1,964 research outputs found
Global child and family-centered care fellowship, education and mentorship for pediatric healthcare professionals: A literature review
Child- and family-centered care (FCC) is increasingly accepted and implemented to optimize the healthcare experience for patients, their families, and healthcare professionals. Standish Foundation for Children, a 501(c)(3) non-profit, has designed and piloted a fellowship to educate pediatric healthcare professionals in FCC & psychosocial care via an inquiry and mentorship model in Tbilisis, Georgia. This review aimed to evaluate and synthesize existing literature on psychosocial and FCC mentorship for pediatric healthcare professionals in four parts: ongoing need, effects on healthcare professionals, effects on children and their families and/or caregivers, and in cross-country healthcare settings. Reviewers searched open-source databases for articles in English published between 2010 and 2021. Opportunities for psychosocial and FCC skills development is both desired and needed by pediatric healthcare professionals, a viewpoint shared by families of pediatric patients. Existing mentorship models varied in design but overall improved provider confidence and ability to provide FCC in clinical settings. Some support for these interventions improving patient and family clinical outcomes is documented, although further research is necessary. In cross-country healthcare settings with varying resource levels, clinical mentorship in general can improve quality and delivery of care without requiring entirely new approaches. This review supports psychosocial mentorship models as an effective tool for child- and family-centered care delivery. Future research into long-term professional and patient outcomes, FCC impact on pediatric patients with non-traditional family units, and in cross-country settings is recommended to gain a more comprehensive understanding of how FCC can improve quality of healthcare.
Experience Framework
This article is associated with the Staff & Provider Engagement lens of The Beryl Institute Experience Framework (https://www.theberylinstitute.org/ExperienceFramework). Access other PXJ articles related to this lens. Access other resources related to this lens
TMCO1 is a novel target for cancer chemotherapy
Transmembrane and coiled-coil domains 1 (TMCO1) is a protein of 22 KDa highly conserved in amino acid sequence among mammalian species and functions as an endoplasmic reticulum (ER) Ca2+load-activated Ca2+channel. Homozygous frameshift mutation in TMCO1 causes distinctive craniofacial dysmorphism, skeletal anomalies, and mental retardation. However, its physiological functions are largely unknown. In this study, we found that TMCO1 was co-localized with microtubules as determined by immunohistostaining and a co-sedimentation assay. Interestingly, TMCO1 was highly expressed in the invasive front of high grade lung cancer and metastatic cancer cells of clinical specimens. To further investigate the biological role of TMCO1 in lung cancer, we knocked it down in A549 cells, a human lung adenocarcinoma cell line, by using shRNA lentiviral particles. Disruption of TMCO1 in the cells resulted in delayed microtubule polymerization and remarkably increased acetylation of -tubulin. In addition, A549 cells lacking of TMCO1 grew significantly slower than the control cells. Taken together, our findings suggest that TMCO1 may be a therapeutic target for lung cancer treatment.https://engagedscholarship.csuohio.edu/u_poster_2018/1031/thumbnail.jp
The effect of cognitive fatigue on prefrontal cortex correlates of neuromuscular fatigue in older women
BACKGROUND: As the population of adults aged 65 and above is rapidly growing, it is crucial to identify physical and cognitive limitations pertaining to daily living. Cognitive fatigue has shown to adversely impact neuromuscular function in younger adults, however its impact on neuromuscular fatigue, and associated brain function changes, in older adults is not well understood. The aim of the study was to examine the impact of cognitive fatigue on neuromuscular fatigue and associated prefrontal cortex (PFC) activation patterns in older women. METHODS: Eleven older (75.82 (7.4) years) females attended two sessions and performed intermittent handgrip exercises at 30Â % maximum voluntary contraction (MVC) until voluntary exhaustion after a 60-min control (watching documentary) and 60-min cognitive fatigue (performing Stroop Color Word and 1-Back tests) condition. Dependent measures included endurance time, strength loss, PFC activity (measured using fNIRS), force fluctuations, muscle activity, cardiovascular responses, and perceived discomfort. RESULTS: Participants perceived greater cognitive fatigue after the 60-min cognitive fatigue condition when compared to the control condition. While neuromuscular fatigue outcomes (i.e., endurance time, strength loss, perceived discomfort), force fluctuations, and muscle activity were similar across both the control and cognitive fatigue conditions, greater decrements in PFC activity during neuromuscular fatigue development after the cognitive fatigue condition were observed when compared to the control condition. CONCLUSION: Despite similar neuromuscular outcomes, cognitive fatigue was associated with blunted PFC activation during the handgrip fatiguing exercise that may be indicative of neural adaptation with aging in an effort to maintain motor performance. Examining the relationship between cognitive fatigue and neuromuscular output by imaging other motor-related brain regions are needed to provide a better understanding of age-related compensatory adaptations to perform daily tasks that involve some levels of cognitive demand and physical exercise, especially when older adults experience them sequentially
Examining Time to Evacuate Dynamically Activated Aircraft Hazard Areas
The growth in launch and reentry operations in the National Airspace System (NAS) presents the Federal Aviation Administration (FAA) with the challenge of integrating them more efficiently while also minimizing effects on other NAS users and maintaining safety. Currently, to maintain safety and account for unforeseen events such as vehicle breakup, the FAA segregates large amounts of airspace, called Aircraft Hazard Areas (AHAs), from traditional NAS users during launch and reentry operations. In order to minimize effects on NAS users, some AHAs during reentry are dynamically activated only if an unexpected event occurs. If a dynamic AHA is activated, then aircraft would have to evacuate from the AHA before debris reaches the NAS. The FAA can determine how long it takes for debris to reach the NAS (60,000 feet and below), but it does not have a capability to statistically examine how long it would take aircraft to evacuate these AHAs while considering different aircraft performance parameters, airspace traffic patterns, and controllers with different response times. The FAA could also implement smaller AHAs for launches by using dynamic AHAs, but only if they can better understand the time needed to evacuate them. The MITRE Corporation’s Center for Advanced Aviation System Development (MITRE CAASD) is developing a flexible, fast-time modeling and simulation capability that examines the time to evacuate these AHAs and quantifies how different factors (e.g., air traffic control notification delay, traffic orientation, and traffic density) affect those times. This paper describes this modeling capability and demonstrates potential use cases
Halo-model Analysis of the Clustering of Photometrically Selected Galaxies from SDSS
We measure the angular 2-point correlation functions of galaxies in a volume
limited, photometrically selected galaxy sample from the fifth data release of
the Sloan Digital Sky Survey. We split the sample both by luminosity and galaxy
type and use a halo-model analysis to find halo-occupation distributions that
can simultaneously model the clustering of all, early-, and late-type galaxies
in a given sample. Our results for the full galaxy sample are generally
consistent with previous results using the SDSS spectroscopic sample, taking
the differences between the median redshifts of the photometric and
spectroscopic samples into account. We find that our early- and late- type
measurements cannot be fit by a model that allows early- and late-type galaxies
to be well-mixed within halos. Instead, we introduce a new model that
segregates early- and late-type galaxies into separate halos to the maximum
allowed extent. We determine that, in all cases, it provides a good fit to our
data and thus provides a new statistical description of the manner in which
early- and late-type galaxies occupy halos.Comment: Accepted to MNRAS 11 pages, 6 figure
Differences in Startle and Prepulse Inhibition in Contactin-associated Protein-like 2 Knock-out Rats are Associated with Sex-specific Alterations in Brainstem Neural Activity
The contactin-associated protein-like 2 (CNTNAP2) gene encodes for the CASPR2 protein, which plays an essential role in neurodevelopment. Mutations in CNTNAP2 are associated with neurodevelopmental disorders, including autism spectrum disorder and schizophrenia. Rats with a loss of function mutation in the Cntnap2 gene show increased acoustic startle response (ASR) and decreased prepulse inhibition (PPI). The neural basis of this altered auditory processing in Cntnap2 knock-out rats is currently unknown. Auditory brainstem recordings previously revealed no differences between the genotypes. The next step is to investigate brainstem structures outside of the primary auditory pathway that mediate ASR and PPI, which are the pontine reticular nucleus (PnC) and pedunculopontine tegmentum (PPTg), respectively. Multi-unit responses from the PnC and PPTg in vivo of the same rats revealed sex-specific effects of loss of CASPR2 expression on PnC activity, but no effects on PPTg activity. Female Cntnap
Evolution of the Clustering of Photometrically Selected SDSS Galaxies
We measure the angular auto-correlation functions (w) of SDSS galaxies
selected to have photometric redshifts 0.1 < z < 0.4 and absolute r-band
magnitudes Mr < -21.2. We split these galaxies into five overlapping redshift
shells of width 0.1 and measure w in each subsample in order to investigate the
evolution of SDSS galaxies. We find that the bias increases substantially with
redshift - much more so than one would expect for a passively evolving sample.
We use halo-model analysis to determine the best-fit
halo-occupation-distribution (HOD) for each subsample, and the best-fit models
allow us to interpret the change in bias physically. In order to properly
interpret our best-fit HODs, we convert each halo mass to its z = 0 passively
evolved bias (bo), enabling a direct comparison of the best-fit HODs at
different redshifts. We find that the minimum halo bo required to host a galaxy
decreases as the redshift decreases, suggesting that galaxies with Mr < -21.2
are forming in halos at the low-mass end of the HODs over our redshift range.
We use the best-fit HODs to determine the change in occupation number divided
by the change in mass of halos with constant bo and we find a sharp peak at bo
~ 0.9 - corresponding to an average halo mass of ~ 10^12Msol/h. We thus present
the following scenario: the bias of galaxies with Mr < -21.2 decreases as the
Universe evolves because these galaxies form in halos of mass ~ 10^12Msol/h
(independent of redshift), and the bias of these halos naturally decreases as
the Universe evolves.Comment: 17 pages, 14 figures, matches version accepted for publication in
MNRA
RHOA GTPase Controls YAP-Mediated EREG Signaling in Small Intestinal Stem Cell Maintenance
RHOA, a founding member of the Rho GTPase family, is critical for actomyosin dynamics, polarity, and morphogenesis in response to developmental cues, mechanical stress, and inflammation. In murine small intestinal epithelium, inducible RHOA deletion causes a loss of epithelial polarity, with disrupted villi and crypt organization. In the intestinal crypts, RHOA deficiency results in reduced cell proliferation, increased apoptosis, and a loss of intestinal stem cells (ISCs) that mimic effects of radiation damage. Mechanistically, RHOA loss reduces YAP signaling of the Hippo pathway and affects YAP effector epiregulin (EREG) expression in the crypts. Expression of an active YAP (S112A) mutant rescues ISC marker expression, ISC regeneration, and ISC-associated Wnt signaling, but not defective epithelial polarity, in RhoA knockout mice, implicating YAP in RHOA-regulated ISC function. EREG treatment or active β-catenin Catnblox(ex3) mutant expression rescues the RhoA KO ISC phenotypes. Thus, RHOA controls YAP-EREG signaling to regulate intestinal homeostasis and ISC regeneration
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