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Abstract Topic: Cellular, Tissue and Genetic Engineering

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Analysis of Contributor Molecule in Dura mater Healing Process
Hendrikus Masang Ban Bolly1,2,3, Yulius Hermanto4, Ahmad Faried2, Muhammad Zafrullah Arifin2, Firman Fuad Wirakusumah5

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Corresponding Author
HENDRIKUS MASANG BAN BOLLY

Institutions
1Doctoral Program in Medicine, Faculty of Medicine Universitas Padjadjaran, Bandung Indonesia
2Department of Neurosurgery, Faculty of Medicine Universitas Padjadjaran-Hasan Sadikin Hospital, Bandung Indonesia
3Lecture in Faculty of Medicine, Cenderawasih University, Paua, Indonesia
4Neurosurgery Division, Surgery Department, Faculty of Medicine Riau University, Riau Indonesia
5Department of Obstetrics and Gynecology, Faculty of Medicine Universitas Padjadjaran- Hasan Sadikin Hospital, Bandung Indonesia

Abstract
OBJECTIVE Dura mater is a special tissue that has a critical function in brain anatomy and physiology. This tissue contained some numerous cells, stem cells, and growth factors. This research investigate the protein interaction that contribute to dura mater healing process. METHOD To identify and predict in silico of functional protein interaction in dura mater healing process, we use available analysis software to perform the protein-protein interaction (PPI) analysis (http://gpsprot.org/index.php). GPS Protein is an interactive platform for visualizing human protein interaction by integrating HIPPIE and CORUM databases. We excluded HIV-1 proteomic and RNAi databases, hence focused on human PPI (Confidence level 0.75). Two proteins were inputted as query to identify the potential protein network in dural healing according to previous studies, i.e fibroblast growth factor-2 (FGF2) and transforming growth factor beta-1 (TGFB1). RESULTS In previous study used dura mater cells culture found the role fibroblast in dura mater healing process, FGF-2 and TGFB as the promoters of dural closure. PPI results showed the more important role of TGFB1 with more interactions of TGFB1 to some remodeling proteins (COL, ITG, MMP etc). TGFB1 encoded regulates cell proliferation, differentiation, growth, modulate expression and activation of other growth factors, also induce epithelial-to-mesenchymal transition (EMT) and cell migration in various cell types. CONCLUSION This bioinformatics approach is an efficient and cheaper method for analyzed the molecular aspect of protein that have a special contribution in dura mater healing process. This results could help to focused the further research in more complex laboratory examinations.

Keywords
Duramater, TGFB1, healing, protein interaction

Topic
Cellular, Tissue and Genetic Engineering

Link: https://ifory.id/abstract/kZRn9PpgLXfB


CALCITRIOL INHIBITS PROLIFERATION AND INDUCES APOPTOSIS IN B16-F10 “POTENTIAL ANTICANCER ADJUVANT”
Daniar Amarassaphira (a*), Ronny Lesmana (b,c), Hanna Goenawan (b,c), Yuni Susanti Pratiwi (b,c), Iwan Setiawan (b), Nova Sylviana (b,c), Eva Krisna Sutedja (d), Budi Setiabudiawan (e), Raden Tina Dewi Judistiani (f), and Unang Supratman (g)

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Corresponding Author
Daniar Amarassaphira

Institutions
a) Undergraduate Program Medical Doctor, Faculty of Medicine, Universitas Padjadjaran, Jatinangor 45363, Indonesia.
b) Physiology Division, Department of Biomedical Sciences, Faculty of Medicine, Universitas Padjadjaran, Jatinangor 45363, Indonesia.
c) Physiology Molecular Laboratory, Biological Activity Division, Central Laboratory, Universitas Padjadjaran, Jatinangor 45363, Indonesia.
d) Departement of Dermatology and Venerology, Faculty of Medicine, Universitas Padjadjaran, Bandung 40161, Indonesia.
e) Departement of Pediatric, Faculty of Medicine, Universitas Padjadjaran, Bandung 40161, Indonesia.
f) Departement of Public Health, Faculty of Medicine, Universitas Padjadjaran, Bandung 40161, Indonesia.
g) Department of Chemistry, Faculty of Mathematics and Natural Sciences, Universitas Padjadjaran, Jatinangor 45363, Indonesia.

Abstract
Melanoma is one of the most aggressive types of cancer. Showing a remarkable surge in the last 50 years, melanoma has been projected to be continuously rising in the future. Therapy for advanced type melanoma still becomes a challenge due to low response rate and survival in 10 years. Interestingly, connected with the survival, several epidemiological and preclinical studies had reported that vitamin D deficiency had an association with the progression in several cancer types. Feldman et al 2014 had reported, both in vivo and in vitro studies revealed antiproliferative, antiangiogenic, apoptosis, and differentiation induction effects of calcitriol in various types of cancers. Unfortunately, the study about the calcitriol (1,25(OH)2D3) effects toward melanoma is still limited and its mechanism remains unclear. In the present study, by utilizing B16-F10 melanoma cell line, we elaborate calcitriol antiproliferative effect using MTS Assay in a dose-dependent manner for 24 hours and potential calcitriol-induced apoptosis signaling pathway using Western Blot. We had observed that calcitriol may inhibit melanoma cell proliferation in IC50 of 93.8 ppm lead to the induction of apoptosis-related proteins such as caspase-3, caspase-9, poly (ADP-ribose) polymerases (PARP), mTOR, and HIF1α. These calcitriol-s effects reflect its potential capability as potent adjuvant therapy for melanoma. Taken together, calcitriol inhibited cell proliferation and induced cell death in B16-F10 cell. Thus, showed its potential to be adjuvant therapy for treating melanoma.

Keywords
calcitriol, caspase-3, caspase-9, PARP, mTOR, HIF1α, B16-F10 cell.

Topic
Cellular, Tissue and Genetic Engineering

Link: https://ifory.id/abstract/yvqBZYHg2pkQ


Gene Mutation Detection for Breast Cancer Disease: A Review
Untari N. Wisesty*, Tati Rajab Mengko, Ayu Purwarianti

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Corresponding Author
Untari Novia Wisesty

Institutions
Institut Teknologi Bandung
Bandung Indonesia
*untarinw[at]telkomuniversity.ac.id

Abstract
Breast cancer is one of the most common diseases suffered, especially by women, in the world, and about 2 billion new cases of patients with breast cancer in 2018. Therefore, it is very important to detect cancer early. Early detection of cancer can be done through the analysis of DNA abnormalities from blood cell samples, where the sampling does not require surgery, non-invasive and painless, and can reduce the sampling cost. DNA abnormalities can occur due to heredity or mutase gene. This mutase gene causes uncontrolled cell division. There are several types of gene mutations that can occur, namely point mutation and base-pair insertion and deletion mutation. Point mutation is the occurrence of changes in one or several specific genes that do not change the length of DNA, while the base-pair mutation is the addition or deletion of several genes so that the length of the DNA becomes different. From several studies that have been conducted in the medical field there are mutations in the BRCA1, BRCA2, and PALB2 genes, where mutations in these genes can cause an increased risk of breast cancer. Other mutase genes associated with cancer risk are ATM, BARD1, CDH1, CHEK2, MRE11A, NBN, TP53, PALB2, PTEN, RAD50, RECQL, RINT1. In this paper a literature review is conducted on the methods used in bioinformatics to detect mutase genes including Fourier Transform, Discrete Wavelet Transform, Support Vector Machine, Bayesian, Decision Tree Regression Model, Neural Network, Stack Autoencoder, Deep Boltzmann Machine and Tumor Covariate Signature Model.

Keywords
Breast Cancer, Gene Mutation, Mutation Detection, Pattern Recognition.

Topic
Cellular, Tissue and Genetic Engineering

Link: https://ifory.id/abstract/JmtyF6h3vUnB


ISOLATION AND CULTURE OF RAT EMBRYONIC FIBROBLAST (REF)
Dwi Budiono1, Ratih Rinendyaputri2 dan Vista Budiariati1

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Corresponding Author
Ratih Rinendyaputri

Institutions
1. Department of Anatomy, Physiology and Pharmacology, Faculty of Veterinary Medicine, Bogor Agricultural University, West Java, Indonesia
2. Center For Research and Development of Biomedical and Basic Health Technology, National Institute Health Research and Development, Ministry of Health Republic of Indonesia
Email : ratihr79[at]yahoo.com

Abstract
Feeder cells are inactivated cells that can not proliferate but have capability to produce growth factors and extracellular matrix for attachment and development of the cell culture. Feeder cells are widely used to support pluripotent stem cell (PSC) cultures which is predicted as one of the future cell therapy. One of the type of PSC is embryonic stem cells. Some of the feeder type which already used in stem cells propagation are mouse embryonic fibroblasts (MEF), rat embryonic fibroblast (REF), cumulus cells and mesenchymal stem cells (MSC). Research using feeder cells can be utilized to analyze various growth factors secreted by this cells that can lead to development of synthetic production of these substances. This paper will discuss REF cell culture by explant method and the inactivation process of REF to be used as feeder cells.

Keywords
feeder cells, REF, fibroblast, pluripotent stem cells, embryonic stem cells

Topic
Cellular, Tissue and Genetic Engineering

Link: https://ifory.id/abstract/JZ97H8FQwdzA


THE EFFECTS OF ETHIONAMIDE ON REGULATING THYROID HORMONE RECEPTOR GENE EXPRESSION IN RATS
Ferdyan Efza, Setiawan, Ronny Lesmana,

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Corresponding Author
Ferdyan Efza

Institutions
Universitas Padjadjaran

Abstract
Background. Hypothyroid is one of the most frequently known complication of MDR-TB Treatment. Treatment of MDR-TB using Ethionamide still becomes a challenge due to high numbers of patients develop hypothyroid as complication. Studies had reported that Ethionamide (C8H10N2S) share similar sturcture with Thioamides such as Propythiouracil (C7H8N2S) and Methimazole (C4H6N2S), it induced the effect of iodide trapping & organification inhibition which leads to hypothyroidism. However, the molecular mechanism of Ethionamide effects on regulation thyroid hormone receptor gene expression (TR) remains unclear. The understanding of this molecular mechanism, open a new perspective and help to understand the best method of tuberculosis treatment in the future. Purpose. The purpose of this study is to understand molecular mechanism of ethionamide on regulating TRα1, TRα2, TRβ1, and TRβ2 gene expression in gastrocnemius, soleus, thigh, and cardiac muscle. Methods. 38 rats were assigned into 3 groups; negative control group (no treatment), positive control group (propylthiouracyl), treatment group (ethionamide). Each group were given its treatment for 12 weeks. On the last day, all group were sacrificed and organs were sampled (gastrocnemius, soleus, thigh, and cardiac muscle). Each sample were undergone RNA extraction, PCR amplification, and electrophoresis consecutively to analyze the TRα1, TRα2, TRβ1, and TRβ2 gene expression. Result. We observed that TRα1, TRα2, TRβ1, and TRβ2 gene expression were upregulated by 1.5 fold in gastrocnemius muscle, and were upregulated significantly by 3 fold in cardiac muscle. Conclusion. This study concludes that prolong ethionamide treatment does upregulate thyroid hormone receptor gene expression.

Keywords
Keywords: Hypothyroid, Ethionamide, TRα1, TRα2, TRβ1, TRβ2, Gastrocnemius, Soleus, Thigh, Cardiac

Topic
Cellular, Tissue and Genetic Engineering

Link: https://ifory.id/abstract/MpxFjuw7rVQC


The Role of FTO Gene Polymorphism in Weight Loss Program: An Evidence-Based Case Report
Maggie Nathania, Lily Indriani Octovia

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Corresponding Author
Maggie Nathania

Institutions
Department of Nutrition, Faculty of Medicine, Universitas Indonesia - Ciptomangunkusumo National Hospital
Jl. Salemba Raya No.5, Jakarta Pusat 10430, Indonesia

Abstract
Background: Obesity and its comorbidities are major health problems throughout the world, which continue to increase. “Fat mass and obesity-associated” (FTO) gene is the strongest genetic predictor of body weight, which alters the regulation of IRX3 and IRX5 homeobox gene expression, affecting the mitochondrial fat metabolism. It is hoped that nutrigenomic findings can answer the urgent need to develop more effective anti-obesity strategies, especially in solving various individual responses to treatment variability. Objective: To determine the effectiveness of lifestyle modification on weight loss in patients with FTO gene polymorphisms. Methods: Literature searching was performed on Pubmed, Science Direct, and Cochrane according to the clinical query. Screening on title, abstract, and full-text was based on eligibility criteria (systematic review or meta-analysis of clinical trials, suitability with the clinical question, English language, full-text availability, and human studies), followed by duplication filter and critical appraisal. Results: A meta-analysis article was obtained with FTO AA genotype results, having significantly greater weight loss compared to TT genotypes with weighted mean difference -0,44 kg (95% CI: 0,09 to 0,79; P=0,015). Conclusion: Individuals carrying homozygous FTO obesity predisposition can lose more weight through lifestyle modification than non-carriers, but these differences might be too small to be clinically important. A further consideration is needed to determine the benefit of FTO gene testing over the cost. In carriers of the TT genotype, more aggressive anti-obesity treatment is needed.

Keywords
nutrigenomics, genetic, obesity, nutrition, FTO

Topic
Cellular, Tissue and Genetic Engineering

Link: https://ifory.id/abstract/2nKZ9Y8vH6mC


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