We propose that pseudoknot induced frameshifting efficiency can be viewed as a balance between two competing effects (as visualized in Figure 7) , the mechanically stronger the pseudoknot, the larger the frameshifting efficiency (25) (26) (27) , however, the stronger the pseudoknot the larger the likelihood of stalling the frameshifted ribosome, thus preventing the translation of full-length frameshift product. Possibly, evolution optimized viral pseudoknots to balance these two effects. Hence, in measurements of frameshifting efficiency it is important to take into account the roadblocking effect of mRNA pseudoknots. Figure 7 . Model of frameshifting efficiency. Increasing the strength of a pseudoknot causes the pseudoknot to induce frameshifting at a higher frequency. However, the stronger the pseudoknot the larger the likelihood that it will act as a roadblock for the ribosome, reducing the amount of frameshifted product produced. The optimal frameshifting efficiency is achieved by balancing the two contributions. Secretory phospholipase A2 pathway in various types of lung injury in neonates and infants: a multicentre translational study BACKGROUND: Secretory phospholipase A2 (sPLA2) is a group of enzymes involved in lung tissue inflammation and surfactant catabolism. sPLA2 plays a role in adults affected by acute lung injury and seems a promising therapeutic target. Preliminary data allow foreseeing the importance of such enzyme in some critical respiratory diseases in neonates and infants, as well. Our study aim is to clarify the role of sPLA2 and its modulators in the pathogenesis and clinical severity of hyaline membrane disease, infection related respiratory failure, meconium aspiration syndrome and acute respiratory distress syndrome. sPLA2 genes will also be sequenced and possible genetic involvement will be analysed. METHODS/DESIGN: Multicentre, international, translational study, including several paediatric and neonatal intensive care units and one coordinating laboratory. Babies affected by the above mentioned conditions will be enrolled: broncho-alveolar lavage fluid, serum and whole blood will be obtained at definite time-points during the disease course. Several clinical, respiratory and outcome data will be recorded. Laboratory researchers who perform the bench part of the study will be blinded to the clinical data. DISCUSSION: This study, thanks to its multicenter design, will clarify the role(s) of sPLA2 and its pathway in these diseases: sPLA2 might be the crossroad between inflammation and surfactant dysfunction. This may represent a crucial target for new anti-inflammatory therapies but also a novel approach to protect surfactant or spare it, improving alveolar stability, lung mechanics and gas exchange. Phospholipase A2 biology Phospholipases A2 are a widely distributed group of enzymes primarily implicated in the turnover of membrane phospholipids and lipid digestion. They are also crucial for the inflammation pathways, as they are the first step for the production of eicosanoids and other inflammatory mediators [1, 2] . Secretory phospholipase A2 (sPLA2) is the low molecular, well conserved and secreted form of the enzyme. It is excreted into the alveoli mainly by macrophages and mast cells [1] [2] [3] . sPLA2 has a dual role, as it contributes to the inflammation pathway and it is also the main enzyme involved in the catabolism of surfactant [1, 2, 4] This complex proteo-lipid mixture is essential for the alveolar opening and the maintenance of an adequate gas exchange.