Many Labs 5:Testing pre-data collection peer review as an intervention to increase replicability

Replication studies in psychological science sometimes fail to reproduce prior findings. If these studies use methods that are unfaithful to the original study or ineffective in eliciting the phenomenon of interest, then a failure to replicate may be a failure of the protocol rather than a challenge to the original finding. Formal pre-data-collection peer review by experts may address shortcomings and increase replicability rates. We selected 10 replication studies from the Reproducibility Project: Psychology (RP:P; Open Science Collaboration, 2015) for which the original authors had expressed concerns about the replication designs before data collection; only one of these studies had yielded a statistically significant effect (p < .05). Commenters suggested that lack of adherence to expert review and low-powered tests were the reasons that most of these RP:P studies failed to replicate the original effects. We revised the replication protocols and received formal peer review prior to conducting new replication studies. We administered the RP:P and revised protocols in multiple laboratories (median number of laboratories per original study = 6.5, range = 3?9; median total sample = 1,279.5, range = 276?3,512) for high-powered tests of each original finding with both protocols. Overall, following the preregistered analysis plan, we found that the revised protocols produced effect sizes similar to those of the RP:P protocols (?r = .002 or .014, depending on analytic approach). The median effect size for the revised protocols (r = .05) was similar to that of the RP:P protocols (r = .04) and the original RP:P replications (r = .11), and smaller than that of the original studies (r = .37). Analysis of the cumulative evidence across the original studies and the corresponding three replication attempts provided very precise estimates of the 10 tested effects and indicated that their effect sizes (median r = .07, range = .00?.15) were 78% smaller, on average, than the original effect sizes (median r = .37, range = .19?.50)

Lower esophageal sphincter relaxation reflex kinetics: effects of peristaltic reflexes and maturation in human premature neonates

We defined the sensory-motor characteristics of the lower esophageal sphincter relaxation (LESR) (stimulus threshold volume, response onset, and relaxation period, relaxation magnitude, nadir) during maturation in human neonates. We hypothesized that LESR kinetics differs during maturation and with peristaltic reflex type. Basal and adaptive esophageal motility testing was performed (N = 20 premature neonates) at 34.7 and 39.1 wk (time 1 and time 2). Effects of midesophageal provocation with graded stimuli (N = 1,267 stimuli, air and liquids) on LESR kinetics during esophagodeglutition response (EDR) and secondary peristalsis (SP) were analyzed by mixed models. Frequency of LESR with basal primary peristalsis were different during maturation (P = 0.03). During adaptive responses with maturation, 1) the frequencies of peristaltic reflexes and LESR were similar; 2) liquid stimuli resulted in a shorter LESR response latency and LESR nadir and greater LESR magnitude (all P < 0.05); 3) media differences were noted with LESR response latency (air vs. liquids, P < 0.02); and 4) infusion flow rate-LESR were different (P < 0.01 for air and liquids). Mechanistically, 1) frequency of LESR was greater during peristaltic reflexes at both times (vs. none, P < 0.0001); 2) LESR response latency, duration, and time to complete LESR were longer with EDR (all P < 0.05, vs. SP at time 2); and 3) graded stimulus volume LESR were different for air and liquids (P < 0.01). In conclusion, sensory-motor characteristics of LESR depend on the mechanosensitive properties of the stimulus (media, volume, flow), type of peristaltic reflex, and postnatal maturation. Maturation modulates an increased recruitment of inhibitory pathways that favor LESR

Drosophila tubulin-binding cofactor B is required for microtubule network formation and for cell polarity

International audienceMicrotubules (MTs) are essential for cell division, shape, intracellular transport, and polarity. MT stability is regulated by many factors, including MT-associated proteins and proteins controlling the amount of free tubulin heterodimers available for polymerization. Tubulin-binding cofactors are potential key regulators of free tubulin concentration, since they are required for α-β-tubulin dimerization in vitro. In this paper, we show that mutation of the Drosophila tubulin-binding cofactor B (dTBCB) affects the levels of both α- and β-tubulins and dramatically destabilizes the MT network in different fly tissues. However, we find that dTBCB is dispensable for the early MT-dependent steps of oogenesis, including cell division, and that dTBCB is not required for mitosis in several tissues. In striking contrast, the absence of dTBCB during later stages of oogenesis causes major defects in cell polarity. We show that dTBCB is required for the polarized localization of the axis-determining mRNAs within the oocyte and for the apico-basal polarity of the surrounding follicle cells. These results establish a developmental function for the dTBCB gene that is essential for viability and MT-dependent cell polarity, but not cell division