Claim Missing Document
Check
Articles

Zinc Administration Affects Bronchial Mucosal NF-κB p105/p50, p-NF-κB p65, IL-8, and IL-1β of Zinc-deficient Rats Reza Gunadi Ranuh; Andy Darma; Alpha Fardah Athiyyah; Ergia Latifolia; Retno Asih Setyoningrum; Boerhan Hidajat; Siti Nurul Hidayati; Anang Endaryanto; Ferry Sandra; Subijanto Marto Sudarmo
The Indonesian Biomedical Journal Vol 12, No 3 (2020)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v12i3.1041

Abstract

BACKGROUND: Risk of acute respiratory infections in children less than 5 years of age is up to 95%. Zinc deficiency is one of the main risk factors. This study aimed to explore the effect of zinc on the bronchial mucosae inflammatory status expressed by nuclear factor (NF)-κB p105/p50, NF-κB p65, interleukin (IL)-8, and IL-1β.METHODS: Twenty-four Wistar rats were divided into 4 groups: normal zinc diet group without zinc supplementation (Z1), normal zinc diet group with zinc supplementation (Z2), zinc deficient diet group without zinc supplementation (Z3), and zinc deficient diet group with zinc supplementation (Z4). NF-κB p105/p50, p-NF-κB p65, IL-8, and IL-1β were measured by immunohistochemical staining.RESULTS: The inflammatory status of bronchial mucosae between Z1 and Z2 groups showed no difference (p=0.055). However, the inflammatory status of bronchial mucosae between Z3 and Z4 groups showed significant difference (p<0.01). Multivariate factorial design showed that zinc supplementation was beneficial when given to zinc deficient diet group with regard to decrease p-NF-κB p65, IL-8 and IL-1β levels (p<0.001) and increase dendritic cell (p=0.022).CONCLUSION: Zinc administration under conditions of zinc deficiency affects the inflammatory status, as shown by the decrease of p-NF-κB p65, IL-8 and IL-1β and the increase of NF-κB p105/p50.KEYWORDS: zinc, NF-κB, p105/p50, p65, IL-8, IL-1β, rat
CAPN10 SNP-19 is Associated with Susceptibility of Type 2 Diabetes Mellitus: A Javanese Case-control Study Yanuarita Tursinawati; Rifqi Fauzan Hakim; Afiana Rohmani; Arum Kartikadewi; Ferry Sandra
The Indonesian Biomedical Journal Vol 12, No 2 (2020)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v12i2.984

Abstract

BACKGROUND: The health data of Central Java, Indonesia showed that diabetes mellitus (DM) was the second most increasing non-communicable disease in the province. More than 20 genes have been reported to be associated with DM. Calpain-10 (CAPN10) polymorphism has been reported to be associated with Type 2 Diabetes Mellitus (T2DM). However, the association between CAPN10 single nucleotide polymorphism (SNP)-19 and T2DM among Javanese ethnics has never been reported. Therefore, this study was conducted to investigate the association.METHODS: After fasting for 8 hours, blood samples were drawn from veins of 107 T2DM and 107 non diabetic subjects. A half of the drawn blood was collected for identification of CAPN10 SNP-19, and another half for measuring triglycerides and fasting blood glucose (FBG). Identification of CAPN10 SNP-19 was performed with polymerase chain reaction (PCR) method, while measurement of triglycerides and FBG with colorimetric enzymatic method.RESULTS: The number of T2DM Javanese subjects with 2R/3R and 3R/3R CAPN10 SNP-19 genotypes was significantly higher than the number of T2DM Javanese subjects with 2R/2R genotype (p=0.002). When each number of 2R/3R and 3R/3R T2DM subjects was compared with the number of 2R/2R T2DM subjects, the number of 2R/3R T2DM subjects was significantly higher than the number of 2R/2R T2DM subjects (p=0.000).CONCLUSION: Javanese subjects with 2R/3R and 3R/3R CAPN10 SNP19 genotypes might have susceptibility of T2DM.KEYWORDS: Calpain-10, CAPN10, polymorphism, type 2 diabetes mellitus, triglycerides, fasting blood glucose
Lactobacillus plantarum IS-20506 Probiotic Restores Galectin-4 and Myosin-1a Expressions in Duodenum, Jejunum and Ileum of Lipopolysaccharide-induced Rats Reza Gunadi Ranuh; Alpha Fardah Athiyyah; Andy Darma; Wibi Riawan; Ingrid Suryanti Surono; Ferry Sandra; Subijanto Marto Sudarmo
The Indonesian Biomedical Journal Vol 12, No 3 (2020)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v12i3.1098

Abstract

BACKGROUND: Galectin-4 and Myosin-1a are important proteins for normal intestinal brush border structure and composition. Damage of these proteins by inflammation may alter digestion, absorption and barrier function. Probiotic has been widely known in maintaining gut health. However, the molecular mechanism of Lactobacillus plantarum IS-2056 probiotic in repairing intestinal brush border is not well defined. Therefore, current study was conducted by investigating the Galectin-4 and Myosin-1a expressions in a rodent model.METHODS: Male Wistar rats were induced with/without lipopolysaccharide (LPS) and treated with/without L. plantarum IS-2056 probiotic. On the seventh day, duodenum, jejunum, and ileum were collected and analyzed with western blot and immunohistochemistry for Galectin-4 and Myosin-1a expressions.RESULTS: Rats administrated with L. plantarum IS-2056 probiotic showed significant increase of Galectin-4 and Myosin-1a expressions in duodenum, jejunum, and ileum compared to the control group (p<0.05). While in control group, Galectin-4 level tended to increase in more distal of intestinal segment and Myosin-1a level tended to decrease in more distal intestinal segment.CONCLUSION: L. plantarum IS-20506 probiotic may facilitate the repairment of damaged intestinal brush border as demonstrated by significant restoration of Galectin-4 and Myosin-1a expressions in duodenum, jejunum, and ileum of LPS-induced rats.KEYWORDS: Lactobacillus plantarum, IS-20506, probiotic, galectin-4, myosin-1a, duodenum, jejunum, ileum
Caffeic Acid Inhibits RANKL and TNFa-induced Osteoclastogenesis by Targeting TAK1-p44/42 MAPK Ferry Sandra; Jennifer Putri; Hilary Limen; Blanca Sarizta
The Indonesian Biomedical Journal Vol 13, No 4 (2021)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v13i4.1593

Abstract

BACKGROUND: The potential of the caffeic acid in other important Receptor Activator Nuclear Factor kB Ligand (RANKL)-Tumor Necrosis Factor (TNF)a-induced osteoclastogenic signaling pathways has not been known. Therefore, the current study was conducted to explore as well as to understand the inhibition potential of caffeic acid.METHODS: RAW264.7 cells were cultured, treated with caffeic acid, RANKL and TNFa. Tartrate Resistant Acid Phosphatase (TRAP) staining was performed to detect TRAP+ osteoclast-like polynuclear cells. To detect the activity of p44/42 Mitogen Activated Protein Kinase (MAPK), Akt, and Transforming Growth Factor-β-activated Kinase (TAK)1, the phosphorylated forms of the proteins were investigated with the immunoblotting assay.RESULTS: Pre-treatment of caffeic acid inhibited the RANKL and TNFa-induced differentiation of RAW264.7 cells into TRAP+ osteoclast-like polynuclear cells. RANKL and TNFa induced phosphorylation of p44/42 MAPK at Thr202/Tyr204, phosphorylation of Akt at both Ser473 and Thr308 and phosphorylation of TAK1 at Ser412. Pre-treatment with caffeic acid prior to the RANKL and TNFa induction, inhibited the phosphorylation of MAPK, and TAK1, but not Akt.CONCLUSION: Caffeic acid might regulate the RANKL-TNFa-induced osteoclastogenic pathway in RAW264.7 by targeting TAK1, which later activation of p44/42 MAPK was abolished.KEYWORDS: caffeic acid, osteoclastogenesis, p44/42, Erk1/2, Akt, TAK1, RAW264.7 
Phosphorylated-Survivin at Ser81 Induced Protein Kinase A (PKA): A Back Loop Ferry Sandra; Roya Khosravi-Far
The Indonesian Biomedical Journal Vol 3, No 2 (2011)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v3i2.145

Abstract

BACKGROUND: Survivin, a bifunctional protein, acts as suppressor of apoptosis and has an essential role in mitosis. Survivin is physically phosphorylated on Thr34, and other important sites such as Thr117, Ser20, Thr48 and Ser81. Our previous report has shown that Ser81 of survivin plays role in cytoprotection. In order to investigate the underlying mechanism, all motifs with medium stringency were scanned. We found that site of survivin at Ser81 was correlated to PKA, which is well reported to many cell signal machineries, including cell survival. Therefore, we focused our current investigation in finding possible correlation and interaction between survivin’s Ser81 site and PKA.METHODS: Wild-type survivin (Survivin), antisense survivin (Survivin-AS), mutated-survivin and mutated-survivin Ser81Ala (Survivin-S81A) were constructed. Each retroviral product was produced. Some cell lysates were prepared and immunoprecipitated. For analysis, we performed immunoblotting and PKA’s activity assays.RESULTS: In our current results, phosphorylated-PKA was correlated with survivin. Infection of survivin could lead to acceleration of PKA’s activity in a viral particle dependent manner. This positive back loop induction by survivin was shown to be correlated to Ser81 site, since survivin-mediated PKA activity was not resulted by mutated form of survivin at Ser81 to nonphosphorylatable Ala (S81A).CONCLUSIONS: Our results suggested a possible back loop of survivin to activate PKA, and Ser81 could be an important site to mediate the survivin-PKA back loop signaling. Survivin-induced activation of PKA might be related to cytoprotection.KEYWORDS: survivin, S81A, L929, PKA
Growth and Osteogenic Differentiation of CD117+ Dental Pulp and Periodontal Ligament Cells Ferry Sandra; Janti Sudiono; Ciptadhi Tri Oka Binartha; Angliana Chouw; Melanie Sadono Djamil
The Indonesian Biomedical Journal Vol 9, No 2 (2017)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v9i2.286

Abstract

BACKGROUND: Dental pulp stem cell (DPSC) and periodontal ligament stem cell (PDLSC) have been suggested as valuable seed cells for bone engineering, suggesting that both stem cells are potential osteogenic sources. Since DPSC and PDLSC seem like to have similar potential in bone formation, we conducted a study to compare morphology, immunophenotype and cell growth of DPSC and PDLSC isolated from the same teeth.METHODS: Human dental pulps and periodontal ligaments were obtained from freshly extracted partial impacted third molar teeth. Collected samples were digested with type I collagenase. Resulted cell suspension was washed and cultured. For biomarker identification, the cells were fixed and bound with anti-fluorescein isothiocyanate (FITC)-cluster of differentiation (CD)117 antibody. For cell growth quantification, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used. Meanwhile for osteogenic differentiation, the cells were cultured in osteogenic medium for 1-3 weeks, fixed and stained with alizarin red.RESULTS: Morphology of dental pulps cell (DPC) and periodontal ligament cell (PDLC) in passage 5 was similar. Clear CD117 green fluorescence of DPC and PDLC in passage 5 was observed. Cell growth rate of PDLC was higher than the one of DPC, 0.3858 and 0.3848 respectively. DPC formed bone nodule on the third week culture in osteogenic medium, while PDLC showed bone nodule formation on the second week culture.CONCLUSION: We suggest that DPC and PDLC are potential seed cells for osteogenic regeneration, since they had cell growth capacity and osteogenic differentiation, particularly PDLC that had faster osteogenic differentiation.KEYWORDS: dental pulp, periodontal ligament, cell, growth, osteogenic differentiation
Measurement of Motor Evoked Potential in Acute Ischemic Stroke: Based on Latency, Amplitude, Central Motoric Conduction Time and Resting Motor Threshold Tugas Ratmono; Andi Wijaya; Cahyono Kaelan; Andi Asadul Islam; Ferry Sandra
The Indonesian Biomedical Journal Vol 8, No 3 (2016)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v8i3.208

Abstract

BACKGROUND: After stroke, there are dynamic changes of motor evoked potential (MEP), including latency, amplitude, central motoric conduction time (CMCT) and resting motor threshold (RMT) in cerebral. However, latency, CMCT, amplitude and RMT have not been clearly shown in acute ischemic stroke patients with motoric function impairment based on Modified Motoric Research Council Scale (MRCs).METHODS: Patients with motoric function impairment after acute ischemic stroke were recruited, scored based on MRCs and grouped. Latency, amplitude, CMCT and RMT (% intensity) was measured using transcranial magnetic stimulation (TMS). Latency, amplitude, CMCT and RMT of subjects based on affected hemisphere (AH) and unaffected hemisphere (UH); stroke onset; and motoric severity; were analyzed and compared statistically.RESULTS: Thirty-seven subjects with complete assessments were selected. Results of MEP size measurement between AH and UH showed that latency, amplitude, CMCT and RMT of AH and UH were significantly different (p<0.05). In accordance to AH and UH results, latency, amplitude, CMCT and RMT of mild, moderate and severe groups based on motoric severity, showed that latency and CMCT were prolonged, RMT was increased, while amplitude was decreased along with severity increment. The amplitude and RMT among the groups were significantly different with p=0.034 and p=0.029, respectively.CONCLUSION: MEP size measurement including latency, amplitude, CMCT and RMT have significant different in AH and UH. In addition, amplitude and RMT were significantly different in MRCs groups, therefore the MEP size measurement could be suggested as prognostic tool.KEYWORDS: MEP, latency, amplitude, CMCT, RMT
Vascular Endothelial Growth Factor Level as A Predictor of Hepatocellular Carcinoma in Liver Cirrhosis Patients Benyamin Lukito; Ivet Suriapranata; Pendrianto Pendrianto; Ali Sulaiman; Irawan Yusuf; FX Budhianto Suhadi; George Mathew; Ferry Sandra
The Indonesian Biomedical Journal Vol 6, No 3 (2014)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v6i3.30

Abstract

BACKGROUND: Alpha-fetoprotein (AFP) has been used for hepatocellular carcinoma (HCC) diagnosis and screening, however, AFP has poor specificity. The extensive hypervascularity associated with HCC could be driven in part by the pro-angiogenic factor known as vascular endothelial growth factor (VEGF). Furthermore, invasiveness of certain HCC lesions has recently been linked to high levels of VEGF. Therefore, circulating VEGF levels of patients with liver cirrhosis (LC) and HCC were investigated and analysed.METHODS: An analytical cross sectional study was designed. Diagnosis of HCC and LC was performed using clinical criteria and findings obtained from B-mode ultrasonography (USG), computed tomography (CT) angiography, or magnetic resonance imaging (MRI). Blood were collected intravenously from all subjects. Obtained serum and plasma were stored in -80°C for following analyses: hepatitis B surface antigen (HBSAg), hepatitis C virus (HCV), alanine aminotransferase (ALT), total bilirubin, albumin, VEGF and AFP.RESULTS: Levels of VEGF and AFP were significantly higher in HCC group compared with LC group with p = 3.05 x 10-6 and p = 8.74 x 10-5, respectively. There was a significant positive correlation (p=0.029, r=0.309) between VEGF level and tumor size in HCC group. The area under curve (AUC) for VEGF level in HCC and LC groups was 0.771. In the level of median 435.6 pg/mL VEGF, the sensitivity was 50% and specificity was 86%. In the level of 199.99 pg/mL VEGF the sensitivity was 74% and specificity was 76%.CONCLUSION: The present findings suggested that VEGF level could be a useful marker for the presence of HCC in patients with LC.KEYWORDS: hepatocellular carcinoma, HCC, liver cirrhosis, LC, vascular endothelial growth factor, VEGF, alpha-fetoprotein, AFP 
Correlation between Homeostatic Model Assessment-estimated Insulin Resistance (HOMA-IR) with Asymmetric Dimethylarginine (ADMA) in Prehypertension Maria Evi Novianti; Syakib Bakri; Mansyur Arif; Ferry Sandra
The Indonesian Biomedical Journal Vol 5, No 3 (2013)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v5i3.67

Abstract

BACKGROUND: Not only hypertension, prehypertension has been reported to be linked with increased cardiovascular morbidity and mortality risks as well. Prehypertension has three-fold hypertension and two-fold cardiovascular risks. Pathomechanism that links hypertension with cardiovascular is related with endothelial dysfunction and insulin resistance. Endothelial dysfunction occurs when nitric oxide (NO) biological function was impaired, whereas shown by asymmetric dimethylarginine (ADMA). Subjects with prehypertension had higher insulin resistance events than normotension, whereas shown by homeostatic model assessment-estimated insulin resistance (HOMA-IR). This research was conducted to investigate the correlation of HOMA-IR with ADMA in prehyper- and normo-tension.METHODS: A cross-sectional comparative research was designed. Subjects were recruited and divided into prehyper- and normo-tensive groups. ADMA was measured using ELISA method, while HOMA-IR was calculated by the ratio of fasting insulin and glucose. Spearman 1-tail and Mann Whitney statistical analyses were performed.RESULTS: Comparing to normotensive group, elevated levels of HOMA-IR and ADMA in prehypertensive group were shown, but not significant. In prehypertensive group, we found significant correlation between HOMA-IR and ADMA.CONCLUSION: Insulin resistance and endothelial dysfunction was elevated in prehyper-compared to normotension.KEYWORDS: prehypertension, insulin resistance, endothelial dysfunction, HOMA-IR, ADMA
Hyaluronic Acid Accelerates VEGF and PDGF Release from Advance Platelet Rich Fibrin in Diabetic Foot Ulcer Ronald Winardi Kartika; Idrus Alwi; Franciscus Dhyanagiri Suyatna; Ferry Sandra; Em Yunir; Sarwono Waspadji; Suzzana Immanuel; Todung Silalahi; Saleha Sungkar; Jusuf Rachmat; Saptawati Bardosono; Mirta Hediyati Reksodiputro
The Indonesian Biomedical Journal Vol 13, No 3 (2021)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v13i3.1523

Abstract

BACKGROUND: Hyaluronic acid (HA) is an essential component of extracellular matrix and mediates signaling in wound healing. HA could induce growth factor release from Advanced Platelet Rich Fibrin (A-PRF), including Vascular Endothelial Growth Factor (VEGF) and Platelet-derived Growth Factor (PDGF). However, concentrations of the released-VEGF and PDGF have not been clearly disclosed. Therefore, current study was conducted to measure the release of these growth factors in HA + A-PRF gel of diabetic foot ulcer (DFU) subjects.METHODS: Twenty DFU subjects were included in the study and treated with A-PRF or HA+A-PRF. A-PRF was derived from autologous peripheral blood and processed with low-speed centrifugation. HA was added with a ratio of 1:0.6. A-PRF or HA + A-PRF was applied topically on DFU. Upper tips of A-PRF or HA + A-PRF gels were collected on day 0, 3 and 7 for measurements of VEGF and PDGF concentrations with Enzyme-linked Immune-sorbent Assay (ELISA) methods.RESULTS: On day-3, both VEGF and PDGF concentrations of HA + A-PRF group were significantly higher than the VEGF (p=0.000) and PDGF (p=0.019) concentrations of A-PRF group. The VEGF and PDGF concentrations were continuously and significantly increased on day-7 of HA + A-PRF group, compared to the VEGF (p=0.000) and PDGF (p=0.004) concentrations of A-PRF group.CONCLUSION: Combination HA+A-PRF induces VEGF and PDGF release from A-PRF. A mixture of A-PRF and HA could be more effective than A-PRF alone for treatment of DFU.KEYWORDS: hyaluronic acid, advanced platelet rich fibrin, PRF, growth factor, VEGF, PDGF, diabetic foot ulcer
Co-Authors Abdul Gani Soulisa Abdul Gani Soulisa Achmad Guntur Hermawan Suryo Adji Achmad Kemal Harzif Addin Trirahmanto Ade Prijanti Dwisaptarini Adriana Todingrante Afiana Rohmani Ahmad Dian Wahyudiono Ahmad Kurnia Ahmad R. Utomo Ahmad R. Utomo Aida Fitri Nazillah Al Mazida Fauzil Aishaqeena Alfred Pakpahan, Alfred Ali Sulaiman Alida Roswita Harahap Alpha Fardah Athiyyah Amalia Isnaeni, Nur Amelia Astriani Putri Aminuddin Aminuddin Amirudin Eso Anang Endaryanto Andayani, Lia H. Andi Asadul Islam Andi Wijaya Andi Wijaya Andon Hestiantoro Andri Sutanto Andrian Nova Fitri Andrijono Andrijono Andy Darma Andy Wirahadikusumah Anggraeni, Rezky Angliana Chouw Angliana Chouw Angliana Chouw Angliana Chouw Ani Retno Prijanti Anie Apriani Anna Fuji Rahimah Annisa Amalia Annisa Putri Ariyani Annistri, Savrinda Anwar Santoso Aprisia, Kartika Dwi Ardian Rizal Aria Kekalih Arief Boediono Ariesanti, Yessy Arif Kurniawan Arif Santoso Arif Satria Arimaswti Arimaswati Ariyani, Annisa Putri Armelia Sari Arum Kartikadewi Arya Nur Ihsan Aryani Hayuningtyas, Ria Aryu Candra Asmarinah Asmarinah Ayasha Hajjar Audreyandra Wahid Ayu Rahadiyanti Ayunita Tri Wirattami Aznan Lelo Bambang Sutrisna Bambang Sutrisna Bastian Nova Benyamin Lukito Bethy Suryawathy Hernowo Bianda Claresta Bianda Claresta Blanca Sarizta Boedi Oetomo Roeslan, Boedi Oetomo Boenjamin Setiawan Britanto Dani Wicaksono Budi Utomo Budiono, Bernardus Parish Bukhari, Agussalim Caecilia Caroline Aliwarga Caesary Cloudya P Caesary Cloudya Panjaitan Cahyono Kaelan Camy F. Surjadi Caroline T. Sardjono Caroline Tan Sardjono Caroline Tan Sardjono Chandra Risdian Chandra Risdian Chantika Amardhia Paramita Putri Ciptadhi Tri Oka Binartha Ciptadhi Tri Oka, Ciptadhi Tri Cloudya P, Caesary Cloudya Panjaitan, Caesary Dea Jane Sungkono Denni Joko Purwanto Devi Nisa Hidayati Deviyanti Pratiwi Dewi Liliany Margaretta, Dewi Liliany Dewi Lilyani Margaretha Dewi Ranggaini Dewi, Dian Andriani Ratna Dhaniar, Afifah Yumna dharma Lindarto, dharma Diah Savitri Ernawati Dian R Laksmitawati Dian Ratih Laksmitawati Diana Nur Afifah, Diana Nur Dina Keumala Sari Djanggan Sargowo Djanggan Sargowo Djanggan Sargowo Djanggan Sargowo Djoko Wahono Soeatmadji Dominica Dian Saraswati Sumantri Dwi Davidson Rihibiha Dwifulqi, Hernindya Edi Handoko Eka Seftiana Indahsari Elina Ardiani Sidharta Elisabeth Pricilia Sunata Elline, Elline Ellyza Nasrul Elvita Rahmi Daulay Em Yunir, Em Enny Probosari Enos Tangke Arung, Enos Tangke Ergia Latifolia Eriawan Agung Nugroho, Eriawan Agung Erizal Sugiono Erlina Sih Mahanani, Erlina Sih Ervi Afifah Fahriza Abid Sonia Farhat, Farhat Farid Sastra Nagara Farid Sastra Nagara, Farid Sastra Fatmawati Fatmawati Fauzia Purnamasari Febriyeni, Febriyeni Felix Wong Fibryanto, Eko Fillah Fithra Dieny Fitriasih Fitriasih Fitriyadi Kusuma Franciscus D. Suyatna Frans D. Suyatna Frisca Frisca FX Budhianto Suhadi George Mathew Gita Pratama Gwendy Aniko Hadrian, Gary Halim, Johni HANA RATNAWATI Hariyono Winarto Harry Akza Putrawan Harry Murti Harryanto Wijaya Harryanto Wijaya Hartono, Tiffany Harun Iskandar Hayatun Nufus Hayuningtyas, Ria A. Hayuningtyas, Ria Aryani Hendradi Surjotomo Hendy Setyo Yudhanto Heri Wibowo Herqutanto Herqutanto Hidajat, Boerhan Hilary Limen Huda Shalahudin Darusman I Gusti Made Reza Gunadi Ranuh I Putu Sudayasa Ibnu Suryatmojo Ichwan, Solachuddin Jauhari Arief Ida Parwati Idrus Alwi Ihsan Rizal, Muhammad Ikhsan Nur Arifin Ilham Jaya Patellongi Ilhamjaya Patellongi Indra Bachtiar Indradewa, Rhian Indrayadi Gunardi Indriyanti Rafi Sukmawati Indriyanti Rafi Sukmawati Ingrid Suryanti Surono Intan Masyfufah Hanim Irawan Yusuf Irawan Yusuf Irianiwati Widodo Irvan Septrian S P R Irvanyuni Japutri Ivet Suriapranata Jackson Jackson, Jackson James Handojo Jamhari Jamhari Janti Sudiono Janti Sudiono Janti Sudiono Janti Sudiono Janti Sudiono Jasmine Shafira Jasmine Shafira, Jasmine Jeanne A. Pawitan Jeanne A. Pawitan Jenifer Christy Hadimartana Jennifer Putri Jessica Nathalia Chandra Jessica Nathalia Chandra, Jessica Nathalia Joceline Setiawan Johan Arief Budiman Juliani Hardja Buntara, Magdalena Juminten Saimin Junita Briskila Jusak Nugraha Jusuf Rachmat Karina Febriani Hudono Karyono Mintaroem Kent Wijaya Setiawan Ketherin Ketherin Ketherin Ketherin Ketherin Ketherin Ketherin, Ketherin Khairun Nisa Kharima Abdullah Kharima Abdullah, Kharima Khilmi Ainun Nadliroh Kirana, Farenza Okta Komariah Komariah Komariah Komariah Komariah Komariah Kusuma, Yohanna Laifa Annisa Hendarmin Laila Nuranna Lee, Kyung H. Lee, Kyung Hoon Lelyana, Shelly Leo Alberto Porjo Lia Hapsari Andayani Lidya Imelda Laksmi Linda Lison Linda Sari Sembiring Livia Alvita Liza Meutia Sari Louise Anastasya Luki Astuti Luthfiatul Khusna M Novo P Lubis Maesaroh Maesaroh Makmun, Armanto Mansyur Arif Mansyur Arif Marcellus Simadibrata Maria Celinna Maria Celinna Maria Evi Novianti Maria Verena Emeralda Marshel Tendean Marshel Tendean MARTHA ARDIARIA Maulanisa, Sinta C. Maurin Merlina Meita Hendrianingtyas Melanie S Djamil Melanie Sadono Djamil Melanie Sadono Djamil Melanie Sadono Djamil Melanie Sadono Djamil, Melanie Sadono Melina Setiawan Melinia Melinia Meta Ariyani Sidharta Meta Ariyani Sidharta, Meta Ariyani Mirta Hediyati Reksodiputro Mohammad Aris Widodo Mohammad Aris Widodo Mohammad Sadikin Mohammad Sadikin Monica Andajana Muhamad Rizki Fadlan Muhammad Diah Muhammad Hamdan Muhammad Ihsan Rizal, Muhammad Ihsan Muhammad Novo Perwira Lubis Muharam, Muharam Muharam, Raden Mulyawati, Sufiah Asri MUTMAINNAH, FITRI Nadhia Sari Afiana Nadhia Sari Afiana, Nadhia Sari Nadiah, Najla Nadya Saputri Halim Najla Nadiah Naliani, Silvia Nani Maharani Nanik Setjowati Nasrul Zubir Neni Susilaningsih Nenni Pratiwi Nova Adrian Noviasti Rahma Utami Novriansyah, Robin Nur Ahmad Tabri Nur Indah Purnamasari Nur Zam Zam Nuralifah Nuralifah, Nuralifah Nurani Hayati Nuri Dyah Indrasari Nurjannah Lihawa Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi, Nurrani Mustika Nurul Fauziah Nyoman Suci Widiastiti Oetomo Roeslan, Boedi Olivia Nauli Komala P Lubis, M Novo Pande Putu Erawijantari Pang, Tiffany Parawansah Parawansah Pendrianto Pendrianto Peter Kabo Peter Sugita Pieri Kumaladewi Prasetya, David Eka Pratitis, Visi Endah Primariadewi Rustamadji Primariadewi Rustamadji Pudji Rahajoe Pudji Rahaju Pukovisa Prawiroharjo, Pukovisa Putri Y Suyanto Putri Y Suyanto, Putri Y Putri, Indah Aprianti Quan Yong Tang Rachma Purwanti Rafika Indah Paramita Rahmawati Rahmawati Rahmawati, Dicha Yuliadewi Rahmi Amtha Rahmi Amtha Rahmi Annisa Ramadhan Karsono Ramadhan Ramadhan Rambu Beppy Hamuaty Rambu Beppy Hamuaty, Rambu Beppy Ranggaini, Dewi Ratna Akbari Ganie Respati, Danendra Rakha Putra Retno Asih Setyoningrum Reynaldo Lambertus Rifqi Fauzan Hakim Riko Nofrizal Rio Auricknaga Kintono Riris L. Puspitasari Riris L. Puspitasari Rita Lahirin Rita Lahirin, Rita Ritawaty Ritawaty Rizal Rizal Rizkia Milladina Hidayatulloh Roihatul Mutiah Ronald Winardi Kartika Rosalina Tjandrawinata Roya Khosravi-Far Roya Khosravi-Far Ryco Giftyan Ardika Saleha Sungkar Saptawati Bardosono Saraswati, Jaya Sari, Armelia Sarwono Waspadji Scania, Alifah Evi Seila Arumwardana Septrian S P R, Irvan Setiawan, Kent Wijaya Siti Mega Komariyah SITI NURUL HIDAYATI Soehartono Soehartono Solachuddin Jauhari Arief Ichwan Sonar Soni Panigoro Soulisa, Abdul Gani Soulissa, Abdul G. Sri Mutya Sekarutami Stefani, Rosita Steffi Kurniawan Steward Hadi Steward Steward Sudarmo, Subijanto Marto Suhendro Suhendro Sukartini, Ninik Susi Tjahyani Susy Tjahyani Suzzana Immanuel Syafiqa Amelia, Dinda Syafira Noor Pratiwi Syakib Bakri Syanindita Puspa Wardhani Syarifin, Andi Noor Kholidha Tadahiko Iijima Tadahiko Iijima Taramalinda, Elizabeth Yuliani Taslim, Nurpudji Astuti Tatsushi Muta Teguh Santoso Teguh, Sharren Timotius Andi Kadrianto Tjandra, Kevin Christian Tjandrawati Mozef Tjandrawati Mozef Tjandrawati Mozef Todung Silalahi Toshio Kukita Toshio Kukita Trijani Suwandi Trisfilha, Pretty Tugas Ratmono Tulandi, Togas Uleng Bahrun Victor Reiner Sutanto, Aldrich Virgi Saputra Wa Ode Siti Rahayu Fathanah WAHYU WIDOWATI Wahyu Widowati Wahyu Widowati Wahyu Widowati Wibi Riawan Widiastiti, Nyoman Suci Widya Wulandari Widyastuti, Wiena Wiena Widyastuti Wijaya, Haryanto William Yusuf, Timotius Winarko Luminturahardjo Wirsma Arif Harahap Yanni Dirgantara Yanni Dirgantara Yanni Dirgantara Yanuarita Tursinawati Yefta Moenadjat Yenti Purnamasari Yohanna Feter Yohanna Feter, Yohanna Yora Nindita Yudi Her Oktaviono, Yudi Her Yuliani Taramalinda, Elizabeth Yusra Yusra Yusrina Lukitasari Yuyus Kusnadi Zulfikar Lubis Zulfikri Muhktar