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In this article, an iterative learning algorithm based on extended state observer (ESO) is proposed to deal with the propeller failure of an underwater vehicle. In this control scheme, the nonlinear feedback mechanism of ESO is transplanted to iterative learning processes; that is, the nonlinear function of the current output residual is used to adjust the value of the virtual fault in the next iteration. Additionally, to ensure the safety of the control torque, a saturated proportional-derivative (PD) controller is proposed. Finally, to achieve online parameter self-tuning, a fuzzy logic controller is employed in this control scheme to fuzzify the parameters of a saturated PD controller and ESO. The obtained results show the favorable speed of tracking convergence and the high precision of fault estimation.

Due to highly maneuverable vessels, dense channels and strong clutter, intermittent track segments are common in large-scale marine monitoring. To solve this problem, we propose a long-term continuous tracking method for high frequency surface wave radar (HFSWR) based on an adaptive filtering algorithm combined with an extreme learning machine (ELM). Via analyzing the features of the vessels and tracks and lots of simulations, we select average velocity, average acceleration, average heading angle, average curvature, ratio of the arc length to the chord length, and wavelet coefficient to compose the multidimensional feature vector to train and test the ELM. Field experiment results show that the proposed method has better performance than conventional algorithms with the correct association probability of 94.7%.

To deal with the fault of the thrusters of AUV, an iterative learning algorithm based on the extended states observer (ESO) is established. In this algorithm, the nonlinear feedback mechanism of the ESO is transplanted to iterative learning processes, that is, the nonlinear function of the current output residual is used to adjust the value of the virtual fault in the next iteration. The obtained result shows the favorable convergence speed and the fault estimation precision of the proposed method.

// Liyuan Guo 1, * , Yan Peng 2, * , Lei Sun 3, * , Xia Han 4 , Juan Xu 4 and Dongwei Mao 4 1 Department of Gynecological Oncology, Cancer Hospital of Harbin Medical University, Harbin, China 2 Disease Prevention Center, First Affiliated Hospital, Heilongjiang University of Chinese Medicine, Harbin, China 3 Department of Gynecology and Obstetrics, The Fourth Hospital of Harbin Medical University, Harbin, China 4 Shenzhen Hospital of Guangzhou University of Chinese Medicine, Shenzhen, China * These authors contributed equally to this work Correspondence to: Dongwei Mao, email: maodongwei2017@126.com Keywords: ovarian cancer, genome-wide association study, gene expression Received: July 17, 2017 Accepted: September 21, 2017 Published: October 13, 2017 ABSTRACT Ovarian cancer (OC) is a common cancer in women and the leading cause of deaths from gynaecological malignancies in the world. In addition to the candidate gene approach to identify OC susceptibility genes, the genome-wide association study (GWAS) methods have reported new variants that are associated with OC risk. The minor allele of rs2072590 at 2q31 was associated with an increased OC risk, and was primarily significant for serous subtype. The OC risk-associated SNP rs2072590 lies in non-coding DNA downstream of HOXD3 and upstream of HOXD1 , and it tags SNPs in the HOXD3 3′ UTR. We think that the non-coding rs2072590 variant may contribute to OC susceptibility by regulating the gene expression of HOXD1 and HOXD3. In order to investigate this association, we performed a bioinformatics analysis by a functional annotation of rs2072590 variant using RegulomeDB (version 1.1), HaploReg (version 4.1), and PhenoScanner (version 1.1). Using HaploReg, we identified 19 genetic variants tagged by rs2072590 variant with with r 2 >= 0.8. Using RegulomeDB, we identified that three genetic variants are likely to affect TF binding + any motif + DNase Footprint + DNase peak. Other genetic variants are likely to affect TF binding + DNase peak. Using PhenoScanner (version 1.1), we identified that these 19 genetic variants could significantly regulate the expression of nearby genes, especially the HOXD1 and HOXD3 in human ovary tissue.

Cervical cancer is a significant cause of morbidity and mortality in gynecological malignancies. Although autophagy plays a critical role in affecting cell apoptosis and proliferation, the role of hsa-miR-211-5p (miR-211) in modulating autophagy of cervical cancer cells remains unclear. In the current study, the level of miR-211 was downregulated in cervical cancer specimens, compared to the paired para-carcinoma tissues. While Bcl-2 was upregulated, LC3-II/I was decreased in the tumors, indicating inhibited apoptosis and autophagy. The forced expression of miR-211 inhibited proliferation, and promoted apoptosis in SiHa cervical cancer cells, evidenced by increased expression of apoptotic proteins, caspase-3, and PARP. While the miR-211 inhibitor exerted reverse effects on C-33A cervical cancer cells. Further, miR-211 induced autophagy in cervical cancer cells, as manifested by the presence of LC3 puncta, increased LC3-II/I and Beclin1 levels, and decreased p62 level. The miR-211-induced apoptosis was alleviated by an autophagy inhibitor 3-methyladenine (3-MA). In addition, Bcl-2 was identified as a target of miR-211. Besides, the apoptosis and autophagy triggered by miR-211 were attenuated by Bcl-2 in SiHa cells. In summary, our work indicates that miR-211 induced autophagy and autophagy-dependent apoptosis by regulating Bcl-2 in cervical cancer cells, which provided further understanding of autophagy in cervical carcinogenesis.

Objective: This study aims to evaluate the relationship between apoptosis and autophagy induced by resveratrol (Res) in SKOV3 human ovarian cancer cell lines. Methods: The experiment was divided into four groups: normal control group, Res group, Res combined with autophagy inhibitor 3-methyladenine (Res+3-MA) group, and Z-VAD-FMK group. SKOV3 cells were cultured and treated with Res and 3-MA for 24 hours. The processing concentration of Res was screened out by the Cell Counting Kit-8 (CCK8) assay. The cell survival rate was measured by the CCK8 assay. The expression of bule-associated protein light chain 3 beta 2 (LC3-II) and Beclin-1 was detected using Western blot analysis. The percentages of apoptotic and autophagic cells were analyzed using flow cytometry. Results: The cell survival rate significantly decreased as Res concentration increased, and the differences were statistically significant (P < 0.05). The processing concentration of Res was 25 μmol/L. After treatment with Res for 24 hours, the expression levels of autophagy-related protein LC3 and Beclin-l were significantly higher than in the other groups. Furthermore, the expression of LC3 and Beclin-l significantly declined in the Res+3-MA group compared with the Res group. However, the percentage of autophagic cells significantly decreased from 37.0% ± 4.24% to 6.1% ± 0.28%, and the percentage of apoptotic cells significantly increased from 24% ± 4.55% to 67.0% ± 4.3%; and the differences were statistically significant ( P < 0.05). Conclusion: Res can induce autophagy to inhibit apoptosis in tumor SKOV3 cells, and inhibition of Res+3-MA could not only enhance the effects of chemotherapy but also prevent normal cells from tumorigenesis.

CLN3 is a recently identified anti-apoptotic gene, which has been demonstrated to be highly expressed in a diverse range of cancer cell lines, including ovarian cancer. In the present study, RNA interference, mediated by a lentivirus expressing CLN3 short hairpin RNA (shRNA) was utilized to knockdown the expression of CLN3 in the A2780 human ovarian cancer cell line, and its cisplatin-resistant and carboplatin-resistant sublines, A2780/DDP and A2780/CBP cells. It was revealed that the mRNA and protein expression levels of CLN3 were significantly reduced in the CLN3-specific shRNA-transduced cells, compared with the untransduced and control shRNA-transduced cells. In addition, specific knockdown of CLN3 in these cells inhibited cell proliferation and led to cell cycle arrest at the G0/G1 phase, with eventual apoptosis. CLN3 knockdown caused increases in the levels of Bax, FAX, cleaved-caspase 3, cleaved-caspase 8 and cleaved-RARP, but decreased the level of Bcl-2. Finally, it was observed that CLN3 depletion markedly reduced the half maximum inhibitory concentration in the A2780/DDP and A2780/CBP cells. Taken together, these data suggested that CLN3 is involved in tumorigenesis and drug resistance in ovarian cancer, and may serve as a promising therapeutic target for its treatment.

Background Interleukin-8 (IL-8), a CXC chemokine that recruits and activates inflammatory cells, plays a critical role in the pathogenesis of ulcerative colitis (UC). There are no studies on the association of single nucleotide polymorphisms (SNPs) of the IL-8 gene with the risk of UC. Methods All 162 unrelated UC patients and 203 control subjects were analyzed for 5 IL-8 SNPs ((− 845 (T/C), − 738 (T/A), − 353 (A/T), − 251 (T/A) and + 678 (T/C)) using polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP) assay and PCR-sequence-specific primers (SSP) method. Serum IL-8 concentrations were measured in all subjects. Results Individual SNPs were not associated with risk for UC. However, the frequency of − 353A/− 251A/+ 678T haplotype was significantly higher in UC patients than in healthy controls (OR = 1.454, p = 0.036). By subgroup analyses, this haplotype tended to be more common in severe UC patients than in those with mild-to-moderate disease (OR = 2.281, p = 0.027). Furthermore, patients with AAT diplotype showed significantly increased serum IL-8 concentrations than those with other diplotypes ( p Conclusion These results suggest that IL-8 is a novel susceptibility gene to UC in Chinese UC patients, and furthermore, that IL-8 polymorphisms may be related to severe clinical subtype of UC.

Monocyte chemoattractant protein-1 (MCP-1) is a chemokine involved in monocyte recruitment to sites of inflammation. Raised level of MCP-1 has been widely demonstrated in the intestinal mucosa of patients with ulcerative colitis (UC), suggesting an important role of MCP-1 in the pathogenesis of UC. The -2518A/G polymorphism in the promoter region of MCP-1 gene affecting its transcriptional activation has been reported recently. In order to assess the potential role of this polymorphism in UC, we examined its distribution in 162 unrelated UC patients and 203 healthy controls. In addition, considering the gene regulatory association between interleukin-1beta (IL-1beta) and MCP-1, we further examined whether the gene polymorphisms between MCP-1 and IL-1beta exert synergetic effects on risk of UC. Our results show that the distribution of MCP-1 genotype or allele frequencies between UC patients and controls was not significantly different; however, the association between the polymorphism of MCP-1 -2518 GG and the polymorphism of IL-1beta-511 T in UC patients is significant (OR 2.062, 95% CI 1.034-4.113, P = 0.038). This is the first report describing the association between MCP-1 polymorphism and UC, and our data suggest that the MCP-1 -2518 polymorphism itself does not represent an independent genetic risk factor for UC. In contrast, the combination polymorphisms between MCP-1 and IL-1beta can increase UC risk significantly, which might help us understand the molecular mechanism underlying the development of UC.

An increased production of macrophage inflammatory proteins 1 alpha (MIP-1alpha) has been reported to be associated with ulcerative colitis (UC). We investigated whether a polymorphism site in MIP-1alpha was associated with UC in a Chinese population. Additionally, considering the abnormal lipoprotein metabolism in subjects with UC, we also sought to determine whether genetic variation in the apolipoprotein E (ApoE) gene may play a role in the development of UC.We examined the MIP-1alpha -906 (TA)(4)/(TA)(6) polymorphism and the ApoE polymorphism in a cohort of 162 unrelated UC patients and 220 healthy controls by using restriction fragment length polymorphism assay.A significantly increased frequency of the MIP-1alpha -906 (TA)(6)/(TA)(6) genotype (P = 0.0031, odds ratio [OR] = 1.851, 95% confidence interval [CI] 1.228-2.791), as well as of the ApoE epsilon4+ genotype (P0.001, OR = 2.869, 95% CI 1.768-4.657), in patients with UC was proven. Moreover, the carriage of both MIP-1alpha -906 (TA)(6)/(TA)(6) genotype and ApoE epsilon4+ genotype confers greater risk for the development of UC (P0.001, OR = 5.432, 95% CI 2.761-10.689).These findings suggest that variation in the MIP-1alpha and ApoE genes and their interaction may increase susceptibility to UC. Identifying these novel susceptibility genes, as well as their interactions, will help our understanding of the disease mechanisms of UC and may identify targets for developing novel treatment measures.

Previous studies on the associations between dietary antioxidant vitamins and the risk of cervical cancer remain inconsistent and little evidence is available for serum antioxidant vitamins, which provide more accurate measurements of these nutrients. We conducted a case-control study of 458 incident cases with invasive cervical cancer and 742 controls to assess the effects of diet or serum antioxidant vitamins. Higher serum antioxidant vitamins were associated with a lower risk of cervical cancer after adjusting for potential confounders. The odds ratios (ORs) for the highest (vs. lowest) quartile were 0.66 (95% confidence interval [CI] = 0.46–0.93; P = 0.024) for α-carotene, 0.63 (95% CI = 0.45–0.90; P = 0.006) for β-carotene, 0.53 (95% CI = 0.37–0.74; P P

Background: Herpes simplex virus (HSV) type 1 has a 152 kb double-stranded DNA genome that may encode more than 80 gene products, many of which remain uncharacterized. The HSV-1 triplex is a complex of three protein subunits, VP19C and a dimer of VP23 that is essential for capsid assembly. Previous studies have demonstrated that HSV-1 VP19C contains an atypical nuclear localization signal and a functional nuclear export signal (NES), which are both important for the nucleocytoplasmic shuttling of VP19C. However, whether the VP19C NES is required for efficient HSV-1 production is unknown. Findings: In the present study, a VP19C NES-mutated recombinant virus was generated by using bacterial artificial chromosome recombineering technology to investigate the role of VP19C nuclear export in HSV-1 replication. Our results demonstrate that the growth curves, plaque areas, subcellular localization and viral gene expression are indistinguishable between the VP19C NES-mutated virus and the wild-type virus. Conclusions: Our findings reported herein indicate abrogation of the nuclear export of VP19C did not affect HSV-1 replication and viral gene expression.

Preeclampsia (PE) is a common pregnancy-specific disorder associated with significant maternal and fetal morbidity and mortality worldwide. The present study was performed to investigate the role of a CXC chemokine interleukin-8 (IL-8), in the pathogenesis of PE. IL-8 expression levels were assessed in placental and serum samples from 160 pregnant women with PE (N = 68 severe, 92 mild) and 140 healthy donors. Results from enzyme-linked immunosorbent assay showed that the concentration of serum IL-8 in PE patients (180.27 ± 5.81 ng/L) was significantly higher than that in healthy controls (41.57 ± 5.67 ng/L). Patients with severe PE had even higher serum IL-8 levels. Similar messenger RNA and protein expression patterns of IL-8 in placental tissues were confirmed by quantitative real-time polymerase chain reaction and immunohistochemical assay (N = 30 each in the mild PE, severe PE, and control groups). In addition, single nucleotide polymorphisms of IL-8 gene were detected with polymerase chain reaction-restricted fragment length polymorphism/SSP. The frequency of IL-8-251A allele was significantly higher than that in controls (58.4% vs 48.9%, P

Endothelial dysfunction underlies the pathogenesis of preeclampsia, but its mechanism has not yet been completely understood. In this study we have aimed to measure homocysteine (Hcy), asymmetric dimethylarginine (ADMA), and nitric oxide (NO) levels as endothelial dysfunction markers in preeclamptic women. Control–case study with 62 preeclamptic patients and 30 controls without pregnancy complications was conducted. Plasma total Hcy, determined by capillary column gas chromatography/mass spectrometry (GC/MS), was correlated with serum ADMA (determined by liquid chromatography/tandem mass spectrometry using 13C6-l-arginine as the internal standard) and NO (analyzed by GC/MS). There was a highly significant increase in the plasma concentration of homocysteine (P < 0.001) and ADMA (P