An important question during the intensive care of patients with subarachnoid hemorrhage and craniocerebral trauma is the evaluation of the cerebral autoregulation (CA). The so called Aaslid-Test is a standard method which allows the cerebral autoregulation to be classified. As the results under repetitive conditions show a high variation, it has not been yet possible to draw statistically proved conclusions concerning the performance of the CA. To improve the test results the measuring conditions are discussed and systematized. The algorithms of the Aaslid-Test have been implemented to an online measuring system. The error bandwidth has been estimated. To avoid systematically occurring errors an enhanced measuring protocol is provided.
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http://dx.doi.org/10.1515/bmte.2002.47.s1b.592 | DOI Listing |
Int J Physiol Pathophysiol Pharmacol
December 2024
Department of Food Science and Nutrition, Nara Women's University Kita-Uoya Nishimachi, Nara 630-8506, Japan.
Metabolic syndrome is a group of pathological disorders increasing the risk of serious diseases including cardiovascular disease, stroke, type 2 diabetes. Global widespread of the metabolic syndrome has put a heavy social burden. Interestingly, a crucial link between the metabolic syndrome and a psychiatric disorder may frequently coexist, in which certain shared mechanisms might play a role for the pathogenesis.
View Article and Find Full Text PDFFluids Barriers CNS
January 2025
Department of Biomedical Engineering, Air Force Medical University, Xi'an, China.
Background: Acute and critical neurological diseases are often accompanied with elevated intracranial pressure (ICP), leading to insufficient cerebral perfusion, which may cause severe secondary lesion. Existing ICP monitoring techniques often fail to effectively meet the demand for real-time noninvasive ICP monitoring and warning. This study aimed to explore the use of electrical impedance tomography (EIT) to provide real-time early warning of elevated ICP by observing cerebral perfusion.
View Article and Find Full Text PDFAnn Nutr Metab
January 2025
Department of Translational Medical Science, University of Naples Federico II, Napoli, Italy.
Background: Knowledge of the complex interplay between gut microbiota and human health is gradually increasing as it has just recently been a field of such great interest.
Summary: Recent studies have reported that communities of microorganisms inhabiting the gut influence the immune system through cellular responses and shape many physiological and pathophysiological aspects of the body, including muscle and bone metabolism (formation and resorption). Specifically, the gut microbiota affects skeletal homeostasis through changes in host metabolism, the immune system, hormone secretion, and the gut-brain axis.
Proc Natl Acad Sci U S A
January 2025
National Institute of Biological Sciences, Beijing 102206, China.
Sleep need accumulates during waking and dissipates during sleep to maintain sleep homeostasis (process S). Besides the regulation of daily (baseline) sleep amount, homeostatic sleep regulation commonly refers to the universal phenomenon that sleep deprivation (SD) causes an increase of sleep need, hence, the amount and intensity of subsequent recovery sleep. The central regulators and signaling pathways that govern the baseline and homeostatic sleep regulations in mammals remain unclear.
View Article and Find Full Text PDFMetab Brain Dis
January 2025
Hepato-Neuro Laboratory, Centre Hospitalier de l'Université de Montréal (CRCHUM), Université de Montréal, 900, Rue Saint-Denis - Pavillon R, R08.422, Montréal (Québec), H2X 0A9, Canada.
Sarcopenia and hepatic encephalopathy (HE) are complications of chronic liver disease (CLD), which negatively impact clinical outcomes. Hyperammonemia is considered to be the central component in the pathogenesis of HE, however ammonia's toxic effects have also been shown to impinge on extracerebral organs including the muscle. Our aim was to investigate the effect of attenuating hyperammonemia with ornithine phenylacetate (OP) on muscle mass loss and associated molecular mechanisms in rats with CLD.
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