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Journal : Narra J

Correlation of miR-150, hsa-let-7e, and miR-146a and gene expression of IL-6, IL-8, IP-10, and MIP-1β during dengue virus infection Sri Masyeni; Kuntaman Kuntaman; Aryati Aryati; Muchlis AU Sofro; Usman Hadi; Gondo Mastutik; Windu Purnomo; Agus Santosa; Benediktus Yohan; Erni Juwita Nelwan; R. Tedjo Sasmono
Narra J Vol. 1 No. 1 (2021): April 2021
Publisher : Narra Sains Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.52225/narraj.v1i1.31

Abstract

Growing evidence suggests that microRNAs (miRNAs) play a pivotal role in viral infection. The objective of this study was to assess the association between the expression of miR-150, hsa-let-7e, and miR-146a on cytokine expression during dengue infection. Dengue virus (DENV) strain SJN-006, a serotype 2 DENV strain of the Cosmopolitan genotype, isolated in Bali, Indonesia, was used to infect peripheral blood mononuclear cells (PBMCs) isolated from healthy individuals. The relative gene expressions of miR-150, hsa-let-7e, and miR-146a as well as the gene expression of cytokines (IL-6, IL-8, IP-10, and MIP-1β) were determined using quantitative real time - polymerase chain reaction (qRT-PCR) at 6, 12 and 24 hours post infection (hpi). Correlations between the microRNAs and cytokines were analyzed by means of causality tests. Our data suggests that miR-150 and hsa-let-7e were significantly higher in infected-PBMCs after 12 hpi compared to the uninfected-PBMCs (p<0.05). The causality tests demonstrated that miR-150 and hsa-let-7e were negatively correlated with IL-8 expression, meanwhile miR-146a was the contrast. DENV infection was negatively and positively correlated with miR-150 and hsa-let-7e, respectively, after 24 hpi. In conclusion, our data demonstrates the vital role of miR-150, hsa-let-7e, and miR-146a in regulating IL-8 expression with possible different pathways.
Correlation of miR-150, hsa-let-7e, and miR-146a and gene expression of IL-6, IL-8, IP-10, and MIP-1β during dengue virus infection Masyeni, Sri; Kuntaman, Kuntaman; Aryati, Aryati; Sofro, Muchlis AU; Hadi, Usman; Mastutik, Gondo; Purnomo, Windu; Santosa, Agus; Yohan, Benediktus; Nelwan, Erni Juwita; Sasmono, R. Tedjo
Narra J Vol. 1 No. 1 (2021): April 2021
Publisher : Narra Sains Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.52225/narraj.v1i1.31

Abstract

Growing evidence suggests that microRNAs (miRNAs) play a pivotal role in viral infection. The objective of this study was to assess the association between the expression of miR-150, hsa-let-7e, and miR-146a on cytokine expression during dengue infection. Dengue virus (DENV) strain SJN-006, a serotype 2 DENV strain of the Cosmopolitan genotype, isolated in Bali, Indonesia, was used to infect peripheral blood mononuclear cells (PBMCs) isolated from healthy individuals. The relative gene expressions of miR-150, hsa-let-7e, and miR-146a as well as the gene expression of cytokines (IL-6, IL-8, IP-10, and MIP-1β) were determined using quantitative real time - polymerase chain reaction (qRT-PCR) at 6, 12 and 24 hours post infection (hpi). Correlations between the microRNAs and cytokines were analyzed by means of causality tests. Our data suggests that miR-150 and hsa-let-7e were significantly higher in infected-PBMCs after 12 hpi compared to the uninfected-PBMCs (p<0.05). The causality tests demonstrated that miR-150 and hsa-let-7e were negatively correlated with IL-8 expression, meanwhile miR-146a was the contrast. DENV infection was negatively and positively correlated with miR-150 and hsa-let-7e, respectively, after 24 hpi. In conclusion, our data demonstrates the vital role of miR-150, hsa-let-7e, and miR-146a in regulating IL-8 expression with possible different pathways.
Challenges and adversities among doctors in the era of healthcare disruption: Reflection from COVID-19 pandemic Sugiyatmi, Tri A.; Hadi, Usman; Chalidyanto, Djazuly; Pathak, Yashwant; Miftahussurur, Muhammad
Narra J Vol. 3 No. 2 (2023): August 2023
Publisher : Narra Sains Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.52225/narra.v3i2.134

Abstract

The doctor's profession is noble and tied up with quite strict rules, both in terms of ethics as well as discipline. Naturally, there is a problem of asymmetrical information between doctors and patients, often leading to misunderstandings. The purpose of this review is to map the available evidence related to the challenges and difficulties faced by doctors in the era of disruption. The evidence indicate that disruption of health services has both positive and negative effects. Many aspects related to the use of technology in the medical practices including innovation, cost-effectiveness, and quality improvement. However, psychologically, the doctors often get frustrated by internal or external triggers. The external factors, ranges from the equipment and work procedures, for instance, using high technology, communication with management, inter-professional relationships, patients, and their families. Volatility, uncertainty, complexity, and ambiguity (VUCA) could cause stress and burnout. In this case, doctors are highly vulnerable, and consequently, have the potential to make mistakes. Therefore, the adversity faced by doctors ought to be mapped. Resilience is a barrier against stress and burnout and the ability to adapt in resilience among doctors is important factor in dealing with the disruption era.
The role of mediator suppressor of cytokine signaling (SOCS), toll-like receptor 3 (TLR-3) and nuclear factor kappa B (NFκB) on cytokine production during dengue virus infection Masyeni, Sri; Kuntaman, Kuntaman; Aryati , Aryati; Sofro, Muchlis AU.; Hadi, Usman; Mastutik, Gondo; Purnomo, Windu; Santosa, Agus; Iqhrammullah, Muhammad; Yohan, Benediktus; Nelwan, Erni J.; Sasmono, R. Tedjo
Narra J Vol. 3 No. 2 (2023): August 2023
Publisher : Narra Sains Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.52225/narra.v3i2.167

Abstract

Inability to understand the pathogenesis of severe dengue, in particular the control mechanism of immune responses, has led to high mortality rate for patients with dengue shock syndrome (DSS). The aim of this study was to determine the control mechanism of cytokine production by mediator suppressor of cytokine signaling (SOCS), toll-like receptor 3 (TLR-3) and nuclear factor kappa B (NFκB) during DENV infection. Peripheral blood mononuclear blood cells (PBMC), isolated from healthy individuals, were infected with dengue virus (DENV)-2 strain SJN-006 Cosmopolitan genotype (isolated from Bali, Indonesia). The relative gene expression of SOCS-3, TLR-3, NFκB, and the cytokine genes (interleukin (IL)-6, IL-8, interferon inducible protein 10 (IP-10), and macrophage inflammatory protein-1 beta (MIP-1β)) were measured using qRT-PCR at 6, 12 and 24 hours post infection (hpi). Student t-test and Mann-Whitney test were used to compare the gene expressions while causal correlations were analyzed using regression test and path analyses. DENV-2 infection increased the gene expression of SOCS-3, TLR-3, and NFκB after 12 and 24 hpi. The expression of IL-6, IL-8, IP-10, and MIP-1β genes was increased and peaked at different times post-infection. NFκB and SOCS-3 genes likely have role in the upregulation of IL-8 and IL-6 gene expression, respectively. MIP-1β gene expression was significantly induced by both NFκB and SOCS-3. In conclusion, our study suggested that SOCS-3, TLR-3, and NFκB are important in regulating the production of IL-6, IL-8, IP-10, MIP-1β during early phase of DENV-2 infection. This enriches our understanding on pathogenesis pathway of DENV-associated cytokine storm.
Effector function and neutrophil cell death in the severity of sepsis with diabetes mellitus Margalin, Brilliant; Arfijanto, Muhammad V.; Hadi, Usman
Narra J Vol. 4 No. 1 (2024): April 2024
Publisher : Narra Sains Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.52225/narra.v4i1.532

Abstract

Sepsis, a life-threatening condition resulting from immune dysregulation, is typically triggered by bacterial infections and commonly coexists with diabetes mellitus. Neutrophils are the first responders to infection and require regulated activation to control pathogen and damage-associated molecular patterns. Dysregulation of neutrophil activation leads to uncontrolled inflammatory responses, often observed in both sepsis and diabetes patients. Neutrophil dysregulation, characterized by effector dysfunction and inadequate cell death processes, can serve as a biomarker for assessing sepsis severity, particularly in diabetic patients. This review article provides information on the relationship between effector function, neutrophil cell death, and the severity of sepsis in individuals with diabetes mellitus, aiming to shed light on the mechanisms underlying sepsis progression. Topics covered in the review include an overview of effector function of neutrophil cells, mechanisms of neutrophil cell death, and dysregulation of effectors and neutrophil cell death processes in sepsis severity with diabetes mellitus.