The Role of Executive Functioning and Technological Anxiety (FOMO) in College Course Performance as Mediated by Technology Usage and Multitasking Habits / El papel del funcionamiento ejecutivo y de la ansiedad tecnológica (FOMO) en el desempeño académico universitario mediatizado por la utilización de la tecnología y los hábitos multi-tarea

This study investigated how technology use impacts academic performance. A proposed model postulated that academic performance could be predicted by a cognitive independent variable-executive functioning problems-and an affective independent variable-technological anxiety or FOMO (fear of missing out)-mediated by how students choose to use technology. An unobtrusive smartphone application called "Instant Quantified Self" monitored daily smartphone s and daily minutes of use. Other mediators d self-reported smartphone use, self-observed studying attention, self-reported multitasking preference, and a classroom digital metacognition tool that assessed the studen's ability to understand the ramifications of technology use in the classroom that is not relevant to the learning process. Two hundred sixteen participants collected an average of 56 days of "Instant" application data, demonstrating that their smartphone was ed more than 60 times a day for three to four minutes each time for a total of 220 daily minutes of use. Results indicated that executive functioning problems predicted academic course performance mediated by studying attention and a single classroom digital metacognition subscale concerning availability of strategies of when to use mobile phones during lectures. FOMO predicted performance directly as well as mediated by a second classroom digital metacognition concerning attitudes toward mobile phone use during lectures. Implications for college students and professors increasing metacognition about technology use in the classroom and taking "tech breaks" to reduce technology anxiety

Este estudio analiza la repercusión del uso de la tecnología en el desempeño académico. Se propuso un modelo que postulaba que el desempeño académico podía predecirse mediante una variable independiente cognitiva (los problemas de funcionamiento ejecutivo) y una variable independiente afectiva (la ansiedad tecnológica o FOMO -el miedo a perderse algo), influido por el modo como los alumnos elegían utilizar la tecnología. Mediante una aplicación para móvil no intrusiva, denominada "Yo cuantificado instantáneo" seguía los desbloqueos diarios del móvil y los minutos de uso. Había otros mediadores, como el uso del móvil según el usuario, la atención en el estudio según la observa el usuario, preferencias de multi-tarea según el usuario y una nueva herramienta de medida digital en el aula para analizar la capacidad del alumno para entender las ramificaciones del uso de la tecnología en el aula que no es relevante para el proceso de aprendizaje. Un total de 216 participantes recogieron datos de la aplicación "instantánea" durante una media de 56 días, mostrando que su teléfono móvil era desbloqueado más de 60 veces al día entre tres y cuatro minutos cada vez durante un total de 220 minutos diarios de uso. Los resultados indicaban que los problemas de funcionamiento ejecutivo predecían el rendimiento académico mediatizado por la atención en el estudio y una única subescala de metacognición digital en el aula relativa a la disponibilidad de estrategias sobre cuándo utilizar el móvil durante las clases. El FOMO predecía el desempeño directamente además de a través de una segunda metacognición digital del aula relativa a las actitudes hacia el teléfono móvil durante las clases. Entre las implicaciones para los alumnos y los profesores está el aumento de la metacognición sobre el uso de la tecnología en el aula y "descansar de la tecnología" para disminuir la ansiedad que produce

The Role of Executive Functioning and Technological Anxiety (FOMO) in College Course Performance as Mediated by Technology Usage and Multitasking Habits.

This study investigated how technology use impacts academic performance. A proposed model postulated that academic performance could be predicted by a cognitive independent variable-executive functioning problems-and an affective independent variable-technological anxiety or FOMO (fear of missing out)-mediated by how students choose to use technology. An unobtrusive smartphone application called "Instant Quantified Self" monitored daily smartphone un-locks and daily minutes of use. Other mediators included self-reported smartphone use, self-observed studying attention, self-reported multitasking preference, and a classroom digital metacognition tool that assessed the student's ability to understand the ramifications of technology use in the classroom that is not relevant to the learning process. Two hundred sixteen participants collected an average of 56 days of "Instant" application data, demonstrating that their smartphone was unlocked more than 60 times a day for three to four minutes each time for a total of 220 daily minutes of use. Results indicated that executive functioning problems predicted academic course performance mediated by studying attention and a single classroom digital metacognition subscale concerning availability of strategies of when to use mobile phones during lectures. FOMO predicted performance directly as well as mediated by a second classroom digital metacognition concerning attitudes toward mobile phone use during lectures. Implications for college students and professors include increasing metacognition about technology use in the classroom and taking "tech breaks" to reduce technology anxiety.

Este estudio analiza la repercusión del uso de la tecnología en el desempeño académico. Se propuso un modelo que postulaba que el desempeño académico podía predecirse mediante una variable independiente cognitiva (los problemas de funcionamiento ejecutivo) y una variable independiente afectiva (la ansiedad tecnológica o FOMO ­el miedo a perderse algo), influido por el modo como los alumnos elegían utilizar la tecnología. Mediante una aplicación para móvil no intrusiva, denominada "Yo cuantificado instantáneo" seguía los desbloqueos diarios del móvil y los minutos de uso. Había otros mediadores, como el uso del móvil según el usuario, la atención en el estudio según la observa el usuario, preferencias de multi-tarea según el usuario y una nueva herramienta de medida digital en el aula para analizar la capacidad del alumno para entender las ramificaciones del uso de la tecnología en el aula que no relevante para el proceso de aprendizaje. Un total de 216 participantes recogieron datos de la aplicación "instantánea" durante una media de 56 días, mostrando que su teléfono móvil era desbloqueado más de 60 veces al día entre tres y cuatro minutos cada vez durante un total de 220 minutos diarios de uso. Los resultados indicaban que los problemas de funcionamiento ejecutivo predecían el rendimiento académico mediatizado por la atención en el estudio y una única subescala de metacognición digital en el aula relativa a la disponibilidad de estrategias sobre cuándo utilizar el móvil durante las clases. El FOMO predecía el desempeño directamente además de a través de una segunda metacognición digital del aula relativa a las actitudes hacia el teléfono móvil durante las clases. Entre las implicaciones para los alumnos y los profesores está el aumento de la metacognición sobre el uso de la tecnología en el aula y "descansar de la tecnología" para disminuir la ansiedad que produce.

Media and technology use predicts ill-being among children, preteens and teenagers independent of the negative health impacts of exercise and eating habits.

The American Academy of Pediatrics recommends no screen time for children under the age of 2 and limited screen time for all children. However, no such guidelines have been proposed for preteens and teenagers. Further, research shows that children, preteens, and teenagers are using massive amounts of media and those with more screen time have been shown to have increased obesity, reduced physical activity, and decreased health. This study examined the impact of technology on four areas of ill-being-psychological issues, behavior problems, attention problems and physical health-among children (aged 4-8), preteens (9-12), and teenagers (13-18) by having 1030 parents complete an online, anonymous survey about their own and their child's behaviors. Measures included daily technology use, daily food consumption, daily exercise, and health. Hypothesis 1, which posited that unhealthy eating would predict impaired ill-being, was partially supported, particularly for children and preteens. Hypothesis 2, which posited that reduced physical activity would predict diminished health levels, was partially supported for preteens and supported for teenagers. Hypothesis 3, that increased daily technology use would predict ill-being after factoring out eating habits and physical activity, was supported. For children and preteens, total media consumption predicted illbeing while for preteens specific technology uses, including video gaming and electronic communication, predicted ill-being. For teenagers, nearly every type of technological activity predicted poor health. Practical implications were discussed in terms of setting limits and boundaries on technology use and encouraging healthy eating and physical activity at home and at school.

Enhanced Ca²+ influx through cardiac L-type Ca²+ channels maintains the systolic Ca²+ transient in early cardiac atrophy induced by mechanical unloading.

Cardiac atrophy as a consequence of mechanical unloading develops following exposure to microgravity or prolonged bed rest. It also plays a central role in the reverse remodelling induced by left ventricular unloading in patients with heart failure. Surprisingly, the intracellular Ca(2+) transients which are pivotal to electromechanical coupling and to cardiac plasticity were repeatedly found to remain unaffected in early cardiac atrophy. To elucidate the mechanisms underlying the preservation of the Ca(2+) transients, we investigated Ca(2+) cycling in cardiomyocytes from mechanically unloaded (heterotopic abdominal heart transplantation) and control (orthotopic) hearts in syngeneic Lewis rats. Following 2 weeks of unloading, sarcoplasmic reticulum (SR) Ca(2+) content was reduced by ~55 %. Atrophic cardiac myocytes also showed a much lower frequency of spontaneous diastolic Ca(2+) sparks and a diminished systolic Ca(2+) release, even though the expression of ryanodine receptors was increased by ~30 %. In contrast, current clamp recordings revealed prolonged action potentials in endocardial as well as epicardial myocytes which were associated with a two to fourfold higher sarcolemmal Ca(2+) influx under action potential clamp. In addition, Cav1.2 subunits which form the pore of L-type Ca(2+) channels (LTCC) were upregulated in atrophic myocardium. These data suggest that in early cardiac atrophy induced by mechanical unloading, an augmented sarcolemmal Ca(2+) influx through LTCC fully compensates for a reduced systolic SR Ca(2+) release to preserve the Ca(2+) transient. This interplay involves an electrophysiological remodelling as well as changes in the expression of cardiac ion channels.

The Media and Technology Usage and Attitudes Scale: An empirical investigation.

Current approaches to measuring people's everyday usage of technology-based media and other computer-related activities have proved to be problematic as they use varied outcome measures, fail to measure behavior in a broad range of technology-related domains and do not take into account recently developed types of technology including smartphones. In the present study, a wide variety of items, covering a range of up-to-date technology and media usage behaviors. Sixty-six items concerning technology and media usage, along with 18 additional items assessing attitudes toward technology, were administered to two independent samples of individuals, comprising 942 participants. Factor analyses were used to create 11 usage subscales representing smartphone usage, general social media usage, Internet searching, e-mailing, media sharing, text messaging, video gaming, online friendships, Facebook friendships, phone calling, and watching television in addition to four attitude-based subscales: positive attitudes, negative attitudes, technological anxiety/dependence, and attitudes toward task-switching. All subscales showed strong reliabilities and relationships between the subscales and pre-existing measures of daily media usage and Internet addiction were as predicted. Given the reliability and validity results, the new Media and Technology Usage and Attitudes Scale was suggested as a method of measuring media and technology involvement across a variety of types of research studies either as a single 60-item scale or any subset of the 15 subscales.

Pathways for Learning from 3D Technology.

The purpose of this study was to find out if 3D stereoscopic presentation of information in a movie format changes a viewer's experience of the movie content. Four possible pathways from 3D presentation to memory and learning were considered: a direct connection based on cognitive neuroscience research; a connection through "immersion" in that 3D presentations could provide additional sensorial cues (e.g., depth cues) that lead to a higher sense of being surrounded by the stimulus; a connection through general interest such that 3D presentation increases a viewer's interest that leads to greater attention paid to the stimulus (e.g., "involvement"); and a connection through discomfort, with the 3D goggles causing discomfort that interferes with involvement and thus with memory. The memories of 396 participants who viewed two-dimensional (2D) or 3D movies at movie theaters in Southern California were tested. Within three days of viewing a movie, participants filled out an online anonymous questionnaire that queried them about their movie content memories, subjective movie-going experiences (including emotional reactions and "presence") and demographic backgrounds. The responses to the questionnaire were subjected to path analyses in which several different links between 3D presentation to memory (and other variables) were explored. The results showed there were no effects of 3D presentation, either directly or indirectly, upon memory. However, the largest effects of 3D presentation were on emotions and immersion, with 3D presentation leading to reduced positive emotions, increased negative emotions and lowered immersion, compared to 2D presentations.

Altered myocardial gene expression reveals possible maladaptive processes in heterozygous and homozygous cardiac myosin-binding protein C knockout mice.

Familial hypertrophic cardiomyopathy (FHC) is an autosomal dominant disease characterized by left ventricular hypertrophy (LVH) predominantly affecting the interventricular septum. Cardiac myosin-binding protein C (cMyBP-C) mutations are common causes of FHC. Gene expression profiling was performed in left ventricles of 9-week-old wild-type mice, heterozygous cMyBP-C KO mice displaying asymmetric septal hypertrophy, and homozygous mice developing eccentric LVH. Knocking out one or two cMyBP-C genes leads primarily to gene expression changes indicating an increased energy demand, activation of the JNK and p38 parts of the MAPK pathway and deactivation of the ERK part, and induction of apoptosis. Altered gene expression for processes related to cardiac structure, contractile proteins, and protein turnover was also identified. Many of the changes were more pronounced in the homozygous KO mice. These alterations point to physiological and pathological adaptations in the prehypertrophic heterozygous KO mice and the hypertrophic homozygous mice.

Effect of cardiac myosin-binding protein C on stability of the thick filament.

In contrast to skeletal muscle isoforms of myosin-binding protein C (MyBP-C), the cardiac isoform has 11 rather than 10 modules (labeled C0-C10, N-C terminus), three phosphorylation sites between C1 and C2, and 28 additional amino acids in C5. Within the C5-C10 region of cardiac MyBP-C (cMyBP-C) there are interactions between C5 and C8 as well as C7 and C10. Isolated skinned cardiac trabeculae were incubated with one of three recombinant fragments of cMyBP-C to interfere with interactions of endogenous C5. 2-10 microM C5 or C5-containing peptide fragments of cMyBP-C reversibly reduced Ca sensitivity without extracting myofibrillar protein. C2-C4 fragments had no effect. This result indicated that the region of cMyBP-C that contains C5 maintains a specific structural arrangement of myosin that helps set its contractile properties. Greater than 10 microM C5 caused skinned trabeculae to lose a substantial amount of cMyBP-C and some myosin heavy chain, resulting in irreversible decline in maximum Ca-activated force. MyBP-C appears to stabilize the structure of the thick filament and modulate the way in which myosin heads extend to the thin filament.

College students' choices of study strategies.

For a closed-book examination, study strategies that could promote deep processing correlated positively with scores but were not likely to be used by the 46 students. For an open-book, open-note examination, strategies that might have led to confusion regarding the locations of material in the textbook and lecture notes correlated negatively with scores, although they were not likely to be used by the 58 students.

Genetic testing and genetic counselling in hypertrophic cardiomyopathy: the French experience.

AIMS: A major breakthrough in the molecular genetics of hypertrophic cardiomyopathy (HCM) has made genetic testing now available in clinical practice, raising new questions about its implications, potential benefits, and the organisation of the procedure. The aim of this work was (1) to discuss the different questions related to genetic testing in HCM, and propose guidelines for the different situations, (2) to report our preliminary experience with a specific procedure. METHODS AND RESULTS: The main questions asked by patients and relatives concern presymptomatic diagnosis and prenatal counselling/diagnosis, while clinicians sometimes discuss diagnostic and prognostic testing. To take into account the complex medical and psychological implications of this new approach, we developed a specific, multidisciplinary, and multiple step procedure, including a cardiologist, a geneticist, and a psychologist. Seventy subjects were examined, including (1) 29 adults for presymptomatic diagnosis (of whom 10 left the procedure after the first visit and 19 continued, among whom six had a mutation and two experienced negative psychological impact, observed during follow up), (2) nine couples of parents for presymptomatic diagnosis in their children (the procedure was stopped after the first visit in eight and continued in one), (3) 22 couples for prenatal counselling (no prenatal genetic testing was asked for after the first visit), and (4) 10 subjects for diagnostic testing. We decided to perform no prognostic testing. CONCLUSION: Our preliminary experience confirms the complexity of the situation and suggests the necessity for a specific procedure to ensure good practice in genetic testing of HCM.

Relation between QT duration and maximal wall thickness in familial hypertrophic cardiomyopathy.

BACKGROUND: QT abnormalities have been reported in left ventricular hypertrophy and hypertrophic cardiomyopathy. OBJECTIVE: To determine the relation between left ventricular hypertrophy and increased QT interval in familial hypertrophic cardiomyopathy. METHODS: The QT interval was measured in 206 genotyped adult subjects with familial hypertrophic cardiomyopathy from 15 unrelated families carrying mutations in the beta myosin heavy chain (beta-MHC) gene (five families, n = 68) or the cardiac myosin binding protein C (MyBPC) gene (10 families, n = 138). Subjects were classified as genetically unaffected (controls, n = 112), affected with left ventricular hypertrophy (penetrants, n = 58), or affected without left ventricular hypertrophy (non-penetrants, n = 36). RESULTS: There was a significant increase in QTmax and QTmin from controls to non-penetrants and penetrants for both the MyBPC group (p < or = 0.001 and p < or = 0.001, respectively) and the beta-MHC group (p < or = 0.001 and p < or = 0.001, respectively). In the MyBPC group, the increase in the QT interval could be explained by increased left ventricular hypertrophy. In the beta-MHC group, non-penetrants had a significantly longer QTmax than controls despite the absence of left ventricular hypertrophy, and a similar QT interval to penetrants despite a lesser degree of left ventricular hypertrophy. CONCLUSIONS: In familial hypertrophic cardiomyopathy, genetically affected subjects without left ventricular hypertrophy may have a prolonged QT duration, which depends not only on the degree of left ventricular hypertrophy, when present, but also on the causative mutation.

COOH-terminal truncated human cardiac MyBP-C alters myosin filament organization.

Myosin-binding protein C (MyBP-C) is thought to play structural and/or regulatory role in striated muscles. The cardiac isoform of MyBP-C is one of the disease genes associated with familial hypertrophic cardiomyopathy and most of the mutations produce COOH truncated proteins. In order to determine the consequences of these mutations on myosin filament organization, we have characterized the effect of a 52-kDa NH2-terminal peptide of human cardiac MyBP-C on the alpha-myosin heavy chain (alpha-MyHC) filament organization. This peptide lacks the COOH-terminal MyHC-binding site and retains the two MyHC-binding domains located in the N-terminal part of MyBP-C. For this characterization, cDNA constructs (rat alpha-MyHC, full-length and truncated human cardiac MyBP-C) were transiently expressed singly or in pairwise combination in COS cells. In conformity with previous works performed on the skeletal isoform of MyBP-C, we observed that full-length cardiac MyBP-C organizes the MyHC into dense structures of uniform width. While the truncated protein is stable and can interact with MyHC in COS cells, it does not result in the same organization of sarcomeric MyHC that is seen with the full-length MyBP-C. These results suggest that the presence of truncated cardiac MyBP-C could, at least partly, disorganize the sarcomeric structure in patients with familial hypertrophic cardiomyopathy.

Homozygotes for a R869G mutation in the beta -myosin heavy chain gene have a severe form of familial hypertrophic cardiomyopathy.

UNLABELLED: Familial Hypertrophic Cardiomyopathy (FHC) is an autosomal dominant disease characterised by ventricular hypertrophy, with predominant involvement of the interventricular septum. It is a monogenic disease with a high level of genetic heterogeneity (nine genes and more than 110 mutations reported so far). We describe a family with a new R869G mutation in the beta -myosin heavy chain gene (MYH7). This mutation was found in the heterozygous status in both parents and in the homozygous status in the two children. A haplotype analysis on the MYH7 locus with microsatellite markers showed that the same haplotype is transmitted within the family, suggesting a founder effect. Clinically, the father was asymptomatic with mild left ventricular hypertrophy on echocardiography. The mother had a mild form of hypertrophic cardiomyopathy and remained asymptomatic until 60 years old when an atrial fibrillation occurred. For the two children, clinical diagnosis was performed at 12 and 8 years and atrial fibrillation occurred at 17 years. For both children, the evolution was characterized by left ventricle (LV) systolic dysfunction and a severe dilatation of the left atrium before 40 years of age. CONCLUSIONS: In this family, a new R869G mutation in the MYH7 gene was found. Interestingly, a mutation was found at the homozygous status for the first time in FHC. This finding suggests that this particular mutation is compatible with life, but for homozygous subjects, age at onset of symptoms was earlier and the disease much more severe than in the heterozygous subjects, suggesting a gene-dose effect.

First description of germline mosaicism in familial hypertrophic cardiomyopathy.

Familial hypertrophic cardiomyopathy is a genetically and phenotypically heterogeneous disease caused by mutations in seven sarcomeric protein genes. It is known to be transmitted as an autosomal dominant trait with rare de novo mutations.A French family in which two members are affected by hypertrophic cardiomyopathy was clinically screened with electrocardiography and echocardiography. Genetic analyses were performed on leucocyte DNA by haplotype analysis with microsatellite markers at the MYH7 locus and mutation screening by single strand conformation polymorphism analysis. Two subjects exhibited severe hypertrophic cardiomyopathy. A mutation in the MYH7 gene was found in exon 14 (Arg453Cys). The two affected patients were carriers of the mutation, which was not found in the circulating lymphocytes of their parents. Haplotype analysis at the MYH7 locus with two intragenic microsatellite markers (MYOI and MYOII) and the absence of the mutation in the father's sperm DNA suggested that the mutation had been inherited from the mother. However, it was not found in either her fibroblasts or hair. This is the first description of germline mosaicism shown by molecular genetic analysis in an autosomal dominant disorder and more especially in hypertrophic cardiomyopathy. This mosaicism had been inherited from the mother but did not affect her somatic cells. Such a phenomenon might account for some de novo mutations in familial hypertrophic cardiomyopathy.

COOH-terminal truncated cardiac myosin-binding protein C mutants resulting from familial hypertrophic cardiomyopathy mutations exhibit altered expression and/or incorporation in fetal rat cardiomyocytes.

Mutations in human cardiac myosin-binding protein C (cMyBP-C) gene are associated with familial hypertrophic cardiomyopathy (FHC), and most of them are predicted to produce COOH-truncated proteins. To understand the molecular mechanism(s) by which such mutations cause FHC, we analyzed (i) the accumulation of human cMyBP-C mutants in fetal rat cardiomyocytes, and (ii) the protein sequence of the human wild-type (wt) cMyBP-C by hydrophobic cluster analysis with the aim of identifying new putative myosin-binding site(s). Accumulation and sarcomeric localization of the wt protein and of four FHC-mutant cMyBP-Cs (E542Q and three COOH-truncated proteins) were studied in cardiomyocytes by immunostaining and confocal microscopy after transfection with myc-tagged constructs. We found that: (i) 10 % of the cells expressing COOH-truncated mutants exhibit an incorporation into the A-band of the sarcomere without any alteration of the myofibrillar architecture versus 76 % of those expressing the wt or E542Q mutant cMyBP-Cs (p<0.001); (ii) 90 % of the cells expressing the truncated mutants show a diffuse localization of these proteins in the cardiomyocytes, out of which 45 % exhibit a significant alteration of the sarcomeric structure (p<0.0001 versus wt); and (iii) the two shortest mutant cMyBP-Cs accumulate at very low levels in fetal rat cardiomyocytes as compared to the wt (p<0.008). Protein sequence analysis indicated that a 45-residue sequence in the NH2-terminal C0 domain of cMyBP-C exhibits a consistent homology (sequence similarity score of 42 %) with a segment of the NH2-terminal domain of myomesin, another myosin-binding protein. This result suggests that the C0 domain of human cMyBP-C contains a novel putative myosin-binding site that could account for the A-band incorporation of the truncated mutants. In addition, the faint accumulation and the diffuse localization of truncated mutants could probably be explained by a low affinity of the C0 domain for myosin. We conclude that COOH-truncated cMyBP-Cs may act as poison polypeptides that disrupt the myofibrillar architecture and result in the defects observed in FHC.

Double heterozygosity for mutations in the beta-myosin heavy chain and in the cardiac myosin binding protein C genes in a family with hypertrophic cardiomyopathy.

Familial hypertrophic cardiomyopathy is a genetically heterogeneous autosomal dominant disease, caused by mutations in several sarcomeric protein genes. So far, seven genes have been shown to be associated with the disease with the beta-myosin heavy chain (MYH7) and the cardiac myosin binding protein C (MYBPC3) genes being the most frequently involved. We performed electrocardiography (ECG) and echocardiography in 15 subjects with hypertrophic cardiomyopathy from a French Caribbean family. Genetic analyses were performed on genomic DNA by haplotype analysis with microsatellite markers at each locus involved and mutation screening by single strand conformation polymorphism analysis. Based on ECG and echocardiography, eight subjects were affected and presented a classical phenotype of hypertrophic cardiomyopathy. Two new mutations cosegregating with the disease were found, one located in the MYH7 gene exon 15 (Glu483Lys) and the other in the MYBPC3 gene exon 30 (Glu1096 termination codon). Four affected subjects carried the MYH7 gene mutation, two the MYBPC3 gene mutation, and two were doubly heterozygous for the two mutations. The doubly heterozygous patients exhibited marked left ventricular hypertrophy, which was significantly greater than in the other affected subjects. We report for the first time the simultaneous presence of two pathological mutations in two different genes in the context of familial hypertrophic cardiomyopathy. This double heterozygosity is not lethal but is associated with a more severe phenotype.

Downsizing, reengineering and patient safety: numbers, newness and resultant risk.

Downsizing and reengineering are facts of life in contemporary healthcare organizations. In most instances, these organizational changes are undertaken in an attempt to increase productivity or cut operational costs with results measured in these terms. Less often considered are potential detrimental effects on patient safety or strategies, which might be used to minimize these risks.