Ilham Rahmanto
Unknown Affiliation

Published : 3 Documents Claim Missing Document
Claim Missing Document
Check
Articles

Found 3 Documents
Search

Amplification genetic engineering strategy by Crispr-Cas13 Enzymes for detection and treatment COVID-19 mediated with gold nanoparticle (AUNP) Salsabila Farah Rafidah; Ilham Rahmanto; Ardellia Bertha Pratiska
Qanun Medika - Jurnal Kedokteran FK UMSurabaya Vol 6, No 2 (2022): Journal Qanun Medika Vol 6 No 02
Publisher : Universitas Muhammadiyah Surabaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.30651/jqm.v6i2.11227

Abstract

WHO declared the disease outbreak due to the COVID-19 coronavirus a global pandemic. Indonesian government's efforts to eradicate the pandemic through mass screening have not been effective due to the limitations of the three main modalities used to detect COVID-19, including Rapid Test Diagnostic (RTD) antibodies, RTD antigens, and Reverse Transcriptase-Polymerase Chain Reaction (RT-RTD PCR), In addition, other detection tools are sometimes used, such as Enzyme-Linked Immunosorbent Assay (ELISA) and rapid molecular tests. To eradicate this pandemic, the government needs COVID-19 detection tools that are effective, cheap, fast, and accessible. To determine the application of the genetic engineering strategy of amplification by the CRISPR-cas13 enzyme for detecting and treating COVID-19 mediated by gold nanoparticles (AuNP). This research uses a qualitative literature study with content analysis, observation development, and literature study; an alternative solution to this problem is CRISPR-Cas13, achieved by the SHERLOCK method. This method designs and screens a targeted group of CRISPR RNAs based on the identification of functional crRNAs of SARS-CoV-2. Amplification of CRISPR-Cas13 by SHERLOCK and PAC-MAN enzymes has the potential to be the latest detection and treatment method for gold nanoparticle-mediated COVID-19 (AuNP) in Indonesia.
CRISPR-Cas9 through AAV delivery system as a gene therapy in Parkinson’s disease Maulana Bagus Adi Cahyono; Ilham Rahmanto; Zahras Azimuth Doman; Galuh Senjani Yulfani Putri; Christopher Surya Lodianto; Pradana Zaky Romadhon
Qanun Medika - Jurnal Kedokteran FK UMSurabaya Vol 7 No 2 (2023): Journal Qanun Medika Vol 07 No 02
Publisher : Universitas Muhammadiyah Surabaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.30651/jqm.v7i2.16117

Abstract

The global population living with Parkinson’s disease is estimated to reach 9.4 million people, which has increased significantly since 2016, with a total of 6 million people. Parkinson's is a neurodegenerative disease of the substantia nigra that causes a decrease in dopamine production and is characterized by the appearance of cytoplasmic misfold proteins called Lewy bodies. The study found that abnormalities or mutations in the SNCA and LRRK2 genes correlated with the overproduction of the ɑ-synuclein protein, which forms Lewy bodies that cause Parkinson's. Current Parkinson's medications only temporarily replace lost dopamine but do not treat the direct cause of Parkinson's; this research used qualitative literature study with content analysis, observation, and development; the use of CRISPR-Cas9 through AAV genetic engineering in repairing SNCA and LRRK2 mutant gene. This genetic therapy works by cutting the mutant DNA base sequences in the SNCA and LRRK2 genes and then replacing them with normal sequences through a homology-direct repair mechanism. As a result, the abnormalities or mutations that cause Parkinson's in these two genes can be corrected, so that dopaminergic levels in the brain can return to normal and excessive accumulation of α-synuclein protein can be suppressed.
Tandem peptide lipid CRISPR-Cas9 complex combating APP and APOE4 gene abnormality in Alzheimer's disease Ilham Rahmanto; Maulana Bagus Adi Cahyono; Husnul Khatimah; Rahmi Nugraningrum; Pionera Seconda Giyanti Putri; Nurul Zulfa Sahiruddin; Nabila Rahmaniah; Pradana Zaky Romadhon
Qanun Medika - Jurnal Kedokteran FK UMSurabaya Vol 8 No 01 (2024): Qanun Medika Vol 08 No 01 January 2024
Publisher : Universitas Muhammadiyah Surabaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.30651/jqm.v8i01.16054

Abstract

Alzheimer's attacks 24 million global population and dominates 60-80% of existing cases of dementia. It causes the accumulation of beta-amyloid (Aβ) plaques in the hippocampus and entorhinal cortex, resulting in decreased mass from the brain. Recent studies have shown that the manifestation of this disease is due to an overaccumulation of abnormal Aβ protein due to abnormalities in the APP and APOE4 genes. Point mutations in the APP gene will create the toxic form of Aβ protein, namely Aβ42, and the toxic APOE4 gene will accelerate the onset of Aβ42 deposition and pro-inflammatory activity that exacerbates the degenerative process of the brain. Gene editing as a potential definitive therapy was recently a concern by researchers. CRISPR-Cas9 repairs the APP gene and substitutes the APOE4 gene with APOE3 by modifying the gene's DNA sequence. Nano complex CRISPR-Cas9 tandem peptide lipid is a model for clinicians to target brain nerve cells. In vivo research on an Alzheimer's mouse model proved the potential of nano-complex-based peptides as carriers of CRISPR-Cas9 in brain nerve cells. This engineering technology offers satisfactory results with high precision, minimal side effects, and a relatively low price for long-term therapeutic effects and even a lifetime.