摘要 :
In this study a binary Mg-Zn magnesium alloy was researched as a degradable biomedical material. An Mg-Zn alloy fabricated with high-purity raw materials and using a clean melting process had very low levels of impurities. After s...
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In this study a binary Mg-Zn magnesium alloy was researched as a degradable biomedical material. An Mg-Zn alloy fabricated with high-purity raw materials and using a clean melting process had very low levels of impurities. After solid solution treatment and hot working the grain size of the Mg-Zn alloy was finer and a uniform single phase was gained. The mechanical properties of this Mg-Zn alloy were suitable for implant applications, i.e. the tensile strength and elongation achieved were approximately 279.5MPa and 18.8%, respectively. The results of in vitro degradation experiments including electrochemical measurements and immersion tests revealed that the zinc could elevate the corrosion potential of Mg in simulated body fluid (SBF) and reduce the degradation rate. The corrosion products on the surface of Mg-Zn were hydroxyapatite (HA) and other Mg/Ca phosphates in SBF. In addition, the influence caused by in vitro degradation on mechanical properties was studied, and the results showed that the bending strength of Mg-Zn alloy dropped sharply in the earlier stage of degradation, while smoothly during the later period. The in vitro cytotoxicity of Mg-Zn was examined. The result 0-1 grade revealed that the Mg-Zn alloy was harmless to L-929 cells. For in vivo experiments, Mg-Zn rods were implanted into the femoral shaft of rabbits. The radiographs illustrated that the magnesium alloy could be gradually absorbed in vivo at about 2.32mm/yr degradation rate obtained by weight loss method. Hematoxylin and eosin (HE) stained section around Mg-Zn rods suggested that there were newly formed bone surrounding the implant. HE stained tissue (containing heart, liver, kidney and spleen tissues) and the biochemical measurements, including serum magnesium, serum creatinine (CREA), blood urea nitrogen (BUN), glutamic-pyruvic transaminase (GPT) and creatine kinase (CK) proved that the in vivo degradation of Mg-Zn did not harm the important organs. Moreover, no adverse effects of hydrogen generated by degradation had been observed and also no negative effects caused by the release of zinc were detected. These results suggested that the novel Mg-Zn binary alloy had good biocompatibility in vivo.
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The objective of our study was to determine granulocyte-macrophage colony-stimulating factor (GM-CSF) activity in the brain following GM-CSF induction. We injected recombinant mouse GM-CSF into the brains of 8-month-old C57BL6 mic...
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The objective of our study was to determine granulocyte-macrophage colony-stimulating factor (GM-CSF) activity in the brain following GM-CSF induction. We injected recombinant mouse GM-CSF into the brains of 8-month-old C57BL6 mice via intracerebroventricular injections and studied the activities of microglia, astrocytes, and neurons. We also sought to determine whether an anti-GM-CSF antibody could suppress endogenous microglial activity in the C57BL6 mice and could also suppress microglial activity induced by the recombinant mouse GM-CSF in another group of C57BL6 mice. Using quantitative real-time RT-PCR, we assessed microglial, astrocytic, and neuronal activity by measuring mRNA expression of pro-inflammatory cytokines, GFAP, and the neuronal marker NeuN in the cerebral cortex tissues from C57BL6 mice. We performed immunoblotting and immunohistochemistry of activated microglia in different regions of the brains from control (phosphate-buffered saline-injected C57BL6 mice) and experimental mice (recombinant GM-CSF-injected C57BL6 mice, GM-CSF antibody-injected C57BL6 mice, and recombinant mouse GM-CSF plus anti-GM-CSF antibody-injected C57BL6 mice). We found increased mRNA expression of CD40 (9.75-fold), tumor necrosis factor-alpha (2.1-fold), CD45 (1.73-fold), and CD11c (1.70-fold) in the cerebral cortex of C57BL6 mice that were induced with recombinant GM-CSF, compared with control mice. Further, the anti-GM-CSF antibody suppressed microglia in mice that were induced with recombinant GM-CSF. Our immunoblotting and immunohistochemistry findings of GM-CSF-associated cytokines in C57BL6 mice induced with recombinant GM-CSF, in C57BL6 mice injected with the anti-GM-CSF antibody, and in C57BL6 mice injected with recombinant mouse GM-CSF plus anti-GM-CSF antibody concurred with our real-time RT-PCR findings. These findings suggest that GM-CSF is critical for microglial activation and that anti-GM-CSF antibody suppresses microglial activity in the CNS. The findings from this study may have implications for anti-inflammatory effects of Alzheimer's disease and experimental autoimmune encephalomyelitis mice (a multiple sclerosis mouse model).
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With increasing data rate and power density, high-performance memories have started to require dynamic thermal management (DTM), following the trend of processor and hard drive. There are also lack of a memory thermal model and si...
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With increasing data rate and power density, high-performance memories have started to require dynamic thermal management (DTM), following the trend of processor and hard drive. There are also lack of a memory thermal model and simulation tools to facilitate the research of memory DTM. This study investigates the approach of coordinating processor, which is the source of memory access requests, and memory to improve system performance and/or power efficiency during memory thermal emergency. Two such schemes, namely adaptive core gating (DTM-ACG) and coordinated DVFS (DTM-CDVFS), are proposed and evaluated on a real server platform. DTM-ACG gates processor cores and DTM-CDVFS scales down the frequency and voltage level of processor cores according to memory thermal emergency level. Their combination, namely DTM-COMB, is also evaluated. The experimental results show that the two schemes, while successfully controlling memory activities and handling thermal emergencies, improve performance significantly under the given thermal envelope. The measurement results from an Intel SR1500AL server testbed show that on average, DTM-ACG and DTM-CDVFS improve performance by 6.7 and 15.3 percent, respectively, over a prior memory bandwidth throttling scheme. DTM-CDVFS also reduces the processor power rate by 15.5 percent and system (including processor and memory) energy by 22.7 percent. Additionally, we propose a DRAM thermal model and validate it with measurement on the instrumented server platform. We find that our proposed model faithfully catches the dynamic DRAM temperature changes; the average difference between the modeled and measured temperature is less than $(1^{circ}{rm C})$.
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This paper incorporates the group sparse representation into the well-known canonical correlation analysis (CCA) framework and proposes a novel discriminant feature extraction technique named group sparse canonical correlation ana...
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This paper incorporates the group sparse representation into the well-known canonical correlation analysis (CCA) framework and proposes a novel discriminant feature extraction technique named group sparse canonical correlation analysis (GSCCA). GSCCA uses two sets of variables and aims at preserving the group sparse (GS) characteristics of data within each set in addition to maximize the global interset covariance. With GS weights computed prior to feature extraction, the locality, sparsity and discriminant information of data can be adaptively determined. The GS weights are obtained from an NP-hard group-sparsity promoting problem that considers all highly correlated data within a group. By defining one of the two variable sets as the class label matrix, GSCCA is effectively extended to multiclass scenarios. Then GSCCA is theoretically formulated as a least-squares problem as CCA does. Comparative analysis between this work and the related studies demonstrate that our algorithm is more general exhibiting attractive properties. The projection matrix of GSCCA is analytically solved by applying eigen-decomposition and trace ratio (TR) optimization. Extensive benchmark simulations are conducted to examine GSCCA. Results show that our approach delivers promising results, compared with other related algorithms.
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BACKGROUND: Prior studies have suggested lower use of guideline-recommended therapy and worse poststroke outcomes in older patients. We sought to examine age-related differences in characteristics, performance measures, temporal t...
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BACKGROUND: Prior studies have suggested lower use of guideline-recommended therapy and worse poststroke outcomes in older patients. We sought to examine age-related differences in characteristics, performance measures, temporal trends, and early clinical outcomes for acute ischemic stroke in a large contemporary cohort. METHODS AND RESULTS: The relationships between age and clinical characteristics, performance measures, and in-hospital outcomes were analyzed in 502 036 ischemic stroke admissions from 1256 hospitals in the Get With the Guidelines-Stroke program from 2003 to 2009. Data were analyzed by age groups (<50, 50 to 59, 60 to 69, 70 to 79, 80 to 89, and >/=90 years) and with age as a continuous variable. Seven predefined performance measures and 2 summary measures were analyzed. Mean age of ischemic stroke patients was 71.0+/-14.6 years; 52.5% were women. Older patients were more likely to have a history of atrial fibrillation or hypertension and less likely to be black, Hispanic, or current/recent smokers. Although modest age-related differences in each individual performance measure were identified, there were substantial temporal improvements in performance measures from 2003 to 2009 in each age group, and many age-related treatment gaps were narrowed or eliminated over time. Older patients were less likely to be discharged home (adjusted odds ratio, 0.69; 95% confidence interval, 0.68 to 0.69) and more likely to die in hospital (adjusted odds ratio, 1.27; 95% confidence interval, 1.25 to 1.29) for each 10-year age increase. CONCLUSIONS: Older patients with ischemic stroke differ in clinical characteristics and experience higher in-hospital mortality than younger patients. Performance measure-based treatment rates improved substantially over time for ischemic stroke patients in all age groups, resulting in smaller age-related treatment gaps.
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Situated in the central part of China, the Han River Basin is undergoing rapid social and economic development with some human interventions to be made soon which will profoundly influence the water environment of the basin. The i...
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Situated in the central part of China, the Han River Basin is undergoing rapid social and economic development with some human interventions to be made soon which will profoundly influence the water environment of the basin. The integrated MIKE 11 model system comprising of a rainfall-runoff model (NAM), a non-point load evaluation model (LOAD), a hydrodynamic model (MIKE 11 HD) and a water quality model (ECOLab) was applied to investigate the impact of the Middle Route of the South-North Water Diversion Project on the Han River and the effectiveness of the 2 proposed mitigation projects, the 22 wastewater treatment plants (WWTPs) and the Yangtze-Han Water Diversion Project. The study concludes that business as usual will lead to a continuing rapid deterioration of the water quality of the Han River. Implementation of the Middle Route of the South-North Water Diversion Project in 2010 will bring disastrous consequence in the form of the remarkably elevated pollution level and high risk of algae bloom in the middle and lower reaches. The proposed WWTPs will merely lower the pollution level in the reach by around 10%, while the Yangtze-Han Water Diversion Project can significantly improve the water quality in the downstream 200-km reach. The results reveal that serious water quality problem will emerge in the middle reach between Xiangfan and Qianjiang in the future. Implementation of the South-North Water Diversion Project (phase II) in 2030 will further exacerbate the problem. In order to effectively improve the water quality of the Han River, it is suggested that nutrient removal processes should be adopted in the proposed WWTPs, and the pollution load from the non-point sources, especially the load from the upstream Henan Province, should be effectively controlled.
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We study the problem of human activity recognition from RGB-Depth (RGBD) sensors when the skeletons are not available. The skeleton tracking in Kinect SDK works well when the human subject is facing the camera and there are no occ...
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We study the problem of human activity recognition from RGB-Depth (RGBD) sensors when the skeletons are not available. The skeleton tracking in Kinect SDK works well when the human subject is facing the camera and there are no occlusions. In surveillance or nursing home monitoring scenarios, however, the camera is usually mounted higher than human subjects, and there may be occlusions. The interest-point based approach is widely used in RGB based activity recognition, it can be used in both RGB and depth channels. Whether we should extract interest points independently of each channel or extract interest points from only one of the channels is discussed in this paper. The goal of this paper is to compare the performances of different methods of extracting interest points. In addition, we have developed a depth map-based descriptor and built an RGBD dataset, called RGBD-SAR, for senior activity recognition. We show that the best performance is achieved when we extract interest points solely from RGB channels, and combine the RGB-based descriptors with the depth map-based descriptors. We also present a baseline performance of the RGBD-SAR dataset.
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Although cancer patients exhibit a generalized immunosuppressive status, substantial evidence indicates that the inflammatory reaction at a tumor site can promote tumor growth and progression. Hepatocellular carcinoma (HCC) is usu...
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Although cancer patients exhibit a generalized immunosuppressive status, substantial evidence indicates that the inflammatory reaction at a tumor site can promote tumor growth and progression. Hepatocellular carcinoma (HCC) is usually derived from inflamed cirrhotic liver with extensive leukocyte infiltration. We recently found that proinflammatory T helper (Th)17 cells are accumulated in HCC tissue, where they promote disease progression by fostering angiogenesis. Here we show that interleukin (IL)-17-producing cells were enriched predominantly in peritumoral stroma of HCC tissues, and their levels were well correlated with monocyte/macrophage density in the same area. Most peritumoral CD68(+) cells exhibited an activated phenotype. Accordingly, tumor-activated monocytes were significantly superior to the suppressive tumor macrophages in inducing expansion of Th17 cells from circulating memory T cells in vitro with phenotypic features similar to those isolated from HCCs. Moreover, we found that tumor-activated monocytes secreted a set of key proinflammatory cytokines that triggered proliferation of functional Th17 cells. Inhibition of monocytes/macrophages inflammation in liver markedly reduced the level of tumor-infiltrating Th17 cells and tumor growth in vivo. CONCLUSION: The proinflammatory Th17 cells are generated and regulated by a fine-tuned collaborative action between different types of immune cells in distinct HCC microenvironments, and allows the inflammatory response of activated monocytes to be rerouted in a tumor-promoting direction. Selectively modulating the "context" of inflammatory response in tumors might provide a novel strategy for anticancer therapy.
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Diffuse large B cell lymphoma (DLBCL) is clinically and biologically heterogeneous. In most cases of DLBCL, lymphoma cells co-express vascular endothelial growth factor (VEGF) and its receptors VEGFR1 and VEGFR2, suggesting autocr...
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Diffuse large B cell lymphoma (DLBCL) is clinically and biologically heterogeneous. In most cases of DLBCL, lymphoma cells co-express vascular endothelial growth factor (VEGF) and its receptors VEGFR1 and VEGFR2, suggesting autocrine in addition to angiogenic effects. We enumerated microvessel density and scored lymphoma cell expression of VEGF, VEGFR1, VEGFR2 and phosphorylated VEGFR2 in 162 de novo DLBCL patients treated with R-CHOP (rituximab, cyclophosphamide, vincristine, doxorubicin and prednisone)-like regimens. VEGFR2 expression correlated with shorter overall survival (OS) independent of International Prognostic Index (IPI) (P = 0.0028). Phosphorylated VEGFR2 (detected in 13% of cases) correlated with shorter progression-free survival (PFS, P = 0.044) and trended toward shorter OS on univariate analysis. VEGFR1 was not predictive of survival on univariate analysis, but it did correlate with better OS on multivariate analysis with VEGF, VEGFR2 and IPI (P = 0.036); in patients with weak VEGFR2, lack of VEGFR1 coexpression was significantly correlated with poor OS independent of IPI (P = 0.01). These results are concordant with our prior finding of an association of VEGFR1 with longer OS in DLBCL treated with chemotherapy alone. We postulate that VEGFR1 may oppose autocrine VEGFR2 signalling in DLBCL by competing for VEGF binding. In contrast to our prior results with chemotherapy alone, microvessel density was not prognostic of PFS or OS with R-CHOP-like therapy.
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Annexin A1 (ANXA1), a mediator of the anti-inflammatory action of glucocorticoids, is important in cancer development and progression, whereas NF-kappaB regulates multiple cellular phenomena, some of them associated with inflammat...
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Annexin A1 (ANXA1), a mediator of the anti-inflammatory action of glucocorticoids, is important in cancer development and progression, whereas NF-kappaB regulates multiple cellular phenomena, some of them associated with inflammation and cancer. We showed that glucocorticoids and chemopreventive modified nonsteroidal anti-inflammatory drugs, such as nitric oxide-donating aspirin (NO-ASA) and phospho-aspirin, induced ANXA1 in cultured human colon and pancreatic cancer cells. ANXA1 associated with NF-kappaB and suppressed its transcriptional activity by preventing NF-kappaB binding to DNA. The induction of ANXA1 by glucocorticoids was proportional to their anti-inflammatory potency, as was the suppression of NF-kappaB activity, which was accompanied by enhanced apoptosis and inhibition of cell growth mediated by changes in NF-kappaB-dependent cell signaling. The proposed novel mechanism was operational in the intestinal mucosa of mice treated with dexamethasone or NO-ASA. ANXA1-based oligopeptides displayed the same effects as ANXA1 on NF-kappaB. One such tripeptide (Gln-Ala-Trp) administered to nude mice inhibited the growth of SW480 human colon cancer xenografts by 58% compared with control (P < 0.01). Our findings reveal that ANXA1 is an inducible endogenous inhibitor of NF-kappaB in human cancer cells and mice, provide a novel molecular mechanism for the action of anti-inflammatory agents, and suggest the possibility of mechanism-driven drug development.
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