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INDONESIA
Molecular and Cellular Biomedical Sciences (MCBS)
Published by Cell and Biopharmaceutical Institute
ISSN : 25274384     EISSN : 25273442     DOI : -
Core Subject : Health, Science,
Biochemistry, Genetics & Molecular Biology Dentistry Immunology & microbiology Medicine & Pharmacology Neuroscience
Molecular and Cellular Biomedical Sciences (MCBS) has been published by Cell and BioPharmaceutical Institute (CBPI), a biannually published scientific journal, is an open access, peer-reviewed journal that supports all topics in Biology, Pathology, Pharmacology, Biochemistry, Histology and Biomedicine in the aspect of molecular and cellular.
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Articles 7 Documents
 1 
Search results for , issue "Vol 8, No 1 (2024)" : 7 Documents clear
Chlorogenic Acid Protects Cell Death in the Cerebellum through Anti-Apoptotic Protein Bcl2 in Transient Global Ischemia Cases Hermawati, Ery; Handini, Mitra; Ilmiawan, Muhammad In'am; Mahyarudin, Mahyarudin
Molecular and Cellular Biomedical Sciences Vol 8, No 1 (2024)
Publisher : Cell and BioPharmaceutical Institute

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21705/mcbs.v8i1.411

Abstract

Background: Cerebellum is one of the vital components of the brain that will be affected by ischemia-reperfusion (IR) injury. IR injury will increase free radicals, which in turn can trigger apoptosis and cell death. Therefore, this study was conducted to examine the effect of chlorogenic acid administration on apoptosis and the number of cells in the cerebellum of rats with global ischemic transients.Materials and methods: Wistar rats were divided into five groups: sham-operated (C1), IR (C2), IR + 15 mg/kgBW chlorogenic acid (T1), IR + 30 mg/kgBW chlorogenic acid (T2), and IR + 60 mg/kgBW chlorogenic acid (T3). C2, T1, T2, and T3 groups received bilateral common carotid occlusion (BCCO) surgery to induce IR injury. Thirty minutes after BCCO surgery, T1, T2, and T3 rats were administered chlorogenic acid in various doses intraperitoneally. RNA extraction and real-time polymerase chain reaction (PCR) measurements were then performed on NeuN, Bcl2, Bax, caspase 3, as well as on GAPDH as housekeeping genes.Results: There were significant differences in NeuN expressions between groups, with the highest expression shown in C1 followed by T3. Bcl2 expressions were also significantly different between groups, and rats in C1 and T3 showed to be significantly higher compared to C2, while T1 was significantly lower than C1. However, Bax and caspase 3 expressions showed no significant differences.Conclusion: Chlorogenic acid in 60 mg/kgBW dose increases NeuN expression and Bcl2 mRNA expression after transient global ischemia. These increases might correlate with the heightened level of protection against apoptosis in the cerebellum, hence showing its potential in protecting neuron cells.Keywords: transient global ischemia, chlorogenic acid, cerebellum, apoptosis
Application of Omics and Bioinformatics Technologies in Response to COVID-19 Pandemic Aga, Abebe Mengesha; Woldesemayat, Adugna Abdi
Molecular and Cellular Biomedical Sciences Vol 8, No 1 (2024)
Publisher : Cell and BioPharmaceutical Institute

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21705/mcbs.v8i1.363

Abstract

The medical biotechnology community has undertaken significant endeavors to gain a comprehensive understanding of SARS-CoV-2’s biology and pathogenesis mechanisms. Omics approaches and technologies have been widely employed in the fight against SARS-CoV-2. Since the onset of the virus outbreak, researchers have demonstrated how recent omics and bioinformatics technological advancements have contributed to the diagnosis, vaccine development, treatment, and control of disease transmission. Studies conducted since the outbreak have been collected and summarized, with a focus on bioinformatics approaches and their contribution to controlling this pandemic. Developments and advanced omics technology in connection to the COVID-19 pandemic have been analyzed. The multi-omics technology, which offers various strategies in identifying potential diagnostics, therapeutics, studies of variants of concern, and drug repurposing approaches, has been assessed. Pandemic response has seen the application of multi-omics and pan-genomics approaches, including genomics, metabolomics, transcriptomics, proteomics, epigenomics, clustered regularly interspaced short palindromic repeats (CRISPR) technology, host-pathogen interactions, artificial intelligence, and machine learning in various research areas. Additionally, bioinformatics and mathematical modeling have played a significant role in disease control. The use of smart technologies to control virus transmission and predict patients’ health conditions and treatment outcomes has also been crucial. Transcriptome analysis has emerged as a major application, contributing to the generation of new knowledge on viral sequences and intracellular signaling pathways that regulate viral infection and pathogenesis mechanisms. The sequencing of the virus has paved the way for the use of omics technologies and an integrative technique in combating the pandemic. In general, the advancement of omics technology during this pandemic has been fascinating and has contributed a significant role to the science of health biotechnology in general and omics and bioinformatics in particular.Keywords: bioinformatics, coronavirus, COVID-19, omics, SARS COV-2
Percutaneous Secundum Atrial Septal Defect Closure: Failure Rate and Procedural Predictors Yuwono, Elien; Gunawijaya, Eka; Yantie, Ni Putu Veny Kartika
Molecular and Cellular Biomedical Sciences Vol 8, No 1 (2024)
Publisher : Cell and BioPharmaceutical Institute

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21705/mcbs.v8i1.442

Abstract

Background: Percutaneous atrial septal defect (ASD) closure is one of therapeutic options for patients with a suitable ASD anatomy, however in developing countries, the exact figure and procedural characteristics remain unknown. Therefore, this study was conducted to identify the failure rate and procedural predictors of the percutaneous ASD closure.Materials and methods: A retrospective study using a database of all patients undergoing percutaneous ASD closure was conducted between March 2010 to November 2023. Patients who developed a pulmonary hypertensive crisis during the procedure were excluded. Procedural and echocardiographic parameter were measured and analyzed.Results: A total of 112 samples were included in this study, 74.1% were female and 55.36% were pediatric patients. The failure rate was 12.5% (n=14) with diameter index was higher in the failed group. Unpaired T-test revealed that ASD size was one of the predictor failure in pediatric patients (mean diameter: 24.7±6.46 mm vs. 16.36±5.94 mm, p=0.001). There were no statistically significant variations in rim diameters, while compared with all patients with appropriate rims (rim ≥7mm), the failure rate was higher in patients with two rims measuring between 5.9 and 6.9 mm and rims less than 5 mm. Two patients presented with device embolization and required surgical device removal.Conclusion: The failure rate of percutaneous ASD closure was 12.5%. A larger ASD increases the risk of failure of percutaneous closure in pediatric patients. Furthermore, patient with 5-6.9 mm on two or more rims as well as those with rim less than 5 mm, have a higher failure rate.Keywords: secundum atrial septal defect, percutaneous closure, failure rate
Molecular Adaptation of Cardiac Remodeling in Metabolic Syndrome: Focus on AMPK, SIRT1 and PGC-1a Ramadhan, Andika Yusuf; Soetikno, Vivian
Molecular and Cellular Biomedical Sciences Vol 8, No 1 (2024)
Publisher : Cell and BioPharmaceutical Institute

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21705/mcbs.v8i1.367

Abstract

Obesity, lack of physical activity, and genetic predisposition might play a pivotal role in pathogenesis of metabolic syndrome. Cardiac function alteration including hemodynamic changes, contractility function, arrhythmia, and cellular respiratory function, might happen due to chronic condition in metabolic syndrome. Insulin resistance, neurohormonal activation and chronic inflammation might contribute to these changes. Cardiomyocyte had capabilities to adapt from these abnormalities, one of them is the activation of cellular pathway to resist cardiac injury from metabolic syndrome. This molecular pathway involves three proteins, including AMP-activated protein kinase (AMPK), sirtuin-1 (SIRT1) and peroxisome proliferator-activated receptor γ coactivator-α (PGC-1α). The aim of this narrative review is to elucidate role of AMPK, SIRT1, and PGC-1α in cardiac adaptation against cardiac dysfunction in metabolic syndrome. AMPK, SIRT-1, and PGC-1α contribute to adapt and to repair the cardiac injury resulting from celullar and mechanical stress from metabolic syndrome and prevent cardiac remodeling event. Several pathological events, such as insulin resistance, induce alteration of switching energy fuel to the heart, causing cardiomyocte to rely on glucose metabolism and lipotoxicity, leading to damages of cardiomyocyte through reactive oxygen species (ROS) generation and lipid peroxidation. Increase of ROS promotes cardiac injury followed by necrotic and apoptotic events. AMPK, SIRT1, and PGC-1α act as cardioprotector molecule against metabolic syndrome insults to several mechanism such as: AMPK play role as counter act of lipotoxicity and insulin resistance through increasing insulin sensitivity and regulate redox reaction. SIRT1 plays role in regulating apoptotic genes and PGC-1α repairs cardiac fuel sources. Activation of AMPK/SIRT1/PGC-1α prevent cardiac remodeling due to metabolic syndrome by increasing insulin sensitivity, increases mitochondrial biogenesis and reduce pro-apoptotic signals in cardiomyocte.Keywords: AMPK/SIRT1/PGC-α, cardiac remodeling, metabolic syndrome
The Role of Hypoxia-inducible Factor in Mycobacterium tuberculosis-infected Macrophages Fitriana, Nina; Iswanti, Febriana Catur; Sadikin, Mohamad
Molecular and Cellular Biomedical Sciences Vol 8, No 1 (2024)
Publisher : Cell and BioPharmaceutical Institute

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21705/mcbs.v8i1.405

Abstract

Tuberculosis is caused by Mycobacterium tuberculosis infection. During M. tuberculosis infection, there is a decrease in the partial pressure of oxygen in the granuloma microenvironment, which causes the hypoxia-inducible factor (HIF) to become stable. HIF functions as a transcription factor that regulates the expression of genes crucial for metabolic adaptation in hypoxic conditions. Recent research suggests that HIF plays a vital role in infectious and inflammatory conditions. Several studies have demonstrated that HIF signaling can enhance macrophages antimicrobial activity and bactericidal effect against M. tuberculosis, such as increasing macrophage autophagy, enhancing the effects of rifampicin, inhibiting p38 MAPK signaling, enhancing the regulation of effector antimicrobial pathways mediated by human β defensin 2 (hBD2) and vitamin D receptor (VDR), redirecting energy metabolism to glycolysis, and producing various cytokines. All these responses ultimately result in the inhibition of intracellular M. tuberculosis growth. HIF has therapeutic implications, potentially being a new candidate for host-directed therapy as a complement to existing antituberculosis drugs. Understanding the role of HIF in macrophages during M. tuberculosis infection and comprehending the host-pathogen relationship with M. tuberculosis is advantageous for developing future therapies.Keywords: Mycobacterium tuberculosis, macrophages, hypoxia-inducible factor
Potency of Peripheral Blood- and Umbilical Cord Blood-derived Dendritic Cells and Their Secretomes as Vaccines for Cancer Haifa, Rima; Sartika, Cynthia Retna; Faried, Ahmad; Hadisaputri, Yuni Elsa; Chouw, Angliana; Wijaya, Andi; Barliana, Melisa Intan
Molecular and Cellular Biomedical Sciences Vol 8, No 1 (2024)
Publisher : Cell and BioPharmaceutical Institute

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21705/mcbs.v8i1.358

Abstract

Dendritic cell (DC) vaccines, as immunotherapy agents, can gather up and transport cancer-related antigens to T lymphocytes, activating anti-tumor effector responses. After being activated by DC, cytotoxic T lymphocyte cells (CTL) will secrete the cytolytic granzyme B that can effectively induce rapid apoptosis of target cells. On the other hand, DC also secrete several cytokines and a large number of exosomes, which together operate as a whole antigen-presenting entity. The efficacy of the vaccine’s treatment may be affected by the sources used for DC vaccines. Umbilical cord blood (UCB) from healthy donors can be employed when autologous cancer patient’s peripheral blood (PB) cannot be used as a source for isolating DC due to genetic abnormalities. Comparing UCB to other sources, there is a painless method of collecting sources as opposed to PB, which necessitates a venipuncture or leukapheresis procedure to isolate the blood. Many studies related to the use of PB-DC have been carried out, but research on potential comparisons between PB-DC and UCB-DC is still very limited. In this review, the potential of PB- and UCB-derived DC and their secretomes for cancer will be discussed.Keywords: dendritic cells, vaccines, umbilical cord blood, peripheral blood
Angiotensin-Converting Enzyme Genetic Polymorphism rs4343 as Risk of Diabetic Nephropathy in Jambi-Malay Population Elfiani, Elfiani; Puspasari, Anggelia; Arif, Cut Wulan; Maharani, Citra; Ali, Zulkhair; Suhaimi, Novadian; Effendi, Ian; Suprapti, Suprapti; Shafira, Nyimas Natasha Ayu
Molecular and Cellular Biomedical Sciences Vol 8, No 1 (2024)
Publisher : Cell and BioPharmaceutical Institute

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21705/mcbs.v8i1.410

Abstract

Background: Diabetic nephropathy (DN) is one of the frequent complications of type II diabetes mellitus (T2DM) in Jambi province. Controlling blood glucose and blood pressure does not guarantee DN prevention, since genetic factors may also contribute to this disease. Multi-ethnic studies showed that one of the strongest genetic factors associated with DN was single nucleotide polymorphism rs4343 of angiotensin-converting enzyme (ACE) gene. Study regarding phenotype-genotype association of ACE rs4343 and DN has not yet been performed in Jambi Province, which is dominated by Malay ethnicity. This study was conducted to reveal the association between ACE rs4343 and the risk of DN in the Jambi-Malay population.Materials and methods: This was a cross-sectional study involving 75 subjects (44 with DN and 31 without DN) who suffered from T2DM and hypertension. DN was defined as albumin to creatinine ratio (ACR) ≥30 mg/g. Genotyping was performed with one-step tetra amplification refractory mutation system-polymerase chain reaction (PCR) using specific primer for ACE rs4343. Bivariate and multivariate analyses were performed to analyze the genetic risk for DN.Results: The bivariate analysis showed the proportion of DN subjects was higher than non-DN within the AG genotype (11:1) than within the AA (33:30) genotype. This difference was statistically significant (p=0.012; OR (95% CI): 10.00 (1.22-82.15)). Multivariate analysis showed that AG genotype (p=0.047; OR (95% CI): 10.04 (1.03-97.31)) and uncontrolled blood pressure (p=0.001; OR (95% CI): 6.72 (2.08-21.71)) were the risk factors of DN in the Jambi-Malay population.Conclusion: Polymorphism of ACE rs4343 is a risk factor of DN in the Jambi-Malay Population.Keywords: rs4343, angiotensin-converting enzyme gene, diabetic nephropathy, Malay, Jambi

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