Mannose Binding Lectin and C3 Serum Levels in Coronary Artery Disease: A Cross-Sectional Study.

Background: The process of tissue injury in coronary artery disease (CAD) has been associated with activation of the complement system, partly due to the action of mannose-binding lectin (MBL) and C3, which are expressed in atherosclerotic lesions.

Objective: The aim of this study was to evaluate the serum levels of MBL and C3 in patients with CAD and to compare them with healthy controls. Additionally, we aim to assess the correlation between MBL and C3 levels and cardiometabolic parameters.

C5a Serum Levels in Patients with Endometriosis: A Cross-Sectional Study.

Endometriosis (EM) is a gynecological disorder that presents significant immune dysregulation in its pathophysiology. Recent studies indicate that the Complement System may play a significant role in the immune processes involved in peritoneal clearance and inflammation in EM patients. C5a is a potent anaphylatoxin molecule of complement associated with the development of inflammatory disorders, however its possible impact on EM development requires further investigation.

Executive functions in migraine patients: a systematic review with meta-analysis.

Migraine, a common neurological disease, is known to impact the quality of life of individuals with this condition. We performed a systematic review with meta-analysis to investigate the abnormalities associated with executive functions of migraineurs as compared with healthy controls. In addition, we investigated the differences between patients with and without aura.

Medical advertising in social networks: awareness and medical school education.

Objective: this study analyzed medicine students' knowledge regarding medical advertising on social media.

Method: this is a cross-sectional study carried out between January and May 2022 with 179 medical students from public and private institutions from Curitiba - PR, using a structured questionnaire with nine problem situations on medical advertising. It was established as "sufficient" knowledge ≥70% of the problem-situations based on current professional codes and resolutions.

Gene Polymorphism and MASP-3 Serum Levels in Patients with Chronic Chagas Disease.

Introduction: Chagas disease (CD), caused by , 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 infection and during the chronic phase of CD; however, the role of the MBL-associated serine protease 1 () gene encoding MASP-1, MASP-3, and MAp44 complement proteins has not yet been reported in CD. This study investigated the possible association between gene polymorphisms and MASP-3 protein serum levels in chronic CD and its clinical forms.

Ficolin activation as a potential biomarker of the severity of schizophrenia.

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.

Ficolin-3 in chronic Chagas disease: Low serum levels associated with the risk of cardiac insufficiency.

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.

Hepatitis B Virus Infection Among Leprosy Patients: A Case for Polymorphisms Compromising Activation of the Lectin Pathway and Complement Receptors.

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 (, ) encoding components of the lectin pathway, and two genes encoding complement receptors () in 190 patients, of which 74 were positive for HBsAg and/or anti-HBc (HBV+, 93.

Ficolin-3 in rheumatic fever and rheumatic heart disease.

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.

Clinical and epidemiological aspects of chronic Chagas disease from Southern Brazil.

Introduction: Patients with Chagas disease (CD), caused by Trypanosoma cruzi, present a higher risk of developing other chronic diseases, which may contribute to CD severity. Since CD is underreported in the southern state of Paraná, Brazil, we aimed to characterize clinical and epidemiological aspects of individuals chronically infected with T. cruzi in Southern Brazil.

Ficolin-1 and ficolin-3 polymorphisms and susceptibility to rheumatoid arthritis.

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 gene in RA is not completely established, while no study evaluated gene polymorphisms in RA to date.

Gene Functional Polymorphisms and C3 Serum Levels in Patients with Rheumatoid Arthritis.

The complement system is a key component of the innate immunity that plays a significant role in the development and clinical presentation of Rheumatoid arthritis (RA). Complement protein C3 is a central molecule in the activation of complement with a significant role in the inflammatory processes of RA. Nevertheless, the impact of C3 gene polymorphisms in the development of RA is still unknown.

Chagas Disease: From Discovery to a Worldwide Health Problem.

Carlos Chagas discovered American trypanosomiasis, also named Chagas disease (CD) in his honor, just over a century ago. He described the clinical aspects of the disease, characterized by its etiological agent () and identified its insect vector. Initially, CD occurred only in Latin America and was considered a silent and poorly visible disease.

Human collectin-11 (COLEC11) and its synergic genetic interaction with MASP2 are associated with the pathophysiology of Chagas Disease.

Chagas Disease (CD) is an anthropozoonosis caused by Trypanosoma cruzi. With complex pathophysiology and variable clinical presentation, CD outcome can be influenced by parasite persistence and the host immune response. Complement activation is one of the primary defense mechanisms against pathogens, which can be initiated via pathogen recognition by pattern recognition molecules (PRMs).

Sickening or Healing the Heart? The Association of Ficolin-1 and Rheumatic Fever.

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 , 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).

Case Report: High Mannose-Binding Lectin Serum Determined by Genotype and Risk for Clinical Progression to Chagasic Cardiomyopathy: A Case Report of Three Patients.

Chagas disease (CD), caused by infection with the parasite , 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.

Complement activation in acute myocardial infarction: An early marker of inflammation and tissue injury?

Background: Acute myocardial infarction (AMI) is a potentially fatal condition, being a major cause of death worldwide. Ischemia suffered during AMI causes tissue damage, leading to an inflammatory process. Moreover, myocardial injury can generate damage-associated molecular patterns that activate pattern recognition molecules including some complement proteins.

Human complement receptor type 1 (CR1) protein levels and genetic variants in chronic Chagas Disease.

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.

Mannose-binding lectin deficiency and miscarriages in rheumatoid arthritis.

Objective: 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.

Methods: 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).

Association of a new FCN3 haplotype with high ficolin-3 levels in leprosy.

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.

[Beta 2-adrenergic receptor gene association with overweight and asthma in children and adolescents and its relationship with physical fitness].

Objective:: To investigate the association of and polymorphisms of β2-adrenergic receptor gene () with the occurrence of asthma and overweight and the gene's influence on anthropometric, clinic, biochemical and physical fitness variables in children and adolescents.

Methods:: Subjects were evaluated for allelic frequencies of the β2-adrenergic receptor gene, height, weight, body mass index (BMI), BMI -score, waist circumference (WC), pubertal stage, resting heart rate (HRres), blood pressure (BP), total cholesterol (TC), glucose, insulin, high density lipoprotein (HDL-C), low density lipoprotein (LDL-C), triglyceride (TG), Homeostasis Metabolic Assessment (HOMA2-IR), Quantitative Insulin Sensitivity Check Index (QUICKI) and maximal oxygen uptake (VO). The participants were divided in four groups: overweight asthmatic (=39), overweight non-asthmatic (=115), normal weight asthmatic (=12), and normal weight non-asthmatic (=40).

Gestational diabetes mellitus (GDM) decreases butyrylcholinesterase (BChE) activity and changes its relationship with lipids.

Many conditions interfere with butyrylcholinesterase (BChE) activity, e.g., pregnancy or presence of the BCHE gene variant -116A can decrease activity whereas obesity and types I and II diabetes mellitus can increase activity.

Amplification and deletion of the RAPH1 gene in breast cancer patients.

Lamellipodin protein (Lpd), encoded by the RAPH1 gene, modulates the assembly of actin cytoskeleton through its binding to the Ena/VASPs proteins, and acts in cellular motility and lamelipodial protrusion. The region where RAPH1 gene is located (2q33) is deleted in various types of cancer and the gene expression changes in tumors when compared to normal tissues. Amplifications and deletions of the RAPH1 gene were investigated in breast carcinoma samples, in order to determine the possible relationship of the gene with breast cancer tumorigenesis and lymph node metastasis.

Association of variants of the -116 site of the butyrylcholinesterase BCHE gene to enzyme activity and body mass index.

Butyrylcholinesterase (BChE) is coded by the BCHE gene that presents four exons. The non-codifying exon 1 presents two variants -116G and -116A, being -116A preferentially in cis conformation with the 539T variant (K) of exon 4 which was associated with lower BChE activity and lower body mass index (BMI) variance. This study analyzed the frequency of -116 variants and the relation of genotypes -116GG;539AA, -116GG;539AT and -116GA;539AT with BChE activity and with BMI in Euro-Brazilian blood donors.