Popular weight-loss drugs like Wegovy may raise risk of complications under anesthesia
Après avoir intégré ce principe au signalement préoccupant actuel, plutôt que de présumer que les agonistes des récepteurs du GLP-1 sontdangereuxÀ notre avis, nous sommes arrivés au moment où le principe de précaution devrait être invoqué et nous devrions considérer les éléments suivants pour toute la patientèle périopératoire prenant des agonistes des récepteurs du GLP-1 :: envisager...
: envisager de consulter un·e endocrinologue au sujet des risques et des avantages d’interrompre la prise du médicament pour au moins trois demi-vies avant l’intervention prévue.Il est peu probable qu’une prolongation du temps de jeûne soit nécessaire chez les personnes prenant des agonistes des récepteurs du GLP-1, car le jeûne a des effets périopératoires négatifsdu jeûne chez cette patientèle.
Les considérations ci-dessus ne sont pas des lignes directrices de pratique clinique, car nous ne disposons actuellement pas de suffisamment de données probantes pour générer des lignes directrices. Plutôt, ce sont des éléments basés sur l’opinion que les prestataires d’anesthésie devraient prendre en compte.
Compte tenu de l’utilisation croissante des agonistes des récepteurs du GLP-1 à l’échelle mondiale et de la disponibilité de formulations orales, s’il existe un risque accru d’aspiration associé à ces médicaments, on pourrait s’attendre à ce que l’incidence du problème s’aggrave considérablement au cours des prochaines années.
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Lysosomal acidification dysfunction in microglia: an emerging pathogenic mechanism of neuroinflammation and neurodegeneration - Journal of NeuroinflammationMicroglia are the resident innate immune cells in the brain with a major role in orchestrating immune responses. They also provide a frontline of host defense in the central nervous system (CNS) through their active phagocytic capability. Being a professional phagocyte, microglia participate in phagocytic and autophagic clearance of cellular waste and debris as well as toxic protein aggregates, which relies on optimal lysosomal acidification and function. Defective microglial lysosomal acidification leads to impaired phagocytic and autophagic functions which result in the perpetuation of neuroinflammation and progression of neurodegeneration. Reacidification of impaired lysosomes in microglia has been shown to reverse neurodegenerative pathology in Alzheimer’s disease. In this review, we summarize key factors and mechanisms contributing to lysosomal acidification impairment and the associated phagocytic and autophagic dysfunction in microglia, and how these defects contribute to neuroinflammation and neurodegeneration. We further discuss techniques to monitor lysosomal pH and therapeutic agents that can reacidify impaired lysosomes in microglia under disease conditions. Finally, we propose future directions to investigate the role of microglial lysosomal acidification in lysosome–mitochondria crosstalk and in neuron–glia interaction for more comprehensive understanding of its broader CNS physiological and pathological implications.
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All you need to know about Harry Styles' rumoured new girlfriend Taylor RussellHarry Styles has been spotted looking cosy with new girlfriend, Canadian actress Taylor Russell, at the press night of her new play The Effect at the National Theatre in London
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Lysosomal acidification dysfunction in microglia: an emerging pathogenic mechanism of neuroinflammation and neurodegeneration - Journal of NeuroinflammationMicroglia are the resident innate immune cells in the brain with a major role in orchestrating immune responses. They also provide a frontline of host defense in the central nervous system (CNS) through their active phagocytic capability. Being a professional phagocyte, microglia participate in phagocytic and autophagic clearance of cellular waste and debris as well as toxic protein aggregates, which relies on optimal lysosomal acidification and function. Defective microglial lysosomal acidification leads to impaired phagocytic and autophagic functions which result in the perpetuation of neuroinflammation and progression of neurodegeneration. Reacidification of impaired lysosomes in microglia has been shown to reverse neurodegenerative pathology in Alzheimer’s disease. In this review, we summarize key factors and mechanisms contributing to lysosomal acidification impairment and the associated phagocytic and autophagic dysfunction in microglia, and how these defects contribute to neuroinflammation and neurodegeneration. We further discuss techniques to monitor lysosomal pH and therapeutic agents that can reacidify impaired lysosomes in microglia under disease conditions. Finally, we propose future directions to investigate the role of microglial lysosomal acidification in lysosome–mitochondria crosstalk and in neuron–glia interaction for more comprehensive understanding of its broader CNS physiological and pathological implications.
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All you need to know about Harry Styles' rumoured new girlfriend Taylor RussellHarry Styles has been spotted looking cosy with new girlfriend, Canadian actress Taylor Russell, at the press night of her new play The Effect at the National Theatre in London
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metaSpectraST: an unsupervised and database-independent analysis workflow for metaproteomic MS/MS data using spectrum clustering - MicrobiomeBackground The high diversity and complexity of the microbial community make it a formidable challenge to identify and quantify the large number of proteins expressed in the community. Conventional metaproteomics approaches largely rely on accurate identification of the MS/MS spectra to their corresponding short peptides in the digested samples, followed by protein inference and subsequent taxonomic and functional analysis of the detected proteins. These approaches are dependent on the availability of protein sequence databases derived either from sample-specific metagenomic data or from public repositories. Due to the incompleteness and imperfections of these protein sequence databases, and the preponderance of homologous proteins expressed by different bacterial species in the community, this computational process of peptide identification and protein inference is challenging and error-prone, which hinders the comparison of metaproteomes across multiple samples. Results We developed metaSpectraST, an unsupervised and database-independent metaproteomics workflow, which quantitatively profiles and compares metaproteomics samples by clustering experimentally observed MS/MS spectra based on their spectral similarity. We applied metaSpectraST to fecal samples collected from littermates of two different mother mice right after weaning. Quantitative proteome profiles of the microbial communities of different mice were obtained without any peptide-spectrum identification and used to evaluate the overall similarity between samples and highlight any differentiating markers. Compared to the conventional database-dependent metaproteomics analysis, metaSpectraST is more successful in classifying the samples and detecting the subtle microbiome changes of mouse gut microbiomes post-weaning. metaSpectraST could also be used as a tool to select the suitable biological replicates from samples with wide inter-individual variation. Conclusions metaSpectraST enables rapid profiling of
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What is Post-Operative Cognitive Decline?Post-operative cognitive decline, or dysfunction (POCD), is a recognized clinical phenomenon in which patients experience lasting cognitive impairment for some time following anesthesia. Read more here: cognition health disease operation
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