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Irko:An Improved Runge-Kutta Optimization Algorithm for Global Optimization Problems

Computers, materials & Continua 2022年第3期70卷 4803-4827页

作者： R.manjula Devi m.Premkumar Pradeep Jangir mohamed Abdelghany Elkotb Rajvikram madurai Elavarasan Kottakkaran Sooppy Nisar Department of Computer Science and Engineering Kongu Engineering CollegePerundurai638060Tamil NaduIndia Department of Electrical&Electronics Engineering Dayananda Sagar College of EngineeringBengaluru560078KarnatakaIndia Rajasthan Rajya Vidyut Prasaran Nigam Sikar332025RajasthanIndia mechanical Engineering Department College of EngineeringKing Khalid UniversityAbha61421Saudi Arabia mechanical Engineering Department Faculty of EngineeringKafrelsheikh UniversityEgypt Clean and Resilient Energy Systems(CARES)Laboratory Texas A&MUniversityGalveston77553TXUSA College of Arts and Sciences Prince Sattam bin Abdulaziz UniversityWadi Aldawaser11991Saudi Arabia

Optimization is a key technique for maximizing or minimizing functions and achieving optimal cost,gains,energy,mass,and so *** order to solve optimization problems,metaheuristic algorithms are *** of these techniques are influenced by collective knowledge and natural *** is no such thing as the best or worst algorithm;instead,there are more effective algorithms for certain ***,in this paper,a new improved variant of a recently proposed metaphorless Runge-Kutta Optimization(rko)algorithm,called Improved Runge-Kutta Optimization(Irko)algorithm,is suggested for solving optimization *** Irko is formulated using the basic rko and local escaping operator to enhance the diversification and intensification capability of the basic rko *** performance of the proposed Irko algorithm is validated on 23 standard benchmark functions and three engineering constrained optimization *** outcomes of Irko are compared with seven state-of-the-art algorithms,including the basic rko *** to other algorithms,the recommended Irko algorithm is superior in discovering the optimal results for all selected optimization *** runtime of Irko is less than 0.5 s for most of the 23 benchmark problems and stands first for most of the selected problems,including real-world optimization problems.

关键词： Engineering design global optimization local escaping operator metaheuristics Runge-Kutta optimization algorithm

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Differential roles of EPS8 in carcinogenesis:Loss of protein expression in a subset of colorectal carcinoma and adenoma

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World Journal of Gastroenterology 2012年第29期18卷 3896-3903页

作者： Wael m Abdel-Rahman Salla Ruosaari Sakari Knuutila Pivi Peltomki Department of medical Laboratory Sciences College of Health SciencesUniversity of SharjahSharjah 27272United Arab Emirates Department of medical Genetics University of HelsinkiFIN-00014 HelsinkiFinland Department of Pathology Haartman InstituteUniversity of HelsinkiFIN-00014 HelsinkiFinland HUSLAB Helsinki University Central HospitalFIN-00014 HelsinkiFinland

AIm:To analyze the epidermal growth factor receptor pathway substrate 8(EPS8) expression status and role in colorectal carcinogenesis given that EPS8 has a conserved actin barbed-end capping function that is required for proper maturation in intestinal ***:We studied 8 colon cancer cell lines and 58 colorectal tumors(19 adenomas and 39 carcinomas).We performed expression microarray analysis of colon cancer cell lines followed by loss of heterozygosity(LOH)analysis and immunohistochemistry for EPS8 expression in colon ***,we performed mutation analysis by direct sequencing and methylation analysis by bisulfite sequencing and methylation-specific polymerase chain reaction ***:Expression microarray analysis of colon cancer cell lines showed overexpression of EPS8 transcript in all lines but *** wide loss of heterozygosity(LOH) analysis of colon tumors,showed considerable LOH at the EPS8 gene ***,EPS8 was constitutively expressed in normal colonic mucosa with a dot-like supranuclear localization with accentuation at the luminal surface supporting its proposed role in epithelial *** colon tumors(4 adenoma,15 carcinoma) out of 51(37%) showed strikingly tumor specific EPS8 protein *** the remaining tumors,5/51(2 adenoma,and 3 carcinoma,10%) showed marked overexpression,while 27/51 tumors(53%) showed retained *** analysis revealed a missense mutation(c.794C>T,p.R265C) in exon 8 in *** EPS8 promoter was also methylated in rko,but there was no significant methylation in other cell lines or carcinoma ***:The loss of EPS8 expression in colorectal adenomas and carcinomas suggests that down regulation of this gene contributes to the development of a subset of colorectal cancers,a finding which could have applications in diagnosis and treatment.

关键词：肿瘤发生大肠癌蛋白子集肠腺基因突变分析甲基化分析表皮生长因子受体

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Role of AXL in invasion and drug resistance of colon and breast cancer cells and its association with p53 alterations

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World Journal of Gastroenterology 2017年第19期23卷 3440-3448页

作者： Wael m Abdel-Rahman Noura A Al-khayyal Vidhya A Nair S R Aravind maha Saber-Ayad Department of medical Laboratory Sciences College of Health Sciences and Sharjah Institute for Medical ResearchUniversity of Sharjah College of medicine and Sharjah Institute for medical Research University of Sharjah Environment and Cancer Research Group Sharjah Institute for Medical ResearchUniversity of Sharjah Department of Basic medical Sciences College of Medicineand Sharjah Institute for medical ResearchUniversity of SharjahSharjah Cairo University

AIm To characterize AXL receptor tyrosine kinase(AXL)expression in relationship to tumor protein P53(TP53gene,p53 protein)and its role in tumor invasion and response to *** We used 14 cell lines,including 3 isogenic pairs carrying mutant/knockout p53,to gain insight into the relationship between AXL and *** included HCT116,HCT116.p53 mutant,rko,and rko.p53-/-lines(all from colon cancers)as well as breast cancer cell lines mCF7 and 1001(mCF7-p53 mutant clone).He La cell line was used as a positive control for epithelial to mesenchymal transition(EmT).AXL expression was determined by Western blotting using rabbit monoclonal antibody clone *** si RNA silencing was performed and followed by collagen invasion *** viability analysis using the sulforhodamine B assay and the invasion assay were performed after exposure to chemotherapeutic agents(doxorubicin for breast cancer cells;5FU or irinotecan for colon cancer cells).RESULTS We showed that the introduction of p53 mutations or knockout increased expression levels of AXL in isogenic cells compared to the matching p53 wild-type parental ***,we found a trend for correlation between the potential EmT candidate AXL,p53 alterations,and EmT markers in colorectal and breast *** expression of AXL in rko cells,a rare colon cancer cell line with inactive Wnt signaling,suggests that the AXL oncogene might provide an alternative genetic pathway for colorectal carcinogenesis in the absence of Wnt signaling activation and TP53 *** silencing in the TP53 mutant isogenic cell lines 1001,HCT116.p53 mutant and rko.P53-/-was>95%efficient and the silenced cells were less invasive compared to the parental TP53 wild-type *** silencing showed a subtle trend to restore colon cancer cell sensitivity to5FU or ***,AXL expressing cells developed more invasive potential after exposure to chemotherapy compared to the AXL-silenced *** AXL is influenced by p

关键词： AXL 乳癌化疗结肠癌侵略

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Preclinical evaluation of azathioprine plus buthionine sulfoximine in the treatment of human hepatocarcinoma and colon carcinoma

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World Journal of Gastroenterology 2011年第34期17卷 3899-3911页

作者： Borja Hernández-Breijo Jorge monserrat Sara Ramírez-Rubio Eva P Cuevas Diana Vara Inés Díaz-Laviada m Dolores Fernández-moreno Irene D Román Javier P Gisbert Luis G Guijarro molecular Hepatic Toxicology Unit Biochemistry and Molecular Biology Department University of Alcalá Networked Biomedical Research Center of Hepatic and Digestive Diseases (CIBEREHD) medicine Department University of Alcalá Neuroendocrinology of Cannabinoid/Vanilloid System Unit Biochemistry and Molecular Biology Department University of Alcalá Gastroenterology Unit Hospital de la Princesa Institute of Health Research Princesa Networked Biomedical Research Center of Hepatic and Digestive Diseases (CIBEREHD)

AIm: To evaluate the efficacy and the safety of azathioprine (AZA) and buthionine sulfoximine (BSO) bylocalized application into HepG2 tumor in ***: Different hepatoma and colon carcinoma cell lines (HepG2, HuH7, Chang liver, LoVo, rko, SW-48, SW-480) were grown in minimal essencial medium supplemented with 10% fetal bovine serum and 1% antibiotic/antimycotic solution and maintained in a humidified 37 ℃ incubator with 5% CO2. These cells were pretreated with BSO for 24 h and then with AZA for different times. We examined the effects of this combination on some proteins and on cellular death. We also studied the eff icacy and the safety of AZA (6 mg/kg per day) and BSO (90 mg/kg per day) in HepG2 tumor growth in vivo using athymic mice. We measured safety by serological markers such as aminotransferases and creatine ***: The in vitro studies revealed a new mechanism of action for the AZA plus BSO combination in the cancer cells compared with other thiopurines (6-mercaptopurine, 6-methylmercaptopurine, 6-thioguanine and 6-methylthioguanine) in combination with BSO. The cytotoxic effect of AZA plus BSO in HepG2 cells resulted from necroptosis induction in a mitochondrial-dependent manner. From kinetic studies we suggest that glutathione (GSH) depletion stimulates c-Jun amino-terminal kinase and Bax translocation in HepG2 cells with subsequent deregulation of mitochondria (cytochrome c release, loss of membrane potential), and proteolysis activation leading to loss of membrane integrity, release of lactate dehydrogenase and DNA degradation. Some of this biochemical and cellular changes could be reversed by N-acetylcysteine (a GSH replenisher). In vivo studies showed that HepG2 tumor growth was inhibited when AZA was combined with ***: Our studies suggest that a combination of AZA plus BSO could be useful for localizedtreatment of hepatocellular carcinoma as in the currently used transarterial chemoembolization method.

关键词：硫唑嘌呤结肠癌肝癌 HepG2细胞评价亚砜肿瘤生长临床

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Identification of anticancer drugs to radiosensitise BRAF-wild-type and mutant colorectal cancer

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Cancer Biology & medicine 2019年第2期16卷 234-246页

作者： Rebecca Carter Azadeh Cheraghchi-Bashi Adam Westhorpe Sheng Yu Yasmin Shanneik Elena Seraia Djamila Ouaret Yasuhiro Inoue Catherine Koch Jenny Wilding Daniel Ebner Anderson J. Ryan Francesca m. Buffa Ricky A. Sharma NIHR University College London Hospitals Biomedical Research Centre/ UCL Cancer Institute University College London London WC1E 6DD UK NIHR Oxford Biomedical Research Centre Department of Oncology University of Oxford Oxford 0X1 2JD UK Computational Biology and Integrative Genomics University of Oxford Oxford 0X1 2JD UK NDm Research Building Nuffield Department of Medicine University of Oxford Oxford 0X1 2JD UK Weatherall Institute of molecular medicine John Radcliffe Hospital University of Oxford Oxford 0X1 2JD UK mie University Graduate School of Medicine Department of Gastrointestinal and Pediatric Surgery Division of Reparative Medicine Institute of Life Sciences Edobashi 2-174 Tsu Japan Departme nt of Biology Massachusetts In stitute of Tech no logy Cambridge Massachusetts 02142 USA Target Discovery Institute National Phenotypic Screening Centre Nuffield Department of Medicine University of OxfordOxford 0X1 2JD UK CRUK & mRC Oxford Institute for Radiation Oncology University of Oxford Oxford 0X1 2JD UK

Objective: Patients with BRAF-mutant colorectal cancer(CRC) have a poor prognosis. molecular status is not currently used to select which drug to use in combination with radiotherapy. Our aim was to identify drugs that radiosensitise CRC cells with known BRAF ***: We screened 298 oncological drugs with and without ionising radiation in colorectal cancer cells isogenic for BRAF. Hits from rank product analysis were validated in a 16-cell line panel of human CRC cell lines, using clonogenic survival assays and xenograft models in ***: most consistently identified hits were drugs targeting cell growth/proliferation or DNA damage repair. The most effective class of drugs that radiosensitised wild-type and mutant cell lines was PARP inhibitors. In clonogenic survival assays, talazoparib produced a radiation enhancement ratio of 1.9 in DLD1(BRAF-wildtype) cells and 1.8 in rko(BRAF V600 E) cells. In DLD1 xenografts, talazoparib significantly increased the inhibitory effect of radiation on tumour growth(P ≤ 0.01).Conclusions: Our method for screening large drug libraries for radiosensitisation has identified PARP inhibitors as promising radiosensitisers of colorectal cancer cells with wild-type and mutant BRAF backgrounds.

关键词： Radiosensitizer colorectal cancer PARP inhibitor radiotherapy

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