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Molecular Diagnosis of Tuberculosis
Fariz Nurwidya,Diah Handayani,Erlina Burhan,Faisal Yunus 전남대학교 의과학연구소 2018 전남의대학술지 Vol.54 No.1
Tuberculosis (TB) is one of the leading causes of adult death in the Asia-Pacific Region,including Indonesia. As an infectious disease caused by Mycobacterium tuberculosis(MTB), TB remains a major public health issue especially in developing nations dueto the lack of adequate diagnostic testing facilities. Diagnosis of TB has entered an eraof molecular detection that provides faster and more cost-effective methods to diagnoseand confirm drug resistance in TB cases, meanwhile, diagnosis by conventional culturesystems requires several weeks. New advances in the molecular detection of TB, includingthe faster and simpler nucleic acid amplification test (NAAT) and whole-genomesequencing (WGS), have resulted in a shorter time for diagnosis and, therefore, fasterTB treatments. In this review, we explored the current findings on molecular diagnosisof TB and drug-resistant TB to see how this advancement could be integrated into publichealth systems in order to control TB.
Nurwidya, Fariz,Damayanti, Triya,Yunus, Faisal The Korean Academy of Tuberculosis and Respiratory 2016 Tuberculosis and Respiratory Diseases Vol.79 No.1
Chronic obstructive pulmonary disease (COPD) is a chronic and progressive inflammatory disease of the airways and lungs that results in limitations of continuous airflow and is caused by exposure to noxious gasses and particles. A major cause of morbidity and mortality in adults, COPD is a complex disease pathologically mediated by many inflammatory pathways. Macrophages, neutrophils, dendritic cells, and CD8+ T-lymphocytes are the key inflammatory cells involved in COPD. Recently, the non-coding small RNA, micro-RNA, have also been intensively investigated and evidence suggest that it plays a role in the pathogenesis of COPD. Here, we discuss the accumulated evidence that has since revealed the role of each inflammatory cell and their involvement in the immunopathogenesis of COPD. Mechanisms of steroid resistance in COPD will also be briefly discussed.
Epithelial Mesenchymal Transition in Drug Resistance and Metastasis of Lung Cancer
Fariz Nurwidya,Fumiyuki Takahashi,Akiko Murakami,Kazuhisa Takahashi 대한암학회 2012 Cancer Research and Treatment Vol.44 No.3
Among all types of cancer, incidence of lung cancer remains the highest with regard to cancerrelated mortality. Problems contributing to recurrence of the disease include metastasis and drug resistance. Mounting evidence has demonstrated involvement of epithelial mesenchymal transition (EMT) in cancer progression. EMT is a critical mechanism ensuring tissue remodeling during morphogenesis of multicellular organisms. Therefore, understanding of the biology of this process for identification of potential EMT-targeted therapeutic strategies for the benefit cancer patients is necessary. This review describes recent evidence of EMT involvement in drug resistance and metastasis of cancers, with an emphasis on lung cancer.
( Fariz Nurwidya ),( Triya Damayanti ),( Faisal Yunus ) 대한결핵 및 호흡기학회 2016 Tuberculosis and Respiratory Diseases Vol.79 No.1
Chronic obstructive pulmonary disease (COPD) is a chronic and progressive inflammatory disease of the airways and lungs that results in limitations of continuous airflow and is caused by exposure to noxious gasses and particles. A major cause of morbidity and mortality in adults, COPD is a complex disease pathologically mediated by many inflammatory pathways. Macrophages, neutrophils, dendritic cells, and CD8+ T-lymphocytes are the key inflammatory cells involved in COPD. Recently, the non-coding small RNA, micro-RNA, have also been intensively investigated and evidence suggest that it plays a role in the pathogenesis of COPD. Here, we discuss the accumulated evidence that has since revealed the role of each inflammatory cell and their involvement in the immunopathogenesis of COPD. Mechanisms of steroid resistance in COPD will also be briefly discussed.
Circulating Tumor Cell and Cell-free Circulating Tumor DNA in Lung Cancer
Fariz Nurwidya,Jamal Zaini,Andika Chandra Putra,Sita Andarini,Achmad Hudoyo,Elisna Syahruddin,Faisal Yunus, M.D., Ph.D. 전남대학교 의과학연구소 2016 전남의대학술지 Vol.52 No.3
Circulating tumor cells (CTCs) are tumor cells that are separated from the primary site or metastatic lesion and disseminate in blood circulation. CTCs are considered to be part of the long process of cancer metastasis. As a ‘liquid biopsy’, CTC molecular examination and investigation of single cancer cells create an important opportunity for providing an understanding of cancer biology and the process of metastasis. In the last decade, we have seen dramatic development in defining the role of CTCs in lung cancer in terms of diagnosis, genomic alteration determination, treatment response and, finally, prognosis prediction. The aims of this review are to understand the basic biology and to review methods of detection of CTCs that apply to the various types of solid tumor. Furthermore, we explored clinical applications, including treatment monitoring to anticipate therapy resistance as well as biomarker analysis, in the context of lung cancer. We also explored the potential use of cell-free circulating tumor DNA (ctDNA) in the genomic alteration analysis of lung cancer.
From tumor hypoxia to cancer progression
Fariz Nurwidya,Fumiyuki Takahashi,Kunihiko Minakata,Akiko Murakami,Kazuhisa Takahashi 대한해부학회 2012 Anatomy & Cell Biology Vol.45 No.2
Hypoxia, defined as a decrease of tissue oxygen levels, represents a fundamental pathophysiological condition in the microenvironment of solid tumors. Tumor hypoxia is known to be associated with radio/chemo-resistance and metastasis that eventually lead to cancer progression contributing to poor prognosis in cancer patients. Among transcription factors that accumulated under hypoxic conditions, hypoxia-inducible factor-1 (HIF-1) is a master transcription factor that has received the most intense attention in this field of research due to its capacity to modulate several hundred genes. With a clearer understanding of the HIF-1 pathway, efforts are directed at manipulation of this complex genetic process in order to ultimately decrease cellular HIF-1 levels. Some novel agents have been shown to have HIF-1 inhibition activity through a variety of molecular mechanisms and have provided promising results in the preclinical setting.