Modified RIFLE criteria in critically ill children with acute kidney injury

A classification system has been proposed to standardize the definition of acute kidney injury in adults. These criteria of risk, injury, failure, loss, and end-stage renal disease were given the acronym of RIFLE. We have modified the criteria based on 150 critically ill pediatric RIFLE (pRIFLE) patients to assess acute kidney injury incidence and course along with renal and/or non-renal comorbidities. Of these children, 11 required dialysis and 24 died. Patients without acute kidney injury in the first week of intensive care admission were less likely to subsequently develop renal Injury or Failure; however, 82% of acute kidney injury occurred in this initial week. Within this group of 123 children, 60 reached pRIFLEmax for Risk, 32 reached Injury, and 31 reached Failure. Acute kidney injury during admission was an independent predictor of intensive care; hospital length of stay and an increased risk of death independent of the Pediatric Risk of Mortality (PRISM II) score (odds ratio 3.0). Our results show that a majority of critically ill children develop acute kidney injury by pRIFLE criteria and do so early in the course of intensive care. Acute kidney injury is associated with mortality and may lead to increased hospital costs. We suggest that the pRIFLE criteria serves to characterize the pattern of acute kidney injury in critically ill children

Data from a pre-publication independent replication initiative examining ten moral judgement effects

We present the data from a crowdsourced project seeking to replicate findings in independent laboratories before (rather than after) they are published. In this Pre-Publication Independent Replication (PPIR) initiative, 25 research groups attempted to replicate 10 moral judgment effects from a single laboratory's research pipeline of unpublished findings. The 10 effects were investigated using online/lab surveys containing psychological manipulations (vignettes) followed by questionnaires. Results revealed a mix of reliable, unreliable, and culturally moderated findings. Unlike any previous replication project, this dataset includes the data from not only the replications but also from the original studies, creating a unique corpus that researchers can use to better understand reproducibility and irreproducibility in science

The pipeline project: Pre-publication independent replications of a single laboratory's research pipeline

This crowdsourced project introduces a collaborative approach to improving the reproducibility of scientific research, in which findings are replicated in qualified independent laboratories before (rather than after) they are published. Our goal is to establish a non-adversarial replication process with highly informative final results. To illustrate the Pre-Publication Independent Replication (PPIR) approach, 25 research groups conducted replications of all ten moral judgment effects which the last author and his collaborators had “in the pipeline” as of August 2014. Six findings replicated according to all replication criteria, one finding replicated but with a significantly smaller effect size than the original, one finding replicated consistently in the original culture but not outside of it, and two findings failed to find support. In total, 40% of the original findings failed at least one major replication criterion. Potential ways to implement and incentivize pre-publication independent replication on a large scale are discussed

New intragenic deletions in the Phex gene clarify X-linked hypophosphatemia-related abnormalities in mice.

X-linked hypophosphatemic rickets (XLH) in humans is caused by mutations in the PHEX gene. Previously, three mutations in the mouse Phex gene have been reported: Phex Hyp , Gy, and Phex Ska1 . Here we report analysis of two new spontaneous mutations in the mouse Phex gene, Phex Hyp-2J and Phex Hyp-Duk . Phex Hyp-2J and Phex Hyp-Duk involve intragenic deletions of at least 7.3 kb containing exon 15, and 30 kb containing exons 13 and 14, respectively. Both mutations cause similar phenotypes in males, including shortened hind legs and tail, a shortened square trunk, hypophosphatemia, hypocalcemia, and rachitic bone disease. In addition, mice carrying the Phex Hyp-Duk mutation exhibit background-dependent variable expression of deafness, circling behavior, and cranial dysmorphology, demonstrating the influence of modifying genes on Phex-related phenotypes. Cochlear cross-sections from Phex Hyp-2J /Y and Phex Hyp-Duk /Y males reveal a thickening of the temporal bone surrounding the cochlea with the presence of a precipitate in the scala tympani. Evidence of the degeneration of the organ of Corti and spiral ganglion also are present in the hearing-impaired Phex Hyp-Duk /Y mice, but not in the normal-hearing Phex Hyp-2J/Y mice. Analysis of the phenotypes noted in Phex Hyp-Duk /Y an Phex Hyp-2J /Y males, together with those noted in Phex Ska1 /Y and Phex Hyp /Y males, now allow XLH-related phenotypes to be separated from non-XLH-related phenotypes, such as those noted in Gy/Y males. Also, identification of the genetic modifiers of hearing and craniofacial dysmorphology in Phex Hyp-Duk /Y mice could provide insight into the phenotypic variation of XLH in humans

The effects of phytase on growth performance and intestinal transit time of broilers fed nutritionally adequate diets and diets deficient in calcium and phosphorus

Five experiments (Exp.) were conducted to determine the effects of phytase on growth performance and intestinal transit time in chicks fed nutritionally adequate diets and diets deficient in Ca and nonphytate P (nPP). In Exp. 1 and 2, chicks were fed a nutritionally adequate diet from 0 to 6 d or from 0 to 4 d posthatching; assay periods were 8 or 10 d; average initial BW were 98 or 79 g; and average final BW were 371 or 369 g, respectively. Treatments were replicated with 12 pens of 5 chicks each. Corn-soybean meal (C-SBM) diets were adequate in all nutrients except Ca and nPP where appropriate. The treatments were 1) C-SBM, 1.0% Ca, and 0.45% nPP; 2) C-SBM, 0.80% Ca, and 0.25% nPP; 3) Diet 1 + 600 phytase units/kg of diet; 4) Diet 2 + 600 phytase units/kg of diet. Experiments 3, 4, and 5 were conducted to determine the effects of phytase on intestinal transit time in broilers. Broilers were fed the same nutritionally adequate diet from 0 to 18, 27, or 23 d posthatching, and the assay periods were 7 d. Treatments were replicated with 18 individually penned broilers. Average initial BW were 768, 1,108, or 838 g, and average final BW were 1,299, 1,704, or 1,392 g in Exp. 3 to 5, respectively. Transit time data were collected on d 1 and 7 of the Exp. Diets were 1) C-SBM, 0.9% Ca, and 0.35% nPP; 2) C-SBM, 0.80% Ca, and 0.25% nPP + 600 phytase units/kg of diet. Transit time was calculated as the difference between the time feed was first ingested and the time of first appearance of solid feces. In Exp. 1 and 2, the reduction in dietary Ca and nPP reduced (P \u3c 0.01) average daily gain (ADG), average daily feed intake (ADFI), and gain:feed. Phytase addition increased (P \u3c 0.02) ADG and ADFI in diets deficient in Ca and nPP and in the nutritionally adequate diets. In Exp. 2, the reduction in Ca and nPP reduced (P \u3c 0.01) toe and tibia ash percentage, but phytase addition increased (P \u3c 0.01) toe and tibia ash percentage. The increase in toe ash percentage was greater in chicks fed the Ca and nPP deficient diet than in chicks fed the nutritionally adequate diet (Ca and nPP x phytase, P \u3c 0.01). In Exp. 3, 4, and 5, transit time on d 1 was faster (P \u3c 0.03) in chicks fed phytase. On d 7, transit time tended to be faster in chicks fed phytase, but the effect was not significant (P = 0.15). These data indicate that phytase increases ADG and ADFI in diets deficient in Ca and nPP and in diets formulated to be adequate (or excess) in all nutrients for broiler chicks. The increase in ADG and ADFI in chicks fed the nutritionally adequate diet may be due to a faster transit time of feed through the digestive tract, resulting in a greater feed intake and gain. ©2006 Poultry Science Association, Inc