The way that multinational businesses in integrated global industries coordinate and control R&D, manufacturing, and marketing functions across borders has significant implications for performance. We propose that, in such global industries, certain integrating modes will be more effective than others in integrating a function globally. We show that each function has a different combination of effective integrating modes. For global R&D integration, people-based and information-based modes are more effective than formalization-based and centralization-based modes. For manufacturing, people, information, and formalization are more effective than centralization. With respect to marketing, information and centralization are more effective than people and formalization. We also demonstrate that the co-alignment between actual and ideal profiles (configurations or patterns) of integrating modes results in superior performance. Our results reveal that people-based and information-based modes are generally more effective than formalization-based and centralization-based modes in coordinating and controlling business functions worldwide. Journal of International Business Studies (2003) 34, 327–344. doi:10.1057/palgrave.jibs.8400035
TMPRSS4 is a novel type II transmembrane serine protease found at the cell surface that is highly expressed in pancreatic, colon and gastric cancer tissues. However, the biological functions of TMPRSS4 in cancer are unknown. Here we show, using reverse transcription-PCR, that TMPRSS4 is highly elevated in lung cancer tissues compared with normal tissues and is also broadly expressed in a variety of human cancer cell lines. Knockdown of TMPRSS4 by small interfering RNA treatment in lung and colon cancer cell lines was associated with reduction of cell invasion and cell-matrix adhesion as well as modulation of cell proliferation. Conversely, the invasiveness, motility and adhesiveness of SW480 colon carcinoma cells were significantly enhanced by TMPRSS4 overexpression. Furthermore, overexpression of TMPRSS4 induced loss of E-cadherin-mediated cell-cell adhesion, concomitant with the induction of SIP1/ZEB2, an Ecadherin transcriptional repressor, and led to epithelialmesenchymal transition events, including morphological changes, actin reorganization and upregulation of mesenchymal markers. TMPRSS4-overexpressing cells also displayed markedly increased metastasis to the liver in nude mice upon intrasplenic injection. Taken together, these studies suggest that TMPRSS4 controls the invasive and metastatic potential of human cancer cells by facilitating an epithelial-mesenchymal transition; TMPRSS4 may be a potential therapeutic target for cancer treatment.
Study design: Anatomical measurement. Objective: To obtain quantitative anatomical data on each spinal cord segment in human, and determine the presence of correlations between the measures. Setting: Department of Rehabilitation Medicine, Pusan National University Hospital, Pusan, Korea. Methods: A total of 15 embalmed Korean adult human cadavers (13 males, two females; mean age 57.3 years) were used. The length of each cord segment was defined as the root attachment length plus the upper inter-root length. After performing a total vertebrectomy, a transverse cut was made at the approximate proximal and distal point of each segment from segment C3 to S5. Sagittal and transverse diameters at the proximal end of each segment, and cross-sectional area, height, and volume of the segment were measured. Results: The transverse diameter was largest at segment C5, and decreased progressively to segment T8. However, the sagittal diameter of each segment did not change distinctly with the segment. The cervical and lumbar enlargements were determined by the transverse diameters of the segments. Segment C5 had the largest cross-sectional area, at 75.0 mm 2 . Segment T6 was the longest, averaging 22.4 mm in length. The longest segment in the cervical spinal cord was segment C5, at 15.5 mm, and segment L1 in the lumbar spinal cord. The volume was largest at segment C5, with a value of 1173.9 mm 3 . Conclusions: We found characteristic quantitative differences in the values of the parameters measured in the thoracic spinal cord compared to those measured in the cervical and lumbar or lumbosacral spinal cords. These measurements of spinal cord segments appear to provide valuable and practical standard quantitative features and may provide basic data for understanding the morphometric characteristics relevant to pathophysiologic conditions of the spinal cord.
Successful synthesis of room-temperature ferromagnetic semiconductors, Zn$_{1-x}$Fe$_{x}$O, is reported. The essential ingredient in achieving room-temperature ferromagnetism in bulk Zn$_{1-x}$Fe$_{x}$O was found to be additional Cu doping. A transition temperature as high as 550 K was obtained in Zn$_{0.94}$Fe$_{0.05}$Cu$_{0.01}$O; the saturation magnetization at room temperature reached a value of $0.75 \mu_{\rm B}$ per Fe. Large magnetoresistance was also observed below $100 $K.Comment: 11 pages, 4 figures; to appear in Appl. Phys. Let
Although curcumin suppresses the growth of a variety of cancer cells, its poor absorption and low systemic bioavailability have limited its translation into clinics as an anticancer agent. In this study, we show that dimethoxycurcumin (DMC), a methylated, more stable analog of curcumin, is significantly more potent than curcumin in inducing cell death and reducing the clonogenicity of malignant breast cancer cells. Furthermore, DMC reduces the tumor growth of xenografted MDA-MB 435S cells more strongly than curcumin. We found that DMC induces paraptosis accompanied by excessive dilation of mitochondria and the endoplasmic reticulum (ER); this is similar to curcumin, but a much lower concentration of DMC is required to induce this process. DMC inhibits the proteasomal activity more strongly than curcumin, possibly causing severe ER stress and contributing to the observed dilation. DMC treatment upregulates the protein levels of CCAAT-enhancer-binding protein homologous protein (CHOP) and Noxa, and the small interfering RNA-mediated suppression of CHOP, but not Noxa, markedly attenuates DMC-induced ER dilation and cell death. Interestingly, DMC does not affect the viability, proteasomal activity or CHOP protein levels of human mammary epithelial cells, suggesting that DMC effectively induces paraptosis selectively in breast cancer cells, while sparing normal cells. Taken together, these results suggest that DMC triggers a stronger proteasome inhibition and higher induction of CHOP compared with curcumin, giving it more potent anticancer effects on malignant breast cancer cells.
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