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23,852 result(s) for "King, J"
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Lobster
Takes us on a journey through the history, biology, and culture of lobsters, including the creature's economic and environmental status worldwide. He describes the evolution of technologies to capture these creatures and addresses the ethics of boiling them alive. Along the way, King also explores the salacious lobster palaces of the 1920s, the animal's thousand-year status as an aphrodisiac, and how the lobster has inspired numerous artists, writers, and thinkers including Aristotle, Dickens, Thoreau, Dali, and Woody Allen.
Multimodal assessment improves neuroprognosis performance in clinically unresponsive critical-care patients with brain injury
Accurately predicting functional outcomes for unresponsive patients with acute brain injury is a medical, scientific and ethical challenge. This prospective study assesses how a multimodal approach combining various numbers of behavioral, neuroimaging and electrophysiological markers affects the performance of outcome predictions. We analyzed data from 349 patients admitted to a tertiary neurointensive care unit between 2009 and 2021, categorizing prognoses as good, uncertain or poor, and compared these predictions with observed outcomes using the Glasgow Outcome Scale–Extended (GOS-E, levels ranging from 1 to 8, with higher levels indicating better outcomes). After excluding cases with life-sustaining therapy withdrawal to mitigate the self-fulfilling prophecy bias, our findings reveal that a good prognosis, compared with a poor or uncertain one, is associated with better one-year functional outcomes (common odds ratio (95% CI) for higher GOS-E: OR = 14.57 (5.70–40.32), P  < 0.001; and 2.9 (1.56–5.45), P  < 0.001, respectively). Moreover, increasing the number of assessment modalities decreased uncertainty (OR = 0.35 (0.21–0.59), P  < 0.001) and improved prognostic accuracy (OR = 2.72 (1.18–6.47), P  = 0.011). Our results underscore the value of multimodal assessment in refining neuroprognostic precision, thereby offering a robust foundation for clinical decision-making processes for acutely brain-injured patients. ClinicalTrials.gov registration: NCT04534777 . Multimodal approaches combining various numbers of behavioral, neuroimaging and electrophysiological markers improves neuroprognosis performance in clinically unresponsive critical-care patients.
Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function
In neurological diseases, the actions of microglia, the resident myeloid cells of the CNS parenchyma, may diverge from, or intersect with, those of recruited monocytes to drive immune-mediated pathology. However, defining the precise roles of each cell type has historically been impeded by the lack of discriminating markers and experimental systems capable of accurately identifying them. Our ability to distinguish microglia from monocytes in neuroinflammation has advanced with single-cell technologies, new markers and drugs that identify and deplete them, respectively. Nevertheless, the focus of individual studies on particular cell types, diseases or experimental approaches has limited our ability to connect phenotype and function more widely and across diverse CNS pathologies. Here, we critically review, tabulate and integrate the disease-specific functions and immune profiles of microglia and monocytes to provide a comprehensive atlas of myeloid responses in viral encephalitis, demyelination, neurodegeneration and ischemic injury. In emphasizing the differential roles of microglia and monocytes in the severe neuroinflammatory disease of viral encephalitis, we connect inflammatory pathways common to equally incapacitating diseases with less severe inflammation. We examine these findings in the context of human studies and highlight the benefits and inherent limitations of animal models that may impede or facilitate clinical translation. This enables us to highlight common and contrasting, non-redundant and often opposing roles of microglia and monocytes in disease that could be targeted therapeutically.
Ahab's rolling sea : a natural history of Moby-Dick
\"This book asks the questions of whether Moby-Dick-the first novel to represent vast metaphorical and spiritual implications for our own behavior through ocean animals- closely conveyed the understanding of whales in the nineteenth century, and what was twisted merely for the fictional purposes. Richard King lays bare the background to Moby-Dick by moving through the voyage of the Pequod, exploring topics in marine biology, oceanography, and the science of navigation as Ishmael raises them in the novel\"-- Provided by publisher.
Cochrane Rapid Reviews Methods Group offers evidence-informed guidance to conduct rapid reviews
To develop methods guidance to support the conduct of rapid reviews (RRs) produced within Cochrane and beyond, in response to requests for timely evidence syntheses for decision-making purposes including urgent health issues of high priority. Interim recommendations were informed by a scoping review of the underlying evidence, primary methods studies conducted, and a survey sent to 119 representatives from 20 Cochrane entities, who were asked to rate and rank RR methods across stages of review conduct. Discussions among those with expertise in RR methods further informed the list of recommendations with accompanying rationales provided. Based on survey results from 63 respondents (53% response rate), 26 RR methods recommendations are presented for which there was a high or moderate level of agreement or scored highest in the absence of such agreement. Where possible, how recommendations align with Cochrane methods guidance for systematic reviews is highlighted. The Cochrane Rapid Reviews Methods Group offers new, interim guidance to support the conduct of RRs. Because best practice is limited by the lack of currently available evidence for some RR methods shortcuts taken, this guidance will need to be updated as additional abbreviated methods are evaluated.
Sailing alone : a history
Sailing on a boat by yourself out at sea and out of sight of land can be exhilarating or terrifying, compelling or tedious - sometimes it can be all of these things just in one morning. It is an adventure at odds with our normal, sociable lives, carried out floating on a medium wholly inimical to our existence. But the deep ocean is also a remarkable place on which to think. Richard King's engaging and curious book is about the debt we owe to solo sailors: women and men, young and old, who have set out alone. Spending weeks and months alone, slowly, quietly, and close to the ocean surface is to create the world's largest laboratory: an endlessly changing, capricious and startling place in which to observe oneself, the weather, the stars and myriad sea creatures, from the tiniest to the most massive and threatening.
Activating AMP-activated protein kinase (AMPK) slows renal cystogenesis
Renal cyst development and expansion in autosomal dominant polycystic kidney disease (ADPKD) involves both fluid secretion and abnormal proliferation of cyst-lining epithelial cells. The chloride channel of the cystic fibrosis transmembrane conductance regulator (CFTR) participates in secretion of cyst fluid, and the mammalian target of rapamycin (mTOR) pathway may drive proliferation of cyst epithelial cells. CFTR and mTOR are both negatively regulated by AMP-activated protein kinase (AMPK). Metformin, a drug in wide clinical use, is a pharmacological activator of AMPK. We find that metformin stimulates AMPK, resulting in inhibition of both CFTR and the mTOR pathways. Metformin induces significant arrest of cystic growth in both in vitro and ex vivo models of renal cystogenesis. In addition, metformin administration produces a significant decrease in the cystic index in two mouse models of ADPKD. Our results suggest a possible role for AMPK activation in slowing renal cystogenesis as well as the potential for therapeutic application of metformin in the context of ADPKD.
Acute effects of exercise on appetite, ad libitum energy intake and appetite-regulatory hormones in lean and overweight/obese men and women
Background: Acute exercise does not elicit compensatory changes in appetite parameters in lean individuals; however, less is known about responses in overweight individuals. This study compared the acute effects of moderate-intensity exercise on appetite, energy intake and appetite-regulatory hormones in lean and overweight/obese individuals. Methods: Forty-seven healthy lean ( n =22, 11 females; mean (s.d.) 37.5 (15.2) years; 22.4 (1.5) kg m −2 ) and overweight/obese ( n =25, 11 females; 45.0 (12.4) years, 29.2 (2.9) kg m −2 ) individuals completed two, 8 h trials (exercise and control). In the exercise trial, participants completed 60 min treadmill exercise (59 (4)% peak oxygen uptake) at 0–1 h and rested thereafter while participants rested throughout the control trial. Appetite ratings and concentrations of acylated ghrelin, peptide YY (PYY) and glucagon-like peptide-1 (GLP-1) were measured at predetermined intervals. Standardised meals were consumed at 1.5 and 4 h and an ad libitum buffet meal was provided at 7 h. Results: Exercise suppressed appetite (95% confidence interval (CI) −3.1 to −0.5 mm, P =0.01), and elevated delta PYY (95% CI 10 to 17 pg ml −1 , P <0.001) and GLP-1 (95% CI 7 to 10 pmol l −1 , P <0.001) concentrations. Delta acylated ghrelin concentrations (95% CI −5 to 3 pg ml −1 , P =0.76) and ad libitum energy intake (95% CI −391 to 346 kJ, P =0.90) were similar between trials. Subjective and hormonal appetite parameters and ad libitum energy intake were similar between lean and overweight/obese individuals ( P ⩾0.27). The exercise-induced elevation in delta GLP-1 was greater in overweight/obese individuals (trial-by-group interaction P =0.01), whereas lean individuals exhibited a greater exercise-induced increase in delta PYY (trial-by-group interaction P <0.001). Conclusions: Acute moderate-intensity exercise transiently suppressed appetite and increased PYY and GLP-1 in the hours after exercise without stimulating compensatory changes in appetite in lean or overweight/obese individuals. These findings underscore the ability of exercise to induce a short-term energy deficit without any compensatory effects on appetite regardless of weight status.