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Blood pressure (BP) is the main biomarker for monitoring patients, as its lack of control above values considered normal is a modifiable risk factor for target organ damage. The aim of this study is to evaluate the accuracy of the wearable electronic device photoplethysmography technology (PPG) Samsung Galaxy Watch 4 in determining BP in young patients compared to manual and automatic methods of BP determination. This is a quantitative and cross-sectional study, following validation protocols for wearable devices and BP measurement. It was carried out with twenty healthy young adults, in which BP was measured using four instruments, namely, standard sphygmomanometer device (manual), automatic arm oscillometric device (reference), wrist oscillometric device, and Smartwatch PPG. Eighty systolic blood pressure (SBP) and diastolic blood pressure (DBP) readings were observed. SBP means manual 118 ± 2.20,arm 113 ± 2.54, wrist 118 ± 2.51, and PPG (smartwatch) 113 ± 2.58. Among means, arm and PPG difference is 0.15, arm and wrist 4.95, arm and manual 4.45 wrist with PPG. The mean DBP manual 76.7 ± 1.84, arm 73.6 ± 1.92, wrist 79.3 ± 1.87, and PPG 72.2 ± 1.38. Among means, the difference between the arm and PPG is 1.4 and arm and hand 3.5 mmHg. The correlation shows PPG with manual, arm, and wrist. There was a strong SBP correlation and a moderate DBP correlation between the methods tested, evidencing the accuracy of the PPG smartwatch in relation to the reference method.
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Hipertensión , Dispositivos Electrónicos Vestibles , Adulto Joven , Humanos , Determinación de la Presión Sanguínea , Estudios Transversales , Presión Sanguínea/fisiología , Esfigmomanometros , Hipertensión/diagnósticoRESUMEN
Type 1 diabetes mellitus is a clinical condition characterized by insufficient insulin production due to progressive loss of pancreatic islet ß-cells mediated by an autoimmune response. This deregulation of the immune system is caused by the action of genetic, epigenetic, and environmental factors in varying combinations for each individual. Although the inflammation of the islets with immune cell infiltration, known as insulitis, is an important element in pathogenesis, other factors are necessary for disease initiation. Associations with variants of HLA and other genes related to immune system function, mainly haplotypes HLA-DR3-DQ2 and HLA-DR4-DQ8, are more evident. The influence of polymorphisms and epigenetic modifications, as well as the microbiome, is convincing proof of the existence of a complex interaction between genetic, immune, and environmental factors in the etiology and pathogenesis of this metabolic disorder. Loss of selftolerance to autoimmunity is a critical point in the development of the disease, and regulatory T cells play a key role in this process. Thus, any failure of these cells, either due to an insufficient number or altered expression of cytokines and transcription factors, may be the trigger for the onset of the disease. The protective action of regulatory T cells is controlled by gene expression that is modulated by epigenetic modifications, including the dysregulation of noncoding RNAs. This review takes an updated approach to the natural history of type 1 diabetes, focusing on the factors involved in the etiology and pathogenesis.
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Diabetes Mellitus Tipo 1 , Humanos , Diabetes Mellitus Tipo 1/genética , Haplotipos , Antígeno HLA-DR3/genéticaRESUMEN
The aim of the present study was to compare pulmonary function among patients with different clinical forms and scores for risk of death and stroke. Patients were recruited from the Chagas Disease Ambulatory Service at the University of Rio Grande do Norte State (Mossoró, Brazil). The evaluation of pulmonary function was performed through spirometry techniques using a digital spirometer, and information about the clinical forms (cardiac, cardiodigestive, digestive and undetermined) and scores for risk of death (Rassi's risk-of-death score) and stroke was subsequently collected. Upon completion of the evaluation, comparisons of the values obtained between the groups for different clinical forms, risk stratification of stroke and Rassi's risk-of-death were made. The study cohort consisted of 72 patients. Individuals with a low risk of death had significantly higher values in the Tiffeneau index and individuals with a low risk of stroke presented with higher percentage values for forced vital capacity and forced expiratory volume in 1 sec. In addition, individuals with heart disease had worse percentage values for FVC and FEV1. In conclusion, the results showed that spirometry was an effective analytical technique and was associated with clinical forms, and death and stroke risk scores, in patients with Chagas disease, adding an important prognostic tool to those currently available.
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Osteosarcoma (OS) is a bone tumor of mesenchymal origin, most frequently occurring during the rapid growth phase of long bones, and usually located in the epiphyseal growth plates of the femur or the tibia. Its most common feature is genome disorganization, aneuploidy with chromosomal alterations, deregulation of tumor suppressor genes and of the cell cycle, and an absence of DNA repair. This suggests the involvement of surveillance failures, DNA repair or apoptosis control during osteogenesis, allowing the survival of cells which have undergone alterations during differentiation. Epigenetic events, including DNA methylation, histone modifications, nucleosome remodeling and expression of non-coding RNAs have been identified as possible risk factors for the tumor. It has been reported that p53 target genes or those genes that have their activity modulated by p53, in addition to other tumor suppressor genes, are silenced in OS-derived cell lines by hypermethylation of their promoters. In osteogenesis, osteoblasts are formed from pluripotent mesenchymal cells, with potential for self-renewal, proliferation and differentiation into various cell types. This involves complex signaling pathways and multiple factors. Any disturbance in this process can cause deregulation of the differentiation and proliferation of these cells, leading to the malignant phenotype. Therefore, the origin of OS seems to be multifactorial, involving the deregulation of differentiation of mesenchymal cells and tumor suppressor genes, activation of oncogenes, epigenetic events and the production of cytokines.
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Persistent infection by high-risk human papillomavirus (HR-HPV) is the main risk factor for uterine cervical cancer (UCC). However, viral infection alone is not sufficient for the development and progression of premalignant cervical lesions for cancer. In previous years it has been suggested that the adaptive immune response triggered by the differentiation of naïve helper T cells in Th17 cells may serve an important role in disease development. It has been hypothesized that Th17 cells may be involved in the promotion of UCC, as high levels of interleukin 17 (IL17) expression have been detected in the mucosa of the uterine cervix of patients affected by the disease. However, the role of Th17 cells in the tumor development and progression remains unclear. It is believed that the immune response of the Th17 type during persistent infection of the genital tract with HR-HPV triggers chronic inflammation with a long duration with the production of IL17 and other pro-inflammatory cytokines, creating a favorable environment for tumor development. These cytokines are produced by immune system cells in addition to tumor cells and appear to function by modulating the host immune system, resulting in an immunosuppressive response as opposed to inducing an effective protective immune response, thus contributing to the growth and progression of the tumor. In the present review, the latest advances are presented about the function of Th17 cells and the cytokines produced by them in the development and progression of UCC.
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Chagas disease (CD) is a public health problem in Latin America. The acute phase presents nonspecific symptoms and most patients recover from acute parasitemia and undergo a prolonged asymptomatic phase. Several years later, about 30% of infected individuals develop chronic cardiopathy with progressive cardiomegaly, arrhythmia, thromboembolic events and heart failure. These symptoms suggest a persistent association with the presence of inflammatory infiltrate and tissue, and cellular destruction in the heart muscle. Nevertheless, few research studies have attempted to understand the role of inflammatory cells, such as neutrophils, in establishing the pathology and progression of CD. Only recently have some studies been performed with this intention. Despite this effort, the role of neutrophils in CD is still considered controversial. This review discusses the morphological and functional characteristics of neutrophils that describes their participation in the establishment and progression of Trypanosoma cruzi infection, through the development of its effector functions, such as release of lithic components, production of oxidative agents and release of inflammatory mediators capable of modulating the host immune response.
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Enfermedad de Chagas/patología , Neutrófilos/inmunología , Trypanosoma cruzi/inmunología , Animales , Enfermedad de Chagas/inmunología , Enfermedad de Chagas/parasitología , Progresión de la Enfermedad , Humanos , Neutrófilos/patología , Trypanosoma cruzi/genética , Trypanosoma cruzi/fisiologíaRESUMEN
Inflammation is a defense strategy against invading agents and harmful molecules that is activated immediately following a stimulus, and involves the release of cytokines and chemokines, which activate the innate immune response. These mediators act together to increase blood flow and vascular permeability, facilitating recruitment of effector cells to the site of injury. Following resolution of the injury and removal of the stimulus, inflammation is disabled, but if the stimulus persists, inflammation becomes chronic and is strongly associated with cancer. This is likely to be due to the fact that the inflammation leads to a wound that does not heal, requiring a constant renewal of cells, which increases the risk of neoplastic transformation. Debris from phagocytosis, including the reactive species of oxygen and nitrogen that cause damage to DNA already damaged by the leukotrienes and prostaglandins, has an impact on inflammation and various carcinogenic routes. There is an association between chronic inflammation, persistent infection and cancer, where oncogenic action is mediated by autocrine and paracrine signals, causing changes in somatic cells under the influence of the microbial genome or of epigenetic factors. Among the infectious agents associated with cancer, certain genotypes of human papillomavirus (HPV) stand out. HPV is responsible for virtually all cases of cervical cancer and a lower proportion of cancers of the vagina, vulva, anus, penis and a number of extragenital cancers. In the present review, recent advances in the mechanisms involved in the inflammatory response are presented with their participation in the process of carcinogenesis, emphasizing the role of chronic inflammation in the development of HPV-induced cervical cancer.
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PURPOSE: This cross-sectional study aimed to estimate the prevalence of Chlamydia trachomatis (CT) infection alone and in combination with human papillomavirus (HPV). Furthermore, the study investigates whether the CT infection increases the risk of contracting HPV and whether the presence of both pathogens is associated with a higher prevalence of cervical lesions. METHODS: Cervical samples of 1,134 asymptomatic women enrolled in a screening program for cervical cancer were analyzed. Two cervical specimens were collected from each patient, one for cytologic examination and the other for detection of CT by polymerase chain reaction (PCR), using a primer pair which amplifies a specific sequence of the DNA plasmid. RESULTS: The overall prevalence rate infection was 10.9%, being 10% in the women with normal cytology, 13.8% in those with atypical squamous cells of undetermined significance (ASC-US), and 25% with low-grade squamous intraepithelial lesion (LSIL). The infection by CT did not increase the risk of acquiring HPV infection. The higher prevalence of LSIL in women co-infected with HPV and CT is possibly due to HPV. CONCLUSION: CT infection was more prevalent in younger women aged up to 32 years, who had an early onset of reproductive activity and a history of having had multiple sexual partners lifelong may be at a greater risk of acquiring infection of the genital tract by C. trachomatis.
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Infecciones por Chlamydia/epidemiología , Chlamydia trachomatis/aislamiento & purificación , Tamizaje Masivo/métodos , Papillomaviridae/aislamiento & purificación , Infecciones por Papillomavirus/epidemiología , Neoplasias del Cuello Uterino/epidemiología , Adolescente , Adulto , Brasil/epidemiología , Chlamydia trachomatis/genética , Estudios Transversales , Detección Precoz del Cáncer , Femenino , Humanos , Persona de Mediana Edad , Papillomaviridae/genética , Infecciones por Papillomavirus/patología , Reacción en Cadena de la Polimerasa , Prevalencia , Infecciones del Sistema Genital/epidemiología , Factores de Riesgo , Neoplasias del Cuello Uterino/patología , Neoplasias del Cuello Uterino/virología , Adulto JovenRESUMEN
Objective. The purpose of this study was to assess the knowledge level about HPV and screening of cervical cancer in women from the metropolitan region of Natal, Brazil. Materials and Methods. A descriptive cross-sectional study involving sexually active women was conducted. The participants were submitted to a face-to-face interview, using a structured questionnaire that permitted the quantification of data and opinions of the respondents. Results. Most participants (70.9%) had poor knowledge about HPV and also the Pap test (53.0%). The high level of knowledge about HPV was associated with age, education, marital status, household income, and pregnancy, while the high level of knowledge about the Pap test proved to be associated only with education and household income. Conclusion. The results highlight the need for performing educational campaigns emphasizing the role of HPV in the etiology of cervical lesions of different degrees, including cervical cancer, as well as the importance of having a Pap test regularly to prevent these diseases.
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ß(S) haplotypes were studied in 47 non-related patients with sickle-cell anemia from the state of Rio Grande do Norte, Brazil. Molecular analysis was conducted by PCR/RFLP using restriction endonucleases XmnI, HindIII, HincII and HinfI to analyze six polymorphic sites from the beta cluster. Twenty-seven patients (57.5%) were identified with genotype CAR/CAR, 9 (19.1%) CAR/BEN, 6 (12.8%) CAR/CAM, 1 (2.1%) BEN/BEN, 2 (4.3%) CAR/Atp, 1 (2.1%) BEN/Atp and 1 (2.1%) with genotype Atp/Atp. The greater frequency of Cameroon haplotypes compared to other Brazilian states suggests the existence of a peculiarity of African origin in the state of Rio Grande do Norte.
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35 unrelated individuals were studied for characterization as either heterozygous or homozygous for beta-thalassemia. Molecular analysis was done by PCR/RFLP to detect the mutations most commonly associated with beta-thalassemia (ß(0)IVS-I-1, ß(+)IVS-I-6, and ß(0)39). In the patients who showed none of these mutations, the beta-globin genes were sequenced. Of the 31 heterozygous patients, 13 (41.9%) had the ß(+)IVS-I-6 mutation, 15 (48.4%) the ß(0)IVS-I-1 mutation, 2 (6.5%) the ß(+)IVS-I-110 mutation and 1 (3.2%) the ß(+)IVS-I-5 mutation. IVS-I-6 was detected in the four homozygotes. The mutation in codon 39, often found in previous studies in Brazil, was not detected in the present case. This is the first study aiming at identifying mutations that determine beta-thalassemia in the state of Rio Grande do Norte.
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We analyzed cervical specimens of 202 women, aged 15 to 64 years, attended at Luis Antonio Hospital, Natal, Brazil, to determine the prevalence of HPV and identify the more frequent genotypes and risk factors for HPV infection in women attended at a cervical cancer screening service. Two specimens were collected from each patient: one for cytological examination and the other to detect HPV DNA by PCR, and typing by dot blot hybridization. A total of 54.5% of the sample had normal cytology and 45.5% had cytological alterations. HPV was detected in 24.5% of the cytologically normal women and in 59.8% of those with altered cytology. Both single and double HPV infection increased the likelihood of cytological alterations. Thirteen types of HPV were identified, most of which were high risk. HPV 16 was the most prevalent single-type infection, followed by HPV 58. The most frequent double infection was the association between HPV 56 and 57. The prevalence of HPV in cytologically normal women was greater than that reported for countries on all the continents except Africa. The inverse was observed in women with cytological alterations. The distribution of HPV types was similar to that described for the Americas, with some differences. Multiple sexual partners was the only risk factor showing an association with the presence of HPV infection.