Articles: function.
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Anesthesia and analgesia · Nov 2024
Using Bibliometric Data to Define and Understand Publishing Network Equity in Anesthesiology.
Anesthesiology departments and professional organizations increasingly recognize the need to embrace diverse membership to effectively care for patients, to educate our trainees, and to contribute to innovative research. 1 Bibliometric analysis uses citation data to determine the patterns of interrelatedness within a scientific community. Social network analysis examines these patterns to elucidate the network's functional properties. Using these methodologies, an analysis of contemporary scholarly work was undertaken to outline network structure and function, with particular focus on the equity of node and graph-level connectivity patterns. ⋯ The highly modular network structure indicates dense author communities. Extracommunity cooperation is limited, previously demonstrated to negatively impact novel scientific work. 2 , 3 Inequitable node influence is seen at both author and institution level, notably an imbalance of information transfer and disparity in connectivity patterns. There is an association between network influence, article publication (authors), and NIH funding (institutions). Female and minority authors are inequitably represented among the most influential authors. This baseline bibliometric analysis provides an opportunity to direct future network connections to more inclusively share information and integrate diverse perspectives, properties associated with increased academic productivity. 3 , 4.
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International Consensus Criteria for Pediatric Sepsis and Septic Shock RELEASE DATE: January 21, 2024 PRIOR VERSION(S): International Pediatric Sepsis Consensus Conference: Definitions for Sepsis and Organ Dysfunction in Pediatrics (2005) DEVELOPER: Society of Critical Care Medicine FUNDING SOURCE: Society of Critical Care Medicine (grant R01HD105939 from the National Institute of Child Health and Human Development) TARGET POPULATION: Children with sepsis and septic shock.
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Neuropeptide Y (NPY) Y2 receptor (Y2) antagonist BIIE0246 can both inhibit and facilitate nociception. The authors hypothesized that Y2 function depends on inflammation or nerve injury status. ⋯ The authors conclude that Y2 at central terminals of primary afferent neurons provides tonic inhibition of mechanical and cold nociception and itch. This switches to the promotion of mechanical and thermal hyperalgesia in models of acute and chronic postsurgical and neuropathic pain, perhaps due to an increase in the population of Y2 that effectively couples to G-proteins. These results support the development of Y2 antagonists for the treatment of chronic postsurgical and neuropathic pain.
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Acta Anaesthesiol Scand · Nov 2024
Observational StudyHealth status and quality of life before critical illness: Northern Finland Birth Cohort 1966 study.
Previous findings support the claim intensive care unit (ICU) patients have a higher rate of comorbidities and reduction of health- and functional status compared with the normal population. ⋯ In this study examining previously un-hospitalized patients, the main factors associated with future critical illness were neurological comorbidities, malignancy, alcohol misuse, smoking, low maximum muscle strength, and less frequent physical exercise compared with those with hospitalization not requiring ICU admission.
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Myofascial trigger points (MTrPs) are the primary etiological characteristics of chronic myofascial pain syndrome. Receptor tyrosine kinases (RTKs) are associated with signal transduction in the central mechanisms of chronic pain, but the role of RTKs in the peripheral mechanisms of MTrPs remains unclear. The current study aimed to identify RTKs expression in MTrPs and elucidate the molecular mechanisms through which platelet-derived growth factor receptor-α (PDGFR-α) induces contraction knots and inflammatory pain-like behavior in a rat model of myofascial trigger points. ⋯ COL1A1-induced phosphorylation of PDGFR-α and the subsequent activation of the JAK2/STAT3 pathway may induce dysfunctional muscle contraction and increased nociception at MTrPs.