Mood disorders mainly affect the patient’s daily life, lead to suffering and disability, increase the incidence rate of many medical illnesses, and even cause a trend of suicide. The glucocorticoid (GC)-mediated hypothalamus–pituitary–adrenal (HPA) negative feedback regulation plays a key role in neuropsychiatric disorders. The balance of the mineralocorticoid receptor (MR)/glucocorticoid receptor (GR) level contributes to maintaining the homeostasis of the neuroendocrine system. Consistently, a chronic excess of GC can also lead to HPA axis dysfunction, triggering anxiety, depression, memory loss, and cognitive impairment. The animal model induced by chronic corticosterone (CORT) administration has been widely adopted because of its simple replication and strong stability. This review summarizes the behavioral changes and underlying mechanisms of chronic CORT administration-induced animal models, including neuroinflammatory response, pyroptosis, oxidative stress, neuroplasticity, and apoptosis. Notably, CORT administration at different doses and cycles can destroy the balance of the MR/GR ratio to make dose-dependent effects of CORT on the central nervous system (CNS). This work aims to offer an overview of the topic and recommendations for future cognitive function research.

Our study offers a novel mechanism in GLA anti-angiogenesis by the microRNA-520a (miR-520a)-mediated inhibition of the NF-κB/IL-6/STAT-3 signal pathway in breast cancer cells.

Research has indicated that general anesthetics may potentially induce neuroapoptosis, resulting in long-term neurological deficits in the developing brain. Fortunately, xenon, a noble gas, emerges as a promising candidate for an ideal anesthetic due to its favorable properties, offering neuroprotection and mitigating the neurotoxic effects of other general anesthetics during early life stages. Nevertheless, it is important to highlight that xenon has also been observed to cause neuroapoptosis in the neonatal brain, suggesting that xenon possesses both neuroprotective qualities (as evidenced by pre-clinical and clinical studies) and neurotoxic potential (based mainly on pre-clinical evidence) during brain development. To gain a comprehensive understanding the effects xenon, this review will explore the anesthetic properties of xenon, examine its effects on anesthesia, and elucidate its mechanisms of potential neuroprotection and neurotoxicity in the developing brain. The primary emphasis will be on xenon’s application in the context of anesthetic-induced developmental neurotoxicity (AIDN), hypoxic-ischemic encephalopathy (HIE), and teratogenicity, aiming to provide valuable insights for pediatricians, pediatric anesthesiologists, and other healthcare professionals involved in the use and study of xenon anesthesia.

General anesthetics may accelerate the neuropathological changes related to Alzheimer’s disease (AD), of which amyloid beta (Aβ)-induced toxicity is one of the main causes. However, the interaction of general anesthetics with different Aβ-isoforms remains unclear. In this study, we investigated the effects of sevoflurane (0.4 and 1.2 maximal alveolar concentration (MAC)) on four Aβ species-induced changes on dendritic spine density (DSD) in hippocampal brain slices of Thy1-eGFP mice and multiple epidermal growth factor-like domains 10 (MEGF10)-related astrocyte-mediated synaptic engulfment in hippocampal brain slices of C57BL/6 mice. We found that both sevoflurane and Aβ downregulated CA1-dendritic spines. Moreover, compared with either sevoflurane or Aβ alone, pre-treatment with Aβ isoforms followed by sevoflurane application in general further enhanced spine loss. This enhancement was related to MEGF10-related astrocyte-dependent synaptic engulfment, only in AβpE3 + 1.2 MAC sevoflurane and 3NTyrAβ + 1.2 MAC sevoflurane condition. In addition, removal of sevoflurane alleviated spine loss in Aβ + sevoflurane. In summary, these results suggest that both synapses and astrocytes are sensitive targets for sevoflurane; in the presence of 3NTyrAβ, 1.2 MAC sevoflurane alleviated astrocyte-mediated synaptic engulfment and exerted a lasting effect on dendritic spine remodeling.

Purpose The coracoid process presents surgical challenges due to its irregular anatomical morphology, further compounded by a paucity of population-specific morphometric data in the Chinese population. This study aimed to systematically analyze the morphometric characteristics of the coracoid process in the Chinese population and simulate mid-axial screw placement through the vertical portion of the coracoid, thereby providing anatomical guidance for surgical fixation of coracoid base fractures. Methods Seven scapular specimens and 12 three-dimensional CT reconstructions were analyzed. Measurements were set the length, width, and thickness of the horizontal portion, the height, width, and thickness of the vertical portion, as well as the length and width of the glenoid cavity. Simulated mid-axial screw trajectories were assessed for angulation relative to the glenoid plane and scapular body plane, and the extreme range of each entry angle was defined. Specimen measurements were compared to the CT data. Entry point distances from anatomical landmarks and screw trajectory lengths were measured. Results In the scapular specimens, the length of the horizontal portion was 37.94 ± 4.02 mm, with a width of 13.74 ± 1.35 mm and a thickness of 9.40 ± 0.90 mm. The height of the vertical portion was 19.14 ± 1.64 mm, with a width of 24.99 ± 1.30 mm and a thickness of 9.97 ± 1.43 mm. The length of the glenoid cavity was 41.21 ± 4.50 mm, and the width was 29.39 ± 4.12 mm. In the glenoid plane, the screw trajectory angle was 51.33° ± 16.04°, and the extreme range of entry angle was 53.53° ± 6.05°. For the scapular body plane, it was 8.67° ± 6.36° and 63.86° ± 6.36°, respectively. The CT data measurements aligned with those of the specimens except for the extreme range of entry angles (P < 0.05). The optimal entry point was 10 mm lateral to the medial border of the horizontal portion, slightly below the midpoint of its superior-inferior axis, with a trajectory length of about 40 mm. Conclusion This study delineates the anatomical dimensions of the coracoid process in the Chinese population and defines safe parameters for mid-axial screw placement through the vertical portion, including entry point localization, trajectory orientation, and angulation limits. These findings enhance the precision and safety of coracoid-related surgical interventions.

Background:Reactive gliosis serves as a characteristic feature of the pathophysiology of Alzheimer’s disease (AD). Nevertheless, the influence of anesthetics on the morphological dynamics of astrocytes remains ambiguous.Methods:Employing ex vivo hippocampal slices, in this study, we explored the impacts of sevoflurane and Amyloid-β peptide 1-42 (Aβ1-42) oligomers on astrocytic morphology. The primary outcomes encompassed the fluorescence intensity of glial fibrillary acidic protein (GFAP), the levels of a 38-kDa GFAP breakdown product (a marker of astroglial injury), and quantitative morphometric analyses (cell volume, surface area, branch complexity, and Sholl intersections).Results:Co-exposure to sevoflurane and Aβ1-42 led to an elevation of the 38-kDa GFAP breakdown product and a significant reduction in the mean fluorescence intensity of GFAP. Moreover, it resulted in a decrease in astrocytic volume, surface area, branch complexity, and Sholl intersections. These synergistic alterations were not observed when either treatment was administered alone.Conclusions:These findings imply that sevoflurane aggravates Aβ1-42-induced astrocytic dysfunction, which has implications for perioperative management in patients with AD or those at risk of developing AD.