https://rjupublisher.com/ojs/index.php/RJHS/issue/feed 2026-08-30T20:55:40+00:00 Dr. Ruth Rize Paas Megahati. S journalhome@rjupublisher.com Open Journal Systems <p>The Radinka Journal of Health Science is a journal that focuses on research articles, reviews, and empirical research. This journal aims to facilitate research in areas of health science. Additionally, the journal has been accredited <a href="https://sinta.kemdiktisaintek.go.id/journals/profile/18401" target="_blank" rel="noopener"><strong data-path-to-node="2" data-index-in-node="234">Sinta 4</strong></a>.</p> <p>Journal Title: Radinka Journal of Health Science<br />Initials: RJHS<br />Journal Abbreviation: Radinka J. Health Scie<br />Frequency: Published four times yearly (February, May, August, and November).<br />DOI:10.56778/RJHS<br />Editor-in-Chief: Dr. Ruth Rize Paas Megahati S<br />Publisher: Radinka Jaya Utama Publisher, Padang, West Sumatra, Indonesia<br />Indexing: <a href="https://sinta.kemdiktisaintek.go.id/journals/profile/18401" target="_blank" rel="noopener">Sinta 4</a>, <a href="https://scholar.google.com/citations?hl=en&amp;user=hMuFwPkAAAAJ" target="_blank" rel="noopener">Google Scholar</a>, <a href="https://search.crossref.org/search/works?q=Radinka+Journal+of+Health+Science&amp;from_ui=yes" target="_blank" rel="noopener">Crossref</a>, <a href="https://portal.issn.org/resource/ISSN/3025-7751" target="_blank" rel="noopener">Road</a>, <a href="https://garuda.kemdikbud.go.id/journal/view/35221" target="_blank" rel="noopener">Garuda</a>, and <a href="https://onesearch.id/Repositories/Repository?library_id=9003" target="_blank" rel="noopener">Onesearch</a><br />Languages: Indonesian and English.</p> <p>Focus and Scope: The Radinka Journal of Health Science (RJHS) accepts manuscripts in the fields of medical laboratory engineering, health information management, pharmacy, midwifery, occupational health and safety, nursing, physiotherapy, health promotion, public health, medicine, environmental health, dental health, dental engineering, radiology, nutrition, sanitation, epidemiological supervision, health psychology, health technology, health information systems, health law, hospital management, etc. RJHS publishes high-quality scientific research results: articles, and systematic, structured literature reviews.</p> <p>Thank you for choosing the Radinka Journal of Health Science</p> https://rjupublisher.com/ojs/index.php/RJHS/article/view/773 2026-08-21T15:50:19+00:00 Ruth Rize Paas Megahati S megahati71@gmail.com Yessy Aprihatin aprihatin23@gmail.com

<p>Human immunodeficiency virus-associated neurocognitive disorders and peripheral neuropathy remain persistent clinical challenges despite effective viral suppression through antiretroviral therapy. Recent evidence suggests that vitamin B1 dyshomeostasis serves as a critical metabolic bottleneck that accelerates axonal degeneration. This study aims to elucidate the molecular interplay between thiamine homeostasis and neurotrophic signaling in human immunodeficiency virus-associated neurodegeneration, specifically identifying metabolic drivers of axonal damage. Following the PRISMA 2020 guidelines, a comprehensive search was conducted across PubMed, Scopus, Web of Science, and Google Scholar for peer-reviewed studies published between 2018 and 2025. Quality assessment was performed using Joanna Briggs Institute tools to ensure high-quality evidence. The analysis revealed that viral proteins, particularly glycoprotein 120, disrupt solute carrier family 19 thiamine transporters, precipitating a mitochondrial adenosine triphosphate failure. This bioenergetic crisis fundamentally impairs the thiamine-neurotrophic axis by hindering the proteolytic cleavage of pro-brain-derived neurotrophic factor into its mature form and silencing the mitogen-activated protein kinase/extracellular signal-regulated kinase survival pathway, driving distal axonal degeneration. Conversely, interventions using high-dose thiamine and lipophilic derivatives, such as benfotiamine, effectively bypass transport barriers via passive diffusion, restore alpha-ketoglutarate dehydrogenase enzymatic activity, and suppress nuclear factor kappa B-mediated neuroinflammation, thereby stabilizing axonal integrity. In conclusion, thiamine dyshomeostasis represents a pivotal metabolic driver of neurodegeneration, and targeted supplementation with benfotiamine offers a promising therapeutic strategy to mitigate neurocognitive and peripheral deficits.</p>

2026-08-30T00:00:00+00:00 Copyright (c) 2026 RADINKA JOURNAL OF HEALTH SCIENCE https://rjupublisher.com/ojs/index.php/RJHS/article/view/746 2026-07-04T06:22:58+00:00 SALISU, Umar Muhammad umsalisu.pg@atbu.edu.ng

<p>Human immunodeficiency virus-associated neurocognitive disorders and peripheral neuropathy remain persistent clinical challenges despite effective viral suppression through antiretroviral therapy. Recent evidence suggests that vitamin B1 dyshomeostasis serves as a critical metabolic bottleneck that accelerates axonal degeneration. This study aims to elucidate the molecular interplay between thiamine homeostasis and neurotrophic signaling in human immunodeficiency virus-associated neurodegeneration, specifically identifying metabolic drivers of axonal damage. Following the PRISMA 2020 guidelines, a comprehensive search was conducted across PubMed, Scopus, Web of Science, and Google Scholar for peer-reviewed studies published between 2018 and 2025. Quality assessment was performed using Joanna Briggs Institute tools to ensure high-quality evidence. The analysis revealed that viral proteins, particularly glycoprotein 120, disrupt solute carrier family 19 thiamine transporters, precipitating a mitochondrial adenosine triphosphate failure. This bioenergetic crisis fundamentally impairs the thiamine-neurotrophic axis by hindering the proteolytic cleavage of pro-brain-derived neurotrophic factor into its mature form and silencing the mitogen-activated protein kinase/extracellular signal-regulated kinase survival pathway, driving distal axonal degeneration. Conversely, interventions using high-dose thiamine and lipophilic derivatives, such as benfotiamine, effectively bypass transport barriers via passive diffusion, restore alpha-ketoglutarate dehydrogenase enzymatic activity, and suppress nuclear factor kappa B-mediated neuroinflammation, thereby stabilizing axonal integrity. In conclusion, thiamine dyshomeostasis represents a pivotal metabolic driver of neurodegeneration, and targeted supplementation with benfotiamine offers a promising therapeutic strategy to mitigate neurocognitive and peripheral deficits.</p> <p> </p>

2026-08-30T00:00:00+00:00 Copyright (c) 2026 RADINKA JOURNAL OF HEALTH SCIENCE