Coordinated probabilistic optimal decision-making model for multi-area ATC with risk control

In the decision-making of multi-area ATC (Available Transfer Capacity) in electricity market environment, the existing resources of transmission network should be optimally dispatched and coordinately employed on the premise that the secure system operation is maintained and risk associated is controllable. The non-sequential Monte Carlo simulation is used to determine the ATC probability density distribution of specified areas under the influence of several uncertainty factors, based on which, a coordinated probabilistic optimal decision-making model with the maximal risk benefit as its objective is developed for multi-area ATC. The NSGA-II is applied to calculate the ATC of each area, which considers the risk cost caused by relevant uncertainty factors and the synchronous coordination among areas. The essential characteristics of the developed model and the employed algorithm are illustrated by the example of IEEE 118-bus test system. Simulative result shows that, the risk of multi-area ATC decision-making is influenced by the uncertainties in power system operation and the relative importance degrees of different areas.

Analysis and control of cracking due to shrinkage in cast-in-place reinforced concrete slabs

The numerical analysis method of cracking in cast-in-place reinforced concrete slabs is presented. T he results agree w ell with the actual conditions. T he current state of knowledge and some new research findings on crack-control are introduced such as increasing the quantities of the distribution steel, adopting fibre reinforced concrete etc. Some recommended crack-control procedures used in design construction is presented based on the investigation and study of cracking in a frame structure.

Serum levels of soluble receptor for advanced glycation end products and of S100 proteins are associated with inflammatory, autoantibody, and classical risk markers of joint and vascular damage in rheumatoid arthritis

Introduction: The receptor for advanced glycation end products (RAGE) is a member of the immunoglobulin superfamily of cell surface receptor molecules. High concentrations of three of its putative proinflammatory ligands, S100A8/A9 complex (calprotectin), S100A8, and S100A12, are found in rheumatoid arthritis (RA) serum and synovial fluid. In contrast, soluble RAGE (sRAGE) may prevent proinflammatory effects by acting as a decoy. This study evaluated the serum levels of S100A9, S100A8, S100A12 and sRAGE in RA patients, to determine their relationship to inflammation and joint and vascular damage. Methods: Serum sRAGE, S100A9, S100A8 and S100A12 levels from 138 patients with established RA and 44 healthy controls were measured by ELISA and compared by unpaired t test. In RA patients, associations with disease activity and severity variables were analyzed by simple and multiple linear regressions. Results: Serum S100A9, S100A8 and S100A12 levels were correlated in RA patients. S100A9 levels were associated with body mass index (BMI), and with serum levels of S100A8 and S100A12. S100A8 levels were associated with serum levels of S100A9, presence of anti-citrullinated peptide antibodies (ACPA), and rheumatoid factor (RF). S100A12 levels were associated with presence of ACPA, history of diabetes, and serum S100A9 levels. sRAGE levels were negatively associated with serum levels of C-reactive protein (CRP) and high-density lipoprotein (HDL), history of vasculitis, and the presence of the RAGE 82Ser polymorphism. Conclusions: sRAGE and S100 proteins were associated not just with RA inflammation and autoantibody production, but also with classical vascular risk factors for end-organ damage. Consistent with its role as a RAGE decoy molecule, sRAGE had the opposite effects to S100 proteins in that S100 proteins were associated with autoantibodies and vascular risk, whereas sRAGE was associated with protection against joint and vascular damage. These data suggest that RAGE activity influences co-development of joint and vascular disease in rheumatoid arthritis patients.

Seminal plasma proteome of eletroejaculated Bos indicus bulls

The present study describes the seminal plasma proteome of Bos indicus bulls. Fifty-six, 24-month old Australian Brahman sires were evaluated and subjected to electroejaculation. Seminal plasma proteins were separated by 2-D SDS-PAGE and identified by mass spectrometry. The percentage of progressively motile and morphologically normal sperm of the bulls were 70.4±2.3 and 64±3.2%, respectively. A total of 108 spots were identified in the 2-D maps, corresponding to 46 proteins. Binder of sperm proteins accounted for 55.8% of all spots detected in the maps and spermadhesins comprised the second most abundant constituents. Other proteins of the Bos indicus seminal plasma include clusterin, albumin, transferrin, metalloproteinase inhibitor 2, osteopontin, epididymal secretory protein E1, apolipoprotein A-1, heat shock 70kDa protein, glutathione peroxidase 3, cathelicidins, alpha-enolase, tripeptidyl-peptidase 1, zinc-alpha-2-glycoprotein, plasma serine protease inhibitor, beta 2-microglobulin, proteasome subunit beta type-4, actin, cathepsins, nucleobinding-1, protein S100-A9, hemoglobin subunit alpha, cadherin-1, angiogenin-1, fibrinogen alpha and beta chain, ephirin-A1, protein DJ-1, serpin A3-7, alpha-2-macroglobulin, annexin A1, complement factor B, polymeric immunoglobulin receptor, seminal ribonuclease, ribonuclease-4, prostaglandin-H2 D-isomarase, platelet-activating factor acetylhydrolase, and phosphoglycerate kinase In conclusion, this work uniquely portrays the Bos indicus seminal fluid proteome, based on samples from a large set of animals representing the Brahman cattle of the tropical Northern Australia. Based on putative biochemical attributes, seminal proteins act during sperm maturation, protection, capacitation and fertilization.

Combining unsupervised and invigilated assessment of introductory programming

We compared student performance on large-scale take-home assignments and small-scale invigilated tests that require competency with exactly the same programming concepts. The purpose of the tests, which were carried out soon after the take home assignments were submitted, was to validate the students' assignments as individual work. We found widespread discrepancies between the marks achieved by students between the two types of tasks. Many students were able to achieve a much higher grade on the take-home assignments than the invigilated tests. We conclude that these paired assessments are an effective way to quickly identify students who are still struggling with programming concepts that we might otherwise assume they understand, given their ability to complete similar, yet more complicated, tasks in their own time. We classify these students as not yet being at the neo-Piagetian stage of concrete operational reasoning.

南黄海浮游植物的固碳强度与污染物胁迫下海水碳源/汇格局的变化

本论文在解析了南黄海生态环境的基础上，首次研究揭示了浮游植物固碳强度的年际变化及生态反馈机制，获得了东中国近海浮游植物固碳强度及对海域源/汇格局的影响程度；同时，用室内模拟实验探讨了重金属和有机污染物胁迫下海水无机碳体系和源汇格局的变化过程，获得了一些新的认识。主要结论如下： 1. 南黄海浮游植物固碳强度具有明显的时空变化特征，与海域光照、流系和水团变化、海水磷的浓度等因素密切相关，并在一定程度上决定海区碳源/汇的性质。2005年秋季浮游植物日固碳量达9.5万吨，1983-2005年间，南黄海浮游植物固碳强度有降低的趋势，与海水关键营养盐－磷的限制有关。东中国近海浮游植物年总固碳量约为2.2亿吨，约占全球近海浮游植物的年固碳量的2.0%。 在综合分析秋季南黄海水文、化学、生物背景的基础上，系统阐明了海域浮游植物固碳体系的生物地球化学机制。结果表明，2005年秋季南黄海浮游植物固碳强度，即初级生产力变化在 97−701 mgC m-2 d-1之间，平均为307 mg C m-2 d-1；与其关系比较密切的环境因子为海水透明度、盐度、pH、氨氮 (NH4-N)、磷酸盐 (PO4-P) 以及Chl a。在这些因素中，PO4-P对初级生产力的影响最大，显然11月份南黄海的磷是浮游植物生长的限制因子，次之的影响因素是Chl a和NH4-N。 对南黄海源汇格局的研究发现，如果除去涌升流较为活跃的站位（A9、B7、B8、B9、C8、C9、 D9和A1），2005年秋季表层海水pCO2与浮游植物固碳强度明显负相关（r=-0.8，n=23, p<0.001）。在南黄海东部浮游植物固碳强度较高，pCO2值较低；而在西部海区浮游植物固碳强度较低的区域，其pCO2值较高。碳源/汇转折点浮游植物固碳强度为230 mgC m-2 d-1，即小于此值，海区为大气二氧化碳的源，反之为汇，并且CO2汇区浮游植物固碳强度平均值约是CO2源区的2倍多；浮游植物固碳作用，在某一时间和空间尺度内，基本决定了海区的源汇格局。估算结果显示，东中国近海浮游植物固碳量约为222×106t a-1，约为东中国近海通过海－气界面总表观碳汇强度每年1369万吨的16.2倍，仅就浮游植物的年固碳量而言，东中国近海约占全球近海浮游植物的年固碳量的2.0%。 研究揭示了近年来南黄海浮游植物固碳强度具有区域与年际变化明显这一显著特点。一般，近岸区（由黄海沿岸水和表层水控制）内，光照是浮游植物固碳的主要限制因子；从2001年后的大多数年份中，中央区（黄海冷水团控制）的浮游植物固碳强度均与磷酸盐浓度显著正相关，但与氮浓度的相关性不大，说明南黄海生态系统普遍存在着磷限制而非氮限制；混合区终年受黄、东海混合水控制，受到光照条件和营养盐浓度同时影响。根据本次观测所获数据，结合以前研究者的调查资料，我们发现从1983年到2005年，南黄海浮游植物优势种由Bacillariophyta变为Pyrrophyta，浮游植物细胞丰度和Chl a明显下降，浮游植物固碳强度几乎下降了二分之一 （由569.50 mgC m-2 d-1下降至306.83 mgC m-2 d-1），说明南黄海在世界边缘海固碳过程中的作用在降低。经过相关水质参数及生态环境变化的分析，以上现象是对关键营养盐磷的限制以及光限制响应的缘故。此外，研究还发现，由于南黄海初级生产者产量下降所引起的一些生态反馈信息，如浮游动物固碳量的下降和鱼类产量的锐减。 2. 室内模拟实验显示，重金属（铅、铜、镉和锌）及有机污染物（乙醇、丙酮、尿素和多灭磷）对水体生物固碳体系有重要影响，较低浓度时可提高水体的固碳能力，相应水体中的DIC、HCO3-和 Pco2 与对照组相比都明显下降 (P<0.01)；当污染物达到一定浓度后，水体生物的固碳能力明显下降，其有机碳可降解转化为无机碳。当污染物小于转折浓度水体为大气二氧化碳的汇，反之为源。 水体固碳体系对于不同种类、不同浓度的污染物质所表现的受胁迫情况不同，低浓度各污染物（包括重金属和有机污染物）添加组中（对于重金属为0.1和1µmol•L-1，醇和酮分别为<0.5 mol L-1和<0.75 mol L-1），藻干重及固碳量均要大于初始值，说明适量的外源污染可能会促进藻类生长，提高水体的固碳能力，相应水体中的DIC、HCO3- 和PCO2与对照组相比都明显下降 (P<0.01)。当污染物达到一定浓度后，由于其毒害作用，使得水体内生物的固碳能力下降，甚至分解并转化为无机碳，从会引起DIC、HCO3- 和PCO2含量的升高，其含量上升幅度会因固碳体系对不同种类污染物耐受程度的差异而不同。对于尿素和多灭磷，二者浓度分别达到80和20mgL-1时，水体中二氧化碳各参数仍呈现下降趋势，说明在该浓度范围内，大型藻类（如石莼）仍可利用添加物中的氮和磷，将其做为氮源或磷源，促进水体总固碳量的增加。 污染物胁迫对水体碳源汇能力及格局可起到一定的调控作用，与污染物的浓度密切相关，污染物存在着一转折浓度，分别为5µmol L-1（铜）、20µmol L-1（镉） 0.75mol L-1（酮），当污染物添加小于转折浓度并排除其他影响因素时，水体表现为大气CO2的汇，并且适量的增加污染物浓度会使海洋碳汇能力有所增强；而当污染物超出转折浓度时，水体成为CO2的源，其CO2的释放量是随着污染物浓度的增加而增大。对与研究中其他种类的污染物，在实验室设计范围内，水体始终表现为大气CO2的汇。

Sensitivity to switching rates in stochastically switched ODEs

We consider a stochastic process driven by a linear ordinary differential equation whose right-hand side switches at exponential times between a collection of different matrices. We construct planar examples that switch between two matrices where the individual matrices and the average of the two matrices are all Hurwitz (all eigenvalues have strictly negative real part), but nonetheless the process goes to infinity at large time for certain values of the switching rate. We further construct examples in higher dimensions where again the two individual matrices and their averages are all Hurwitz, but the process has arbitrarily many transitions between going to zero and going to infinity at large time as the switching rate varies. In order to construct these examples, we first prove in general that if each of the individual matrices is Hurwitz, then the process goes to zero at large time for sufficiently slow switching rate and if the average matrix is Hurwitz, then the process goes to zero at large time for sufficiently fast switching rate. We also give simple conditions that ensure the process goes to zero at large time for all switching rates. © 2014 International Press.

Thrombopoietin, flt3-ligand and c-kit-ligand modulate HOX gene expression in expanding cord blood CD133(+) cells

Haemopoietic stem/progenitor cell (HSPC) development is regulated by extrinsic and intrinsic stimuli. Extrinsic modulators include growth factors and cell adhesion molecules, whereas intrinsic regulation is achieved with many transcription factor families, of which the HOX gene products are known to be important in haemopoiesis. Umbilical cord blood CD133(+) HSPC proliferation potential was tested in liquid culture with 'TPOFLK' (thrombopoietin, flt-3 ligand and c-kit ligand, promoting HSPC survival and self-renewal), in comparison to 'K36EG' (c-kit-ligand, interleukins-3 and -6, erythropoietin and granulocyte colony-stimulating factor, inducing haemopoietic differentiation). TPOFLK induced a higher CD133(+) HSPC proliferation (up to 60-fold more, at week 8) and maintained a higher frequency of the primitive colony-forming cells than K36EG. Quantitative polymerase chain reaction analysis revealed opposite expression patterns for specific HOX genes in expanding cord blood CD133(+) HSPC. After 8 weeks in liquid culture, TPOFLK increased the expression of HOX B3, B4 and A9 (associated with uncommitted HSPC) and reduced the expression of HOX B8 and A10 (expressed in committed myeloid cells) when compared to K36EG. These results suggest that TPOFLK induces CD133(+) HSPC proliferation, self-renewal and maintenance, up-regulation of HOX B3, B4 and A9 and down-regulation of HOX B8 and A10 gene expression.

Differential Hox Expression in Murine Embryonic Stem Cell Models of Normal and Malignant Hematopoiesis.

The Hox family are master transcriptional regulators of developmental processes, including hematopoiesis. The Hox regulators, caudal homeobox factors (Cdx1-4), and Meis1, along with several individual Hox proteins, are implicated in stem cell expansion during embryonic development, with gene dosage playing a significant role in the overall function of the integrated Hox network. To investigate the role of this network in normal and aberrant, early hematopoiesis, we employed an in vitro embryonic stem cell differentiation system, which recapitulates mouse developmental hematopoiesis. Expression profiles of Hox, Pbx1, and Meis1 genes were quantified at distinct stages during the hematopoietic differentiation process and compared with the effects of expressing the leukemic oncogene Tel/PDGFRß. During normal differentiation the Hoxa cluster, Pbx1 and Meis1 predominated, with a marked reduction in the majority of Hox genes (27/39) and Meis1 occurring during hematopoietic commitment. Only the posterior Hoxa cluster genes (a9, a10, a11, and a13) maintained or increased expression at the hematopoietic colony stage. Cdx4, Meis1, and a subset of Hox genes, including a7 and a9, were differentially expressed after short-term oncogenic (Tel/PDGFRß) induction. Whereas Hoxa4-10, b1, b2, b4, and b9 were upregulated during oncogenic driven myelomonocytic differentiation. Heterodimers between Hoxa7/Hoxa9, Meis1, and Pbx have previously been implicated in regulating target genes involved in hematopoietic stem cell (HSC) expansion and leukemic progression. These results provide direct evidence that transcriptional flux through the Hox network occurs at very early stages during hematopoietic differentiation and validates embryonic stem cell models for gaining insights into the genetic regulation of normal and malignant hematopoiesis.

FPGA Prototyping of Emerging Manycore Architectures for Parallel Programming Research using Formic Boards

Performance evaluation of parallel software and architectural exploration of innovative hardware support face a common challenge with emerging manycore platforms: they are limited by the slow running time and the low accuracy of software simulators. Manycore FPGA prototypes are difficult to build, but they offer great rewards. Software running on such prototypes runs orders of magnitude faster than current simulators. Moreover, researchers gain significant architectural insight during the modeling process. We use the Formic FPGA prototyping board [1], which specifically targets scalable and cost-efficient multi-board prototyping, to build and test a 64-board model of a 512-core, MicroBlaze-based, non-coherent hardware prototype with a full network-on-chip in a 3D-mesh topology. We expand the hardware architecture to include the ARM Versatile Express platforms and build a 520-core heterogeneous prototype of 8 Cortex-A9 cores and 512 MicroBlaze cores. We then develop an MPI library for the prototype and evaluate it extensively using several bare-metal and MPI benchmarks. We find that our processor prototype is highly scalable, models faithfully single-chip multicore architectures, and is a very efficient platform for parallel programming research, being 50,000 times faster than software simulation.