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| 1 | The Performance of Maximum Likelihood, Spectral Angle Mapper, Neural Net- work and Decision Tree Classifiers in Hyperspectral Image Analysis显示文摘 | Helmi Z M Affendi Suhaili and Shattri Mansor | 2007 | Journal of Computer Science2007，3，6： | 1 |
| 2 | Comparative study of wear performance of particulate and fiber-reinforced nano-ZnO/ultra-high molecular weight polyethylene hybrid composites using response surface methodology显示文摘 | Boon Peng Chang Hazizan Md Akil Muhammad Ghaddafy Affendy | 2014 | Materials and Design2014，63，： | 1 |
| 3 | The Performance of Maximum Likelihood, Spectral Angle Mapper, Neural Network and Decision Tree Classifier in Hyperspectral Image Analysis 显示文摘 | Helmi Zulhaidi Mohd Shafri Affendi Suhaili Shattri Mansor | 2007 | Journal of Computer Science (S1549-3636)2007，3，6： | 1 |
| 4 | Documentation of EWS gene rearrangements by fluorescence in situ hybridization in frozen sections of Ewing' s sarcoma-peripheral primitive neuroectodermal tumor显示文摘 | Monforte-Munoz H Lopez-Terrada D Affendie H | 1999 | Am J Surg Pathol1999，23，3： | 1 |
| 5 | The Performance of Maximum Likelihood,Spectral Angle Mapper,Neural Network and Decision Tree Classifiers in Hyperspectral Image Analysis显示文摘 | Helmi Z M Affendi Suhaili Shattri Mansor | | 0，，06： | 1 |
| 6 | Gastroesophageal reflux disease in pregnancy显示文摘 | Raja Affendi Raja Ali | 2007 | Best Practice & Research Clinical Gastroenterology2007，，5： | 1 |
| 7 | 软珊瑚Sarcophyton glaucum中新型细胞毒性寡肽的纯化与鉴定(英文)显示文摘目的:纯化和鉴定软珊瑚Sarcophyton glaucum蛋白水解物中的细胞毒性肽。创新点:首次从软珊瑚S. glaucum中发现具有癌细胞毒性的寡肽,开发了一种有潜力的新型抗癌药物。方法:通过碱性蛋白酶、胰凝乳蛋白酶、木瓜蛋白酶和胰蛋白酶产生软珊瑚S. glaucum蛋白质水解物,并通过MTT法评估其对人宫颈癌HeL a细胞的毒性。通过膜超滤、凝胶过滤色谱、固相萃取和反相高效液相色谱等技术进一步提纯肽;采用从头测序法(de novo sequencing)进行肽鉴定;根据所鉴定的序列,进一步确定合成肽的细胞毒性。结论:从软珊瑚S. glaucum的木瓜蛋白酶水解物中鉴定出三种新型肽序列:AGAPGG、AERQ和RDTQ(分子量分别为428.45、502.53和518.53 Da)。此三种寡肽具有对HeLa的细胞毒性,其半最大效应浓度(EC50)值各为8.6、4.9和5.6 mmol/L,为抗癌药物5-氟尿嘧啶的3.3、5.8和5.1倍。当测试对非癌细胞Hek293的毒性时,这三种肽仅显示16%、25%和11%的细胞毒性。因此,AERQ、AGAPGG和RDTQ有很大的潜力成为肽类抗癌药物。 | Yixian QUAH Nor Ismaliza MOHD ISMAIL Jillian Lean Sim OOI Yang Amri AFFENDI Fazilah ABD MANAN Lai-Kuan TEH Fai-Chu WONG Tsun-Thai CHAI | 2019 | Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)2019，20，1： | 0 |
| 8 | Roles of phosphatidylinositol-3-kinases signaling pathway in inflammation-related cancer:Impact of rs10889677 variant and buparlisib in colitis-associated cancer显示文摘BACKGROUND Phosphatidylinositol-3-kinases(PI3K)is a well-known route in inflammationrelated cancer.Recent discovery on PI3K-related genes revealed a potential variant that links ulcerative colitis(UC)and colorectal cancer(CRC)with colitisassociated cancer(CAC).PI3K/AKT pathway has been recommended as a potential additional therapeutic option for CRC due to its substantial role in modifying cellular processes.Buparlisib is a pan-class I PI3K inhibitor previously shown to reduce tumor growth.AIM To investigate the regulation of rs10889677 and the role of buparlisib in the PI3K signaling pathway in CAC pathogenesis.METHODS Genomic DNA from 32 colonic samples,including CAC(n=7),UC(n=10)and CRC(n=15),was sequenced for the rs10889677 mutation.The mutant and wildtype fragments were amplified and cloned in the pmirGLO vector.The luciferase activity of cloned vectors was assessed after transfection into the HT29 cell line.CAC mice were induced by a mixture of a single azoxymethane injection and three cycles of dextran sulphate sodium,then buparlisib was administered after 14 d.The excised colon was subjected to immunohistochemistry for Ki67 and Cleaved-caspase-3 markers and quantitative real-time polymerase chain reaction analysis for Pdk1 and Sgk2.RESULTS Luciferase activity decreased by 2.07-fold in the rs10889677 mutant,confirming the hypothesis that the variant disrupted miRNA binding sites,which led to an increase in IL23R expression and the activation of the PI3K signaling pathway.Furthermore,CAC-induced mice had a significantly higher disease activity index(P<0.05).Buparlisib treatment significantly decreased mean weight loss in CAC-induced mice(P<0.05),reduced the percentage of proliferating cells by 5%,and increased the number of apoptotic cells.The treatment also caused a downward trend of Pdk1 expression and significantly decreased Sgk2 expression.CONCLUSION Our findings suggested that the rs10889677 variant as a critical initiator of the PI3K signaling pathway,and buparlisib had the ability to prevent PI3K-non-AKT activation in the pathophysiology of CAC. | Nurul Nadirah Razali Raja Affendi Raja Ali Khairul Najmi Muhammad Nawawi Azyani Yahaya Norshafila Diana Mohd Rathi Norfilza Mohd Mokhtar | 2023 | World Journal of Gastroenterology2023，29，40： | 0 |
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