Effects of etomidate versus propofol for total intravenous anaesthesia on postoperative quality of recovery in patients undergoing day-case laparoscopic cholecystectomy: protocol for a multicentre, randomised controlled non-inferiority trial.

Background: The choice of anaesthetic agents may influence specific aspects of postoperative recovery, such as haemodynamic stability, recovery times and the incidence of adverse events, in patients undergoing day-case laparoscopic cholecystectomy. Propofol is widely used in total intravenous anaesthesia (TIVA) for its favourable recovery profile, while etomidate, valued for its haemodynamic stability, is less commonly used due to concerns about adrenal suppression. This study aims to compare etomidate-based and propofol-based TIVA on postoperative quality of recovery in patients undergoing day-case laparoscopic cholecystectomy, hypothesising that etomidate is non-inferior to propofol.

Persistent depressive-symptom trajectories predict conversion from mild cognitive impairment to Alzheimer's disease: A longitudinal ADNI study.

Background: Depressive symptoms are increasingly recognized as a modifiable risk factor for Alzheimer's disease (AD). However, most studies have assessed these symptoms at a single time point or within overlapping symptom-outcome windows, limiting temporal inference.

Methods: We analyzed 397 participants with baseline mild cognitive impairment (MCI) from the Alzheimer's Disease Neuroimaging Initiative.

A Genome-wide study on the genetic and causal effects of smoking in neurodegeneration.

Background: Smoking represents the largest preventable risk factor for human health, yet previous studies have failed to establish conclusive evidence regarding the causal relationship between smoking and neurodegenerative diseases. This study employs genetic correlation and Mendelian randomization analyses to investigate the potential association between smoking and neurodegenerative disorders.

Methods: This study analyzed summary data from genome-wide association studies (GWAS) on smoking and neurodegenerative diseases.

ω-3 PUFAs Alleviate GJ-Cx43 Uncoupling Induced by Long-Term Isoflurane Exposure by Activating the Wnt/β-catenin Signaling Pathway in Astrocytes.

Isoflurane, a widely used anesthetic, has raised concerns due to its potential neurotoxic effects, including oxidative stress and astrocytic gap junction (GJ) dysfunction. This study investigates whether ω-3 polyunsaturated fatty acids (PUFAs), particularly docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), can mitigate these effects by activating the Wnt/β-catenin signaling pathway. Using primary astrocytes, we found that long-term isoflurane exposure uncoupled GJ-Cx43, increased reactive oxygen species (ROS), and inhibited Wnt/β-catenin signaling.

Temporal patterns of cognitive decline after hypertension onset among middle-aged and older adults in China.

Individuals with prevalent hypertension are at an increased risk of developing dementia and tend to exhibit lower cognitive function. However, the magnitude of cognitive change following the onset of new hypertension remains uncertain. A cohort of 7949 adults aged 45 and older without hypertension at baseline was followed prospectively for 7 years.

Mitochondria-targeting Bimetallic Cluster Nanozymes Alleviate Neuropathic Pain Through Scavenging ROS and Reducing Inflammation.

Neuropathic pain is a significant public health concern. Inflammatory mediators and reactive oxygen species (ROS) are recognized as primary contributors to pain perception. In this study, a mitochondria-targeted modification of bimetallic cluster nanozyme (TPP-Au-Ru) is developed.

Deciphering the CREB-NR2B axis: Unraveling the crosstalk of insulin and TGF-β signalling in ameliorating postoperative cognitive dysfunction.

Postoperative cognitive dysfunction (POCD) is a significant postoperative complication, particularly in the elderly, linked to inflammation-mediated neural dysfunction. Insulin resistance and disruptions in transforming growth factor beta (TGF-β) signalling are associated with cognitive decline in aging, yet their roles in POCD are not fully understood. Here, we demonstrated that both insulin and TGF-β pathways were disrupted in POCD mouse models, with recombinant insulin and TGF-β treatments improving cognitive outcomes.

Novel drug targets for delirium based on genetic causality.

Background: Effective treatment and prevention of delirium remain challenging, largely due to the limited efficiency in identifying and validating drug targets. To address this gap, we performed a systematic Mendelian Randomization (MR) study of the druggable genome to identify potential therapeutic targets for delirium.

Methods: To identify therapeutic targets for delirium, we conducted MR and colocalization analyses using cis-eQTL data (31,684 blood samples and 1387 brain samples) and genome-wide association study (GWAS) data for delirium (discovery cohort N = 431,880; validation cohort N = 403,037).

The role of clock control of DRP1 activity involved in postoperative cognitive dysfunction.

Postoperative cognitive dysfunction (POCD) is a prevalent clinical issue following anesthesia and surgery. The onset of POCD, which is closely linked to circadian rhythm disturbance in previous studies, yet the underlying mechanism remains elusive. There is increasing evidence showed that mitochondrial architecture is coordinated by the circadian clock which DRP1 playing a crucial role.

Microglia mediate memory dysfunction via excitatory synaptic elimination in a fracture surgery mouse model.

Cognitive impairment is a common issue among human patients undergoing surgery, yet the neural mechanism causing this impairment remains unidentified. Surgical procedures often lead to glial cell activation and neuronal hypoexcitability, both of which are known to contribute to postoperative cognitive dysfunction (POCD). However, the role of neuron-glia crosstalk in the pathology of POCD is still unclear.

Recombinant chitinase-3-like protein 1 alleviates learning and memory impairments via M2 microglia polarization in postoperative cognitive dysfunction mice.

JOURNAL/nrgr/04.03/01300535-202509000-00032/figure1/v/2024-11-05T132919Z/r/image-tiff Postoperative cognitive dysfunction is a severe complication of the central nervous system that occurs after anesthesia and surgery, and has received attention for its high incidence and effect on the quality of life of patients. To date, there are no viable treatment options for postoperative cognitive dysfunction.

LanCL1 protects developing neurons from long-term isoflurane anesthesia-induced neurotoxicity.

Research has revealed that prolonged or repeated exposure to isoflurane, a common general anesthetic, can lead to cognitive and behavioral deficiencies, particularly in early life. The brain contains a wealth of LanCL1, an antioxidant enzyme that is thought to mitigate oxidative stress. Nevertheless, its precise function in mammals remains uncertain.

HuR promotes triglyceride synthesis and intestinal fat absorption.

Triacylglyceride (TAG) synthesis in the small intestine determines the absorption of dietary fat, but the underlying mechanisms remain to be further studied. Here, we report that the RNA-binding protein HuR (ELAVL1) promotes TAG synthesis in the small intestine. HuR associates with the 3' UTR of Dgat2 mRNA and intron 1 of Mgat2 pre-mRNA.

Long-term isoflurane anesthesia induces cognitive deficits via AQP4 depolarization mediated blunted glymphatic inflammatory proteins clearance.

Perioperative neurocognitive disorders (PND) refer to cognitive deterioration that occurs after surgery or anesthesia. Prolonged isoflurane exposure has potential neurotoxicity and induces PND, but the mechanism is unclear. The glymphatic system clears harmful metabolic waste from the brain.

Carbon quantum dots assisted BiFeO@BiOBr S-scheme heterojunction enhanced peroxymonosulfate activation for the photocatalytic degradation of imidacloprid under visible light: Performance, mechanism and biotoxicity.

A novel S-scheme heterojunction photocatalyst carbon quantum dots (CQDs)/BiFeO/BiOBr (CBB) was synthesized via a facile hydrothermal method, which was highly effective in activating peroxymonosulfate (PMS) to photodegrade imidacloprid (IMD) (one of the typical neonicotinoid insecticides (NEOs)) under visible light irradiation. Based on the physicochemical and photoelectrochemical analysis, the super photocatalytic performance of the CBB photocatalyst was contributed to the enhanced separation and transfer of photogenerated electrons (e) and holes (h), the activation of PMS by reactive species, and the wider light absorption range induced by CQDs. Moreover, the intermediate products and possible photodegradation pathways of IMD were confirmed through high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS) detection and density functional theory (DFT) calculations.

PPARα agonist fenofibrate prevents postoperative cognitive dysfunction by enhancing fatty acid oxidation in mice.

Background: Due to high rates of incidence and disability, postoperative cognitive dysfunction (POCD) currently receives a lot of clinical attention. Disturbance of fatty acid oxidation is a potential pathophysiological manifestation underlying POCD. Peroxisome proliferator-activated receptor α (PPARα) is a significant transcription factor of fatty acid oxidation that facilitates the transfer of fatty acids into the mitochondria for oxidation.

Nicotinamide mononucleotide pretreatment improves long-term isoflurane anesthesia-induced cognitive impairment in mice.

Postoperative cognitive dysfunction (POCD) is characterized by impaired cognitive function following general anesthesia and surgery. Oxidative stress is a significant pathophysiological manifestation underlying POCD. Previous studies have reported that the decline of nicotinamide adenine dinucleotide (NAD) -dependent sirtuin 1 (SIRT1) contributes to the activation of oxidative stress.

Long-term sevoflurane exposure relieves stress-enhanced fear learning and anxiety in PTSD mice.

Objectives: Post-traumatic stress disorder (PTSD) is characterized by recurrent episodes of severe anxiety after exposure to traumatic events. It is believed that these episodes are triggered at least in part by environmental stimuli associated with the precipitating trauma through classical conditioning, termed conditioned fear. However, traditional methods of conditioned fear memory extinction are frequently ineffective for PTSD treatment due to the contribution of non-associative sensitization caused by trauma.

Activating ryanodine receptor improves isoflurane-induced cognitive dysfunction.

Background: Postoperative cognitive dysfunction (POCD) is characterized by impaired learning and memory. 6 h duration isoflurane anesthesia is an important factor to induce POCD, and the dysfunction of ryanodine receptor (RyR) in the hippocampus may be involved in this process. We investigated the expression of RyR3 in the hippocampus of mice after 6-h duration isoflurane anesthesia, as well as the improvement of RyR receptor agonist caffeine on POCD mice, while attempting to identify the underlying molecular mechanism.

Transformation of graphene oxide affects photodegradation of imidacloprid in the aquatic environment: Mechanism and implication.

Graphene oxide (GO) is a representative novel carbonaceous nanomaterial, and neonicotinoid insecticides (NEOs) are currently the insecticides with the highest market share in the world. Their widespread application deservedly leads to their release to the environment. Thus, the complex interactions of these two types of organic compounds have attracted extensive attention.

Mild acute stress prevents the memory impairment induced by long-term isoflurane anesthesia.

Objectives: Long-term isoflurane anesthesia exposure could result in postoperative cognitive dysfunction (POCD). Preoperative stress is also reported to be a risk factor of POCD. However, it is unknown whether acute stress could impair memory after long-term isoflurane anesthesia.

Inhibition of the integrated stress response reverses oxidative stress damage-induced postoperative cognitive dysfunction.

Postoperative cognitive dysfunction (POCD) is a common complication following anesthesia and surgery that might lead to a decline in learning and memory. Oxidative stress damage is one of the pathogenic mechanisms underlying POCD. Recent studies had shown that the integrated stress response (ISR) is closely related to oxidative stress.

Enhancement of astrocytic gap junctions Connexin43 coupling can improve long-term isoflurane anesthesia-mediated brain network abnormalities and cognitive impairment.

Aim: Astrocytes are connected by gap junctions Connexin43 (GJs-Cx43) forming an extensive intercellular network and maintain brain homeostasis. Perioperative neurocognitive disorder (PND) occurs frequently after anesthesia/surgery and worsens patient outcome, but the neural circuit mechanisms remain unclear. This study aimed to determine the effects of the GJs-Cx43-mediated astrocytic network on PND and ascertain the underlying neural circuit mechanism.