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INDONESIA
The Indonesian Biomedical Journal
ISSN : -     EISSN : -     DOI : -
Core Subject : Health, Science,
Arjuna Subject : -
Articles 621 Documents
Phylogeny of HPV-16 and HPV-18 Multiple Infection of a Patient with Cervical Cancer from Dr. Hasan Sadikin General Hospital, Bandung: A Case Report Vera Amalia Lestari; Ika Agus Rini; Gita Widya Pradini; Edhyana Sahiratmadja; Herman Susanto
The Indonesian Biomedical Journal Vol 10, No 3 (2018)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v10i3.383

Abstract

BACKGROUND: From all of human papillomaviruses (HPV) genotypes capable of causing cervical cancer, it is estimated that 70 percent are HPV-16 and HPV-18. HPV-16 can infect the tissues in single infection or together with other high-risk types of HPV, and the most common is with HPV-18. The origin of HPV can be identified by its phylogenetic tree. The aim of this study was to determine the phylogeny of HPV-16 and HPV-18 multiple infection in cervical cancer, whether both HPVs were from the same origin.METHODS: Cervical tissue biopsies (n=33) were obtained from Hasan Sadikin Hospital in the period of September to November 2016. HPV genotyping test was performed to confirm the HPV-16 and HPV-18 multiple infection. L1 gene of both HPV-16 and HPV-18 were sequenced for phylogenetic analysis.RESULTS: Phylogenetic analysis of L1 HPV-16 and HPV-18 showed the closest relationship with sequence from China and Thailand, respectively.CONCLUSION: HPV-16 and HPV-18 multiple infection of a cervical cancer patient from Dr. Hasan Sadikin General Hospital Bandung showed a very close L1 phylogeny relationship with isolate from Asian region.KEYWORDS: HPV-16, HPV-18, multiple infection, cervical cancer, Bandung
Telomeres and Telomerase in The Aging Heart Anna Meiliana; Nurrani Mustika Dewi; Andi Wijaya
The Indonesian Biomedical Journal Vol 9, No 3 (2017)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v9i3.389

Abstract

BACKGROUND: Aging per se is a risk factor for reduced cardiac function and heart diseases, even when adjusted for aging-associated cardiovascular risk factors. Accordingly, aging-related biochemical and cell-biological changes lead to pathophysiological conditions, especially reduced heart function and heart disease.CONTENT: Telomere dysfunction induces a profound p53-dependent repression of the master regulators of mitochondrial biogenesis and function, peroxisome proliferator-activated receptor gamma coactivator (PGC)-1a and PGC-1b in the heart, which leads to bioenergetic compromise due to impaired oxidative phosphorylation and ATP generation. This telomere-p53-PGC mitochondrial/metabolic axis integrates many factors linked to heart aging including increased DNA damage, p53 activation, mitochondrial, and metabolic dysfunction and provides a molecular basis of how dysfunctional telomeres can compromise cardiomyocytes and stem cell compartments in the heart to precipitate cardiac aging.SUMMARY: The aging myocardium with telomere shortening and accumulation of senescent cells restricts the tissue regenerative ability, which contributes to systolic or diastolic heart failure. Moreover, patients with ion-channel defects might have genetic imbalance caused by oxidative stress-related accelerated telomere shortening, which may subsequently cause sudden cardiac death. Telomere length can serve as a marker for the biological status of previous cell divisions and DNA damage with inflammation and oxidative stress. It can be integrated into current risk prediction and stratification models for cardiovascular diseases and can be used in precise personalized treatments.KEYWORDS: aging, telomere, telomerase, aging heart, mitochondria, cardiac stem cell
High VEGF Level is Produced by Human Umbilical Cord- Mesenchymal Stem Cells (hUC-MSCs) in Amino Acid-Rich Medium and under Hypoxia Condition Veronika Maria Sidharta; Elizabeth Henny Herningtyas; Christine Ayu Lagonda; Dilafitria Fauza; Yuyus Kusnadi; Rina Susilowati; Ginus Partadiredja
The Indonesian Biomedical Journal Vol 10, No 3 (2018)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v10i3.457

Abstract

BACKGROUND: Secretome production by stem cells depends on their culture conditions such as oxygen concentration and the composition of the culture media. In this study, we investigated the secretion of neurotrophic growth factors of human umbilical cord mesenchymal stem cells (hUC-MSCs) in amino acid-rich culture medium and under hypoxic condition.METHODS: hUC-MSCs were cultured in normoxic and various hypoxic (1%, 5%, 10%) conditions in an amino acid-rich culture medium. The end-point parameters (cell proliferation and survival, cell morphology and growth factor secretion) were measured at 3 time-points (48 hours, 72 hours and 96 hours). ELISA-based methods were used for neurotrophic factors detection, including neurotrophic growth factor (NGF), vascular endothelial factor (VEGF), and brain-derived neurotrophic factor (BDNF).RESULTS: NGF secretion was not detectable at any time points both in normoxia and hypoxia. BDNF secretion under normoxia was induced at 48 h time point and reached the highest level at an average of 181.9±13.01 pg/mL at 96 hours, whereas hypoxia exposure to hUC-MSCs only induced the BDNF secretion at low level. VEGF secretion was barely detectable in normoxic condition. However, VEGF secretion reached the highest level at an average of 7707.55±2110.85 pg/mL in 5% hypoxia at 96 hours.CONCLUSION: Combination of amino acid-rich culture medium and hypoxia condition dramatically induced high VEGF secretion by hUC-MSCs, especially at 5% hypoxia, induced mild BDNF secretion and had no effect toward NGF secretion.KEYWORDS: human umbilical cord mesenchymal stem cells, neurotrophic growth factor, amino acid-rich, hypoxia
Genome Editing with Crispr-Cas9 Systems: Basic Research and Clinical Applications Anna Meiliana; Nurrani Mustika Dewi; Andi Wijaya
The Indonesian Biomedical Journal Vol 9, No 1 (2017)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v9i1.272

Abstract

BACKGROUND: Recently established genome editing technologies will open new avenues for biological research and development. Human genome editing is a powerful tool which offers great scientific and therapeutic potential.CONTENT: Genome editing using the clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPRassociated protein 9 (Cas9) technology is revolutionizing the gene function studies and possibly will give rise to an entirely new degree of therapeutics for a large range of diseases. Prompt advances in the CRISPR/Cas9 technology, as well as delivery modalities for gene therapy applications, are dismissing the barriers to the clinical translation of this technology. Many studies conducted showed promising results, but as current available technologies for evaluating off-target gene modification, several elements must be addressed to validate the safety of the CRISPR/Cas9 platform for clinical application, as the ethical implication as well.SUMMARY: The CRISPR/Cas9 system is a powerful genome editing technology with the potential to create a variety of novel therapeutics for a range of diseases, many of which are currently untreatable.KEYWORDS: genome editing, CRISPR-Cas, guideRNA, DSB, ZFNs, TALEN
Modulation of Caspase-3 Expression by Arcangelisia flava Post Acetaminophen-Induced Hepatotoxicity in Rat’s Liver Steffi Liem; Tina Rostinawati; Ronny Lesmana; Sri Adi Sumiwi; Tiana Milanda; Mutakin Mutakin; Irma Melyani Puspitasari; Jutti Levita
The Indonesian Biomedical Journal Vol 10, No 2 (2018)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v10i2.412

Abstract

BACKGROUND: Acetaminophen, when used at low doses is a safe drug, but at higher doses it induces apoptosis in hepatoma cells. Arcangelisia flava that grows widely in Kalimantan Island, Indonesia, contains berberine which is effective in protecting the liver. This work was aimed to study the effect of A. flava extract on the modulation of caspase-3 in acetaminophen-induced hepatotoxicity.METHODS: Thirty-five Wistar male rats were divided into groups: I the normal control (water); II the negative control (Arabic gum powder or PGA, 2% in suspension); III the positive control (silymarin); IV-VII (A. flava extract 100, 200, 400, and 800 mg/Kg of body weight (BW), respectively) for 14 days. At day 15th, group II-VII were induced with acetaminophen 1000 mg/Kg of BW per oral for 7 days along with the extracts. At day 22nd, the animals were measured for their serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT) and gamma-glutamyl transferase (GGT), histological examination, and Western blotting.RESULTS: Acetaminophen elevated the SGOT and SGPT (3x compared to normal group), and GGT (5x compared to normal group) of the animals in group II. Pre-treatment with higher doses of A. flava extract (group VI and VII) significantly prevented the biochemical changes induced by acetaminophen. Normal histology of the liver was showed by group I, III, VII, whereas dilated sinusoids, central vein (CV) lesion, and local haemorrage were observed in group II, IV, V and VI. Western blotting showed an inhibition of caspase-3 expression by A. flava extract in dose-dependent manner.CONCLUSION: A. Higher dose A. flava extract shows hepatoprotective activity by preventing the elevation of serum transaminases and transferase levels. Eventually, no damage in the acetaminophen-induced rat’s liver was observed. This plant modulates the expression of caspase 3 protein in dose-dependent manner.KEYWORDS: Arcangelisia sp, caspase-3, berberine, hepatoprotective activity, NSAIDs, yellow root
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
The Blockade of Glutamate N-methyl-D-aspartate Receptors into the Prelimbic of Prefrontal Cortex Decreases Morphine-induced Conditioned Place Preference in Rat Samad Javadi; Hojjatallah Alaei; Ebrahim Hosseini; Mohammad Amin Edalatmanesh
The Indonesian Biomedical Journal Vol 9, No 3 (2017)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v9i3.343

Abstract

BACKGROUND: The prelimbic area (PL) of the prefrontal cortex is susceptible to abnormal developmental stimuli that raises the risk of addiction. Glutamate receptors play a key role in opiate reinforcement and reward functions in this area. Therefore, we examined the effect of the DL-2-amino-5-phosphonopentanoic acid (AP5), as N-methyl-D-aspartate (NMDA) receptor antagonist into the PL on the phases of conditioned place preference (CPP) induced by morphine.METHODS: Male Wistar rats were divided into 12 groups (3 surgical groups for each dose of morphine in any phase of CPP) and anaesthetized with chloral hydrate. Cannula was implanted into the PL and the AP5 was injected into this area and morphine-induced CPP was investigated. Data were processed with the commercially available SPSS 22 software using one-way ANOVA and Tukey's test. p<0.05 were considered statistically significant.RESULTS: Our findings indicated, morphine in doses of 2.5 to 10 mg/kg induced CPP. Microinjection of various doses of the AP5 into the PL before the administration of the effective dose of morphine significantly reduced place preference in the acquisition and the expression phases of the CPP test compared to the sham group (p<0.001). In another set of our experiments was seen that, different doses of the AP5 with the ineffective dose of morphine only reduced the expression phase of the CPP (p<0.001) while, produced neither preference nor aversion effect on the acquisition phase (p=0.147).CONCLUSION: It seems that the glutamate NMDA receptors in the PL through memory formation and morphine-related reward signals play a critical role in addiction process during morphine-induced CPP.KEYWORDS: N-methyl-aspartate, morphine, glutamate receptor, prefrontal cortex, reward
Anthropometry-based Body Fat Percentage Predicts High hs-CRP in Chronic Kidney Disease Patients Mochammad Thaha; Maulana Antiyan Empitu; Ika Nindya Kadariswantiningsih; Cahyo Wibisono Nugroho; Nurina Hasanatuludhhiyah; Haerani Rasyid; Zaky El Hakim; Maulana Muhtadin Suryansyah; Rieza Rizqi Alda; Mohammad Yusuf Alsagaff; Mochammad Amin; Djoko Santoso; Yusuke Suzuki
The Indonesian Biomedical Journal Vol 10, No 2 (2018)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v10i2.397

Abstract

BACKGROUND: Obesity is an important cardiovascular risk factor and associated with low grade inflammation in chronic kidney disease (CKD) patients. This study aims to assess the association between body fat with serum high sensitivity C-reactive protein (hs-CRP) level in CKD patients.METHODS: A cross-sectional study was performed in 71 CKD patients. Anthropometric measurements included body weight, height, body mass index (BMI), body fat percentage (BFP), skinfold thickness (SKF) of triceps and biceps were performed by trained physician. BFP was calculated using Kwok’s Formula and hs-CRP was measured by Particle enhanced Turbidimetry.RESULTS: The averaged BMI of our subjects was 25.8±4.4. There was no significant difference in BMI between pre-dialysis and hemodialysis CKD patients. Positive correlation was found between BFP and hs-CRP (r=0.266; p<0.05), while there was no significant correlation between BMI and hs-CRP.CONCLUSION: Body fat percentage was associated with hs-CRP. Hence, it will be more beneficial to assess nutritional status in CKD using BFP rather than BMI alone since it was demonstrated to correlate with hs-CRP in our studyKEYWORDS: CKD, obesity, inflammation, body fat, hs-CRP
The Correlation Between TP53 Expression and Ki-67 Proliferation with Bartl Malignancy Degree of Plasma Cell Neoplasm Isabelle Deli Lestadi; Nurjati Chaerani Siregar; Puspita Eka Wuyung
The Indonesian Biomedical Journal Vol 9, No 1 (2017)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v9i1.236

Abstract

BACKGROUND: Plasma cell neoplasm (PCN) is a neoplastic plasma cell proliferation which includes solitary bone plasmacytoma (SBP), extramedullary plasmacytoma (EMP) and multiple myeloma (MM). Bartl classifies the degrees of PCN as low, intermediate and high. The aim of this study is to find the correlation between tumor suppressor gene p53 (TP53) expression and Ki-67 proliferation with Bartl malignancy degree of PCN. Therefore earlier PCN diagnostic method to prevent the development of PCN into MM can be found.METHODS: Thirty-two PCN cases were classified into three groups based on Bartl’s degrees of malignancy. TP53 and Ki-67 immunohistochemical staining were performed on samples and the percentage of positivity was evaluated.RESULTS: The Bartl’s low degree of malignancy was found in 10 MM cases (31.2%), intermediate degree in  5 SBP cases (15.6%) and high in 2 SBP and EMP cases (6.2%). TP53 expression was obtainable at 4% of low, 16% of intermediate and 10% of high degree. There was a significant difference between TP53 expression in low and intermediate degree (p=0.004). Mean proliferation index of Ki-67 was 57% in low, 44.6% in intermediate, and 32.6% in high degree. There was no significant difference of Ki-67 proliferation indexes among the group (p=0.339).CONCLUSION: Increasing expression TP53 was in accord with Bartl’s degrees of malignancy, especially in low and intermediate degree, but there was no significant difference between Ki-67 proliferation index and Bartl’s degrees of malignancy.KEYWORDS: plasmacytoma, myeloma, TP53, Ki-67, Bartl classification
The Role of Ceftazidime as a Photosensitizer in Human Erythrocytes Through Oxidative Stress Mechanism Mashuri Mashuri; Mustofa Ruhullah; Bayu Diertama Putera; Vicky Pramudinta Mega; Fadillah Alma Putra; Eko Suhartono
The Indonesian Biomedical Journal Vol 10, No 2 (2018)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v10i2.355

Abstract

BACKGROUND: Ceftazidime was known to cause photosensitization reactions. However, how it plays the role remained unclear. In our study, we aim to investigate the photosensitization effect of ceftazidime in erythrocytes via oxidative stress.METHODS: Samples were divided into six different groups: negative control group, positive control group and four experimental groups with 10%, 20%, 30%, and 40% ceftazidime, respectively. The positive control and experimental groups were exposed to ultraviolet (UV)-light for 2 hours. Superoxide radical, malondialdehyde (MDA), carbonyl compounds (CC) and methemoglobin (Met-Hb) levels were then measured.RESULTS: The results showed a significant increased of superoxide radical, MDA, CC and Met-Hb levels in all experimental groups compared to both negative or positive control groups (p< 0.05).CONCLUSION: In conclusion, our study confirmed the role of ceftazidime as a photosensitizer in erythrocytes via the oxidative stress mechanisms.KEYWORDS: ceftazidime, oxidative stress, photosensitizer, photosensitization.