The resilience of interdependent transportation networks under targeted attack

Modern world builds on the resilience of interdependent infrastructures characterized as complex networks. Recently, a framework for analysis of interdependent networks has been developed to explain the mechanism of resilience in interdependent networks. Here we extend this interdependent network model by considering flows in the networks and study the system's resilience under different attack strategies. In our model, nodes may fail due to either overload or loss of interdependency. Under the interaction between these two failure mechanisms, it is shown that interdependent scale-free networks show extreme vulnerability. The resilience of interdependent SF networks is found in our simulation much smaller than single SF network or interdependent SF networks without flows.Comment: 5 pages, 4 figure

The Role of Paragus quadri-fasciatus Meigen on Aphid Control and the Observations of its Biological Characteristics

Four-strip small syrphid fly, Paragus quadri-fasciatus Meigen is the important natural enemy of aphids in our region. A fly can eat about 800 aphids during its whole life. There are more than 10 kinds of aphids can be food of this fly, such as soybean aphid, Chinese sorghum aphid and radish aphid etc. The fly has 3~4 generations each year in Tonghua county, Jilin province. The adult of the first generation appears after the last ten-day period of April each year. It takes 30~35 days to complete one generation. The fly can oviposit 84~124 eggs in its whole life. Major natural enemies of the fly are ichneumon wasps, spiders, lacewings and etc.Originating text in Chinese.Citation: Gao, Junfeng, Jiang, Lianfeng, Zhang, Guangxin, Li, Chunshan, Zhao, Guangquan. (1996). The Role of Paragus quadri-fasciatus Meigen on Aphid Control and the Observations of its Biological Characteristics. Journal of Jilin Agricultural Sciences, 5(2), 60-61

TTSVD: an efficient sparse decision making model with two-way trust recommendation in the AI enabled IoT systems

The convergence of AI and IoT enables data to be quickly explored and turned into vital decisions, and however, there are still some challenging issues to be further addressed. For example, lacking of enough data in AI-based decision making (so called Sparse Decision Making, SDM) will decrease the efficiency dramatically, or even disable the intelligent IoT networks. Taking the intelligent IoT networks as the network infrastructure, the recommendation systems have been facing such SDM problems. A naive solution is to introduce so-called trust information. However, trust information also maybe face the difficulty of sparse trust evidence (a.k.a sparse trust problem). In our work, an accurate sparse decision making model with two-way trust recommendation in the AI enabled IoT systems is proposed by us, named TT-SVD. Our model incorporates both trust information and rating information more completely, which can efficiently alleviate the above mentioned sparse trust problem and therefore be able to solve the cold start and data sparsity problems. Specifically, we first consider the two-fold trust influences from both trustees and trustors, which can be represented by a factor called trust propensity. To this end, we propose a dual model, including the trustor model (TrustorSVD) and a trustee model (TrusteeSVD) based on an existing rating-only recommendation model called SVD++, which are integrated by the weighted average and yield the final model, TT-SVD. The experimental results show that our model outperforms the state of the art including SVD and TrustSVD in both the ”all users” and ”cold start users” cases, and the accuracy improvement can reach a maximum of 29%. Complexity analysis shows that our model is equally suitable for the case of large sparse datasets. In a word, our model can effectively solve the sparse decision problem by introducing the two-way trust recommendation, and hence improve the efficiency of the intelligent recommendation systems

MRl of Prostate Cancer Antigen Expression for Diagnosis and lmmunotherapy

BACKGROUND: Tumor antigen (TA)-targeted monoclonal antibody (mAb) immunotherapy can be effective for the treatment of a broad range of cancer etiologies; however, these approaches have demonstrated variable clinical efficacy for the treatment of patients with prostate cancer (PCa). An obstacle currently impeding translational progress has been the inability to quantify the mAb dose that reaches the tumor site and binds to the targeted TAs. The coupling of mAb to nanoparticle-based magnetic resonance imaging (MRI) probes should permit in vivo measurement of patient-specific biodistributions; these measurements could facilitate future development of novel dosimetry paradigms wherein mAb dose is titrated to optimize outcomes for individual patients. METHODS: The prostate stem cell antigen (PSCA) is broadly expressed on the surface of prostate cancer (PCa) cells. Anti-human PSCA monoclonal antibodies (mAb 7F5) were bound to Au/Fe(3)O(4) (GoldMag) nanoparticles (mAb 7F5@GoldMag) to serve as PSCA-specific theragnostic MRI probe permitting visualization of mAb biodistribution in vivo. First, the antibody immobilization efficiency of the GoldMag particles and the efficacy for PSCA-specific binding was assessed. Next, PC-3 (prostate cancer with PSCA over-expression) and SMMC-7721 (hepatoma cells without PSCA expression) tumor-bearing mice were injected with mAb 7F5@GoldMag for MRI. MRI probe biodistributions were assessed at increasing time intervals post-infusion; therapy response was evaluated with serial tumor volume measurements. RESULTS: Targeted binding of the mAb 7F5@GoldMag probes to PC-3 cells was verified using optical images and MRI; selective binding was not observed for SMMC-7721 tumors. The immunotherapeutic efficacy of the mAb 7F5@GoldMag in PC-3 tumor-bearing mice was verified with significant inhibition of tumor growth compared to untreated control animals. CONCLUSION: Our promising results suggest the feasibility of using mAb 7F5@GoldMag probes as a novel paradigm for the detection and immunotherapeutic treatment of PCa. We optimistically anticipate that the approaches have the potential to be translated into the clinical settings

Maneuvering Route Safety Planning for Military Vehicles during Wartime

Maneuvering route planning for the military vehicles during wartime is a noteworthy problem in the field of military transportation. Existing research paid little attention to security of vehicles, which we consider as a non-ignorable aspect with the military background. Based on scenarios, we build a k-th shortest paths planning model aiming at vehicles safety improving. A genetic algorithm with specific encoding rules is proposed. And two groups of computational experiments based on the real road network of Fujian, China are performed. The results of the experiments show this is an effective algorithm to improve the vehicles’ safety during maneuvering

Maneuvering Route Safety Planning for Military Vehicles during Wartime

Maneuvering route planning for the military vehicles during wartime is a noteworthy problem in the field of military transportation. Existing research paid little attention to security of vehicles, which we consider as a non-ignorable aspect with the military background. Based on scenarios, we build a k-th shortest paths planning model aiming at vehicles safety improving. A genetic algorithm with specific encoding rules is proposed. And two groups of computational experiments based on the real road network of Fujian, China are performed. The results of the experiments show this is an effective algorithm to improve the vehicles’ safety during maneuvering

Expression of GITR Enhances Multiple Myeloma Cell Sensitivity to Bortezomib.

Recently tumor necrosis factor receptor super family member 18 (TNFRSF18, also called GITR) has been identified as a novel tumor suppressor gene in Multiple Myeloma (MM), undergoing aberrant DNA methylation-mediated gene expression silencing. Furthermore, the expression of GITR blocks canonical NF-κB activation in MM cells in response to TNFα. Bortezomib, a proteasome inhibitor, can induce NF-κB activation, which may significantly influence the drug response in MM patients. In this study, we aim to elucidate if GITR status is associated with response to Bortezomib in MM cells through regulating GITR mediated NF-κB blockade. We found that GITR was significantly downregulated in MM patients and cell lines. Overexpression of GITR inhibited non-canonical NF-κB activation induced by TNFα. Moreover, NF-κB inhibitor induced apoptosis in GITR-deficient MM cells in response to TNFα. In addition, overexpression of GITR could inhibit Bortezomib-induced NF-κB activation and enhance the cytotoxicity of Bortezomib in GITR-deficient MM cell line (MM1.S). In contrast, knockdown of GITR attenuated the cytotoxic effect of Bortezomib on GITR proficient MM (RPMI) cell line and increased NF-κB activation. Finally, overexpression of GITR enhanced the sensitivity to Bortezomib in co-culture with bone marrow stromal cells and significantly reduced the tumor growth in MM1.S xenograft mice. In conclusion, we demonstrated that GITR expression can enhance the sensitivity to Bortezomib by inhibiting Bortezomib-induced NF-κB activation

Expression of GITR Enhances Multiple Myeloma Cell Sensitivity to Bortezomib.

Recently tumor necrosis factor receptor super family member 18 (TNFRSF18, also called GITR) has been identified as a novel tumor suppressor gene in Multiple Myeloma (MM), undergoing aberrant DNA methylation-mediated gene expression silencing. Furthermore, the expression of GITR blocks canonical NF-κB activation in MM cells in response to TNFα. Bortezomib, a proteasome inhibitor, can induce NF-κB activation, which may significantly influence the drug response in MM patients. In this study, we aim to elucidate if GITR status is associated with response to Bortezomib in MM cells through regulating GITR mediated NF-κB blockade. We found that GITR was significantly downregulated in MM patients and cell lines. Overexpression of GITR inhibited non-canonical NF-κB activation induced by TNFα. Moreover, NF-κB inhibitor induced apoptosis in GITR-deficient MM cells in response to TNFα. In addition, overexpression of GITR could inhibit Bortezomib-induced NF-κB activation and enhance the cytotoxicity of Bortezomib in GITR-deficient MM cell line (MM1.S). In contrast, knockdown of GITR attenuated the cytotoxic effect of Bortezomib on GITR proficient MM (RPMI) cell line and increased NF-κB activation. Finally, overexpression of GITR enhanced the sensitivity to Bortezomib in co-culture with bone marrow stromal cells and significantly reduced the tumor growth in MM1.S xenograft mice. In conclusion, we demonstrated that GITR expression can enhance the sensitivity to Bortezomib by inhibiting Bortezomib-induced NF-κB activation