Murti Andriastuti, Melita Adiwidjaja, Hindra Irawan Satari,
Volume 11, Issue 4 ( December 2019 2019)
Abstract
Background: Iron deficiency (ID) is the most common micronutrient deficiency in the world. If left untreated, ID will lead to iron deficiency anemia (IDA) and other irreversible consequences. The American Academy of Pediatrics recommended reticulocyte hemoglobin content (Ret-He) as an alternative laboratory examination to screen and detect ID. We aimed to compare Ret-He with other laboratory parameters to screen for iron status in healthy children.
Methods: This is a cross-sectional study comprising 207 children aged 6-18 years in Jakarta, Indonesia. Children were divided according to their iron status. Ret-He was compared with hemoglobin (Hb), mean corpuscular volume (MCV), ferritin, and transferrin saturation (TS) to assess iron status in children. Receiver operating characteristic (ROC) curve was performed to determine the optimal cut-off value for Ret-He using SPSS software.
Results: Ret-He had a positive correlation with MCV (r=0.690, n=207, P<0.001), Hb (r=0.491, n=207, P<0.01), and ferritin (r=0.336, n= 207, P<0.001). Ret-He can not be used to detect iron depletion with the cut-off value of 30.3 pg with 100% sensitivity, 19.7% specificity, 100% negative predictive value (NPV), and 5.4% positive predictive value (PPV). A Ret-He cut-off value of 28.9 pg was established as optimal to identify ID (78.9% sensitivity, 56.2% specificity, 92.2% NPV, and 28.9% PPV) and 27 pg to detect IDA (75% sensitivity, 80% specificity, 98.1% NPV, and 18.7% PPV).
Conclusion: Ret-He can be used as an alternative screening parameter to detect ID and IDA in children aged 6-18 years. Screening for IDA with Ret-He has to be done with other parameters, such as Hb examination.
Ulfatun Nisa, Indwiani Astuti, Ronny Martien, Dhani Rinaldi Maulana, Ysrafil Ysrafil, Leonny Dwi Rizkita,
Volume 18, Issue 1 (March-2026 2026)
Abstract
Background: Hepatocellular carcinoma (HCC) is one of the most lethal malignancies worldwide, and dysregulation of microRNAs has been increasingly recognized as a critical driver in its pathogenesis. Among them, miR-217-5p has been reported as a tumor-suppressive miRNA, yet its molecular role and therapeutic potential in HCC remain largely unclear.
Methods: In silico analyses were performed using a network pharmacology approach to construct a protein–protein interaction (PPI) network of hepatocellular carcinoma (HCC)-associated genes targeted by miR-217-5p, followed by hub gene identification using CytoHubba. Functional enrichment analyses, including Gene Ontology (GO) and KEGG pathways, were conducted using ShinyGO, while expression and survival analyses were validated using UALCAN, GEPIA2, and the Human Protein Atlas. In vitro validation was performed by delivering miR-217-5p mimics into HepG2 cells using chitosan nanoparticles (CS-NPs), followed by qRT-PCR analysis of endogenous miRNA expression, KRAS suppression, and p53 restoration.
Results: A total of 152 potential target genes of miR-217-5p in HCC were identified, which were predominantly enriched in key biological processes related to regulation of cell population proliferation, as well as cancer-associated pathways including PI3K–Akt signaling and hepatocellular carcinoma pathways. PPI analysis, following the removal of disconnected nodes, generated a highly interconnected network comprising 146 nodes and 1042 edges, indicating extensive molecular interactions among the identified targets. Furthermore, hub gene analysis of the PPI network identified PTEN, KRAS, ESR1, HIF1A, and CDH1 as central regulatory genes. Notably, in vitro validation demonstrated that miR-217-5p delivered via chitosan nanoparticles (CS-NPs) successfully restored endogenous miR-217-5p expression and significantly suppressed KRAS expression, exhibiting a strong inverse correlation (r = −0.937, p < 0.0001). In addition, p53 protein levels were markedly increased following treatment.
Conclusion: Our findings demonstrate that miR-217-5p exerts tumor-suppressive effects in HCC by directly targeting KRAS and restoring p53 expression. Delivery of miR-217-5p using chitosan nanoparticles represents a promising miRNA replacement therapy strategy and highlights its potential as both a therapeutic agent in HCC.
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