Repair Path Research Articles

Research and Application of the Optimal Repair Path Based on BP-Dijkstra in the Distribution Network

The existing power system emergency repair system mainly relies on manual scheduling and selection of traffic paths based on experiences. Also, the existing traffic navigation has only one-time route planning, which may not be intelligent enough to fit the traffic changes. In order to solve the above problems, this paper establishes a power emergency repair system based on GPRS wireless communication technology, on-board GPS terminal equipment, transportation and power system GIS. Based on the current traffic information, BP neural network is used to predict the average speed of different paths and to calculate the running time of each path. The Dijkstra algorithm was introduced in the later stage to find the optimal repair path with the shortest time duration. The updates of time settings during optimization are introduced. The original optimal repair path is maintained within the set time limits; otherwise the new path will be updated. In this paper, a complex traffic network analysis and simulation verification are presented. The results show that the algorithm is feasible and applicable.

Smart Power Evolution of Food Refrigerated based on Particle Swarm Optimization Algorithm

Particle Swarm Optimization (PSO) algorithm is a new evolutionary computation technique. This article has conducted the thorough research to the PSO algorithm, analyses the algorithm principle, basic steps, application steps and parameter settings and other content. This study introduces the idea of random inertia weight and the discrete PSO algorithm is improved, which makes it easy to jump out of local optima and discrete optimization problem. The establishment of the best repair path and the best routing model of electric power communication network, the improved algorithm is applied to power communication network management in the two aspects, it can quickly find the optimal path and the routing request, prove the feasibility and effectiveness of PSO algorithm for solving the discrete problem. The establishment of the optimal route choice model, based on local search and memory unit in the algorithm, the optimal route selection program using the improved PSO algorithm simulation, the results show the effectiveness of the PSO algorithm for solving the discrete problem and potential.

Potential Use of Dietary Antioxidant to Prevent Radiation-Induced Genomic Instability

Irradiation induces DNA strand breaks within milliseconds of exposure. Cellular DNA repair machineries immediately sense and locate the broken parts of DNA and activate a variety of DNA repair path ways to restore normal genetic makeup after radiation damage. During this active process of DNA repair, broken strands may improperly rejoin in some of the irradiated cells and are propagated through cell generations. These cells, with altered genetic composition, may eventually result in path physiological conditions. This phenomenon of development of delayed genetic alterations is widely known as genomic instability. Genomic instability is associated with the progression and development of plethora of diseases including cancer, hematological, neurological and cardiovascular disorders[1,2]. However, the mechanistic link between radiation-induced DNA breaks and subsequent development of genomic instability has not been clearly elucidated.

CB1 cannabinoid receptor agonist inhibits matrix metalloproteinase activity in spinal cord injury: A possible mechanism of improved recovery

Increased matrix metalloproteinase (MMP) activity contributes to glial scar formation that inhibits the repair path after spinal cord injury (SCI). We examined whether treatment with N-​(2-​chloroethyl)-​5Z,​8Z,​11Z,​14Z-​eicosatetraenamide (ACEA), a selective synthetic cannabinoid receptor (CB1R) agonist, inhibits MMP and improves functional and histological recovery in a mouse spinal cord compression injury model. Injured mice randomly received either intraperitoneal ACEA (3mg/kg/day) or vehicle for up to 3 weeks. Behavioral, histological and biochemical assays were performed. Rotarod assessment and the Basso Mouse Scale score showed an improved performance following ACEA treatment concomitant with a decrease in compression lesion volume. MMP-9 and MMP-2 activity was measured at 1, 7 and 14 days post-SCI. SCI markedly increased MMP-9, but had negligible effect on MMP-2 activity. ACEA-treatment decreased MMP-9 activity by 80%, 49%, and 56%, respectively (P<0.05) and had a smaller effect on MMP-2 activity. The CB1R antagonist SR141716, but not the CB2R antagonist SR144528, blocked ACEA-mediated decrease in MMP-9 activity confirming the role of the CB1R in the process. Collectively these data demonstrate that post-injury CB1R agonism can improve SCI outcome and also indicate marked attenuation of MMP-9 proteolytic enzyme activity as a biochemical mechanism.

The Research on Slices’ Data Repair and Filling Path Optimization

Fused deposition modeling (FDM) is one of rapid prototyping process, which process includes Common Layer Interface (CLI) file generation and rapid prototyping. This paper focuses on algorithm to repair error datum of slices to generate CLI file and arithmetic-zoning scanning algorithm based intersection sorting which were used to FDM process. Conclusions of experiment show that the algorithm to repair error datum of slices can correct repair the error datum and fast extraction of contour information, and it provides an efficient method for generating CLI file from Stereo lithography(STL) slices; that arithmetic-zoning scanning method can reduce the possibility of model wrapping and shrinkage stress. The two algorithms improve production efficiency of FDM and are worth promoting.

Electronic Structure of (6−4) DNA Photoproduct Repair Involving a Non-Oxetane Pathway

Mutagenic pyrimidine-pyrimidone (6-4) photoproducts are one of the main DNA lesions induced by solar UV radiation. These lesions can be photoreversed by (6-4) photolyases. The originally published repair mechanism involves rearrangement of the lesion into an oxetane intermediate upon binding to the (6-4) photolyase, followed by light-induced electron transfer from the reduced flavin cofactor. In a recent crystallographic study on a (6-4) photoproduct complexed with (6-4) photolyase from Drosophila melanogaster no oxetane was observed, raising the possibility of a non-oxetane repair mechanism. Using quantum-chemical calculations we find that in addition to repair via an oxetane, a direct transfer of the hydroxyl group results in reversal of the radical anion (6-4) photoproduct. In both mechanisms, the transition states have high energies and correspond to avoided crossings of the ground and excited electronic states. To study whether the repair can proceed via these state crossings, the excited-state potential energy curves were computed. The radical excitation energies and accessibility of the nonadiabatic repair path were found to depend on hydrogen bonds and the protonation state of the lesion. On the basis of the energy calculations, a nonadiabatic repair of the excited (6-4) lesion radical anion via hydroxyl transfer is probable. This repair mechanism is in line with the recent structural data on the (6-4) photolyase from D. melanogaster .

Slipped (CTG)•(CAG) repeats can be correctly repaired, escape repair or undergo error-prone repair

Expansion of (CTG)*(CAG) repeats, the cause of 14 or more diseases, is presumed to arise through escaped repair of slipped DNAs. We report the fidelity of slipped-DNA repair using human cell extracts and DNAs with slip-outs of (CAG)(20) or (CTG)(20). Three outcomes occurred: correct repair, escaped repair and error-prone repair. The choice of repair path depended on nick location and slip-out composition (CAG or CTG). A new form of error-prone repair was detected whereby excess repeats were incompletely excised, constituting a previously unknown path to generate expansions but not deletions. Neuron-like cell extracts yielded each of the three repair outcomes, supporting a role for these processes in (CTG)*(CAG) instability in patient post-mitotic brain cells. Mismatch repair (MMR) and nucleotide excision repair (NER) proteins hMSH2, hMSH3, hMLH1, XPF, XPG or polymerase beta were not required-indicating that their role in instability may precede that of slip-out processing. Differential processing of slipped repeats may explain the differences in mutation patterns between various disease loci or tissues.