Organ crosstalk during acute lung injury, acute respiratory distress syndrome, and mechanical ventilation.

PURPOSE OF REVIEW: Multiple organ failure is the main cause of morbidity and mortality in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) patients. Moreover, survivors of both ALI and ARDS often show significant neurocognitive decline at discharge. These data suggest a deleterious organ crosstalk between lungs and distal organs. This article reviews the recent literature concerning the role of this organ crosstalk during ALI, ARDS, and mechanical ventilation, especially focusing on brain-lung communication. RECENT FINDINGS: Numerous pulmonary and extrapulmonary disorders could predispose critically ill patients to ALI and ARDS. Mechanical ventilation, although a lifesaving intervention, could contribute by modulating the mechanisms involved in the pathophysiology of lung damage and their impact on remote organs. Emerging clinical and experimental evidence supports the hypothesis of a multidirectional organ crosstalk between lungs and distal organs. SUMMARY: Organ crosstalk is an emerging area of research in lung disease in critically ill patients. The findings of these studies are clinically relevant and show the importance of an integrative approach in the management of critical patients. However, further studies are necessary to understand the complex interactions concurring in these pathologies.

Cross-sectional study of human coding- and non-coding RNAs in progressive stages of Helicobacter pylori infection.

Helicobacter pylori infects 4.4 billion individuals worldwide and is considered the most important etiologic agent for peptic ulcers and gastric cancer. Individual response to H. pylori infection is complex and depends on complex interactions between host and environmental factors. The pathway towards gastric cancer is a sequence of events known as Correa's model of gastric carcinogenesis, a stepwise inflammatory process from normal mucosa to chronic-active gastritis, atrophy, metaplasia and gastric adenocarcinoma. This study examines gastric clinical specimens representing different steps of the Correa pathway with the aim of identifying the expression profiles of coding- and non-coding RNAs that may have a role in Correa's model of gastric carcinogenesis. We screened for differentially expressed genes in gastric biopsies by employing RNAseq, microarrays and qRT-PCR. Here we provide a detailed description of the experiments, methods and results generated. The datasets may help other scientists and clinicians to find new clues to the pathogenesis of H. pylori and the mechanisms of progression of the infection to more severe gastric diseases. Data is available via ArrayExpress.

Expression profile of circulating microRNAs in the Correa pathway of progression to gastric cancer.

BACKGROUND: Helicobacter pylori infection causes long-term chronic active gastritis, a risk factor for the intestinal and diffuse forms of gastric cancer. Most gastric cancers develop in a stepwise progression from chronic active gastritis to precursor lesions of gastric cancer. The early detection of gastric cancer improves survival. Studies with recent evidence have proposed circulating-microRNAs as biomarkers of cancer. OBJECTIVE: The purpose of this study was to explore the circulating-microRNA profile from H. pylori infection to gastric adenocarcinoma. METHODS: One hundred and twenty-three patients were enrolled and assigned to the discovery or the validation sets. In the discovery phase, circulating-microRNAs were measured by dye-based quantitative polymerase chain reaction and a selection of circulating-microRNAs was validated by probe-based quantitative polymerase chain reaction. A quality control protocol was used. RESULTS: One hundred and sixty-seven circulating-microRNAs were detected. Precursor lesions of gastric cancer and gastric cancer patients showed the downregulation of eight and five circulating-microRNAs, respectively. We further validated the deregulation of miR-196a-5p in precursor lesions of gastric cancer and the deregulation of miR-134-5p, miR-144-3p and miR-451a in gastric cancer. However, circulating-microRNAs exhibited moderate diagnostic performance due to the overlap of circulating-microRNA expression between non-cancer and cancer patients. miR-144-3p/miR-451a expression levels were correlated. Interestingly, these microRNAs are in 17q11.2, a site of rearrangements associated with gastric cancer. CONCLUSION: Circulating-microRNAs are deregulated in precancerous and gastric cancer patients but efforts are needed to improve their diagnostic accuracy.