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Recent research has highlighted the indispensability of traditional molecular biology and imaging techniques in pain research. However, the mechanisms underlying pain empathy remain unclear. Consequently, a deeper understanding of these mechanisms would greatly enhance pain management. This article aimed to scrutinize previous research findings on pain empathy, with a particular emphasis on the correlation between empathy for pain and distinct anatomical structures, such as mirror neurons, the anterior cingulate cortex, insular cortex, prefrontal cortex, and amygdala. Additionally, this study explored the involvement of endogenous systems, including oxytocin and the locus coeruleus norepinephrine system, hypothalamic–pituitary–adrenal axis, opioid system, and 5-hydroxylamine signaling. In conclusion, the mechanisms of pain empathy are complex and diverse, and research on pain empathy and target treatment will contribute to pain treatment.

Amyotrophic lateral sclerosis (ALS) causes progressive motor neuron degeneration, but an in vivo understanding of its early pathology remains limited. A recent study used topographic layer imaging to investigate iron and calcium accumulation in the primary motor cortex (M1) of patients with ALS compared with controls. Despite the preserved cortical thickness, ALS patients showed increased iron in layer 6 and calcium accumulation in layer 5a and the superficial layer. Calcium accumulation was particularly prominent in the low-myelin borders, potentially preceding the demyelination. This study reveals a novel in vivo pathology in ALS, suggesting that calcium dysregulation may precede iron accumulation and contribute to early M1 cell degeneration. Further investigation using quantitative susceptibility mapping and complementary techniques, such as diffusion kurtosis imaging, along with ultrahigh-field magnetic resonance imaging, into the role of calcium and early intervention strategies is warranted.

This study aimed to evaluate the efficacy and safety of remimazolam for intraoperative sedation during regional anesthesia. It was a phase II-multicenter, randomized, single-blind, parallel-group, active-controlled clinical trial (No. ChiCTR2100054956). From May 6, 2021 to July 4, 2021, patients were randomly enrolled from 17 hospitals in China. A total of 105 patients aged 18–65 years who underwent selective surgery under regional anesthesia were included. Patients received different sedatives with different dosages: 0.1 mg/kg remimazolam (HR), 0.05 mg/kg remimazolam (LR), or 1.0 mg/kg propofol (P) group, followed by a maintenance infusion. Main outcome measures included the efficacy of sedation measured by Modified Observer's Assessment of Alertness/Sedation Scale (MOAA/S) levels (1–4, 1–3, 2–3, 3, and 2–4) during the sedation procedure (the duration percentage) and incidence of adverse reactions. It showed that the duration percentage of MOAA/S levels 1–4 was 100.0 [8.1]% (median [interquartile range]), 89.9 [20.2]%, 100.0 [7.7]% in the HR, LR, and P groups, respectively. The percentage of patients in the HR, LR, and P groups who achieved MOAA/S levels 1–4 within 3 min after administration was 85.7%, 58.8%, and 82.9%, respectively. However, the time to recovery from anesthesia after withdrawal of sedatives (7.9 ± 5.7 min), incidence of anterograde amnesia (75%), and adverse effects were not statistically significant among the three groups. These findings suggest that a loading dose of remimazolam 0.1 mg/kg followed by a maintenance infusion of 0–3 mg/kg/h provides adequate sedation for patients under regional anesthesia without increasing adverse reactions.

This review comprehensively assesses the epidemiology, interaction, and impact on patient outcomes of perioperative sleep disorders (SD) and perioperative neurocognitive disorders (PND) in the elderly. The incidence of SD and PND during the perioperative period in older adults is alarmingly high, with SD significantly contributing to the occurrence of postoperative delirium. However, the clinical evidence linking SD to PND remains insufficient, despite substantial preclinical data. Therefore, this study focuses on the underlying mechanisms between SD and PND, underscoring that potential mechanisms driving SD-induced PND include uncontrolled central nervous inflammation, blood–brain barrier disruption, circadian rhythm disturbances, glial cell dysfunction, neuronal and synaptic abnormalities, impaired central metabolic waste clearance, gut microbiome dysbiosis, hippocampal oxidative stress, and altered brain network connectivity. Additionally, the review also evaluates the effectiveness of various sleep interventions, both pharmacological and nonpharmacological, in mitigating PND. Strategies such as earplugs, eye masks, restoring circadian rhythms, physical exercise, noninvasive brain stimulation, dexmedetomidine, and melatonin receptor agonists have shown efficacy in reducing PND incidence. The impact of other sleep-improvement drugs (e.g., orexin receptor antagonists) and methods (e.g., cognitive-behavioral therapy for insomnia) on PND is still unclear. However, certain drugs used for treating SD (e.g., antidepressants and first-generation antihistamines) may potentially aggravate PND. By providing valuable insights and references, this review aimed to enhance the understanding and management of PND in older adults based on SD.

Alzheimer's disease (AD) is a chronic and progressive neurodegenerative condition that is influenced by multiple factors along with neuroinflammation and oxidative stress. Our previous study proved that Lithocarpus polystachyus Rehd. aqueous extract (sweet tea aqueous extract, STAE) effectively inhibits hydrogen peroxide-induced neuronal cell injury. However, it is not clear whether STAE can protect against AD, and its underlying mechanisms are still uncertain. Therefore, the present study was designed to evaluate the possible behavioral and neurochemical effects of STAE on Aβ_25-35-induced AD rats administered STAE (20, 40, 80 mg/mL) for 14 days. We showed that STAE administration significantly and dose-dependently ameliorated the cognitive deficits in the AD rat models, assessed in the Morris water maze (MWM) test, Y-maze test, and novel object recognition (NOR) test. The results of hematoxylin and eosin (H&E) staining and Nissl staining showed that after treatment with STAE, the pathological damage to the hippocampal CA1, CA3, and dentate gyrus (DG) neurons of rats was significantly improved. Furthermore, STAE dose-dependently inhibited microglia and astrocyte activation in the hippocampus of rats accompanied by increased protein expression of silent mating-type information regulation 2 homolog 6 (SIRT6) and decreased protein expression of nod-like receptor thermal protein domain-associated protein 3 (NLRP3) and its downstream pyroptosis-related genes after following Aβ_25-35. In summary, our findings indicate that STAE effectively inhibits Aβ_25-35-induced learning and memory impairment in rats, and the mechanism is, at least partially, related to the regulation of SIRT6/NLRP3 signaling pathway.

Ischemic stroke is the most prevalent cerebrovascular disorder in the clinical setting. It results in associated neurological abnormalities due to a variety of factors, including disruption of cerebral arterial blood flow, hypoxia, and ischemic necrosis of local brain tissues. The neurovascular unit (NVU) is a dynamic structural complex that consists of neurons, glial cells, pericytes, vascular endothelial cells, and the extracellular matrix. Many cells work together to preserve the integrity of the central nervous system (CNS) under physiological conditions. However, following ischemic stroke, NVU homeostasis is disrupted along with the development of tissue ischemia and hypoxia, as well as impaired interactions between various components of the NVU. Collectively, the changes result in increased blood–brain barrier permeability, neuronal dysfunction, and functional destruction of nerve conduction bundles, ultimately leading to the clinical manifestation of neurological deficits including motor, cognitive, and speech impairments that hinder the rehabilitation process. In recent years, with continuously expanding research on ischemic cerebrovascular disease, the role of interconnections between different cells in the NVU in ischemic stroke has received increasing attention. To describe new concepts for the prevention and treatment of ischemic cerebrovascular illnesses, this article reviews the interplay between NVU in the pathogenesis of ischemic stroke.

This study aims to investigate the systemic mechanism of Panax notoginseng saponins (PNS) in antiaging using network pharmacology combined with experimental validation. String database and Cytoscape3.7.2 were used to perform the protein–protein interaction (PPI) and construct genes network. The key target genes were analyzed using gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). Then, the aging-related genes were verified by reverse-transcription polymerase chain reaction in SAM-P/8 mice, and performed molecular docking with the main components of PNS. Moreover, it produced cluster between Hub genes and differential genes. A total of 169 crossover genes were obtained, and the results of GO and KEGG indicated that the antiaging effect of PNS was mediated by apoptosis, cancer, and neurodegeneration and that five of the eight Hub genes had good binding activity with the main components of PNS. In addition, animal experiments reported that MAP2, MAPKK4, RAB6A, and Sortilin-1 have different levels of expression in the brain tissues of aging mice, and bind well docking with the main active components of PNS. However, there was no crossover between the 169 PNS intersecting genes and the four differential genes, while they yielded a link from PPI in which MAP2K4 was only linked to AKT1 and CASP3; MAP2 was only linked to AKT1 and CASP3; RAB6A was only linked to AKT1; but Sortlin-1 did not link to the Hub genes. In summary, the antiaging effect of PNS is associated with the eight Hub genes and four differential genes. All of them consist of a cluster or group that is possibly related to the antiaging effect of PNS.

Epilepsy is an abnormal neurologic disorder distinguished by the recurrent manifestation of seizures, and the precise underlying mechanisms for its development and progression remain uncertain. In recent years, the hypothesis that inflammatory mediators and corresponding pathways contribute to seizures has been supported by experimental results. The potential involvement of neuroinflammation in the development of epilepsy has garnered growing interest. This review centers attention on the involvement of inflammatory mediators in the emergence and progression of epilepsy within recent years, focusing on both clinical research and animal models, to enhance comprehension of the intricate interplay between brain inflammation and epileptogenesis.

This study aims to provide a clinical reference for the management of endocrine complications in pituitary tumor patients by synthesizing recent evidence for domestic and international management strategies. Based on the PIPOST (Population, Intervention, Professional, Outcome, Setting, and Type of Evidence) framework, evidence-based medicine targets were determined. Electronic decision support systems, guideline websites, and databases were searched to identify the best evidence on postoperative endocrine complications in pituitary tumors. The PICO (Patient, Intervention, Comparison, Outcome) principle was used to construct the search strategy, and the studies from the past 10 years (July 2013 to July 2023) were included. A total of 11 articles were included, including four guidelines, two expert consensus statements, one systematic review, one best practice article, and three randomized controlled trials. We obtained evidence on five aspects (endocrine assessment, secondary adrenal insufficiency management, water metabolism disorder management, special population management, and follow-up management) with a total of 30 pieces of evidence. Clinical healthcare professionals should focus on the care and follow-up of patients with postoperative complications, such as adrenal insufficiency, temporary or permanent diabetes insipidus, and hyponatremia. Future research should involve large sample sizes, long-term follow-ups, and multicenter studies to further clarify the protocols for fluid restriction, diet, and hormone use.

Neurodegenerative diseases represent an increasingly burdensome challenge of the past decade, primarily driven by the global aging of the population. Ongoing efforts focus on implementing diverse strategies to mitigate the adverse effects of neurodegeneration, with the goal of decelerating the pathology progression. Notably, in recent years, it has emerged that the use of nanoparticles (NPs), particularly those obtained through green chemical processes, could constitute a promising therapeutic approach. Green NPs, exclusively sourced from phytochemicals, are deemed safer compared to NPs synthetized through conventional chemical route. In this study, the effects of green chemistry-derived silver NPs (AgNPs) were assessed in neuroblastoma cells, SHSY-5Y, which are considered a pivotal model for investigating neurodegenerative diseases. Specifically, we used two different concentrations (0.5 and 1 µM) of AgNPs and two time points (24 and 48 h) to evaluate the impact on neuroblastoma cells by observing viability reduction and intracellular calcium production, especially using 1 µM at 48 h. Furthermore, investigation using atomic force microscopy (AFM) unveiled an alteration in Young's modulus due to the reorganization of cortical actin following exposure to green AgNPs. This evidence was further corroborated by confocal microscopy acquisitions as well as coherency and density analyses on actin fibers. Our in vitro findings suggest the potential efficacy of green AgNPs against neurodegeneration; therefore, further in vivo studies are imperative to optimize possible therapeutic protocols.