Approximation algorithms for fault tolerant facility allocation

Given nf sites, each equipped with one facility, and n c cities, fault tolerant facility location (FTFL) [K. Jain and V. V. Vazirani, APPROX '00: Proceedings of the Third International Workshop on Approximation Algorithms for Combinatorial Optimization, Spinger, New York, 2000, pp. 177-183] requires computing a minimum-cost connection scheme such that each city connects to a specified number of facilities. When each city connects to exactly one facility, FTFL becomes the classical uncapacitated facility location problem (UFL) that is well-known NP hard. The current best solution to FTFL admits an approximation ratio 1.7245 due to Byrka, Srinivasan, and Swamy applying the dependent rounding technique announced recently [Proceedings of IPCO, 2010, pp. 244-257], which improves the ratio 2.076 obtained by Swamy and Shmoys based on LP rounding [ACM Trans. Algorithms, 4 (2008), pp. 1-27]. In this paper, we study a variant of the FTFL problem, namely, fault tolerant facility allocation (FTFA), as another generalization of UFL by allowing each site to hold multiple facilities and show that we can obtain better solutions for this problem. We first give two algorithms with 1.81 and 1.61 approximation ratios in time complexity O(mRlogm) and O(Rn3), respectively, where R is the maximum number of facilities required by any city, m = nfnc, and n = max{ nf, nc}. Instead of applying the dual-fitting technique that reduces the dual problem's solution to fit the original problem as used in the literature [K. Jain et al., Journal of the ACM, 50 (2003), pp. 795-824; K. Jain, M. Mahdian, and A. Saberi, STOC'02: Proceedings of the 34th Annual ACM Symposium on the Theory of Computing, New York, 2002, pp. 731-740; A. Saberi et al., Approximation, Randomization, and Combinatorial Optimization: Algorithms and Techniques, Springer, New York, 2001, pp. 127-137], we propose a method called inverse dual-fitting that alters the original problem to fit the dual solution and show that this method is more effective for obtaining solutions of multifactor approximation. We show that applying inverse dual-fitting and factor-revealing techniques our second algorithm is also (1.11,1.78)- And (1,2)-approximation simultaneously. These results can be further used to achieve solutions of 1.52-approximation to FTFA and 4-approximation to the fault tolerant k-facility allocation problem in which the total number of facilities is bounded by k. These are currently the best bifactor and single-factor approximation ratios for the problems concerned. ©2013 Society for Industrial and Applied Mathematics.Hong Shen and Shihong X

Deep functional analysis of synII, a 770-kilobase synthetic yeast chromosome

INTRODUCTION Although much effort has been devoted to studying yeast in the past few decades, our understanding of this model organism is still limited. Rapidly developing DNA synthesis techniques have made a “build-to-understand” approach feasible to reengineer on the genome scale. Here, we report on the completion of a 770-kilobase synthetic yeast chromosome II (synII). SynII was characterized using extensive Trans-Omics tests. Despite considerable sequence alterations, synII is virtually indistinguishable from wild type. However, an up-regulation of translational machinery was observed and can be reversed by restoring the transfer RNA (tRNA) gene copy number. RATIONALE Following the “design-build-test-debug” working loop, synII was successfully designed and constructed in vivo. Extensive Trans-Omics tests were conducted, including phenomics, transcriptomics, proteomics, metabolomics, chromosome segregation, and replication analyses. By both complementation assays and SCRaMbLE (synthetic chromosome rearrangement and modification by loxP -mediated evolution), we targeted and debugged the origin of a growth defect at 37°C in glycerol medium. RESULTS To efficiently construct megabase-long chromosomes, we developed an I- Sce I–mediated strategy, which enables parallel integration of synthetic chromosome arms and reduced the overall integration time by 50% for synII. An I- Sce I site is introduced for generating a double-strand break to promote targeted homologous recombination during mitotic growth. Despite hundreds of modifications introduced, there are still regions sharing substantial sequence similarity that might lead to undesirable meiotic recombinations when intercrossing the two semisynthetic chromosome arm strains. Induction of the I- Sce I–mediated double-strand break is otherwise lethal and thus introduced a strong selective pressure for targeted homologous recombination. Since our strategy is designed to generate a markerless synII and leave the URA3 marker on the wild-type chromosome, we observed a tenfold increase in URA3 -deficient colonies upon I- Sce I induction, meaning that our strategy can greatly bias the crossover events toward the designated regions. By incorporating comprehensive phenotyping approaches at multiple levels, we demonstrated that synII was capable of powering the growth of yeast indistinguishably from wild-type cells (see the figure), showing highly consistent biological processes comparable to the native strain. Meanwhile, we also noticed modest but potentially significant up-regulation of the translational machinery. The main alteration underlying this change in expression is the deletion of 13 tRNA genes. A growth defect was observed in one very specific condition—high temperature (37°C) in medium with glycerol as a carbon source—where colony size was reduced significantly. We targeted and debugged this defect by two distinct approaches. The first approach involved phenotype screening of all intermediate strains followed by a complementation assay with wild-type sequences in the synthetic strain. By doing so, we identified a modification resulting from PCRTag recoding in TSC10 , which is involved in regulation of the yeast high-osmolarity glycerol (HOG) response pathway. After replacement with wild-type TSC10 , the defect was greatly mitigated. The other approach, debugging by SCRaMbLE, showed rearrangements in regions containing HOG regulation genes. Both approaches indicated that the defect is related to HOG response dysregulation. Thus, the phenotypic defect can be pinpointed and debugged through multiple alternative routes in the complex cellular interactome network. CONCLUSION We have demonstrated that synII segregates, replicates, and functions in a highly similar fashion compared with its wild-type counterpart. Furthermore, we believe that the iterative “design-build-test-debug” cycle methodology, established here, will facilitate progression of the Sc2.0 project in the face of the increasing synthetic genome complexity. SynII characterization. ( A ) Cell cycle comparison between synII and BY4741 revealed by the percentage of cells with separated CEN2-GFP dots, metaphase spindles, and anaphase spindles. ( B ) Replication profiling of synII (red) and BY4741 (black) expressed as relative copy number by deep sequencing. ( C ) RNA sequencing analysis revealed that the significant up-regulation of translational machinery in synII is induced by the deletion of tRNA genes in synII. </jats:sec

A Vessel Flow Detection System based on Laser Sensors

A system using two laser sensors for vessel flow detection was introduced. Mathematical morphology on ship contour detection was studied and vesselâ??s contour was reconstructed based on geometric space projection, vesselâ??s width threshold filtering and connected graph merging. Also, the necessity of vesselâ??s contour reconstruction is verified by experiments. A data fusion method based on two laser sensors was researched for vesselâ??s length detection, which using spatial adjustment and data correlation to calculate the speed, and to estimate the length of a vessel. Finally, a vessel flow detection system was built and worked fine

Ginsenoside Rh4 Suppresses Metastasis of Gastric Cancer via SIX1-Dependent TGF-&beta;/Smad2/3 Signaling Pathway

Gastric cancer (GC) is the leading causes of cancer-related death worldwide. Surgery remains the cornerstone of gastric cancer treatment, and new strategies with adjuvant chemotherapy are currently gaining more and more acceptance. Ginsenoside Rh4 has excellent antitumor activity. Conversely, the mechanisms involved in treatment of GC are not completely understood. In this study, we certified that Rh4 showed strong anti-GC efficiency in vitro and in vivo. MTT and colony formation assays were performed to exhibit that Rh4 significantly inhibited cellular proliferation and colony formation. Results from the wound healing assay, transwell assays, and Western blotting indicated that Rh4 restrained GC cell migration and invasion by reversing epithelial&ndash;mesenchymal transition (EMT). Further validation by proteomic screening, co-treatment with disitertide, and SIX1 signal silencing revealed that SIX1, a target of Rh4, induced EMT by activating the TGF-&beta;/Smad2/3 signaling pathway. In summary, our discoveries demonstrated the essential basis of the anti-GC metastatic effects of Rh4 via suppressing the SIX1&ndash;TGF-&beta;/Smad2/3 signaling axis, which delivers a new idea for the clinical treatment of GC

Improvement of arc burn defect of initial contact loss of electric hot incremental sheet forming

Electric hot incremental sheet forming, which is used to form hard-to-form sheet metal, is viewed as the one of rapid prototyping manufacturing technologies. However, the non-uniform stress distribution of forming regions would cause an initial contact loss phenomenon between the tool and the sheet, and an electric arc burn of the part surface is obtained due to the contact loss. In this work, a control method of axial pressure response was proposed to judge the stability of the initial contact between forming the tool and the sheet. A power supply on-off device was designed for electric hot incremental forming, and the calculation model of the initial axial force was established during deformation. Meanwhile, two response pressure values were proposed to control the power supply starting and the current intervention and to ensure the stability of the power supply during the forming process. In addition to this, the axial force and the surface of part were analyzed further in electric hot incremental sheet forming

UPLC-Q-TOF/MS-Based Plasma Metabolomics to Evaluate the Effects of Aspirin Eugenol Ester on Blood Stasis in Rats

Aspirin eugenol ester (AEE) is a novel compound that is formed from the esterification of aspirin (acetylsalicylic acid (ASA)) and eugenol. This study aimed to investigate the effects of AEE on blood stasis in rats and to characterize the underlying mechanisms using a plasma metabolomic study. The results indicate that AEE and ASA could modulate whole blood viscosity (WBV), plasma viscosity (PV), blood coagulation parameters, platelet count, platelet aggregation, lactate dehydrogenase (LDH), creatinine (CR) and the levels of thromboxane A2 (TXA2) and 6-keto prostaglandin F1&alpha; (6-keto-PGF1&alpha;). The metabolic profiles of the plasma samples from all groups were clearly separated in the score plots. Nineteen potential metabolites were selected and identified, and disordered levels of these metabolites could be regulated by AEE and ASA. Pathway analysis showed that the mechanism of action of AEE on blood stasis might be principally related to the metabolism of amino acid, fatty acid, energy and glycerophospholipid. The above results indicate that AEE protected the rats against blood stasis, and that this effect might have been caused by the anticoagulation activity of AEE and its abilities to maintain a balance between TXA2 and PGI2, reduce blood viscosity, inhibit platelet aggregation and normalize the plasma metabolic profile