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Abstrak :
Identifikasi Pneumocystis jirovecii pada pasien dengan koinfeksi tuberkulosis (TB) paru masih menjadi tantangan karena gambaran klinis maupun radiologis keduanya yang mirip dan P. jirovecii tidak dapat dikultur. Identifikasi P. jirovecii di Indonesia masih berdasarkan pemeriksaan mikroskopik yang seringkali kurang sensitif. Oleh karena itu, dikembangkan teknik real time PCR yang lebih sensitif dan spesifik dengan gen target mitochondrial large subunit (mtLSU) dan mitochondrial small subunit (mtSSU) rRNA. Penelitian ini bertujuan untuk mengoptimasi deteksi gen mitochondrial large dan small subunit rRNA dalam mengidentifikasi P. jirovecii pada pasien terkait TB paru. Penelitian ini menggunakan 26 sampel sputum pasien terkait TB paru. Optimasi teknik real time PCR berupa optimasi konsentrasi primer, probe, suhu penempelan, volume cetakan DNA dan uji reaksi silang dilakukan untuk mendapatkan kondisi yang optimal dalam amplifikasi gen mtLSU dan mtSSU rRNA. Hasil penelitian menunjukkan hasil optimasi deteksi kedua gen tersebut dapat mengidentifikasi P. jirovecii 1 dari 26 sampel (3,84%). Uji real time PCR yang telah di optimasi dalam penelitian ini dapat mendeteksi P. jirovecii pada sampel klinis pasien terkait TB paru. ......Identification of Pneumocystis jirovecii in patients with co-infected pulmonary tuberculosis (TB) is still a challenge because the clinical and radiological features of both are similar and P. jirovecii cannot be cultured. Identification of P. jirovecii in Indonesia is still based on microscopic examination which is often less sensitive. Therefore, a more sensitive and specific real time PCR technique was developed with mitochondrial large subunit (mtLSU) and mitochondrial small subunit (mtSSU) rRNA target genes. This study aimed to optimize the detection of mitochondrial large and small subunit rRNA genes to identify P. jirovecii in pulmonary TB-related patients. A total of 26 sputum samples of pulmonary TB-related patients were collected. Real time PCR technique optimization including the optimization of primer and probe concentrations, annealing temperature, DNA template volume and cross-reaction testing, was carried out to obtain optimal conditions for mtLSU and mtSSU rRNA gene amplification.  The results showed that the optimization of detection for both genes could identify P. jirovecii in 1 out of 26 samples (3.84%). The optimized real time PCR test in this study can detect P. jirovecii in clinical samples of pulmonary TB-related patients.

Abstrak :
Andrografolida telah terbukti memiliki efek kardioproteksi, namun masih belum diketahui mekanismenya. Penelitian ini bertujuan untuk melihat mekanisme dari andrografolida pada tikus dengan kardiotoksisitas doksorubisin, fokus pada biogenesis mitokondria. Tikus Sprague-Dawley jantan sebanyak 24 ekor dibagi secara acak menjadi empat kelompok: Normal (N); dosis kumulatif doksorubisin 16 mg/kgBB i.p. (Dox); Dox 16 mg/kgBB + andrografolida 30 mg/kgBB (Dox+And30); dan Dox 16 mg/kgBB + andrografolida 60 mg/kgBB (Dox+And60). Gejala toksisitas dan berat badan dicatat setiap harinya. Dianalisis ekspresi NF-κB dengan metode Western Blot, bersamaan dengan ekspresi dari PGC-1α dan TFAM dengan metode qRT-PCR dan pewarnaab HE pada jaringan jantung. Diamati bahwa doksorubisin menurunkan aktivitas LDH dan CKMB, dan lebih lanjut menurunkan ekspresi PGC-1α dan TFAM, dengan penurunan pada intesitas pita NF-κB. Pemberian bersama dengan andrografolida mengurangi efek tersebut. Selain itu, analisis histopatologi dari jaringan jantung menunjukkan perbaikan. Temuan ini menunjukkan andrografolida memiliki potensi kardioporteksi setidaknya dalam bagian melalui peningkatan fungsi mitokondria. ......Andrographolide has been proved to exert cardioprotective effects, but little is known about its mechanism. This study aimed to assess the mechanism of andrographolide in rats with doxorubicin cardiotoxicity, focus on mitochondrial biogenesis. Twenty-four male rat Sprague-Dawley were randomized into: Normal (N); doxorubicin 16 mg/kg BW i.p. (Dox); Dox 16 mg/kgBW+andrographolide 30 mg/kg BW (Dox+And30); Dox 16 mg/kg BW+andrographolide 60 mg/kg (Dox+And60). We analyzed the expression of NF-κB by Western Blotting method, along with mRNA expression of PGC-1α and TFAM by qRT-PCR method, and HE staining of heart tissues. We observed that doxorubicin enhanced LDH and CK-MB activities, and further decreased the expression of PGC-1α and TFAM with decreased the intensity of NF-κB band. Co-treatment with andrographolide ameliorated those effects. In addition, the histopathology feature of heart tissues were also improved. These findings showed that andrographolide has a cardioprotective effect at least in part through augmentation of mitochondrial function.

Abstrak :
This is the definitive, one-stop resource on preclinical drug evaluation for potential mitochondrial toxicity, addressing the issue upfront in the drug development process. It discusses mitochondrial impairment to organs, skeletal muscle, and nervous systems and details methodologies used to assess mitochondria function. It covers both in vitro and in vivo methods for analysis and includes the latest models.

Abstrak :
Mitokondria merupakan organel yang memetabolisme besi secara ekstensif, sehingga menjadi target kerusakan yang diinduksi besi pada kondisi hemosiderosis. Produksi reactive oxygen species (ROS) yang tinggi di mitokondria dapat lebih meningkat saat ada besi bebas yang kemudian memicu reaksi Fenton. Produksi ROS yang tinggi dapat menyebabkan stres oksidatif, sehingga regulasi konsentrasi besi harus diatur dengan ketat. Phaleria macrocarpa diketahui mengandung senyawa aktif mangiferin yang telah terbukti memiliki aktivitas kelasi besi, namun belum diketahui apakah dapat bekerja di mitokondria. Penelitian ini bertujuan untuk mengetahui efektivitas ekstrak etanol buah Phaleria macrocarpa dalam melindungi mitokondria hati dari kerusakan akibat besi dan kaitannya dengan transporter influks dan efluks besi di hati tikus model hemosiderosis. Penelitian ini menggunakan organ hati tersimpan dari tikus Sprague-Dawleyjantan sebanyak 30 ekor yang dibagi secara acak ke dalam 6 kelompok, yaitu normal (N) dan kelompok hemosiderosis tanpa terapi (Fe), diterapi deferiprone 462,5 mg/kgBB (Fe+DFP), mangiferin 50 mg/kgBB (Fe+M), serta ekstrak etanol buah Phaleria macrocarpa dosis 100 mg/kgBB (Fe+PM100) dan 200 mg/kgBB (Fe+PM200). Dilakukan analisis kadar MnSOD, copy number mtDNA, dan analisis ekspresi mRNA DMT1, ZIP14, MFRN1, MFRN2, ABCB7, dan ABCB8 yang dilaporkan berperan dalam transpor besi ke dalam sel dan mitokondria. Hasil penelitian menunjukkan bahwa ekstrak Phaleria macrocarpa memengaruhi ekspresi gen transporter besi namun tidak dapat memperbaiki penanda kerusakan mitokondria pada organ hati hemosiderosis. ......Mitochondria are organelles that metabolize iron extensively, making them targets for iron-induced damage. The high production of reactive oxygen species (ROS) in mitochondria can be further increased when there is free iron which then triggers the Fenton reaction. High ROS production can cause oxidative stress, so iron concentration regulation must be strictly regulated. Phaleria macrocarpa is known to contain the active compound mangiferin which has been shown to have iron chelation activity, but it is not yet known whether it can work in mitochondria. This study aims to determine the effectiveness of the ethanol extract of Phaleria macrocarpa fruit in protecting liver mitochondria from iron-induced damage and its relation to iron influx and efflux transporters in the liver of hemosiderosis rat models. This study used stored liver organs from 30 male Sprague-Dawley rats which were randomly divided into 6 groups, namely normal (N) and hemosiderosis groups without therapy (Fe), treated with deferiprone 462.5 mg/kgBW (Fe+DFP), mangiferin 50 mg/kgBW (Fe+M), and Phaleria macrocarpa fruit ethanolic extract at a dose of 100 mg/kgBW (Fe+PM100) and 200 mg/kgBW (Fe+PM200). Analysis of MnSOD levels, mtDNA copy number, and analysis of relative mRNA expression of DMT1, ZIP14, MFRN1, MFRN2, ABCB7, and ABCB8 were performed which were reported to play a role in iron transport into cells and mitochondria. The results showed that Phaleria macrocarpa extract has the potential to modulate the expression of iron transporter genes but was not able to ameliorate the mitochondrial damage marker in hemosiderosis liver.

Abstrak :
Mitochondria are far more than the “powerhouse” of the cell as they have classically been described. In fact, mitochondria biological activities have progressively expanded to include not only various bioenergetic processes but also important biosynthetic pathways, calcium homeostasis and thermogenesis, cell death by apoptosis, several different signal transduction pathways mainly related to redox control of gene expression and so on. This functional and structural complexity may undergo important derangements so to justify the definition of ‘mitochondrial medicine’, which should include all the clinical consequences of congenital or acquired mitochondrial dysfunctions. There are actually a growing number of studies which assign a significant pathogenic role to damaged mitochondria in different diseases: ischemia/reperfusion injury, neurodegenerative diseases, cancer with its dramatic sequelae (i.e, metastasis), metabolic syndrome, hyperlipidemias, just to mention a few of the most important pathologies. In this context, a further aspect that should not be disregarded is the interaction of pharmacological agents with mitochondria, not only in regard of the toxicological aspects but, above all, of the potential therapeutic applications. In fact, it is interesting to note that, while the properties of different so-called “mitoxicants” are well-known, the subtle linkages between drugs and mitochondria is still in need of a real pharmacological and therapeutic control at the clinical level.

Abstrak :
This book will describe the nuclear encoded genes and their expressed proteins of mitochondrial oxidative phosphorylation. Most of these genes occur in eukaryotic cells, but not in bacteria or archaea.

Abstrak :
As age related diseases increase in prevalence and impact more significantly on medical resources it is imperative to understand these diseases and the mechanisms behind their progression. New research has stimulated a growing interest in mitochondrial involvement in neurodegenerative disorders such as parkinson’s disease, alzheimer’s disease and multiple sclerosis and the mechanisms which lead from mitochondrial dysfunction to neurodegeneration. Mitochondrial dysfunction in neurodegenerative disorders brings together contributions from leaders in the field internationally on the various ways in which mitochondrial dysfunction contributes to the pathogenesis of these diseases, guiding the reader through the basic functions of mitochondria and the mechanisms that lead to their dysfunction, to the consequences of this dysfunction on neuronal function before finishing with the modelling of these disorders and discussion of new potential therapeutic targets.