FACTORS AFFECTING THE TRANSFER OF INTER-ORGANIZATIONAL SYSTEMS TO CHINA: A CASE STUDY OF HIGH-TECH ENTERPRISES

Due to the huge market potentiality, profuse production resource such as workforce and land, and low production costs in China, many international high-tech enterprises are moving their production line to China. Accompanying production offshoring is the transfer of Information Technology (IT) to ensure that the production processes remain efficient and effective at home and abroad. Many enterprises however encounter problems in transferring their IT to China, especially when the IT is an inter-organizational system (IOS), which is across organizational boundaries and involves the management of relationships among participants. In order to understand how to successfully transfer IOS to China, we aim to find out key relational factors of IOS performance in China through an observation of a binary relationship built upon an e-procurement system between a Taiwanese PC ODM (Original Design Manufacturer) and its Chinese suppliers. Based on the relational view of the firm, four relational factors are proposed and examined. The results show that IOS specific investments and effective IOS governance most strongly affects the result of IOS transfer to China, whereas complementary resource endowment has least influence

Second generation Dirac cones and inversion symmetry breaking induced gaps in graphene/hexagonal boron nitride

Graphene/h-BN has emerged as a model van der Waals heterostructure, and the band structure engineering by the superlattice potential has led to various novel quantum phenomena including the self-similar Hofstadter butterfly states. Although newly generated second generation Dirac cones (SDCs) are believed to be crucial for understanding such intriguing phenomena, so far fundamental knowledge of SDCs in such heterostructure, e.g. locations and dispersion of SDCs, the effect of inversion symmetry breaking on the gap opening, still remains highly debated due to the lack of direct experimental results. Here we report first direct experimental results on the dispersion of SDCs in 0$^\circ$ aligned graphene/h-BN heterostructure using angle-resolved photoemission spectroscopy. Our data reveal unambiguously SDCs at the corners of the superlattice Brillouin zone, and at only one of the two superlattice valleys. Moreover, gaps of $\approx$ 100 meV and $\approx$ 160 meV are observed at the SDCs and the original graphene Dirac cone respectively. Our work highlights the important role of a strong inversion symmetry breaking perturbation potential in the physics of graphene/h-BN, and fills critical knowledge gaps in the band structure engineering of Dirac fermions by a superlattice potential.Comment: Nature Physics 2016, In press, Supplementary Information include

A novel role of sesamol in inhibiting NF-κB-mediated signaling in platelet activation

<p>Abstract</p> <p>Background</p> <p>Platelet activation is relevant to a variety of coronary heart diseases. Our previous studies revealed that sesamol possesses potent antiplatelet activity through increasing cyclic AMP formation. Although platelets are anucleated cells, they also express the transcription factor, NF-κB, that may exert non-genomic functions in platelet activation. Therefore, we further investigated the inhibitory roles of sesamol in NF-κB-mediated platelet function.</p> <p>Methods</p> <p>Platelet aggregation, Fura 2-AM fluorescence, and immunoblotting analysis were used in this study.</p> <p>Results</p> <p>NF-κB signaling events, including IKKβ phosphorylation, IκBα degradation, and p65 phosphorylation, were markedly activated by collagen (1 μg/ml) in washed human platelets, and these signaling events were attenuated by sesamol (2.5~25 μM). Furthermore, SQ22536 and ODQ, inhibitors of adenylate cyclase and guanylate cyclase, respectively, strongly reversed the sesamol (25 μM)-mediated inhibitory effects of IKKβ phosphorylation, IκBα degradation, and p65 phosphorylation stimulated by collagen. The protein kinase A (PKA) inhibitor, H89, also reversed sesamol-mediated inhibition of IκBα degradation. Moreover, BAY11-7082, an NF-κB inhibitor, abolished IκBα degradation, phospholipase C (PLC)γ2 phosphorylation, protein kinase C (PKC) activation, [Ca²⁺]i mobilization, and platelet aggregation stimulated by collagen. Preincubation of platelets with the inhibitors, SQ22536 and H89, both strongly reversed sesamol-mediated inhibition of platelet aggregation and [Ca²⁺]i mobilization.</p> <p>Conclusions</p> <p>Sesamol activates cAMP-PKA signaling, followed by inhibition of the NF-κB-PLC-PKC cascade, thereby leading to inhibition of [Ca²⁺]i mobilization and platelet aggregation. Because platelet activation is not only linked to hemostasis, but also has a relevant role in inflammation and metastasis, our data demonstrating that inhibition of NF-κB interferes with platelet function may have a great impact when these types of drugs are considered for the treatment of cancer and various inflammatory diseases.</p

Effect of Antrodia

Antrodia camphorata is a rare Taiwanese medicinal mushroom. Antrodia camphorata extract has been reported to exhibit antioxidant, anti-inflammation, antimetastasis, and anticancer activities and plays a role in liver fibrosis, vasorelaxation, and immunomodulation. Critical vascular inflammation leads to vascular dysfunction and cardiovascular diseases, including abdominal aortic aneurysms, hypertension, and atherosclerosis. Platelet activation plays a crucial role in intravascular thrombosis, which is involved in a wide variety of cardiovascular diseases. However, the effect of Antrodia camphorata on platelet activation remains unclear. We examined the effects of Antrodia camphorata on platelet activation. In the present study, Antrodia camphorata treatment (56–224 μg/mL) inhibited platelet aggregation induced by collagen, but not U46619, an analogue of thromboxane A2, thrombin, and arachidonic acid. Antrodia camphorata inhibited collagen-induced calcium (Ca2+) mobilization and phosphorylation of protein kinase C (PKC) and Akt. In addition, Antrodia camphorata significantly reduced the aggregation and phosphorylation of PKC in phorbol-12, 13-dibutyrate (PDBu) activated platelets. In conclusion, Antrodia camphorata may inhibit platelet activation by inhibiting of Ca2+ and PKC cascade and the Akt pathway. Our study suggests that Antrodia camphorata may be a potential therapeutic agent for preventing or treating thromboembolic disorders

Xanthohumol, a Prenylated Flavonoid from Hops (Humulus lupulus), Prevents Platelet Activation in Human Platelets

Xanthohumol is the principal prenylated flavonoid in the hop plant (Humulus lupulus L.). Xanthohumol was found to be a very potent cancer chemopreventive agent through regulation of diverse mechanisms. However, no data are available concerning the effects of xanthohumol on platelet activation. The aim of this paper was to examine the antiplatelet effect of xanthohumol in washed human platelets. In the present paper, xanthohumol exhibited more-potent activity in inhibiting platelet aggregation stimulated by collagen. Xanthohumol inhibited platelet activation accompanied by relative [Ca2+]i mobilization, thromboxane A2 formation, hydroxyl radical (OH●) formation, and phospholipase C (PLC)γ2, protein kinase C (PKC), mitogen-activated protein kinase (MAPK), and Akt phosphorylation. Neither SQ22536, an inhibitor of adenylate cyclase, nor ODQ, an inhibitor of guanylate cyclase, reversed the xanthohumol-mediated inhibitory effect on platelet aggregation. Furthermore, xanthohumol did not significantly increase nitrate formation in platelets. This study demonstrates for the first time that xanthohumol possesses potent antiplatelet activity which may initially inhibit the PI3-kinase/Akt, p38 MAPK, and PLCγ2-PKC cascades, followed by inhibition of the thromboxane A2 formation, thereby leading to inhibition of [Ca2+]i and finally inhibition of platelet aggregation. Therefore, this novel role of xanthohumol may represent a high therapeutic potential for treatment or prevention of cardiovascular diseases

MeCP2 binding to DNA depends upon hydration at methyl-CpG

MeCP2 is an essential transcriptional repressor that mediates gene silencing through binding to methylated DNA. Binding specificity has been thought to depend on hydrophobic interactions between cytosine methyl groups and a hydrophobic patch within the methyl-CpG-binding domain (MBD). X-ray analysis of a methylated DNA-MBD cocrystal reveals, however, that the methyl groups make contact with a predominantly hydrophilic surface that includes tightly bound water molecules. This suggests that MeCP2 recognizes hydration of the major groove of methylated DNA rather than cytosine methylation per se. The MeCP2-DNA complex also identifies a unique structural role for T158, the residue most commonly mutated in Rett syndrome

Structure and Luminescence Properties of Eu3+-Doped Cubic Mesoporous Silica Thin Films

Eu3+ ions-doped cubic mesoporous silica thin films with a thickness of about 205 nm were prepared on silicon and glass substrates using triblock copolymer as a structure-directing agent using sol–gel spin-coating and calcination processes. X-ray diffraction and transmission electron microscopy analysis show that the mesoporous silica thin films have a highly ordered body-centered cubic mesoporous structure. High Eu3+ ion loading and high temperature calcination do not destroy the ordered cubic mesoporous structure of the mesoporous silica thin films. Photoluminescence spectra show two characteristic emission peaks corresponding to the transitions of5D0-7F1 and 5D0-7F2 of Eu3+ ions located in low symmetry sites in mesoporous silica thin films. With the Eu/Si molar ratio increasing to 3.41%, the luminescence intensity of the Eu3+ ions-doped mesoporous silica thin films increases linearly with increasing Eu3+ concentration

Transplantation of canine umbilical cord blood-derived mesenchymal stem cells in experimentally induced spinal cord injured dogs

This study was to determine the effects of allogenic umbilical cord blood (UCB)-derived mesenchymal stem cells (MSCs) and recombinant methionyl human granulocyte colony-stimulating factor (rmhGCSF) on a canine spinal cord injury model after balloon compression at the first lumbar vertebra. Twenty-five adult mongrel dogs were assigned to five groups according to treatment after a spinal cord injury: no treatment (CN); saline treatment (CP); rmhGCSF treatment (G); UCB-MSCs treatment (UCB-MSC); co-treatment (UCBG). The UCB-MSCs isolated from cord blood of canine fetuses were prepared as 106 cells/150 µl saline. The UCB-MSCs were directly injected into the injured site of the spinal cord and rmhGCSF was administered subcutaneously 1 week after the induction of spinal cord injury. The Olby score, magnetic resonance imaging, somatosensory evoked potentials and histopathological examinations were used to evaluate the functional recovery after transplantation. The Olby scores of all groups were zero at the 0-week evaluation. At 2 week after the transplantation, the Olby scores in the groups with the UCB-MSC and UCBG were significantly higher than in the CN and CP groups. However, there were no significant differences between the UCB-MSC and UCBG groups, and between the CN and CP groups. These comparisons remained stable at 4 and 8 week after transplantation. There was significant improvement in the nerve conduction velocity based on the somatosensory evoked potentials. In addition, a distinct structural consistency of the nerve cell bodies was noted in the lesion of the spinal cord of the UCB-MSC and UCBG groups. These results suggest that transplantation of the UCB-MSCs resulted in recovery of nerve function in dogs with a spinal cord injury and may be considered as a therapeutic modality for spinal cord injury