21 results on '"Fabiana Antunes Andrade"'
Search Results
2. Insights into the role of complement system in the pathophysiology of endometriosis
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Fabiana Antunes Andrade, Renato Nisihara, and Danilo Rahal
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0301 basic medicine ,Immunology ,Endometriosis ,Disease ,Bioinformatics ,Pathogenesis ,03 medical and health sciences ,0302 clinical medicine ,Immune system ,Humans ,Immunology and Allergy ,Medicine ,Molecular Targeted Therapy ,Complement Activation ,Innate immune system ,business.industry ,Disease Management ,Complement System Proteins ,medicine.disease ,Combined Modality Therapy ,Complement system ,Complement (complexity) ,Biomarker (cell) ,Treatment Outcome ,030104 developmental biology ,Gene Expression Regulation ,Female ,Disease Susceptibility ,business ,Biomarkers ,Signal Transduction ,030215 immunology - Abstract
Endometriosis (EM) is a gynecologic disorder characterized by the presence of endometrium-like tissue outside of normal location that affects up to 10 % of all women in reproductive age. The pathogenesis of endometriosis is not completely known. The relationship between complement and EM has already been demonstrated in some studies, indicating an important role in the pathophysiology of the disease, however, researches are scarce and sometimes controversial. The objective of this review is to bring state-of-the-art knowledge on the subject and promote better understanding of the complement system role in the pathophysiology of EM. We searched in databases up to December 2020 and found 1213 articles that were screened, from which were selected 54 articles from title and abstract. We found that there is a dysfunction of the immune system on endometriosis, including the complement system. Apparently, the complement system is dysregulated in endometriosis and several proteins of the three complement pathways presented serum levels altered in women with endometriosis compared with those without the disease. The most studied protein is C3. Future investigations on the innate immune response and complement system could offer a further understanding on the inflammatory pathogenesis of EM, which will support a new therapeutic plan.
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- 2021
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3. Ficolin-3 in rheumatic fever and rheumatic heart disease
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Fabiana Antunes Andrade, Lorena Bavia, Sandra Jeremias Catarino, Iara Messias-Reason, and Luiza Guilherme
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Adult ,Male ,0301 basic medicine ,Genotype ,Heart disease ,Immunology ,Single-nucleotide polymorphism ,medicine.disease_cause ,Polymorphism, Single Nucleotide ,Autoimmunity ,03 medical and health sciences ,0302 clinical medicine ,Lectins ,medicine ,Humans ,Immunology and Allergy ,Genetic Predisposition to Disease ,Alleles ,business.industry ,Rheumatic Heart Disease ,Genetic Variation ,Middle Aged ,Prognosis ,medicine.disease ,Complement system ,030104 developmental biology ,Lectin pathway ,Streptococcus pyogenes ,Rheumatic fever ,Female ,Disease Susceptibility ,Rheumatic Fever ,business ,Ficolin ,Biomarkers ,030215 immunology - Abstract
Rheumatic fever (RF) and chronic rheumatic heart disease (RHD) are complications of oropharyngeal infection caused by Streptococcus pyogenes. Despite the importance of the complement system against infections and autoimmunity diseases, studies on the role of the lectin pathway in RF and RHD are scarce. Thus, our aim was to evaluate the association of ficolin-3 serum levels, FCN3 polymorphisms and haplotypes with the susceptibility to RF and RHD. We investigated 179 patients with a history of RF (126 RHD and 53 RF only) and 170 healthy blood donors as control group. Ficolin-3 serum concentrations were measured using enzyme-linked immunosorbent assay (ELISA). Three FCN3 single nucleotide polymorphisms (SNPs rs532781899, rs28362807 and rs4494157) were genotyped through the sequence-specific PCR method. Lower ficolin-3 serum levels were observed in RF patients when compared to controls (12.81 μg/mL vs. 18.14 μg/mL respectively, p 0.0001, OR 1.22 [1.12-1.34]), and in RHD in comparison to RF only (RFo) (12.72 μg/mL vs. 14.29 μg/mL respectively, p = 0.016, OR 1.38 [1.06-1.80]). Low ficolin-3 levels (10.7 μg/mL) were more common in patients (39.5 %, 30/76) than controls (20.6 %, 13/63, p = 0.018, OR = 2.51 [1.14-5.31]), and in RHD (44.4 %, 28/63) than RFo (15.4 %, 2/13, p = 0.007, OR = 3.08 [1.43-6.79]). On the other hand, FCN3 polymorphism/haplotypes were not associated with ficolin-3 serum levels or the disease. Low ficolin-3 levels might be associated with RF, being a potential marker of disease progression.
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- 2021
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4. MASP1 Gene Polymorphism and MASP-3 Serum Levels in Patients with Chronic Chagas Disease
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Ednéia Oliveira Cavalcanti, Kárita Cláudia Freitas Lidani, Camila de Freitas Oliveira Toré, Iara José de Messias Reason, and Fabiana Antunes Andrade
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Immunology ,General Medicine - Abstract
Chagas disease (CD), caused by Trypanosoma cruzi, is a major public health issue worldwide affecting 6–7 million people, mainly in Latin America. The complement system plays a crucial role in host immune defense against T. cruzi infection and during the chronic phase of CD; however, the role of the MBL-associated serine protease 1 (MASP1) gene encoding MASP-1, MASP-3, and MAp44 complement proteins has not yet been reported in CD. This study investigated the possible association between MASP1 gene polymorphisms and MASP-3 protein serum levels in chronic CD and its clinical forms. Five polymorphisms of MASP1 gene regulatory regions were genotyped in 214 patients with CD and 197 healthy controls (rs7609662 G>A, rs13064994 C>T, rs72549262 C>G, rs1109452 C>T and rs850314 G>A). MASP-3 serum levels were assessed in 70 patients and 66 healthy controls. Clinical data, serum levels of complement proteins (ficolin-2, ficolin-3 and MBL) and inflammatory markers (pentraxin-3 and hsCRP) were also included in the analyses. A significant association of the MASP1 GC_CCA haplotype with CD (padj= 0.002; OR 3.17 [1.19–8.39]) and chronic chagasic cardiomyopathy (CCC) (padj= 0.013; OR 4.57 [1.37–15.16] was observed. MASP-3 and pentraxin-3 levels were positively correlated in the patients (rho = 0.62; p = 0.0001). MASP-3 levels were not associated with MASP1 polymorphisms or CD and its clinical forms. Furthermore, no correlation was observed between MASP-3 levels and that of ficolin-2, ficolin-3, MBL and hsCRP. Our findings suggest a possible role for the MASP1 GC_CCA haplotype in susceptibility to chronic CD and CCC clinical forms.
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- 2022
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5. Ficolin‐3 in chronic Chagas disease: Low serum levels associated with the risk of cardiac insufficiency
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Indira Chakravarti, Maria Regina Tizzot, Paola Rosa Luz, Iara Messias-Reason, Thaisa Lucas Sandri, Edneia Oliveira Cavalcanti, Marcia Holsbach Beltrame, Fabiana Antunes Andrade, and Kárita Cláudia Freitas Lidani
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0301 basic medicine ,Chagas disease ,medicine.medical_specialty ,Heart Diseases ,030231 tropical medicine ,Immunology ,Inflammation ,Disease ,Biology ,Asymptomatic ,Gastroenterology ,Ventricular Function, Left ,03 medical and health sciences ,0302 clinical medicine ,Lectins ,Internal medicine ,medicine ,Humans ,Chagas Disease ,Ejection fraction ,Stroke Volume ,Heterozygote advantage ,medicine.disease ,Pathophysiology ,030104 developmental biology ,Parasitology ,medicine.symptom ,Ficolin - Abstract
Aims To investigate whether FCN3 polymorphisms and circulating ficolin-3 levels were associated with clinical forms of chronic Chagas disease (CD) and to assess their potential use as biomarkers for the disease or its severity. Methods and results FCN3 polymorphisms (g.1637delC (rs532781899) in exon 5; g.3524_3532insTATTTGGCC (rs28362807) in intron 5 and g.4473C > A) (rs4494157) in intron 7) were determined in 178 chronic CD patients (65 asymptomatic, 68 cardiac, 21 digestive and 24 cardiodigestive), and 285 healthy controls by sequence-specific PCR. Ficolin-3 serum levels, measured by ELISA in 80 patients and 80 controls, did not differ between groups. On the other hand, ficolin-3 levels were positively correlated with left ventricular ejection fraction (P = .002; r = .5), with lower levels associated with increased risk of cardiac insufficiency (P = .033; OR 7.21, 95%IC 1.17-44.4). Ficolin-3 levels were positively correlated with ficolin-2 (P = .021; r = .63), and negatively with MBL (P = .002; r = -.36) and pentraxin-3 (P = .04; r = -.32) levels. No significant results were observed for the investigated FCN3 polymorphisms and CD. The g.1637del/1637C heterozygotes presented lower ficolin-3 levels than g.1637C/1637C homozygotes in the control group (P = .023). Conclusion Low ficolin-3 levels may play a role in the pathophysiology of cardiac insufficiency associated with CD.
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- 2021
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6. Hepatitis B Virus Infection Among Leprosy Patients: A Case for Polymorphisms Compromising Activation of the Lectin Pathway and Complement Receptors
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Angelica Beate Winter Boldt, Camila de Freitas Oliveira-Toré, Gabriela Canalli Kretzschmar, Hellen Weinschutz Mendes, Sérvio Túlio Stinghen, Fabiana Antunes Andrade, Valéria Bumiller-Bini, Letícia Boslooper Gonçalves, Anna Carolina de Moraes Braga, Ewalda von Rosen Seeling Stahlke, Thirumalaisamy P. Velavan, Steffen Thiel, and Iara José Taborda de Messias-Reason
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0301 basic medicine ,Male ,HBsAg ,Complement receptor 1 ,complement system proteins ,medicine.disease_cause ,0302 clinical medicine ,Immunology and Allergy ,mannose-binding protein-associated serine proteases ,Mannan-binding lectin ,Original Research ,Aged, 80 and over ,Coinfection ,Middle Aged ,Hepatitis B ,Receptors, Complement ,Mycobacterium leprae ,Lectin pathway ,ficolin ,Female ,Ficolin ,MASP2 ,leprosy ,lcsh:Immunologic diseases. Allergy ,Adult ,Hepatitis B virus ,Genotype ,030231 tropical medicine ,Immunology ,Biology ,Polymorphism, Single Nucleotide ,03 medical and health sciences ,Young Adult ,complement 3b receptors ,genetic polymorphisms ,Leprosy ,medicine ,Humans ,Genetic Predisposition to Disease ,mannose-binding lectin ,Genetic Association Studies ,Aged ,Complement Pathway, Mannose-Binding Lectin ,medicine.disease ,030104 developmental biology ,Haplotypes ,biology.protein ,biology.gene ,lcsh:RC581-607 - Abstract
Thousands of leprosy patients not only suffer from physical deformities, but also either have or have had hepatitis B virus (HBV) coinfection. Polymorphisms of the complement system modulate susceptibility to leprosy, but genetic susceptibility to past or present HBV infection is unknown. We used sequencing and multiplex sequence-specific PCR to genotype 72 polymorphisms of seven genes (MBL2, FCN1, FCN2, FCN3, MASP1, MASP2, C3) encoding components of the lectin pathway, and two genes encoding complement receptors (CR1, VSIG4) in 190 patients, of which 74 were positive for HBsAg and/or anti-HBc (HBV+, 93.2% with a resolved infection) and 116 lepromatous patients, and 408 HBV-blood donors. In addition, we tested for levels of proteins of the lectin pathway. We found no difference between serum concentrations of mannan-binding lectin (MBL), MBL-associated serine proteins (MASP-1, MASP-2, MASP-3, MAp44), ficolin-3 (FCN-3), soluble complement receptor 1 (sCR1) and MBL mediated C4 activation, measured by ELISA or TRIFMA in up to 167 HBV+ and HBV− patients. Haplotypes lowering protein levels or encoding dysfunctional proteins increased susceptibility to HBV infection: MBL2*LYQC (OR = 3.4, p = 0.02), MASP1*AC_CC (OR = 4.0, p = 0.015) and MASP2*1C2-l (OR = 5.4, p = 0.03). Conversely, FCN1*3C2 haplotype, associated with higher gene expression, was protective (OR = 0.56, P = 0.033). Other haplotypes associated with HBV susceptibility were: MASP2*2B1-i (OR = 19.25, P = 0.003), CR1*3A (OR = 2.65, P = 0.011) and VSIG4*TGGRCG (OR = 12.55, P = 0.014). Some polymorphisms in ficolin genes associated with lower protein levels increased susceptibility to leprosy/HBV infection: FCN*1 (OR = 1.66, P = 0.029), FCN2*GGGCAC (OR = 6.73, P = 0.008), and FCN3*del_del_C (OR = 12.54, P = 0.037), and to lepromatous disease/HBV infection: FCN2*TA (OR = 2.5, P = 0.009), whereas FCN2*MAG was associated with increased FCN-2 expression and resistance against coinfection (OR = 0.29, P = 0.026). These associations were independent of demographic factors and did not increase susceptibility to leprosy per se, except MASP2*1C2-l. Associations for FCN2, FCN3, MASP1, MASP2, and VSIG4 variants were also independent of each other. In conclusion, polymorphisms compromising activation of the lectin pathway of complement increase susceptibility to HBV infection, with ficolin polymorphisms playing a major role in modulating the susceptibility among leprosy patients.
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- 2021
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7. Impact of VSIG4 gene polymorphisms on susceptibility and functional status of rheumatoid arthritis
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Thirumalaisamy P. Velavan, Hoang Van Tong, Shirley Ramos da Rosa Utiyama, Fabiana Antunes Andrade, Leia Sena, Cristhine Pieczarka, Iara Messias-Reason, Isabela Goeldner Eibofner, and Thelma L. Skare
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0301 basic medicine ,Adult ,Adolescent ,Immunology ,Arthritis ,Complement receptor ,Polymorphism, Single Nucleotide ,Arthritis, Rheumatoid ,03 medical and health sciences ,Young Adult ,0302 clinical medicine ,Immune system ,Genetics ,medicine ,Humans ,Genetic Predisposition to Disease ,Allele ,Receptor ,Molecular Biology ,Genetics (clinical) ,Alleles ,Genetic Association Studies ,Aged ,business.industry ,General Medicine ,Middle Aged ,medicine.disease ,Receptors, Complement ,030104 developmental biology ,Rheumatoid arthritis ,Immunoglobulin superfamily ,Gene polymorphism ,business ,Brazil ,030215 immunology - Abstract
The complement receptor of the immunoglobulin superfamily (CRIg, encoded by the VSIG4 gene) is a macrophage receptor involved in the clearance of immune complexes and autologous cells. Our results suggest that the VSIG4 rs1044165T allele is a risk factor for severe functional status of rheumatoid arthritis in women, possibly by affecting VSIG4 gene expression.
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- 2021
8. Author response for 'Ficolin‐3 in chronic Chagas disease: low serum levels associated with the risk of cardiac insufficiency'
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Kárita Cláudia Freitas Lidani, Indira Chakravarti, Marcia Holsbach Beltrame, Thaisa Lucas Sandri, Maria Regina Tizzot, Iara de Messias-Reason, Paola Rosa Luz, Edneia Oliveira Cavalcanti, and Fabiana Antunes Andrade
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business.industry ,Immunology ,Chronic Chagas' disease ,Medicine ,business ,Ficolin - Published
- 2020
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9. Ficolin-1 and ficolin-3 polymorphisms and susceptibility to rheumatoid arthritis
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Kárita Cláudia Freitas Lidani, Thelma Larocca Skare, Regina Tizzot, Cristhine Pieczarka, Iara Messias-Reason, Fabiana Antunes Andrade, Sandra Jeremias Catarino, and Lorena Bavia
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0301 basic medicine ,Genotype ,Immunology ,Gene Expression ,Inflammation ,Polymorphism, Single Nucleotide ,Arthritis, Rheumatoid ,03 medical and health sciences ,0302 clinical medicine ,Lectins ,medicine ,Immunology and Allergy ,Humans ,Genetic Predisposition to Disease ,Promoter Regions, Genetic ,Alleles ,Genetic Association Studies ,030203 arthritis & rheumatology ,Autoimmune disease ,business.industry ,Complement System Proteins ,medicine.disease ,Complement system ,030104 developmental biology ,medicine.anatomical_structure ,Haplotypes ,Lectin pathway ,Rheumatoid arthritis ,Gene polymorphism ,Synovial membrane ,medicine.symptom ,business ,Ficolin ,Brazil - Abstract
Rheumatoid arthritis (RA) is an autoimmune disease, which compromises the synovial membrane resulting in chronic inflammation. Ficolins are key proteins of the lectin pathway of complement able to recognize pathogen-associated molecular patterns, apoptotic cells, and cellular debris mediating the clearance by phagocytes. High ficolin-1 and ficolin-3 levels have been observed in RA patients, however, the influence of polymorphisms in the
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- 2020
10. Case Report: High Mannose-Binding Lectin Serum Determined by MBL2 Genotype and Risk for Clinical Progression to Chagasic Cardiomyopathy: A Case Report of Three Patients
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Paola Rosa Luz, Kárita Cláudia Freitas Lidani, Fabiana Antunes Andrade, Ronaldo Kiviatcoski Kozlowski, and Iara Messias-Reason
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Chagas disease ,biology ,business.industry ,030231 tropical medicine ,Cardiomyopathy ,Lectin ,biology.organism_classification ,medicine.disease ,Asymptomatic ,03 medical and health sciences ,0302 clinical medicine ,Infectious Diseases ,Polymorphism (computer science) ,Virology ,Genotype ,Immunology ,medicine ,biology.protein ,Parasitology ,medicine.symptom ,Trypanosoma cruzi ,business ,Genotyping - Abstract
Chagas disease (CD), caused by infection with the parasite Trypanosoma cruzi, leads to severe cardiomyopathy in 20-30% of patients, whereas the remainder may stay asymptomatic and never develop cardiomyopathy or other clinical manifestations. The underlying cause for this variable outcome is not fully characterized, although previous studies have found high levels of circulating mannose-binding lectin (MBL) to be associated with cardiac failure echocardiographic changes. We report three indeterminate (asymptomatic) chronic Chagas patients who were followed up for 10 years. Two of these patients developed chronic chagasic cardiomyopathy (CCC) during this follow-up period and, when genotyped, were found to be carriers of the high MBL producer HYPA/HYPA genotype, suggesting that genetically determined high MBL serum might be associated with the risk of CCC development. These results suggest the use of MBL quantification and MBL2 genotyping as tools for clinical assessment in patients with chronic CD.
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- 2019
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11. Ficolin activation as a potential biomarker of the severity of schizophrenia
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Marcelo Alves Carriello, Tamires Amelotti Coelho, Raffael Massuda, Lorena Bavia, Iara Messias-Reason, Diego Fabian Karvat Gracia, Eloisa Maria Pontarolo Gomes, and Fabiana Antunes Andrade
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education.field_of_study ,Complement component 3 ,Positive and Negative Syndrome Scale ,biology ,business.industry ,Population ,C-reactive protein ,medicine.disease ,Complement system ,Psychiatry and Mental health ,Schizophrenia ,Lectins ,Lectin pathway ,mental disorders ,Immunology ,biology.protein ,Humans ,Medicine ,business ,education ,Ficolin ,Biomarkers ,Biological Psychiatry - Abstract
Several studies have examined the complement system in schizophrenia, suggesting an involvement of the lectin pathway. We analyzed 49 patients with schizophrenia and explored the association between psychopathology of schizophrenia and complement component 3 (C3) serum levels, C-reactive protein (CRP) serum levels, ficolin activation, and mannose-binding lectin (MBL) activation. In the multiple regression analysis, a negative association was observed between the Positive and Negative Syndrome Scale (PANSS) total score and ficolin activation. Body mass index (BMI) was positively associated with the serum levels of C3 and CRP. MBL activation was not associated with any independent variables. Our findings facilitate a better understanding of the complement system in schizophrenia. Additional studies with a large sample population are needed to confirm our results.
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- 2021
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12. Sickening or Healing the Heart? The Association of Ficolin-1 and Rheumatic Fever
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Sandra Jeremias Catarino, Fabiana Antunes Andrade, Angelica Beate Winter Boldt, Luiza Guilherme, and Iara Jose Messias-Reason
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lcsh:Immunologic diseases. Allergy ,Adult ,Male ,0301 basic medicine ,haplotype ,Adolescent ,Heart disease ,Streptococcus pyogenes ,Immunology ,Inflammation ,medicine.disease_cause ,Polymorphism, Single Nucleotide ,polymorphism ,Young Adult ,03 medical and health sciences ,ficolin-1 ,Lectins ,Genotype ,medicine ,Humans ,Mitral Valve Stenosis ,Immunology and Allergy ,Genetic Predisposition to Disease ,FCN1 ,Allele ,Child ,Promoter Regions, Genetic ,Aged ,Original Research ,business.industry ,Haplotype ,Rheumatic Heart Disease ,Middle Aged ,rheumatic fever ,medicine.disease ,030104 developmental biology ,Haplotypes ,Child, Preschool ,Disease Progression ,Rheumatic fever ,Female ,medicine.symptom ,lcsh:RC581-607 ,business ,Ficolin - Abstract
Rheumatic fever (RF) and its subsequent progression to rheumatic heart disease (RHD) are chronic inflammatory disorders prevalent in children and adolescents in underdeveloped countries, and a contributing factor for high morbidity and mortality rates worldwide. Their primary cause is oropharynx infection by Streptococcus pyogenes, whose acetylated residues are recognized by ficolin-1. This is the only membrane-bound, as well as soluble activator molecule of the complement lectin pathway (LP). Although LP genetic polymorphisms are associated with RF, FCN1 gene's role remains unknown. To understand this role, we haplotyped five FCN1 promoter polymorphisms by sequence-specific amplification in 193 patients (138 with RHD and 55, RF only) and 193 controls, measuring ficolin-1 serum concentrations in 78 patients and 86 controls, using enzyme-linked immunosorbent assay (ELISA). Patients presented lower ficolin-1 serum levels (p < 0.0001), but did not differ according to cardiac commitment. Control's genotype distribution was in the Hardy-Weinberg equilibrium. Four alleles (rs2989727: c.−1981A, rs10120023: c.−542A, rs10117466: c.−144A, and rs10858293: c.33T), all associated with increased FCN1 gene expression in whole blood or adipose subcutaneous tissue (p = 0.000001), were also associated with increased protection against the disease. They occur within the *3C2 haplotype, associated with an increased protection against RF (OR = 0.41, p < 0.0001) and with higher ficolin-1 levels in patient serum (p = 0.03). In addition, major alleles of these same polymorphisms comprehend the most primitive *1 haplotype, associated with increased susceptibility to RF (OR = 1.76, p < 0.0001). Nevertheless, instead of having a clear-cut protective role, the minor c.−1981A and c.−144A alleles were also associated with additive susceptibility to valvar stenosis and mitral insufficiency (OR = 3.75, p = 0.009 and OR = 3.37, p = 0.027, respectively). All associations were independent of age, sex or ethnicity. Thus, minor FCN1 promoter variants may play a protective role against RF, by encouraging bacteria elimination as well as increasing gene expression and protein levels. On the other hand, they may also predispose the patients to RHD symptoms, by probably contributing to chronic inflammation and tissue injury, thus emphasizing the dual importance of ficolin-1 in both conditions.
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- 2018
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13. Ficolin-1 and Ficolin-3 Plasma Levels Are Altered in HIV and HIV/HCV Coinfected Patients From Southern Brazil
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Hellen Weinschutz Mendes, Marcia Holsbach Beltrame, Maria Regina Tizzot, Edna Reiche, Steffen Thiel, Fabiana Antunes Andrade, Jens C. Jensenius, Kárita Cláudia Freitas Lidani, and Iara Messias-Reason
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Male ,0301 basic medicine ,hepatitis C virus ,Ficolin-3 ,Ficolin-1 ,HIV Infections ,COMPLEMENT ,0302 clinical medicine ,Lectins ,Immunology and Allergy ,Medicine ,SYSTEMIC-LUPUS-ERYTHEMATOSUS ,Original Research ,Mannan-binding lectin ,Coinfection ,virus diseases ,Middle Aged ,Acquired immune system ,Hepatitis C ,Lectin pathway ,Female ,Ficolin ,Viral load ,CHRONIC HEPATITIS-C ,Brazil ,Adult ,lcsh:Immunologic diseases. Allergy ,Complement system ,DEFENSE ,Immunology ,Collectin ,VIRUS-INFECTION ,LECTIN PATHWAY ,03 medical and health sciences ,INFLAMMATION ,Acquired immunodeficiency syndrome (AIDS) ,Humans ,complement system ,Aged ,Glycoproteins ,business.industry ,medicine.disease ,HIV infection ,030104 developmental biology ,HAKATA ANTIGEN ,UPDATE ,VIRAL-HEPATITIS ,business ,lcsh:RC581-607 ,030215 immunology - Abstract
The complement system is a key component of the innate immune system, participating in the surveillance against infectious agents. Once activated by one of the three different pathways, complement mediates cell lysis, opsonization, signalizes pathogens for phagocytosis and induces the adaptive immune response. The lectin pathway is constituted by several soluble and membrane bound proteins, called pattern recognition molecules (PRM), including mannose binding lectin (MBL), Ficolins-1, -2, and -3, and Collectin 11. These PRMs act on complement activation as recognition molecules of pathogen-associated molecular patterns (PAMPs) such as N-acetylated, found in glycoproteins of viral envelopes. In this study, Ficolin-1 and Ficolin-3 plasma levels were evaluated in 178 HIV patients (93 HIV; 85 HIV/HCV) and 85 controls from southern Brazil. Demographic and clinical-laboratory findings were obtained during medical interview and from medical records. All parameters were assessed by logistic regression, adjusted for age, ancestry, and sex. Significantly lower levels of Ficolin-1 were observed in HIV/HCV coinfected when compared to HIV patients (p = 0.005, median = 516 vs. 667 ng/ul, respectively) and to controls (p < 0.0001, 1186 ng/ul). Ficolin-1 levels were lower in males than in females among HIV patients (p = 0.03) and controls (p = 0.0003), but no association of Ficolin-1 levels with AIDS was observed. On the other hand, Ficolin-3 levels were significantly lower in controls when compared to HIV (p < 0.0001, medians 18,240 vs. 44,030 ng/ml, respectively) and HIV/HCV coinfected (p < 0.0001, 40,351 ng/ml) patients. There was no correlation between Ficolin-1 and Ficolin-3 levels and age, HIV viral load or opportunistic infections. However, Ficolin-3 showed a positive correlation with T CD4 cell counts in HIV monoinfected patients (p = 0.007). We provide here the first assessment of Ficolin-1 and-3 levels in HIV and HIV/HCV coinfected patients, which indicates a distinct role for these pattern recognition molecules in both viral infections.
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- 2018
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14. Complement Factor H as a potential atherogenic marker in chronic Chagas' disease
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Thaisa Lucas Sandri, Kárita Cláudia Freitas Lidani, Lorena Bavia, Renato Nisihara, Iara Messias-Reason, and Fabiana Antunes Andrade
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0301 basic medicine ,Chagas disease ,Adult ,Male ,medicine.medical_specialty ,Immunology ,Inflammation ,030204 cardiovascular system & hematology ,Biology ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Internal medicine ,medicine ,Humans ,Chagas Disease ,Aged ,Ejection fraction ,Cholesterol ,Middle Aged ,medicine.disease ,030104 developmental biology ,Endocrinology ,Blood pressure ,chemistry ,Factor H ,Complement Factor H ,Chronic Disease ,Alternative complement pathway ,Parasitology ,Female ,medicine.symptom ,Body mass index ,Biomarkers - Abstract
We aimed to investigate the association between plasma levels of complement Factor H (FH) with cardiac involvement, inflammatory and cardiometabolic parameters in patients with chronic Chagas' disease (CD). FH plasmatic levels were determined in 80 chronic CD patients. Glycaemic index, lipidogram (high-density lipoprotein cholesterol HDL-C, low-density lipoprotein cholesterol LDL-C, triglycerides and total cholesterol) and Ultrasensitive C-Reactive Protein (uCRP) values were obtained from medical records. Height, weight, body mass index (BMI) blood pressure and left ventricular ejection fraction (LVEF) were obtained from echocardiography examinations. Comparisons between chronic CD clinical forms were performed using Mann-Whitney test and correlation Spearman's test. FH levels were correlated positively with triglycerides (P = .001, r = .39), LDL-C (P = .009, r = .3), cholesterol (P = .02, r = .28), uCRP (P = .029, r = .31) and BMI (P = .008, r = .34); and negatively with HDL-C (P = .03, r = -.25) levels. Dyslipidemic patients showed higher FH levels compared to normolipidemic, although no difference for FH levels was observed between chronic CD clinical forms. Alternative pathway of complement may be a link between immune response and metabolic disorders, with important immunoregulatory role in chronic CD.
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- 2018
15. Human complement receptor type 1 (CR1) protein levels and genetic variants in chronic Chagas Disease
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Thaisa Lucas, Sandri, Kárita Cláudia Freitas, Lidani, Fabiana Antunes, Andrade, Christian G, Meyer, Peter G, Kremsner, Iara J, de Messias-Reason, and Thirumalaisamy P, Velavan
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Adult ,Male ,0301 basic medicine ,Chagas disease ,Complement receptor 1 ,lcsh:Medicine ,030204 cardiovascular system & hematology ,Polymorphism, Single Nucleotide ,Linkage Disequilibrium ,Article ,03 medical and health sciences ,Exon ,0302 clinical medicine ,Complement Receptor Type 1 ,Humans ,Medicine ,Chagas Disease ,lcsh:Science ,Opsonin ,Aged ,Multidisciplinary ,biology ,business.industry ,lcsh:R ,Haplotype ,Middle Aged ,Acquired immune system ,medicine.disease ,Pathophysiology ,030104 developmental biology ,Haplotypes ,Case-Control Studies ,Immunology ,Receptors, Complement 3b ,Female ,lcsh:Q ,biology.gene ,business - Abstract
Complement is an essential element in both innate and acquired immunity contributing to the immunopathogenesis of many disorders, including Chagas Disease (CD). Human complement receptor 1 (CR1) plays a role in the clearance of complement opsonized molecules and may facilitate the entry of pathogens into host cells. Distinct CR1 exon 29 variants have been found associated with CR1 expression levels, increased susceptibility and pathophysiology of several diseases. In this study, CR1 plasma levels were assessed by ELISA and CR1 variants in exon 29 by sequencing in a Brazilian cohort of 232 chronic CD patients and 104 healthy controls. CR1 levels were significantly decreased in CD patients compared to controls (p CR1 rs1704660G, rs17047661G and rs6691117G variants were significantly associated with CD and in high linkage disequilibrium. The CR1*AGAGTG haplotype was associated with T. cruzi infection (p = 0.035, OR 3.99, CI 1.1-14.15) whereas CR1*AGGGTG was related to the risk of chagasic cardiomyopathy (p = 0.028, OR 12.15, CI 1.13-113). This is the first study that provides insights on the role of CR1 in development and clinical presentation of chronic CD.
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- 2018
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16. Mannose-binding lectin deficiency and miscarriages in rheumatoid arthritis
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Iara Messias-Reason, Thelma L. Skare, Juliana Z Cieslinski, Shirley Ramos da Rosa Utiyama, Isabela Goeldner, Thirumalaisamy P. Velavan, Renato Nisihara, and Fabiana Antunes Andrade
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Untranslated region ,Adult ,Male ,medicine.medical_specialty ,Genotype ,Immunology ,Gastroenterology ,Mannose-Binding Lectin ,Miscarriage ,Arthritis, Rheumatoid ,03 medical and health sciences ,Exon ,0302 clinical medicine ,Internal medicine ,medicine ,Odds Ratio ,Immunology and Allergy ,Humans ,Allele ,Alleles ,Mannan-binding lectin ,030203 arthritis & rheumatology ,biology ,business.industry ,Lectin ,Middle Aged ,medicine.disease ,MBL deficiency ,Abortion, Spontaneous ,Amino Acid Substitution ,Haplotypes ,Rheumatoid arthritis ,biology.protein ,Female ,business ,Biomarkers ,Metabolism, Inborn Errors ,030215 immunology - Abstract
To investigate the association between mannose-binding lectin (MBL) serum level and MBL2 polymorphisms, and the frequency of spontaneous miscarriages in rheumatoid arthritis (RA) patients.One hundred seventy seven women (mean age 50 years) with RA from Southern Brazil were studied and 4.5% had a history of abortion (8/177). The MBL levels were determined by ELISA. MBL2 polymorphisms in the promoter (-550H/L, -221X/Y), 5' untranslated region (4 P/Q) and exon 1 (p.Gly54Asp: B allele, p.Arg52Cys: D allele and p.Gly57Glu: C allele; collectively labelled O) were genotyped by sequencing.Mannose-binding lectin levels of RA patients ranged from ≤100 ng/mL to 6640 ng/mL (median 541.5 ng/mL). There was a significant difference in MBL median levels (100 ng/mL vs. 625 ng/mL, respectively, p = .001) and frequency of MBL deficiency (75.0% vs. 24.1%, p = .007, OR = 10.3, 95%CI = 1.9-55.4), in patients with a history of miscarriage vs those without it. Patients with RA and miscarriage had more frequently haplotypes related with low MBL levels (p = .007, OR = 10.5, 95%CI = 1.3-84) than high producers. Moreover, LYPB haplotype and O allele were significantly associated with the occurrence of miscarriage (p = .001, OR = 9.7, 95%CI = 2.4-39.1 and p = .009, OR = 5.9, 95%CI = 1.4-23.4, respectively).The results suggest that MBL deficiency and the presence of MBL2 gene polymorphisms that lead to MBL deficiency are risk factors for the occurrence of miscarriage in patients with RA.
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- 2017
17. Association of a new FCN3 haplotype with high ficolin-3 levels in leprosy
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Fabiana Antunes Andrade, Letícia Boslooper Gonçalves, Angelica Beate Winter Boldt, Iara Messias-Reason, Marcia Holsbach Beltrame, and Valéria Bumiller Bini
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Bacterial Diseases ,Male ,Serum ,0301 basic medicine ,Heredity ,Artificial Gene Amplification and Extension ,Disease ,Polymerase Chain Reaction ,Biochemistry ,law.invention ,law ,Lectins ,Medicine and Health Sciences ,Medicine ,10. No inequality ,Mycobacterium leprae ,Polymerase chain reaction ,Aged, 80 and over ,biology ,lcsh:Public aspects of medicine ,Genomics ,Middle Aged ,Mycobacterium Leprae ,3. Good health ,Actinobacteria ,Genetic Mapping ,Infectious Diseases ,Lectin pathway ,Female ,Leprosy ,Ficolin ,Research Article ,Neglected Tropical Diseases ,Adult ,lcsh:Arctic medicine. Tropical medicine ,Adolescent ,lcsh:RC955-962 ,Variant Genotypes ,Enzyme-Linked Immunosorbent Assay ,Genome Complexity ,Research and Analysis Methods ,Polymorphism, Single Nucleotide ,Young Adult ,03 medical and health sciences ,Genetics ,Humans ,Genetic Predisposition to Disease ,Allele ,Molecular Biology Techniques ,Molecular Biology ,Alleles ,Aged ,Glycoproteins ,Bacteria ,business.industry ,Haplotype ,Organisms ,Public Health, Environmental and Occupational Health ,Biology and Life Sciences ,Computational Biology ,Proteins ,lcsh:RA1-1270 ,Tropical Diseases ,biology.organism_classification ,medicine.disease ,Introns ,030104 developmental biology ,Haplotypes ,Genetic Loci ,Immunology ,business - Abstract
Leprosy is a chronic inflammatory disease caused by Mycobacterium leprae that mainly affects the skin and peripheral nervous system, leading to a high disability rate and social stigma. Previous studies have shown a contribution of genes encoding products of the lectin pathway of complement in the modulation of the susceptibility to leprosy; however, the ficolin-3/FCN3 gene impact on leprosy is currently unknown. The aim of the present study was to investigate if FCN3 polymorphisms (rs532781899: g.1637delC, rs28362807: g.3524_3532insTATTTGGCC and rs4494157: g.4473C>A) and ficolin-3 serum levels play a role in the susceptibility to leprosy. We genotyped up to 190 leprosy patients (being 114 (60%) lepromatous), and up to 245 controls with sequence-specific PCR. We also measured protein levels using ELISA in 61 leprosy and 73 controls. FCN3 polymorphisms were not associated with disease, but ficolin-3 levels were higher in patients with FCN3 *2B1 (CinsA) haplotype (p = 0.032). Median concentration of ficolin-3 was higher in leprosy per se (26034 ng/mL, p = 0.005) and lepromatous patients (28295 ng/mL, p = 0.016) than controls (18231 ng/mL). In addition, high ficolin-3 levels (>33362 ng/mL) were more common in leprosy per se (34.4%) and in lepromatous patients (35.5%) than controls (19.2%; p = 0.045 and p = 0.047, respectively). Our results lead us to suggest that polymorphisms in the FCN3 gene cooperate to increase ficolin-3 concentration and that it might contribute to leprosy susceptibility by favoring M. leprae infection., Author summary Leprosy is considered a neglected disease and still a public health problem in many countries where it was not yet eliminated, leading to a high disability rate and social stigma. The molecular mechanisms of M. leprae infection and immune evasion are still poorly known, raising the need for studies that may contribute to a better understanding of leprosy etiology, as well as improvement in diagnosis and treatment. Ficolin-3 is a soluble molecule of the innate immune system that recognizes a wide range of pathogen-associated molecular patterns leading to complement activation and phagocytosis. We observed high concentration of ficolin-3 in leprosy patients, likely caused by polymorphisms present in intronic regions of FCN3 gene, which may contribute to leprosy susceptibility by favoring M. leprae infection. This is the first study addressing FCN3 polymorphisms and ficolin-3 levels in leprosy, indicating it as a good candidate biomarker associated with the host response against M. leprae.
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- 2017
18. Geographical distribution of complement receptor type 1 variants and their associated disease risk
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Thaisa, Lucas Sandri, Selorme, Adukpo, Dao Phuong, Giang, Christian N, Nguetse, Fabiana, Antunes Andrade, Hoang van, Tong, Nguyen Linh, Toan, Le Huu, Song, Preetham, Elumalai, Kumarasamy, Thangaraj, Vijaya Lakshmi, Valluri, Francine, Ntoumi, Christian G, Meyer, Iara, Jose de Messias Reason, Peter G, Kremsner, and Thirumalaisamy P, Velavan
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Male ,0301 basic medicine ,Linkage disequilibrium ,Heredity ,Physiology ,Complement System ,lcsh:Medicine ,Ghana ,Biochemistry ,Linkage Disequilibrium ,0302 clinical medicine ,Gene Frequency ,Complement Receptor Type 1 ,Polymorphism (computer science) ,Immune Physiology ,Genotype ,Medicine and Health Sciences ,Ethnicities ,lcsh:Science ,Genetics ,Immune System Proteins ,Multidisciplinary ,Exons ,Middle Aged ,Body Fluids ,Genetic Mapping ,Blood ,Infectious Diseases ,Vietnam ,Female ,Anatomy ,Brazil ,Research Article ,Adult ,Adolescent ,Immunology ,India ,Variant Genotypes ,Kongo People ,Single-nucleotide polymorphism ,Biology ,Polymorphism, Single Nucleotide ,03 medical and health sciences ,Parasitic Diseases ,Humans ,Genetic Predisposition to Disease ,Selection, Genetic ,Allele ,Allele frequency ,Racial Groups ,Haplotype ,lcsh:R ,Biology and Life Sciences ,Proteins ,Tropical Diseases ,Malaria ,030104 developmental biology ,Haplotypes ,Immune System ,People and Places ,Receptors, Complement 3b ,Population Groupings ,lcsh:Q ,Blood Groups ,030217 neurology & neurosurgery ,Africans - Abstract
Background Pathogens exert selective pressure which may lead to substantial changes in host immune responses. The human complement receptor type 1 (CR1) is an innate immune recognition glycoprotein that regulates the activation of the complement pathway and removes opsonized immune complexes. CR1 genetic variants in exon 29 have been associated with expression levels, C1q or C3b binding and increased susceptibility to several infectious diseases. Five distinct CR1 nucleotide substitutions determine the Knops blood group phenotypes, namely Kna/b, McCa/b, Sl1/Sl2, Sl4/Sl5 and KCAM+/-. Methods CR1 variants were genotyped by direct sequencing in a cohort of 441 healthy individuals from Brazil, Vietnam, India, Republic of Congo and Ghana. Results The distribution of the CR1 alleles, genotypes and haplotypes differed significantly among geographical settings (p≤0.001). CR1 variants rs17047660A/G (McCa/b) and rs17047661A/G (Sl1/Sl2) were exclusively observed to be polymorphic in African populations compared to the groups from Asia and South-America, strongly suggesting that these two SNPs may be subjected to selection. This is further substantiated by a high linkage disequilibrium between the two variants in the Congolese and Ghanaian populations. A total of nine CR1 haplotypes were observed. The CR1*AGAATA haplotype was found more frequently among the Brazilian and Vietnamese study groups; the CR1*AGAATG haplotype was frequent in the Indian and Vietnamese populations, while the CR1*AGAGTG haplotype was frequent among Congolese and Ghanaian individuals. Conclusion The African populations included in this study might have a selective advantage conferred to immune genes involved in pathogen recognition and signaling, possibly contributing to disease susceptibility or resistance.
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- 2017
19. Ficolin-3 serum levels and FCN3 polymorphisms in chronic Chagas disease
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Marcia Holsbach Beltrame, Thaisa Lucas Sandri, Kárita Cláudia Freitas Lidani, Iara Messias-Reason, and Fabiana Antunes Andrade
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business.industry ,Immunology ,Chronic Chagas' disease ,Immunology and Allergy ,Medicine ,Hematology ,business ,Ficolin - Published
- 2016
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20. C3 gene polymorphism and cardiometabolic risk factors in chronic Chagas disease
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Cesar Maistro Guimarães, Vanessa Picceli, Iara Messias-Reason, Kárita Cláudia Freitas Lidani, Thaisa Lucas Sandri, and Fabiana Antunes Andrade
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Cardiometabolic risk ,business.industry ,Immunology ,Chronic Chagas' disease ,Immunology and Allergy ,Medicine ,Hematology ,Gene polymorphism ,business - Published
- 2016
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21. The role of Complement Receptor 1 (CD35) in chronic Chagas Disease
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Thaisa Lucas Sandri, Hoang Van Tong, Kárita Cláudia Freitas Lidani, Fabiana Antunes Andrade, Christina Schieber, Iara Messias-Reason, and Thirumalaisamy P. Velavan
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biology ,business.industry ,Complement receptor 1 ,Immunology ,Chronic Chagas' disease ,Immunology and Allergy ,Medicine ,Hematology ,biology.gene ,business - Published
- 2016
- Full Text
- View/download PDF
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