An ADMM-based Distributed Optimization Method for Solving Security-Constrained AC Optimal Power Flow

In this paper, we study efficient and robust computational methods for solving the security-constrained alternating current optimal power flow (SC-ACOPF) problem, a two-stage nonlinear optimization problem with disjunctive constraints, that is central to the operation of electric power grids. The first-stage problem in SC-ACOPF determines the operation of the power grid in normal condition, while the second-stage problem responds to various contingencies of losing generators, transmission lines, and transformers. The two stages are coupled through disjunctive constraints, which model generators' active and reactive power output changes responding to system-wide active power imbalance and voltage deviations after contingencies. Real-world SC-ACOPF problems may involve power grids with more than 30k buses and 22k contingencies and need to be solved within 10-45 minutes to get a base case solution with high feasibility and reasonably good generation cost. We develop a comprehensive algorithmic framework to solve SC-ACOPF that meets the challenge of speed, solution quality, and computation robustness. In particular, we develop a smoothing technique to approximate disjunctive constraints into a smooth structure which can be handled by interior-point solvers; we design a distributed optimization algorithm to efficiently generate first-stage solutions; we propose a screening procedure to prioritize contingencies; and finally, we develop a reliable and parallel architecture that integrates all algorithmic components. Extensive tests on industry-scale systems demonstrate the superior performance of the proposed algorithms

Numerical analysis of thermoelectric power generation coupled with temperature-dependent material properties

Thermoelectric generator (TEG) with improved performance is a promising technology in power supply and energy harvesting. Existing studies primarily adopt constant material properties to investigate TEG performance. However, thermoelectric (TE) material properties are subjected to considerable variations with temperature. Thus, reasonable doubts have risen concerning the influence level of temperature-dependent material properties on TEG performance. To solve this problem, an efficient and a comprehensive one-dimensional numerical model is developed to fully consider the third-order polynomial temperature-dependent thermal conductivity, Seebeck coefficient, and electrical resistivity. Control volume and finite difference algorithms are compared, and experiments are conducted to verify the developed numerical model. The temperature distribution along the TE leg obviously differs from the parabolic shape, which is a classic temperature distribution under the assumption of constant material properties. Insights find that the local change rate of thermal conductivity and Thomson effect are the essential reasons for the abovementioned phenomenon. It has been found that Thomson heat is released in the part of the leg near the cold-end, whereas it is absorbed in the remaining parts of the leg near the hot-end. The electric power on the basis of constant material properties is confirmed to be accurate enough by the developed numerical model, but the parabolic shape of the TE efficiency can be only obtained when temperature-dependent material properties are considered. Furthermore, it is wise to improve the TE efficiency by structural optimization. The present work provides an efficient and a comprehensive one-dimensional numerical model to include temperature-dependent material properties. New insights into the temperature and heat flux distribution, Thomson influence, and structural optimization potential are also presented for the in-depth understanding of the TE conversion process

Cytoplasmic p21 is a potential predictor for cisplatin sensitivity in ovarian cancer

<p>Abstract</p> <p>Background</p> <p>P21^(WAF1/Cip1)binds to cyclin-dependent kinase complexes and inhibits their activities. It was originally described as an inhibitor of cancer cell proliferation. However, many recent studies have shown that p21 promotes tumor progression when accumulated in the cell cytoplasm. So far, little is known about the correlation between cytoplasmic p21 and drug resistance. This study was aimed to investigate the role of p21 in the cisplatin resistance of ovarian cancer.</p> <p>Methods</p> <p>RT-PCR, western blot and immunofluorescence were used to detect p21 expression and location in cisplatin-resistant ovarian cancer cell line C13* and its parental line OV2008. Regulation of cytoplasmic p21 was performed through transfection of p21 siRNA, Akt2 shRNA and Akt2 constitutively active vector in the two cell lines; their effects on cisplatin-induced apoptosis were evaluated by flow cytometry. Tumor tissue sections of clinical samples were analyzed by immunohistochemistry.</p> <p>Results</p> <p>p21 predominantly localizes to the cytoplasm in C13* compared to OV2008. Persistent exposure to low dose cisplatin in OV2008 leads to p21 translocation from nuclear to cytoplasm, while it had not impact on p21 localization in C13*. Knockdown of cytoplasmic p21 by p21 siRNA transfection in C13* notably increased cisplatin-induced apoptosis through activation of caspase 3. Inhibition of p21 translocation into the cytoplasm by transfection of Akt2 shRNA into C13* cells significantly increased cisplatin-induced apoptosis, while induction of p21 translocation into the cytoplasm by transfection of constitutively active Akt2 in OV2008 enhanced the resistance to cisplatin. Immunohistochemical analysis of clinical ovarian tumor tissues demonstrated that cytoplasmic p21 was negatively correlated with the response to cisplatin based treatment.</p> <p>Conclusions</p> <p>Cytoplasmic p21 is a novel biomarker of cisplatin resistance and it may represent a potential therapeutic target for ovarian tumors that are refractory to conventional treatment.</p

Plexin-B1 silencing inhibits ovarian cancer cell migration and invasion

BACKGROUND: Elevated Plexin-B1 expression has been found in diverse human cancers and in non-neoplastic tissues, and it mediates diverse biological and pathological activities. However, whether or not Plexin-B1 expression is involved in human ovarian tumors remains unclear. In the present study, Plexin-B1 expression was explored in benign and malignant human ovarian tumor tissues. In addition, the impact of Plexin-B1 expression on ovarian cancer cell proliferation, migration and invasion were investigated in vitro. METHODS: Plexin-B1 expression was analyzed in normal and benign ovarian tissues and serous ovarian tumors (both borderline and malignant) by immunohistochemical staining, as well as in four human ovarian cancer cell lines (A2780, C13*, SKOV3, and OV2008) by RT-PCR and western blot analyses. Furthermore, endogenous Plexin-B1 expression was suppressed by Plexin-B1 siRNA in SKOV3 cells, which overexpress Plexin-B1. Protein levels of Plexin-B1, AKT and AKT(Ser473 )were examined by western blot analysis. Cell proliferation, migration and invasion were measured with MTT, wound healing and boyden chamber assays, respectively, and the cytoskeleton was monitored via F-actin staining. RESULTS: Expression levels of Plexin-B1 protein were significantly higher in serous ovarian carcinomas than in normal ovaries or benign ovarian neoplasms, and in the former, Plexin-B1 expression was positively correlated with lymphatic metastasis, and the membrane and cytoplasm of cancer cells stained positively. SKOV3 cells displayed the highest Plexin-B1 expression at both the mRNA and protein levels among the four tested human ovarian cancer cell lines and was selected as a cell model for further in vitro experiments. Plexin-B1 siRNA significantly suppressed phosphorylation of AKT at Ser473 in SKOV3 cells, but it did not alter total AKT expression. In addition, silencing of Plexin-B1 in SKOV3 cells inhibited cell migration and invasion and reorganized the cytoskeleton, whereas cell proliferation was not affected. CONCLUSION: Plexin-B1 expression correlates with malignant phenotypes of serous ovarian tumors, probably via phosphorylation of AKT at Ser473, suggesting that Plexin-B1 might be a useful biomarker and/or a novel therapeutic target

Mesenchymal stem cells as carriers and amplifiers in CRAd delivery to tumors

<p>Abstract</p> <p>Background</p> <p>Mesenchymal stem cells (MSCs) have been considered to be the attractive vehicles for delivering therapeutic agents toward various tumor diseases. This study was to explore the distribution pattern, kinetic delivery of adenovirus, and therapeutic efficacy of the MSC loading of E1A mutant conditionally replicative adenovirus Adv-Stat3(-) which selectively replicated and expressed high levels of anti-sense Stat3 complementary DNA in breast cancer and melanoma cells.</p> <p>Methods</p> <p>We assessed the release ability of conditionally replicative adenovirus (CRAd) from MSC using crystal violet staining, TCID₅₀assay, and quantitative PCR. In vitro killing competence of MSCs carrying Adv-Stat3(-) toward breast cancer and melanoma was performed using co-culture system of transwell plates. We examined tumor tropism of MSC by Prussian blue staining and immunofluorescence. In vivo killing competence of MSCs carrying Adv-Stat3(-) toward breast tumor was analyzed by comparison of tumor volumes and survival periods.</p> <p>Results</p> <p>Adv-Stat3(-) amplified in MSCs and were released 4 days after infection. MSCs carrying Adv-Stat3(-) caused viral amplification, depletion of Stat3 and its downstream proteins, and led to significant apoptosis in breast cancer and melanoma cell lines. In vivo experiments confirmed the preferential localization of MSCs in the tumor periphery 24 hours after tail vein injection, and this localization was mainly detected in the tumor parenchyma after 72 hours. Intravenous injection of MSCs carrying Adv-Stat3(-) suppressed the Stat3 pathway, down-regulated Ki67 expression, and recruited CD11b-positive cells in the local tumor, inhibiting tumor growth and increasing the survival of tumor-bearing mice.</p> <p>Conclusions</p> <p>These results indicate that MSCs migrate to the tumor site in a time-dependent manner and could be an effective platform for the targeted delivery of CRAd and the amplification of tumor killing effects.</p

Inhibition of PC cell-derived growth factor (PCDGF)/granulin-epithelin precursor (GEP) decreased cell proliferation and invasion through downregulation of cyclin D and CDK 4 and inactivation of MMP-2

BACKGROUND: PC cell-derived growth factor (PCDGF), also called epithelin/granulin precursor (GEP), is an 88-kDa secreted glycoprotein with the ability to stimulate cell proliferation in an autocrine fashion. In addition, some studies indicated that PCDGF participated in invasion, metastasis and survival of cancer cells by regulating cell migration, adhesion and proliferation. Yet the effects of PCDGF on proliferation and invasion of ovarian cancer cells in vitro and the mechanisms by which PCDGF mediates biological behaviors of ovarian cancer have rarely been reported. In the present study we investigated whether and how PCDGF/GEP mediated cell proliferation and invasion in ovarian cancer. METHODS: PCDGF/GEP expression level in three human ovarian cancer cell lines of different invasion potential were detected by RT-PCR and western blot. Effects of inhibition of PCDGF expression on cell proliferation and invasion capability were determined by MTT assay and Boyden chamber assay. Expression levels of cyclin D1 and CDK4 and MMP-2 activity were evaluated in a pilot study. RESULTS: PCDGF mRNA and protein were expressed at a high level in SW626 and A2780 and at a low level in SKOV3. PCDGF expression level correlated well with malignant phenotype including proliferation and invasion in ovarian cancer cell lines. In addition, the proliferation rate and invasion index decreased after inhibition of PCDGF expression by antisense PCDGF cDNA transfection in SW626 and A2780. Furthermore expression of CyclinD1 and CDK4 were downregulated and MMP-2 was inactivated after PCDGF inhibition in the pilot study. CONCLUSION: PCDGF played an important role in stimulating proliferation and promoting invasion in ovarian cancer. Inhibition of PCDGF decreased proliferation and invasion capability through downregulation of cyclin D1 and CDK4 and inactivation of MMP-2. PCDGF could serve as a potential therapeutic target in ovarian cancer

Lymphoma endothelium preferentially expresses Tim-3 and facilitates the progression of lymphoma by mediating immune evasion

Angiogenesis is increasingly recognized as an important prognosticator associated with the progression of lymphoma and as an attractive target for novel modalities. We report a previously unrecognized mechanism by which lymphoma endothelium facilitates the growth and dissemination of lymphoma by interacting with circulated T cells and suppresses the activation of CD4+ T cells. Global gene expression profiles of microdissected endothelium from lymphoma and reactive lymph nodes revealed that T cell immunoglobulin and mucin domain–containing molecule 3 (Tim-3) was preferentially expressed in lymphoma-derived endothelial cells (ECs). Clinically, the level of Tim-3 in B cell lymphoma endothelium was closely correlated to both dissemination and poor prognosis. In vitro, Tim-3+ ECs modulated T cell response to lymphoma surrogate antigens by suppressing activation of CD4+ T lymphocytes through the activation of the interleukin-6–STAT3 pathway, inhibiting Th1 polarization, and providing protective immunity. In a lymphoma mouse model, Tim-3–expressing ECs promoted the onset, growth, and dissemination of lymphoma by inhibiting activation of CD4+ T cells and Th1 polarization. Our findings strongly argue that the lymphoma endothelium is not only a vessel system but also a functional barrier facilitating the establishment of lymphoma immune tolerance. These findings highlight a novel molecular mechanism that is a potential target for enhancing the efficacy of tumor immunotherapy and controlling metastatic diseases

The Rural Development and the Environment of Eastern China

Since China’s reform started from 1978, Eastern China developed rapidly. The agriculture had been substituted by other industries seriously as the reform implemented deeply, while land and labors also moved to other industries. At the beginning of reform, there was an integration between urban and rural area in Eastern China. In this process, the rural development and the environment have interactions between them. Therefore, I mentioned some measures to promote rural development and improve the environment in Eastern China, according to the interactions between them.MSc/MAInternational Economy and Busines

HISTORY THROUGH LOANWORDS: THE LOAN CORRESPONDENCES BETWEEN HANI AND CHINESE

National audiencethe stratification of Chinese loanwords into Dazhai Hani, a Tibeto-Burman language, has been studied. The basic principles (principle of coherence; extended principleof coherence) guiding analysis are presented in a methodological section. Two main strata of borrowings from SW Mandarin, a modern layer reflecting the phonology of Lüchun Mandarin, and the other from another, earlier source (contemporary with the introduction of the potato and tobacco), are distinguished. A set of early Chinese borrowings is also identified but the sound correspondences in that layer are incomplete. The words for ‘eggplant' and ‘tea' are shared with Chinese but appear to be Tibeto-Burman loanwords to Chinese rather than the opposite.on a étudié la stratification des emprunts lexicaux faits par le hani de Dazhai, une langue tibéto-birmane, au chinois. Les principes de l'analyse (principe de cohérence, principe étendu de cohérence) sont exposés dans une partie méthodologique. Deux grandes couches d'emprunts au mandarin du sud-ouest, l'une constituée d'emprunts contemporains au dialecte mandarin de Lüchun, l'autre datant de l'introduction de la pommede terre et du tabac, sont distinguées. Des emprunts anciens (en nombre limité) sont identifiés, mais seulement une partie des correspondances phonétiques peut être dégagée. Deux termes: “aubergine” et “thé” semblent être des emprunts tibéto-birmans en chinois