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Background Gliomas are the most malignant and aggressive form of brain tumors, and account for the majority of brain cancer related deaths. Previous studies have reported that SUB1 serves as a novel RBP, which is highly expressed in tumors. Aim In our research, we aimed at exploring the regulatory mechanism of SUB1 in glioma cells. Methods RT-qPCR was conducted to measure the expression of SUB1, HSP90β and MYC in glioma cells in U87 cell. Cell function tests were conducted to identify how the ectopic SUB1 expression influenced the proliferation and migration of glioma cells. Also, functional assays and mechanism experiments were carried out to figure out the relationship among circVCAN, SUB1 and MYC/HSP90β. Results SUB1 expression was up-regulated in glioma cells. The inhibition of SUB1 expression suppressed the proliferation and migration of glioma cells, while the up-regulation of that accelerated the proliferation and migration of glioma cells. CircVCAN could up-regulate the expression of MYC/HSP90β by recruiting SUB1, thereby promoting glioma progression. Conclusion SUB1 plays a significant role in the survival and migration of glioma cells.

Glioma is a common invasive cancer with unfavorable prognosis in patients. Long non-coding RNAs (lncRNAs) exert significant functions in carcinogenesis of various cancers including glioma. Among them, long intergenic non-coding RNA 668 (LINC00668) was reported to function as oncogene in various cancers, but its molecular mechanism in glioma has not been thoroughly researched. Our current study aimed to investigate the role and molecular mechanism of LINC00668 in glioma cells. We initially found out that LINC00668 was up-regulated in glioma cells. Through a series of function assays, LINC00668 was verified to facilitate cell proliferation and inhibit apoptosis in glioma. Then, by means of online databases, RNA pull down assay and RIP assay, we verified the binding relation between LINC00668 and miR-518c-3p. Also, the next function assays exposed that miR-518c-3p was the tumor suppressor in glioma cells. Similarly, SOCS5 (suppressor of cytokine signaling 5) was found to bind with miR-518c-3p, which repressed glioma tumorigenesis by targeting SOCS5. Moreover, rescue assays manifested that LINC00668 modulated expression of SOCS5 in a miR-518c-3p-dependent way and further regulated glioma tumorigenesis. Overall, LINC00668 modulates SOCS5 expression through competitively sponging miR-518c-3p to facilitate glioma cell proliferation.

Description, Circulating tumor cells with high levels of adhesion proteins survive more easily in circulation and form metastatic tumors., To study how cancer cells can withstand fluid shear stress (SS), we isolated SS-resistant breast and lung cancer cells using a microfluidic circulatory system. These SS-resistant cells showed higher abilities to form clusters, survive in circulation, and metastasize in mice. These SS-resistant cells expressed 4.2- to 5.3-fold more desmocollin-2 (DSC2) and plakophilin-1 (PKP1) proteins. The high expression of DSC2 and PKP1 facilitated cancer cells to form clusters in circulation, and also activated PI3K/AKT/Bcl-2–mediated pathway to increase cell survival. The high levels of DSC2 and PKP1 are also important for maintaining high expression of vimentin, which stimulates fibronectin/integrin β1/FAK/Src/MEK/ERK/ZEB1–mediated metastasis. Moreover, higher levels of DSC2 and PKP1 were detected in tumor samples from patients with breast and lung cancer, and their high expression was correlated with lower overall survival and worse disease progression. DSC2 and PKP1 may serve as new biomarkers for detecting and targeting metastatic circulating tumor cells.

Background Signal regulatory protein β1 (SIRPB1) is a signal regulatory protein member of the immunoglobulin superfamily and is capable of modulating receptor tyrosine kinase-coupled signaling. Copy number variations at the SIRPB1 locus were previously reported to associate with prostate cancer aggressiveness in patients, however, the role of SIRPB1 in prostate carcinogenesis is unknown. Methods Fluorescence in situ hybridization and laser-capture microdissection coupled with quantitative polymerase chain reaction was utilized to determine SIRPB1 gene amplification and messenger RNA expression in prostate cancer specimens. The effect of knockdown of SIRPB1 by RNA interference in PC3 prostate cancer cells on cell growth in colony formation assays and cell mobility in wound-healing, transwell assays, and cell cycle analysis was determined. Overexpression of SIPRB1 in C4-2 prostate cancer cells on cell migration, invasion, colony formation and cell cycle progression and tumor take rate in xenografts was also determined. Western blot assay of potential downstream SIRPB1 pathways was also performed. Results SIRPB1 gene amplification was detected in up to 37.5% of prostate cancer specimens based on in silico analysis of several publicly available datasets. SIRPB1 gene amplification and overexpression were detected in prostate cancer specimens. The knockdown of SIRPB1 significantly suppressed cell growth in colony formation assays and cell mobility. SIRPB1 knockdown also induced cell cycle arrest during the G0 /G1 phase and enhancement of apoptosis. Conversely, overexpression of SIPRB1 in C4-2 prostate cancer cells significantly enhanced cell migration, invasion, colony formation, and cell cycle progression and increased C4-2 xenograft tumor take rate in nude mice. Finally, this study presented evidence for SIRPB1 regulation of Akt phosphorylation and showed that Akt inhibition could abolish SIRPB1 stimulation of prostate cancer cell proliferation. Conclusions These results suggest that SIRPB1 is a potential oncogene capable of activating Akt signaling to stimulate prostate cancer proliferation and could be a biomarker for patients at risk of developing aggressive prostate cancer.

Attitude Dilution of Precision (ADOP) is an important indicator that reflects the relationship between attitude errors and noise in carrier phase observations for Global Navigation Satellite System (GNSS) attitude determination. Several definitions of the ADOP have been put forward by some scholars so far. However, there is no widely accepted standard ADOP definition currently. Therefore, the most exact ADOP definition need to be selected to compare the attitude determination performance of BDS and GPS stand-alone and integrated system. In this paper, three representative ADOP definitions are studied. Theoretical analysis and data simulation show that the ADOP definition proposed by Gomez is the best among these three definitions. After that, the ADOP for BDS and GPS integrated attitude determination is defined based on the ADOP-Gomez definition. BDS and GPS stand-alone and integrated ADOP are calculated in a three-antenna static attitude determination experiment. The experimental results demonstrate that the ADOP for GPS stand-alone system is on the whole lower than BDS stand-alone system, which means the geometry strength of GPS for attitude determination is stronger than BDS. Even so, the ADOP for BDS is nearly close to GPS in the condition that the visible satellite numbers of BDS and GPS are almost the same. It is also concluded that the ADOP for BDS and GPS integrated system significantly decreases compared with their stand-alone system.

Cancer immunotherapy based on carbon-quantum-dots (CQDs) has proven effective. The CQDs composited cancer cell (CM-cancer) exhibit robust customized immunogenicity, which can recruit macrophages and dendritic cells to effectively deliver the cancer antigens into lymph nodes to activate CD8+ T cells, and eventually leads to an anti-cancer immune response all over the body. The CM-cancer is not only able to inhibit primary tumors, but also clearly eliminate metastatic tumors. Our research demonstrates a promising personalized cancer immunotheraputic technology for potential clinical applications.

Cancer immunotherapy based on carbon-quantum-dot (CQD) modified cancer cells (CM-cancer) has proven effective. The CQDs non-distinctively modify the conformational structure of proteins by hydrogen bonding between the protein chains and the permeated CQDs via a thermal treatment. CM-cancer vaccines exhibit robust immunogenicity, which can recruit macrophages and dendritic cells to effectively deliver the cancer antigens into lymph nodes to activate CD8+ T cells, and eventually leads to an anti-cancer immune response all over the body. The CM-cancer vaccinations are not only able to inhibit primary tumors, but also clearly eliminate metastatic tumors. Our research demonstrates a promising personalized cancer immunotheraputic technology for potential clinical applications.

Traumatic brain injury (TBI) represents a major public health concern worldwide, with no significant change in its epidemiology over the last 30 years. After TBI, the primary injury induces irreversible brain damage, which is untreatable. The subsequent secondary injury plays a critical role in the clinical prognosis because without effective treatment it will provide additional tissue damage. The resulting scenario is the rise in intracranial pressure (ICP) with the development of progressive neurological deficits. Current optimal management is based on a progressive, target-driven approach combining both medical and surgical treatment strategies among which is decompressive hemicraniectomy. With the advent of technology, research in the glymphatic pathways, and advances in microscopic surgery, a novel surgical technique—the cisternostomy—has emerged that holds promise in managing rising ICP in TBI-affected patients. In this article we describe the rationale for cisternostomy, an emerging microneurosurgical approach for the management of moderate to severe TBI. © 2019 Elsevier Inc.

Glioma is the most common malignant brain tumors with poor prognosis. The molecular events involved in the development and progression of glioma remain unclear. In this study, the expression levels of miR-302c-3p were examined in glioma tissues by qRT-PCR. The in vitro and in vivo functional effects of miR-302c-3p were examined further. Luciferase reporter assays were conducted to confirm the targeting associations. Results showed that the expression level of miR-302c-3p in glioma tissues was significantly lower than those in normal brain tissues (P < 0.001). The decreased expression of mi-302c-3p in glioma was positively associated with WHO grade (P < 0.001). Up-regulation of MTDH was also detected in glioma tumors compared with normal brain tissues (P = 0.0027) and is inversely correlated with miR-302c-3p expression (P = 0.003, R2 = 0.4065). MTDH mRNA is a direct target of miR-302c-3p, whose ectopic expression decreases MTDH expression through binding to its 3′-untranslated region. Overexpression of miR-302c-3p results in a dramatic inhibition of glioma cells proliferation and invasion in vitro and in vivo. These data suggest that miR-302c-3p play a pivotal role in the progression of glioma by targeting MTDH and is a potential inhibitor in glioma treatment.

Substituted gold(III) tetraarylporphyrins have been synthesised. The analogues TPPAuCl (TPP = tetraphenylporhyrin), MeOTPPAuCl, TMOPPAuCl, MeO2CTPPAuCl, O2NTPPAuCl and PyTPPAuCl were evaluated for their in vitro cytotoxic activity against the Sarcoma 180 mouse tumour cell line panel. Compound MeO2CTPPAuCl exhibited good growth inhibitory properties against Sarcoma 180 and afforded IC50 values 2CTPPAuCl as cytotoxic agents.

The Zn(OAc)22H2O-catalyed Michael addition reaction of indole to electron-deficient nitroolefins to afford the corresponding adducts in good to excellent yields with high selectivity is reported.

Overexpression of the tumor-derived monocyte chemotactic protein-1 (MCP-1) has been suggested to partially promote prostate cancer bone metastasis, but the function for host-derived MCP-1 in these processes is not well established. To understand the function of host-derived MCP-1 on bone metastasis, we developed a mouse model using intracardiac injection and in vivo selection to obtain tumor cell subpopulations with a higher propensity for bone metastasis. Here, we found that a loss of host MCP-1 (MCP-1 knockout) retarded tumor growth in bone and prolonged survival of mice by intracardiac injection of tumor cells in vivo. Moreover, a decrease in osteolytic bone lesion was observed in MCP-1 knockout mice by bone density analysis, as compared to wild-type control. Systemically, MCP-1 deficiency inhibited the proportion of PMN-and M-MDSC populations with immunosuppressive function. Together, this study indicates that the dysregulated immunity resulting from a loss of host MCP-1 signaling is sufficient to drive PCa bone metastasis, and provides a new perspective for targeting the endogenous MCP-1 pathway as an antimetastatic strategy. Supported by NSFC Key Project 81130046; NSFC projects 81773146, 81272415; JCYJ20170412152943794, JCYJ20170412154619484, JCYJ20170307105128101, JCYJ2017030711041760; Guangxi Key Projects 2013GXNSFEA053004. Citation Format: Jie Meng, Weiping Liang, Haibo Tong, Evan T. Keller, Jian Zhang, Yi Lu. Host-derived MCP-1 dictates prostate cancer skeletal metastasis in vivo [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 996.

Chemoresistance, in various types of cancer including prostate cancer (PCa), is one of the major challenges in cancer therapy. Others and our lab have reported that the epithelial-to-mesenchymal transition (EMT) plays critical roles in development of chemoresistance and metastasis. The calcium-sensing receptor (CaSR) plays important roles in maintenance of calcium homeostasis and altered CaSR expression, and functional changes are involved in certain diseases, including tumorigenesis and its development. However, the mechanism of CaSR in PCa chemoresistance remains unclear. In current study, the CaSR expression level was detected in parental PC3 and DU145 cells and their chemoresistant PC3-TxR and DU145-TxR cells. We found the CaSR was highly expressed in chemoresistant PC3-TxR and DU145-TxR cells. Then by using siRNA technique, CaSR expression was transiently knocked down in chemoresistant cells. The tumor cell migration, invasion, and colony formation were evaluated by wound healing, transwell, and colony formation assays, respectively. The drug sensitivity was evaluated using MTS assay. We observed that the abilities of tumor cell migration and invasion were significantly diminished in CaSR knockdown PC3-TxR and DU145-TxR cells. The ability of colony formation was also reduced. Interestingly, the sensitivity to paclitaxel was reactivated in CaSR knockdown PC3-TxR and DU145-TxR cells. We finally observed that E-cadherin expression was increased in CaSR knockdown chemoresistant cells, and Snail, Vimentin and β-catenin were decreased; these results are consistent with EMT phenotypic alterations. Taken together, we conclude that downregulation of CaSR enhances MET-mediated prostate cancer chemosensitivity. Supported by NSFC Key Project 81130046; NSFC projects 81773146,81272415; JCYJ20170412152943794, JCYJ20170412154619484, JCYJ20170307105128101, JCYJ2017030711041760; Guangxi Key Projects 2013GXNSFEA053004. Citation Format: Luying Huang, Fuhao Wang, Haibo Tong, Atsushi Mizokami, Evan T. Keller, Yi Lu, Jian Zhang. Downregulation of calcium-sensing receptor enhances MET-mediated prostate cancer chemosensitivity [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 5896.

In view of the problem of the long-term variation of code multipath error (called code multipath bias) in the IGSO and MEO satellite observable, code multipath bias of BDS is analyzed using iGMAS data of multiple earth stations. In addition, the GPS and BDS multipath error variation is analyzed comparatively. The results show that the variation of BDS multipath error is related to the elevation angle, satellite orbit type and carrier frequency, but independent with the location of the receivers. And for the carrier frequency B1, B2, and B3, the code multipath bias for MEO satellite is 1.66, 1.05 and 0.53 m, respectively. For IGSO satellite the code multipath bias is 0.65, 0.44, and 0.31 m accordingly, which are smaller than that reported by earlier papers. Especially, for IGSO at frequency B2 and B3, the code multipath bias is smaller than half of that reported earlier. At the same time, in order to reduce the multipath bias, a two-order polynomial fitting algorithm is proposed in this paper. The results show that: compared with the results of piecewise linear model with 10 correction parameters, the two-order polynomial correction algorithm with three correction parameters can correct the multipath error and reduce the RMS of the multipath error more effectively. The two-order polynomial model in this paper is more convenient considering broadcasting the correction information to the users.

Metastasis is the major cause of treatment failure in various malignancies, including prostate cancer (PCa). Accumulating data has suggested that primary cancer cells prefer to spread to certain distant organs. To explore the mechanisms of different cancer cells preferentially metastasizing to certain organs, we established a prostate cancer lung metastasis model. Murine prostate cancer cells (RM1), which labeled with luciferase, were used in this study. RM1 cells were injected into left tibia of mouse (C57BL/6J), and monitored the tumor growth and metastasis every week by Bioluminescence Imaging. The mice would be sacrificed when metastatic tumor appeared in multi-organs. We isolated the lung metastatic tumor, made single cell suspension and amplified. The lung metastatic tumor cells were specifically metastasized to lung when the tumor cells were injected intratibially again. After several cycles we obtained highly lung metastatic tumor cells, named RM1-LM cells. Further, we investigated property and function changes in RM1-LM cells compared to parental cells (RM1) using in vitro assays. We firstly found the highly lung metastatic tumor cells showed more mesenchymal properties. Western blot results showed that hallmarks of EMT including E-cadherin, vimentin, snail, and ZO-1 were altered significantly in RM1-LM cells. Then, we observed that the highly lung metastatic tumor cells exhibited increased proliferative, colony formation, migratory and invasive abilities. Mechanistic analyses indicated that prostate cancer organ-specific metastasis mediated by the activation of GSK-3β/β-catenin pathway. The current study may provide potential therapeutic targets and diagnostic biomarkers of PCa metastasis. This work was supported by Natural Science Foundation of China (NSFC) Key Project (81130046); NSFC (81171993; 81272415); Guangxi Projects of China (2013GXNSFEA053004; 2012GXNSFCB053004). Note: This abstract was not presented at the meeting. Citation Format: Siyuan Qin, Qiong Song, Jinlu Dai, Haibo Tong, Evan Keller, Jian Zhang, Yi Lu. Activation of GSK3β/β-catenin pathway promotes organ-specific metastasis in prostate cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 4939. doi:10.1158/1538-7445.AM2017-4939

Signal-regulatory-protein beta 1(SIRPB1) is a member of the signal-regulatory-protein (SIRP) family that belongs to the immunoglobulin superfamily and is capable of modulating receptor tyrosine kinase-coupled signaling. The copy-number variations (CNV) at the SIRPB1 locus were associated with aggressiveness of prostate cancer in patients. To test if SIRPB1 could affect prostate cancer development and progression, we investigated the potential role and mechanisms of SIRPB1 action in prostate cancer cell lines in vitro and in xenograft tumors. Knockdown of SIRPRB1 by RNA interference resulted in significant suppression of cell colony formation, cell mobility, cell migration, and invasion. The knockdown also induced cell cycle arrest during the G0/G1 phase and a remarkable enhancement of apoptosis in PC3 prostate cancer cells. In contrast, overexpression of SIPRB1 significantly induced cell migration, invasion, colony formation and cell cycle in C4-2 prostate cancer cells. Furthermore, overexpression of SIRPB1 in C4-2 cell model enhanced its tumor take rate in nude mice. Also, SIRPB1 mRNA expression was increased in up to 39% of the prostate cancer specimens based on in silico analysis of several public databases. These results suggest that SIRPB1 is a potential oncogene in the prostate and could be used as a biomarker to identify patients at risk of developing aggressive prostate cancer. Citation Format: Qiong Song, Siyuan Qin, Chunlin Zou, Wenchu Wang, Lihui Wang, Haibo Tong, William J. Catalona, Jian Zhang, Yi Lu, Zhou Wang. SIRPB1 promotes prostate cancer cell proliferation & migration [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 331. doi:10.1158/1538-7445.AM2017-331

A hierarchical control architecture for mission re-planning of autonomous underwater vehicle (AUV) navigating in uncertain ocean environment is presented in this paper. The proposed component-oriented control architecture structured is made of three parts: situation reasoning, re-planning trigger and hierarchical re-planning layer. Situation reasoning using the unstructured real-word information obtained by sorts of sensor detectes and recognizes uncertain event.The re-planning trigger decides the re-planning level by the event types and influence degree. Hierarchical re-planning layer contains mission re-planning, task re-planning and behavior re-planning. Different re-planning level depends on the result of re-planning trigger. Preliminary versions of the architecture have been integrated and tested in a simulation environment. Experiment indicates that the novel control architecture can implement mission re-planning steady and safty. DOI : http://dx.doi.org/10.11591/telkomnika.v12i6.5442 Full Text: PDF

In recent years, navigation signal simulator with different functions has been playing a very important role in meeting the performance requirement of the research, test and evaluation of the different navigation receiver, such as RDSS, RNSS and dual-mode receivers. Compared with the simulator of GPS, BeiDou Navigation Satellite System (BDS) have some different unique characteristics, especially in RDSS determination. First, the principle of comprehensive RDSS position and report is elaborated and then requirements of the dynamic navigation signal simulation are analyzed. Finally, two key mathematical models are established to simulate the signals arriving at the receiver antenna for dual-mode receiver test, which are: the transmitting time iterative model and satellite orbit approximation model. The results show that the BDS dual-mode simulator can satisfy dual-mode receiver’s test requirements.

For tracking the weak and high dynamic Global Positioning System (GPS) signals, the vector delay lock loop (VDLL) performs better than the traditional scalar based methods. The navigation states of the VDLL always converge to the biased solution when more than 4 satellites are available. In order to reduce the position bias caused by the code tracking bias, the modified VDLL with unbiased code tracking is proposed and implemented in the software defined receiver. The detector of the code phase is introduced to keep the unbiased code tracking adaptively. Simulation results show that the estimated code phase errors of the modified VDLL have zero mean when the redundant satellites are available.

The receiver autonomous integrity monitoring (RAIM) is the straightforward way to handle the outlier, but the protection levels are vulnerable to the satellite geometry. A robust protection level is proposed. Firstly, a robust positioning solution based on MM-estimation is introduced. Then the protection level of the robust solution is presented. Finally, the experiments with actual GPS data demonstrate that the robust protection levels are less affected by the geometry. Moreover, the robust protection levels are more stringent to bound the maximum error than the conventional protection levels.

As the satellite navigation system BD-2 comes to be more and more sophisticated, the RDSS/RNSS dual-mode user receiver covering two work modes of RDSS and RNSS are developing rapidly. It is demanded to simulate the satellite signals in different conditions to test the behaviors of the dual-mode user receiver. RDSS is an active positioning system. Otherwise, RNSS is a passive positioning system, without transmitting signals. The key point in developing a RDSS/RNSS dual-mode signal simulator is how to guarantee the synchronization of these two different kinds of systems. A signal simulation method adapted to RDSS and RNSS is proposed here; the formulae for the Doppler frequency shift are derived, which have solved the pseudorange consistency problem of RDSS and RNSS signal in the same GEO. The experiment results validate the algorithms developed here. The results in practical use show that the RDSS/RNSS dual-mode signal simulator developed here is meeting all the test requirements.

Title compounds (Ia)—(Id) exhibit significant inhibitory effects on the growth of S180 tumor cells, derivative (Id) displays even more potent activity than cisplatin.

The Zn(OAc)22H2O-catalyed Michael addition reaction of indole to electron-deficient nitroolefins to afford the corresponding adducts in good to excellent yields with high selectivity is reported.

The synthesis of novel substituted gold(III) tetraarylporphyrins with aqueous solubility has been carried out. The analogs ClAuTPP(CH(3)Py(+)·I(-)), ClAuTCPPNa, ClAuTPPCO(2)Na, ClAuTSPPNa and ClAuTPPNH(2)·HCl were evaluated for their in vitro cytotoxic activity against sarcoma 180 mouse tumor and SGC-7901 human gastric cancer cell line panel. Compound ClAuTCPPNa exhibited significant growth inhibitory properties against sarcoma 180 mouse tumor and SGC-7901 human gastric cancer cell examined, and afforded IC(50) values

A novel research apparatus is developed to measure the fluid thermal conductivity while in shearing flow, and to determine its dependence on the shearing itself, contrary to the current state-of-the-art of measuring thermal conductivity under the condition of motionless fluid. A concentric cylinders’ apparatus was developed to provide controlled heat transfer in the radial direction, orthogonal to the circumferential fluid velocity, thus virtually preserving pure conductive heat transfer mode. The measurement and control are accomplished and integrated by using a computerized data acquisition system and a comprehensive virtual instrument, developed using the LabVIEW application software. It was found that the thermal conductivity of a Newtonian fluid, such as distilled water, was virtually independent of the fluid motion, as expected. However, for non-Newtonian fluids such as 1000 and 2000 wppm aqueous polyacrylamide (Praestol) solutions, there was up to 10–20% increase of thermal conductivity in the operating shear rate range (40 ≤ γ ≤ 510 sec−1) at 27°C average fluid temperature.

A robust GPS positioning algorithm with high efficiency is presented to reduce the positioning error caused by the outlier. First, the robustness is obtained by the outlier-insensitive initial estimate. The robust initial estimate is selected from the separated group estimates under the stringent criterion. Secondly, the weights of the pseudo-ranges are calculated with the initial estimate. Finally, the efficiency of the initial estimate is improved by performing the iterative reweighted recursive least squares with the updated weights. Experimental data-processing results show that the proposed algorithm is effective to resist the outlier which has contaminated the high leverage observation.