Search

The global economy has undergone a paradigm shift because of the convergence of digital technology, intellectual property and customer supremacy. The concept of e-business refers to a business phenomenon in which digital technology, intellectual property and customer supremacy are seatniessly integrated with business activities, which alters, and often replaces, the conventional business paradigm at both industrial and corporate levels. Put differently, e-business is about the commitment and capability of companies in various industries to utilize digital technology (particularly the Internet), emphasize intellectual property, and enhance customer satisfaction across the business functions, thus changing the way of doing business from a traditional company-centric, stand-alone paradigm to a new network-leveraged synchronized paradigm. Thus, the Internet-enabled and Internet-transformed companies and industries will become e-companies and e-industries. In the context of e-business and the new economy, the boundaries, of space and time will be increasingly elastic in responding to market changes.

Background: The purpose of this study is to propose a novel method for assessing dynamic elastance of the superficial arterial wall using the sinusoidal minute vibration method.Methods: A sinusoidal signal was used to drive a vibrator which induced a displacement of 0.15 mm with a frequency range between 40 and 85 Hz. The vibrator closely contacted with the wall of a superficial radial artery, and caused the arterial wall to shift simultaneously. A force sensor attached to the tip of the vibrator was used to pick up the reactive force exerted by the radial arterial wall. According to the Voigt and Maxwell models, a linear relationship was found between the maximum reactive force and the squared angular frequency of the vibration. The intercept of the linear function represents the arterial wall elastance. In order to validate the feasibility of our method, twenty-nine healthy subjects were recruited and the wall elastances of their radial arteries were measured at room temperature (25 °C), after a 5-min cold stress (4 °C) and a 5-min hot stress (42 °C), respectively.Results: After the 5-min cold stimulation, the maximum radial wall elastance significantly increased from 0.441 ± 0.182 × 10(6) dyne/cm to 0.611 ± 0.251 × 10(6) dyne/cm (p = 0.001). In the 5-min hot stress, the maximum radial wall elastance significantly decreased to 0.363 ± 0.106 × 10(6) dyne/cm (p = 0.013).Conclusions: The sinusoidal minute vibration method proposed can be employed to obtain the quantitative elastance of a superficial artery under different thermal conditions, and to help assess the severity of arterial stiffness in conduit arteries. [ABSTRACT FROM AUTHOR]

Aquaporins (AQPs) have previously been associated with increased expression in solid tumors. However, its expression in hematologic malignancies including CML has not been described yet. Here, we report the expression of AQP5 in CML cells by RT-PCR and immunohistochemistry. While normal bone marrow biopsy samples (n = 5) showed no expression of AQP5, 32% of CML patient samples (n = 41) demonstrated AQP5 expression. In addition, AQP5 expression level increased with the emergence of imatinib mesylate resistance in paired samples (p = 0.047). We have found that the overexpression of AQP5 in K562 cells resulted in increased cell proliferation. In addition, small interfering RNA (siRNA) targeting AQP5 reduced the cell proliferation rate in both K562 and LAMA84 CML cells. Moreover, by immunoblotting and flow cytometry, we show that phosphorylation of BCR-ABL1 is increased in AQP5-overexpressing CML cells and decreased in AQP5 siRNA-treated CML cells. Interestingly, caspase9 activity increased in AQP5 siRNA-treated cells. Finally, FISH showed no evidence of AQP5 gene amplification in CML from bone marrow. In summary, we report for the first time that AQP5 is overexpressed in CML cells and plays a role in promoting cell proliferation and inhibiting apoptosis. Furthermore, our findings may provide the basis for a novel CML therapy targeting AQP5. [ABSTRACT FROM AUTHOR]