Detection of Epstein-Barr Virus DNA in Gastric Biopsies of Pediatric Patients with Dyspepsia.

In this study, we assessed the presence of (EBV) in gastric samples derived from pediatric patients with dyspeptic symptoms, aiming to understand whether EBV participates in the development of early gastric lesions influencing chronic inflammation, in conjunction with the (Hp) bacterium. We analyzed EBV load in 236 gastric biopsies derived from 186 pediatric patients with chronic dyspepsia and compared it with EBV serology, Hp load and serology, and with immune cell infiltration. We found that 7.

Differential expression of coxsackievirus and adenovirus receptor in endomyocardial tissue of patients with myocarditis.

Recent studies demonstrated that the expression of coxsackievirus and adenovirus receptor (CAR) is implicated in the pathophysiology of myocarditis. The aim of the present study was to assess the association between active and borderline myocarditis and CAR expression in endomyocardial tissues, and analyze the association between CAR expression and treatment response. An analytic, cross‑sectional, retrospective study was performed in 26 patients with myocarditis and 10 control subjects without heart disease.

Elevated Levels of Interferon- Are Associated with High Levels of Epstein-Barr Virus Reactivation in Patients with the Intestinal Type of Gastric Cancer.

Background: The inflammatory response directed against () is believed to be one of the main triggers of the appearance of gastric lesions and their progression to gastric cancer (GC). Epstein-Barr virus (EBV) has been found responsible for about 10% of all GCs, but the inflammatory response has not been studied in GC patients with evidence of high levels of EBV reactivation.

Objective: To determine the relationship between inflammation and antibodies against EBV reactivation antigens, , and the bacterium virulence factor CagA in patients with GC.

Transcriptional Profiling of Type II Toxin-Antitoxin Genes of under Different Environmental Conditions: Identification of HP0967-HP0968 System.

is a Gram-negative bacterium that colonizes the human gastric mucosa and is responsible for causing peptic ulcers and gastric carcinoma. The expression of virulence factors allows the persistence of in the stomach, which results in a chronic, sometimes uncontrolled inflammatory response. Type II toxin-antitoxin (TA) systems have emerged as important virulence factors in many pathogenic bacteria.

Epstein-Barr virus association with peptic ulcer disease.

Background. Helicobacter pylori (HP) infection and nonsteroidal anti-inflammatory drugs (NSAID) use are considered the main risk to develop peptic ulcer disease (PUD). However, PUD also occurs in the absence of HP infection and/or NSAID use.

Preeclampsia is associated with lower production of vascular endothelial growth factor by peripheral blood mononuclear cells.

Background: Recent studies show that vascular endothelial growth factor (VEGF) downregulation is implicated in preeclampsia (PE) pathophysiology. This study assessed the relationship between PE and VEGF levels produced by peripheral blood mononuclear cells (PBMCs) and their serum levels.

Methods: A cross-sectional design was performed in 36 patients who had hypertensive disorders during pregnancy.

Correction: Epstein Barr Virus and Helicobacter pylori Co-Infection Are Positively Associated with Severe Gastritis in Pediatric Patients.

[This corrects the article DOI: 10.1371/journal.pone.

Epstein Barr virus and Helicobacter pylori co-infection are positively associated with severe gastritis in pediatric patients.

Background: H. pylori infection is acquired during childhood and causes a chronic inflammatory response in the gastric mucosa, which is considered the main risk factor to acquire gastric cancer (GC) later in life. More recently, infection by Epstein-Barr virus (EBV) have also been associated with GC.

Relation of antimyocardium antibodies to mortality in patients with acute myocardial infarction.

Background: Antimyocardium antibodies (AMA) have been observed in patients with acute myocardial infarction (AMI). At present it is unknown if these AMA play a role in the pathogenesis of acute or chronic myocardial damage or if they are only produced as a result of tissue destruction, disappearing later without clinical manifestations. However, some studies have shown that patients with AMI and AMA have higher possibilities of presenting heart failure and death.