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"Simpson, John"
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In the forests of the night : encounters in Peru with terrorism, drug-running and military oppression
In one of the most dangerous and thrilling investigations of his distinguished career, world-renowned journalist John Simpson journeyed into Peru's heart of darkness on the trail of Abimael Guzman, who, at the time of his arrest, was the leader of the Shining Path guerrilla movement. This vivid, disturbing book reveals how violence breeds violence in a police state whose economy revolves around cocaine, and how, amid all the casual torture and slaughter, certain brave individuals are prepared to put their lives at risk to tell the truth. John Simpson's expedition into the heart of South America is structured in two parts. First, he traveled to the rainforests of Brazil, where he visited the Ashaninca tribe of Indians in the Amazonian jungle, had a harrowing experience when his canoe capsized in a piranha-infested river, and was persuaded to sample a native hallucinogenic drink called dime. The second and most hazardous part of his journey was to Peru, a country that provides more than 70 percent of the raw material of the entire world's cocaine supply. There Simpson penetrated a hinterland of violence and despair. Simpson spoke to families whose children had been taken away in the middle of the night by the Peruvian army and were never seen or heard from again. He met with people whose lives had been torn apart by Shining Path terrorists. Helped by a few brave friends who risked their lives to provide information and guidance, Simpson and his BBC documentary team were introduced to men and women who testified against army officers involved in the smuggling of coca to Colombia. This is an inspiring story, written with all the color and pace of a thriller, but showing the hard facts about one of the world's most brutal regimes and its equally brutal opponents.
A human model of bilateral pulmonary vein sampling to assess the effects of one-lung ventilation on neutrophil function
Neutrophil activation drives lung complications after cardiopulmonary bypass (CPB). Evidence suggests the healthy, ventilated lung may beneficially re-condition pro-inflammatory neutrophils. However, evidence in humans is lacking, due to a paucity of good models. CPB with simultaneous central venous and bilateral pulmonary vein sampling provides an opportunity to model effects of one-lung ventilation. The study's primary objectives were to establish a model of intra-operative, bilateral pulmonary vein sampling and to determine whether neutrophil function differed after passing through inflated or deflated lungs.
Seventeen patients having \"on pump\" coronary artery bypass grafting (CABG) with one-lung ventilation (in two cohorts with tidal volume 2ml kg-1 and FiO2 0.21, or tidal volume 4 ml kg-1 and FiO2 0.5 respectively) were recruited. Cohort 1 consisted of 9 patients (7 male, median age 62.0 years) and Cohort 2 consisted of 8 male patients (median age 65.5 years). Recruitment was via prospective screening of scheduled elective and non-elective CABG procedures with cardiopulmonary bypass. Each patient had five blood samples taken-central venous blood pre-operatively; central venous blood pre-CPB; central venous blood post-CPB; pulmonary venous blood draining the ventilated lung post-CPB; and pulmonary venous blood draining the deflated lung post-CPB. Neutrophil phagocytosis and priming status were quantified. Plasma cytokines were measured.
Phagocytosis and priming were not significantly different in neutrophils returning from the ventilated lung as compared to the non-ventilated lung. Plasma IL-6, IL-8 and IL-10 were significantly elevated by CPB.
The intra-operative, bilateral pulmonary vein sampling model provides unique opportunities to assess biological effects of interventions to one lung, with the other lung acting as an internal control. Single-lung ventilation during CPB had no significant effects on neutrophil function.
Journal Article
We chose to speak of war and strife : the world of the foreign correspondent
In corners of the globe where fault-lines erupt into bloodshed and civil war, foreign correspondents have, for hundreds of years, been engaged in uncovering the latest news and--despite obstacles bureaucratic, political, and violent--reporting it by whatever means available. It's a working life that is difficult, exciting, and undeniably glamorous. These stories celebrate an endangered tradition. Where once despatches were trusted to the hands of a willing sea-captain, telegraph operator, or stranger in an airport queue prepared to spirit a can of undeveloped film back to London, today the digital realm has transformed the relaying of the news--even if the work of gathering it in the field has changed little.
Book
Voltage collapse in complex power grids
A large-scale power grid’s ability to transfer energy from producers to consumers is constrained by both the network structure and the nonlinear physics of power flow. Violations of these constraints have been observed to result in voltage collapse blackouts, where nodal voltages slowly decline before precipitously falling. However, methods to test for voltage collapse are dominantly simulation-based, offering little theoretical insight into how grid structure influences stability margins. For a simplified power flow model, here we derive a closed-form condition under which a power network is safe from voltage collapse. The condition combines the complex structure of the network with the reactive power demands of loads to produce a node-by-node measure of grid stress, a prediction of the largest nodal voltage deviation, and an estimate of the distance to collapse. We extensively test our predictions on large-scale systems, highlighting how our condition can be leveraged to increase grid stability margins.
A power grid is constrained by both its nonlinear physics and network structure, and violations of these constraints may lead to voltage collapse blackouts, which have been studied mostly numerically. Here the authors derive a closed-form condition to provide an analytic test for voltage collapse.
Journal Article
The world of Achaemenid Persia : history, art and society in Iran and the ancient Near East : proceedings of a conference at the British Museum 29th September-1st October 2005
\"A Major Guide To and an explanation of the whole Phenomenon of the Persian Empire, from the acknowledged experts.\" -- Book Jacket.
BOOK
Delayed induction of type I and III interferons mediates nasal epithelial cell permissiveness to SARS-CoV-2
The nasal epithelium is a plausible entry point for SARS-CoV-2, a site of pathogenesis and transmission, and may initiate the host response to SARS-CoV-2. Antiviral interferon (IFN) responses are critical to outcome of SARS-CoV-2. Yet little is known about the interaction between SARS-CoV-2 and innate immunity in this tissue. Here we apply single-cell RNA sequencing and proteomics to a primary cell model of human nasal epithelium differentiated at air-liquid interface. SARS-CoV-2 demonstrates widespread tropism for nasal epithelial cell types. The host response is dominated by type I and III IFNs and interferon-stimulated gene products. This response is notably delayed in onset relative to viral gene expression and compared to other respiratory viruses. Nevertheless, once established, the paracrine IFN response begins to impact on SARS-CoV-2 replication. When provided prior to infection, recombinant IFNβ or IFNλ1 induces an efficient antiviral state that potently restricts SARS-CoV-2 viral replication, preserving epithelial barrier integrity. These data imply that the IFN-I/III response to SARS-CoV-2 initiates in the nasal airway and suggest nasal delivery of recombinant IFNs to be a potential chemoprophylactic strategy.
The innate immune response in epithelial cells after SARS-CoV-2 infection is not fully understood. Here the authors use human air-liquid interface culture and show single cell transcription changes and delayed type I Interferon responses after SARS-CoV-2 infection compared with other respiratory viruses.
Journal Article
The Oxford dictionary of modern slang
Features slang words and expressions from throughout the English-speaking world, providing a stonking good read for all word lovers and English students.
Book
Regulation of Transforming Growth Factor-β1–driven Lung Fibrosis by Galectin-3
Abstract
Rationale
Idiopathic pulmonary fibrosis (IPF) is a chronic dysregulated response to alveolar epithelial injury with differentiation of epithelial cells and fibroblasts into matrix-secreting myofibroblasts resulting in lung scaring. The prognosis is poor and there are no effective therapies or reliable biomarkers. Galectin-3 is a β-galactoside binding lectin that is highly expressed in fibrotic tissue of diverse etiologies.
Objectives
To examine the role of galectin-3 in pulmonary fibrosis.
Methods
We used genetic deletion and pharmacologic inhibition in well-characterized murine models of lung fibrosis. Further mechanistic studies were performed in vitro and on samples from patients with IPF.
Measurements and Main Results
Transforming growth factor (TGF)-β and bleomycin-induced lung fibrosis was dramatically reduced in mice deficient in galectin-3, manifest by reduced TGF-β1–induced EMT and myofibroblast activation and collagen production. Galectin-3 reduced phosphorylation and nuclear translocation of β-catenin but had no effect on Smad2/3 phosphorylation. A novel inhibitor of galectin-3, TD139, blocked TGF-β–induced β-catenin activation in vitro and in vivo and attenuated the late-stage progression of lung fibrosis after bleomycin. There was increased expression of galectin-3 in the bronchoalveolar lavage fluid and serum from patients with stable IPF compared with nonspecific interstitial pneumonitis and controls, which rose sharply during an acute exacerbation suggesting that galectin-3 may be a marker of active fibrosis in IPF and that strategies that block galectin-3 may be effective in treating acute fibrotic exacerbations of IPF.
Conclusions
This study identifies galectin-3 as an important regulator of lung fibrosis and provides a proof of principle for galectin-3 inhibition as a potential novel therapeutic strategy for IPF.
Journal Article
