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  • 1
    Online Resource
    Online Resource
    Vietnam National University Journal of Science ; 2019
    In:  VNU Journal of Science: Medical and Pharmaceutical Sciences Vol. 35, No. 1 ( 2019-06-21)
    In: VNU Journal of Science: Medical and Pharmaceutical Sciences, Vietnam National University Journal of Science, Vol. 35, No. 1 ( 2019-06-21)
    Abstract: The metabolism of Isoniazid, one of the first-line antituberculosis drugs for TB treatment and prophylaxis, depends on the acetyltransferase 2 acetylation (NAT2) phenotype. Different phenotypes of NAT2 will lead to differences in drug concentration and the risk of uncontrolled side effects, such as hepatitis, peripheral neuropathy, gastrointestinal disorders (nausea, vomiting, and stomach pain). These risks are related to the presence of mutant NAT2 alleles such as NAT2*5 (c.341T 〉 C), *6 (c.590G 〉 A) and *7 (c.857G 〉 A), that reduce the N- acetyltransferase activity. Therefore, the genotyping method for NAT2 polymorphism using RFLP and Sanger sequencing was established. The method was successfully applied to determine the polymorphism of 84 TB patients. This study provides a better tool for analyzing NAT2 gene to assist clinicians in treating isoniazid. Keywords Enzyme NAT2, isoniazid, single nucleotide polymorphism, RFLP, Sanger sequencing. References [1] U.A. Boelsterli, K.K. Lee, Mechanisms of isoniazid-induced idiosyncratic liver injury: emerging role of mitochondrial stress, J. Gastroenterol. Hepatol. 29 (2014) 678–687.[2] A. Zabost, S. Brzezinska, M. Kozinska, M. Blachnio, J. Jagodzinski, Z. Zwolska, E. Augustynowicz-Kopec, Correlation of N-acetyltransferase 2 genotype with isoniazid acetylation in Polish tuberculosis patients, Biomed Res Int. 2013 (2013) 1-5.[3] M. Kinzig-Schippers, D. Tomalik-Scharte, A. Jetter, B. Scheidel, V. Jakob, M. Rodamer, I. Cascorbi, O. Doroshyenko, F. Sorgel, U. Fuhr, Should we use N-acetyltransferase type 2 genotyping to personalize isoniazid doses? Antimicrob Agents Chemother. 49 (2005) 1733-8[4] K. Walker, G. Ginsberg, D. Hattis, D.O. Johns, K.Z. Guyton, B. Sonawane, Genetic polymorphism in N-Acetyltransferase (NAT): Population distribution of NAT1 and NAT2 activity, J Toxicol Environ Health B Crit Rev. 12 (2009) 440-472. [5] G. Ramachandran, S. Swaminathan, Role of pharmacogenomics in the treatment of tuberculosis: a review, Pharmgenomics Pers Med. 5 (2012) 89-98.[6] J. Azuma, M. Ohno, R. Kubota, S. Yokota, T. Nagai, K. Tsuyuguchi, Y. Okuda, T. Takashima, S. Kamimura, Y. Fujio, I. Kawase, Pharmacogenetics-based tuberculosis therapy research group, NAT2 genotype guided regimen reduces isoniazid-induced liver injury and early treatment failure in the 6-month four-drug standard treatment of tuberculosis: a randomized controlled trial for pharmacogenetics-based therapy, Eur J Clin Pharmacol. 69 (2013) 1091-1101.[7] P.S. Adole, P.S. Kharbanda, S. Sharma, N-acetyltransferase 2 (NAT2) gene polymorphism as a predisposing factor for phenytoin intoxication in tuberculous meningitis or tuberculoma patients having seizures - A pilot study, Indian J Med Res. 143 (2016) 581-590.[8] WHO Scientific Group on Pharmacogenetics and World Health Organization, Pharmacogenetics: report of a WHO scientific group,World Health Organization Technical Report Series. (1973)[9] T.D. Da Silva, A.V. Felipe, J.M. De Lima, C.T. Oshima, N.M. Forones, N-Acetyltransferase 2 genetic polymorphisms and risk of colorectal cancer, World J Gastroenterol. 17 (2011) 760-765. [10] E.Y. Lau, J.S. Felton, F.C. Lightstone, Insights into the o-acetylation reaction of hydroxylated heterocyclic amines by human arylamine N-acetyltransferases: a computational study, Chem Res Toxicol. 19 (2006) 182-1190.[11] Ensembl - EBI, http://asia.ensembl.org/Homo_sapiens/Variation/Population?db=core;r=8:18399844-18400844;v=rs1801280;vdb=variation;vf=1243314,2019 (Ensembl release 96 - April 2019).[12] I.B. Kuznetsov, M. McDuffie, R. Moslehi, A web server for inferring the human N-acetyltransferase-2 (NAT2) enzymatic phenotype from NAT2 genotype, Bioinformatics. 25 (2009) 1185-1186. [13] P. Wang, K. Pradhan, X.B. Zhong, X. Ma, Isoniazid metabolism and hepatotoxicity, Acta Pharm Sin B. 6 (2016) 384-392.[14] M. Ohno, I. Yamaguchi, I. Yamamoto, T. Fukuda, S. Yokota, Slow N-acetyltransferase 2 genotype affects the incidence of isoniazid and rifampicin-induced hepatotoxicity, Int J Tuberc Lung Dis. 4 (2000) 256-261. [15] G.M. Lower, T. Nilsson, C.E. Nelson, H. Wolf, T.E. Gamsky, G.T. Bryan, N-acetyltransferase phenotype and risk in urinary bladder cancer: approaches in molecular epidemiology. Preliminary results in Sweden and Denmark, Int J Epidemiol. 36 (2007) 11-18.      
    Type of Medium: Online Resource
    ISSN: 2588-1132 , 2615-9309
    Language: Unknown
    Publisher: Vietnam National University Journal of Science
    Publication Date: 2019
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  • 2
    In: Vietnam Journal of Hydrometeorology, Vietnam Meteorological and Hydrological Administration, Vol. 10, No. 741 ( 2022-9-25), p. 85-97
    Type of Medium: Online Resource
    ISSN: 2525-2208
    URL: Issue
    Language: Unknown
    Publisher: Vietnam Meteorological and Hydrological Administration
    Publication Date: 2022
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  • 3
    In: VNU Journal of Science: Medical and Pharmaceutical Sciences, Vietnam National University Journal of Science, Vol. 35, No. 1 ( 2019-06-21)
    Abstract: Though the ivy (Hedera nepalensis K. Koch.) has long been utilized in traditional medicine, its genome information is very limited. For plants, an effective method of DNA extraction is a very important step which greatly affects subsequent genetic analyses. In this study, four different methods of DNA extraction from dry leaves were used. A comparison of different protocols resulted in the yield of extracted DNA that ranged from 10.5 to 437.4 ng/μl and with a purity ranged from 1.8 to 2.2. Based on the PCR results of GBSSI gene, Gene JET Plant Genomic DNA Purification Mini Kit is the most optimal extraction method for Vietnam ivy’s dry leaves. A preliminary analysis of the phylogenetic tree based on the GBSSI marker showed that ivy growing in a number of northern mountainous provinces of Vietnam belonged to the H. nepalensis K. Koch species. The high - quality total DNA will allow us to amplify different DNA markers, providing valuable genetic information to preserve and develop medicinal resources in Vietnam. Keywords GBSSI, Hedera nepalensis K. Koch, DNA extraction. References [1] J. Ackerfield, J. Wen, A morphometric analysis of Hedera L. (the ivy genus, Araliaceae) and its taxonomic implications, Adansonia Sér. 24 (2002) 187-212.[2] U.S. National Plant Germplasm System, Taxon: Hedera nepalensis K. Koch, https://npgsweb.ars -grin.gov/gringlobal/taxonomydetail.aspx?id= 18567, 2019 (accessed 21 March 2019). [3] L. Jafri, S. Saleem, T.P. Kondrytuk, I.Q. Haq, N. Ullah, J.M. Pezzuto, B. Mirza, Hedera nepalensis K. Koch: A Novel Source of Natural Cancer Chemopreventive and Anticancerous Compounds, Phytotherapy Reserch. 30 (2016) 447-453.[4] S. Saleem, L. Jafri, I. Haq, L.C. Chang, D. Calderwood, B.D. Green, B. Mirza, Plants Fagonia cretica L. and Hedera nepalensis K. Koch contain natural compounds with potent dipeptidyl peptidase-4 (DPP-4) inhibitory activity, Journal of Ethnopharmacology. 156 (2014) 26-32.[5] W.J. Hashmi, H. Ismail, F. Mehmood, B. Mirza, Neuroprotective, antidiabetic and antioxidant effect of Hedera nepalensis and lupeol against STZ+ AlCl3 induced rats model, DARU: Journal of faculty of Pharmacy, Tehran University of Medical Sciences. 26 (2018) 179-190.[6] H. Ismail, A. Rasheed, I.U. Haq, L. Jafri, N. Ullah, E. Dilshad, M. Sajd, B. Mirza, Five indigenous plants of Pakistan with Antinociceptive, anti-inflammatory, antidepressant, and anticoagulant properties in Sprague Dawley rats, Evidence-based Complementary and alternative medicine 2017 (2017) 1-10.[7] A. Mitchell, J. Wen. Phylogenetic utility and evidence for multiple copies of granule-bound starch synthase I (GBSSI) in Araliaceae, Taxon 53 (2004) 29-44.[8] M.A. Saghai-Maroof, K.M. Soliman, R.A. Jorgensen, R.W.L. Allard, Ribosomal DNA spacer-length polymorphisms in barley: Mendelian inheritance, chromosomal location, and population dynamics, Proceeding of the National Academy of Sciences of the USA. 81 (1984) 8014-8018.[9] M. Elias, G.S. Mühlen, D. McKey, A.C. Roa, J. Tohme, Genetic diversity of traditional South American landraces of cassava (Manihot esculenta Crantz): an analysis using microsatellites, Economic Botany. 58 (2004) 242-256.[10] B.D. Lade, A.S. Patil, H.M. Paikrao, Efficient genomic DNA extraction protocol from medicinal rich Passiflora foetida containing high level of polysaccharide and polyphenol, Springerplus. 3 (2014) 1-7.[11] J.H. Cota-Sánchez, K. Remarchuk, K. Ubayasena, Ready-to-use DNA extracted with a CTAB method adapted for herbarium specimens and mucilaginous plant tissue, Plant Molecular Biology Reporter. 24 (2006) 161.[12] J. Zhang, J.M. Stewart, Economical and rapid method for extracting cotton genomic DNA, Journal of Cotton Science. 4 (2000) 193-201.[13] T. Li, H. Pan, Y. Feng, H. Li, Y. Zhao, Bioactivity-guided isolation of anticancer constituents from Hedera nepalensis K. Koch, South African Journal of Botany. 100 (2015) 87-93.[14] L. Jafri, S. Saleem, N. Ullah, B. Mirza, In vitro assessment of antioxidant potential and determination of polyphenolic compounds of Hedera nepalensis K. Koch, Arabian Journal of Chemistry. 10 (2017) S3699-S3706.[15] B. Ahmad, N. Munir, S. Bashir, S. Azam, I. Khan, M. Ayub, Biological screening of Hedera nepalensis, Journal of Medicinal Plants Research. 6 (2012) 5250-5257.[16] K.H.E. Koch, Hortus Dendrologicus, F. Schneider & Co., Berlin, 1985, pp 250.[17] A. Rehder, New species, varieties and combinations from the herbarim and the collections of the Arnold arboretum, Journal of the Arnold Arboretum. 4 (1923) 250.  
    Type of Medium: Online Resource
    ISSN: 2588-1132 , 2615-9309
    Language: Unknown
    Publisher: Vietnam National University Journal of Science
    Publication Date: 2019
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  • 4
    In: Journal of 108 - Clinical Medicine and Phamarcy, 108 Institute of Clinical Medical and Pharmaceutical Sciences, ( 2022-12-01)
    Abstract: Hội chứng huỷ myelin do thẩm thấu (Osmotic Demyelination Syndrome - ODS) được ghi nhận là một biến chứng của việc điều chỉnh quá nhanh tình trạng hạ natri máu. Sinh lý bệnh của ODS được lý giải là do rối loạn thẩm thấu ở tế bào não gây phá huỷ myelin ở các tế bào thần kinh. Bệnh có tỷ lệ tử vong cao và việc điều trị thường được thực hiện chủ yếu ở các trung tâm hồi sức. Chúng tôi báo cáo trường hợp lâm sàng hội chứng huỷ myelin do thẩm thấu, hậu quả của việc điều chỉnh quá mức tình trạng hạ natri máu. Các triệu chứng lâm sàng về thần kinh cũng như tổn thương trên chẩn đoán hình ảnh của bệnh nhân sau điều trị hồi phục gần hoàn toàn. Kết luận: Hội chứng huỷ myelin do thẩm thấu là biến chứng của việc điều trị quá nhanh tình trạng hạ natri máu. Việc điều trị ODS đều chỉ dừng ở các báo cáo lâm sàng tuy nhiên với sự kết hợp của immunoglobulin, steroid và lọc huyết tương cho thấy hiệu quả không chỉ trong giai đoạn cấp mà còn giúp cải thiện kết cục thần kinh sau này.
    Type of Medium: Online Resource
    ISSN: 1859-2872
    URL: Issue
    Language: Unknown
    Publisher: 108 Institute of Clinical Medical and Pharmaceutical Sciences
    Publication Date: 2022
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  • 5
    Online Resource
    Online Resource
    Vietnam National University Journal of Science ; 2020
    In:  VNU Journal of Science: Medical and Pharmaceutical Sciences Vol. 36, No. 3 ( 2020-09-25)
    In: VNU Journal of Science: Medical and Pharmaceutical Sciences, Vietnam National University Journal of Science, Vol. 36, No. 3 ( 2020-09-25)
    Abstract: This study develops procedures for cloning ITS and matK genes on six specimens in order to exploit and conserve the genetic resources of H. nepalensis and evaluate its genetic diversity based on molecular markers. The study methods include DNA extraction from dried leaf samples, amplification of ITS and matK regions using PCR, sequencing and comparing with the sequences on Genbank. The study results include a successfully-established process of cloning ITS and matK genes; successful amplification and sequencing of the ITS and matK regions. The results also show that four samples (N1-N4) were 100% homologous to H. nepalensis and H1and H2 samples were 100% homologous to H. helix. The results provide data and tools for further studies of exploitation and development of the H. nepalensis K. Koch genetic resources in Vietnam. Keywords ITS, matK, Hedera nepalensis K. Koch, PCR References [1] V.V. Chi. Dictionary of Vietnamese Medicinal Plants, Publ. House Medicine, Ho Chi Minh City, 2012 (in Vietnamese).[2] D.H. Bich, D.Q. Cuong, B.X. Chuong, N. Thuong, D. T. Dam. The medicinal plants and animals in Vietnam, Hanoi Sci. Technol. Publ. House Hanoi, 2006 (in Vietnamese).[3] A. Sadat, M. Alam, A. Rauf, W. Ullah, Biological screening of ethyl acetate extract of Hedera nepalensis stem, Afr J Pharm Pharmacol, 6 (2012) 2934-2937. https://doi.org/10.5897/AJPP12.828.[4] T. Li, H. Pan, Y. Feng, H. Li, Y. Zhao, Bioactivity-guided isolation of anticancer constituents from Hedera nepalensis K. Koch, S Afr J Bot, 100 (2015) 87-93. https://doi.org/10.1016/j.sajb.2015.05.011.[5] L. Jafri, S. Saleem, N. Ullah, B. Mirza, In vitro assessment of antioxidant potential and determination of polyphenolic compounds of Hedera nepalensis K. Koch, Arab J Chem, 10 (2017) 3699-3706. https://doi.org/10.1016/j.arabjc.2014.05.002. [6] S. Saleem, L. Jafri, I. ul Haq, L.C. Chang, D. Calderwood, B.D. Green, B. Mirza, Plants Fagonia cretica L. and Hedera nepalensis K. Koch contain natural compounds with potent dipeptidyl peptidase-4 (DPP-4) inhibitory activity, J Ethnopharmacol, 156 (2014) 26-32. https://doi.org/10.1016/j.jep.2014.08.017.[7] W.J. Hashmi, H. Ismail, F. Mehmood, B. Mirza, Neuroprotective, antidiabetic and antioxidant effect of Hedera nepalensis and lupeol against STZ+ AlCl 3 induced rats model, DARU, 26 (2018) 179-190. https://doi.org/10.1007/s40199-018-0223-3.[8] H. Ismail, A. Rasheed, I.-u. Haq, L. Jafri, N. Ullah, E. Dilshad, M. Sajid, B. Mirza, Five indigenous plants of Pakistan with Antinociceptive, anti-inflammatory, antidepressant, and anticoagulant properties in Sprague Dawley rats, Evid Based Complement Alternat Med, 2017 (2017). https://doi.org/10.1155/2017/7849501[9] N.D. Thanh. DNA marker techniques in study and selection of plant. Journal of Biology. 36 (2014) 265-294 (in Vietnamese). https://doi.org/10.15625/0866-7160/v36n3.5974.[10] P.Z. Goldstein, R. DeSalle, Review and interpretation of trends in DNA barcoding, Front Ecol Evol, 7 (2019) 302. https://doi.org/10.3389/fevo.2019.00302.[11] S. Abugalieva, L. Volkova, Y. Genievskaya, A. Ivaschenko, Y. Kotukhov, G. Sakauova, Y. Turuspekov, Taxonomic assessment of Allium species from Kazakhstan based on ITS and matK markers, BMC plant biol, 17 (2017) 258. https://doi.org/10.1186/s12870-017-1194-0.[12] R.M. Bhagwat, B.B. Dholakia, N.Y. Kadoo, M. Balasundaran, V.S. Gupta, Two new potential barcodes to discriminate Dalbergia species, PloS one, 10 (2015) e0142965. https://doi.org/10.1371/journal.pone.0142965[13] D. Grivet, R. Pe tit, Phylogeography of the common ivy (Hedera sp.) in Europe: genetic differentiation through space and time, Mol Ecol, 11 (2002) 1351-1362. https://doi.org/10.1046/j.1365294x.2002.01522.x.[14] R. Li, J. Wen, Phylogeny and biogeography of Dendropanax (Araliaceae), an amphi-Pacific disjunct genus between tropical/subtropical Asia and the Neotropics, Syst Bot, 38 (2013) 536-551. https://doi.org/10.1600/036364413X666606.[15] Y. Sun, D. Skinner, G. Liang, S. Hulbert, Phylogenetic analysis of Sorghum and related taxa using internal transcribed spacers of nuclear ribosomal DNA, ‎Theor Appl Genet, 89 (1994) 26-32. https://doi.org/10.1007/BF00226978[16] P. Cuénoud, V. Savolainen, L.W. Chatrou, M. Powell, R.J. Grayer, M.W. Chase, Molecular phylogenetics of Caryophyllales based on nuclear 18S rDNA and plastid rbcL, atpB, and matK DNA sequences, Am J Bot, 89 (2002) 132-144. https://doi.org/10.3732/ajb.89.1.132.[17] D. Bošeľová, J. Žiarovská, L. Hlavačková, K. Ražná, M. Bežo, Comparative analysis of different methods of Hedera helix DNA extraction and molecular evidence of the functionality in PCR Acta fytotechn zootechn, 19 (2016) 144-149. https://doi.org/10.15414/afz.2016.19.04.144-149.[18] D.D. Long, Comparative analysis of different DNA extraction methods and preliminary analysis of genetic diversity of Hedera nepalensis K. Koch. in Vietnam based on GBSSI marker, VNU Journal of Science: Medical and Pharmaceutical Sciences, 35 (2019) 88-95 (in Vietnamese). https://doi.org/10.25073/2588-1132/vnumps.4165 [19] J.H. Cota-Sánchez, K. Remarchuk, K. Ubayasena, Ready-to-use DNA extracted with a CTAB method adapted for herbarium specimens and mucilaginous plant tissue, Plant Mol Biol Rep, 24 (2006)161. https://doi.org/10.1007/BF02914055.[20] S. Xu, D. Li, J. Li, X. Xiang, W. Jin, W. Huang, X. Jin, L. Huang, Evaluation of the DNA barcodes in Dendrobium (Orchidaceae) from mainland Asia, PloS one, 10 (2015) e0115168. https://doi.org/10.1371/journal.pone.0115168.[21] P. Vargas, H.A. McAllister, C. Morton, S.L. Jury, M.J. Wilkinson, Polyploid speciation in Hedera (Araliaceae): Phylogenetic and biogeographic insights based on chromosome counts and ITS sequences, Pl Syst Evol, 219 (1999) 165-179. https://doi.org/10.1007/BF00985577[22] X. Lei, Y.W. Wang, S.Y. Guan, L.J. Xie, L. Xin, C.Y. Sun, Prospects and problems for identification of poisonous plants in China using DNA barcodes, Biomed Environ Sci, 27 (2014) 794-806. https://doi.org/10.3967/bes2014.115.[23] H. Sun, W. McLewin, M.F. Fay, Molecular phylogeny of Helleborus (Ranunculaceae), with an emphasis on the East Asian‐Mediterranean disjunction, Taxon, 50 (2001) 1001-1018. https://doi.org/10.2307/1224717.    
    Type of Medium: Online Resource
    ISSN: 2588-1132 , 2615-9309
    Language: Unknown
    Publisher: Vietnam National University Journal of Science
    Publication Date: 2020
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  • 6
    Online Resource
    Online Resource
    Vietnam National University Journal of Science ; 2019
    In:  VNU Journal of Science: Medical and Pharmaceutical Sciences Vol. 35, No. 1 ( 2019-06-21)
    In: VNU Journal of Science: Medical and Pharmaceutical Sciences, Vietnam National University Journal of Science, Vol. 35, No. 1 ( 2019-06-21)
    Abstract: Drug resistant TB is currently a global challenge causing high risk of death and expanding the disease. This study explores the prevalence of drug resistance in newly diagnosed and recurrent TB patients and identifies the association between NAT2 gene polymorphism distribution and acetylator phenotype of NAT2 gene and the two study groups. The study results show that the newly diagnosed TB had l lower male ratio and younger age in comparison to the recurrent TB. Newly diagnosed group was more sensitive to first line TB drugs. However, both groups had significant resistance ratio in relation to INH and SM. Finally, the allele and acetylator phenotype frequency of NAT2 showed the significant association with TB status. The study concludes that the newly diagnosed and recurrent TB patients expressed differently in their profiles concerning patient’s background, drug resistance and NAT2 allele distribution. Keywords Drug resistance, INH, NAT2 polymorphism, newly diagnosed TB, recurrent TB1. References [1] WHO, Global Tuberculossi report, https://www.who.int/tb/publications/global_report/en/, 2018 (accessed 16 April 2019).[2] Hoàng Thị Phượng, Nghiên cứu đặc điểm lâm sàng, cận lâm sàng, tính kháng thuốc của vi khuẩn ở bệnh nhân lao phổi mới kết hợp bệnh đái tháo đường, Luận văn tiến sĩ Y học, trường Đại học Y Hà Nội, 2009.[3] S. Guaoua, I. Ratbi, F.Z. Laarabi, S.A. Elalaoui, IC. Jaouad, A. Barkat, A. Sefiani, Distribution of allelic and genotypic frequencies of NAT2 and CYP2E1 variants in Moroccan population, BMC Genet. 15 (2014) 156.[4] A. Toure, M. Cabral, A. Niang, C. Diop, A. Garat, L. Humbert, M. Fall, A. Diouf, F. Broly, M. Lhermitte, D. Allorge, Prevention of isoniazid toxicity by NAT2 genotyping in Senegalese tuberculosis patients, Toxicol Rep. 3 (2016) 826-831.[5] M. Majumder, N. Sikdar, S. Ghosh, B. Roy, Polymorphisms at XPD and XRCC1 DNA repair loci and increased risk of oral leukoplakia and cancer among NAT2 slow acetylators, Int J Cancer. 120(10) (2007) 2148-2156.[6] S. Morita, M. Yano, T. Tsujinaka, Y. Akiyama, M. Taniguchi, K. Kaneko, H. Miki, T. Fujii, K. Yoshino, H. Kusuoka, M. Monden, Genetic polymorphisms of drug-metabolizing enzymes and susceptibility to head-and-neck squamous-cell carcinoma, Int J Cancer. 80(5) (1999) 685-688.[7] Hoàng Hà, Nghiên cứu một số đặc điểm lâm sàng, cận lâm sàng, sinh học của vi khuẩn ở bệnh nhân lao phổi điều trị lại, Luận án tiến sỹ Y học, Trường Đại học Y Hà Nội, 2009.[8] S. Wattanapokayakit, T. Mushiroda, H. Yanai, N. Wichukchinda, C. Chuchottawon, S. Nedsuwan, A. Rojanawiwat, S. Denjanta, T. Kantima, J. Wongyai, W. Suwankesawong, W. Rungapiromnan, R. Kidkeukarun, W. Bamrungram, A. Chaiwong, S. Suvichapanich, S. Mahasirimongkol, K. Tokunaga, NAT2 slow acetylator associated with anti-tuberculosis drug-induced liver injury in Thai patients, Int J Tuberc Lung Dis. 20(10) (2016) 1364-1369.[9] Đinh Ngọc Sỹ, Chiến lược quản lý bệnh lao đa kháng thuốc tại Việt Nam, Tạp chí khoa học Hội Phổi Pháp - Việt. 2(3) (2011) 40-42.[10] Nguyễn Thu Hà, Trần Văn Sáng, Đinh Ngọc Sỹ, Lâm sàng, cận lâm sàng và tính kháng thuốc của vi khuẩn lao ở bệnh nhân lao phổi tái phát, JFran Viet Pneu. 2(3) (2011) 63-67.[11] D. Tu, L. Zhang, J. Su, Resistance and efficacy of treatment in relapse pulmonary tuberculosis, Zhonghua Jie He He Hu Xi Za Zhi. 23 (11) (2000) 666-668    
    Type of Medium: Online Resource
    ISSN: 2588-1132 , 2615-9309
    Language: Unknown
    Publisher: Vietnam National University Journal of Science
    Publication Date: 2019
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  • 7
    Online Resource
    Online Resource
    Springer Science and Business Media LLC ; 2015
    In:  KSCE Journal of Civil Engineering Vol. 19, No. 6 ( 2015-9), p. 1566-1572
    In: KSCE Journal of Civil Engineering, Springer Science and Business Media LLC, Vol. 19, No. 6 ( 2015-9), p. 1566-1572
    Type of Medium: Online Resource
    ISSN: 1226-7988 , 1976-3808
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2015
    detail.hit.zdb_id: 2446036-9
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  • 8
    In: Tạp chí Y học Việt Nam, Vietnam Medical Journal, Vietnam Medical Association, Vol. 500, No. 1 ( 2021-06-08)
    Abstract: Đặt vấn đề: Bệnh cơ tim phì đại (BCTPĐ) là bệnh di truyền phổ biến, do gen trội trên nhiễm sắc thể thường quy định. Đột biến trên các gen mã hóa protein đốt cơ (sacromere) của sợi cơ tim được cho là nguyên nhân di truyền chính gây ra BCTPĐ. Trong đó, đa hình rs36211723 thuộc gen mã hóa protein C liên kết myosin (MYBPC3) chiếm tỉ lệ lớn trong các đa hình gây bệnh cơ tim phì đại ở người Việt Nam. Vì vậy, việc tiến hành xây dựng quy trình phân tích đa hình di truyền rs36211723 ở người mắc BCTPĐ là thực sự cần thiết. Phương pháp: Tách chiết DNA tổng số từ mẫu máu tĩnh mạch, khuếch đại gen bằng PCR, xác định kiểu gen bằng giải trình tự Sanger. Kết quả và kết luận: Quy trình phân tích đa hình rs36211723 đã được hoàn thiện. Nghiên cứu được áp dụng thành công để phân tích kiểu gen của một gia đình bệnh nhân mắc BCTPĐ. Ngoài bệnh nhân, bố của bệnh nhân có mang đa hình này nhưng biểu hiện bệnh lý không rõ ràng, được bác sĩ khuyến cáo nên theo dõi tiến triển bệnh lý chặt chẽ để hạn chế biến chứng nặng xảy ra.
    Type of Medium: Online Resource
    ISSN: 1859-1868
    Language: Unknown
    Publisher: Vietnam Medical Journal, Vietnam Medical Association
    Publication Date: 2021
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  • 9
    Online Resource
    Online Resource
    Vietnam National University Journal of Science ; 2021
    In:  VNU Journal of Science: Medical and Pharmaceutical Sciences Vol. 37, No. 4 ( 2021-12-05)
    In: VNU Journal of Science: Medical and Pharmaceutical Sciences, Vietnam National University Journal of Science, Vol. 37, No. 4 ( 2021-12-05)
    Abstract: To achieve high therapeutic efficacy in the patient, information on pharmacokinetics, pharmacodynamics, and pharmacogenetics is required. With the development of science and technology, especially genetic sequencing technology, more and more research on pharmacogenomics has been conducted. The relationship between the genome and the response of a person to drugs is being explored to support personalized medicine, which shows efficacy in clinical treatment. In particular, the IL28B gene polymorphisms have been studied and shown to have impacts on drug responses in the treatment of many diseases, such as chronic hepatitis C, chronic hepatitis B, and myeloproliferative neoplasms. However, pharmacogenetic studies of the IL28B gene have not given exact recommendations for dose adjustment in treatment; they only show the impact tendency that individuals with an unfavorable genotype (usually the genotype of the mutant allele) show poor response to treatment compared to those with a favorable genotype. The frequency of mutant alleles varies among different ethnic groups and between different viral genotypes. Identifying and predicting the possibility of successful treatment helps both clinicians and patients make better choices of treatment decisions to optimize treatment possibilities, and reduce side effects and treatment costs. Keywords IL28B polymorphism, drug response, hepatitis C, hepatitis B, myeloproliferative disorders. References [1] V. M. Lauschke, M. I. Sundberg, The Importance of Patient - Specific Factors for Hepatic Drug Response and Toxicity, International Journal of Molecular Sciences, Vol. 17, No. 10, 2016, pp. 1714, https://doi.org/10.3390/ijms17101714.[2] E. Vesell et al., Genetic and Environmental Factors Affecting Drug Disposition in man, Clinical Pharmacology & Therapeutics, Vol. 22, No. 5, 1977, pp. 659-679, https://doi.org/10.1002/cpt1977225part2659.[3] M. J Sorich, R. A McKinnon, Personalized Medicine: Potential, Barriers and Contemporary Issues, Current Drug Metabolism, Vol. 13, No. 7, 2012, pp. 1000-1006, https://doi.org/10.2174/138920012802138615.[4] C. M. Lange, S. Zeuzem, IL28B Single Nucleotide Polymorphisms in the Treatment of Hepatitis C, Journal of Hepatology, Vol. 55, No. 3, 2011, pp. 692-701, https://doi.org/10.1016/j.jhep.2011.03.006.[5] Y. Luo, C. Jin, Z. Ling, X. Mou, Q. Zhang, C. Xiang, Association Study of IL28B: Rs12979860 and Rs8099917 Polymorphisms With SVR in Patients Infected with Chronic HCV Genotype 1 to PEG-INF/RBV Therapy using Systematic Meta-Analysis, Gene, Vol. 513, No. 2, 2013, pp. 292-296, https://doi.org/10.1016/j.gene.2012.10.030.[6] A. Muir et al., Clinical Pharmacogenetics Implementation Consortium (CPIC) Guidelines for IFNL3 (IL28B) Genotype and PEG Interferon‐Α-Based Regimens, Clinical Pharmacology Therapeutics, Vol. 95, No. 2, 2014, pp. 141-146, https://doi.org/10.1038/clpt.2013.203.[7] The Pharmacogenomics Knowledgebase (PharmGKB), Drug Label Annotations, https://www.pharmgkb.org/gene/PA134952671/labelAnnotation/, 2020 (accessed on: April 10th, 2020).[8] A. Jazwinski, A. Muir, IL28B: Implications for Clinical Practice, Current Hepatitis Reports, Vol. 11, No. 1, 2012, pp. 15-22, https://doi.org/10.1007/s11901-011-0118-y.[9] Ensembl, Variant Table https://asia.ensembl.org/Homo_sapiens/Gene/Variation_Gene/Table?db=core;g=ENSG00000197110;r=19:39243553-39245129/, 2020 (accessed on: April 20th, 2020).[10] Ensembl, Explore This Variant, https://asia.ensembl.org/index.html/,02020 2020 (accessed on: April 20th, 2020).[11] Ministry of Health, Technical Guidelines on HCV Diagnosis and Treatment, Ministry of Health, Hanoi, 2016 (in Vietnamese).[12] A. J. V. D. Meer et al., Association between Sustained Virological Response and All-Cause Mortality Among Patients with Chronic Hepatitis C and Advanced Hepatic Fibrosis, Jama, Vol. 308, No. 24, 2012, pp. 2584-2593, https://doi.org/10.1001/jama.2012.144878.[13] J. J. Feld, J. H. Hoofnagle, Mechanism of Action of Interferon and Ribavirin in Treatment of Hepatitis C, Nature Genetics, Vol. 436, No. 7053, 2005, pp. 967-972, https://doi.org/10.1038/nature04082.[14] D. Ge et al., Genetic Variation in IL28B Predicts Hepatitis C Treatment-Induced Viral Clearance, Nature Genetics, Vol. 461, No. 7262, 2009, pp. 399-401, https://doi.org/10.1038/nature08309.[15] J. Fischer et al., Combined Effects of Different Interleukin‐28B Gene Variants on the Outcome of Dual Combination Therapy in Chronic Hepatitis C Virus Type 1 Infection, Hepatology, Vol. 55, No. 6, 2012, pp. 1700-1710, https://doi.org/10.1002/hep.25582.[16] E. Cariani et al., Interleukin 28B Polymorphisms As Predictors of Sustained Virological Response in Chronic Hepatitis C: Systematic Review and Meta-Analysis, The Pharmacogenomics Journal, Vol. 16, No. 1, 2016, pp. 18-29, https://doi.org/10.1038/tpj.2015.28.[17] Z. Jia, Y. Ding, S. Tian, J. Niu, J. Jiang, Test of IL28B Polymorphisms in Chronic Hepatitis C Patients Treated with Pegifn and Ribavirin Depends on HCV Genotypes: Results from A Meta-Analysis, Plos One, Vol. 7, No. 9, 2012, pp. e45698, https://doi.org/10.1371/journal.pone.0045698.[18] A. Moghaddam et al., IL28B Genetic Variation and Treatment Response in Patients with Hepatitis C Virus Genotype 3 Infection, Hepatology, Vol. 53, No. 3, 2011, pp. 746-754, https://doi.org/10.1002/hep.24154.[19] E. Mohammed et al., IFNL3 Polymorphisms Predict Response to Therapy in Chronic Hepatitis C Genotype 2/3 Infection, Journal of Hepatology, Vol. 61, No.2, 2014, pp. 235-241, https://doi.org/10.1016/j.jhep.2014.03.039.[20] T. M. Scherzer et al., Early Virologic Response and IL28B Polymorphisms in Patients with Chronic Hepatitis C Genotype 3 Treated with Peginterferon Alfa-2a and Ribavirin, Journal of Hepatology, Vol. 54, No. 5, 2011, pp. 866-871, https://doi.org/10.1016/j.jhep.2010.08.024.[21] J. Stenkvist, A. Sönnerborg, O. Weiland, HCV RNA Decline in Chronic HCV Genotype 2 and 3 During Standard of Care Treatment According to IL28B Polymorphism, Journal of Viral Hepatitis, Vol. 20, No. 3, 2013, pp. 193-199, https://doi.org/10.1111/j.1365-2893.2012.01645.x.[22] T. Asselah et al., IL28B Polymorphism is Associated with Treatment Response in Patients with Genotype 4 Chronic Hepatitis C, Journal of Hepatology, Vol. 56, No. 3, 2012, pp. 527-532, https://doi.org/10.1016/j.jhep.2011.09.008.[23] S. D. Nicola et al., Interleukin 28B Polymorphism Predicts Pegylated Interferon Plus Ribavirin Treatment Outcome in Chronic Hepatitis C Genotype 4, Hepatology, Vol. 55, No. 2, 2012, pp. 336-342, https://doi.org/10.1002/hep.24683.[24] M. Derbala et al., Interleukin-28 and Hepatitis C Virus Genotype-4: Treatment-Induced Clearance and Liver Fibrosis, World Journal of Gastroenterology, Vol. 18, No. 47, 2012, pp. 7003-7008, https://doi.org/10.3748/wjg.v18.i47.7003.[25] N. Antaki et al., IL28B Polymorphisms do not Predict Response to Therapy in Chronic Hepatitis C with HCV Genotype 5, Gut, Vol. 61, No. 11, 2012, pp. 1640-1641, http://dx.doi.org/10.1136/gutjnl-2012-302019.[26] S. Akkarathamrongsin et al., Early Viral Kinetics During Hepatitis C Virus Genotype 6 Treatment According to IL28B Polymorphisms, World Journal of Gastroenterology, Vol. 20, No. 30, 2014, pp. 10599-10605, https://doi.org/10.3748/wjg.v20.i30.10599.[27] C. Bucci et al., Favourable IL28B Polymorphisms Are Associated with A Marked Increase in Baseline Viral Load In Hepatitis C Virus Subtype 3a Infection and Do Not Predict A Sustained Virological Response After 24 Weeks of Therapy, Journal of General Virology, Vol. 94, No. 6, 2013, pp. 1259-1265, https://doi.org/10.1099/vir.0.051052-0.[28] M. L. Yu et al., Role of Interleukin‐28B Polymorphisms in the Treatment of Hepatitis C Virus Genotype 2 Infection in Asian Patients, Hepatology, Vol. 53, No. 1, 2011, pp. 7-13, https://doi.org/10.1002/hep.23976.[29] O. G. Shaker, N. A. Sadik, Polymorphisms in Interleukin‐10 and Interleukin‐28 B Genes in E Gyptian Patients with Chronic Hepatitis C Virus Genotype 4 and Their Effect on the Response to Pegylated Interferon/Ribavirin‐Therapy, Journal of Gastroenterology Hepatology, Vol. 27, No. 12, 2012, pp. 1842-1849, https://doi.org/10.1111/j.14401746.2012.07273.x.[30] W. K. Seto et al., Role of IL 28B and Inosine Triphosphatase Polymorphisms in the Treatment of Chronic Hepatitis C Virus Genotype 6 Infection, Journal of Viral Hepatitis, Vol. 20, No. 7, 2013, pp. 470-477, https://doi.org/10.1111/jvh.12047.[31] H. Zheng, M. Li, B. Chi, X. X. Wu, J. Wang, D. W. Liu, IL28B Rs12980275 Variant As A Predictor of Sustained Virologic Response to Pegylated-Interferon and Ribavirin in Chronic Hepatitis C Patients: A Systematic Review and Meta-Analysis, Clinics Research in Hepatology Gastroenterology, Vol. 39, No. 5, 2015, pp. 576-583, https://doi.org/10.1016/j.clinre.2015.01.009.[32] J. Chen et al., IL28B Genetic Variations Are Associated with High Sustained Virological Response (SVR) of Interferon-Α Plus Ribavirin Therapy in Taiwanese Chronic HCV Infection, Genes Immunity, Vol. 12, No. 4, 2011, pp. 300-309, https://doi.org/10.1038/gene.2011.1.[33] Y. Tanaka et al., Genome-Wide Association of IL28B with Response to Pegylated Interferon-Α and Ribavirin Therapy for Chronic Hepatitis C, Nature Genetics, Vol. 41, No. 10, 2009, pp. 1105-1109, https://doi.org/10.1038/ng.449.[34] [34] M. P. Vincent Soriano et al., Care Of Patients Coinfected with HIV and Hepatitis C Virus: 2007 Updated Recommendations from the HCV-HIV International Panel, Aids, Vol. 21, No. 9, 2007, pp. 1073-1089, https://doi.org/10.1097/QAD.0b013e3281084e4d.[35] C. S. Graham et al, Influence of Human Immunodeficiency Virus Infection on the Course of Hepatitis C Virus Infection: A Meta-Analysis, Clinical Infectious Diseases, Vol. 33, No. 4, 2001, pp. 562-569, https://doi.org/10.1086/321909.[36] M. D. Castellarnau et al., Deciphering the Interleukin 28B Variants That Better Predict Response to Pegylated Interferon-Α And Ribavirin Therapy in HCV/HIV-1 Coinfected Patients, Plos One, Vol. 7, No. 2, 2012, pp. e31016, https://doi.org/10.1371/journal.pone.0031016.[37] I. M. Jacobson et al., Telaprevir for Previously Untreated Chronic Hepatitis C Virus Infection, The New England Journal of Medicine, Vol. 364, No. 25, 2011, pp. 2405-2416, https://doi.org/10.1056/NEJMoa1012912.[38] V. Vadwai, B. R. Das, IL28B Genotyping: A Step Towards HCV-Personalized Therapy, International Journal of Gastroenterology Research and Practice, Vol. 2014, No. 2014, pp. 16, https://doi.org/10.5171/2014.212341.[39] F. About et al., Impact of IL28B, APOH and ITPA Polymorphisms on Efficacy and Safety pf TVR-Or BOC-Based Triple Therapy in Treatment-Experienced HCV-1 Patients with Compensated Cirrhosis from the ANRS CO20-CUPIC Study, PloS One, Vol. 10, No. 12, 2015, pp. e0145105, https://doi.org/10.1371/journal.pone.0145105.[40] G. Calisti et al., IL28B Genotype Predicts Response to Chronic Hepatitis C Triple Therapy with Telaprevir or Boceprevir in Treatment Naïve and Treatment-Experienced Patients Other Than Prior Partial-and Null-Responders, Springer Plus, Vol. 4, No. 1, 2015, pp. 1-9, https://doi.org/10.1186/s40064-015-1137-x.[41] S. Susser et al., Predictive Value of Interferon-Lambda Gene Polymorphisms for Treatment Response in Chronic Hepatitis C, Plos One, Vol. 9, No. 11, 2014, pp. e112592, https://doi.org/10.1371/journal.pone.0112592.[42] A. Tsubota et al., Impact of IL28B Polymorphisms on 24‐Week Telaprevir‐Based Combination Therapy for A Sian Chronic Hepatitis C Patients with Hepatitis C Virus Genotype 1b, Journal of Gastroenterology Hepatology, Vol. 29, No. 1, 2014, pp. 144-150, https://doi.org/10.1111/jgh.12402.[43] M. Manns et al., Simeprevir with Pegylated Interferon Alfa 2a or 2b Plus Ribavirin in Treatment-Naive Patients with Chronic Hepatitis C Virus Genotype 1 Infection (QUEST-2): A Randomised, Double-Blind, Placebo-Controlled Phase 3 Trial, The Lancet, Vol. 384, No. 9941, 2014, pp. 414-426, https://doi.org/10.1016/S0140-6736(14)60538-9.[44] M. Nakayama, H. Kobayashi, K. Fukushima, M. Ishido, Y. Komada, K. Yoshizawa, Predictive Factors for 24 Weeks Sustained Virologic Response (SVR24) and Viral Relapse in Patients Treated with Simeprevir Plus Peginterferon and Ribavirin, Hepatology International, Vol. 10, No. 1, 2016, pp. 158-168, https://doi.org 10.1007/s12072-015-9654-9.[45] F. Poordad et al., Factors that Predict Response of Patients with Hepatitis C Virus Infection to Boceprevir, Gastroenterology, Vol. 143, No. 3, 2012, pp. 608-618, https://doi.org/10.1053/j.gastro.2012.05.011.[46] C. Hézode et al., Daclatasvir Plus Peginterferon Alfa and Ribavirin for Treatment-Naive Chronic Hepatitis C Genotype 1 or 4 Infection: A Randomised Study, Gut, Vol. 64, No. 6, 2015, pp. 948-956, http://dx.doi.org/10.1136/gutjnl-2014-307498.[47] A Thompson et al., GS-5885 + GS-9451 + Peginterferon and Ribavrin (Pr) for Six or 12 Weeks Achieves A High SVR12 in Treatment Naïve Genotype 1 IL28B CC Patients, Journal of Hepatology, Vol. 58, No. Suppl 1, 2013, pp. S29, https://doi.org/10.1016/S0168-8278(13)60066-5.[48] S. Zeuzem et al., Pegylated Interferon-Lambda (Pegifn-Λ) Shows Superior Viral Response with Improved Safety and Tolerability Versus Pegifn-Α-2a In HCV Patients (G1/2/3/4): EMERGE Phase Iib Through Week 12, Journalof Hepatology, Vol. 54, No. Suppl 1, 2011, pp. S538, https://doi.org/10.1016/S0168-8278(11)61362-7.[49] S. Zeuzem et al., Faldaprevir and Deleobuvir for HCV Genotype 1 Infection, The New England Journal of Medicine, Vol. 369, No. 7, 2013, pp. 630-639, https://doi.org/10.1056/NEJMoa1213557.[50] T. R. O'Brien, S. Kottilil, J. J. Feld, T. R. Morgan, R. M. Pfeiffer, Race or Genetic Makeup for Hepatitis C Virus Treatment Decisions?, Hepatology, Vol. 65, No. 6, 2017, pp. 2124-2125, https://doi.org/10.1002/hep.29057.[51] R. M. Pfeiffer et al, Subgroup Differences in Response to 8 Weeks of Ledipasvir/Sofosbuvir for Chronic Hepatitis C, Open Forum Infectious Diseases, Vol. 1, No. 3, 2014, pp.1-4 ofu110, https://doi.org/10.1093/ofid/ofu110.[52] N. Akuta et al., Retreatment Efficacy and Predictors of Ledipasvir Plus Sofosbuvir to HCV Genotype 1 in Japan, Journal of Medical Virology, Vol. 89, No. 2, 2017, pp. 284-290, https://doi.org/10.1002/jmv.24617.[53] T. R. O’Brien, S. Kottilil, R. M. Pfeiffer, IFNL4 Genotype is Associated with Virologic Relapse After 8-Week Treatment with Sofosbuvir, Velpatasvir, and Voxilaprevir, Gastroenterology, Vol. 153, No. 6, 2017, pp. 1694-1695, https://doi.org/10.1053/j.gastro.2017.06.069.[54] A. J. Khan, V. A. Saraswat, P. Ranjan, D. Parmar, T. S. Negi, S. Mohindra, Polymorphism in Interferon Λ3/Interleukin‐28B Gene and Risk to Noncirrhotic Chronic Hepatitis C Genotype 3 Virus Infection and Its Effect on the Response to Combined Daclatasvir and Sofosbuvir Therapy, Journal of Medical Virology, Vol. 91, No. 4, 2019, pp. 659-667, https://doi.org/10.1002/jmv.25359.[55] A. Vasanthakumar et al., Reduced Itpase Activity and Favorable Il28b Genetic Variant Protect Against Ribavirin-Induced Anemia in Interferon-Free Regimens, Plos One, Vol. 13, No. 5, 2018, pp. e0198296, https://doi.org/10.1371/journal.pone.0198296.[56] H. Ahmed et al., Meta-Analysis of Grazoprevir Plus Elbasvir for Treatment of Hepatitis C Virus Genotype 1 Infection, Annals of Hepatology, Vol. 17, No. 1, 2018, pp. 18-32, https://doi.org/10.5604/01.3001.0010.7532 [57] J. J. Feld et al., Treatment of HCV with ABT-450/R–Ombitasvir and Dasabuvir with Ribavirin, New England Journal of Medicine, Vol. 370, No. 17, 2014, pp. 1594-1603, https://doi.org/10.1056/NEJMoa1315722.[58] S. Padmanabhan, Handbook of Pharmacogenomics and Stratified Medicine, Elsevier, London, 2014.[59] A. Osinusi, S. Naggie, The Role of IL28B Genotype Testing in The Era of Direct Acting Antiviral Agents, European Gastroenterology Hepatology Review, Vol. 1, No. 2, 2012, pp. 33-39. [60] Ministry of Health, Technical Guidelines on HBV Diagnosis and Treatment, Ministry of Health, Hanoi, 2019 (in Vietnamese).[61] Y. Yano et al., Factors Associated with the Decrease in Hepatitis B Surface Antigen Titers Following Interferon Therapy in Patients with Chronic Hepatitis B: Is Interferon and Adefovir Combination Therapy Effective?, Biomedical Reports, Vol. 7, No. 3, 2017, pp. 257-262, https://doi.org/10.3892/br.2017.944.[62] H. L. Y. Chan et al., A Randomized, Controlled Trial of Combination Therapy for Chronic Hepatitis B: Comparing Pegylated Interferon-Α2b and Lamivudine with Lamivudine Alone, Annals Of Internal Medicine, Vol. 142, No. 4, 2005, pp. 240-250, https://doi.org/10.7326/0003-4819-142-4-200502150-00006.[63] H. L. Janssen et al., Pegylated Interferon Alfa-2b Alone or in Combination with Lamivudine for Hbeag-Positive Chronic Hepatitis B: A Randomised Trial, The Lancet, Vol. 365, No. 9454, 2005, pp. 123-129, https://doi.org/10.1016/S0140-6736(05)17701-0.[64] G. K. Lau et al., Peginterferon Alfa-2a, Lamivudine, and The Combination for Hbeag-Positive Chronic Hepatitis B, New England Journal of Medicine, Vol. 352, No. 26, 2005, pp. 2682-2695, https://doi.org/10.1056/NEJMoa043470.[65] Z. Zhao et al., The Impact Of IFNL3 Genotype on Interferon Treatment Outcome in Patients Chronically Infected with Hepatitis B Virus: A Meta-Analysis, Microbial Pathogenesis, Vol. 134, 2019, pp. 103598, https://doi.org/10.1016/j.micpath.2019.103598.[66] M. Lindgren et al., Genetic Variation in IL 28B (IFNL 3) and Response to Interferon‐Alpha Treatment in Myeloproliferative Neoplasms, European Journal of Haematology, Vol. 100, No. 5, 2018, pp. 419-425, https://doi.org/10.1111/ejh.13034.[67] P. J. Campbell, A. R. Green, The Myeloproliferative Disorders, New England Journal of Medicine, Vol. 355, No. 23, 2006, pp. 2452-2466, https://doi.org/10.1056/NEJMra063728.[68] R. T. Silver, J. J. Kiladjian, H. C. Hasselbalch, Interferon and The Treatment of Polycythemia Vera, Essential Thrombocythemia and Myelofibrosis, Expert Rev Hematol, Vol. 6, No. 1, 2013, pp. 49-58, https://doi.org/10.1586/ehm.12.69.[69] R. T. Silver, K. Vandris, J. J. Goldman, Recombinant Interferon-Alpha May Retard Progressionof Early Primary Myelofibrosis: A Preliminary Report, Blood, Vol. 117, No. 24, 2011, pp. 6669-6672, https://doi.org/10.1182/blood-2010-11-320069.[70] M. Lindgren et al., A Retrospective Cohort Study of Interferon-Α Therapy in Myeloproliferative Neoplasms; Adverse Events, Thromboembolic Incidence and Causes of Termination of Therapy, Blood, Vol. 124, No. 21, 2014, pp. 1861, https://doi.org/10.1182/blood.V124.21.1861.1861.[71] P. H. Phiet et al., Rs12979860 and Rs8099917 Single Nucleotide Polymorphism of IL28B Gene in South Vietnam Patients Infected with Hepatitis C Virus, Journal of Hepatobiliary Vietnam, Vol. 21, 2012, pp. 9-16 (in Vietnamese).[72] P. T. T. Thuy et al., The Different Impacts of IL28B Genotype in Treatment Vietnamese Patients with Chronic Hepatitis C Genotype 1 and 6, Journal of Hepatobiliary Vietnam, Vol. 29, 2014, pp. 108-109 (in Vietnamese).        
    Type of Medium: Online Resource
    ISSN: 2588-1132 , 2615-9309
    Language: Unknown
    Publisher: Vietnam National University Journal of Science
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    Online Resource
    SAGE Publications ; 2018
    In:  RELC Journal Vol. 49, No. 3 ( 2018-12), p. 339-352
    In: RELC Journal, SAGE Publications, Vol. 49, No. 3 ( 2018-12), p. 339-352
    Abstract: At the implementation level of the national project ‘ Teaching and Learning Foreign Language in the Public-Sector Educational System for the 2008–2020 Period’, the Vietnamese Ministry of Education and Training (MOET) provided large-scale general English proficiency training for key English teachers and classroom English training for a pilot group of teachers. This research explores in-service teachers’ perceptions of the usefulness of the training and of the changes which occurred in their classrooms as a result of the training. The findings have shown that although in-service teachers across different levels of proficiency appreciate both sets of training, they found classroom English training more relevant and practical to their teaching context. The results of the study also suggest that in contexts with insufficient numbers of qualified foreign language teachers, high proficiency standards for teachers compared with their current level of proficiency, and limited support for in-service teachers to achieve and maintain the required proficiency, classroom English training can be considered as a strategic choice and hence, should be prioritized.
    Type of Medium: Online Resource
    ISSN: 0033-6882 , 1745-526X
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2018
    detail.hit.zdb_id: 2169714-0
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    SSG: 7,11
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