Soroprevalência da infecção por Helicobacter pylori em crianças de diferentes níveis sócio-econômicos em Porto Velho, Estado de Rondônia Seroprevalence of Helicobacter pylori infection among children of different socioeconomic levels in Porto Velho, State of Rondônia

O estudo investigou a soroprevalência de infecção pelo Helicobacter pylori em 200 (subdivididas em 2 grupos) crianças da Cidade de Porto Velho, Rondônia. A prevalência da soropositividade variou consideravelmente de acordo com o nível sócio-econômico, onde 51% das crianças de baixo nível e 24% de classe média eram positivas. As características da população infantil relacionadas ao sexo, raça e dieta alimentar não representaram fatores de risco para a aquisição da infecção; porém, a maioria das infectadas pertencia à faixa etária de cinco ou mais anos, independente do nível sócio-econômico. A distribuição fenotípica dos grupos sanguíneos ABO, entre os indivíduos infectados e não infectados, mostrou4 que a sororeatividade ao Helicobacter pylori foi maior entre as crianças do grupo sanguíneo O, sugerindo que há uma maior susceptibilidade genética destas crianças para a infecção pelo Helicobacter pylori.<br>This study investigated the seroprevalence of Helicobacter pylori infection in 200 children in the city of Porto Velho, State of Rondônia, divided in two groups of 100 children. The prevalence of seropositivity varied considerably according to socioeconomic level, such that 51% of the lower-level children and 24% of the middle-class children were positive. The characteristics of the child population relating to sex, ethnicity and diet did not represent risk factors for acquiring the infection. However, most of the infected children were in the age group of five years or older, independent of socioeconomic level. The phenotypic distribution of ABO blood groups among the infected and uninfected individuals showed that the seroreactivity to Helicobacter pylori was greater among the children with the O blood type, thus suggesting that these children have greater genetic susceptibility to infection by Helicobacter pylori

Coagulation, Protease-Activated Receptors, and Viral Myocarditis

The coagulation protease cascade plays an essential role in hemostasis. In addition, a clot contributes to host defense by limiting the spread of pathogens. Coagulation proteases induce intracellular signaling by cleavage of cell surface receptors called protease-activated receptors (PARs). These receptors allow cells to sense changes in the extracellular environment, such as infection. Viruses activate the coagulation cascade by inducing tissue factor expression and by disrupting the endothelium. Virus infection of the heart can cause myocarditis, cardiac remodeling and heart failure. Recent studies using a mouse model have shown that tissue factor, thrombin and PAR-1 signaling all positively regulate the innate immune during viral myocarditis. In contrast, PAR-2 signaling was found to inhibit interferon-β expression and the innate immune response. These observations suggest that anticoagulants may impair the innate immune response to viral infection and that inhibition of PAR-2 may be a new target to reduce viral myocarditis.

Mode and Characteristics of Arrhythmia Initiation in Idiopathic Ventricular Fibrillation: A THESIS Substudy.

There is limited information on the mode of arrhythmia initiation in idiopathic ventricular fibrillation (IVF). A non-pause-dependent mechanism has been suggested to be the rule. The aim of this study was to assess the mode and characteristics of initiation of polymorphic ventricular tachycardia (PVT) in patients with short or long-coupled PVT/IVF included in THESIS (THerapy Efficacy in Short or long-coupled idiopathic ventricular fibrillation: an International Survey), a multicenter study involving 287 IVF patients treated with drugs or radiofrequency ablation. We reviewed the initiation of 410 episodes of ≥1 PVT triplet in 180 patients (58.3% females; age 39.6 ± 13.6 years) with IVF. The incidence of pause-dependency arrhythmia initiation (prolongation by &gt;20 ms of the preceding cycle length) was assessed. Most arrhythmias (n = 295; 72%) occurred during baseline supraventricular rhythm without ambient premature ventricular complexes (PVCs), whereas 106 (25.9%) occurred during baseline rhythm including PVCs. Nine (2.2%) arrhythmias occurred during atrial/ventricular pacing and were excluded from further analysis. Mode of PVT initiation was pause-dependent in 45 (15.6%) and 64 (60.4%) of instances in the first and second settings, respectively, for a total of 109 of 401 (27.2%). More than one type of pause-dependent and/or non-pause-dependent initiation (mean: 2.6) occurred in 94.4% of patients with ≥4 events. Coupling intervals of initiating PVCs were &lt;350 ms, 350-500 ms, and &gt;500 ms in 76.6%, 20.72%, and 2.7% of arrhythmia initiations, respectively. Pause-dependent initiation occurred in more than a quarter of arrhythmic episodes in IVF patients. PVCs having long (between 350 and 500 ms) and very long (&gt;500 ms) coupling intervals were observed at the initiation of nearly a quarter of PVT episodes