number: HI15C1535)

Plasma membrane calcium ATPase regulates bone mass by fine-tuning osteoclast differentiation and survival.

The precise regulation of Ca2+ dynamics is crucial for proper differentiation and function of osteoclasts. Here we show the involvement of plasma membrane Ca2+ ATPase (PMCA) isoforms 1 and 4 in osteoclastogenesis. In immature/undifferentiated cells, PMCAs inhibited receptor activator of NF-B ligand–induced Ca2+ oscillations and osteoclast differentiation in vitro. Interestingly, nuclear factor of activated T cell c1 (NFATc1) directly stimulated PMCA transcription, whereas the PMCA-mediated Ca2+ efflux prevented NFATc1 activation, forming a negative regulatory loop. PMCA4 also had an anti-osteoclastogenic effect by reducing NO, which facilitates preosteoclast fusion. In addition to their role in immature cells, increased expression of PMCAs in mature osteoclasts prevented osteoclast apoptosis both in vitro and in vivo. Mice heterozygous for PMCA1 or null for PMCA4 showed an osteopenic phenotype with more osteoclasts on bone surface. Furthermore, PMCA4 expression levels correlated with peak bone mass in premenopausal women. Thus, our results suggest that PMCAs play important roles for the regulation of bone homeostasis in both mice and humans by modulating Ca2+ signaling in osteoclasts.OAIID:oai:osos.snu.ac.kr:snu2012-01/102/0000026258/8SEQ:8PERF_CD:SNU2012-01EVAL_ITEM_CD:102USER_ID:0000026258ADJUST_YN:NEMP_ID:A076310DEPT_CD:861CITE_RATE:10.264FILENAME:J Cell Biol-2012-Kim-ATPase.pdfDEPT_NM:치의학과EMAIL:[email protected]_YN:YCONFIRM:

The ubiquitin-mediated degradation of Jak1 modulates osteoclastogenesis by limiting interferon-beta-induced inhibitory signaling.

Interferons (IFNs) have been shown to negatively regulate osteoclastogenesis. In a proteomic study to assess protein expression during osteoclastogenesis, we discovered that the expression level of Jak1 was significantly decreased during the early stage of osteoclast differentiation from mouse bone marrow macrophages (BMMs) upon stimulation with receptor activator of nuclear factor kappaB ligand (RANKL). RANKL induced Jak1 ubiquitination, and a proteasome inhibitor MG132 efficiently blocked the RANKL-induced degradation of Jak1. The expression level of Jak1 correlated with the susceptibility of osteoclast precursors to the negative regulatory effects of IFN-beta on osteoclastogenesis, since preosteoclasts (pOCs) in which Jak1 expression is significantly reduced could proceed with osteoclastogenesis in the presence of IFN-beta. Forced down-regulation of Jak1 by small interfering RNA (siRNA) resulted in the efficient osteoclast differentiation of BMMs in the presence of inhibitory IFN-beta, while overexpression of Jak1 in pOCs elicited IFN-beta-dependent inhibition of osteoclastogenesis. Furthermore, we found that the IFN-beta-induced inhibition of osteoclastogenesis required STAT3 downstream of Jak1. These data suggest that the regulation of Jak1 expression during osteoclast differentiation might serve as an intrinsic mechanism that determines osteoclast lineage commitment by modulating the negative regulation by IFN-beta

Plasma membrane calcium ATPase regulates bone mass by fine-tuning osteoclast differentiation and survival

The precise regulation of Ca(2+) dynamics is crucial for proper differentiation and function of osteoclasts. Here we show the involvement of plasma membrane Ca(2+) ATPase (PMCA) isoforms 1 and 4 in osteoclastogenesis. In immature/undifferentiated cells, PMCAs inhibited receptor activator of NF-κB ligand–induced Ca(2+) oscillations and osteoclast differentiation in vitro. Interestingly, nuclear factor of activated T cell c1 (NFATc1) directly stimulated PMCA transcription, whereas the PMCA-mediated Ca(2+) efflux prevented NFATc1 activation, forming a negative regulatory loop. PMCA4 also had an anti-osteoclastogenic effect by reducing NO, which facilitates preosteoclast fusion. In addition to their role in immature cells, increased expression of PMCAs in mature osteoclasts prevented osteoclast apoptosis both in vitro and in vivo. Mice heterozygous for PMCA1 or null for PMCA4 showed an osteopenic phenotype with more osteoclasts on bone surface. Furthermore, PMCA4 expression levels correlated with peak bone mass in premenopausal women. Thus, our results suggest that PMCAs play important roles for the regulation of bone homeostasis in both mice and humans by modulating Ca(2+) signaling in osteoclasts

Prohibitin modulates periodontium differentiation in mice development

Introduction: Prohibitin (PHB) is an essential scaffold protein that modulates signaling pathways controlling cell survival, metabolism, inflammation, and bone formation. However, its specific role in periodontium development remains less understood. This study aims to elucidate the expression pattern and function of PHB in periodontium development and its involvement in alveolar bone formation.Methods: Immunolocalization of PHB in the periodontium of postnatal (PN) mice were examined. Phb morpholino was micro-injected into the right-side mandible at PN5, corresponding to the position where the alveolar bone process forms in relation to the lower first molar. The micro-injection with a scramble control (PF-127) and the left-side mandibles were used as control groups. Five days post-micro-injection, immunohistochemical analysis and micro-CT evaluation were conducted to assess bone mass and morphological changes. Additionally, expression patterns of signaling molecules were examined following Phb downregulation using 24-h in vitro cultivation of developing dental mesenchyme at E14.5.Results: The immunostaining of PHB showed its localization in the periodontium at PN5, PN8, and PN10. The in vitro cultivation of dental mesenchyme resulted in alterations in Bmps, Runx2, and Wnt signalings after Phb knock-down. At 5 days post-micro-injection, Phb knocking down showed weak immunolocalizations of runt-related transcription factor (RUNX2) and osteocalcin (OCN). However, knocking down Phb led to histological alterations characterized by decreased bone mass and stronger localizations of Ki67 and PERIOSTIN in the periodontium compared 1 to control groups. The micro-CT evaluation showed decreased bone volume and increased PDL space in the Phb knock-down specimens, suggesting its regulatory role in bone formation.Discussion: The region-specific localization of PHB in the margin where alveolar bone forms suggests its involvement in alveolar bone formation and the differentiation of the periodontal ligament. Overall, our findings suggest that Phb plays a modulatory role in alveolar bone formation by harmoniously regulating bone-forming-related signaling molecules during periodontium development

The role of interleukin-17 in bone metabolism and inflammatory skeletal diseases

The balance between osteoblast-dependent bone formationand osteoclast-dependent bone resorption maintains bonehomeostasis. In inflammatory conditions, this balance shiftstoward bone resorption, causing osteolytic bone lesionsobserved in rheumatoid arthritis and periodontitis. A recentlydiscovered family of cytokine IL-17 is widely reported tomediate diverse inflammatory processes. During the lastdecade, novel roles for IL-17 in skeletal homeostasis have beendiscovered indicating the potential importance of this cytokinein bone metabolism. This review will summarize and discussthe involvement of IL-17 during bone homeostasis in bothphysiologic and pathologic conditions. A better understandingof the role of IL-17 in skeletal systems warrants an advance inbone biology, as well as development of therapeutic strategiesagainst bone-lytic diseases, such as rheumatoid arthritis andperiodontitis. [BMB Reports 2013; 46(10): 479-483

Investigation of Densification Behavior of Contacting Particles Using a 2d Monte Carlo Potts Model

Densification behavior of solid-pore systems during final stage of solid-state sintering is explored by a spin-exchange-path-dependent rate-controlled Monte Carlo (MC) Potts model. Especially, two-dimensional circular particles, contacting with each other, are digitally prepared as inputs for the proposed MC algorithm. Diffusivities in the context of pore-solid exchange along the grain boundaries, on the hetero-interfaces and through the bulk are controlled in order to elucidate the relative contribution of the different diffusion mode to the densification. The effect of grain boundary energy anisotropy on the densification behavior will be also discussed. The results indicate the proposed model generically have a potential to predict the realistic evolution polycrystalline microstructures during the solid-state sintering