VNU Journal of Science: Medical and Pharmaceutical Sciences

CYP2C19 is one of the pricipal enzymes involed in the antiplatelet prodrug in patients with acute myocardial infraction. Different genotypes can cause various responses to platelet aggregation inhibitors. Therefore, we conduct research to evaluate the relationship between CYP2C19 polymorphisms and platelet aggregation in patients with acute myocardial infraction. The study was processed with a cross-sectional study of patients diagnosed acute myocardial infraction had blood samples tested for the gene CYP2C19 and platelet aggregation. The results in 64 consecutive patients, phenotypes based on genotypes: 59,3% poor and intermediate metabolizer, 40,7% extensive metabolizer. The average platelet aggregation of (poor, intermediate) metabolizer and extensive metabolizer were 29,79±13,6 and 23,27±11,6, respectively, there was a high similarity between the groups (p>0,05). The average platelet aggregation of (poor, intermediate) metabolier and extensive metabolizer on the group with Clopidogrel were 26,2±10,5 and 29,9±13,6 (p>0,05), the average with Ticagrelor were 10,8±6,5 and 18,4±8,7 (p>0,05), respectively. The group treated with Ticagrelor had a lower platelet aggregation than the remaining one with Clopidogrel (p<0,01). The study got some initial results that would be important for further studies on the relationship between CYP2C19 polymorphisms and platelet aggregation on Viet Namese patients with acute myocardial infraction.

This study aims to assess effectiveness and tolerance with neoadjuvant chemotherapy in patients with locally advanced gastric cancer in the period of 2018-2020. The study used the descriptive cross-sectional method to investigate 70 patients diagnosed with locally advanced gastric cancer, assigned to ECX/ECF or FLOT neoadjuvant chemotherapy regimens at Vietnam National Cancer Hospital. The results show that the partial response rates in the ECX/ECF and FLOT groups were 69.70% and 89.20%, respectively. There was no significant difference in the response level between the two groups (p = 0.716). 78.79% in the ECX/ECF group and 88.56% in the FLOT group underwent surgery. Neutropenia was an adverse event with the highest rate of grades 3 and 4 in both regimens (FLOT regimen was 10.81%, ECX/ECF regimen was 24.24%). There is a statistically significant difference in the incidence of events between the groups with prophylaxis and non-prophylaxis by granulocyte colony-stimulating factor. Taken together, there was no significant difference in the response level between the two groups; regarding the event of neutropenia, it could be controlled by prophylaxis in terms of benefits and risks for each patient. Keywords: Gastric cancer, effectiveness, safety, neoadjuvant chemotherapy. References [1] International Agency for Research on Cancer Global Cancer Observatory, 2020.[2] Ministry of Health, Guidelines for the Diagnosis and Treatment of Stomach Cancer, 2020 (in Vietnamese).[3] K. Liu, G. Li, C. Fan, C. Zhou, J. Li, Adapted Choi response Criteria for Prediction of Clinical Outcome in Locally Advanced Gastric Cancer Patients Following Preoperative Chemotherapy, Acta Radiologica, Vol. 53, No. 2, 2012, pp.127-34, https:// doi.org/10.1258/ar.2011.110273.[4] D. Cunningham, W. H. Allum, S. P. Stenning,J. N. Thompson, C. J. H. V. Velde, M. Nicolson,J. H. Scarffe, F. J. Lofts, S. J. Falk, T. J. Iveson,D. B. Smith, R. E. Langley, M. Verma, S. Weeden,Y. J. Chua, MAGIC Trial Participants. Perioperative Chemotherapy Versus Surgery Alone for Resectable Gastroesophageal Cancer, New England Journal of Medicine, Vol. 355, No.1, 2006, pp. 11-20, https://doi.org/10.1056/ NEJMoa055531.[5] S. E. A. Batran, N. Homann, C. Pauligk,T. O. Goetze, J. Meiler, S. Kasper, H. G. Koppet, et al., FLOT4-AIO Investigators, Perioperative Chemotherapy with Fluorouracil Plus Leucovorin, Oxaliplatin, and Docetaxel Versus Fluorouracil or Capecitabine Plus Cisplatin and Epirubicin for Locally Advanced, Resectable Gastric or Gastro-Oesophageal Junction Adenocarcinoma (FLOT4): A Randomised, Phase 2/3 Trial, Lancet, Vol. 393, No. 10184, 2019, pp. 1948-1957, https://doi.org/ 10.1016/S0140-6736(18)32557-1.[6] L. Sung, P. C. Nathan, S. M. Alibhai, G. A. Tomlinson, J. Beyene, Meta-analysis: Effect of Prophylactic Hematopoietic Colony-Stimulating Factors on Mortality and Outcomes of Infection, Annals of Internal Medicine, Vol. 147, No. 6, 2007, pp. 400-411, https://doi.org/10.7326/0003 - 4819 - 147 - 6-200709180 - 00010.

BK polyomavirus (BKV), a ubiquitous opportunistic infection among humans, causes BKV-associated nephropathy (BKVN) after renal transplantation. BKV strains worldwide are classified into 4 genotypes (I-IV), among which genotype I and IV are subdivided into 4 and 6 subtypes, respectively. Based on 580 bp-long VP1 sequences, this study analyzed the genotypes of 6 BKV strains from 20 specimens including plasma and urine from renal allograft recipients in Northern Vietnam. The VP1 genes of the BKV strains were analyzed by BLAST (NCBI), Bioedit, combined with MEGA7.0 software to construct and analyze the phylogenetic tree. Several mutations (8-39/ 580 nucleotides) were identified in all the 6 BKV strains compared to reference Dunlop BKV strain, among which BKV1 strain’s subtype IVc1 (isolated from the BKVN patients) had the most mutation nucleotides (39/ 580). The remaining 5 strains of BKV belonged to genotype I. The study provides a valuable fundamental molecular database contributing to monitoring as well as screening strategies and treatment options for BKV in kidney allograft recipients in Vietnam.  Keywords: BK polyomavirus, BKV-associated nephropathy (BKVN), renal transplantation, genotype. References [1] Gardner, S.D., et al., New human papovavirus (B.K.) isolated from urine after renal transplantation. Lancet, 1971. 1(7712): p. 1253-7.[2] Reploeg, M.D., G.A. Storch, and D.B. Clifford, Bk virus: a clinical review. Clin Infect Dis, 2001. 33(2): p. 191-202.[3] Randhawa, P.S., et al., Human polyoma virus-associated interstitial nephritis in the allograft kidney. Transplantation, 1999. 67(1): p. 103-9.[4] Sawinski, D. and S. Goral, BK virus infection: an update on diagnosis and treatment. Nephrol Dial Transplant, 2015. 30(2): p. 209-17.[5] Hirsch, H.H., et al., Polyomavirus-associated nephropathy in renal transplantation: critical issues of screening and management. Adv Exp Med Biol, 2006. 577: p. 160-73.[6] Bechert, C.J., et al., Monitoring of BK viral load in renal allograft recipients by real-time PCR assays. Am J Clin Pathol, 2010. 133(2): p. 242-50.[7] Takasaka, T., et al., Subtypes of BK virus prevalent in Japan and variation in their transcriptional control region. J Gen Virol, 2004. 85(Pt 10): p. 2821-7.[8] Boukoum, H., et al., Distribution of BK polyomavirus genotypes in Tunisian renal transplant recipients. J Med Virol, 2011. 83(4): p. 725-30.[9] Ledesma, J., et al., BK polyomavirus genotyping at inter- and intra-patient level in Spain. J Med Virol, 2013. 85(8): p. 1402-8.[10] Schwarz, A., et al., Viral Origin, Clinical Course, and Renal Outcomes in Patients With BK Virus Infection After Living-Donor Renal Transplantation. Transplantation, 2016. 100(4): p. 844-53.[11] An, H.P.H., et al., Ca lâm sàng nhiễm virus BK ở bệnh nhân sau ghép thận. Tạp chí Nghiên cứu Y học, 2015. 93(1): p. 142-148.[12] Hùng, T. http://benhvien198.vn/thong-bao-hai-truong-hop-nhiem-virus-bk-tren-benh-nhan-sau-ghep-than-tai-benh-vien-19-8. 2016.[13] Sharma, R., et al., BK Virus in Kidney Transplant: Current Concepts, Recent Advances, and Future Directions. Exp Clin Transplant, 2016. 14(4): p. 377-84.[14] Hayden, R.T., et al., Factors contributing to variability of quantitative viral PCR results in proficiency testing samples: a multivariate analysis. J Clin Microbiol, 2012. 50(2): p. 337-45.[15] Zhong, S., et al., Distribution patterns of BK polyomavirus (BKV) subtypes and subgroups in American, European and Asian populations suggest co-migration of BKV and the human race. J Gen Virol, 2009. 90(Pt 1): p. 144-52.[16] Matsuda, Y., Y. Qazi, and Y. Iwaki, A rapid and efficient method BK polyomavirus genotyping by high-resolution melting analysis. J Med Virol, 2011. 83(12): p. 2128-34.[17] Pastrana, D.V., et al., BK polyomavirus genotypes represent distinct serotypes with distinct entry tropism. Journal of virology, 2013. 87(18): p. 10105-10113.[18] Nishimoto, Y., et al., An Asian origin for subtype IV BK virus based on phylogenetic analysis. J Mol Evol, 2007. 65(1): p. 103-11.[19] Luo, C., et al., Genotyping schemes for polyomavirus BK, using gene-specific phylogenetic trees and single nucleotide polymorphism analysis. J Virol, 2009. 83(5): p. 2285-97.[20] Jin, L. and P.E. Gibson, Genomic Function and Variation of Human Polyomavirus BK (BKV). Rev Med Virol, 1996. 6(4): p. 201-214.

This article aims to establish a novel cytochrome b real-time PCR assay using Taqman probe for identification of P. malariae and its discrimination from other Plasmodium human infecting species. The optimization of real-time PCR assay with 1X QuantiTect Probe PCR Master Mix, primers and probe used at concentrations of 0.4 μM and 0.1 μM, respectively; and 2.5 mM MgCl2, 5 μl DNA template and deionized H2O of 20 μl, was performed using a real-time PCR instrument. The developed real-time PCR assay was evaluated for the limit of detection, stability on standard panels (109-100 copies/ µl), as well as the sensitivity, specificity on control groups. The probit analysis demonstrates that the 95% detection limit was <0.5 parasite/μl, both the sensitivity and specificity of the assay were 100% when evaluated on the control groups.  Additionally, the assay initially evaluated on 41 clinical samples including 21 malaria samples and 20 samples of volunteer blood donors, identified 1 positive sample with P. malariae from the disease group, which shows a concordant result with nested PCR. This novel Cyt b real-time PCR assay for identifying P. malariae may also facilitate earlier discrimination of P. malariae from other Plasmodium parasites with high sensitivity. Keywords Cytochrome b, malaria parasite, plasmodium malariae, mitochondria, real-time PCR. References [1] B. Singh, C. Daneshvar, Human infections and detection of Plasmodium knowlesi, Clinical microbiology reviews 26(2) (2013) 165-84. https://doi.org/10.1128/cmr.00079-12.[2] World Health Organization, Regional and global trends in burden of malaria cases and deaths, World malaria report 2019, Geneva, pp. 4-12.[3] World Health Organization, Progress towards elimination during the RBM decade 2000-2010, Eliminating malaria: learning from the past, looking ahead, Geneva (2011), pp. 39-70.[4] J.M. Vinetz, J. Li, T.F. McCutchan, et al., Plasmodium malariae infection in an asymptomatic 74-year-old Greek woman with splenomegaly, N Engl J Med 338(6) (1998) 367-71. https://doi.org/10.1056/NEJM199802053380605.[5] E. Lo, K. Nguyen, J. Nguyen, et al., Plasmodium malariae Prevalence and csp Gene Diversity, Kenya, 2014 and 2015, Emerg Infect Dis 23(4) (2017) 601-610. https://doi.org/10.3201/eid2304.161245.[6] W.E. Collins, G.M. Jeffery, Plasmodium malariae: parasite and disease, Clinical microbiology reviews 20(4) (2007) 579-92. https://doi.org/10.1128/CMR.00027-07.[7] M. Adams, S.N. Joshi, G. Mbambo, et al., An ultrasensitive reverse transcription polymerase chain reaction assay to detect asymptomatic low-density Plasmodium falciparum and Plasmodium vivax infections in small volume blood samples, Malar J 14 (2015) 520. https://doi.org/10.1186/s12936-015-1038-z.[8] W. Xu, U. Morris, B. Aydin-Schmidt, et al., SYBR Green real-time PCR-RFLP assay targeting the plasmodium cytochrome B gene-a highly sensitive molecular tool for malaria parasite detection and species determination, PloS one 10(3) (2015) e0120210. https://doi.org/10.1371/journal.pone.0120210.[9] E.M. Burd, Validation of laboratory-developed molecular assays for infectious diseases, Clinical microbiology reviews 23(3) (2010) 550-76. https://doi.org/10.1128/CMR.00074-09.[10] G. Snounou, S. Viriyakosol, X.P. Zhu, et al., High sensitivity of detection of human malaria parasites by the use of nested polymerase chain reaction, Molecular and biochemical parasitology 61(2) (1993) 315-20. https://doi.org/10.1016/0166-6851(93)90077-b.[11] C.G. Haanshuus, K. Morch, B. Blomberg, et al., Assessment of malaria real-time PCR methods and application with focus on low-level parasitaemia, PloS one 14(7) (2019) e0218982. https://doi.org/10.1371/journal.pone.0218982.[12] F. Perandin, N. Manca, A. Calderaro, et al., Development of a real-time PCR assay for detection of Plasmodium falciparum, Plasmodium vivax, and Plasmodium ovale for routine clinical diagnosis, Journal of clinical microbiology 42(3) (2004) 1214-9. https://doi.org/10.1128/jcm.42.3.1214-1219.2004.[13] C.E. Oriero, J.P. van Geertruyden, J. Jacobs, et al., Validation of an apicoplast genome target for the detection of Plasmodium species using polymerase chain reaction and loop mediated isothermal amplification, Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases 21(7) (2015) 686 e1-7. https://doi.org/10.1016/j.cmi.2015.02.025.[14] D.F. Echeverry, N.A. Deason, J. Davidson, et al., Human malaria diagnosis using a single-step direct-PCR based on the Plasmodium cytochrome oxidase III gene, Malaria journal 15 (2016) 128. https://doi.org/10.1186/s12936-016-1185-x.[15] P. Li, Z. Zhao, H. Xing, et al., Plasmodium malariae and Plasmodium ovale infections in the China-Myanmar border area, Malaria journal 15(1) (2016) 557. https://doi.org/10.1186/s12936-016-1605-y.[16] E.T.J. Chong, J.W.F. Neoh, T.Y. Lau, et al., Genetic and haplotype analyses targeting cytochrome b gene of Plasmodium knowlesi isolates of Malaysian Borneo and Peninsular Malaysia, Acta tropica 181 (2018) 35-39. https://doi.org/10.1016/j.actatropica.2018.01.018.[17] C. Farrugia, O. Cabaret, F. Botterel, et al., Cytochrome b gene quantitative PCR for diagnosing Plasmodium falciparum infection in travelers, Journal of clinical microbiology 49(6) (2011) 2191-5. https://doi.org/10.1128/JCM.02156-10.[18] C. Wongsrichanalai, M.J. Barcus, S. Muth, et al., A review of malaria diagnostic tools: microscopy and rapid diagnostic test (RDT), The American journal of tropical medicine and hygiene 77(6 Suppl) (2007) 119-27.[19] H.V. Nguyen, P.V.D. Eede, C. van Overmeir, et al., Marked age-dependent prevalence of symptomatic and patent infections and complexity of distribution of human Plasmodium species in central Vietnam, The American journal of tropical medicine and hygiene 87(6) (2012) 989-995. https://doi.org/10.4269/ajtmh.2012.12-0047.  

Thoái hóa khớp gối là bệnh khớp rất thường gặp phụ nữ sau mãn kinh, do béo phì và tăng phì đại xương và mọc gai xương ở khớp gối. Trái lại, loãng xương là hiện tượng mất xương dần dần sau mãn kinh. Tuy nhiên, trên lâm sàng hai bệnh thường phối hợp với nhau. Mục tiêu nghiên cứu: Xác định tỷ lệ bệnh nhân nữ thoái hóa khớp gối phối hợp loãng xương và tìm hiểu một số yếu tố ảnh hưởng loãng xương ở bệnh nhân nữ thoái hóa khớp gối. Đối tượng và phương pháp nghiên cứu: Gồm 68 bệnh nhân thoái hóa khớp gối, được đánh giá loãng xương và các yếu tố nguy cơ loãng xương. Kết quả: Tỷ lệ bệnh nhân nữ thoái hóa khớp gối phối hợp với loãng xương chiếm 37/68 (54,4%) .Chỉ số khối cơ thấp –SMI< 6,75 chiếm 46/68 (67,6%), ở nhóm loãng xương chỉ số khối cơ là là 6,25 ± 0,75 và tỷ lệ bệnh nhân thiếu vitamine D là 57/68 (83,8%). Kết luận: Tỷ lệ bệnh nhân nữ thoái hóa khớp gối phối hợp với loãng xương chiếm 54,4% .Các yếu tố  tuổi cao, cân nặng thấp và  chỉ số  khốí cơ  thấp  ảnh  hưởng đến loãng  xương ở bệnh  nhân  nữ thoái  hóa  khớp gối.

Berberine (BBR) is a plant-origin alkaloid with a long history, commonly used for treating infectious diarrhea. In recent years, BBR has been found with many pharmacological effects such as lowering blood glucose, anti-hyperlipidemia, liver protection, kidney protection, anti-atherosclerosis, antioxidants, etc. However, several studies revealed that the oral bioavailability of BBR was very low. Therefore, drug delivery systems have been studied to improve the absorption of BBR through an intestinal epithelial barrier such as liposomes, proliposomes, phytosomes, and nano lipids. The finding of new drug delivery systems has great potential in developing new medicines with a traditional active substance – BBR. Besides, BBR is also an important lead compound with different pharmacological effects, promising to form many new drug discovery programs with high feasibility.  

 Apolipoprotein C3 (APOC3) plays an important role in regulating lipid levels. This study aimed to assess whether the polymorphism APOC3-rs2854116 is associated with lipid profiles in primary school children in Hanoi. A case-control study was designed including 161 cases with dyslipidemia and 406 controls without dyslipidemia. Genotype for APOC3-rs2854116 polymorphism was determined by the polymerase chain reaction and restriction fragment length polymorphism method (PCR-RFLP). The results showed that there were differences in the effect of APOC3-rs2854116 polymorphism to lipid profiles among children with dyslipidemia. In comparison with A/G and A/A carriers, the G/G carriers had the higher concentration of serum TC, TG, and LDL-C (P < 0.05). APOC3-rs2854116 polymorphism was related to hypercholesterolemia in children with the most appropriate genetic model being additive model. Increasing each of the G alleles increased the risk of hypercholesterolemia by 2.2 times (P = 0.005) after adjustment for age and sex. This relationship was almost unchanged after adjustment for obesity-related traits. The study suggested that the APOC3-rs2854116 polymorphism significantly associated with hypercholesterolemia in primary school children in Hanoi independent of obesity-related traits. Keywords APOC3, rs2854116, hypercholesterolemia, primary school children. References [1] A. Kawakami, M. Yoshida, Apolipoprotein CIII links dyslipidemia with atherosclerosis, Journal of atherosclerosis and thrombosis 16(1) (2009) 6-11. https://doi.org/10.5551/jat.e607.[2] D. Gaudet, D. Brisson, K. Tremblay, V.J. Alexander, W. Singleton, S.G. Hughes, J.L. Witztum, Targeting APOC3 in the familial Chylomicronemia syndrome, New England Journal of Medicine 371(23) (2014) 2200-2206. https://doi.org/10.1056/NEJMoa1400284.[3] P. Libby, Triglycerides on the rise: should we swap seats on the seesaw?, European heart journal 36 (2015) 774-776. https://doi.org/10.1093/eurheartj/ehu500.[4] W.W. Li, M.M. Dammerman, J.D. Smith, S. Metzger, J.L. Breslow, T. Leff, Common genetic variation in the promoter of the human apoC-III gene abolishes regulation by insulin and may contribute to hypertriglyceridemia, Journal of Clinical Investigation 96(6) (1995) 2601-2605. https://doi.org/10.1172/JCI118324.[5] C. Couillard, M.C. Vohl, J.C. Engert, I. Lemieux, A. Houde, N. Alméras, J. Bergeron, Effect of apoC-III gene polymorphisms on the lipoprotein-lipid profile of viscerally obese men, Journal of lipid research 44(5) (2003) 986-993. https://doi.org/10.1194/jlr.M300043-JLR200.[6] J. Dallongeville, A. Meirhaeghe, D. Cottel, J.C. Fruchart, P. Amouyel, N. Helbecque, Gender related association between genetic variations of APOC-III gene and lipid and lipoprotein variables in northern France, Atherosclerosis 150(1) (2000) 149-157. https://doi.org/10.1016/s0021-9150(99)00362-7.[7] C.A. Rocco, D. Mecikovsky, P. Aulicino., R. Bologna, L. Sen, A. Mangano, Hypercholesterolemia Is Associated with the Apolipoprotein C-III (APOC3) Genotype in Children Receiving HAART: An Eight-Year Retrospective Study, PLos One 7(7) (2012) e39678. https://doi.org/10.1371/journal.pone.0039678.[8] S. Li, Y. Yang, X. Ouyang, J. Shen, M. Zhou, Y.Y. Song, Associations of the APOC3 rs2854116 and rs2854117 polymorphisms with plasma APOC3 and lipid levels: a meta-analysis, Int J Clin Exp Med 9(8) (2016) 15972. http://www.ijcem.com/files/ijcem0025065.pdf[9] N.C. Khan, L.B. Mai, D.T.P. Ha, N.D. Minh, L.D. Tuyen, H.H Tue, Overweight, obesity and related association in adults aged 25-54 years, Nutrition status and intervention strategy in Vietnam (2007) 49-72. (in Vietnamese).[10] T.T. Mai, L.T. Hop, N.T. Lam, N.T. Xuan, Overweight, obesity and dyslipidemia in children aged 4-9 years in some primary schools of Hoan Kiem District, Hanoi. Journal of Food and Nutrition 9(3) (2013) 9-18. (in Vietnamese).[11] P.O. Kwiterovich, Recognition and management of dyslipidemia in children and adolescents, The Journal of clinical endocrinology and metabolism 93(11) (2008) 4200-4209. https://doi.org/10.1210/jc.2008-1270.[12] National Cholesterol Education Program, Report of the Expert Panel on Blood Cholesterol Levels in Children and Adolescents, Pediatrics 89(S) (1992) 525-584. https://pediatrics.aappublications.org/content/pediatrics/89/3/495.full.pdf.[13] T.G. Lohman, A.F. Roche, R. Martorell, Anthropometric standardization reference manual, Champaign, IL: Human Kinetics Book, UK (1988).[14] N.T.H. Hanh, P.T. Phuong, T.Q. Binh, APOC3 rs2854116 single nucleotide polymorphism in Hanoi primary school children, The 2nd National Scientific Conference on Biological Research and Teaching in Vietnam, Vietnam National University Publishing House (2016) 287-294.[15] X. Solé, E. Guinó, J. Valls, R. Iniesta, V. Monero, SNPStats: a web tool for the analysis of association studies, Bioinformatics 22(15) (2006) 1928-1929. https://doi.org/10.1093/bioinformatics/btl268.[16] R.L. Pollex, M.R. Ban, T.K. Young, P. Bjerregaard, S.S. Anand, S. Yusuf, M.W. Huff, Association between the-455T>C promoter polymorphism of the APOC3 gene and the metabolic syndrome in a multi-ethnic sample, BMC medical genetics 8(1) (2007) 80-87. https://dx.doi.org/10.1186%2F1471-2350-8-80.[17] N.T.H. Hanh, B.T. Nhung, L.T. Hop, T.Q. Binh, Association of nutritional status, family and neonatal characteristics with hypertriglycemia in primary school children in Hanoi. VNU Journal of Science: Natural Sciences and Technology 31(4S) (2015) 94-101 (in Vietnamese).[18] N.T.H. Hạnh, B.T. Nhung, T.Q. Binh, L.T. Hop, Optimal model on association of some environmental factors with Hyperalphalipoproteinemia in primary school children in Hanoi. Second National Conference on study and education of biology in Vietnam VNU publishing house (2016) 295-303 (in Vietnamese).[19] N.T.H. Hanh, B.T. Nhung, L.T. Hop, T.Q. Binh, Relationship between some environmental factors and hyperbetalipoproteinemia in 6 - 11 year-old children in Hanoi, Journal of Science, Hanoi National University of Education 61(9) (2016) 185-192. https://doi.org/10.18173/2354-1059.2016-0072.[20] M. Larsson, E. Vorrsjö, P. Talmud, A. Lookene, G. Olivecrona, Apolipoproteins CI and C-III inhibit lipoprotein lipase activity by displacement of the enzyme from lipid droplets, Journal of Biological Chemistry 288(47) (2013) 33997-34008. https://doi.org/10.1074/jbc.M113.495366.[21] M. Miller, J. Rhyne, H. Chen, V. Beach, R. Ericson, K. Luthra, A. Misra, APOC3 promoter polymorphisms C-482T and T-455C are associated with the metabolic syndrome, Archives of medical research 38(4) (2007) 444-451. https://doi.org/10.1016/j.arcmed.2006.10.013.[22] E.D. França, J.G.B. Alves, M.H. Hutz, APOA1/C3/A4 gene cluster variability and lipid levels in Brazilian children, Brazilian journal of medical and biological research 38(4) (2005) 535-541. http://dx.doi.org/10.1590/S0100-879X2005000400006.[23] F. Sentinelli, S. Romeo, C. Maglio, M. Incani, M.A. Burza, F. Scano, M.G. Baroni, Lack of effect of apolipoprotein C3 polymorphisms on indices of liver steatosis, lipid profile and insulin resistance in obese Southern Europeans, Lipids in health and disease 10(1) (2011). http://doi.org/10.1186/1476-511X-10-9.      

The pharmacokinetics of clarithromycin (CLR) conventional tablets (T1/2: 5-7 h) demand 2 or 3 doses per day, which is inconvenient for patients. Therefore, a sustained-release CLR tablet is necessary. Based on Klacid MR tablets (AbbVie) composed of citric acid and sodium alginate (Na-ALG), we developed a 24-hour extended-release CLR tablet. Although citric acid had a significant effect on the CLR release profile, the incompatibility of citric acid and CLR was reported (via FT-IR and stability study). Based on the function of Na-ALG in controlling the release and reducing the incompatibility of citric acid and CLR, a process (CLR and citric acid were granulated separately) was proposed. The final tablet formulation showed 1-month stability and dissolution similarity to standard tablets in pH 6.8 medium (f2 > 50).  

Niacin (nicotinic acid) is a highly water-soluble vitamin, which has been used as a lipid-lowering agent. Sustained release (SR) niacin tablet was  developed in oder to maintain a constant drug concentration for a specific period of time with minimum side effects. In this study, the once daily extended release matrix tablets of niacin using a hydrophilic polymer of HPMC K100M as matrix excipient were prepared by wet granulation method. The results of the dissolution study indicated that the release of the drug was found to be dependent on the proportions of HPMC used in the tablets. The dissolution profile of the optimal formula was similar to that of the predict and attained the requirements of USP 37. The dug incorporated in the matrix released by diffusion and fitted the first order kinetic. Keyword Niacin, sustained release, hydrophilic matrix, HPMC References [1] Bộ Y tế, Dược điển Việt Nam IV, NXB Y học, 2009. [2] Harol E. Bays, Carlos A. Dujovne, (2003), “Comparison of one - daily, Niacin extended-release/ Lovastatin with Standard doses of Atorvastatin and Simvastatin (The advicor Versus othe cholesterol-Modulating Agents Trial Evaluation)”, Am J Cardiol., 91, pp. 667-672.[3] Juergen Siepmann, F. Siepmann (2008), “Mathematical modeling of drug delivery”, International Journal of Pharmaceutics, 364, pp. 328-343.[4] Patel D.N., Ghelani T.K. (2011), “Formulation and evaluation of once daily niacin extended release matrix tablets”, Pharma Science Monitor, 2(4), pp.145-153.[5] Rezowanur Rahman, Sheikh Tasnim Jahan (2010), “Preparation and evaluation of mucoadhesive hydrophilic hydroxy propyl methyl cellulose based extended release matrix tablets of Niacin (Nicotinic acid)”, American Journal of Scientific and Industrial Research, pp. 558-564.[6] Paulo Costa, José Manuel Sousa Lobo (2001), “Modeling and comparison of dissolution profiles”, European Journal of Pharmaceutical Sciences, 13, pp. 123-133.[7] USP 37, pp. 3980-3981.

Rutin is a natural flavonoid that has many effects on human health and beauty. However, rutin has low solubility and bioavailability. Niosomes are drug delivery system that enhance drug permeation of drug through the skin. Aloe is widly used in cosmetic preparations due to its anti-aging, moisturizing and essential skin nutrients. Therefore, the aim of study is preparation of nano niosomes, loaded with rutin and aloe gel extraction (rutin-aloe niosomes) by thin film hydration method. Rutin niosomes was reduced size by ultrasonic method. The size and distribution of vesicles were determined by dynamic light scattering method.  Drug content in niosomal suspension was determined by UV-Vis absorption spectroscopy. The results showed that rutin-aloe niosomes were prepared by thin-film hydration method using Span 60, cholesterol and rutin in molar ratio of 7:3:4 using aloe gel extract as hydration solvent. Mixture of methanol-chloroform (volume ratio 1:1) was used as solvent for solution of membrane companents for evaporation. The manufactured rutin-aloe niosomes had size of about 160 nm, the entrapment efficiency was 95,57% and drug loading was 32,06%. Keywords Rutin, aloe, niosomes, nano, entrapment efficiency, drug loading. References [1] A. Ganeshpurkar, A.K. Saluja, The Pharmacological Potential of Rutin, Saudi pharmaceutical journal 2 (2017) 149-164. https://doi.org/10.1016/j.jsps.2016.04.025.[2] N.B. Mahale, P.D. Thakkar, Niosomes: novel sustained release nonionic stable vesicular systems—an overview, Advances in colloid and interface science 183 (2012) 46-54. https://doi.org/10.1016/j.cis.2012.08.002[3] V.B. Junyaprasert, P. Singhsa, Physicochemical properties and skin permeation of Span 60/Tween 60 niosomes of ellagic acid, International journal of pharmaceutics 2 (2012) 303-311. https://doi.org/10.1016/j.ijpharm.2011.11.032.[4] A. Manosroi, P. Jantrawut et al, In vitro and in vivo skin anti-aging evaluation of gel containing niosomes loaded with a semi-purified fraction containing gallic acid from Terminalia chebula galls, Pharmaceutical biology 11 (2011) 1190-1203.https://doi.org/10.3109/13880209.2011.576347.[5] A. Surjushe, R. Vasani et al, Aloe vera: a short review, Indian journal of dermatology 4 (2008) 163 - 166. https://doi.org/10.4103/0019-5154.44785.[6] M. Takahashi, D. Kitamoto et al, Liposomes encapsulating Aloe vera leaf gel extract significantly enhance proliferation and collagen synthesis in human skin cell lines, Journal of oleo science 12 (2009) 643-650. https://doi.org/ 10.5650/jos.58.643.