Articles: human.
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Curr Opin Anaesthesiol · Feb 2025
ReviewThe climate crisis - actions to prioritize for anaesthesiologists.
Climate change is the biggest threat to human health and survival in the twenty-first century. Emissions associated with healthcare contribute to climate change and there are many personal and professional actions that can reduce carbon emissions. This review highlights why action is necessary and what anaesthetists and healthcare workers can do. ⋯ This article shows that, while patient safety and quality of care must remain healthcare's top priority, considering the climate implications of care is part of that duty. Many actions that reduce the carbon impact of care simultaneously improve the quality of care and reduce financial cost. More research into sustainable healthcare is needed. Departments and hospitals and must create environments in which climate conversations are welcomed and can result in positive advancements.
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We examined de-functionalization and temporal functional recovery of C-nociceptor evoked pain after topical 8% capsaicin applied for 4 consecutive days. ⋯ Sinusoidal electrical stimulation can still activate small diameter axons desensitized to heat after 4 consecutive days of topical 8% capsaicin application and reveals differential temporal functional regeneration of C-nociceptor sub-types. Electrical sinusoidal stimulation may detect such axons that no longer respond to heat stimuli in neuropathic skin.
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Biomarkers are becoming crucial in ever more medical tasks and are proposed to change medicine in profound ways. By biomarking ever more attributes of human life, they tend to blur the distinction between health and disease and come to characterize life as such. Not only do biomarkers strongly influence the professional conception of disease by pervading ever more diagnoses, but they also impact patients' experience of illness. To manage how biomarkers influence patients, professionals, and societies, we urgently need to move from identifying potentially relevant biomarkers to determine their meaning and value to individuals, professionals, and public health.
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Translational models of the sensitized pain system are needed to progress the understanding of involved mechanisms. In this study, long-term potentiation was used to develop a mechanism-based large-animal pain model. Event-related potentials to electrical stimulation of the ulnar nerve were recorded by intracranial recordings in pigs, 3 weeks before, immediately before and after, and 3 weeks after peripheral high-frequency stimulation (HFS) applied to the ulnar nerve in the right forelimb (7 pigs) or in control animals (5 pigs). ⋯ The relative increase in N1 30 minutes after HFS and the degree of mechanical hyperalgesia 2 weeks post-HFS was correlated ( P < 0.033). These results show for the first time that the pig HFS model resembles the human HFS model closely where the profile of sensitization is comparable. Interestingly, the degree of sensitization was associated with the cortical signs of hyperexcitability at HFS induction.
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Na v 1.9 is of interest to the pain community for a number of reasons, including the human mutations in the gene encoding Na v 1.9, SCN11a , that are associated with both pain and loss of pain phenotypes. However, because much of what we know about the biophysical properties of Na v 1.9 has been learned through the study of rodent sensory neurons, and there is only 76% identity between human and rodent homologs of SCN11a , there is reason to suggest that there may be differences in the biophysical properties of the channels in human and rodent sensory neurons, and consequently, the contribution of these channels to the control of sensory neuron excitability, if not pain. Thus, the purpose of this study was to characterize Na v 1.9 currents in human sensory neurons and compare the properties of these currents with those in rat sensory neurons recorded under identical conditions. ⋯ However, we noted a number of potentially important differences between the currents in human and rat sensory neurons including a lower threshold for activation, higher threshold for inactivation, slower deactivation, and faster recovery from slow inactivation. Human Na v 1.9 was inhibited by inflammatory mediators, whereas rat Na v 1.9 was potentiated. Our results may have implications for the role of Na v 1.9 in sensory, if not nociceptive signaling.