Five-Point Likert Items: t test versus Mann-Whitney-Wilcoxon (\u3ci\u3eAddendum added October 2012\u3c/i\u3e)

Likert questionnaires are widely used in survey research, but it is unclear whether the item data should be investigated by means of parametric or nonparametric procedures. This study compared the Type I and II error rates of the t test versus the Mann-Whitney-Wilcoxon (MWW) for five-point Likert items. Fourteen population distributions were defined and pairs of samples were drawn from the populations and submitted to the t test and the t test on ranks, which yields the same results as MWW. The results showed that the two tests had equivalent power for most of the pairs. MWW had a power advantage when one of the samples was drawn from a skewed or peaked distribution. Strong power differences between the t test and MWW occurred when one of the samples was drawn from a multimodal distribution. Notably, the Type I error rate of both methods was never more than 3% above the nominal rate of 5%, even not when sample sizes were highly unequal. In conclusion, for five-point Likert items, the t test and MWW generally have similar power, and researchers do not have to worry about finding a difference whilst there is none in the population.Accessed 61,170 times on https://pareonline.net from October 06, 2010 to December 31, 2019. For downloads from January 1, 2020 forward, please click on the PlumX Metrics link to the right

Localization and density of phoretic deutonymphs of the mite Uropoda orbicularis (Parasitiformes : Mesostigmata) on Aphodius beetles (Aphodiidae) affect pedicel length

The phoretic stage of Uropodina mites is a deutonymph with developed morphological adaptations for dispersal by insects. Phoretic deutonymphs are able to produce a pedicel, a stalk-like temporary attachment structure that connects the mite with the carrier. The aim of our study was to determine whether localization and density of phoretic deutonymphs on the carrier affect pedicel length. The study was conducted on a common phoretic mite-Uropoda orbicularis (Uropodina) and two aphodiid beetles-Aphodius prodromus and Aphodius distinctus. Our results show that pedicel length is influenced by the localization of deutonymphs on the body of the carrier. The longest pedicels are produced by deutonymphs attached to the upper part of elytra, whereas deutonymphs attached to femora and trochanters of the third pair of legs and the apex of elytra construct the shortest pedicels. In general, deutonymphs attached to more exposed parts of the carrier produce longer pedicels, whereas shorter pedicels are produced when deutonymphs are fixed to non-exposed parts of the carrier. A second factor influencing pedicel length is the density of attached deutonymphs. Mean pedicel length and deutonymph densities were highly correlated: higher deutonymph density leads to the formation of longer pedicels. The cause for this correlation is discussed, and we conclude that pedicel length variability can increase successful dispersal

Early KPC-Producing Klebsiella pneumoniae Bacteremia among Intensive Care Unit Patients Non-Colonized upon Admission

Among 140 patients colonized by KPC-producing Klebsiella pneumoniae (KPC-Kp) between fourth and seventh day of Intensive Care Unit stay, 24 developed bacteraemia immediately after colonization. Colistin-resistance of the colonizing isolate was the factor significantly associated with early KPC-Kp bacteraemia (P < 0.001; OR 6.6, 95% CI 2.4–18.4), a worrisome finding since infections by colistin-resistant isolates is associated with increased mortality due to limited remaining therapeutic options

Broad targeting of resistance to apoptosis in cancer

Apoptosis or programmed cell death is natural way of removing aged cells from the body. Most of the anti-cancer therapies trigger apoptosis induction and related cell death networks to eliminate malignant cells. However, in cancer, de-regulated apoptotic signaling, particularly the activation of an anti-apoptotic systems, allows cancer cells to escape this program leading to uncontrolled proliferation resulting in tumor survival, therapeutic resistance and recurrence of cancer. This resistance is a complicated phenomenon that emanates from the interactions of various molecules and signaling pathways. In this comprehensive review we discuss the various factors contributing to apoptosis resistance in cancers. The key resistance targets that are discussed include (1) Bcl-2 and Mcl-1 proteins; (2) autophagy processes; (3) necrosis and necroptosis; (4) heat shock protein signaling; (5) the proteasome pathway; (6) epigenetic mechanisms; and (7) aberrant nuclear export signaling. The shortcomings of current therapeutic modalities are highlighted and a broad spectrum strategy using approaches including (a) gossypol; (b) epigallocatechin-3-gallate; (c) UMI-77 (d) triptolide and (e) selinexor that can be used to overcome cell death resistance is presented. This review provides a roadmap for the design of successful anti-cancer strategies that overcome resistance to apoptosis for better therapeutic outcome in patients with cancer

Congenital Heart Disease–Causing Gata4 Mutation Displays Functional Deficits In Vivo

Defects of atrial and ventricular septation are the most frequent form of congenital heart disease, accounting for almost 50% of all cases. We previously reported that a heterozygous G296S missense mutation of GATA4 caused atrial and ventricular septal defects and pulmonary valve stenosis in humans. GATA4 encodes a cardiac transcription factor, and when deleted in mice it results in cardiac bifida and lethality by embryonic day (E)9.5. In vitro, the mutant GATA4 protein has a reduced DNA binding affinity and transcriptional activity and abolishes a physical interaction with TBX5, a transcription factor critical for normal heart formation. To characterize the mutation in vivo, we generated mice harboring the same mutation, Gata4 G295S. Mice homozygous for the Gata4 G295S mutant allele have normal ventral body patterning and heart looping, but have a thin ventricular myocardium, single ventricular chamber, and lethality by E11.5. While heterozygous Gata4 G295S mutant mice are viable, a subset of these mice have semilunar valve stenosis and small defects of the atrial septum. Gene expression studies of homozygous mutant mice suggest the G295S protein can sufficiently activate downstream targets of Gata4 in the endoderm but not in the developing heart. Cardiomyocyte proliferation deficits and decreased cardiac expression of CCND2, a member of the cyclin family and a direct target of Gata4, were found in embryos both homozygous and heterozygous for the Gata4 G295S allele. To further define functions of the Gata4 G295S mutation in vivo, compound mutant mice were generated in which specific cell lineages harbored both the Gata4 G295S mutant and Gata4 null alleles. Examination of these mice demonstrated that the Gata4 G295S protein has functional deficits in early myocardial development. In summary, the Gata4 G295S mutation functions as a hypomorph in vivo and leads to defects in cardiomyocyte proliferation during embryogenesis, which may contribute to the development of congenital heart defects in humans

Participation of Candida albicans transcription factor Rlm1 in cell wall biogenesis and virulence

Candida albicans cell wall is important for growth and interaction with the environment. RLM1 is one of the putative transcription factors involved in the cell wall integrity pathway, which plays an important role in the maintenance of the cell wall integrity. In this work we investigated the involvement of RLM1 in the cell wall biogenesis and in virulence. Newly constructed C. albicans Δ/Δrlm1 mutants showed typical cell wall weakening phenotypes, such as hypersensitivity to Congo Red, Calcofluor White, and caspofungin (phenotype reverted in the presence of sorbitol), confirming the involvement of RLM1 in the cell wall integrity. Additionally, the cell wall of C. albicans Δ/Δrlm1 showed a significant increase in chitin (213%) and reduction in mannans (60%), in comparison with the wild-type, results that are consistent with cell wall remodelling. Microarray analysis in the absence of any stress showed that deletion of RLM1 in C. albicans significantly down-regulated genes involved in carbohydrate catabolism such as DAK2, GLK4, NHT1 and TPS1, up-regulated genes involved in the utilization of alternative carbon sources, like AGP2, SOU1, SAP6, CIT1 or GAL4, and genes involved in cell adhesion like ECE1, ALS1, ALS3, HWP1 or RBT1. In agreement with the microarray results adhesion assays showed an increased amount of adhering cells and total biomass in the mutant strain, in comparison with the wild-type. C. albicans mutant Δ/Δrlm1 strain was also found to be less virulent than the wild-type and complemented strains in the murine model of disseminated candidiasis. Overall, we showed that in the absence of RLM1 the modifications in the cell wall composition alter yeast interaction with the environment, with consequences in adhesion ability and virulence. The gene expression findings suggest that this gene participates in the cell wall biogenesis, with the mutant rearranging its metabolic pathways to allow the use of alternative carbon sources.This work was supported by CBMA (Centre of Molecular and Environmental Biology) through the FCT (Fundacao para a Ciencia e Tecnologia) project PEst-C/BIA/UI4050/2011. Yolanda Delgado-Silva was supported by an ALbAN scholarship (No E07D400922PE), and Alexandra Correia by SFRH/BD/31354/2006 fellowship. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

Identification and Characterization of a Mef2 Transcriptional Activator in Schistosome Parasites

Myocyte enhancer factor 2 protein (Mef2) is an evolutionarily conserved activator of transcription that is critical to induce and control complex processes in myogenesis and neurogenesis in vertebrates and insects, and osteogenesis in vertebrates. In Drosophila, Mef2 null mutants are unable to produce differentiated muscle cells, and in vertebrates, Mef2 mutants are embryonic lethal. Schistosome worms are responsible for over 200 million cases of schistosomiasis globally, but little is known about early development of schistosome parasites after infecting a vertebrate host. Understanding basic schistosome development could be crucial to delineating potential drug targets. Here, we identify and characterize Mef2 from the schistosome worm Schistosoma mansoni (SmMef2). We initially identified SmMef2 as a homolog to the yeast Mef2 homolog, Resistance to Lethality of MKK1P386 overexpression (Rlm1), and we show that SmMef2 is homologous to conserved Mef2 family proteins. Using a genetics approach, we demonstrate that SmMef2 is a transactivator that can induce transcription of four separate heterologous reporter genes by yeast one-hybrid analysis. We also show that Mef2 is expressed during several stages of schistosome development by quantitative PCR and that it can bind to conserved Mef2 DNA consensus binding sequences

Megabase deletions of gene deserts result in viable mice

The functional importance of the approximately 98 percent of mammalian genomes not corresponding to protein coding sequences remain largely un-scrutinized 1. To test experimentally whether some extensive regions of non-coding DNA, referred to as gene deserts 2-4, contain critical functions essential for the viability of the organism, we deleted two large non-coding intervals, 1,511 kb and 845 kb in length, from the mouse genome. Viable mice homozygous for the deletions were generated and were indistinguishable from wild-type littermates with regards to morphology, reproductive fitness, growth, longevity and a variety of parameters assaying general homeostasis. Further in-depth analysis of the expression of genes bracketing the deletions revealed similar expression characteristics in homozygous deletion and wild-type mice. Together, the two deleted segments harbour 1,243 non-coding sequences conserved between humans and rodents (>100bp, 70 percent identity). These studies demonstrate that some large-scale deletions of non-coding DNA can be well tolerated by an organism, bringing into question the role of many human-mouse conserved sequences 5,6, and further supports the existence of potentially "disposable DNAi" in the genomes of mammals