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"Reynolds, James"
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Robert Lepage/Ex Machina : revolutions in theatrical space
\"Robert Lepage/Ex Machina: Revolutions in Theatrical Space provides an ideal introduction to one of our most innovative companies - and a much-needed and timely reappraisal of Lepage's oeuvre. International, interdisciplinary and intercultural to the core, Ex Machina have negotiated some of the most complex creative and cultural challenges of our time. This book maps the story of that journey by analysing the full spectrum of their richly varied work. Through a comprehensive historiography of productions since 1994, Robert Lepage/Ex Machina offers a detailed picture of the relationship between director and company, while connecting Ex Machina to culturally specific features of Quâebec, and its theatre. This book reveals for the first time how overlooked aspects of creativity and culture shaped the company's early work, while installing a dynamic interplay between director and company that would spark a unique and ongoing evolution of praxis. Central to this re-evaluation of practice is the book's identification of an architectural aesthetic at the heart of Ex Machina's work, an aesthetic which provides its artistic and political centres of gravity. Moreover, this architectural aesthetic powers the emergence of concrete narrative as a new and distinctive mode of theatrical storytelling - uniting story and space, body and technology, content and form - and demanding that we discover the politics of these performances in the energetic gestures of theatre design, and space itself. Drawing on extensive interviews with Lepage, Ex Machina personnel and collaborative partners, Robert Lepage/Ex Machina calls upon us to revise both our creative and critical perceptions of this vital and distinctive practice\"-- Provided by publisher.
Book
Astrocytes mediate neurovascular signaling to capillary pericytes but not to arterioles
Active neurons increase their energy supply by dilating nearby arterioles and capillaries to increase blood flow, but the mechanisms underlying neurovascular coupling are debated. In this paper, the authors show that different calcium-dependent signaling pathways regulate blood flow at the level of capillary pericytes and arteriole smooth muscle.
Active neurons increase their energy supply by dilating nearby arterioles and capillaries. This neurovascular coupling underlies blood oxygen level–dependent functional imaging signals, but its mechanism is controversial. Canonically, neurons release glutamate to activate metabotropic glutamate receptor 5 (mGluR5) on astrocytes, evoking Ca
2+
release from internal stores, activating phospholipase A2 and generating vasodilatory arachidonic acid derivatives. However, adult astrocytes lack mGluR5, and knockout of the inositol 1,4,5-trisphosphate receptors that release Ca
2+
from stores does not affect neurovascular coupling. We now show that buffering astrocyte Ca
2+
inhibits neuronally evoked capillary dilation, that astrocyte [Ca
2+
]
i
is raised not by release from stores but by entry through ATP-gated channels, and that Ca
2+
generates arachidonic acid via phospholipase D2 and diacylglycerol lipase rather than phospholipase A2. In contrast, dilation of arterioles depends on NMDA receptor activation and Ca
2+
-dependent NO generation by interneurons. These results reveal that different signaling cascades regulate cerebral blood flow at the capillary and arteriole levels.
Journal Article
Ranibizumab versus laser therapy for the treatment of very low birthweight infants with retinopathy of prematurity (RAINBOW): an open-label randomised controlled trial
Despite increasing worldwide use of anti-vascular endothelial growth factor agents for treatment of retinopathy of prematurity (ROP), there are few data on their ocular efficacy, the appropriate drug and dose, the need for retreatment, and the possibility of long-term systemic effects. We evaluated the efficacy and safety of intravitreal ranibizumab compared with laser therapy in treatment of ROP.
This randomised, open-label, superiority multicentre, three-arm, parallel group trial was done in 87 neonatal and ophthalmic centres in 26 countries. We screened infants with birthweight less than 1500 g who met criteria for treatment for retinopathy, and randomised patients equally (1:1:1) to receive a single bilateral intravitreal dose of ranibizumab 0·2 mg or ranibizumab 0·1 mg, or laser therapy. Individuals were stratified by disease zone and geographical region using computer interactive response technology. The primary outcome was survival with no active retinopathy, no unfavourable structural outcomes, or need for a different treatment modality at or before 24 weeks (two-sided α=0·05 for superiority of ranibizumab 0·2 mg against laser therapy). Analysis was by intention to treat. This trial is registered with ClinicalTrials.gov, NCT02375971.
Between Dec 31, 2015, and June 29, 2017, 225 participants (ranibizumab 0·2 mg n=74, ranibizumab 0·1 mg n=77, laser therapy n=74) were randomly assigned. Seven were withdrawn before treatment (n=1, n=1, n=5, respectively) and 17 did not complete follow-up to 24 weeks, including four deaths in each group. 214 infants were assessed for the primary outcome (n=70, n=76, n=68, respectively). Treatment success occurred in 56 (80%) of 70 infants receiving ranibizumab 0·2 mg compared with 57 (75%) of 76 infants receiving ranibizumab 0·1 mg and 45 (66%) of 68 infants after laser therapy. Using a hierarchical testing strategy, compared with laser therapy the odds ratio (OR) of treatment success following ranibizumab 0·2 mg was 2·19 (95% Cl 0·99–4·82, p=0·051), and following ranibizumab 0·1 mg was 1·57 (95% Cl 0·76–3·26); for ranibizumab 0·2 mg compared with 0·1 mg the OR was 1·35 (95% Cl 0·61–2·98). One infant had an unfavourable structural outcome following ranibizumab 0·2 mg, compared with five following ranibizumab 0·1 mg and seven after laser therapy. Death, serious and non-serious systemic adverse events, and ocular adverse events were evenly distributed between the three groups.
In the treatment of ROP, ranibizumab 0·2 mg might be superior to laser therapy, with fewer unfavourable ocular outcomes than laser therapy and with an acceptable 24-week safety profile.
Novartis.
Journal Article
The egg book : see how baby animals hatch, step by step!
Watch every remarkable stage of baby animals hatching from their eggs. Many animals start life inside eggs and this book explores these magical capsules in detail, with stunning photographs of the moment the creatures emerge. Featuring more than 20 animals - including a penguin, a tortoise, and even a slug - this book documents the moment of hatching step by step. Learn how birds, reptiles, amphibians, fish, and invertebrates hatch from their eggs, as well as what happens inside an egg's shell. See the biggest egg in the world hatching, find out which animals have jellylike eggs, and which animals' egg cases are known as 'mermaids' purses'. With expert information and jaw-dropping photography, 'The Egg Book' is the ideal gift for any child with a love of nature and baby animals.
BOOK
Astrocytes regulate brain extracellular pH via a neuronal activity-dependent bicarbonate shuttle
Brain cells continuously produce and release protons into the extracellular space, with the rate of acid production corresponding to the levels of neuronal activity and metabolism. Efficient buffering and removal of excess H
+
is essential for brain function, not least because all the electrogenic and biochemical machinery of synaptic transmission is highly sensitive to changes in pH. Here, we describe an astroglial mechanism that contributes to the protection of the brain milieu from acidification. In vivo and in vitro experiments conducted in rodent models show that at least one third of all astrocytes release bicarbonate to buffer extracellular H
+
loads associated with increases in neuronal activity. The underlying signalling mechanism involves activity-dependent release of ATP triggering bicarbonate secretion by astrocytes via activation of metabotropic P2Y
1
receptors, recruitment of phospholipase C, release of Ca
2+
from the internal stores, and facilitated outward HCO
3
−
transport by the electrogenic sodium bicarbonate cotransporter 1, NBCe1. These results show that astrocytes maintain local brain extracellular pH homeostasis via a neuronal activity-dependent release of bicarbonate. The data provide evidence of another important metabolic housekeeping function of these glial cells.
Several mechanisms contribute to the maintenance of constant extracellular pH, essential for normal brain function. Here the authors show that astrocytes help to control local brain pH via a neuronal activity-dependent release of bicarbonate by the electrogenic sodium bicarbonate cotransporter 1.
Journal Article
Disentangling astroglial physiology with a realistic cell model in silico
Electrically non-excitable astroglia take up neurotransmitters, buffer extracellular K
+
and generate Ca
2+
signals that release molecular regulators of neural circuitry. The underlying machinery remains enigmatic, mainly because the sponge-like astrocyte morphology has been difficult to access experimentally or explore theoretically. Here, we systematically incorporate multi-scale, tri-dimensional astroglial architecture into a realistic multi-compartmental cell model, which we constrain by empirical tests and integrate into the NEURON computational biophysical environment. This approach is implemented as a flexible astrocyte-model builder ASTRO. As a proof-of-concept, we explore an in silico astrocyte to evaluate basic cell physiology features inaccessible experimentally. Our simulations suggest that currents generated by glutamate transporters or K
+
channels have negligible distant effects on membrane voltage and that individual astrocytes can successfully handle extracellular K
+
hotspots. We show how intracellular Ca
2+
buffers affect Ca
2+
waves and why the classical Ca
2+
sparks-and-puffs mechanism is theoretically compatible with common readouts of astroglial Ca
2+
imaging.
Astrocytes have gained increasing attention for their roles in regulating neural circuits via neurotransmitter uptake, K + buffering, and ability to signal via Ca
2 +
transients. Here, the authors develop a computational modelling environment for astrocytes, akin to the NEURON environment, called ASTRO.
Journal Article
100 things to know about : numbers, computers & coding
When was the webcam invented and why? Do imaginary numbers exist? What is fuzzy logic? Find the answers these questions about the amazing world of numbers, computers and coding, along with loads of other curious, amazing and mind-boggling facts, in this eye-catching book that is absolutely bursting with information.
BOOK
Population-based prevalence of fetal alcohol spectrum disorder in Canada
Background
Fetal alcohol spectrum disorder (FASD) is one of the most disabling potential outcomes of prenatal alcohol exposure. The population-based prevalence of FASD among the general population of Canada was unknown. The objective of this study was to determine the population-based prevalence of FASD among elementary school students, aged 7 to 9 years, in the Greater Toronto Area (GTA) in Ontario, Canada.
Methods
This screening study used a cross-sectional, observational design utilizing active case ascertainment, along with retrospective collection of prenatal alcohol exposure information. Data collection involved two phases. Phase I consisted of taking growth measurements, a dysmorphology examination, and obtaining a history of behavioral and/or learning problems. Phase II consisted of a neurodevelopmental assessment, maternal interview, and behavioral observations/ratings by parents/guardians. Final diagnostic screening conclusions were made by consensus by a team of experienced multidisciplinary experts during case conferences, using the 2005 Canadian guidelines for FASD diagnosis. The prevalence of FASD was estimated, taking into consideration the selection rate, which was used to account for students who dropped out or were lost to follow-up during each phase. Monte Carlo simulations were employed to derive the confidence interval (CI) for the point estimates.
Results
A total of 2555 students participated. A total of 21 cases of suspected FASD were identified. The prevalence of FASD was estimated to be 18.1 per 1000, or about 1.8%. Using a less conservative approach (sensitivity analysis), the prevalence of FASD was estimated to be 29.3 per 1000, or about 2.9%. Therefore, the population-based prevalence of FASD is likely to range between 2 and 3% among elementary school students in the GTA in Ontario, Canada.
Conclusions
This study provides the first population-based estimate of the prevalence of FASD in Canada. The estimate is approximately double or possibly even triple previous crude estimates. FASD prevalence exceeds that of other common birth defects such as Down’s syndrome, spina bifida, trisomy 18, as well as autism spectrum disorder in Canada. More effective prevention strategies targeting alcohol use during pregnancy, surveillance of FASD, and timely interventions and support to individuals with FASD and their families are urgently needed.
Journal Article