Κυριακή 21 Μαΐου 2017
Dynamic chromatin technologies: from individual molecules to epigenomic regulation in cells
A full understanding of chromatin in diverse cellular processes requires the consideration of its dynamics, but most standard chromatin assays provide only a static snapshot. This Review describes various emerging methods for probing chromatin dynamics across a wide range of temporal and spatial scales, and discusses the resulting biological insights.
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Alzheimer’s disease: the state of the art in resting-state magnetoencephalography
Worldwide, approximately 35.6 million people are estimated to have dementia (WHO, 2012). Dementia prevalence ranges between 1.6% and 6.4% in subjects over age 60 and increases disproportionally with advancing age (Ferri et al., 2005). Alzheimer's disease (AD) is the most common form of dementia and is known to be accompanied by abnormal neuronal activity that has been linked to amyloid beta depositions between neurons (Bero et al 2011; Walker and Jucker, 2011). Although studies have indicated several potentially modifiable risk factors for AD (Norton et al., 2014), at this moment, no curative interventions are available.
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Compensatory and decompensatory alterations in cardiomyocyte Ca2+ dynamics in hearts with diastolic dysfunction following aortic banding
Key points
- At the cellular level cardiac hypertrophy causes remodelling, leading to changes in ionic channel, pump and exchanger densities and kinetics.
- Previous studies have focused on quantifying changes in channels, pumps and exchangers without quantitatively linking these changes with emergent cellular scale functionality.
- Two biophysical cardiac cell models were created, parameterized and validated and are able to simulate electrophysiology and calcium dynamics in myocytes from control sham operated rats and aortic-banded rats exhibiting diastolic dysfunction.
- The contribution of each ionic pathway to the calcium kinetics was calculated, identifying the L-type Ca2+ channel and sarco/endoplasmic reticulum Ca2+ATPase as the principal regulators of systolic and diastolic Ca2+, respectively.
- Results show that the ability to dynamically change systolic Ca2+, through changes in expression of key Ca2+ modelling protein densities, is drastically reduced following the aortic banding procedure; however the cells are able to compensate Ca2+ homeostasis in an efficient way to minimize systolic dysfunction.
Abstract
Elevated left ventricular afterload leads to myocardial hypertrophy, diastolic dysfunction, cellular remodelling and compromised calcium dynamics. At the cellular scale this remodelling of the ionic channels, pumps and exchangers gives rise to changes in the Ca2+ transient. However, the relative roles of the underlying subcellular processes and the positive or negative impact of each remodelling mechanism are not fully understood. Biophysical cardiac cell models were created to simulate electrophysiology and calcium dynamics in myocytes from control rats (SHAM) and aortic-banded rats exhibiting diastolic dysfunction. The model parameters and framework were validated and the fitted parameters demonstrated to be unique for explaining our experimental data. The contribution of each ionic pathway to the calcium kinetics was calculated, identifying the L-type Ca2+ channel (LCC) and the sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) as the principal regulators of systolic and diastolic Ca2+, respectively. In the aortic banding model, the sensitivity of systolic Ca2+ to LCC density and diastolic Ca2+ to SERCA density decreased by 16-fold and increased by 23%, respectively, relative to the SHAM model. The energy cost of ionic homeostasis is maintained across the two models. The models predict that changes in ionic pathway densities in compensated aortic banding rats maintain Ca2+ function and efficiency. The ability to dynamically alter systolic function is significantly diminished, while the capacity to maintain diastolic Ca2+ is moderately increased.
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Significance and Nature of Bystander Responses Induced by Various Agents
Publication date: Available online 21 May 2017
Source:Mutation Research/Reviews in Mutation Research
Author(s): Neha Verma, Ashu Bhan Tiku
Bystander effects in a biological system are the responses shown by non-targeted neighbouring cells/tissues/organisms. These responses are triggered by factors released from targeted cells when exposed to a stress inducing agent. The biological response to stress inducing agents is complex, owing to the diversity of mechanisms and pathways activated in directly targeted and bystander cells. These responses are highly variable and can be either beneficial or hazardous depending on the cell lines tested, dose of agent used, experimental end points and time course selected. Recently non-targeted cells have even been reported to rescue the directly exposed cells by releasing protective signals that might be induced by non-targeted bystander responses. The nature of bystander signal/s is not yet clear. However, there are evidences suggesting involvement of ROS, RNS, protein factors and even DNA molecules leading to the activation of a number of signaling pathways. These can act independently or in a cascade, to induce events leading to changes in gene expression patterns that could elicit detrimental or beneficial effects.Many review articles on radiation induced bystander responses have been published. However, to the best of our knowledge, a comprehensive review on bystander responses induced by other genotoxic chemicals and stress inducing agents has not been published so far. Therefore, the aim of the present review is to give an overview of the literature on different aspects of bystander responses: agents that induce these responses, factors that can modulate bystander responses and the mechanisms involved.
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Communicative Access Measures for Stroke: Development and Evaluation of a Quality Improvement Tool
Publication date: Available online 20 May 2017
Source:Archives of Physical Medicine and Rehabilitation
Author(s): Aura Kagan, Nina Simmons-Mackie, J. Charles Victor, Melodie T.Y. Chan
Objective1) To develop a systems level quality improvement tool targeting communicative access to information and decision-making for stroke patients with language disorders and 2) to evaluate the resulting tool – Communicative Access Measures for Stroke (CAMS).DesignSurvey development and evaluation was in line with accepted guidelines, and included item generation and reduction, survey formatting and composition, pre-testing, pilot-testing, and reliability assessment.SettingDevelopment and evaluation were carried out in hospital and community agency settings.ParticipantsThe project utilized a convenience sample of 31 participants for the survey development, and 63 participants for the CAMS reliability study (broken down into 6 administrators/managers, 32 frontline staff, 25 participants with aphasia). The number of eligible participants invited to the reliability study included 45 community-based organizations in Ontario as well as 4400 individuals from communities of practice.InterventionsNot applicable.Main Outcome Measure(s)Data were analyzed using kappa statistics and intraclass correlations for each item score on all surveys.ResultsA tool, the Communicative Access Measures for Stroke (CAMS), comprising three surveys, was developed for health facilities from the perspectives of 1) administrators/policy makers, 2) staff/frontline health care providers, and 3) patients with aphasia (using a communicatively accessible version). Reliability for items on the CAMS Administrator and CAMS Staff surveys was moderate to high (Kappa/ICCs ranging from 0.54 to 1.00). As expected, reliability was lower for the CAMS Patient survey with most items having ICCs between 0.4 and 0.6.Conclusion(s): These findings suggest that CAMS may provide useful quality improvement information for health care facilities with an interest in improving care for patients with stroke and aphasia.
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Are you smarter than the average paramedic? Test your EMS smarts!
Take our 10-question quiz to test your knowledge, then share your results and challenge your colleagues to prove their expertise
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