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  • 1
    In: The Lancet Regional Health - Western Pacific, Elsevier BV, Vol. 37 ( 2023-08), p. 100801-
    Type of Medium: Online Resource
    ISSN: 2666-6065
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2023
    detail.hit.zdb_id: 3052289-4
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  • 2
    In: Tạp chí Y học Việt Nam, Vietnam Medical Journal, Vietnam Medical Association, Vol. 505, No. 1 ( 2021-09-11)
    Abstract: Đái tháo đường (ĐTĐ) tuýp 2 là một trong những căn bệnh có xu hướng ngày càng tăng với nhiều biến chứng nguy hiểm, trong đó có nguy cơ gia tăng các tổn thương hệ tim mạch. Ước tính khoảng 75% bệnh nhân ĐTĐ tuýp 2 tử vong do hậu quả của các bệnh tim mạch. Tuy nhiên, ở Việt Nam chưa có nhiều nghiên cứu đánh giá nguy cơ mắc bệnh tim mạch trong 10 năm theo thang điểm Framingham (Framingham Risk Score - FRS) ở bệnh nhân ĐTĐ tuýp 2. Để dự đoán nguy cơ mắc bệnh tim mạch trong 10 năm và các yếu tố liên quan đến tình trạng này, chúng tôi tiến hành nghiên cứu theo phương pháp mô tả, cắt ngang trên 139 bệnh nhân (62 nam và 77 nữ) ĐTĐ tuýp 2, có độ tuổi trung bình 66,31 ± 8,88, cho thấy chủ yếu các bệnh nhân thuộc nhóm nguy cơ rất cao (41,7%), nguy cơ cao (17,3%), nguy cơ trung bình (20,9%) và nguy cơ thấp (20,1%). Nguy cơ mắc bệnh tim mạch cao hơn ở bệnh nhân nam, trên 60 tuổi, chỉ số khối cơ thể cao, có tình trạng rối loạn lipid máu. Với bệnh nhân ĐTĐ tuýp 2 kèm theo tăng huyết áp có khả năng làm tăng nguy cơ ở mức rấtcao lên 10,784 lần.
    Type of Medium: Online Resource
    ISSN: 1859-1868
    Language: Unknown
    Publisher: Vietnam Medical Journal, Vietnam Medical Association
    Publication Date: 2021
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  • 3
    In: Tạp chí Y học Cộng đồng, Institute of Community Health, Vol. 64, No. 4 ( 2023-07-28)
    Abstract: Mục tiêu: Mô tả chất lượng cuộc sống liên quan đến thị giác của bệnh nhân đái tháo đường tại Bệnh viện E và một số yếu tố liên quan. Đối tượng và phương pháp nghiên cứu: Nghiên cứu mô tả cắt ngang có phân tích được thực hiện trên 119 người bệnh mắc đái tháo đường được quản lý và điều trị tại Bệnh viện E năm 2020. Kết quả: Điểm NEI-VFQ-25 của người bệnh ĐTĐ trung bình là 83,25 ± 13,35 điểm. Trong đó khía cạnh sự phụ thuộc vào người khác đạt điểm cao nhất là 94,46 ± 13,03 điểm. Khía cạnh sức khỏe tổng quát đạt điểm trung bình thấp nhất là 37,39 ± 17,78 điểm. Tuổi cao,nữ giới, sống ở thành thị là những yếu tố nhân khẩu học có liên quan tới chất lượng cuộc sống liên quan tới thị giác thấp (p 〈 0,05). Điểm chất lượng cuộc sống liên quan tới thị giác lần lượt là 91±4,85, 86,69±11,84 và 77,9±14,6 ở các nhóm mắc bệnh dưới 5 năm, 5 – 10 năm và trên 10 năm (p 〈 0,01). Điểm trung bình chất lượng cuộc sống liên quan đến thị giác của nhóm đối tượng có biến chứng võng mạc, tăng huyết áp, suy giảm thị giác thấp hơn nhiều so với các nhóm không bị (p 〈 0,05) Kết luận: CLCS liên quan tới thị giác ở người bệnh đái tháo đường điều trị tại bệnh viện E năm 2020 tương đối cao đặc biệt là khía cạnh sự phụ thuộc vào người khác. CLCS liên quan tới thị giác ở người ĐTĐ có liên quan tới tuổi, giới, nơi sống, thời gian mắc ĐTĐ, tình trạng mắc THA, võng mạc ĐTĐ và suy giảm thị giác.
    Type of Medium: Online Resource
    ISSN: 2354-0613
    URL: Issue
    Language: Unknown
    Publisher: Institute of Community Health
    Publication Date: 2023
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  • 4
    Online Resource
    Online Resource
    Vietnam National University Journal of Science ; 2020
    In:  VNU Journal of Science: Medical and Pharmaceutical Sciences Vol. 36, No. 1 ( 2020-03-24)
    In: VNU Journal of Science: Medical and Pharmaceutical Sciences, Vietnam National University Journal of Science, Vol. 36, No. 1 ( 2020-03-24)
    Abstract: Malignant hyperthermia (MH) is a clinical response happened to patient who is sensitive with inhaled anesthesia drug that could cause suddently death. Many previous studies showed that malignant hyperthermia strongly related to genetic background of patients including RYR1, CACNA1S or STAC3 gene polymorphisms. With the development of high technology such as next generation sequencing, scientists found that 37 to 86 percents of MH cases had RYR1 mutations and approximately 1 percent of those had CACNA1S mutations. Gene analysis testing was recommended to apply for patient with MH medical history or MH patient’s family relations. Keywords Malignant hyperthermia, inhaled anesthesia, RYR1, CACNA1S, STAC3. References [1] G. Torri, Inhalation anesthetics: a review, Minerva Anestesiologica 76 (2010) 215–228. [2] N. Kassiri, S. Ardehali, F. Rashidi, S. Hashemian, Inhalational anesthetics agents: The pharmacokinetic, pharmacodynamics, and their effects on human body, Biomed. Biotechnol. Res. J. BBRJ 2 (2018) 173. https://doi.org/10.4103/bbrj.bbrj_6618.[3] H. Rosenberg, N. Sambuughin, S. Riazi, R. Dirksen, Malignant Hyperthermia Susceptibility, in: M.P. Adam, H.H. Ardinger, R.A. Pagon, S.E. Wallace, L.J. Bean, K. Stephens, A. Amemiya (Eds.), GeneReviews, University of Washington, Seattle, Seattle (WA), 19932020. http://www.ncbi.nlm.nih.gov/books/NBK1146/ (accessed February 2, 2020).[4] H. Rosenberg, N. Pollock, A. Schiemann, T. Bulger, K. Stowell, Malignant hyperthermia: a review, Orphanet J. Rare Dis 10 (2015) 93. https://doi.org/10.1186/s13023-015-0310-1.[5] D. Carpenter, C. Ringrose, V. Leo, A. Morris, R.L. Robinson, P.J. Halsall, P.M. Hopkins, M.-A. Shaw, The role of CACNA1S in predisposition to malignant hyperthermia, BMC Med. Genet 10 (2009) 104. https://doi.org/10.1186/1471-2350-10-104.[6] S. Riazi, N. Kraeva, P.M. Hopkins, Updated guide for the management of malignant hyperthermia, Can. J. Anaesth. J. Can. Anesth 65 (2018) 709–721. https://doi.org/10.1007/s12630-018-1108-0.[7] S. Riazi, N. Kraeva, P.M. Hopkins, Malignant Hyperthermia in the Post-Genomics Era: New Perspectives on an Old Concept, Anesthesiology 128 (2018) 168–180. https://doi.org/10.1097/ALN.0000000000001878.[8] [D.M. Miller, C. Daly, E.M. Aboelsaod, L. Gardner, S.J. Hobson, K. Riasat, S. Shepherd, R.L. Robinson, J.G. Bilmen, P.K. Gupta, M.-A. Shaw, P.M. Hopkins, Genetic epidemiology of malignant hyperthermia in the UK, BJA Br. J. Anaesth 121 (2018) 944–952. https://doi.org/10.1016/j.bja.2018.06.028.[9] T.A. Beam, E.F. Loudermilk, D.F. Kisor, Pharmacogenetics and pathophysiology of CACNA1S mutations in malignant hyperthermia, Physiol. Genomics 49 (2017) 81–87. https://doi.org/10.1152/physiolgenomics.00126.2016.[10] I.T. Zaharieva, A. Sarkozy, P. Munot, A. Manzur, G. O’Grady, J. Rendu, E. Malfatti, H. Amthor, L. Servais, J.A. Urtizberea, O.A. Neto, E. Zanoteli, S. Donkervoort, J. Taylor, J. Dixon, G. Poke, A.R. Foley, C. Holmes, G. Williams, M. Holder, S. Yum, L. Medne, S. Quijano-Roy, N.B. Romero, J. Fauré, L. Feng, L. Bastaki, M.R. Davis, R. Phadke, C.A. Sewry, C.G. Bönnemann, H. Jungbluth, C. Bachmann, S. Treves, F. Muntoni, STAC3 variants cause a congenital myopathy with distinctive dysmorphic features and malignant hyperthermia susceptibility, Hum. Mutat 39 (2018) 1980–1994. https://doi.org/10.1002/humu.23635.[11] A.F. Dulhunty, The voltage-activation of contraction in skeletal muscle, Prog. Biophys. Mol. Biol 57 (1992) 181–223. https://doi.org/10.1016/0079-6107(92)90024-Z.[12] C. Franzini-Armstrong, A.O. Jorgensen, Structure and Development of E-C Coupling Units in Skeletal Muscle, Annu. Rev. Physiol 56 (1994) 509–534. https://doi.org/10.1146/annurev.ph.56.030194.002453.[13] D.H. MacLennan, M. Abu-Abed, C. Kang, Structure-function relationships in Ca(2+) cycling proteins, J. Mol. Cell. Cardiol 34 (2002) 897–918. https://doi.org/10.1006/jmcc.2002.2031.[14] H. Rosenberg, M. Davis, D. James, N. Pollock, K. Stowell, Malignant hyperthermia, Orphanet J. Rare Dis 2 (2007) 21. https://doi.org/10.1186/1750-1172-2-21.[15] S.M. Karan, F. Crowl, S.M. Muldoon, Malignant hyperthermia masked by capnographic monitoring, Anesth. Analg 78 (1994) 590–592. https://doi.org/10.1213/00000539-199403000-00029.[16] M.G. Larach, G.A. Gronert, G.C. Allen, B.W. Brandom, E.B. Lehman, Clinical presentation, treatment, and complications of malignant hyperthermia in North America from 1987 to 2006, Anesth. Analg 110 (2010) 498–507. https://doi.org/10.1213/ANE.0b013e3181c6b9b2.[17] M.G. Larach, A.R. Localio, G.C. Allen, M.A. Denborough, F.R. Ellis, G.A. Gronert, R.F. Kaplan, S.M. Muldoon, T.E. Nelson, H. Ording, H. Rosenberg, B.E. Waud, D.J. Wedel, A Clinical Grading Scale to Predict Malignant Hyperthermia Susceptibility, Anesthesiology 80 (1994) 771–779. https://doi.org/10.1097/00000542-199404000-00008.[18] D. Schneiderbanger, S. Johannsen, N. Roewer, F. Schuster, Management of malignant hyperthermia: diagnosis and treatment, Ther. Clin. Risk Manag 10 (2014) 355–362. https://doi.org/10.2147/TCRM.S47632.[19] R. Robinson, D. Carpenter, M.-A. Shaw, J. Halsall, P. Hopkins, Mutations in RYR1 in malignant hyperthermia and central core disease, Hum. Mutat 27 (2006) 977–989. https://doi.org/10.1002/humu.20356.[20] M.L. Alvarellos, R.M. Krauss, R.A. Wilke, R.B. Altman, T.E. Klein, PharmGKB summary: very important pharmacogene information for RYR1, Pharmacogenet. Genomics 26 (2016) 138–144. https://doi.org/10.1097/FPC.0000000000000198.[21] A. Merritt, P. Booms, M.-A. Shaw, D.M. Miller, C. Daly, J.G. Bilmen, K.M. Stowell, P.D. Allen, D.S. Steele, P.M. Hopkins, Assessing the pathogenicity of RYR1 variants in malignant hyperthermia, BJA Br. J. Anaesth 118 (2017) 533–543. https://doi.org/10.1093/bja/aex042.[22] P.M. Hopkins, H. Rüffert, M.M. Snoeck, T. Girard, K.P.E. Glahn, F.R. Ellis, C.R. Müller, A. Urwyler, European Malignant Hyperthermia Group, European Malignant Hyperthermia Group guidelines for investigation of malignant hyperthermia susceptibility, Br. J. Anaesth 115 (2015) 531–539. https://doi.org/10.1093/bja/aev225.[23] N.T. Thuy, L.N. Thanh, N.T.T. Mau, N.H. Hoang, N.T.K. Lien, D.D. Long, N.T. Bình, D.A. Tien, N.C. Huu, N.T. Hieu, P.T.H. Nhung, V.T. Thom, Whole exome sequencing revealed a pathogenic variant in a gene related to malignant hyperthermia in a Vietnamese cardiac surgical patient: A case report, Ann. Med. Surg 48 (2019) 88–90. https://doi.org/10.1016/j.amsu.2019.10.030.[24] B. Neuhuber, U. Gerster, F. Döring, H. Glossmann, T. Tanabe, B.E. Flucher, Association of calcium channel α1S and β1a subunits is required for the targeting of β1a but not of α1S into skeletal muscle triads, Proc. Natl. Acad. Sci. U. S. A 95 (1998) 5015–5020. https://doi.org/10.1073/pnas.95.9.5015.[25] M. Whirl-Carrillo, E.M. McDonagh, J.M. Hebert, L. Gong, K. Sangkuhl, C.F. Thorn, R.B. Altman, T.E. Klein, Pharmacogenomics Knowledge for Personalized Medicine, Clin. Pharmacol. Ther 92 (2012) 414–417. https://doi.org/10.1038/clpt.2012.96.[26] N. Monnier, V. Procaccio, P. Stieglitz, J. Lunardi, Malignant-hyperthermia susceptibility is associated with a mutation of the alpha 1-subunit of the human dihydropyridine-sensitive L-type voltage-dependent calcium-channel receptor in skeletal muscle, Am. J. Hum. Genet 60 (1997) 1316–1325 . https://doi.org/10.1086/515454.[27] S.L. Stewart, K. Hogan, H. Rosenberg, J.E. Fletcher, Identification of the Arg1086His mutation in the alpha subunit of the voltage-dependent calcium channel (CACNA1S) in a North American family with malignant hyperthermia, Clin. Genet 59 (2001) 178–184. https://doi.org/10.1034/j.1399 0004.2001.590306.x.[28] P.J. Toppin, T.T. Chandy, A. Ghanekar, N. Kraeva, W.S. Beattie, S. Riazi, A report of fulminant malignant hyperthermia in a patient with a novel mutation of the CACNA1S gene, Can. J. Anaesth. J. Can. Anesth 57 (2010) 689–693. https://doi.org/10.1007/s12630-010-9314-4.[29] E.J. Horstick, J.W. Linsley, J.J. Dowling, M.A. Hauser, K.K. McDonald, A. Ashley-Koch, L. Saint-Amant, A. Satish, W.W. Cui, W. Zhou, S.M. Sprague, D.S. Stamm, C.M. Powell, M.C. Speer, C. Franzini-Armstrong, H. Hirata, J.Y. Kuwada, Stac3 is a component of the excitation-contraction coupling machinery and mutated in Native American myopathy, Nat. Commun 4 (2013) 1952. https://doi.org/10.1038/ncomms2952.[30] D.S. Stamm, A.S. Aylsworth, J.M. Stajich, S.G. Kahler, L.B. Thorne, M.C. Speer, C.M. Powell, Native American myopathy: Congenital myopathy with cleft palate, skeletal anomalies, and susceptibility to malignant hyperthermia, Am. J. Med. Genet. A 146A (2008) 1832–1841. https://doi.org/10.1002/ajmg.a.32370.[31] A. Polster, B.R. Nelson, S. Papadopoulos, E.N. Olson, K.G. Beam, Stac proteins associate with the critical domain for excitation–contraction coupling in the II–III loop of CaV1.1, J. Gen. Physiol 150 (2018) 613–624. https://doi.org/10.1085/jgp.201711917.[32] S.M. Wong King Yuen, M. Campiglio, C.-C. Tung, B.E. Flucher, F. Van Petegem, Structural insights into binding of STAC proteins to voltage-gated calcium channels, Proc. Natl. Acad. Sci 114 (2017) E9520–E9528. https://doi.org/10.1073/pnas.1708852114.[33] M. Grabner, R.T. Dirksen, N. Suda, K.G. Beam, The II-III loop of the skeletal muscle dihydropyridine receptor is responsible for the Bi-directional coupling with the ryanodine receptor, J. Biol. Chem 274 (1999) 21913–21919. https://doi.org/10.1074/jbc.274.31.21913.[34] J. Nakai, T. Tanabe, T. Konno, B. Adams, K.G. Beam, Localization in the II-III loop of the dihydropyridine receptor of a sequence critical for excitation-contraction coupling, J. Biol. Chem 273 (1998) 24983–24986. https://doi.org/10.1074/jbc.273.39.24983.[35] C.J. Morton, I.D. Campbell, SH3 domains. Molecular “Velcro,” Curr. Biol. CB 4 (1994) 615–617. https://doi.org/10.1016/s0960-9822(00)00134-2.[36] A. Zafra-Ruano, I. Luque, Interfacial water molecules in SH3 interactions: Getting the full picture on polyproline recognition by protein-protein interaction domains, FEBS Lett 586 (2012) 2619–2630. https://doi.org/10.1016/j.febslet.2012.04.057.        
    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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  • 5
    Online Resource
    Online Resource
    Vietnam National University Journal of Science ; 2021
    In:  VNU Journal of Science: Medical and Pharmaceutical Sciences Vol. 37, No. 2 ( 2021-06-28)
    In: VNU Journal of Science: Medical and Pharmaceutical Sciences, Vietnam National University Journal of Science, Vol. 37, No. 2 ( 2021-06-28)
    Abstract: Today, the incidence of type 2 diabetes mellitus is increasing rapidly on global. This disease is shown with many complications that significantly affect public health. One of them is kidney complications, which have a high incidence among diabetic patients in Vietnam (25.6-33.1%). Age, history of hypertension, and dyslipidemia are considered to be the main risk factors for diabetic nephropathy. Thus, early detection of these factors for kidney damage is significant for diagnosing, monitoring, treatment, and prognosis of diabetic patients. Our descriptive, cross-sectional study conducting on 120 diabetic patients at E Hospital has observed that blood cholesterol levels, HbA1c levels were independently related to eGFR decline below 60 mL/min/1.73m2. From those data, an equation to predict the risk of diabetic kidney disease was estimated as p =  with k = Keyword: Type 2 diabetes, Diabetic nephropathy, Risk factor Today, the incidence of type 2 diabetes mellitus is increasing rapidly on global. This disease is shown with many complications that significantly affect public health. One of them is kidney complications, which have a high incidence among diabetic patients in Vietnam (25.6-33.1%). Age, history of hypertension, and dyslipidemia are considered to be the main risk factors for diabetic nephropathy. Thus, early detection of these factors for kidney damage is significant for diagnosing, monitoring, treatment, and prognosis of diabetic patients. Our descriptive, cross-sectional study conducting on 120 diabetic patients at E Hospital has observed that blood cholesterol levels, HbA1c levels were independently related to eGFR decline below 60 mL/min/1.73m2. From those data, an equation to predict the risk of diabetic kidney disease was estimated as p =  with k = Keyword Type 2 diabetes, Diabetic nephropathy, Risk factor. References [1] N. H. Cho, J. Kirigia, J. C. Mnanya, K. Ogurstova, L. Guraiguata, W. Rathmann, G. Roglic, N. Forouhi, R. Dajani, A. Esteghmati, E. Boyko, L. Hambleton, O. L. M. Neto, P. A. Montoya, S. Joshi, J. Chan, J. Shaw, T.A. Samuels, M. Pavkov, A. Reja, IDF Diabetes Atlas Eight Edition, International Diabete Federation, England, 2017.[2] N. T. Khue, Diabetes – General Endocrinology, Ho Chi Minh Publisher, Ho Chi Minh city, 2003 (in Vietnamese). [3] H. H. Kiem, Clinical Nephrology, Medical Publishing House, Hanoi, 2010 (in Vietnamese). [4] T. H. Quang, Practice Diabetes - Endocrine Disease, Medical Publishing House Hanoi, Hanoi, 2010 (in Vietnamese). [5] D. T. M. Hao, T. T. A. Thu, Diabetic Kidney Disease: Attention Problems, Vietnam Journal of Diabetes and Endocrinology, Vol. 38, 2020, pp. 12-17 (in Vietnamese), https://doi.org/10.47122/vjde.2020.38.2. [6] K. Tziomalos, A. Vasilios G, Diabetic Nephropathy: New Risk Factors and Improvements in Diagnosis, The Review of Diabetic Studies: RDS, Vol. 12, No. 1-2, 2015, pp. 110-118, https://doi.org/10.1900/RDS.2015.12.110.[7] American Diabetes Association, 2. Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes-2020, Journal Diabetes Care, Vol. 43, No. 1, 2020, pp. S14, https://doi.org/10.2337/dc20-S002.[8] A. S. Levey, J. Coresh, E. Balk, A. T. Kausz, A. Levin, M. W. Steffes, R. J. Hogg, R. D. Perrone, J. Lau, G. Eknoyan, National Kidney Foundation Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification, Ann Intern Med, Vol. 139, 2003, pp. 137-147, https://doi.org/10.7326/0003-4819-139-2-200307150-00013.[9] D. S. Freedman, M. Horlick, G. S. Berenson, A Comparison of The Slaughter Skinfold-thickness Equations and BMI in Predicting Body Fatness and Cardiovascular Disease Risk Factor Levels in Children, The American Journal of Clinical Nutrition, Vol. 98, No. 6, 2013, pp. 1417-1424, https://doi.org/10.3945/ajcn.113.065961.[10] National Heart, Lung and Blood Institutes, National Cholesterol Education Program: ATP III Guidelines at-a-glance Quick Desk Reference, https://www.nhlbi.nih.gov/files/docs/guidelines/atglance.pdf, (accessed on: 5th April 2021).[11] K. Eckardt, B. Kasiske, D. Wheeler, K. Uhlig, D. Miskulin, A. Earley, S. Haynes, J. Lamont, KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease: Definition and Classification of CKD, Kidney International Supplements, Vol. 3, 2013, pp. 5-14, https://doi.org/10.1038/kisup.2012.77.[12] I. H. Boer, M. L. Caramori, J. C. N. Chan, H. J. L. Heerspink, C. Hurst, K. Khunti, A. Liew, E. D. Michos, S. D. navaneethan, P. Rossing, W. A. Olowu, T. Sadusky, N. Tandon, K. R. Tuttle, C. Wanner, K. G. Wilkens, S. Zoungas, KDIGO 2020 Clinical Practice Guideline for Diabetes Management in Chronic Kidney Disease, Kidney international, Vol. 98, No. 4S, 2020, pp. S1-S115, http://dx.doi.org/10.1016/j.kint.2020.06.019.[13] B. T. T. Huong, N. T. Giang, Values of Cystatin C in Early Diagnosis of Renal Disease in Patients with Typ 2 Diabetes in Thai Nguyen National Hospital, Vietnam Medical Journal, Vol. 498, No. 2, 2021, pp. 13-17 (in Vietnamese).[14] L. X. Truong, N. D. Tai, T. Q. P. Linh, T. T. Nhung, The Prevalence of The Positive Microalbumin Urine in The Type 2 Diabetic Patients at District 2 Hospital, Y Hoc TP. Ho Chi Minh, Vol. 22, No. 2, 2018, pp. 139-143 (in Vietnamese).[15] S. Yi, S. Park, Y. Lee, H Park, B. Balkau, J. Yi, Association Between Fasting Glucose and All-cause Mortality According to Sex and Age: A Prospective Cohort Study, Scientific Reports, Vol. 7, No. 1, 2017, pp. 1-9, https://doi.org/10.1038/s41598-017-08498-6.[16] R. Gupta, M. Sharma, N. K. Goyal, P. S. Lodha, K. K. Sharma, Gender Differences in 7 Years Trends in Cholesterol Lipoproteins and Lipids in India: Insights From A Hospital Database, Indian Journal of Endocrinology Metabolism, Vol. 20, No. 2, 2016, pp. 211-8, https://doi.org/10.4103/2230-8210.176362.[17] X. Zhang, Z. Meng, X. Li, M. Liu, X. Ren, M. Zhu, Q. He, Q Zhang, K. Song, Q. Jia, C. Zhang, X Wang, X. Liu, The Association Between Total Bilirubin and Serum Triglyceride in Both Sexes in Chinese, Lipids In Health and Disease, Vol. 17, No. 1, 2017, pp. 1-8, https://doi.org/10.1186/s12944-018-0857-7.[18] S. Palazhy, V. Viswanathan, Lipid Abnormalities in Type 2 Diabetes Mellitus Patients with Overt Nephropathy, Diabetes Metabolism Journal, Vol. 41, No. 2, 2017, pp. 128-134, https://doi.org/ 10.4093/dmj.2017.41.2.128.[19] R. I. Papacocea, D. Timofte, M. Tanasescu, A. Balcangiu stroescu, D. G. Balan, A. Tulin, O. Stiru, I. A. Vacaroiu, A. Mihai, C. C. Popa, C. Cosconel, M. Enyedi, D. Miricescu, L. Raducu, D. Ionescu, Kidney Aging Process and The Management of The Elderly Patient with Renal Impairment, Experimental and Therapeutic Medicine, Vol. 21, 2021, pp. 266, https://doi.org/10.3892/etm.2021.9697.[20] R. D. Lindeman, Overview: Renal Physiology and Pathophysiology of Aging, Am J Kidney Dis, Vol. 16, 1990, pp. 275–282, https://doi.org/10.1016/s0272-6386(12)80002-3.[21] G. Zoppini, G. Targher, M. Chonchol, V. Ortalda, C. Negri, V. Stoicio, E. Bonora, Predictors of Estimated GFR Decline in Patients With Type 2 Diabetes and Preserved Kidney Function, Clinical Journal of the American Society of Nephrology, Vol. 7, No. 3, 2012, pp. 401-408, https://doi.org/10.2215/CJN.07650711.[22] R. Trevisan, A. R. Dodesini, G. Lepore, Lipids and Renal Disease, Journal of the American Society of Nephrology, Vol. 17, No. 2-4, 2006, pp. S145-S147. https://doi.org/10.1681/ASN.2005121320.[23] V. T. Samuel, G. I. Shulman, Mechanisms for Insulin Resistance: Common Threads and Missing Links, Cell, Vol. 148, No. 5, 2012, pp. 852-871, https://doi.org/10.1016/j.cell.2012.02.017.[24] W. Patricia, D. Gloria Michelle, F. Alessia, Systemic and Renal Lipids in Kidney Disease Development and Progression, American Journal of Physiology-Renal Physiology, Vol. 310, No. 6, 2016, pp. F433-F445, https://doi.org/ 10.1152/ajprenal.00375.2015.[25] F. M. Sacks, M. P. Hermans, P. Fioretto, P. Valensi, T. Davis, E. Horton, C. Wanner, K. A. Rubeaan, I. Barzon, L. Bishop, E. Bonora, P. Bunnag, L. Chuang, C. Deerochanawong, R. Goldenberg, B. Harshfiled, C. Hernandez, S. H. Botein, H. Itoh, W. Jia, Y. Jiang, T. Kadowaki, N. Laranjo, L. Leiter, T. Miwwa, M. Odawara, K. Ohashi, A. Ohno, C. Pan, J. Pan, J. P. Botet, Z. Reiner, C. M. Rotella, R. Simo, M. Tanaka, E. T. Reiner, D. T. Barima, G. Zoppini, V. J. Carey, Association between Plasma Triglycerides and High-density Lipoprotein Cholesterol and Microvascular Kidney Disease and Retinopathy in Type 2 Diabetes Mellitus: A Global Case–control Study In 13 Countries, Circulation. Vol. 129, No. 9, 2014, pp. 999-1008, https://doi.org/10.1161/CIRCULATIONAHA.113.002529.[26] Y. Wang, X. Qiu, L. Lv, C. Wang, Z. Ye, S. Li, Q. Liu, T. Lou, X. Liu, Correlation Between Serum Lipid Levels and Measured Glomerular Filtration Rate In Chinese Patients With Chronic Kidney Disease, PLoS One, Vol. 11, No. 10, 2016, pp. e0163767, https://doi.org/10.1371/journal.pone.0163767.[27] N. J. Radcliffe, J. Seah, M. Clarke, R. J. Maclsaac, G. Jerrums, E. I. Ekinci, Clinical Predictive Factors in Diabetic Kidney Disease Progression, Journal of Diabetes Investigation, Vol. 8, No. 1, 2017, pp. 6-18, https://doi.org/10.1111/jdi.12533.[28] D. D. Miao, E. C. Pan, Q. Zhang, Z. M. Sun, Y. Qin, M. Wu, Development and Validation of A Model for Predicting Diabetic Nephropathy in Chinese People, Biomedical and Environmental Sciences, Vol. 30, No. 2, 2017, pp. 106-112, https://doi.org/10.3967/bes2017.014.[29] R. G. Nelson, M. E. Grams, S. H. Ballew, Y. Sang, F. Azizi, S. J. Chadban, L. Chaker, S. C. Dunning, C. Fox, Y. Hirakawa, K. Iseki, J. Ix, T. H. Jafar, A. Kottgen, D. M. J. Naimark, T. Ohjubo, G. J. Prescott, C. M. Bebholz, C. Sabanayagam, T. Sairenchi, B. Schottker, Y. Shibagaki, M. Tonelli, L. Zhang, R. T. Gansevoort, K. Matsushita, M. Woodward, J. Coresh, V. Shalev, Development of Risk Prediction Equations For Incident Chronic Kidney Disease, Jama, Vol. 322, No. 21, 2019, pp. 2104-2114, https://doi.org/10.1001/jama.2019.17379.    
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  • 6
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    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: Cardiovascular disease is the leading cause of death in the world. Cardiovascular risk assessment is an important step in preventing and treating the disease. The current study assesses the 10-year risk of cardiovascular disease in 306 VNU’s office workers in 2016-2017 based on the 2008 Framingham Risk Score. The study results show that the average risk score was 4.05 ± 4.76%; low risk was 90.52%; moderate risk: 7.85 %; and high to very high risk was 1.63%. Men have a higher risk score than women (p 〈 0.001). The ten-year cardiovascular risk score shows that age and systolic blood pressure correlated with the risk at a medium level, and cholesterol and HDL correlated with it at a low level. Keywords Framingham Risk Score 2008, 10-year cardiovascular risk score, hypertension, blood cholesterol, blood HDL. References [1] Cardiovasculardiseases, http://www.who.int/en/newsroom/factsheets/detail/cardiovascular diseases-(cvds), (truy cập ngày 22/03/2019).[2] A.R. Gregory et al, Global, regional, and national burden of cardiovascular diseases for 10 Causes, 1990 to 2015, Journal of the American college of cardiology. 70(1) (2017) 1–25.[3] E. Gresham, T.E. Fitzpatrick , P.A. Wolf et al, Residual disability in survivors of stroke--the Framingham study, N Engl J Med. 293(19) (1975) 954–956.[4] T.A. Pearson, S.N. Blair, S.R. Danielset et al, AHA guidelines for primary prevention of cardiovascular disease and stroke: 2002 update: consensus panel guide to comprehensive risk reduction for adult patients without coronary or other atherosclerotic vascular diseases, American heart association science advisory and coordinating committee, Circulation. 106(3) (2002) 388–391.[5] I. Graham, D. Atar, K. B. Johnsen et al, European guidelines on cardiovascular disease prevention in clinical practice: full text - Fourth joint task force of the European society of cardiology and other societies on cardiovascular disease prevention in clinical practice constituted by representatives of nine societies and by invited experts, Euro heart J. 28(19) (2007) 2375-2414.[6] S.S. Mahmood, D. Levy, R.S. Vasanet et al, The Framingham heart study and the epidemiology of cardiovascular diseases: a historical perspective, Lancet. 383(9921) (2014) 999–1008.[7] J.A.A.G. Damen, L. Hooft, E. Schuit et al, Prediction models for cardiovascular disease risk in the general population: systematic review, BMJ. 353(2016) 1-10.[8] L.Q.H. Goh, T.A. Welborn, S.S. Dhaliwal, Independent external validation of cardiovascular disease mortality in women utilising Framingham and SCORE risk models: a mortality follow-up study, BMC women health. 14 (2014) 118-129.[9] L.M. A. Rodenas, J.A. C. Herencia, J.A. D. Garrote et al, Framingham risk score for prediction of cardiovascular diseases: a population-based study from southern Europe, PLoS One. 8(9) (2013) 1-10.[10] G.M. Park, Y.H. Kim, Model for predicting cardiovascular disease: insights from a Korean cardiovascular risk model, Pulse (Basel). 3(2) (2015) 153–157.[11] Trần Kim Trang, Nguy cơ 10 năm của bệnh tim mạch ở nữ giới tăng huyết áp, Y học thành phố Hồ Chí Minh. 16(1) (2012) 181-185.[12] Trương Thanh Sơn, Nguyễn Văn Trí, Trương Quang Bình, Nghiên cứu áp dụng thang điểm Framingham nhằm định nguy cơ bệnh động mạch vành trong 10 năm tới tại bệnh viện đa khóa Bình Dương, Y học thành phố Hồ Chí Minh. 15(1) (2011) 207-212. [13] Nguyễn Thị Kim Thủy, Dự báo nguy cơ mắc bệnh động mạch vành trong 10 năm theo thang điểm Frammingham ở bệnh nhân tăng huyết áp nguyên phát, Y học thực hành. 802(1) (2012) 27-29. [14] Nguyễn Hồng Huệ, Nguyễn Đức Công, Nghiên cứu ước tính nguy cơ bệnh động mạch vành trong 10 năm tới theo thang điểm Framingham qua 500 trường hợp, Y học thành phố Hồ Chí Minh. 15(2) (2011) 38-44. [15] C.V. Aram et al, The seventh report of the joint national committee on prevention, detection, evaluation, and treatment of high blood pressure, National heart, lung and blood institute - National institutes of health, NIH publication no. 04-5230, US, (2014), pp 13.[16] National Heart, Lung and Blood Institute, Third Report of the national cholesterol education program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult treatment panel III) Final report, National institutes of health, part II, US, (2002), pp 5-10. [17] World Health Organization, The Asia-Pacific perspective: redefining obesity and its treatment, Geneva: World health organization western pacific regional office, (2000), 18-19.[18] N.Q. Nguyen, S.T. Pham, L.D. Do et al, Cardiovascular disease risk factor patterns and their implications for intervention strategies in Vietnam, Int J Hypertens, ID. 560397, (2012), 1-11.[19] M. Nakhaie, B. Koor, S. Salehiet al, Prediction of cardiovascular disease risk using framingham risk score among office workers, Iran, 2017, Saudi journal of kidney diseases and transplantation. 29(3) (2018) 608-614. [20] Trịnh Xuân Thắng, Nghiên cứu các yếu tố nguy cơ bệnh tim mạch ở người 〉 25 tuổi tại 2 quận huyện Hà Nội, Luận văn thạc sỹ, Đại học Y Hà Nội, (2013). [21] Nguyễn Hoàng Liên, Văn Thế Trung, Xác định nguy cơ tim mạch theo thang điểm Framingham trên bệnh nhân vẩy nến tại bệnh viện da liễu TP. Hồ Chí Minh, Y Học TP. Hồ Chí Minh, 18(1), (2014), 79-85. [22] R. Gupta, V. Kaul, A. Agrawalet et al, Cardiovascular risk according to educational status in India, Preventive medicine. 51(5) (2010) 408–411.[23] C.A. Jones, L. Ross, N. Suraniet al, Framingham ten-year general cardiovascular disease risk: agreement between BMI-based and cholesterol-based estimates in a South Asian convenience sample, PLOS ONE. 10(3) (2015) e0119183.[24] K.S. Tyrrell, H.C. Lassila, E. Meilahn et al, Carotid atherosclerosis in premenopausal and postmenopausal women and its association with risk factors measured after menopause, Stroke. 29(6) (1998) 1116–1121.[25] Margaret Kelly Hayes et al, Influence of age and health behaviors on stroke risk: lessons from longitudinal studies, J Am Geriatr Soc. 58(2) (2010) 325–328.[26] D. Sugiyama, T. Okamura, M. Watanabe et al, Risk of hypercholesterolemia for cardiovascular disease and the population attributable fraction in a 24-year Japanese cohort study, J Atheroscler Thromb. 22(1) (2015) 95–107.[27] M.R. Law, N.J. Wald, S.G. Thompson, By how much and how quickly does reduction in serum cholesterol concentration lower risk of ischaemic heart disease, BMJ. 308(6925) (1994) 367–372.[28] Abolfazl Mohammadbeigi et al, Dyslipidemia prevalence in Iranian adult men: the impact of population-based screening on the detection of undiagnosed patients, World J men health. 33(3) (2015) 167-173. [29] R.S. Joshi et al, Prevalence of dyslipidemia in urban and rural India: The ICMR–INDIAB Study, PloS ONE. 9(5) (2014) 1-9.[30] Wichai Aekplakorn et al, Prevalence of dyslipidemia and management in the Thai population: national health examination survey IV, 2009, Journal of lipids. (2014) 1-13.[31] Asia Pacific, Cohort Studies Collaboration, cholesterol, diabetes and major cardiovascular diseases in the Asia-pacific region, Diabetologia. 50(11) (2003) 2289-2297.[32] S. Lewington, R. Clarke, N. Qizilbash, R. Peto, R. Collins et al, Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies, Lancet. 360(9349) (2002) 1903–1913.[33] Viet Nam national STEPS Survey 2015, https://www.who.int/ncds/un-task-force/steps-survey-vietnam2015.pdf, (2015), (truy cập ngày 09/03/2019).[34] Nguyễn Lân Việt, Kết quả mới nhất điều tra tăng huyết áp toàn quốc năm 2015 – 2016, Hội tim mạch Việt Nam, http://www.yhth.vn/hoinghitanghuyetapvietnamlanthuii_d3378.aspx, (2016) (truy cập ngày 11/02/2019).[35] M. Satoh, et al, Combined effect of blood pressure and total cholesterol levels on long-term risks of subtypes of cardiovascular death: evidence for cardiovascular prevention from observational cohorts in Japan, hypertension. 65(3) (2015) 517–524.  
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  • 7
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    Online Resource
    Vietnam National University Journal of Science ; 2019
    In:  VNU Journal of Science: Medical and Pharmaceutical Sciences Vol. 35, No. 2 ( 2019-12-17)
    In: VNU Journal of Science: Medical and Pharmaceutical Sciences, Vietnam National University Journal of Science, Vol. 35, No. 2 ( 2019-12-17)
    Abstract:  The incidence of type 2 diabetes mellitus is rapidly increasing, with many complications pressured on the health care system. Complications of diabetes due to chronic hyperglycemia related to other metabolic disorders, causing damage to the microvascular system. Among them, damaged kidney vessels lead to impair the renal function as diabetic nephropathy is the most common cause of end-stage renal disease. Measurement of glomerular filtration rate (GFR) is an important parameter in assessing renal function. In Vietnam’s hospital, serum creatinine is the biomarker mostly used to assess GFR. However, this biomarker is affected many factors such as gender, age, ... Many studies showed that serum Cystatin C is another biomarker that can detect early decline in GFR, less affected by other factors. Therefore, we conducted this study to explore serum cystatin C and creatinine levels in patients with type 2 diabetes and initially compare GFR in applying formulas of CKD.EPI 2012 and age and sex factors with these two biomarkers on those patient groups. The prospective, descriptive, cross-sectional study was performed on 50 patients with type 2 diabetes. Serum Cystatin C, serum creatinine test was performed and GFR was estimated by CKD.EPI 2012 equation. The results showed that the average serum Cystatin C level of the study group was 0.87 ± 0.24 mg/L that expressed no difference between two genders, and significant difference between age groups. Whereas, the average serum creatinine level of the study group was 81.30 ± 19.70 µmol/L, significant difference between male and female but not difference between age groups. In patients with GFR 〈 60 mL/min/1.73m2, serum creatinine and cystatin C levels were higher than normal but there was no difference with the upper limit in the normal reference range of the two indications. Keyword Type 2 diabetes, serum cystatin C, serum creatinine, glomerular filtration rate. References [1] N.H. Cho, J. Kirigia, J.C. Mnanya, K. Ogurstova, L. Gủaiguata, W. Rathmann, G. Roglic, N. Forouhi, R. Dajani, A. Esteghmati, E. Boyko, L. Hambleton, O.L.M. Neto, P.A. Montoya, S. Joshi, J. Chan, J. Shaw, T.A. Samuels, M. Pavkov, A. Reja, IDF Diabetes Atlas eight edition, International Diabete Federation, 2017. http://fmdiabetes.org/wp-content/uploads/2018/03/IDF-2017.pdf (access 15 july 2019).[2] G. Xu, B. Liu, Y. Sun, Y. Du, L.G. Snetselaar, F.B. Hu, W. Bao, Prevalence of diagnosed type 1 and type 2 diabetes among US adults in 2016 and 2017: population based study, British Medical Journal 361 (2018) k1497. https://doi.org/ 10.1136/bmj.k1497.[3] N.T.T. Minh, N.K. Luong, N.K. Son, The clinical and subclinical characteristics in patients with diabetes mellitus treated at Thai Nguyen General hospital, Journal of pratical medicine 787 (2011) 25-8.[4] N.T.H. Lan, L.D. Tuan, Survey characteristics of renal complication in elderly type 2 diabetes outpatients treated at National Hospital of Endocrinology, Journal of Military Pharmaco-medicine 6 2017 55-62. [5] Mohsen Pourghasem, Hamid Shafi, Zahra, Histological changes of kidney in diabetic nephropathy, Caspian J Intern Med 6(3) (2015) 120-7. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4650785/pdf/cjim-6-120.pdf (access 16 july 2019).[6] D.W. Powell, D.N. Kenagy, S. Zheng, S.C. Coventry, J. Xu, L. Cai, E.C. Carlson, P.N. Epstein, Associations between Structural and Functional Changes to the Kidney in Diabetic Humans and Mice, Life Sci 93(7) (2013) 257-64. https://doi.org/ 10.1016/j.lfs.2013.06.016.[7] Natalie Ebert, Elke Schaeffner, New biomarkers for estimating glomerular filtration rate, Journal of Laboratory and Precision Medicine 3(75) (2018. https://doi.org/10.21037/jlpm.2018.08.07.[8] L.A. Inker, C.H. Schmid, H. Tighiouart, J.H. Eckfeldt, H.I. Feldman, T. Greene, J.W. Kusek, J. Manzi, F.V. Lente, Y.L. Zhang, J. Coresh, A.S. Levey, Estimating Glomerular Filtration Rate from Serum Creatinine and Cystatin C, The new England Journal of Medicine 367 (2012) 20-9. https://doi.org/ 10.1056/NEJMoa1114248.[9] Ashwin Kumar, Anil Kumar, Serum cystatin C and serum creatinine levels in type 2 diabetes mellitus, International Journal of Research in Medical Sciences 3(1) (2015) 174-7. https://doi.org/10.5455/2320-6012.ijrms20150130.[10] X. Jianguo, D.I. Broadhurst, M. Wilson, D.S. Wishart, Translational biomarker discovery in clinical metabolomics:an introductory tutorial, Metabolomics 9 (2013) 280–99. https://doi.org/ 10.1007/s11306-012-0482-9.[11] B.T. Anh, Estimate the glomerular filtration rate by plasma creatinine and cystatin C concentration, Journal of Vietnam Medicine 2 (2012) 12-18.[12] S. Kakde, S. Alexander, V.G. David, S. Jacob, A. Mohapatra, A.T. Valson, B. Gopal, C.K. Jacob, J. Hephzibah, V. Tamilarasi, S. Varughese, Relationship of creatinine and cystatin C-based estimated glomerular filtration rates with measured glomerular filtration rate in healthy kidney donors from South Asia, Indian J Nephrol 28 (2018) 345-50. https://doi.org/ 0.4103/ijn.IJN 249_17[13] Olympus life science research europa GmbH, Olympus clinical chemistry reagent guide, Olympus Diagnostic, American, 2009.[14] International Society of Nephrology, KDIGO 2012 clinical practice guideline for the evaluation and Management of chronic kidney disease, Kidney Int, Kidney International Supplements 3(1) (2012) 5-14. https://kdigo.org/wp-content/uploads/2017/02/KDIGO_2012_CKD_GL.pdf (access 19 july 2019).[15] American Diabete Association, Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes 2018. Diabetes Care, (41(Supplement 1)) (2018) S13-S27. https://diabetesed.net/wp-content/uploads/2017/12/2018-ADA-Standards-of-Care.pdf (access 18 july 2019).[16] L.S. Weinert, A.B. Prates, F.B. do Amaral, M.Z. Vaccoro, J.L. Camargo, S.P. Silveiro, Gender does not influence cystatin C concentrations in healthy volunteers, Clin Chem Lab Med 48(3) (2010) 405-8. https://doi.org/10.1515/CCLM.2010.068.[17] N.T. Ly, T.T.C. Mai, Serum cystatin C and renal function in type 2 diabetic patients, Journal of medical Research 80(3B) (2012) 17-O.Al.[18] Musaimia, A.H. Abu-Nawwas, D.Al. Shaera, N.Y.Khaleela, M.Fawzi, Influence of age, gender, smoking, diabetes, thyroid and cardiac dysfunctions on cystatin C biomarker, Medicina de Familia Semergen 45(1) (2019) 44-51. https://doi.org/ 10.1016/j.semerg.2018.07.005.[19] M.C. Odden, I.B. Tager, R.T. Gansevoort, S.J.L. Bakker, R. Katz, L.F. Fried, et al, Age and cystatin C in healthy adults: a collaborative study, Nephrol Dial Transplant 25(2) (2010) 463-9. https://doi.org/10.1093/ndt/gfp474.[20] E.D. O’ Sullivan, J. Hughes, D.A. Ferenbach, Renal Aging: Causes and Consequences, J Am Soc Nephrol 28 (2017) 407–20. https://doi.org/10.1681/ASN.2015121308.[21] E.D. O’ Sullivan, J. Hughes, D.A. Ferenbach, Renal Aging: Causes and Consequences, J Am Soc Nephrol 28 (2017) 407–20. https://doi.org/10.1681/ASN.2015121308.[22] Christiane Oddoze, Henri Portugal, Yvon Berland, Bertrand Dussol, Cystatin C Is Not More Sensitive Than Creatinine for Detecting Early Renal Impairment in Patients With Diabetes. American Journal of Kidney Diseases, 38(2 (August)), (2001) 310-6. https://doi.org/ 10.1053/ajkd.2001.26096.      
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  • 8
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    Online Resource
    Vietnam National University Journal of Science ; 2017
    In:  VNU Journal of Science: Medical and Pharmaceutical Sciences Vol. 33, No. 2 ( 2017-12-01)
    In: VNU Journal of Science: Medical and Pharmaceutical Sciences, Vietnam National University Journal of Science, Vol. 33, No. 2 ( 2017-12-01)
    Abstract: Podocin protein is encoded by the NPHS2 gene is largely responsible for resistance to corticosteroid in pharmacological treatment of nephrotic syndrome. Therefore, we have constructed the genotyping test of NPHS2 polymorphisms on 149 pediatric patients with primary nephrotic syndrome. Main methods consisted of DNA extraction from peripheral blood samples, polymerase chain reaction (PCR) and Sanger sequencing. In my study, 251 SNPs from 6 exons and 2 new mutations have detected by genotyping test. These results will provide helpful tool and data for further research to determine the role of NPHS2 polymorphisms with corticosteroid response in the treatment of nephrotic syndrome.
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  • 9
    In: Letters in Drug Design & Discovery, Bentham Science Publishers Ltd., Vol. 20, No. 3 ( 2023-03), p. 353-364
    Abstract: 〈 p 〉 Background: Mimosa pudica Linn has been used in traditional medicine to support the treatment of type 2 diabetes. In the present study, we aimed to isolate and evaluate & #945;-glucosidase and Protein Tyrosine Phosphatase 1B (PTP1B) inhibitory activities of bioactive compounds from Mimosa pudica’s leaf extract. 〈 p 〉 Methods: Mimosa pudica leaves were extracted with 80% of ethanol. Bioactive compounds were isolated using a column chromatographic technique and elucidated the structure based on the nuclear magnetic resonance and electrospray ionization mass spectrometry spectral data. The & #945;- glucosidase and PTP1B inhibitory activities of the isolated compounds were evaluated using pnitrophenyl phosphate and p-nitrophenyl- & #945;-D-glucopyranoside as a substrate, respectively. Molecular docking and molecular dynamics are used to study the interaction between isolated compounds and proteins. Lipinski’s rule of five was used to evaluate the drug-like properties of isolated compounds. Predict pharmacokinetic parameters were evaluated using the pkCSM tool. 〈 p 〉 Results: Protocatechuic acid and syringic acid were isolated and identified using spectroscopic methods. Protocatechuic acid and syringic acid considerably inhibited & #945;-glucosidase enzyme at IC 〈 sub 〉 50 〈 /sub 〉 values of 416.17 ± 9.41 μM and 490.78 ± 9.28 μM, respectively. Furthermore, protocatechuic acid and syringic acid expressed strong PTP1B inhibitory activity at IC 〈 sub 〉 50 〈 /sub 〉 values of 248.83 ± 7.66 μM and 450.31 ± 7.77 μM, respectively. Molecular docking and molecular dynamics results showed the interactions of protocatechuic acid and syringic acid with amino acids of PTP1B and & #945;-glucosidase enzyme. Lipinski’s rule of five and absorption, distribution, metabolism, excretion, and toxicity studies predicted that protocatechuic acid and syringic acid have drug-likeness properties. In molecular docking simulation, protocatechuic acid and syringic acid gave relatively negative free binding energies and interacted with many amino acids in the active sites of PTP1B and & #945;-glucosidase. The molecular dynamics simulation results of the complexes were also relatively stable. 〈 p 〉 Conclusion: Our results showed that protocatechuic and syringic acids could be promising compounds for type 2 diabetes treatment. 〈 /p 〉
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    ISSN: 1570-1808
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    Publisher: Bentham Science Publishers Ltd.
    Publication Date: 2023
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  • 10
    In: Journal of Global Antimicrobial Resistance, Elsevier BV, Vol. 27 ( 2021-12), p. 200-211
    Type of Medium: Online Resource
    ISSN: 2213-7165
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2021
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