Not Enough? An Examination of China’s Compliance with the Intentions of the TRIPS Accord

As China is in its third year as a member of the World Trade organization, there is much anticipation as to whether its protection of intellectual property rights is up to international standards. Being one of the largest trading nations in the world, much attention has been given to China’s development since its accession to the WTO. The US Chamber of Commerce has recently made a visit to China in order to examine its progress on implementing WTO rules and the WTO’s Sixth Session of the Ministerial Conference will be hosted by Hong Kong, China. As an increasing amount of foreign direct investment is being poured into the PRC, there remains much concern as to protection of intellectual property rights within the state. This paper examines the development and efforts China has made to its intellectual property laws and whether it lives up to the intentions of the WTO’s Trade Related Agreement on Intellectual Property Rights

Literature Mapping with PubAtlas — extending PubMed with a ‘BLASTing interface’ *

PubAtlas (www.pubatlas.org) is a web service and standalone program providing literature maps for the biomedical research literature. It accepts user-defined sets of terms (PubMed queries) as input, and permits ‘BLASTing’ of one set against another: for all terms x and y in these sets, deriving the results of the pairwise intersections x AND y. This all vs. all capability extends PubMed with a literature analysis interface. Correspondingly, the basic form of literature map that PubAtlas provides for exploring associations among sets of terms is an interactive tabular display, in heatmap/microarray format

Iso-spectral deformations of general matrix and their reductions on Lie algebras

We study an iso-spectral deformation of general matrix which is a natural generalization of the Toda lattice equation. We prove the integrability of the deformation, and give an explicit formula for the solution to the initial value problem. The formula is obtained by generalizing the orthogonalization procedure of Szeg\"{o}. Based on the root spaces for simple Lie algebras, we consider several reductions of the hierarchy. These include not only the integrable systems studied by Bogoyavlensky and Kostant, but also their generalizations which were not known to be integrable before. The behaviors of the solutions are also studied. Generically, there are two types of solutions, having either sorting property or blowing up to infinity in finite time.Comment: 25 pages, AMSLaTe

The profile of cardiac cytochrome c oxidase (COX) expression in an accelerated cardiac-hypertrophy model

The contribution of the mitochondrial components, the main source of energy for the cardiac hypertrophic growth induced by pressure overload, is not well understood. In the present study, complete coarctation of abdominal aorta was used to induce the rapid development of cardiac hypertrophy in rats. One to two days after surgery, we observed significantly higher blood pressure and cardiac hypertrophy, which remained constantly high afterwards. We found an early increased level of cytochrome c oxidase ( COX) mRNA determined by in-situ hybridization and dot blotting assays in the hypertrophied hearts, and a drop to the baseline 20 days after surgery. Similarly, mitochondrial COX protein level and enzyme activity increased and, however, dropped even lower than baseline 20 days following surgery. In addition, in natural hypertension- induced hypertrophic hearts in genetically hypertensive rats, the COX protein was significantly lower than in normotensive rats. Taken together, the lower efficiency of mitochondrial activity in the enlarged hearts of long-term complete coarcted rats or genetically hypertensive rats could be, at least partially, the cause of hypertensive cardiac disease. Additionally, the rapid complete coarctation-induced cardiac hypertrophy was accompanied by a disproportionate COX activity increase, which was suggested to maintain the cardiac energy-producing capacity in overloaded hearts

Roles of insulin-like growth factor II in cardiomyoblast apoptosis and in hypertensive rat heart with abdominal aorta ligation

Although IGF-II activating the IGF-II receptor signaling pathway has been found to stimulate cardiomyocyte hypertrophy, the role of IGF-II in cardiac cell apoptosis remains unclear. This study aimed to identify the roles of IGF-II and/or IGF-II receptors (IGF-II/IIR) in cardiomyoblast apoptosis and in hypertensive rat hearts with abdominal aorta ligation. Cultured rat heart-derived H9c2 cardiomyoblasts and excised hearts from Sprague-Dawley rats with 0- to 20-day complete abdominal aorta ligation, a model of ANG II elevation and hypertension, were used. IGF-II/IIR expression, caspase activity, DNA fragmentation, and apoptotic cells were measured by RT-PCR, Western blot, agarose gel electrophoresis, and TUNEL assay following various combinations of ANG II, IGF-II/IIR antibody, CsA (calcineurin inhibitor), SP-600125 (JNK inhibitor), SB-203580 (p38 inhibitor), U-0126 (MEK inhibitor), or Staurosporine (PKC inhibitor) in H9c2 cells. ANG II-induced DNA fragmentation and TUNEL-positive cells were blocked by IGF-II/IIR antibodies and antisense IGF-II, but not by IGF-II sense. IGF-II-induced apoptosis was blocked by IGF-IIR antibody and CsA. The increased gene expressions of IGF-II and -IIR induced by ANG II were reversed by U-0126 and Sp600125, respectively. Caspase 8 activities induced by ANG II were attenuated by U-0126, SP-600125, and CsA. DNA fragmentation induced by ANG II was totally blocked by SP-600125, and CsA and was attenuated by U-0126. In rats with 0- to 20-day complete abdominal aorta ligation, the increases in IGF-II/IIR levels in the left ventricle were accompanied by hypertension as well as increases in caspase 9 activities and TUNEL-positive cardiac myocytes. ANG II-induced apoptosis was reversed by IGF-II/IIR blockade and coexisted with increased transactivation of IGF-II and -IIR, which are mediated by ERK and JNK pathways, respectively, both of which further contributed to cardiomyoblast apoptosis via calcineurin signaling. The increased cardiac IGF-II, IGF-IIR, caspase 9, and cellular apoptosis were also found in hypertensive rats with abdominal aorta ligation

Cardiomyoblast apoptosis induced by insulin-like growth factor (IGF)-I resistance is IGF-II dependent and synergistically enhanced by angiotensin II

Objective: This study explores the synergistic effect of cardiomyoblast apoptosis induced by angiotensin II (Ang II) and Insulin-like growth factor (IGF)-I resistance, and elucidates the role of IGF-II via IGF-II receptor (R) and calcineurin pathways in apoptosis induced by Ang II and IGF-I resistance. Methods: Apoptosis of cultured cardiomyoblast H9c2 cells was assessed by DNA fragmentation on agarose gel electrophoresis, nuclear condensation stained with DAPI, and Western blot analysis of pro-apoptotic Bad and cytochrome c in various combinations of control, Ang II, antisense IGF (I or II), IGF (I or II) antibody, IGF (I or II) receptor (R) antibody, or calcineurin inhibitor (Cyclosporine A, (CsA)). Results: We found the following: (I) The combination of Ang II and IGF-I deficiencies had a synergistic effect on apoptosis, confirmed by DNA fragmentation, nuclei condensation, and increases in such proapoptotic proteins as Bad, cytochrome c, caspase 9, and caspase 3 in H9c2 cells. (2) IGF-II and IGF-IIR protein products were increased by antisense IGF-I and IGF-I resistance, but these IGF-II protein products were not affected by sense IGF-I and non-specific antibody IgG in H9c2 cells. (3) The alteration of Bad protein level and the release of cytochrome c, both induced by treatments containing combinations of Ang II and antisense IGF-I, IGF-I antibody or IGF-IR antibody, were inhibited by IGF-II antibody. (4) DNA fragmentation, Bad, and cytochrome c which was induced by treatments combining IGF-IR antibody with Ang II or combining IGF-IR antibody with IGF-II were remarkably attenuated by CsA. Conclusion: IGF-I deficiency and/or IGF-IR resistance induced apoptosis in cardiomyoblast cells. The apoptosis, which might have been caused by the upregulation of IGF-II and IGF-IIR genes possibly activated the downstream calcineurin pathway, was synergistically augmented by Ang II

Space Vehicle Terrestrial Environment Design Requirements Guidelines

The terrestrial environment is an important driver of space vehicle structural, control, and thermal system design. NASA is currently in the process of producing an update to an earlier Terrestrial Environment Guidelines for Aerospace Vehicle Design and Development Handbook. This paper addresses the contents of this updated handbook, with special emphasis on new material being included in the areas of atmospheric thermodynamic models, wind dynamics, atmospheric composition, atmospheric electricity, cloud phenomena, atmospheric extremes, and sea state. In addition, the respective engineering design elements are discussed relative to terrestrial environment inputs that require consideration. Specific lessons learned that have contributed to the advancements made in the application and awareness of terrestrial environment inputs for aerospace engineering applications are presented

Modeling of remote sensing image content using attributed relational graphs

Automatic content modeling and retrieval in remote sensing image databases are important and challenging problems. Statistical pattern recognition and computer vision algorithms concentrate on feature-based analysis and representations in pixel or region levels whereas syntactic and structural techniques focus on modeling symbolic representations for interpreting scenes. We describe a hybrid hierarchical approach for image content modeling and retrieval. First, scenes are decomposed into regions using pixel-based classifiers and an iterative split-and-merge algorithm. Next, spatial relationships of regions are computed using boundary, distance and orientation information based on different region representations. Finally, scenes are modeled using attributed relational graphs that combine region class information and spatial arrangements. We demonstrate the effectiveness of this approach in query scenarios that cannot be expressed by traditional approaches but where the proposed models can capture both feature and spatial characteristics of scenes and can retrieve similar areas according to their high-level semantic content. © Springer-Verlag Berlin Heidelberg 2006

Experimental investigation and validation of neutral beam current drive for ITER through ITPA Joint Experiments

Joint experiments investigating the off-axis neutral beam current drive (NBCD) capability to be utilized for advanced operation scenario development in ITER were conducted in four tokamaks (ASDEX Upgrade (AUG), DIII-D, JT-60U and MAST) through the international tokamak physics activity (ITPA). The following results were obtained in the joint experiments, where the toroidal field, B t, covered 0.4-3.7 T, the plasma current, Ip, 0.5-1.2 MA, and the beam energy, Eb, 65-350 keV. A current profile broadened by off-axis NBCD was observed in MAST. In DIII-D and JT-60U, the NB driven current profile has been evaluated using motional Stark effect diagnostics and good agreement between the measured and calculated NB driven current profile was observed. In AUG (at low δ ∼ 0.2) and DIII-D, introduction of a fast-ion diffusion coefficient of Db ∼ 0.3-0.5 m2 s-1 in the calculation gave better agreement at high heating power (5 MW and 7.2 MW, respectively), suggesting anomalous transport of fast ions by turbulence. It was found through these ITPA joint experiments that NBCD related physics quantities reasonably agree with calculations (with Db = 0-0.5 m2 s-1) in all devices when there is no magnetohydrodynamic (MHD) activity except ELMs. Proximity of measured off-axis beam driven current to the corresponding calculation with Db = 0 has been discussed for ITER in terms of a theoretically predicted scaling of fast-ion diffusion that depends on Eb/Te for electrostatic turbulence or βt for electromagnetic turbulence. © 2011 IAEA, Vienna