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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 621 Documents
 12   13   14   15   16 
Association Between Cathepsin S, Cystatin C and High Sensitivity C-Reactive Protein (hsCRP) with Oxidized LDL (Ox-LDL) in Men with Central Obesity Emmy F Harefa; Ilhamjaya Patellongi; Marita Kaniawati
The Indonesian Biomedical Journal Vol 4, No 1 (2012)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v4i1.162

Abstract

BACKGROUND: Inflammation is a central feature of the atherosclerotic process particularly in obesity. hsCRP, a marker of inflammation, may be directly involved in all phases of atheroslerosis by complement activation, apoptosis, vascular cell activation, monocyte recruitment, lipid accumulation and thrombosis. Inflammation has a causal relationship with cysteine proteases including cathepsin S. Therefore, cathepsin S is considered as a molecular link between obesity and atherosclerosis. An imbalance between elastolytic cysteine proteases, cathepsin S and its inhibitor, cystatin C, is involved in the pathogenesis of atherosclerosis. Some studies have shown that increased circulating levels of cathepsin S, hsCRP and cystatin C in inflammatory conditions contribute to atherosclerosis. This study was conducted to investigate the associations between ox-LDL and cathepsin S, and cystatin C and hsCRP in men with central obesity.METHODS: This was a cross-sectional study involving 71 male subjects with central obesity (waist circumference ≥90 cm), with no renal dysfunction, aged 30-60 years.RESULTS: Cathepsin S did not have a significant correlation with ox-LDL (r=0.158, p=0.096). ox-LDL had positive correlation with cystatin C (r=0.156; p=0.029) and hsCRP (r=0.204; p=0.045), and cathepsin S/cystatin C ratios (r=0.360; p=0.024) at level >91 U/L (median ox-LDL).CONCLUSIONS: There were associations between ox-LDL and cystatin C, hsCRP and cathepsin S/cystatin C ratios in men with central obesity.KEYWORDS: obesity, inflammation, atherosclerosis, hsCRP, cystatin C, cathepsin S, ox-LDL
Habitual Coffee Consumption Does Not Correlate with Blood Pressure, Inflammation and Endothelial Dysfunction but Partially Correlates with Oxidative Stress Erizal Sugiono; Mansyur Arif; Anwar Santoso
The Indonesian Biomedical Journal Vol 5, No 1 (2013)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v5i1.51

Abstract

BACKGROUND: Coffee is the most widely consumed beverage in the world and has been known to have effects on cardiovascular system. Many researchers have examined the effects of coffee consumption on blood pressure (BP) and risk of cardiovascular disease (CVD), but their results were inconsistent and still remain a subject of controversy. Oxidative stress, inflammation, and endothelial dysfunction have been known as risk factors of hypertension and CVD. Those factors are also known to be affected by coffee consumption. The aim of this study was to examine the relationship between the effects of habitual coffee consumption on BP and to examine the role of oxidative stress (F2 isoprostane), inflammation (high sensitive C-reactive protein (hsCRP)) and endothelial dysfunction (asymmetric dimethylarginine (ADMA)).METHODS: This was a cross-sectional study in which 47 healthy, non-smoking men aged 30-60 years with varying coffee-drinking habits were enrolled. BP and blood/urine analysis of biomarkers were measured in the morning before activity. Coffee consumption was assessed using a questionnaire. The differences among variables were analyzed using ANOVA and the correlations between variables were analyzed using Kendall’s Tau correlation analysis.RESULTS: Habitual coffee consumption did not correlate with systolic/diastolic BP (r=-0.02; p=0.856 and r=0.15; p=0.230, respectively). Concentrations of ADMA and hsCRP were also not correlated with coffee consumption (r=0.03; p=0.764 and r=0.04; p=0.701, respectively). Coffee consumption only showed significant correlation with F2 isoprostane (r=0.34; p=0.004).CONCLUSION: BP was not affected by coffee consumption although coffee consumption has a significant correlation with F2 isoprostane. These findings suggest that correlation between coffee consumption and BP might be explained by other factors that were not included in this study.KEYWORDS: coffee, caffeine, cardiovascular disease, blood pressure, oxidative stress, inflammation, endothelial dysfunction
Peroxisome Proliferator–Activated Receptors and The Metabolic Syndrome Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 1, No 1 (2009)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v1i1.79

Abstract

BACKGROUND: Obesity is a growing threat to global health by virtue of its association with insulin resistance, inflammation, hypertension, and dyslipidemia, collectively known as the metabolic syndrome (MetS). The nuclear receptors PPARα and PPARγ are therapeutic targets for hypertriglyceridemia and insulin resistance, respectively, and drugs that modulate these receptors are currently in clinical use. More recent work on the PPARδ has uncovered a dual benefit for both hypertriglyceridemia and insulin resistance, highlighting the broad potential of PPARs in the treatment of metabolic disease.CONTENT: We have learned much about PPARs, the metabolic fat sensors, and the molecular pathways they regulate. Through their distinct tissue distribution and specific target gene activation, the three PPARs together control diverse aspects of fatty acid metabolism, energy balance, insulin sensitivity glucose homeostasis, inflammation, hypertension and atherosclerosis. These studies have advanced our understanding of the etiology for the MetS. Mechanisms revealed by these studies highlight the importance of emerging concepts, such as the endocrine function of adipose tissue, tissue-tissue cross-talk and lipotoxicity, in the pathogenesis of type 2 diabetes mellitus and CVD.SUMMARY: The elucidation of key regulators of energy balance and insulin signaling have revolutionized our understanding of fat and sugar metabolism and their intimate link. The three ‘lipidsensing’ (PPARα, PPARγ and PPARδ) exemplify this connection, regulating diverse aspects of lipid and glucose homeostasis, and serving as bonafide therapeutic targets.KEYWORDS: Peroxisome Proliferator, Activated Receptor, Metabolic Syndrome
Circadian Clock and The Cardiometabolic Risk Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 2, No 2 (2010)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v2i2.116

Abstract

BACKGROUND: Epidemiological data reveal parallel trends of decreasing sleep duration and increases in metabolic disorders such as obesity, diabetes and hypertension. There is growing evidence that these trends are mechanistically related.CONTENT: The circadian system orchestrates the temporal organization of many aspects of physiology, including metabolism, in synchrony with the 24 hours rotation of the Earth. The circadian system is a complex feedback network that involves interactions between the central nervous system and peripheral tissues. Circadian regulation is intimately linked to metabolic homeostasis and that dysregulation of circadian rhythms can contribute to disease. Conversely, metabolic signals also feed back into the circadian system, modulating circadian gene expression and behavior.SUMMARY: Both inter- and intraorgan desynchrony may be involved in the pathogenesis of cardiometabolic disease attributable to effects in brain and multiple metabolic tissues including heart, liver, fat, muscle, pancreas and gut. Efforts to dissect the molecular mediators that coordinate circadian, metabolic, and cardiovascular systems may ultimately lead to both improved therapeutics and preventive interventions.KEYWORDS: circadian rhythms, clock genes, nuclear receptor, sleep, obesity, cardiometabolic risk
Aloe Gel Enhances Angiogenesis in Healing of Diabetic Wound Djanggan Sargowo; Adeodatus Yuda Handaya; Mohammad Aris Widodo; Diana Lyrawati; Askandar Tjokroprawiro
The Indonesian Biomedical Journal Vol 3, No 3 (2011)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v3i3.152

Abstract

BACKGROUND: Diabetic micro and macroangiophathy lead to the incident of diabetic foot ulcers characterized by an increased number of circulating endothelial cells (CECs) and decreased function of endothelial progenitor cells (EPCs). This fact is correlated with ischemia and diabetic wound healing failure. Aloe vera gel is known to be able to stimulate vascular endothelial growth factor (VEGF) expression and activity by enhancing nitric oxide (NO) production as a result of nitric oxide synthase (NOS) enzyme activity. Aloe vera is a potential target to enhancing angiogenesis in wound healing.OBJECTIVE: The objective of this study was to explore the major role of Aloe vera gel in wound healing of diabetic ulcers by increasing the level of EPCs, VEGF, and endothelial nitric oxide synthase (eNOS), as well as by reducing the level of CECs involved in angiogenesis process of diabetic ulcers healing.METHODS: The experimental groups was divided into five subgroups consisting of non diabetic wistar rats, diabetic rats without oral administration of aloe gel, and treatment subgroup (diabetic rats) with 30, 60 and 120 mg/day of aloe gel doses for 14 days. All subgroups were wounded and daily observation was done on the wounds areas. Measurement of the number of EPCs (CD34), and CECs (CD45 and CD146) was done by flowcytometry, followed by measurement of VEGF and eNOS expression on dermal tissue by immunohistochemical method on day 0 and day 14 after treatment. The quantitative data were analyzed by One-Way ANOVA and Linear Regression, with a cofidence interval 5% and significance level (p<0.05) using SPSS 16 software to compare the difference and correlation between wound diameters, number of EPCs and CECs as well as the levels of VEGF and eNOS.RESULTS: The results of this study showed that aloe gel oral treatment in diabetic wistar rats was able to accelerate the wound healing process. It was shown by significant reduction of wound diameter (0.27±0.02); the increased number of CECs (0.42±0.57), respectively (p<0.05). On the other hand, the wound diameter and eNOS indicators showed significant differences at the dose of 60 mg, while the number of EPCs and CECs and the level of VEGF showed significantly different results at a dose of 120 mg. Aloe gel oral therapy showed a positive indication of wound healing acceleration at the optimum dose range 60-120 mg a day.CONCLUSIONS: Aloe gel is potential to be a herbal therapy candidate for diabetic wound healing through enhancing EPCs homing, decreasing the CECs number, and stimulating the increase of VEGF and eNOS levels,hence proving to be a dominant factor in the angiogenesis process.KEYWORDS: aloe gel, diabetes, wound healing, angiogenesis
Comparison between Carotid Intima-Media Thickness and Coronary Artery Calcification in the Prediction of Atherosclerosis in Diabetic Patients Rusli Muljadi; Bachtiar Murtala; Peter Kabo; FX Budhianto Suhadi
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.v6i1.42

Abstract

BACKGROUND: Cardiovascular disease is one of the atherosclerosis etiologies that can lead to death. Diabetes mellitus increases the risk of atherosclerosis. Screening tool is very beneficial for detecting atherosclerotic plaque, especially in subclinical atherosclerotic cases. Carotid intima-media thickness (CIMT) and coronary artery calcification score (CACS) are two kinds of tools that are widely used, and each of these tools has its own superiority. This study was aimed to investigate the sensitivity and specificity of both of these tools as screening tools.METHODS: The study was conducted with a cross sectional design involving 43 diabetic and 68 non-diabetic male subjects aged above 45 years old. All subjects fulfilled inclusion criteria. Carotid artery ultrasonography and CACS measurement were performed.RESULTS: Fischer exact test was used to show a significant correlation between CIMT and CACS (p<0.05). Diagnostic test was used to assess the sensitivity of CIMT toward CACS in above 75 percentile. The left common carotid artery (LCCA) showed the highest sensitivity either in diabetic (76.4%) or non-diabetic male subjects (90%).CONCLUSION: CIMT has the same sensitivity with CACS. CIMT can be used as the preferred screening tool for high risk patients and as a substitution tool to CACS for low risk patients in subclinical atherosclerosis detection.KEYWORDS: atherosclerosis, diabetes mellitus, carotid intima-media thickness, coronary artery calciication score
Lung Function Status of Workers Exposed to Welding Fume: A Preliminary Study Mulyana Mulyana; Nuri Purwito Purwito Adi; Meily L Kurniawidjaja; Andi Wijaya; Irawan Yusuf
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.v8i1.196

Abstract

BACKGROUND: Exposure to welding fume in the workplace was associated with lung function disorders and occupational asthma. In this study, we determined lung function parameters in men workers exposed to welding fumes from heavy equipment manufacturer. This study is a preliminary study of biomonitoring program in worker exposed to welding fume as our main study. METHODS: A study with case-control design, random study, was conducted among welder (59 subjects) and non-welder (34 subjects) with more than one year experience in the same job task in a heavy equipment manufacturer. All subjects completed physical examination, informed consent, questionnaire and lung function status. Lung function status was measured by spirometer with vital capacity (VC), forced vital capacity (FCV), forced expiratory volume in one second (FEV1) and ratio of FEV1/FVC as test parameters. Linear regression model was developed to identify the risk factor of lung function parameter status using age, working period and smoking status as variables. RESULTS: This study showed that there were significant lower VC, FVC and FEV1 in welder than non-welder, but not difference in ratio of FEV1/FVC. However, there was no significant difference among welder from foundry and fabrication plan. By multivariate analysis, working period was found as a risk factor for lower parameters in lung function among welder. CONCLUSION: Lung function parameters status were significantly lower in welder than non-welder, and working period was the most important indicator for lung function status evaluation among welder. KEYWORDS: vital capacity, VC, forced vital capacity, FCV, forced expiratory volume in one second, FEV1, lung function, ratio of FEV1/FVC, working period 
Caffeic Acid Inhibited Receptor Activator of Nuclear Factor kappaB Ligand (RANKL)-Tumor Necrosis Factor (TNF) alpha-TNF Receptor Associated Factor (TRAF) 6 induced Osteoclastogenesis Pathway Ferry Sandra; Toshio Kukita; Tatsushi Muta; Tadahiko Iijima
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.v5i3.68

Abstract

BACKGROUND: Caffeic acid was reported in our previous study to have potential in inhibiting osteoclastogenesis through inhibition of nuclear factor κB (NFκB). Here in our current study, we would like to investigate further the caffeic acid-affected signaling pathway leading to NFκB inhibition. Since tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6) plays important role in osteoclastogenesis, we applied TRAF6- transfected RAW264 cells D-Clone (RAW-D) cells as model in this study.METHODS: Caffeic acid in various concentrations was added to in vitro osteoclastogenesis of receptor activator nuclear factor κB ligand (RANKL)-TNFα-induced TRAF6-transfected RAW-D cells. Cells were collected, lysed and immunoblotted to detect TRAF6 expression. To detect tartrate resistant acid phosphatase (TRAP)+ polynucleated cells (PNCs), TRAP staining was performed. Meanwhile, to measure NFκB Activity, cells were transfected with pNFκB-TA-Luc and subjected to Dual Luciferase Reporter Assay System.RESULTS: Caffeic acid did not influence TRAF6 expression of RANKL-TNFα-induced TRAF6-transfected RAW-D cells. Caffeic acid diminished NFκB activity of RANKL-TNFα-induced TRAF6-transfected RAW-D cells in a concentration dependent manner. Significant NFκB activity inhibitions were seen under treatment of 1 and 10 μg/ml caffeic acid. By adding 10 μg/ml caffeic acid in RANKL-TNFα-induced TRAF6-transfected RAW-D cells, TRAP+ PNCs number was significantly suppressed.CONCLUSION: Caffeic acid inhibited RANKL-TNFα-TRAF6-induced osteoclastogenesis pathway. Since caffeic acid did not influence TRAF6 expression, TRAF6-RANK interactions and/or TRAF6 downstream signaling pathway should be further pursued to disclose inhibition mechanism of caffeic acid.KEYWORDS: caffeic acid, osteoclastogenesis, TRAF6, RANKL, TNFα, NFκB, RAW-D
Porphyromonas gingivalis Induced Fragmentation of Type IV Collagen Through Macrophage-Activated MMP-9: (In Vitro Study of Collagenolytic Mechanism in Pathogenesis of Atherosclerotic Plaque Rupture) Siti Nurul Mubarokah; I Dewa Agung Susilawati; Sumarno Sumarno; I Ketut Gedhe Muliartha; Djanggan Sargowo
The Indonesian Biomedical Journal Vol 1, No 3 (2009)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v1i3.105

Abstract

BACKGROUND: Periodontitis is caused mostly by Porphyromonas gingivalis (P.gingivalis) and it is related to acute coronary syndrome. P.gingivalis  readily invades blood circulation and potentially induces collagenolytic activity of inflammatory cells that results in collagen vascular degradation leading to atherosclerotic plague rupture (APR). APR is responsible for the occurence of fatal cardiovascular events such as acute myocardial infraction (AMI).AIMS: To show that P.gingivalis potentially induces fragmentation of the type IV vascular collagen due to macrophage-activated MMP-9.MATERIAL AND METHODS: The ability of P.gingivalis to induce the type IV collagen fragmentation, shown by digesting type IV collagen with the supernatant of monocyte-derived macrophage activated by exposure to P.gingivalis suspension for 18 hours, 37oC, 5%CO2. The type IV collagen fragments were analyzed by SDS-PAGE and confirmed by Western-blotting. Antibody of type IV collagen produced and confirmed by dot-blotting prior to its being used as primary antibody of Western-blotting. The existence of MMP-9 was detected by Dot-blot and Western-blot technique, while the MMP-9 activity was assessed by SDS-PAGE and zymograms.RESULTS: Our data showed that P.gingivalis induced macrophage to produce MMP-9 as one of collagenolytic components, and interaction with P.gingivalis proteases enhanced the proteolytic activity and resulted in degradation of type IV collagen with molecular weight of 88 kDa into two smaller fragments with molecular weight of 80 kDa and 60 kDa. CONCLUSION: P.gingivalis induced macrophage to activate its MMP-9 that led to fragmentation of vascular type IV collagen in the pathogenesis of atherosclerotic plaque rupture. KEYWORDS: P.gingivalis, macrophage, type IV collagen fragmentation, atherosclerotic plaque rupture, AMI
Correlation between hsCRP and Anti-beta2GPI Antibody in Metabolic Syndrome Meiriza Djohari; Mansyur Arif; Burhanuddin Bahar
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.v3i2.142

Abstract

BACKGROUND: Several researches reported that inflammatory and immunological mechanism such as autoantibody to β2-glycoprotein I (anti β2GPI) appear as related factors in initiation and progress of atherosclerosis lesion in patient with autoimmune disease. Antibody to β2GPI titers are correlated with atherosclerosis and in vitro studies showed that they enhance oxidized low density lipoprotein (ox-LDL) uptake by macrophages. Immunization with auto-antigen β2GPI elicits an immune response to influence lesion progression that mostly happens in autoimmune subjects. The metabolic syndrome (MetS) is combination of several metabolic disorders such as obesity, dyslipidemia, Diabetes Mellitus (DM) and conditions due to inflammation and stress oxidative. The Correlation between inflammatory markers such as High sensitivity C-Reactive Protein (hsCRP) and anti-β2GPI antibody in MetS needs to be further investigated.METHODS: This was an observational study with cross sectional design on subject with MetS as determined by the International Diabetes Federation (IDF) 2005’s criteria.RESULTS:There was a positive and significant correlation between hsCRP and anti-β2GPI antibody in MetS group (r=0.406; p≤0.05) as compared to non-MetS group. We found that there was elevated level of anti-β2GPI antibody in hsCRP of 3-10 mg/L.CONCLUSIONS: Anti-β2GPI antibody may be elevated in subjects with MetS who have low grade of inflammation as shown by hsCRP.KEYWORDS: metabolic syndrome, inflammation, autoantigen, atherosclerosis, obesity

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