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All Journal e-GIGI Prosiding Seminar Biologi Indonesian Journal of Cancer Chemoprevention Journal of Mathematical and Fundamental Sciences Indonesian Journal of Cancer Dental Journal (Majalah Kedokteran Gigi) The Indonesian Biomedical Journal Padjadjaran Journal of Dentistry Molecular and Cellular Biomedical Sciences (MCBS) Jurnal Kreativitas PKM SONDE (Sound of Dentistry) Jurnal Muara Sains, Teknologi, Kedokteran dan Ilmu Kesehatan Indonesian Journal of Clinical Pathology and Medical Laboratory (IJCPML) Poltekita: Jurnal Pengabdian Masyarakat ABDI MOESTOPO: Jurnal Pengabdian pada Masyarakat Narra J Proceeding Biology Education Conference Indonesian Journal of Cancer Jurnal Kedokteran Gigi Terpadu JURNAL ABDI MASYARAKAT INDONESIA (JAMIN) Jurnal Abdimas Kesehatan Terpadu
Ferry Sandra
Department Of Biochemistry And Molecular Biology, Division Of Oral Biology, Faculty Of Dentistry, Universitas Trisakti
Agriculture, Biological Sciences & Forestry Humanities Astronomy Biochemistry, Genetics & Molecular Biology Chemistry Civil Engineering, Building, Construction & Architecture Computer Science & IT Dentistry Earth & Planetary Sciences Education Energy Engineering Environmental Science Health Professions Immunology & microbiology Materials Science & Nanotechnology Mathematics Medicine & Pharmacology Neuroscience Nursing Physics Public Health Other

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Journal : The Indonesian Biomedical Journal

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Ser81 Survivin Induced Protein Kinase A (PKA)-dependent Phosphatidylinositol 3-kinase (PI3K) Activity Ferry Sandra; Roya Khosravi-Far
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.v6i3.28

Abstract

BACKGROUND: Our previous report showed that phosphorylated-survivin at Ser81 induces survivin back loop to activate protein kinase A (PKA) in the cytoprotection mechanism. Activated PKA could possibly induce the cytoprotection via Phosphatydilinositol 3-kinase (PI3K). Therefore our current study was conducted to investigate the possibility of survivin-PKA-PI3K signaling pathway.METHODS: Viral productions by BOSC23 cells of Survivin, Antisense Survivin (Survivin-AS) and Ser81Ala mutant (Survivin-S81A) in pMSCV-IRES-GFP vector with cytomegalovirus (CMV) promoter were conducted. L929 cells were pretreated with/without PKI 6-22 amide and infected with viral particle of Survivin, Survivin-AS, Survivin-S81A or vector only. Cells were harvested, lysed and immunoprecipitated with anti-PI3K (p85) antibody and immunoblotted to detect PI3K (p85) and phospho-(Tyr) p85 PI3K. To confirm PI3K activation, PI3K Activity Assay was conducted by using phosphoinositide fraction containing PtdIns(4,5)P2 and [32P]ATP.RESULTS: Immunoblot and PI3K activity results showed similar results. Upon infection of virus with survivin, a markedly increased level of tyrosine phosphorylation of p85 PI3K or PI3K activity in L929 cells was seen. Low levels of tyrosine phosphorylation of p85 PI3K or PI3K activity were observed for Survivin-AS and Survivin-S81A-viral-infected L929 cells. With higher concentrations of Survivin-viral-infection, levels of tyrosine phosphorylation of p85 PI3K or PI3K activity in L929 cells were gradually increased. However, when L929 cells were pretreated with PKI 6-22 amide, prior to Survivin-viral-infection, level of tyrosine phosphorylation level of p85 PI3K or PI3K activity was detected much lower.CONCLUSION: Our result suggest that Ser81 Survivin play role in inducing PI3K activation and the Survivin-PI3K signaling pathway was PKA-dependent.KEYWORDS: Ser81, Survivin, PKA, PI3K, L929
Combination of Fibrinogen and High-sensitivity C-reactive Protein Measurements is Potential in Identification of Acute Coronary Syndrome Djanggan Sargowo; Ferry Sandra
The Indonesian Biomedical Journal Vol 7, No 1 (2015)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v7i1.19

Abstract

BACKGROUND: Acute myocardial infarction (AMI) is one of cardiovascular diseases with high morbidity and mortality rates. Novel biomarkers that can detect accurately acute coronary syndrome (ACS) at early stage, are necessary to improve current strategies and/or to identify subjects who are at risk. Fibrinogen and high-sensitivity C-reactive protein (hs-CRP) roles in inflammation process could be potential for ACS early detection. This study was conducted to evaluate measurements of fibrinogen and hs-CRP on ACS.METHODS: An analytic observational study with cross sectional approach was conducted on patients with Troponin I positive. After signing informed consent, anamnesis and complete blood count were conducted. Besides that, liver function, renal function, and blood glucose tests were conducted as well. Samples of selected subjects were quantified with enzyme-linked immunosorbent assay (ELISA) for Troponin I, fibrinogen and hs-CRP. Then statistical analyses were performed.RESULTS: There were 76 subjects in each ACS and non-ACS groups. ACS group showed significant higher levels of both fibrinogen and hs-CRP compared to Non-ACS group (p=0.000). Among evaluated risk factors, diabetes mellitus (DM) (p=0.003) and hypertension (p=0.000) were significantly higher in ACS group than in non-ACS group. Among evaluated clinical factors, blood glucose (p=0.001) and age (p=0.000) were significantly higher in ACS group than in non-ACS group. Combination of fibrinogen and hs-CRP measurements showed the highest sensitivity (75.00%), specificity (80.26%), accuracy (77.63%), positive predictive value (79.19%) and negative predictive value (76.25%).CONCLUSION: Since fibrinogen and hs-CRP were increased in ACS group and combination of fibrinogen and hs-CRP measurements showed the highest sensitivity, specificity, accuracy, positive predictive value and negative predictive value, we suggest that combination of fibrinogen and hs-CRP measurements could give added value to identify ACS.KEYWORDS: fibrinogen, hs-CRP, biomarker, ACS, acute coronary syndrome, atherosclerosis, inflammation
Conditioned Media of Human Umbilical Cord Blood Mesenchymal Stem Cell-derived Secretome Induced Apoptosis and Inhibited Growth of HeLa Cells Ferry Sandra; Janti Sudiono; Elina Ardiani Sidharta; Elisabeth Pricilia Sunata; Dea Jane Sungkono; Yanni Dirgantara; Angliana Chouw
The Indonesian Biomedical Journal Vol 6, No 1 (2014)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v6i1.44

Abstract

BACKGROUND: Secreted factors contained in conditioned media (CM) of human umbilical cord blood mesenchymal stem cells (hUCB-MSCs) known as secretome, was suspected to have important roles in regulating cells. This study was conducted to investigate the role of CM-hUCB-MSCs-derived secretome in apoptosis and growth of HeLa cells.METHODS: HeLa cells were treated with secretome in various concentrations (0, 0.2, 2 and 20%) for 24 and 48 hours. Trypan blue exclusion assay was performed to detect cell viability. Meanwhile sub-G1 apoptotic assay was performed to detect apoptotic cells. The transition of mitochondrial transmembrane potential (TMP), which occurs in the apoptotic process, was analyzed by mitochondrial membrane potential (ΔΨM) assay. Both sub-G1 and ΔΨM assays were performed using FACSCanto flow cytometer. Statistical analyses were conducted using IBM SPSS Statistics to detect significance level at p<0.05.RESULTS: Secretome significantly induced cell death starting at concentration of 0.2% within a 24-hour period (p<0.05). Secretome significantly induced cell death in concentration and time dependent manner (p<0.05). The cell death was then confirmed as apoptosis through sub-G1 analysis. Due to the underlying apoptotic mechanism, we found distinct decrease of TMP, indicating an increase in mitochondrial membrane permeability of HeLa cells. In addition, we found that HeLa cell growth was inhibited partially by secretome.CONCLUSION: Taken together, we conclude that CMhUCB-MSCs-derived secretome significantly induced apoptosis of HeLa cells in a concentration and time dependent manner through mitochondrial apoptotic pathway. The secretome might also play important role in inhibiting HeLa cell growth.KEYWORDS: umbilical cord blood, mesenchymal stem cell, secretome, apoptosis, growth, cancer
Brucea javanica Leaf Extract Activates Caspase-9 and Caspase-3 of Mitochondrial Apoptotic Pathway in Human Oral Squamous Cell Carcinoma Muhammad Ihsan Rizal; Ferry Sandra
The Indonesian Biomedical Journal Vol 8, No 1 (2016)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v8i1.198

Abstract

BACKGROUND: We previously reported Brucea javanica leaf extract (BJLE) induced apoptosis in human oral squamous cell carcinoma (HSC2) cells by attenuation of mitochondrial membrane permeability. However, further underlying mechanism is not known yet. Therefore, we conducted a study to investigate activation of Caspases related to attenuation of mitochondrial membrane permeability in BJLE-treated human oral squamous cell carcinoma.METHODS: B. javanica leaves were collected, identified, minced, dried, extracted with distilled ethanol at room temperature for 24 hours, filtered and evaporated. Resulted BJLE was stored at 4°C. HSC-2 and HSC-3 cells were fasted for 12 hours and treated with BJLE in various concentrations for 24 hours. Treated HSC-2 and HSC-3 cells were lysed and subjected to western blot, to detect cleaved-Caspase-9, cleaved-Caspase-3 and β-actin. All visualized bands were captured and quantified.RESULTS: Low numbers and morphological alterations of adherent HSC-2 and HSC-3 cells were observed in the group of cells treated with 500, 100 and 10 μg/mL BJLE. Numbers of adherent HSC-2 and HSC-3 cells treated with BJLE were shown decreased along with the increase of BJLE concentrations. Meanwhile, numbers of floating HSC-2 and HSC-3 cells were increased. Bands of cleaved-Caspase-9 and cleaved-Caspase-3 were observed in HSC-2 and HSC-3 cells treated with 500 and 100 μg/mL BJLE. Higher-density bands of cleaved-Caspase-9 and cleaved-Caspase-3 were observed in HSC-2 and HSC-3 cells treated with 500 μg/mL BJLE than 100 μg/mL BJLE. CONCLUSION: BJLE could induce apoptosis by activation of Caspase 9 and Caspase 3 of mitochondrial apoptotic pathway in human oral squamous cell carcinoma. KEYWORDS: Brucea javanica, leaf, apoptosis, HSC-2, HSC-3, Caspase 9, Caspase 3
Proliferation of Peripheral Blood-derived Endothelial Progenitor Cells from Stable Angina Subjects Yudi Her Oktaviono; Djanggan Sargowo; Mohammad Aris Widodo; Yanni Dirgantara; Angliana Chouw; Ferry Sandra
The Indonesian Biomedical Journal Vol 6, No 2 (2014)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v6i2.34

Abstract

BACKGROUND: A population of circulating Endothelial Progenitor Cells (EPCs) has been reported to play important role in maintaining endothelial function and integrity. Since EPCs culture is crucial and an optimized medium is currently available. Therefore we conducted a study to investigate whether stable angina subjects peripheral blood-derived EPCs could be cultured in this medium. Here, we performed study to detect EPCs characteristics and extracellular signalregulated kinase (Erk)1/2 Mitogen-Activated Protein Kinase (MAPK) pathway as possible underlying pathway for EPCs proliferation.METHODS: Peripheral blood EPCs from 8 stable angina subjects were cultured in an optimized medium with/without addition of supplement for 1 or 3 days. Then, the membrane of cultured EPCs were detected with immunofluorescence method for CD34, Vascular Endothelial Growth Factor Receptor 2 (VEGFR-2) and CD133. Colony forming unit (CFU) enumeration was performed. XTT Cell proliferation assay was performed to assess EPCs growth after 1 and 3-days culture. The western blot analysis was performed to detect possible activation of Erk1/2 MAPK.RESULTS: Number of EPCs and CFU cultured for 3 days were significantly higher than the ones cultured for 1 day (p=0.012). EPCs membrane markers from stable angina subjects were detected as well as CFUs were formed. There were significant increase of EPCs number, CFUs number and phosphorylated-Erk2 amount when the groups with and without supplement were compared (p<0.05). Meanwhile U0126, a MAPK Erk1/2 (MEK1/2) inhibitor, significantly inhibited the supplement-induced EPCs number, CFUs number and phosphorylated-Erk2 amount (p<0.05).CONCLUSION: Our results showed that ERK2 MAPK signaling pathway might play an important role in supplement-induced peripheral blood EPCs proliferation in subjects with stable angina.KEYWORDS: endothelial progenitor cell, EPC, p42, Erk2, proliferation
A Pilot Study on Immunohistochemical Expressions of NF-ĸB, Cyclin-D1, VEGF, and Cox-2 in Advanced Stage Laryngeal Carcinoma Pudji Rahaju; Ayunita Tri Wirattami; Ferry Sandra; Steffi Kurniawan; Khairun Nisa; Soehartono Soehartono; Edi Handoko; Ahmad Dian Wahyudiono; Hendradi Surjotomo; Hendy Setyo Yudhanto; Nanik Setjowati
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.v13i4.1580

Abstract

BACKGROUND: Progression of laryngeal carcinoma can be classified with the clinical staging, however there are different patterns of progressions observed in the patient with the same clinical stage which also affects their prognoses. Therefore biomarkers should be used. Nuclear factor (NF)-ĸB, Cyclin-D1, vascular endothelial growth factor (VEGF), cyclooxygenase (Cox)-2 have been reported for laryngeal carcinoma. However, it is still unclear how these markers are expressed and correlated in advanced stage laryngeal carcinoma. Therefore current study was conducted to investigate the expressions of NF-ĸB, Cyclin-D1, VEGF and Cox-2 and their correlations in advanced stage laryngeal carcinoma.METHODS: Subjects were recruited and laryngeal biopsies were collected, fixed in formalin and prepared for immunohistochemistry. The immunohistochemistry was performed using mouse monoclonal anti-NF-kB p65, anti-Cyclin-D12 anti-VEGF, and anti-Cox-2 antibodies. The immunohistochemistry results were documented and measured using ImmunoRatio. Pearson or Spearman correlation test was used based on the results of Shapiro-Wilk test of normality. A p-value of less than 0.05 is considered statistically significant.RESULTS: Twelve male subjects were included in this study. Expressions of NF-ĸB, Cyclin-D1, VEGF dan Cox-2 were clearly observed. Mean of NF-ĸB, Cyclin-D1, VEGF dan Cox-2 IHC expression levels measured with ImmunoRatio were 57.50±20.06%, 45.00±24.31%, 43.33±17.23% and 40.42±16.98%, respectively. There was significant correlation between the expressions of VEGF dan Cox-2 (p=0.031, r=0.622).CONCLUSION: Since correlation between the VEGF and Cox-2 expressions was statistically significant, VEGF and Cox-2 might have important roles in the growth, invasion and metastasis of laryngeal carcinoma.KEYWORDS: advanced stage laryngeal carcinoma, immunohistochemistry, NF-ĸB, Cyclin-D1, VEGF, Cox-2
Targeting Ameloblatoma into Apoptosis Ferry Sandra
The Indonesian Biomedical Journal Vol 10, No 1 (2018)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v10i1.354

Abstract

BACKGROUND: Generally ameloblastoma is a locally aggressive, slow growing, non-metastatic epithelial odontogenic benign tumor. However, rarely some ameloblastoma can metastasize in spite of a benign histologic appearance. Targeting ameloblastoma by inducing it into apoptosis could be a beneficial strategy, since many ameloblastoma cases were reported recurrent after surgical therapy.CONTENT: To investigate ameloblastoma in cellular aspect,cytological pattern of ameloblastoma was divided intoouter layer/peripheral and inner layer/central cells. Tumor necrosis factor (TNF)-α, Fas ligand (FasL), TNF receptor (TNFR)1/death receptor (DR)1, TNFR2/DR2, DR4, DR5andFas were highly expressed in central than peripheral cells. Despite inducing apoptosis, TNF-α can induce PI3K leading to Akt and p44/42 mitogen-activated protein kinases (MAPK) activation in AM-1 cells, which later induce cell survival and proliferation. Therefore apoptotic induction in ameloblastoma should be suggested in higher TNF-α concentration. Expression of FasL and Fas are closely associated with squamous metaplasia and  granular transformation of the tumor cells, suggesting that apoptosis induced by FasL may play a role in the terminally differentiated or degenerative ameloblastoma cells. TNF-related apoptosis-inducing ligand (TRAIL) has emerged as an apoptotic inducing anticancer agent in tumor cells specifically. TRAIL induced activation of caspases, lowering mitochondrial membrane potential, high number of apoptotic cells in ameloblastoma cells. Therefore, TRAIL could be a potential agent for targeting ameloblastoma, although further study should be explored.SUMMARY: Targeting ameloblastoma by inducing it into apoptosis could be achieved effectively, although some criteria should be considered. Therefore understanding the underlying apoptosis signaling pathways are necessary for inducing ameloblasotma into apoptosis. Investigations on other apoptosis-related molecules, potential apoptosis-inducing natural products, and novel approach in reprogramming, are important in the future for a better anagement of ameloblastoma.KEYWORDS: ameloblastoma, apoptosis, TNF, Fas, TRAIL, Akt, MAPK, caspase
Ganoderma lucidum Polysaccharide Peptide Reduce Inflammation and Oxidative Stress in Patient with Atrial Fibrillation Ardian Rizal; Ferry Sandra; Muhamad Rizki Fadlan; Djanggan Sargowo
The Indonesian Biomedical Journal Vol 12, No 4 (2020)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v12i4.1244

Abstract

BACKGROUND: Atrial fibrillation (AF) could be triggered by inflammation and oxidative stress. Ganoderma lucidum has an active substance in the form of β-glucan that can reduce inflammatory process and oxidative stress in rats. The objective of this study was to evaluate the effect of Ganoderma lucidum polysaccharide peptide (GLPP) in paroxysmal AF subjects with parameters of anti-inflammatory antioxidant, electrocardiography and health-related quality of life (HRQoL).METHODS: A randomized closed-label clinical trial with pre- and post-test design was conducted. After AF subjects selection, the subjects were randomized, interviewed and veni-punctured to isolate blood plasma. AF Subjects were then treated with placebo or GLPP for 90 days. Post-test blood plasma was collected on the following day after the 90th day. Then anti-inflammatory and antioxidant parameters were measured. After that, echocardiographic and HRQoL assessments were performed.RESULTS: A total of 38 subjects, 11 males and 27 females, completed the study with no significant changes in diets, physical activities, or medications. Comparing to control, the 90-days GLPP-treated subject characteristics were significant difference in systolic blood pressure, heart rate, malondialdehyde, high-sensitivity C-reactive protein, tumor necrosis factor-a, interleukin (IL)-1b, IL-6, primary (P)-wave dispersion, P-max, physical functioning, limitation to physical health, energy/fatigue, pain, and physical limitation.CONCLUSION: GLPP has several potential effects in AF subjects, including anti-inflammatory, antioxidant, and atrial remodelling, so that HRQoL of AF subjects could be improved. Hence, GLPP could suggested as a potential supplementing agent for AF management.KEYWORDS: atrial fibrillation, Ganoderma lucidum, inflammation, antioxidant, atrial remodelling, quality of life
N-Cadherin as An Important Marker in Colorectal Cancer: An investigation of b-Catenin and Cadherin Expressions of SW-480 and HCT-116 Cell Lines Winarko Luminturahardjo; Djoko Wahono Soeatmadji; Karyono Mintaroem; Pudji Rahajoe; Ferry Sandra
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.v13i3.1562

Abstract

BACKGROUND: The absence of potential biomarkers to detect the metastatic process at an early stage will consequently delay colorectal cancer (CRC) treatment. Some biomarkers including β-Catenin, E-Cadherin and N-Cadherin have been suggested as potential markers. However, there were opposite reports regarding expressions of these markers. Therefore, current study was conducted using CRC cell lines for early stage (SW-480 cells) and late stage (HCT-116 cells) of CRC.METHODS: SW-480 and HCT-116 cells were cultured and seeded on coverslip glasses for immunofluorescence staining to detect β-Catenin, E-cadherin, and N-cadherin. Expressions of β-Catenin, E-cadherin, and N-cadherin were observed and documented under a fluorescent microscope and analyzed with Image J software. Measured results were then statistically analyzed. RESULTS: All β-catenin, E-Cadherin and N-Cadherin expressions were observed in SW-480 and HCT-116 cells. β-catenin MFI averages of SW-480 (47.157±3.479) and HCT-116 (47.240±4.107) cells were similar. E-Cadherin MFI average of SW-480 cells (45.104±4.107) was higher than the one of HCT-116 cells (40.191±3.702). N-Cadherin MFI average of HCT-116 cells (43.702±8.219) was significantly higher (p=0.009) than the one of SW-480 cells (72.506±5.297).CONCLUSION: Taken together, N-Cadherin could be suggested as an important metastasis marker in CRC since the N-Cadherin expression was significantly higher in HCT-116 cells as the late-stage CRC model than SW-480 as the early-stage of CRC model. Further research is still needed by comparing several biomarkers from various clinical samples at all clinical stages of CRC.KEYWORDS: CRC, β-Catenin, E-Cadherin, N-Cadherin, Metastasis, Biomarker
Study of Low-grade Chronic Inflammatory Markers in Men with Central Obesity: Cathepsin S was Correlated with Waist Circumference Adriana Todingrante; Mansyur Arif; Uleng Bahrun; Ferry Sandra
The Indonesian Biomedical Journal Vol 5, No 2 (2013)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v5i2.60

Abstract

BACKGROUND: There is a prevalence increase of overweight and obesity in Indonesia. Central obesity can lead a variety of chronic diseases through the inflammatory process. There are some markers for low-grade chronic inflammatory, such as cathepsin S, high sensitivity C-reactive protein (hs-CRP), interleukin-1- beta (IL-1β). To our current interest that central obesity can lead to various chronic diseases through the inflammatory process, we conducted a study to investigate correlation of Cathepsin S, hs-CRP, IL-1β in men with central obesity.METHODS: A cross-sectional study was conducted. Seventy-eight selected subjects were examined to collect anthropometric data and prepared for sample collection. Collected samples were processed for the following biochemical analyses: fasting glucose, high density lipoprotein (HDL)-cholesterol, triglyceride, serum glutamic oxaloacetic transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), cathepsin S, hs-CRP, and IL-1β. Data distribution and variable correlation were then statistically analyzed.RESULTS: There were significant correlations between waist circumference (WC) and cathepsin S (p=0.030; r=0.214), hs-CRP and cathepsin S (p=0.007; r=0.276), triglyceride and IL-1β (p=0.019; r=-0.235), WC and systolic blood pressure (SBP) (p=0.003; r=-0.312), WC and fasting glucose (p=0.000; r=0.380), WC and body mass index (BMI) (p=0.000; r=0.708).CONCLUSION: Our study showed that cathepsin S was correlated with central obesity, suggesting that cathepsin S could be a potential inflammatory marker in central obesity in the future.KEYWORDS: obesity, inflammation, hs-CRP, cathepsin S, IL-1β, waist circumference
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 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 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 Danendra Rakha Putra Respati 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 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 Fitri Mutmainnah Fitriani, Sabina 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 Hariani, Lynda 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 Shalahuddin 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 Indah Aprianti Putri 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 Johni Halim Juliani Hardja Buntara, Magdalena Juminten Saimin Junita Briskila Jusak Nugraha Jusuf Rachmat Karina Febriani Hudono Kartika Dwi Aprisia Karyono Mintaroem Kent Wijaya Setiawan Ketherin Ketherin Ketherin Ketherin Ketherin Ketherin Ketherin, Ketherin Kevin Christian Tjandra Khairun Nisa Kharima Abdullah Kharima Abdullah, Kharima Khilmi Ainun Nadliroh Kirana, Farenza Okta Komariah Komariah Komariah Komariah Komariah Komariah Kyung Hoon Lee 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 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 Mulyawati, Sufiah Asri 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 Noer Halimatus Syakdiyah Nova Adrian Noviasti Rahma Utami 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 Dewi, Nurrani Mustika Nurul Fauziah Nyoman Suci Widiastiti Oetomo Roeslan, Boedi Olivia Nauli Komala P Lubis, M Novo Pande Putu Erawijantari Pang, Tiffany Paramita, Anindya Parawansah Parawansah Pendrianto Pendrianto Peter Kabo Peter Sugita Pieri Kumaladewi Prasetya, David Eka Primariadewi Rustamadji Primariadewi Rustamadji Pudji Rahajoe Pudji Rahaju Pukovisa Prawiroharjo Putri Y Suyanto Putri Y Suyanto, Putri Y Quan Yong Tang Rachma Purwanti Raden Muharam Natadisastra 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 Reksodiputro, Mirta Hediyati 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 Robin Novriansyah 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 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 Visi Endah Pratitis 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 Yohanna Kusuma Yora Nindita Yudi Her Oktaviono, Yudi Her Yuliani Taramalinda, Elizabeth Yusra Yusra Yusrina Lukitasari Yuyus Kusnadi Zarasade, Lobredia Zulfikar Lubis Zulfikri Muhktar