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Genetic and Molecular Susceptibility in Human Diseases: 2nd Edition
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Genetic and Molecular Susceptibility in Human Diseases: 2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (20 February 2025) | Viewed by 17622

Special Issue Editor

Prof. Dr. Roberto Madeddu

E-Mail Website
Guest Editor
Department of Biomedical Sciences, University of Sassari, Sassari, Italy
Interests: trace elements; cadmium; toxicity; neurodegenerative disorders; cancer stem cells; oncology; miRNA
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Genetic susceptibility refers to the tendency of different populations and individuals to be susceptible to polygenic diseases, such as tumors, under the influence of the external environment, and due to the presence of different genetic structures. Some environmental factors and personal living habits can affect tumor development. All environmental factors that alter cell cycle gene expression, apoptosis, and DNA damage repair are tumor-induced risk factors, including food, natural and artificial radiation, chemicals, and viruses.

This journal welcomes the publication of all findings pertaining to molecular susceptibility in human disease. Pure clinical studies are not within the scope of this Special Issue; however, clinical submissions with biomolecular experiments are welcome.

Dr. Roberto Madeddu
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • genetic susceptibility
  • proteomics
  • gene expression
  • apoptosis

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Related Special Issues

Published Papers (9 papers)

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Research

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19 pages, 4538 KiB  
Article
Functional Characterization of miR-216a-5p and miR-125a-5p on Pancreatic Cancer Stem Cells
by Grazia Fenu, Carmen Griñán-Lisón, Federica Etzi, Aitor González-Titos, Andrea Pisano, Belén Toledo, Cristiano Farace, Angela Sabalic, Esmeralda Carrillo, Juan Antonio Marchal and Roberto Madeddu
Int. J. Mol. Sci. 2025, 26(7), 2830; https://doi.org/10.3390/ijms26072830 - 21 Mar 2025
Viewed by 404
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is the third leading cause of cancer-related death. Its poor prognosis is closely related to late-stage diagnosis, which results from both nonspecific symptoms and the absence of biomarkers for early diagnosis. MicroRNAs (miRNAs) exert a regulatory role in numerous [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is the third leading cause of cancer-related death. Its poor prognosis is closely related to late-stage diagnosis, which results from both nonspecific symptoms and the absence of biomarkers for early diagnosis. MicroRNAs (miRNAs) exert a regulatory role in numerous biological processes and their aberrant expression has been found in a broad spectrum of diseases, including cancer. Cancer stem cells (CSCs) represent a driving force for PDAC initiation, progression, and metastatic spread. Our previous research highlighted the interesting behavior of miR-216a-5p and miR-125a-5p related to PDAC progression and the CSC phenotype. The present study aimed to evaluate the effect of miR-216a-5p and miR-125a-5p on the acquisition or suppression of pancreatic CSC traits. BxPC-3, AsPC-1 cell lines, and their CSC-like models were transfected with miR-216a-5p and miR-125a-5p mimics and inhibitors. Following transfection, we evaluated their impact on the expression of CSC surface markers (CD44/CD24/CxCR4), ALDH1 activity, pluripotency- and EMT-related gene expression, and clonogenic potential. Our results show that miR-216a-5p enhances the expression of CD44/CD24/CxCR4 while negatively affecting the activity of ALDH1 and the expression of EMT genes. MiR-216a-5p positively influenced the clonogenic property. MiR-125a-5p promoted the expression of CD44/CD24/CxCR4 while inhibiting ALDH1 activity. It enhanced the expression of Snail, Oct-4, and Sox-2, while the clonogenic potential appeared to be affected. Comprehensively, our results provide further knowledge on the role of miRNAs in pancreatic CSCs. Moreover, they corroborate our previous findings about miR-216a-5p’s potential dual role and miR-125a-5p’s promotive function in PDAC. Full article
(This article belongs to the Special Issue Genetic and Molecular Susceptibility in Human Diseases: 2nd Edition)
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17 pages, 3373 KiB  
Article
Genetic Polymorphisms in MHC Classes I and II Predict Outcomes in Metastatic Colorectal Cancer
by Pooja Mittal, Francesca Battaglin, Yan Yang, Shivani Soni, Sebastian Stintzing, Aparna R. Parikh, Karam Ashouri, Sandra Algaze, Priya Jayachandran, Lesly Torres-Gonzalez, Wu Zhang, Chiara Cremolini, Volker Heinemann, Joshua Millstein, Indrakant K. Singh and Heinz-Josef Lenz
Int. J. Mol. Sci. 2025, 26(6), 2556; https://doi.org/10.3390/ijms26062556 - 12 Mar 2025
Viewed by 640
Abstract
The immune system is alerted for virally infected cells in the body by the antigen presentation pathway, which is in turn mediated by the major histocompatibility complex (MHC) class I and II molecules. Cancer cells overcome immune evasion as a major hallmark by [...] Read more.
The immune system is alerted for virally infected cells in the body by the antigen presentation pathway, which is in turn mediated by the major histocompatibility complex (MHC) class I and II molecules. Cancer cells overcome immune evasion as a major hallmark by downregulation of the antigen presentation pathway. Therefore, the present study aimed to explore the effect of genetic variants in genes involved in MHC class I and II pathways in patients treated with first-line chemotherapy in combination with targeted antibodies in metastatic colorectal cancer (mCRC) patients. Genomic DNA from the blood samples of 775 patients enrolled in three independent, randomized, first-line trials, namely TRIBE (FOLFIRI-bevacizumab, N = 215), FIRE-3 (FOLFIRI-bevacizumab, N = 107; FOLFIRI-cetuximab, N = 129), and MAVERICC (FOLFIRI-bevacizumab, N = 163; FOLFOX6-bevacizumab, N = 161), was genotyped through OncoArray, a custom array manufactured by Illumina including approximately 530K SNP markers. The impact on the outcome of 40 selected SNPs in 22 genes of MHC class I and II pathways was analyzed. We identified several SNPs in multiple genes associated with targeted treatment benefits across different treatment arms in our study population (p < 0.05). Treatment–SNP interaction analyses confirmed a significant treatment interaction with the targeted agents (bevacizumab vs. cetuximab) and the chemotherapy backbone (FOLFIRI vs. FOLFOX) in certain selected SNPs. Our results highlight a potential role for MHC SNPs as prognostic and predictive biomarkers for first-line treatment in mCRC, with differential effects based on the biologic agent and chemotherapy backbone. These biomarkers, when further validated, may contribute to personalized treatment strategies for mCRC patients. Full article
(This article belongs to the Special Issue Genetic and Molecular Susceptibility in Human Diseases: 2nd Edition)
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21 pages, 2753 KiB  
Article
Genetic Variants Associated with Suspected Neonatal Hypoxic Ischaemic Encephalopathy: A Study in a South African Context
by Caroline J. Foden, Kevin Durant, Juanita Mellet, Fourie Joubert, Jeanne van Rensburg, Khomotso Masemola, Sithembiso C. Velaphi, Firdose L. Nakwa, Alan R. Horn, Shakti Pillay, Gugu Kali, Melantha Coetzee, Daynia E. Ballot, Thumbiko Kalua, Carina Babbo and Michael S. Pepper
Int. J. Mol. Sci. 2025, 26(5), 2075; https://doi.org/10.3390/ijms26052075 - 27 Feb 2025
Viewed by 625
Abstract
Neonatal encephalopathy suspected to be due to hypoxic ischaemic encephalopathy (NESHIE) carries the risk of death or severe disability (cognitive defects and cerebral palsy). Previous genetic studies on NESHIE have predominantly focused on exomes or targeted genes. The objective of this study was [...] Read more.
Neonatal encephalopathy suspected to be due to hypoxic ischaemic encephalopathy (NESHIE) carries the risk of death or severe disability (cognitive defects and cerebral palsy). Previous genetic studies on NESHIE have predominantly focused on exomes or targeted genes. The objective of this study was to identify genetic variants associated with moderate–severe NESHIE through whole-genome, unbiased analysis. Variant filtering and prioritization were performed, followed by association testing both on a case–control basis and to compare the grades of severity and/or progression. Association testing on neonates with NESHIE (N = 172) and ancestry-matched controls (N = 288) produced 71 significant genetic variants (false discovery rate corrected p-value < 6.2 × 10−4), all located in non-coding regions and not previously implicated in NESHIE. Disease-associated variants in non-coding regions are considered to affect regulatory functions, possibly by modifying gene expression, promoters, enhancers, or DNA structure. The most significant variant was at position 6:162010973 in the Parkin RBR E3 ubiquitin protein ligase (PRKN) intron. Intronic variants were also identified in genes involved in inflammatory processes (SLCO3A1), DNA repair (ZGRF1), synaptogenesis (CNTN5), haematopoiesis (ASXL2), and the transcriptional response to hypoxia (PADI4). Ten variants were associated with a higher severity or lack of improvement in NESHIE, including one in ADAMTS3, which encodes a procollagen amino protease with a role in angiogenesis and lymphangiogenesis. This analysis represents one of the first efforts to analyze whole-genome data to investigate the genetic complexity of NESHIE in diverse ethnolinguistic groups of African origin and provides direction for further study. Full article
(This article belongs to the Special Issue Genetic and Molecular Susceptibility in Human Diseases: 2nd Edition)
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23 pages, 5592 KiB  
Article
Genetic Manipulation of Caveolin-1 in a Transgenic Mouse Model of Aortic Root Aneurysm: Sex-Dependent Effects on Endothelial and Smooth Muscle Function
by Tala Curry-Koski, Brikena Gusek, Ross M. Potter, T. Bucky Jones, Raechel Dickman, Nathan Johnson, John N. Stallone, Roshanak Rahimian, Johana Vallejo-Elias and Mitra Esfandiarei
Int. J. Mol. Sci. 2024, 25(23), 12702; https://doi.org/10.3390/ijms252312702 - 26 Nov 2024
Viewed by 1063
Abstract
Marfan syndrome (MFS) is a systemic connective tissue disorder stemming from mutations in the gene encoding Fibrillin-1 (Fbn1), a key extracellular matrix glycoprotein. This condition manifests with various clinical features, the most critical of which is the formation of aortic root aneurysms. Reduced [...] Read more.
Marfan syndrome (MFS) is a systemic connective tissue disorder stemming from mutations in the gene encoding Fibrillin-1 (Fbn1), a key extracellular matrix glycoprotein. This condition manifests with various clinical features, the most critical of which is the formation of aortic root aneurysms. Reduced nitric oxide (NO) production due to diminished endothelial nitric oxide synthase (eNOS) activity has been linked to MFS aortic aneurysm pathology. Caveolin-1 (Cav1), a structural protein of plasma membrane caveolae, is known to inhibit eNOS activity, suggesting its involvement in MFS aneurysm progression by modulating NO levels. In this study, we examined the role of Cav1 in aortic smooth muscle and endothelial function, aortic wall elasticity, and wall strength in male and female MFS mice (FBN1+/Cys1041Gly) by generating developing Cav1-deficient MFS mice (MFS/Cav1KO). Our findings reveal that Cav1 ablation leads to a pronounced reduction in aortic smooth muscle contraction in response to phenylephrine, attributable to an increase in NO production in the aortic wall. Furthermore, we observed enhanced aortic relaxation responses to acetylcholine in MFS/Cav1KO mice, further underscoring Cav1’s inhibitory impact on NO synthesis within the aorta. Notably, van Gieson staining and chamber myography analyses showed improved elastin fiber structure and wall strength in male MFS/Cav1KO mice, whereas these effects were absent in female counterparts. Cav1’s regulatory influence on aortic root aneurysm development in MFS through NO-mediated modulation of smooth muscle and endothelial function, with notable sex-dependent variations. Full article
(This article belongs to the Special Issue Genetic and Molecular Susceptibility in Human Diseases: 2nd Edition)
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19 pages, 2635 KiB  
Article
Association of Cytotoxic T-Lymphocyte Antigen-4 (CTLA-4) Genetic Variants with Risk and Outcome of Cutaneous Melanoma
by Ana Maria Castro Ferreira, Juliana Carron, Gabriela Vilas Bôas Gomez, Vinicius de Lima Vazquez, Sergio Vicente Serrano, Gustavo Jacob Lourenço and Carmen Silvia Passos Lima
Int. J. Mol. Sci. 2024, 25(22), 12327; https://doi.org/10.3390/ijms252212327 - 17 Nov 2024
Viewed by 1178
Abstract
This study aimed to verify whether germline single nucleotide variants (SNV) in CTLA-4 gene, c.-1765C>T, c.-1661A>G, c.-1577G>A, and c.-1478G>A, influence the risk, clinicopathological aspects, and survival of patients with CM, as well as its functional consequences. A total of 432 patients with CM [...] Read more.
This study aimed to verify whether germline single nucleotide variants (SNV) in CTLA-4 gene, c.-1765C>T, c.-1661A>G, c.-1577G>A, and c.-1478G>A, influence the risk, clinicopathological aspects, and survival of patients with CM, as well as its functional consequences. A total of 432 patients with CM and 504 controls were evaluated. CTLA-4 genotypes were identified by real-time polymerase chain reaction (RT-PCR) and expression of CTLA-4 by quantitative PCR (qPCR) and luciferase assay. Cell cycle, proliferation, apoptosis/necrosis, and migration analyses were performed in SK-MEL-28 and A-375 cell lines modified to present homozygous ancestral or variant genotypes by CRISPR technique. Individuals with the CTLA-4 c.-1577 AA genotype and the combined CTLA-4 c.-1577 and c.-1478 AA + AA genotypes were at 1.60- and 3.12-fold higher risk of developing CM, respectively. The CTLA-4 c.-1577 AA genotype was seen as an independent predictor of worse event-free survival and was also associated with higher gene expression, higher cell proliferation, lower cell apoptosis, and higher cell migration. Our data present, for the first time, evidence that CTLA-4 c.-1577G>A alters the risk and clinical aspects of CM treated with conventional procedures and may be used for selecting individuals for tumor prevention and patients for distinct treatment. Full article
(This article belongs to the Special Issue Genetic and Molecular Susceptibility in Human Diseases: 2nd Edition)
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21 pages, 7694 KiB  
Article
CD4+ Effective Memory T Cell Markers GBP2 and LAG3 Are Risk Factors for PTB and COVID-19 Infection: A Study Integrating Single-Cell Expression Quantitative Trait Locus and Mendelian Randomization Analyses
by Liangyu Zhu, Hanxin Wu, Li Peng, Xun Huang, Rui Yang, Weijie Ma, Lei Zhong, Bingxue Li, Jieqin Song, Suyi Luo, Li Gao, Xinya Wu, Weijiang Ma, Fukai Bao and Aihua Liu
Int. J. Mol. Sci. 2024, 25(18), 9971; https://doi.org/10.3390/ijms25189971 - 16 Sep 2024
Cited by 1 | Viewed by 2296
Abstract
Observational studies indicate that variations in peripheral blood mononuclear cell (PBMC) subsets are associated with an increased risk of pulmonary tuberculosis (PTB) and coronavirus disease 2019 (COVID-19), but causal validation is lacking. Here, we combined single-cell expression quantitative trait locus (sc-eQTL) and two-sample [...] Read more.
Observational studies indicate that variations in peripheral blood mononuclear cell (PBMC) subsets are associated with an increased risk of pulmonary tuberculosis (PTB) and coronavirus disease 2019 (COVID-19), but causal validation is lacking. Here, we combined single-cell expression quantitative trait locus (sc-eQTL) and two-sample mendelian randomization (MR) analyses to elucidate the causal relationship between PBMC subsets and the occurrence of PTB and COVID-19 and verified by RT-qPCR. We observed an increase in the CD4+ Effective Memory T Cell (CD4+ TEM) cluster in both PTB and COVID-19 patients according to the single-cell transcriptional landscape of PBMC. Through MR analysis using an inverse variance weighted (IVW) method, we found strong evidence of positive correlations between CD4+ TEM cell markers (GBP2, TRAV1-2, and ODF2L) and PTB, and between markers (LAG3 and SLFN5) and COVID-19, especially highlighted by lead eQTL-SNPs of GBP2 (rs2256752, p = 4.76321 × 10−15) and LAG3 (rs67706382, p = 6.16× 10−16). Similar results were observed in validation sets, and no pleiotropy was detected in sensitivity analyses including weighted median (WM), MR-Egger, MR-pleiotropy residual sum and outlier, and leave-one-out analyses (all p > 0.05). We visualized the colocalization of marker-eQTLs and markers of PTB and COVID-19 genome-wide association study (GWAS) associations. Based on CellChat analyses, monocytes communicated predominantly with CD4+ TEM cells positively expressing PTB markers (GBP2, TRAV1-2, and ODF2L) and COVID-19 markers (LAG3 and SLFN5) in both PTB and COVID-19. Our data suggest a causal effect between two key CD4+ TEM cell markers (GBP2 and LAG3) and the risk for PTB and COVID-19 infection. Our findings provide novel insights into the biological mechanism for PTB and COVID-19 infection, but future single-cell studies are necessary to further enhance understanding of this find. Full article
(This article belongs to the Special Issue Genetic and Molecular Susceptibility in Human Diseases: 2nd Edition)
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Review

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40 pages, 1068 KiB  
Review
Genetic Determinants of Endurance: A Narrative Review on Elite Athlete Status and Performance
by Barkın Bıçakçı, Paweł Cięszczyk and Kinga Humińska-Lisowska
Int. J. Mol. Sci. 2024, 25(23), 13041; https://doi.org/10.3390/ijms252313041 - 4 Dec 2024
Cited by 1 | Viewed by 4984
Abstract
This narrative review explores the relationship between genetics and elite endurance athletes, summarizes the current literature, highlights some novel findings, and provides a physiological basis for understanding the mechanistic effects of genetics in sport. Key genetic markers include ACTN3 R577X (muscle fiber composition), [...] Read more.
This narrative review explores the relationship between genetics and elite endurance athletes, summarizes the current literature, highlights some novel findings, and provides a physiological basis for understanding the mechanistic effects of genetics in sport. Key genetic markers include ACTN3 R577X (muscle fiber composition), ACE I/D (cardiovascular efficiency), and polymorphisms in PPARA, VEGFA, and ADRB2, influencing energy metabolism, angiogenesis, and cardiovascular function. This review underscores the benefits of a multi-omics approach to better understand the complex interactions between genetic polymorphisms and physiological traits. It also addresses long-standing issues such as small sample sizes in studies and the heterogeneity in heritability estimates influenced by factors like sex. Understanding the mechanistic relationship between genetics and endurance performance can lead to personalized training strategies, injury prevention, and improved health outcomes. Future studies should focus on standardized classification of sports, replication studies involving diverse populations, and establishing solid physiological associations between polymorphisms and endurance traits to advance the field of sports genetics. Full article
(This article belongs to the Special Issue Genetic and Molecular Susceptibility in Human Diseases: 2nd Edition)
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19 pages, 525 KiB  
Review
Genes, Gene Loci, and Their Impacts on the Immune System in the Development of Multiple Sclerosis: A Systematic Review
by Borros Arneth
Int. J. Mol. Sci. 2024, 25(23), 12906; https://doi.org/10.3390/ijms252312906 - 30 Nov 2024
Viewed by 1153
Abstract
Multiple sclerosis (MS) is a condition that is characterized by damage to the central nervous system (CNS) that causes patients to experience cognitive and physical difficulties. Although the disease has a complex etiology that involves genetic and environmental factors, little is known about [...] Read more.
Multiple sclerosis (MS) is a condition that is characterized by damage to the central nervous system (CNS) that causes patients to experience cognitive and physical difficulties. Although the disease has a complex etiology that involves genetic and environmental factors, little is known about the role of genes and gene loci in its development. Aims: This study aimed to investigate the effects of genes and gene loci on the immune system during the development of MS. We aimed to identify the main genes and gene loci that play roles in MS pathogenesis and the implications for the future development of clinical treatment approaches. A systematic review of articles published over the last decade was conducted. This review focused on studies about the genetic and epigenetic mechanisms underlying MS onset and progression. Genome-wide association studies (GWASs) as well as papers describing the role of the immune system in disease development were prioritized. Key genetic loci and immune system-related genes, such as HLA class II genes, are associated with MS susceptibility. Studies have also shown that epigenetic modifications, such as DNA methylation, influence disease progression via the immune system. Full article
(This article belongs to the Special Issue Genetic and Molecular Susceptibility in Human Diseases: 2nd Edition)
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17 pages, 3016 KiB  
Review
Loss of the Y Chromosome: A Review of Molecular Mechanisms, Age Inference, and Implications for Men’s Health
by Itzae Adonai Gutiérrez-Hurtado, Astrid Desireé Sánchez-Méndez, Denisse Stephania Becerra-Loaiza, Héctor Rangel-Villalobos, Norma Torres-Carrillo, Martha Patricia Gallegos-Arreola and José Alonso Aguilar-Velázquez
Int. J. Mol. Sci. 2024, 25(8), 4230; https://doi.org/10.3390/ijms25084230 - 11 Apr 2024
Cited by 4 | Viewed by 4410
Abstract
Until a few years ago, it was believed that the gradual mosaic loss of the Y chromosome (mLOY) was a normal age-related process. However, it is now known that mLOY is associated with a wide variety of pathologies in men, such as cardiovascular [...] Read more.
Until a few years ago, it was believed that the gradual mosaic loss of the Y chromosome (mLOY) was a normal age-related process. However, it is now known that mLOY is associated with a wide variety of pathologies in men, such as cardiovascular diseases, neurodegenerative disorders, and many types of cancer. Nevertheless, the mechanisms that generate mLOY in men have not been studied so far. This task is of great importance because it will allow focusing on possible methods of prophylaxis or therapy for diseases associated with mLOY. On the other hand, it would allow better understanding of mLOY as a possible marker for inferring the age of male samples in cases of human identification. Due to the above, in this work, a comprehensive review of the literature was conducted, presenting the most relevant information on the possible molecular mechanisms by which mLOY is generated, as well as its implications for men’s health and its possible use as a marker to infer age. Full article
(This article belongs to the Special Issue Genetic and Molecular Susceptibility in Human Diseases: 2nd Edition)
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