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All Journal The Indonesian Biomedical Journal Molecular and Cellular Biomedical Sciences (MCBS)
Anna Meiliana
Department Of Pharmacology And Clinical Pharmacy, Faculty Of Pharmacy, Universitas Padjadjaran, Jl. Raya Bandung-Sumedang Km 21, Jatinangor 45363
Biochemistry, Genetics & Molecular Biology Dentistry Immunology & microbiology Medicine & Pharmacology Neuroscience Public Health

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Relationship between Circulating Protein p53 and High Sensitivity C-Reactive Protein in Central Obesity Men with Inflammaging Rina Triana; Anna Meiliana; Eli Halimah; Andi Wijaya
The Indonesian Biomedical Journal Vol 11, No 1 (2019)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v11i1.436

Abstract

BACKGROUND: The mechanism of aging goes along with age, one of which is characterized by cellular senescent, which occurs mostly in adipose tissue. Adipose tissue is the site of accumulation of large cell senescent, in the regulation of obesity and aging. Proteins p53 is marker for cell senescent, which are also known to induce inflammation. This study was aimed to determine the relationship between circulating protein p53 and high sensitivity C-reactive protein (hsCRP) in central obese men with inflammaging.METHODS: The study design is an observational study with cross-sectional approach. The subjects were 75 central obese men (waist circumference/WC > 90 cm), aged ≥ 45 years old. Subjects were divided into 2 age groups, those are middle age group: 45-59 years old (50.7%) and elderly group: ≥ 60 years old (49.3%). Examination of circulating p53 was done using enzyme-linked immunosorbent assay (ELISA) method, and the hsCRP examination was done by chemiluminescent method.RESULTS: It was found that there was a correlation between circulating p53 and hsCRP in elderly (r=-0.414; p<0.05) but not in middle age (r=-0.127; p=0.449).CONCLUSION: From this study, it is assumed that more senescence cells in elderly are resulting in increased chronic inflammation.KEYWORDS: aging, senescent, inflammaging, protein p53, hsCRP
Apoptosis and Efferocytosis in Inflammatory Diseases Chandra Agung Purnama; Anna Meiliana; Melisa Intan Barliana; Keri Lestari Dandan; Andi Wijaya
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.v13i3.1608

Abstract

BACKGROUND: Millions of cells in multicellular organisms regenerate every day to replace aged and died cells. Effective cell clearance (efferocytosis) is critical for tissue homeostasis, as the human body recycles its cellular components. We summarize what is known about the mechanisms of efferocytosis and how it impacts the physiology of the organism, effects on inflammation and the adaptive immune response, as well as the consequences of defects in this critical homeostatic mechanism in this review.CONTENT: Cell death is the process by which the human body replaces aged or damaged cells with new ones. It can be triggered by genetically encoded machinery or regulated cell death, or by specific pharmacologic or genetic interventions, resulting in accidental cell death. Dying cells release signals that entice phagocytes to engulf them in a process known as efferocytosis. Efferocytosis is a multistep process involving the release of “find me” and “eat me” signals and destruction of death cells by phagocytes. Different types of cell death including apoptosis and necroptosis can express pro- or anti-inflammatory signals via macrophage activity modulation.SUMMARY: Failed or ineffective efferocytosis can result in disruption of tissue homeostasis, which can contribute to the development of chronic inflammatory diseases such as atherosclerosis, obesity, diabetes, and heart failure. Therefore, any therapeutic strategy that enhances efferocytosis will have a beneficial effect on the treatment of these metabolic disorders.KEYWORDS: apoptosis, necroptosis, phagocytosis, efferocytosis, macrophage.
Red Meats and Processed Meat as the Carcinogenic Foods and Phytochemical-chemoprevention Anna Meiliana; Nurrani Mustika Dewi; Andi Wijaya
The Indonesian Biomedical Journal Vol 11, No 3 (2019)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v11i3.965

Abstract

BACKGROUND: Along with its increased prevalence, in the past decade, cancer had joined the list of chronic debilitating diseases. Nutrition become substantial aspects, due to its time-dependent effect to modulate inflammation thus trigger carcinogenic effects by altering the immune check point. Thus, nutrition contributes to the progression and therapeutic response of cancer, both in human or animal models.CONTENT: Meat is well favored food with appreciable appealing. Due to its high nutritional values it plays a central role in human development. Meat or meat derivate are important sources of proteins, minerals and vitamins. Their nutritional importance is worth compare to their economic impact but recent publication of WHO has set the social alarm about the relationship between red and/or processed meat consumption and cancer. On the other side, some natural or biologic agents may inhibit or reverse tumor growth. Some phytochemical agents including curcumin, resveratrol, lycopene, folates and tea polyphenols clinically proved to tune the signaling pathways regulating cell proliferation and apoptosis in transformed cells, enhance the host immune system and sensitize malignant cells to cytotoxic agents.SUMMARY: Recent studies on chemopreventive agents involves a wide range of molecules, natural (plants, fruits and vegetables) or synthetic will provide better insights for cancer early pathogenesis, important end-point biomarker, and finally potential for reducing the burden of cancer.KEYWORDS: blocking agents, suppressing agents, red meat, processed meat, chemoprevention, phytochemicals
Stem Cell Therapy in Wound Healing and Tissue Regeneration Anna Meiliana; Nurrani Mustika Dewi; Andi Wijaya
The Indonesian Biomedical Journal Vol 8, No 2 (2016)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v8i2.191

Abstract

BACKGROUND: Recent advances in our basic knowledge of the tissue damage and regeneration pathology have combined with a remarkable progress in stem cell biology so the prospect of clinical tissue repair strategies is a tangible reality. We tried to describe a better view about mesenchymal stem cell (MSC) mechanisms in wound healing and tissue regeneration, sending any ideas for next advanced therapies.CONTENT: Sustaining injury, whether minor or major, is part of every organism life. Therefore, efficient response mechanisms to damage have developed. Wound healing is a perplexing multi-step processes which can be divided into three major phases: inflammation, proliferation, and scar formation/remodeling. Though the compartementalization of this process into discrete stages give the illusion of simplicity, but in reality it is much more complicated. So that efficient healing can occur, complex interactions between multiple cell types, soluble factors and extracellular matrix components are required to rebuild the tissue. Even under optimal conditions, the healing process drives to fibrosis or scar. The latest technology that makes a huge difference in the wound healing process is stem cell therapy, which offers a novel approach to many diseases.SUMMARY: Wound healing therapies continue to rapidly evolve, with advances in basic science and engineering research heralding the development of new therapies, as well as ways to modify existing treatments. Stem cell-based therapy is one of the most promising therapeutic concepts for wound healing. Advances in stem cell biology have enabled researchers and clinicians alike with access to cells capable of actively modulating the healing response. KEYWORDS: wound healing, tissue regeneration, stem cells therapy
Novel Biomarkers in Cardiovascular Disease: A Review Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 2, No 3 (2010)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v2i3.122

Abstract

BACKGROUND: The investigation of novel circulating serum and plasma biomarkers in patients with cardiovascular disease has been accelerating at a remarkable pace. New markers or tests are often presented too early to the medical profession, potentially leading to overuse and, thus, extra burden and costs to patients, the healthcare industry, and the economy. The challenge for clinicians and medical researchers is how to optimally apply existing and new markers/tests.CONTENT: Biomarkers are biological parameters that can be objectively measured and quantified as indicators of normal biologic processes, pathogenic processes, or responses to a therapeutic intervention. Typically thought of as disease process screening, diagnosing, or monitoring tools, biomarkers may also be used to determine disease susceptibility and eligibility for specific therapies. Cardiac biomarkers are protein components of cell structures that are released into circulation when myocardial injury occurs. They play a pivotal role in the diagnosis, risk stratification, and treatment of patients with chest pain and suspected acute coronary syndrome (ACS) as well as those with acute exacerbations of heart failure.SUMMARY: Active investigation has brought forward an increasingly large number of novel candidate markers but few have withstood the test of time and become integrated into contemporary clinical care because of their readily apparent diagnostic, prognostic, and/or therapeutic utility. With regard to the more novel biomarkers, careful thought is needed with regard to the appropriate target populations for discovery and validation, as well as the criteria used to sort out the contenders from the pretenders.KEYWORDS: biomarker, cardiovascular disease, atherosclerosis, acute myocardial infarction, heart failure, risk stratification, diagnosis, prognosis
Metaflammation, NLRP3 Inflammasome Obesity and Metabolic Disease Anna Meiliana; Andi Wijaya
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.v3i3.148

Abstract

BACKGROUND: Increasing prevalence of obesity gives rise to many problems associated with multiple morbidities, such as diabetes, hypertension, heart disease, sleep apnea and cancer. The mechanism of obesity is very complex, thus its link to various disease is poorly understood. This review highlights important concepts in our understanding of the pathogenesis of obesity and related complications.CONTENT: Many studies have tried to explore the exciting and puzzling links between metabolic homeostasis and inflammatory responses. A form of subclinical, low-grade systemic inflammation is known to be associated with both obesity and chronic disease. This, later called as "metaflammation", refers to metabolically triggered inflammation. The nutrient-sensing pathway and the immune response coordination are facilitated by these molecular sites in order to maintain homeostasis under diverse metabolic and immune conditions. Recent studies have found that the NLRP3 inflammasome during metabolic stress forms a tie linking TXNIP, oxidative stress, and IL-1β production. This provides new opportunities for research and therapy for the disease often described as the next global pandemic: type 2 diabetes mellitus (T2DM).SUMMARY: The crucial role of metaflammation in many complications of obesity shown by the unexpected overlap between inflammatory and metabolic sensors and their downstream tissue responses. Then great interest arose to explore the pathways that integrate nutrient and pathogen sensing, give more understanding in the mechanisms of insulin resistance type 2 diabetes, and other chronic metabolic pathologies. A family of intracellular sensors called NLR family is a critical component of the innate immune system. They can form multiprotein complexes, called inflammasome which is capable of responding to a wide range of stimuli including both microbial and self molecules by activating the cysteine protease caspase-1, leading to processing and secretion of the proinflammatory cytokines IL-1β and IL-18, which play crucial roles in host defense. Inflammasome dysregulation has been linked to some autoinflammatory and metabolic diseases. These provide opportunities to continue to improve our understanding of the nature of metaflammation in the hope of modifying it to prevent and treat diseasese.KEYWORDS: Inflammation, metaflammation, inflammasome, metabolic disease, obesity
Potential Biomarkers for Diagnosis and Screening of Autism Spectrum Disorders Anna Meiliana; Andi Wijaya
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.v6i3.27

Abstract

BACKGROUND: Autism spectrum disorder (ASD) is a highly heritable neurodevelopmental condition, which is typically characterized by a triad of symptoms: impaired social communication, social reciprocity and repetitive stereotypic behavior. While the behavioral phenotype of ASD is well described, the search for reliable ‘autism biomarkers’ continues.CONTENT: Insulin growth factor (IGF) is essential for the myelination of developing fetal neurons; this is in addition to the well-known links between IGF, maternal inflammation, infection and autism supporting IGF as a potential marker. Combining IGF data with data regarding levels of the known markers, serotonin and anti-myelin basic protein, in order to calculate an autism index, could provide a new diagnostic method for at-risk neonates. Disruptions to multiple pathophysiological systems, including redox, folate, methylation, tryptophan metabolism, and mitochondrial metabolism, have been well documented in autistic patients. Maternal infection and inflammation have known links with autism. Autoimmunity has therefore been a well-studied area of autism research. The potential of using autoantibodies as novel biomarkers for autism, in addition to providing insights into the neurodevelopmental processes that lead to autism.SUMMARY: The six proposed causes of autism involve both metabolic and immunologic dysfunctions and include: increased oxidative stress; decreased methionine metabolism and trans-sulfuration: aberrant free and bound metal burden; gastrointestinal (GI) disturbances; immune/inflammation dysregulation; and autoimmune targeting. A newborn screening program for early-onset ASD should be capable of utilizing a combination of ASD-associated biomarkers representative of the six proposed causes of autism in order to identify newborns at risk. The biomarkers discussed in this article are useful to guide the selection, efficacy and sufficiency of biomedical interventions, which would likely include nutritional supplementation, dietary changes and specific medications for treating GI pathogens and reducing inflammation.KEYWORDS: ASD, autism, biomarkers, newborn screening, diagnosis
Molecular Mechanisms of Cardiovascular Aging Anna Meiliana; Andi Wijaya
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.v5i3.64

Abstract

BACKGROUND: The average lifespan of humans is increasing, and with it the percentage of people entering the 65 and older age group is growing rapidly and will continue to do so in the next 20 years. Within this age group, cardiovascular disease will remain the leading cause of death, and the cost associated with treatment will continue to increase. Aging is an inevitable part of life and unfortunately poses the largest risk factor for cardiovascular disease.CONTENT: We provide an overview of some of the molecular mechanisms involved in regulating lifespan and health, including mitochondria, telomeres, stem cells, sirtuins, Adenosine Monophosphate-activated Protein Kinase, Mammalian Target of Rapamycin and Insulin-like Growth Factor 1. We also provide future perspectives of lifespan and health, which are intimately linked fields.SUMMARY: Aging remains the biggest non-modifiable risk factor for cardiovascular disease. The biological, structural and mechanical changes in senescent cardiovascular system are thought to contribute in increasing incidence of cardiovascular disease in aging. Understanding the mechanisms contributing to such changes is therefore crucial for both prevention and development of treatment for cardiovascular diseases.KEYWORDS: cardiovascular aging, mitochondria, telomeres, sirtuin, stem cells
New Insight in The Molecular Mechanisms of Neurodegenerative Disease Anna Meiliana; Nurrani Mustika Dewi; Andi Wijaya
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.v10i1.448

Abstract

BACKGROUND: Redox and proteotoxic stress contributes to age-dependent accumulation of dysfunctional mitochondria and protein aggregates, and is associated with neurodegeneration. The free radical theory of aging inspired many studies using reactive species scavengers such as alpha-tocopherol, ascorbate and coenzyme-Q to suppress the initiation of oxidative stress. However, clinical trials have had limited success in the treatment of neurodegenerative diseases (NDDs).CONTENT: The misfolding and aggregation of specific proteins is a seminal occurrence in a remarkable variety of NDDs. In Alzheimer’s disease, the two principal aggregating proteins are β-amyloid (Aβ) and tau. The abnormal assemblies formed by conformational variants of these proteins range in size from small oligomers to the characteristic lesions that are visible by optica lmicroscopy, such as senile plaques and neurofibrillary tangles. Pathologic similarities with prion disease suggest that the formation and spread of these proteinaceous lesions might involve a common molecular mechanism, corruptive protein templating. The accumulation of redox modified proteins or organelles cannot be reversed by oxidant intercepting antioxidants and must then be removed by alternative mechanisms. Autophagy serves this essential function in removing damaged or dysfunctional proteins and organelles thus preserving neuronal function and survival.SUMMARY: Senescent cells and their senescence-associated secretory phenotypes (SASPs) may constitute a novel, understudied, and potentially important contributor to neuro-inflammation and subsequent neurodegeneration. Characterization of cellular senescence in the brain could uncover novel therapeutic targets for the prevention and treatment of chronic age-related NDDs.KEYWORDS: brain, aging, neurodegeneration, DNA damage, senescence, neuro-inflammation, mitochondria, lysosome, proteostasis, prion, amyloidosis
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
Co-Authors Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya ANDI WIJAYA Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Arifin, Arief Riadi Babikian, Haig Chandra Agung Purnama Eli Halimah Erizal Sugiono, Erizal Ferdy Ferdian Gatot S. Lawrence Gatot Susilo Lawrence Iceu Dimas Kulsum Ida Paulina Sormin Ilhamjaya Patellongi Ilhamjaya Patellongi Irma Ruslina Defi Ismail, Efriadi Keri Lestari lhamjaya Patellongi Lucia Herminawati Melisa Intan Barliana Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi, Nurrani Mustika Prayudi Santoso Qiantori, Adziqa Ammara Rina Triana Rosalia E Napitupulu Rosdianto, Aziiz Mardanarian Setiawan Setiawan Sumalim, Yelsen Suryani As&#039;ad Suryani As&#039;ad Suryani As’ad Yovita Hartantri