Researchers often lack knowledge about how to deal with outliers when analyzing their data. Even more frequently, researchers do not pre-specify how they plan to manage outliers. In this paper we aim ...to improve research practices by outlining what you need to know about outliers. We start by providing a functional definition of outliers. We then lay down an appropriate nomenclature/classification of outliers. This nomenclature is used to understand what kinds of outliers can be encountered and serves as a guideline to make appropriate decisions regarding the conservation, deletion, or recoding of outliers. These decisions might impact the validity of statistical inferences as well as the reproducibility of our experiments. To be able to make informed decisions about outliers you first need proper detection tools. We remind readers why the most common outlier detection methods are problematic and recommend the use of the median absolute deviation to detect univariate outliers, and of the Mahalanobis-MCD distance to detect multivariate outliers. An R package was created that can be used to easily perform these detection tests. Finally, we promote the use of pre-registration to avoid flexibility in data analysis when handling outliers. 'Publishers note: due to a typesetting error, this paper was originally published with incorrect table numbering, where tables 2, 3, and 4 were incorrectly labelled. This was corrected soon after publication.'
When comparing two independent groups, psychology researchers commonly use Student’s 't'-tests. Assumptions of normality and homogeneity of variance underlie this test. More often than not, when ...these conditions are not met, Student’s 't'-test can be severely biased and lead to invalid statistical inferences. Moreover, we argue that the assumption of equal variances will seldom hold in psychological research, and choosing between Student’s 't'-test and Welch’s 't'-test based on the outcomes of a test of the equality of variances often fails to provide an appropriate answer. We show that the Welch’s 't'-test provides a better control of Type 1 error rates when the assumption of homogeneity of variance is not met, and it loses little robustness compared to Student’s 't'-test when the assumptions are met. We argue that Welch’s 't'-test should be used as a default strategy.
This article details a correction to: Delacre, M., Lakens, D., & Leys, C. (2017). Why Psychologists Should by Default Use Welch’s 't'-test Instead of Student’s t-test. 'International Review of Social ...Psychology', 30(1), 92–101. DOI: https://doi.org/10.5334/irsp.82.
Student’s 't'-test and classical 'F'-test ANOVA rely on the assumptions that two or more samples are independent, and that independent and identically distributed residuals are normal and have equal ...variances between groups. We focus on the assumptions of normality and equality of variances, and argue that these assumptions are often unrealistic in the field of psychology. We underline the current lack of attention to these assumptions through an analysis of researchers’ practices. Through Monte Carlo simulations, we illustrate the consequences of performing the classic parametric 'F'-test for ANOVA when the test assumptions are not met on the Type I error rate and statistical power. Under realistic deviations from the assumption of equal variances, the classic 'F'-test can yield severely biased results and lead to invalid statistical inferences. We examine two common alternatives to the 'F'-test, namely the Welch’s ANOVA ('W'-test) and the Brown-Forsythe test ('F'*-test). Our simulations show that under a range of realistic scenarios, the 'W'-test is a better alternative and we therefore recommend using the 'W'-test by default when comparing means. We provide a detailed example explaining how to perform the 'W'-test in SPSS and R. We summarize our conclusions in practical recommendations that researchers can use to improve their statistical practices.
To move beyond the limitations of null-hypothesis tests, statistical approaches have been developed where the observed data are compared against a range of values that are equivalent to the absence ...of a meaningful effect. Specifying a range of values around zero allows researchers to statistically reject the presence of effects large enough to matter, and prevents practically insignificant effects from being interpreted as a statistically significant difference. We compare the behavior of the recently proposed second generation p-value (Blume, D’Agostino McGowan, Dupont, & Greevy, 2018) with the more established Two One-Sided Tests (TOST) equivalence testing procedure (Schuirmann, 1987). We show that the two approaches yield almost identical results under optimal conditions. Under suboptimal conditions (e.g., when the confidence interval is wider than the equivalence range, or when confidence intervals are asymmetric) the second generation p-value becomes difficult to interpret. The second generation p-value is interpretable in a dichotomous manner (i.e., when the SGPV equals 0 or 1 because the confidence intervals lies completely within or outside of the equivalence range), but this dichotomous interpretation does not require calculations. We conclude that equivalence tests yield more consistent p-values, distinguish between datasets that yield the same second generation p-value, and allow for easier control of Type I and Type II error rates.
In association with innate and adaptive immunity, the microbiota controls the colonisation resistance against intestinal pathogens. Caspase recruitment domain 9 (
), a key innate immunity gene, is ...required to shape a normal gut microbiota.
mice are more susceptible to the enteric mouse pathogen
that mimics human infections with enteropathogenic and enterohaemorrhagic
. Here, we examined how
controls
infection susceptibility through microbiota-dependent and microbiota-independent mechanisms.
infection was assessed in conventional and germ-free (GF) wild-type (WT) and
mice. To explore the impact of
microbiota in infection susceptibility, GF WT mice were colonised with WT (WT→GF) or
(
→GF) microbiota before
infection. Microbiota composition was determined by 16S rDNA gene sequencing. Inflammation severity was determined by histology score and lipocalin level. Microbiota-host immune system interactions were assessed by quantitative PCR analysis.
controls pathogen virulence in a microbiota-independent manner by supporting a specific humoral response. Higher susceptibility to
-induced colitis was observed in
→GF mice. The microbiota of
mice failed to outcompete the monosaccharide-consuming
, worsening the infection severity. A polysaccharide-enriched diet counteracted the ecological advantage of
and the defective pathogen-specific antibody response in
mice.
CARD9 modulates the susceptibility to intestinal infection by controlling the pathogen virulence in a microbiota-dependent and microbiota-independent manner. Genetic susceptibility to intestinal pathogens can be overridden by diet intervention that restores humoural immunity and a competing microbiota.
Here, we show that autophagy is activated in the intestinal epithelium in murine and human colorectal cancer and that the conditional inactivation of Atg7 in intestinal epithelial cells inhibits the ...formation of pre-cancerous lesions in Apc(+/-) mice by enhancing anti-tumour responses. The antibody-mediated depletion of CD8(+) T cells showed that these cells are essential for the anti-tumoral responses mediated by the inhibition of autophagy. We show that Atg7 deficiency leads to intestinal dysbiosis and that the microbiota is required for anticancer responses. In addition, Atg7 deficiency resulted in a stress response accompanied by metabolic defects, AMPK activation and p53-mediated cell-cycle arrest in tumour cells but not in normal tissue. This study reveals that the inhibition of autophagy within the epithelium may prevent the development and progression of colorectal cancer in genetically predisposed patients.
Full text
Available for:
DOBA, IJS, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SBMB, UILJ, UKNU, UL, UM, UPUK
Over 90% of epidemic non-bacterial gastroenteritis are caused by human noroviruses (NoVs), which persist in a substantial subset of people allowing their spread worldwide. This has led to a ...significant number of endemic cases and up to 70,000 children deaths in developing countries. NoVs are primarily transmitted through the fecal-oral route. To date, studies have focused on the influence of the gut microbiota on enteric viral clearance by mucosal immunity. In this study, the use of mouse norovirus S99 (MNoV_S99) and CR6 (MNoV_CR6), two persistent strains, allowed us to provide evidence that the norovirus-induced exacerbation of colitis severity relied on bacterial sensing by nucleotide-binding oligomerization domain 2 (Nod2). Consequently, Nod2-deficient mice showed reduced levels of gravity of Dextran sodium sulfate (DSS)-induced colitis with both viral strains. And MNoV_CR6 viremia was heightened in Nod2
-/-
mice in comparison with animals hypomorphic for Atg16l1, which are prone to aggravated inflammation under DSS. Accordingly, the infection of macrophages derived from WT mice promoted the phosphorylation of Signal Transducer and Activator of Transcription 1 (STAT1) and NOD2's expression levels. Higher secretion of Tumor Necrosis Factor alpha (TNF
$\alpha $
α
) following NOD2 activation and better viral clearance were measured in these cells. By contrast, reduced levels of pSTAT1 and blunted downstream secretion of TNF
$\alpha $
α
were found in Nod2-deficient macrophages infected by MNoV_S99. Hence, our results uncover a previously unidentified virus-host-bacterial interplay that may represent a novel therapeutic target for treating noroviral origin gastroenteritis that may be linked with susceptibility to several common illnesses such as Crohn's disease.
Over 90% of epidemic non-bacterial gastroenteritis are caused by human noroviruses (NoVs), which persist in a substantial subset of people allowing their spread worldwide. This has led to a ...significant number of endemic cases and up to 70,000 children deaths in developing countries. NoVs are primarily transmitted through the fecal-oral route. To date, studies have focused on the influence of the gut microbiota on enteric viral clearance by mucosal immunity. In this study, the use of mouse norovirus S99 (MNoV_S99) and CR6 (MNoV_CR6), two persistent strains, allowed us to provide evidence that the norovirus-induced exacerbation of colitis severity relied on bacterial sensing by nucleotide-binding oligomerization domain 2 (Nod2). Consequently, Nod2-deficient mice showed reduced levels of gravity of Dextran sodium sulfate (DSS)-induced colitis with both viral strains. And MNoV_CR6 viremia was heightened in Nod2-/- mice in comparison with animals hypomorphic for Atg16l1, which are prone to aggravated inflammation under DSS. Accordingly, the infection of macrophages derived from WT mice promoted the phosphorylation of Signal Transducer and Activator of Transcription 1 (STAT1) and NOD2's expression levels. Higher secretion of Tumor Necrosis Factor alpha (TNFα) following NOD2 activation and better viral clearance were measured in these cells. By contrast, reduced levels of pSTAT1 and blunted downstream secretion of TNFα were found in Nod2-deficient macrophages infected by MNoV_S99. Hence, our results uncover a previously unidentified virus-host-bacterial interplay that may represent a novel therapeutic target for treating noroviral origin gastroenteritis that may be linked with susceptibility to several common illnesses such as Crohn's disease.
PDF
