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INDONESIA
The Indonesian Biomedical Journal
Published by The Prodia Education and Research Institute
ISSN : -     EISSN : -     DOI : -
Core Subject : Health, Science,
Biochemistry, Genetics & Molecular Biology Public Health
Arjuna Subject : -
Articles 15 Documents
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Search results for , issue "Vol 11, No 2 (2019)" : 15 Documents clear
Artificial Intelligent in Healthcare Anna Meiliana; Nurrani Mustika Dewi; Andi Wijaya
The Indonesian Biomedical Journal Vol 11, No 2 (2019)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v11i2.844

Abstract

BACKGROUND: Giant transformations are going on currently in health care, and the greatest force behind this phenomenon is data.CONTENT: Big data has arrived into medicine field, lead to potential enhancement in accountability, quality, efficiency, and innovation. Most updated, artificial intelligence (AI) and machine-learning (ML) techniques rapidly developed, bring forth the big data analysis into more useful applications, from resource allocation to complex disease diagnosis. To realize this, a very large set of health-care data is needed for algorithms training and evaluation, including patients’ treatment data, patients respond to treatment, and personal patient information, such as genetic data, family history, health behavior, and vital signs.SUMMARY: Precision Health involving preventive, predictive, personalized and precise. The arrival of AI and ML will enhance and facilitates the improvement of this relationship through better accuracy, productivity, and workflow, thus develop a health system that will go beyond just curing disease, but further into wellness that preventing disease before it strikes, thus the patient–doctor bond is expected to be reformed and not be eroded.KEYWORDS: artificial intelligence, machine learning, deep learning, electronic health records, big data
Severe Hyperthermia Induces Apoptosis Mediated by Caspases Activation and Suppression of Hsp90-alpha Expression in Osteosarcoma Cells Mohammed Ali Nashiry; Gabriele Ruth Anisah Froemming; Yeap Swee Keong; Aletza Binti Mohd Ismail; Aisha Mohd Din; Alyaa Mahmood Al-Khateeb
The Indonesian Biomedical Journal Vol 11, No 2 (2019)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v11i2.594

Abstract

BACKGROUND: Hyperthermia is used as an adjuvant treatment to sensitize cancer cells to subsequent radiotheraphy or chemotherapy. The aim of this study was to study the effect of severe hyperthermia on osteosarcoma cells and its underlying causes.METHODS: Short-term (1 h) severe hyperthermia (45°C) was applied to osteoblast-like osteosarcoma cells (MG-63) and the heat shock response and cell death mechanisms were investigated after recovery at 37°C for 72 h.RESULTS: Cell viability was significantly reduced (p<0.05) and apoptosis was significantly induced by severe hyperthermia in MG-63 cells (p<0.001). Caspase 3/7, 4 and 12 activities were significantly increased after 72 h of recovery at 37°C, indicating that severe hyperthermia induced endoplasmic reticulum (ER) stress and apoptosis (p<0.05). Heat shock protein 90 alpha (Hsp90α) was significantly down regulated at the protein level after recovery, in association with apoptosis induction (p<0.01). Additionally, caspase 8 and 9 were activated, possibly as a result of ER stress or other stimuli while, B-cell leukemia 2 family protein (BCL-2) mRNA was down regulated (p<0.01).CONCLUSION: Severe hyperthermia could cause prolonged cell cytotoxicity by inducing apoptosis in association with inhibition of Hsp90α. This indicates the therapeutic potential of severe hyperthermia for the treatment of osteosarcoma.KEYWORDS: hyperthermia, apoptosis, endoplasmic reticulum, stress, heat shock proteins, osteosarcoma
beta-Glucan Increases IFN-gamma and IL-12 Production of Peripheral Blood Mononuclear Cells with/without Induction of Mycobacterium tuberculosis Wild-type/Mutant DNA Meira Erawati; Nyoman Suci Widyastiti; Tri Indah Winarni; Edi Dharmana
The Indonesian Biomedical Journal Vol 11, No 2 (2019)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v11i2.688

Abstract

BACKGROUND: In tuberculosis infections, the immune system is weakened and cannot produce enough cytokines to against the infection. b-glucan is a potent immunomodulator that induces cytokine production in various bacterial infections. This study aimed to determine the effects of b-glucan on the production of interferon (IFN)-γ and interleukin (IL)-12 in peripheral blood mononuclear cells (PBMCs) induced by Mycobacterium tuberculosis DNA.METHODS: PBMCs were isolated from 11 healthy subjects. PBMCs were treated with/without 5 μg/mL b-glucan and M. tuberculosis rpoB wild-type or mutant DNA. The production of IFN-γ and IL-12 in the supernatant was performed with enzyme-linked immune-sorbent assay (ELISA).RESULTS: b-glucan increased significantly (p<0.05) IFN-γ of M. tuberculosis mutant DNA-induced PBMCs, M. tuberculosis wild-type DNA-induced PBMCs, and non-induced PBMCs. b-glucan also increased significantly (p<0.05) IL-12 of M. tuberculosis mutant DNA-induced PBMCs, M. tuberculosis wild-type DNA-induced PBMCs, and non-induced PBMCs. There were not any significant difference between male and female groups for IL-12 and IFN-γ in all treatment groups (p>0.05, ANOVA test).CONCLUSION: This in vitro study indicates that b-glucan increases the performance of PBMCs to produce IFN-γ and IL-12, with/without induction of M. tuberculosis wild-type/ mutant DNA.KEYWORDS: b-glucan, IFN-γ, IL-12, M. tuberculosis, rpoB
Dextrose Hydration May Promote Cisplatin-induced Nephrotoxicity in Rats: Gender-related Difference Farzaneh Karimi; Sayyedehnikta Kasaei; Azar Baradaran; Farzaneh Ashrafi; Ardeshir Talebi; Zahra Lak; Mehdi Nematbakhsh
The Indonesian Biomedical Journal Vol 11, No 2 (2019)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v11i2.502

Abstract

BACKGROUNDS: Cisplatin (CP) as an anticancer drug may affect the plasma glucose level while diabetic subjects are protected against CP-induced nephrotoxicity. In the current study, the role of dextrose hydration during CP therapy on CP-induced nephrotoxicity was evaluated.METHODS: Sixty-nine male and female rats were divided into 12 groups. The rats were hydrated with 15 mL/kg vehicle or different doses of 2%, 10% and 20% dextrose before and after 7.5 mg/kg CP administration. One week later, the biochemical and kidney function markers, and histology finding were determined.RESULTS: All the animals co-treated with CP and 20% dextrose, were dead during one week of the experiment. Administration of CP alone increased kidney tissue damage score (KTDS) and kidney weight (KW). It also elevated the blood urea nitrogen (BUN) and BUN-creatineine ratio (BUN/Cr) levels in the serum. In addition, CP decreased body weight and creatinine (Cr) clearance (ClCr) significantly in both male and female rats (p<0.05). However, 2% and 10% dextrose did not alter the mentioned parameters in male, but 10% dextrose supplement increased the serum levels of BUN, Cr and BUN/Cr ratio, KW and KTDS significantly in female rats (p<0.05).CONCLUSION: Our data suggest that not only do not support the nephro-protective role of dextrose hydration during CP therapy, the dextrose hydration can act as risk factor to promote CP-induced nephrotoxicity in female rats. Prohibition of high carbohydrate (glucose) diet during CP therapy is recommended.KEYWORDS: cisplatin, nephrotoxicity, dextrose, rat, gender
N-Acetyltransferase 2 (NAT2) Acetylator Status among Systemic Lupus Erythematosus Patients from A Tuberculosis Endemic Area in Bandung, Indonesia Laniyati Hamijoyo; Sasfia Candrianita; Ika Agus Rini; Endang Sutedja; Budi Setiabudiawan; Edhyana Sahiratmadja
The Indonesian Biomedical Journal Vol 11, No 2 (2019)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v11i2.553

Abstract

BACKGROUND: Systemic lupus erythematosus (SLE) patients living in Indonesia are prone to tuberculosis (TB) infection, since this country ranks second globally for TB prevalence. Isoniazid, an anti-tuberculosis (TB) drug, is metabolized by enzyme N-acetyltransferase 2 (NAT2) that is encoded by NAT2 gene. NAT2 haplotype, referring as acetylator status, may predispose as genetic factor in SLE development or complicate SLE therapy. This study explored the NAT2 haplotypes and acetylator status among SLE patients living in a TB endemic area.METHODS: Genomic DNA of 260 registered SLE patients at The Rheumatology Clinic of Dr. Hasan Sadikin General Hospital, Bandung, Indonesia were isolated. NAT2 gene was amplified and sequenced, then NAT2 haplotypes and the acetylator status among SLE patients with or without TB history were determined and presented.RESULTS: Most of SLE patients registered were female (n=250; 96.2%). The median age of patients when SLE was diagnosed for the first time was 27 years old (8-69 years), with organ involvement predominantly in musculoskeletal (80.8%) and mucocutaneous (73.1%). TB history, mostly pulmonary TB, was present in 23.1% of SLE patients of whom TB was diagnosed before SLE (10.4%) or after SLE (10.7%) or both before and after SLE (2%). The acetylator status was mostly intermediate (61.5%) with the NAT2*4/*6B was the most prevalent haplotype (25.8%).CONCLUSION: There is a high number of intermediate and low acetylator status among SLE patients. Since these SLE patients live in TB endemic area, the NAT2 acetylator status determination among SLE patients before starting TB therapy may have clinical benefit to decrease a possible drug induced liver injury, and this warrants further study.KEYWORDS: NAT2, acetylator, systemic lupus erythematosus, tuberculosis

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