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Kumboyono K, Chomsy IN, Iskandar A, Aryati A, Parwati I, Wihastuti TA. Infect Drug Resist. 2022;15:821–829. The authors have advised the author and affiliation list on page 821 is incorrect. The correct author list and affiliations are as follows. Agustin Iskandar,1,2 Khoirunisah Dwi Hartanti,2 Theresia Maharani Sari Nastiti,2 Sandy Wijaya,2 Kumboyono Kumboyono,3 Aryati Aryati,4 Ida Parwati,5 Titin Andri Wihastuti6 1Doctoral Program in Medical Science, Faculty of Medicine, University of Brawijaya, Malang, 65145, Indonesia; 2Department of Clinical Pathology, Faculty of Medicine, University of Brawijaya-Saiful Anwar General Hospital, Malang, 65145, Indonesia; 3Nursing Department, Faculty of Health Sciences, University of Brawijaya, Malang, 65151, Indonesia; 4Department of Clinical Pathology, Faculty of Medicine, Universitas Airlangga, Surabaya, 60131, Indonesia; 5Department of Clinical Pathology, Faculty of Medicine, Universitas Padjadjaran, Bandung, 40161, Indonesia; 6Basic Nursing Department, Faculty of Health Sciences, University of Brawijaya, Malang, 65151, Indonesia Page 823, Ethical Clearance section, the text “The institutional ethics committee of University of Brawijaya approved the study (No. 09/EC/KEPK/07/2021) and also ethical committee of Saiful Anwar General Hospital (No. 4000/011/K.3/302/2021). All of the patients participate in this study provided informed consent that has been accordanced with the Declaration of Helsinki” should read “The institutional ethics committee of Saiful Anwar General Hospital approved the study with reference No. 4000/011/K.3/302/2021 and No. 400/161/K.3/102.7/2022”. Page 828, Acknowledgments section, the text “The authors are thankful for the Ministry of Culture and Education; the Republic of Indonesia sponsored this research financially through “Program Penelitian Kolaborasi Indonesia” World Class University with grant numbers: 342.2/UN10

Teuku Heriansyah,1 Herlina Dimiati,1 Tjut Farahiya Hadi,1 Dimas Arya Umara,1 Lian Varis Riandi,2 Fauzan Fajri,3 Sukmawan Fajar Santosa,4 Titin Andri Wihastuti,5 Kumboyono Kumboyono6 1Department of Cardiology and Vascular Medicine, Faculty of Medicine, Universitas Syiah Kuala, Banda Aceh, Aceh, Indonesia; 2Department of Parasitology, Faculty of Veterinary Medicine, Universitas Syiah Kuala, Banda Aceh, Aceh, Indonesia; 3Department of Animal Model, Faculty of Veterinary Medicine, Universitas Syiah Kuala, Banda Aceh, Aceh, Indonesia; 4Integrated Research Laboratory, Faculty of Veterinary Medicine, Universitas Syiah Kuala, Banda Aceh, Aceh, Indonesia; 5Department of Basic Nursing, Faculty of Health Sciences, Universitas Brawijaya, Malang, Jawa Timur, Indonesia; 6Department of Nursing, Faculty of Health Sciences, Universitas Brawijaya, Malang, IndonesiaCorrespondence: Tjut Farahiya Hadi, Email tjut@mhs.unsyiah.ac.idIntroduction: Ascorbic acid and calcitriol were frequently utilized in conjunction as therapy during the COVID-19 pandemic, and individuals with minor symptoms had notable improvements. There have been a few studies, often with conflicting findings, that examine the use of them for endothelium restoration and numerous clinical trial studies that failed to establish the efficacy. The aim of this study was to find the efficacy of ascorbic acid compared to calcitriol on the inflammatory markers monocyte chemoattractant protein-1 (MCP-1), nitric oxide (NO), and superoxide dismutase (SOD), as protective agents which play an important role in the early stages of atherosclerosis formation. This study was an experimental in vivo study.Methods: The total of 24 male Rattus norvegicus strain Wistar rats were divided into 4 groups, namely: control/normal group (N), atherosclerosis group (DL) given atherogenic diet, atherosclerosis group given atherogenic diet and ascorbic acid (DLC), and atherosclerosis group given atherogenic diet and calcitriol (DLD) treatment for 30 day

Kumboyono Kumboyono,1 Indah Nur Chomsy,2 Agustin Iskandar,3 Aryati Aryati,4 Ida Parwati,5 Titin Andri Wihastuti6 1Nursing Department, Faculty of Health Sciences, University of Brawijaya, Malang, 65151, Indonesia; 2Doctoral Program of Medical Science, Faculty of Medicine, University of Brawijaya, Malang, 65145, Indonesia; 3Department of Clinical Pathology, Faculty of Medicine, University of Brawijaya, Malang, 65145, Indonesia; 4Department of Clinical Pathology, Faculty of Medicine, Universitas Airlangga, Surabaya, 60131, Indonesia; 5Department of Clinical Pathology, Faculty of Medicine, Universitas Padjadjaran, Bandung, 40161, Indonesia; 6Basic Nursing Department, Faculty of Health Sciences, University of Brawijaya, Malang, 65151, IndonesiaCorrespondence: Titin Andri Wihastuti, Basic Nursing Department, Faculty of Health Sciences, University of Brawijaya, Malang, 65151, Indonesia, Email titinwihastuti@gmail.comBackground: Tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and monocyte chemoattractant protein-1 (MCP-1) are early phase cytokines often encountered when the body is exposed to severe acute respiratory syndrome-associated-coronavirus-2. TNF-α, IL-1β, and MCP-1 are pro-inflammatory cytokines critical in the defence response against systemic infection and injury. Therefore, TNF-α, IL-1β, and MCP-1 are the most aggressive responses to viral infections in the acute phase, so they can be used to determine the survival of coronavirus disease 2019 (COVID-19) patients.Purpose: The study aimed to determine the levels of TNF-α, IL-1β, and MCP-1 as predictors of survival for COVID-19 patients.Patients and Methods: A prospective cohort study was conducted on confirmed COVID-19 by a reverse-transcriptase-polymerase-chain-reaction (RT-PCR) in 84 adults admitted to the hospital in Indonesia. TNF-α, IL-1β, and MCP-1 level were measured from serum subjects using the enzyme-linked immunosorbent assay.Results: The results from logistic regression modelling

Kumboyono Kumboyono,1 Indah Nur Chomsy,2 Ardhi Khoirul Hakim,3 Hidayat Sujuti,4,5 Tita Hariyanti,5,6 Arie Srihardyastutie,7 Titin Andri Wihastuti8 1Department of Nursing, Faculty of Health Sciences, University of Brawijaya, Malang, Indonesia; 2Doctoral Program of Medical Science, Faculty of Medicine, University of Brawijaya, Malang, Indonesia; 3Master Program of Biomedical Science, Faculty of Medicine, University of Brawijaya, Malang, Indonesia; 4Department of Biomolecular-Ophtalmology, Faculty of Medicine, University of Brawijaya, Malang, Indonesia; 5Saifur Anwar General Hospital, Malang, Indonesia; 6Department of Public Health, Faculty of Medicine, University of Brawijaya, Malang, Indonesia; 7Department of Chemistry, Faculty of Mathematics and Natural Science, University of Brawijaya, Malang, Indonesia; 8Basic Nursing Department, Faculty of Health Sciences, University of Brawijaya, Malang, IndonesiaCorrespondence: Titin Andri Wihastuti, Email titinwihastuti@gmail.comPurpose: Smoking is a significant risk factor in developing cardiovascular disease pathogenesis through oxidative stress and inflammation mechanisms. This study used cotinine as a biomarker of nicotine exposure levels in the body, which was associated with levels of Interleukin-6 (IL-6) and Superoxide Dismutase (SOD) as markers of oxidative stress and vascular inflammation. The research aimed to analyze the effect of cotinine levels on the expression of IL-6 and SOD.Methods: This study used a cross-sectional design on 200 subjects, consisting 100 smokers and 100 non-smokers. Cotinine levels, IL-6 expression, and SOD were measured from the blood serum of each subject using the Enzyme-Linked Immunosorbent Assay (ELISA) method. Then the data were analyzed using Generalized Structured Component Analysis (GSCA).Results: There was a significant effect of cotinine levels on the reduction of SOD mediated by IL-6 (CR = 4.006). Cotinine levels also increased IL-6 mediated by SOD (CR = 4.292). The structural mode

Kumboyono Kumboyono,1 Wiwit Nurwidyaningtyas,2 Indah Nur Chomsy,2 Titin Andri Wihastuti3 1Nursing Department, Faculty of Medicine, University of Brawijaya, Malang, 65145, Indonesia; 2Doctoral Program of Medical Science, Faculty of Medicine, University of Brawijaya, Malang, 65145, Indonesia; 3Department of Biomedicine, Faculty of Medicine, University of Brawijaya, Malang, 65145, IndonesiaCorrespondence: Kumboyono Kumboyono Email publikasikoe@gmail.comIntroduction: Smoking can cause vascular damage in the form of an inflammatory reaction characterized by endothelial activation. Endothelial activation forms a pathological adaptation pattern so that it can induce the atherogenesis process. Several markers, such as E-selectin, platelet-derived micro particles (PMPs) and hematopoietic stem cell (HSC) can identify the activation of endothelial in circulating blood. Therefore, the deviation of vascular adaptation due to smoking can be detected early through the feedback mechanism between E-selectin, PMPs, and HSC.Purpose: This study aims to analyze the initial picture of the negative impact of smoking on vascular adaptation by measuring E-selectin, PMPs, and HSC in the peripheral blood circulation. Participant criteria and methods: Peripheral blood samples (5 mL) were taken from each participant, both the smoking group (n = 30) and the non-smoker group (n = 31) to obtain peripheral blood mononuclear cells (PBMNC). PBMNC was isolated using ficoll-based gradient centrifugation. The flow cytometry assay method used to measure the E-selectin, PMPs and hematopoietic stem cells.Results: The mean of circulating E-selectin in smokers was higher than that of non-smokers. On the other hand, the average number of PMPs and HSCs in smokers was lower than non-smokers.Conclusion: Smoking increases the risk of accelerated vascular block formation, as indicated by an increase in the amount of circulating E-selectin. The increase in E-selectin in the blood vessels mediates the increased adhe