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INDONESIA
The Indonesian Biomedical Journal
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Core Subject : Health, Science,
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Articles 8 Documents
Search results for , issue "Vol 3, No 2 (2011)" : 8 Documents clear
Correlation between Inflammation and Fibrinolysis Impairment on Central Obesity: A Study for hsCRP, PAI-1, PAP and TAFI Winni Agustiani; Mansyur Arif; Ilhamjaya Patellongi
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.v3i2.143

Abstract

BACKGROUND: Inflammation in the vascular wall plays an important role in the pathogenesis of atherosclerosis. Current studies have shown that increase of systemic inflammatory marker like the acute phase component C-reactive protein (CRP) are associated with an unfavorable progression of disease and an increased risk for acute cardiovascular events. Recently, a close association of Metabolic Syndrome (MetS) with hemostatic abnormalities has been reported. Among hemostatic abnormalities, an increase in plasminogen activator inhibitor (PAI)-1, a strong inhibitor of fibrinolysis, is considered a core feature of MetS. High PAI-1 concentrations may be associated with thrombus formation, also causing cardiovascular events. Therefore, we investigated the association between markers for chronic inflammation (CRP) and the markers of fibrinolytic impairment (PAI-1, PAP, TAFI) in subjects with central obesity.METHODS: This was a cross-sectional study in 80 male Indonesian subjects, aged 30-60 years old with central obesity, conducted from January to March 2008 in Bandung.RESULTS: The study results showed that there was a difference of PAI-1 levels between MetS and Non-MetS group. There were significant correlations between hsCRP and PAI-1 (r=0.252, p=0.024 ), hsCRP and PAP (r=0.253, p=0.024), and also between PAI-1 and PAP (r=-0.239, p=0.033 ) respectively. But, no correlation found between hsCRP and TAFI.CONCLUSIONS: There was correlation between inflammation and fibrinolysis impairment on central obesity. Concentrations oh hsCRP, PAI-1 and TAFI were significantly higher in MetS.KEYWORDS: inflammation, fibrinolysis impairment, hsCRP, PAI-1, PAP, TAFI
Epigenetic Reprogramming Induced Pluripotency Anna Meiliana; Andi Wijaya
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.v3i2.139

Abstract

BACKGROUND: The ability to reprogram mature cells to an embryonic-like state by nuclear transfer or by inducing the expression of key transcription factors has provided us with critical opportunities to linearly map the epigenetic parameters that are essential for attaining pluripotency.CONTENT: Epigenetic reprogramming describes a switch in gene expression of one kind of cell to that of another unrelated cell type. Early studies in frog cloning provided some of the first experimental evidence for reprogramming. Subsequent procedures included mammalian somatic cell nuclear transfer, cell fusion, induction of pluripotency by ectopic gene expression, and direct reprogramming. Through these methods it becomes possible to derive one kind of specialized cell (such as a brain cell) from another, more accessible tissue, such as skin in the same individual. This has potential applications for cell replacement without the immunosuppression treatments commonly required when cells are transferred between genetically different individuals.SUMMARY: Reprogramming with transcription factors offers tremendous promise for the future development of patient-specific pluripotent cells and for studies of human disease. The identification of optimized protocols for the differentiation of iPS cells and ES cells into multiple functional cell types in vitro and their proper engraftment in vivo will be challenged in the coming years. Given that the first small molecule approaches aimed at activating pluripotency genes have already been devised and that murine iPS cells have recently been derived by using non-integrative transient expression strategies of the reprogramming factors, we expect that human iPS cells without permanent genetic alterations will soon be generated.KEYWORDS: epigenetics, reprogramming, pluripotency, stem cells, iPS cells, chromatin, DNA methylation
Correlation of Ghrelin and Obestatin with Waist Circumference in Central Obese Men Widya Kurniawati; Marsetio Donosepoetro; Andi Wijaya
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.v3i2.144

Abstract

BACKGROUND: Central obesity is known as the cause of many metabolic disorders called Metabolic Syndrome. Accumulation of adipocytes in central obesity increases production of cytokines proinflammation. Free fatty acid increases in obesity that drives atherogenic dyslipidemia and insulin resistance. IDF 2005 states that waist circumference (WC) is regarded as the simple criteria of obesity. Energy imbalance lasting for a long period is a determinant factor for obesity, e.g. when energy intake is greater than energy expenditure. The brain and gastrointestinal tract work together to maintain this system. Ghrelin and Obestatin are two gut hormones that work in different ways to keep the energy balance. Ghrelin increases appetite but Obestatin decreases it. The two hormones play an important role in maintaining the dynamic equilibrium of energy balance. This study was aimed to determine correlation of Ghrelin and Obestatin with WC in central obese men.METHODS: This was a cross sectional study involving 53 central obese men. Based on IDF 2005 central obesity is most easily measured by waist circumference using the guidelines ethnic group (not country of residence) specific. We used South Asia ethnic which including Chinese, Malay and Asian Indian population as criteria for this study, that was WC >90 cm, aged 20-60 years. Subjects who had smoking habit, any infectious disease, and ACS were excluded from the study. No restriction was applied on the kind of meals the subjects were having or activities they were doing. The correlation of waist circumference with ghrelin and obestatin was assessed with a significance level of 95% (α=0,05).RESULTS: Patient's age was 40.9623±7.9080 year, waist circumferences was 102.1981±10.2696 cm, weight was 85.8679±16.5475 kg, height was 168.8066±6.3535 cm, BMI was 29.9723±2.4937 kg/m2. Concentration of Ghrelin were 0.70-13.72 ng/mL, and Obestatin 16.66-148.84 pg/mL. Pearson correlation showed that Ghrelin (r=-0.1114, p=0.4271) and Obestatin (r=-0.1781, p=0.2020) had no significant correlation with WC. But in patients WC ≥120 cm had significant negative correlation with Obestatin (r=-0.375, p=0.049).CONCLUSIONS: There was no significant correlation of Ghrelin and Obestatin with WC in obese men. However, there was a negative correlation tendency found in patients with greater WC (≥102 cm).KEYWORDS: obesity, ghrelin, obestatin, waist circumference (WC)
Inflammation is Associated with Vascular Remodeling - Repairing Balances in Hypertensive Obese Subjects Lies Gantini; Syakib Bakri; Andi Wijaya; Anwar Santoso
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.v3i2.140

Abstract

BACKGROUND: Hypertension and obesity are proinflammatory conditions. Vascular remodeling is one of the pathomechanisms reflecting increased cardiovascular (CV) risks and represented as ratio of MMP-9 and sVEGFR-2 concentration. There is no association confirmed between inflammation and remodeling yet. This study was conducted to investigate the correlation between inflammation and vascular remodeling-repairing balances in hypertensive obese subjects.METHODS: This was a cross–sectional study recruited 34 hypertensive obese subjects and 10 hypertensive non obese subjects. They had no antihypertensive medications, neither diabetics nor renal disease and nor acute inflammation detected. Inflammation was assessed as increased hsCRP concentration. Vascular remodeling and repairing were consecutively represented by ratio of MMP-9 and sVEGFR-2.RESULTS: Concentration of hsCRP and MMP-9 were significantly higher in hypertensive obese group than non obese group (2.094±1.90 vs. 0.714±0.40 mg/L; p=0.029; 363.43±143.64 vs. 261.15±61.13 ng/mL, p=0.035, respectively), nonetheless no significant differences of sVEGFR-2 concentration (9.77±2.30 vs. 9.76±1.38 pg/mL, p=0.980) found in both groups. Ratio of MMP-9/sVEGFR-2 was significantly higher in hypertensive obese group than those in non-obese group (38.67±16 vs. 27.22±10, p=0.038). Likewise, they had more subjects with ratio of MMP-9/sVEGFR-2 ≥31.53. This figure is considered as cut-off point of vascular remodeling versus repairing.CONCLUSION: In hypertensive obese subjects, inflammation was activated and vascular remodeling more dominant than repairing process. Inflammation was associated with increased remodeling-repairing balances.KEYWORDS: Matrix Metalloproteinase-9 (MMP-9), soluble Vascular Endothelial Growth Factor Receptor-2 (sVEGFR-2), high sensitivity C-Reactive Protein (hsCRP).
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
Association of Aldosterone, Plasma Renin Activity (PRA) and Superoxide Dismutase (SOD) with Inflammation and Insulin Resistance in Adult Men with Central Obesity Hera Yuliana Intantri; Andi Wijaya; Ilhamjaya Patellongi
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.v3i2.141

Abstract

BACKGROUND: Visceral Obesity is related with chronic low grade inflammation, and is the main component of metabolic syndrome (MetS). MetS is associated with increased cardiovascular disease (CVD). Furthermore, superoxide dismutase (SOD) is correlated with insulin resistance. Several studies have reported a strong correlation between Renin Angiotensin Aldosterone System (RAAS) and CVD, but the association of Aldosterone, Plasma Renin Activity (PRA) and SOD with inflammation, insulin resistance and MetS have not been fully elucidated. The aim of this study was to investigate the correlation of Aldosterone, PRA, and SOD with inflammation (high sensitivity c-reactive protein/hsCRP) and insulin resistance (homeostasis model assessment-insulin resistance/HOMA-IR) in adult men with central obesity.METHODS: This was a cross-sectional study, which was carried out on 80 male subjects with central obesity who were divided into 2 groups: the group of subjects who had fulfilled the MetS criteria and the other group of subjects who did not. After an overnight fasting, blood pressure (BP) was measured on all subjects and laboratory examinations were done for measurement of the concentration of fasting glucose, high density lipoprotein cholesterol (HDL-C), triglyceride, hsCRP, insulin, aldosterone, PRA, and SOD.RESULTS: We found aldosterone had positive correlation with PRA (r = 0.389; p < 0.001) and triglycerides (r =0.234; p=0.036). PRA had positive correlation with SOD (r=0.220; p=0.05) and HDL-C (r=0.273; p=0.014), but not with hsCRP (r=-0.044; p=0.696) and HOMA-IR (r=0.168 p=0.136). PRA correlated with HOMA-IR in MetS (r=0.471; p=0.01). Aldosterone and PRA were correlated with diastolic pressure in those with hypertension (r=0.680; p=0.003 and r=0.608; p=0.01).CONCLUSIONS: There is no direct correlation between aldosterone or SOD and Insulin resistance, and inflammation in men with central obesity. The correlation between PRA and MetS might be through insulin resistance mechanism. We found significant correlation between PRA, HDL-C and SOD. Increased aldosterone was ccorrelated with elevated triglycerides, thus possibly increasing the risk of MetS.KEYWORDS: central obesity, aldosterone, plasma renin activity, superoxide dismutase, inflammation, insulin resistance
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
Progress and Future Challenges of Human Induced Pluripotents Stem Cell in Regenerative Medicine Anna Meiliana; Andi Wijaya
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.v3i2.138

Abstract

BACKGROUND: Less than a decade ago the prospect for reprogramming the human somatic cell looked bleak at best. It seemed that the only methods at our disposal for the generation of human isogenic pluripotent cells would have to involve somatic cell nuclear transfer (SCNT). Shinya Yamanaka in August 2006 in his publication (Cell) promised to change everything by showing that it was apparently very simple to revert the phenotype of a differentiated cell to a pluripotent one by overexpressing four transcription factors in murine fibroblasts.CONTENT: Mouse and human somatic cells can be genetically reprogrammed into induced pluripotent stem cells (iPSCs) by the expression of a defined set of factors (Oct4, Sox2, c-Myc, and Klf4, as well as Nanog and LIN28). iPSCs could be generated from mouse and human fibroblasts as well as from mouse liver, stomach, pancreatic, neural stem cells, and keratinocytes. Similarity of iPSCs and embryonic stem cells (ESCs) has been demonstrated in their morphology, global expression profiles, epigenetic status, as well as in vitro and in vivo differentiation potential for both mouse and human cells. Many techniques for human iPSCs (hiPSCs) derivation have been developed in recent years, utilizing different starting cell types, vector delivery systems, and culture conditions. A refined or perfected combination of these techniques might prove to be the key to generating clinically applicable hiPSCs.SUMMARY: iPSCs are a revolutionary tool for generating in vitro models of human diseases and may help us to understand the molecular basis of epigenetic reprogramming. Progress of the last four years has been truly amazing, almost verging on science fiction, but if we can learn to produce such cells cheaply and easily, and control their differentiation, our efforts to understand and fight disease will become more accessible, controllable and tailored. Ability to safely and efficiently derive hiPSCs may be of decisive importance to the future of regenerative medicine.KEYWORDS: iPSCs, ESC, reprogramming factor, reprogramming efficiency, somatic cell

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