Support Vector Machine to Detect Hypertension

Development of tools to facilitate diagnosis of some disease such as cancer, cardiovascular, hypertension, diabetes, is of great relevance in the medical field. In this paper, we will present a method based on Support Vector Machine regression model to detect the hypertension based on some risk factors including obesity, stress, systolic and diastolic blood pressure, physical exercises, cigaret consumption and diet lifestyle. Data represents a group of students from the Lebanese universities. After the data pre-processing, two Support Vector Machine models are designed and implemented in order to estimate systolic and diastolic blood pressure. The outcomes of the methods are diastolic and systolic blood pressure. Accurate results have been obtained which proves the effectiveness of the proposed Support Vector Machine for preliminary detection of hypertension

Recent Developments on the Crosstalk Between STAT3 and Inflammation in Heart Function and Disease

The transcription factor STAT3 has a protective function in the heart. Until recently, the role of STAT3 in hypertension-induced cardiac hypertrophy was unsettled. Earlier studies revealed that global reduction of STAT3 activity reduced cardiac hypertrophy with hypertension, but caused a disruption of myofilaments and increased contractile dysfunction. However, newer studies with cardiomyocyte-specific deletion of STAT3 indicate that STAT3 does not cause cardiac hypertrophy with increased blood pressure. Rather, cardiac STAT3 is important for maintaining metabolic homeostasis, and loss of STAT3 in cardiomyocytes makes the heart more susceptible to chronic pathological insult, for example by disrupting glucose metabolism and protective signaling networks via the upregulation of certain microRNAs. This scenario has implications for understanding peripartum cardiomyopathy as well. In viral myocarditis, STAT3 opposes the initiation of the dilated phenotype by maintaining membrane integrity via the expression of dystrophin. STAT3 signaling was also found to attenuate myocarditis by polarizing macrophages to a less inflammatory phenotype. On the other hand, STAT3 contributes to immune-mediated myocarditis due to IL-6-induced complement component C3 production in the liver, as well as the differentiation of Th17 cells, which play a role in initiation and development of myocarditis. Besides canonical signaling pathways, unphosphorylated STAT3 (U-STAT3) and redox-activated STAT3 have been shown to couple to transcription in the heart. In addition, tissue signaling cytokines such as IL-22 and IL-17 have been proposed to have actions on the heart that involve STAT3, but are not fully defined. Understanding the novel and often protective aspects of STAT3 in the myocardium could lead to new therapeutic approaches to treat heart disease

Hypertrophie ventriculaire gauche dans l'hypertension artérielle (analyse transcriptomique et gènes candidats chez le rat)

L'objectif de ce travail était d'identifier de nouveaux gènes impliqués dans l'hypertrophie ventriculaire gauche (HVG) associée à l'hypertension artérielle (HTA). Trois souches de rats hypertendus ont été étudiées : TGR(mRen2)27, SHR et LH. L'étude de l'expression des cytokines de la famille de l'IL-6 et de leurs sous-unités réceptrices montre qu'in vivo l'IL-6 et le LIF, mais non pas la CT-1, pourraient être impliqués lors du développement de l'HVG rénine-dépendante. L'analyse transcriptomique a permis de mettre en évidence une interaction entre la rénine et la famille de la protéine précurseur du peptide -amyloïde. La classification des rats a montré que le fond génétique est plus discriminant que la pression artérielle ou les facteurs humoraux. La confrontation des résultats obtenus chez les différents modèles a permis de mettre en évidence l'absence de gènes communs aux 3 modèles d'HVG et donc, l'absence d'un mécanisme moléculaire unique dans l'HVG associée à l'HTALYON1-BU.Sciences (692662101) / SudocSudocFranceF

Evidence That IL-6-Type Cytokine Signaling in Cardiomyocytes Is Inhibited by Oxidative Stress: Parthenolide Targets JAK1 Activation by Generating ROS

Parthenolide, an anti-inflammatory compound, was reported to inhibit signal transducer and activator of transcription 3 (STAT3) activation by the interleukin (IL)-6-type cytokines by an undefined process, which was the focus of our study. Here we report that parthenolide reduced both basal and leukemia inhibitory factor (LIF)-induced STAT3 tyrosine 705 (Y705) phosphorylation in cardiomyocytes in a dose-dependent manner, but stimulated the MAP kinase signaling pathways. Activation of Janus kinase I (JAK1) tyrosine kinase was markedly reduced by parthenolide. Pretreatment with parthenolide inhibited JAK1-mediated phosphorylation of the LIF receptor subunits LIF receptor (LIFR) α and glycoprotein 130 (gp130), and reduced the LIF-induced increase in JAK1 association with both components. In addition, we documented that parthenolide, over the same concentration range, does not have a direct inhibitory effect on JAK1 autophosphorylation. However, we observed that parthenolide increased intracellular reactive oxygen species (ROS). Pretreatment with the antioxidant, N-acetyl-L-cysteine, completely suppressed the effect of parthenolide on JAK1 and STAT3. From these results, we conclude ROS generation in cardiomyocytes blocks STAT3 signaling of the IL-6-type cytokines by targeting JAK1. The finding that signaling by the IL-6-type cytokine may be redox-sensitive defines a novel mechanism of regulation that has implications for exploiting their therapeutic potential

Stress and Heart Rate Variability during University Final Examination among Lebanese Students

Real-life stressors, such as university examination, cause an increase in sympathetic activity of the nervous system innervating the heart, and thus an increase in heart rate (HR). Our study aimed to detect changes in heart rate variability (HRV) during different stages of an exam in a group of 90 healthy university students (30 males and 60 females), over 4 h of monitoring divided into 1 h before, 2 h during, and 1 h after the examination. HRV was significantly highest after the exam, indicating release from stress, as compared to before and during the examination when stress was observable. Undergraduate students in different academic years did not differ in terms of stress, indicating the absence of adaptation to exam procedures. However, HR and R-R interval after the exam showed significant difference between first year undergraduate studies and first year of a graduate program, indicating a higher degree of confidence in graduate students. Results also suggest that HRV in females is significantly lower than that in males before and after examination, despite men having greater sympathetic input. In conclusion, the results of our novel study assessing stress in real-time examination show important gender differences, and lack of adaptation with academic study year

Impaired cardiac structure and systolic function in athletes using supra-physiological doses of anabolic androgenic steroids

Objectives: Athletes are increasingly using supra-physiological doses of anabolic androgenic steroids without weighing health side effects. This study aims to conjointly evaluate the effect of supraphysiological doses of anabolic androgenic steroids on global cardiovascular structure and functional capacity. Design: Cross-sectional study. Methods: 92 males enrolled in the study, including 18 sedentary subjects, 26 anabolic androgenic steroid non-user athletes, and 48 anabolic androgenic steroid-user athletes. Two-dimensional echocardiography was done to evaluate the cardiovascular structure and function. Results: Anabolic androgenic steroid-users presented increased cardiac remodeling of the left ventricle and left atrium compared to control groups (p < 0.001). Anabolic androgenic steroid-users showed increased left ventricular mass/body surface area versus control groups (p < 0.001), with 28 steroid-users (58.3 %) having cardiac remodeling, which is more than control groups (p < 0.001). Anabolic androgenic steroid-users presented lower diastolic function (E and E/A) compared to non-users (p = 0.003 and < 0.001, respectively). Ejection fraction was decreased among anabolic androgenic steroid-users versus the sedentary group only (p = 0.020), while anabolic androgenic steroid-users presented reduced global longitudinal strain of 15.43 % compared to both control groups (p < 0.001). Moreover, anabolic androgenic steroid-users experienced more tricuspid valve regurgitation (p = 0.001). Conclusions: Anabolic androgenic steroid consumption is associated with global cardiac remodeling with increased dimensions of the left ventricle, and atrium. Anabolic androgenic steroid-users present left ventricular hypertrophy with reduced subclinical systolic function. Moreover, anabolic androgenic steroid consumption is correlated with valve regurgitation and dilation of the sino-tubular junction