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All Journal Syntax Literate: Jurnal Ilmiah Indonesia Proceedings Book of International Conference and Exhibition on The Indonesian Medical Education and Research Institute
Purbasari, Bethasiwi
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Humanities Education Environmental Science Health Professions Law, Crime, Criminology & Criminal Justice Medicine & Pharmacology Neuroscience Public Health Social Sciences Other

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Effect of Laser Therapy on Inflammation in Pneumonia or Pneumonia Sepsis through the Nf-Kb Regulatory Pathway: A Literature Review Study Rahmad, Rahmad; Djaharuddin, Irawati; Fauzi, Yanuar Rahmat; Purbasari, Bethasiwi; Hakimah, Annisatul; Waluyo, Yose
Proceedings Book of International Conference and Exhibition on The Indonesian Medical Education Research Institute Vol. 8 No. - (2024): Proceedings Book of International Conference and Exhibition on The Indonesian M
Publisher : Writing Center IMERI FMUI

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.69951/proceedingsbookoficeonimeri.v8i-.242

Abstract

Pneumonia is the most frequent cause of death from infectious diseases is the eighth leading cause of death in the United States. Meanwhile, sepsis and septic shock remain the leading causes of death among critical patients despite decades of significant advances in supportive therapy. A major factor leading to high morbidity and mortality from septic shock is the lack of effective treatment. Many different options have been proposed, among which the prospect of low-level laser therapy is being discussed quite actively. Laser therapy is a viable way to treat pneumonia or sepsis pneumonia. It is known for its benefits as an anti-inflammatory effect that can reduce the levels of pro-inflammatory cytokines, namely IL-6, as well as increase TNFα levels and enhance the balance of inflammatory processes. Additional research is required to confirm the effect of laser therapy on inflammation, especially the NF-kB pathway in cases of pneumonia or sepsis pneumonia in vitro, in vivo and in clinical studies.
Evaluating Human Immunodeficiency Virus (HIV) Neuropathogenesis on HIV -Associated Neurocognitive Disorder (HAND): Role of Virology, Cellular and Immunology Aspects Purbasari, Bethasiwi
Syntax Literate Jurnal Ilmiah Indonesia
Publisher : Syntax Corporation

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.36418/syntax-literate.v9i11.52376

Abstract

Human Immunodeficiency Virus (HIV) became a worldwide pandemic with a global prevalence of 36.9 million in 2014. One of the neurological complications of HIV infection is HIV-associated neurocognitive disorder (HAND). The administration of antiretroviral (ARV) therapy to HIV patients in general contributed to lowering HIV mortality and morbidity. However, ARV therapy did not provide complete protection for neurons. The cumulative prevalence of severe HAND in the lifetime of HIV patients is estimated to be 15%. HAND is classified into three categories: asymptomatic neurocognitive impairment (ANI), mild neurocognitive disorder (MND), and HIV-associated dementia (HAD). HAND remains a significant cause of morbidity in HIV patients. Recent findings on research using animal models have shown new concept development, both viral and cellular-related, on HAND neuropathogenesis, including other clinical factors contributing to HAND progression. Factors contributing to HAND neuropathogenesis consist of the cellular aspect, shown by the role of macrophages and astrocytes, and the viral aspect, shown by the role of neurotoxic HIV proteins and inflammatory molecules. HAND progression comprised chronic neuroinflammation, postsynaptic density decrements, and neurogenesis impairment. A better understanding of HAND neuropathogenesis will increase the optimization of HAND therapy.
The Role Of Exosomes In Diabetic Polyneuropathy: Pathogenesis And Emerging Therapies Purbasari, Bethasiwi
Syntax Literate Jurnal Ilmiah Indonesia
Publisher : Syntax Corporation

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.36418/syntax-literate.v10i7.60687

Abstract

Diabetic polyneuropathy (DPN) is a common and debilitating complication of diabetes mellitus, characterized by progressive nerve damage, chronic pain, and impaired quality of life. Despite advances in glycemic management, current treatments remain largely symptomatic, underscoring the need for novel therapeutic strategies targeting the underlying pathophysiology. Recent research highlights the critical role of exosomes—nanoscale extracellular vesicles that mediate intercellular communication—in the pathogenesis of DPN. These vesicles transport bioactive molecules (e.g., microRNAs, proteins, lipids) that influence metabolic dysfunction, neuroinflammation, microvascular damage, and impaired nerve regeneration. Exosomes derived from immune cells, Schwann cells, and mesenchymal stem cells (MSCs) exhibit dual roles: propagating nerve injury through pro-inflammatory signaling while also offering therapeutic potential via immunomodulation and neuroprotection. Emerging evidence suggests that exosome-based therapies—such as MSC-derived or engineered exosomes—can promote axonal regeneration, suppress NLRP3 inflammasome activation, and restore nerve function in preclinical models. Furthermore, exosomal biomarkers (e.g., miR-29a, miR-125b) hold promise for non-invasive DPN diagnosis. This review explores the pathogenic mechanisms of exosomes in DPN, their diagnostic potential, and the latest advances in exosome-based therapeutics, while addressing challenges in clinical translation.
Co-Authors Djaharuddin, Irawati Fauzi, Yanuar Rahmat Hakimah, Annisatul Rahmad Rahmad Waluyo, Yose