► Short-term load forecasting is achieved using a lifting scheme and autoregressive integrated moving average (ARIMA) models. ► Lifting scheme is embedded into the ARIMA models to enhance forecasting ...accuracy. ► The Coeflet 12 wavelet is factored into lifting scheme steps. ► Apply the proposed algorithm to different practical load data types. ► Forecasting performance of the proposed approach is superior to that of the back-propagation network (BPN) algorithm and traditional ARIMA models.
Short-term load forecasting is achieved using a lifting scheme and autoregressive integrated moving average (ARIMA) models. The lifting scheme is a general and flexible approach for constructing bi-orthogonal wavelets that are usually in the spatial domain. The lifting scheme is embedded into the ARIMA models to enhance forecasting accuracy. Based on wavelet multi-revolution analysis (MRA) results, the lifting scheme decomposes the original load series into different sub-series at different revolution levels, which display the different frequency characteristic of a load. The sub-series are then forecast using properly fitted ARIMA models. Finally, forecasting results at different levels are reconstructed to generate an original load prediction by the inverse lifting scheme. In this study, the Coeflet 12 wavelet is factored into lifting scheme steps. The proposed algorithm was tested by applying it to different practical load data types from the Taipower Company in 2007 for one-day-ahead load forecasting. Simulation results indicate that the forecasting performance of the proposed approach is superior to that of the back-propagation network (BPN) algorithm and traditional ARIMA models.
Designing secure and efficient multivariate public key cryptosystems multivariate cryptography (MVC) to strengthen the security of RSA and ECC in conventional and quantum computational environment ...continues to be a challenging research in recent years. In this paper, we will describe multivariate public key cryptosystems based on extended Clipped Hopfield Neural Network (CHNN) and implement it using the MVC (CHNN-MVC) framework operated in <inline-formula> <tex-math notation="LaTeX">\text {GF}(p) </tex-math></inline-formula> space. The Diffie-Hellman key exchange algorithm is extended into the matrix field, which illustrates the feasibility of its new applications in both classic and postquantum cryptography. The efficiency and security of our proposed new public key cryptosystem CHNN-MVC are simulated and found to be NP-hard. The proposed algorithm will strengthen multivariate public key cryptosystems and allows hardware realization practicality.
Breast cancer is a heterogeneous disease, and the survival rate of patients with breast cancer strongly depends on their stage and clinicopathological features. Chemoradiation therapy is commonly ...employed to improve the survivability of patients with advanced breast cancer. However, the treatment process is often accompanied by the development of drug resistance, which eventually leads to treatment failure. Metabolism reprogramming has been recognized as a mechanism of breast cancer resistance. In this study, we established a doxorubicin-resistant MCF-7 (MCF-7-D500) cell line through a series of long-term doxorubicin in vitro treatments. Our data revealed that MCF-7-D500 cells exhibited increased multiple-drug resistance, cancer stemness, and invasiveness compared with parental cells. We analyzed the metabolic profiles of MCF-7 and MCF-7-D500 cells through liquid chromatography−mass spectrometry. We observed significant changes in 25 metabolites, of which, 21 exhibited increased levels (>1.5-fold change and p < 0.05) and 4 exhibited decreased levels (<0.75-fold change and p < 0.05) in MCF-7 cells with doxorubicin resistance. These results suggest the involvement of metabolism reprogramming in the development of drug resistance in breast cancer, especially the activation of glycolysis, the tricarboxylic acid (TCA) cycle, and the hexamine biosynthesis pathway (HBP). Furthermore, most of the enzymes involved in glycolysis, the HBP, and the TCA cycle were upregulated in MCF-7-D500 cells and contributed to the poor prognosis of patients with breast cancer. Our findings provide new insights into the regulation of drug resistance in breast cancer, and these drug resistance-related metabolic pathways can serve as targets for the treatment of chemoresistance in breast cancer.
Niclosamide is an FDA‑approved anthelmintic drug, and may elicit antineoplastic effects through direct STAT3 inhibition, which has been revealed in numerous human cancer cells. Chemotherapy is the ...standard treatment for advanced esophageal cancers, but also causes severe systemic side effects. The present study represents the first study evaluating the anticancer efficacy of niclosamide in esophageal cancers. Through western blot assay, it was demonstrated that niclosamide suppressed the STAT3 signaling pathway in esophageal adenocarcinoma cells (BE3) and esophageal squamous cell carcinoma cells (CE48T and CE81T). In addition, niclosamide inhibited cell proliferation as determined by 3‑(4,5‑dimethylthiazol‑2‑yl)‑5‑(3‑carboxymethoxyphenyl)‑ 2‑(4‑sulfophenyl)‑-2H‑tetrazolium)‑5‑(3‑carboxymethoxyphenyl)‑ 2‑(4‑sulfophenyl)‑2H‑tetrazolium (MTS) assay and soft agar colony forming assay, and induced cell apoptosis as determined by Annexin V and PI staining. The induction of p21 and G1 arrest of the cell cycle also was revealed in niclosamide‑treated CE81T cells by qPCR and flow cytometric assays, respectively. Furthermore, in the combination analysis of niclosamide and chemotherapeutic agents by MTS assay, low IC50 values were detected in cells co‑treated with niclosamide, with the exception of cisplatin‑treated CE81T cells. To confirm the results using an apoptosis assay, the apoptotic enhancement of niclosamide was only demonstrated in CE48T cells co‑treated with 5‑FU, cisplatin, or paclitaxel, and in BE3 cells co‑treated with paclitaxel, but not in CE81T cells. These findings indicate a future clinical application of niclosamide in esophageal cancers.
Vasculitic peripheral neuropathy (VPN) arises from an inflammatory obstruction in the blood vessels supplying peripheral nerves and subsequent ischaemic insults, which exhibits the clinical features ...of neuropathic pain and impaired peripheral nerve function. VPN induced by ischaemia–reperfusion (IR) has been reported to involve nuclear factor‐κB (NF‐κB)‐mediated neuroinflammation. Recent studies have suggested that endoplasmic reticulum (ER) stress has been implicated in the development of peripheral neuropathies. Resveratrol possesses a potent anti‐inflammatory capacity. We hypothesized that resveratrol may exert a protective effect against VPN through modulating the interrelated ER stress and NF‐κB pathways. Male Sprague‐Dawley rats were allocated into five groups: sham, sham + resveratrol 40 mg/kg (R40), IR, IR + R20 and IR + R40. VPN was induced by occluding the right femoral artery for 4 hours followed by reperfusion. Our data have shown that VPN induced by IR led to hind paw mechanical allodynia, heat hyperalgaesia, and impaired motor nerve conduction velocity (MNCV). With resveratrol intervention, the behavioural parameters were improved in a dose‐dependent manner and the MNCV levels were increased as well. The molecular data revealed that VPN induced by IR significantly increased the expression of NF‐κB as well as the ER stress sensor proteins, protein kinase RNA‐like endoplasmic reticulum kinase, inositol‐requiring enzyme 1 and activating transcription factor 6 in the sciatic nerves. More importantly, resveratrol significantly attenuated the expression of NF‐κB and the ER stress sensor proteins after IR. In conclusion, resveratrol alleviates VPN induced by IR. The mechanisms may involve modulating NF‐κB‐mediated neuroinflammation via suppressing ER stress.
Growth differentiation factor 15 (GDF15) is a strong predictor of cardiovascular events and mortality in individuals with or without cardiovascular diseases. Single nucleotide polymorphisms (SNPs) in ...microRNA (miRNA) target sites, also known as miRSNPs, are known to enhance or weaken miRNA-mRNA interactions and have been linked to diseases such as cardiovascular disease and cancer. In this study, we aimed to elucidate the functional significance of the miRSNP rs1054564 in regulating GDF15 levels. Two rs1054564-containing binding sites for hsa-miR-873-5p and hsa-miR-1233-3p were identified in the 3' untranslated region (UTR) of the GDF15 transcript using bioinformatics tools. Their activities were further characterized by in vitro reporter assays. Bioinformatics prediction suggested that miRNA binding sites harboring the rs1054564-G allele had lower free energies than those with the C allele and therefore were better targets with higher affinities for both hsa-miR-873-5p and hsa-miR-1233-3p. Reporter assays showed that luciferase activity was significantly decreased by rs1054564-G-containing 3' UTRs for both miRNAs (P < 0.05) and was restored by miRNA inhibitors. Comparing the fold suppression of the two miRNAs, only that of hsa-miR-1233-3p showed significant changes between the rs1054564-G- and C-containing 3' UTRs (P = 0.034). In addition, western blots showed that transfection of both miRNA mimics significantly decreased endogenous GDF15 expression in a melanoma cell line (P < 0.05). Taken together, our findings demonstrate that GDF15 is a target of hsa-miR-873-5p and hsa-miR-1233-3p and that the rs1054564-C allele partially abolishes hsa-miR-1233-3p-mediated translational suppression of GDF15. These results suggest that rs1054564 confers allele-specific translational repression of GDF15 via hsa-miR-1233-3p. Our work thus provides biological insight into the previously reported clinical association between rs1054564 and plasma GDF15 levels.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Phospholipase A and acyltransferase 4 (PLAAT4) is a member of the HREV107 tumor suppressor gene family. The expression of PLAAT4 has been shown to induce cell death; however, the underlying mechanism ...remains unknown. Here, we found that RPLP0, a ribosomal protein, can interact with PLAAT4, as determined by yeast two-hybrid screening, coimmunoprecipitation, and colocalization. The level of RPLP0 was suppressed in HtTA cervical cancer cells expressing PLAAT4. In PLAAT4-expressing or RPLP0-silenced cells, decreased cell viability and cell proliferation combined with increased cell death were observed. Furthermore, the levels of cell cycle-associated proteins and anti-apoptotic proteins decreased in PLAAT4-expressing or RPLP0-silenced cells. Similar patterns of cell viability and expression levels of cell-cycle-associated proteins and apoptosis-related proteins were observed in PLAAT4-expressing and RPLP0-knockdown cells, indicating that RPLP0 deficiency might be involved in PLAAT4-mediated growth inhibition and cellular apoptosis.
Glycine N-methyltransferase (GNMT) is a tumor suppressor for hepatocellular carcinoma (HCC). High rates of Gnmt knockout mice developed HCC. Epigenetic alteration and dysregulation of several ...pathways including wingless-type MMTV integration site (Wnt), mitogen-activated protein kinase (MAPK) and Janus kinase and signal transducer and activator of transcription (JAK-STAT) are associated with HCC development in Gnmt knockout mice. We hypothesized that GNMT may regulate signal transduction through interacting with other proteins directly. In this report, we identified a mammalian target of rapamycin (mTOR) inhibitor (DEP domain containing MTOR-interacting protein DEPDC6/DEPTOR) as a GNMT-binding protein by using yeast two-hybrid screening. Fluorescence resonance energy transfer assay demonstrated that the C-terminal half of GNMT interact with the PSD-95/Dlg1/ZO-1 (PDZ) domain of DEPDC6/DEPTOR. Immunohistochemical staining showed that 27.5% (14/51) of HCC patients had higher expression levels of DEPDC6/DEPTOR in the tumorous tissues than in tumor-adjacent tissues, especially among HCC patients with hepatitis B viral infection (odds ratio 10.3, 95% confidence interval CI 1.05-11.3) or patients with poor prognosis (death hazard ratio 4.51, 95% CI 1.60-12.7). In terms of molecular mechanism, knockdown of DEPDC6/DEPTOR expression in HuH-7 cells caused S6K and 4E-BP activation, but suppressed Akt. Overexpression of DEPDC6/DEPTOR activated Akt and increased survival of HCC cells. Overexpression of GNMT caused activation of mTOR/raptor downstream signaling and delayed G2/M cell cycle progression, which altogether resulted in cellular senescence. Furthermore, GNMT reduced proliferation of HuH-7 cells and sensitized them to rapamycin treatment both in vitro and in vivo. In conclusion, GNMT regulates HCC growth in part through interacting with DEPDC6/DEPTOR and modulating mTOR/raptor signaling pathway. Both GNMT and DEPDC6/DEPTOR are potential targets for developing therapeutics for HCC.
A reinforcement learning algorithm is proposed to improve the accuracy of short-term load forecasting (STLF) in this article. The proposed model integrates radial basis function neural network ...(RBFNN), support vector regression (SVR), and adaptive annealing learning algorithm (AALA). In the proposed methodology, firstly, the initial structure of RBFNN is determined by using an SVR. Then, an AALA with time-varying learning rates is used to optimize the initial parameters of SVR-RBFNN (AALA-SVR-RBFNN). In order to overcome the stagnation for searching optimal RBFNN, a particle swarm optimization (PSO) is applied to simultaneously find promising learning rates in AALA. Finally, the short-term load demands are predicted by using the optimal RBFNN. The performance of the proposed methodology is verified on the actual load dataset from the Taiwan Power Company (TPC). Simulation results reveal that the proposed AALA-SVR-RBFNN can achieve a better load forecasting precision compared to various RBFNNs.
The design of unified, efficient, and lightweight cryptographic platform for resource-constrained on-board devices such as sensors, microcontrollers, and actuators in the context of Internet of ...Vehicles remains an open and challenging problem, for both academic and industry. Elliptic curve cryptography (ECC) is considered as a promising encryption algorithm for the next generation communications, as it could provide the same strong security level using relatively smaller key size when compared to the currently used Rivest-Shamir-Adleman algorithm. However, traditional ECCs have the disadvantage of using a fixed curve, making it very easy to be intensively analyzed while being hard to construct a united platform for on-board devices with processors of different instruction lengths. To mitigate the above problem, this paper suggests a dynamic scalable elliptic curve cryptosystem. To synchronize the curve in use, a curve list of different security levels is generated and preserved on both parties. Since both parties randomly choose the curve and the prime number, a extra security level could be provided, so that the security level can still remain the same even using smaller key sizes, while the computation efficiency will be enhanced and the power consumption will be reduced, which is especially suitable for the application in on-board embedded devices. Detailed experimental results illustrate that the presented scheme improves the efficiency by 30% in average when compared with traditional ECC implementations on a similar security level. Therefore, the proposed scalable ECC scheme as a unified cryptographic platform is more economic for these on-board devices in vehicles.
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