Publications by authors named "Yu-qing Wu"

Article Synopsis
  • * Propofol, an anesthetic, enhances the action of the inhibitory neurotransmitter GABA but its specific effects on fear memory and neuronal balance in the BLA are not fully understood.
  • * Research using optogenetics and chemogenetics found that reducing glutamatergic neuron activity or activating GABAergic interneurons decreased glutamatergic neuron excitability, which in turn diminished propofol’s ability to enhance fear memory, suggesting a complex interaction between these neuron types in regulating memory and anxiety responses.
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Background: Cardiac lymphatic vessels are important channels for cardiac fluid circulation and immune regulation. In myocardial infarction and chronic heart failure, promoting cardiac lymphangiogenesis is beneficial in reducing cardiac edema and inflammation. However, the specific involvement of cardiac lymphangiogenesis in viral myocarditis (VMC) has not been studied.

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Background: Previous observational studies have suggested that there appears to be a close association between mitochondrial function and psychiatric disorders, but whether a causal role exists remains unclear.

Methods: We extracted genetic instruments for 67 mitochondrial-related proteins and 10 psychiatric disorders from publicly available genome-wide association studies, and employed five distinct MR methods and false discovery rate correction to detect causal associations between them. Additionally, we conducted a series of sensitivity tests and additional model analysis to ensure the robustness of the results.

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Aims: Type 2 diabetes mellitus (T2DM) is related to an increased risk of postoperative cognitive dysfunction (POCD), which may be caused by neuronal hyperexcitability. Astrocyte glutamate transporter 1 (GLT-1) plays a crucial role in regulating neuron excitability. We investigated if T2DM would magnify the increased neuronal excitability induced by anesthesia/surgery (A/S) and lead to POCD in young adult mice, and if so, determined whether these effects were associated with GLT-1 expression.

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Aims: Postoperative delirium (POD) is a common neurological complication in elderly patients after anesthesia/surgery. The main purpose of this study is to explore the effect of circRNA-targeted miRNA regulating SIRT3 on mitochondrial function through ceRNA mechanism under the surgical model of tibial fracture and to further explore the potential mechanism of postoperative delirium mediated by circRNA, so as to provide new ideas for clinical diagnosis and prevention of POD.

Methods: The surgical model of tibial fracture under sevoflurane anesthesia caused acute delirium-like behavior in elderly mice.

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Background: Breast cancer (BC) exhibits a high incidence rate, imposing a substantial burden on healthcare systems. Novel drug targets are urgently needed for BC. Mendelian randomization (MR) has gained widespread application for identifying fresh therapeutic targets.

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The full mechanism of action of propofol, a commonly administered intravenous anesthetic drug in clinical practice, remains elusive. The focus of this study was the role of GABAergic neurons which are the main neuron group in the ventral pallidum (VP) closely associated with anesthetic effects in propofol anesthesia. The activity of VP GABAergic neurons following propofol anesthesia in Vgat-Cre mice was observed via detecting c-Fos immunoreactivity by immunofluorescence and western blotting.

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The basolateral amygdala (BLA) is the subregion of the amygdala located in the medial of the temporal lobe, which is connected with a wide range of brain regions to achieve diverse functions. Recently, an increasing number of studies have focused on the participation of the BLA in many neuropsychiatric disorders from the neural circuit perspective, aided by the rapid development of viral tracing methods and increasingly specific neural modulation technologies. However, how to translate this circuit-level preclinical intervention into clinical treatment using noninvasive or minor invasive manipulations to benefit patients struggling with neuropsychiatric disorders is still an inevitable question to be considered.

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Background: Postoperative cognitive dysfunction (POCD) is a common complication after anesthesia/surgery, especially among elderly patients, and poses a significant threat to their postoperative quality of life and overall well-being. While it is widely accepted that elderly patients may experience POCD following anesthesia/surgery, the exact mechanism behind this phenomenon remains unclear. Several studies have indicated that the interaction between silent mating type information regulation 2 homologue 1 (SIRT1) and brain-derived neurotrophic factor (BDNF) is crucial in controlling cognitive function and is strongly linked to neurodegenerative disorders.

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The mechanism of ketamine-induced neurotoxicity development remains elusive. Mitochondrial fusion/fission dynamics play a critical role in regulating neurogenesis. Therefore, this study was aimed to evaluate whether mitochondrial dynamics were involved in ketamine-induced impairment of neurogenesis in neonatal rats and long-term synaptic plasticity dysfunction.

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Article Synopsis
  • - Glycolytic metabolites, like 3-phosphoglycerate (3-PGA), are not just for energy but can regulate cell fate by influencing p53 activity related to apoptosis.
  • - Low 3-PGA levels shift phosphoglycerate dehydrogenase (PHGDH) function from serine synthesis to activating p53, promoting apoptosis through interactions with proteins like AXIN and HIPK2.
  • - PHGDH mutations can either hinder or enhance p53 activation and apoptosis in liver cancer cells, with caloric restriction providing a potential method to control cancer growth by lowering glucose levels and affecting PHGDH activity.
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Article Synopsis
  • * Techniques like immunofluorescence, western blotting, and patch-clamp recordings were used to assess NAc GABAergic neuron activity during propofol anesthesia, revealing decreased neuron firing and c-Fos expression after propofol treatment.
  • * Chemogenetic and optogenetic experiments showed that stimulating NAc GABAergic neurons during propofol anesthesia reduced sensitivity and prolonged induction, while inhibiting them had the opposite effects, indicating their crucial role in anesthesia induction and recovery.
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With the ageing of the population, the health problems of elderly individuals have become particularly important. Through a large number of clinical studies and trials, it has been confirmed that elderly patients can experience postoperative cognitive dysfunction after general anesthesia/surgery. However, the mechanism of postoperative cognitive dysfunction is still unknown.

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Vitamin B (VB) is a vital micronutrient to maintain the normal state of the hematopoietic system. It must be obtained from the diet since the human body cannot synthesize it. Moreover, the absorption of VB needs to be mediated by intrinsic factor on the gastrointestinal (GI) track.

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Background: Internet gaming addiction (IGA) is a global concern, especially among young children. There have been some suggestions that childhood psychological maltreatment influences the development of IGA, but evidence for this has thus far been lacking.

Objective: The goal of this study was to investigate the association between childhood psychological maltreatment and IGA in adolescents and the mediation roles of maladaptive emotion regulation strategies and psychosocial problems (depression and social anxiety).

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It has been widely demonstrated by numerous preclinical studies and clinical trials that the neonates receiving repeated or long-time general anesthesia (GA) could develop prolonged cognitive dysfunction. However, the definite mechanism remains largely unknown. Epigenetics, which is defined as heritable alterations in gene expression that are not a result of alteration of DNA sequence, includes DNA methylation, histone post-translational modifications, non-coding RNAs (ncRNAs), and RNA methylation.

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Article Synopsis
  • Neonatal exposure to propofol negatively impacts neurogenesis and cognitive function in rats, potentially leading to long-term neurocognitive decline.
  • Propofol exposure inhibits Akt phosphorylation and increases p27 expression, which adversely affects neural stem cell proliferation and differentiation.
  • Treatment with the Akt activator SC79 can reverse some of the negative effects caused by propofol, suggesting a potential therapeutic pathway for mitigating neurocognitive deficits.
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Aim: To identify the predictive factors and laser photocoagulation associated with the use of silicone oil as endotamponade during primary diabetic vitrectomy.

Methods: The medical and surgical records of 690 patients (798 eyes) who underwent primary diabetic vitrectomy at a tertiary eye hospital in China from January 2018 to December 2018 were reviewed in this retrospective cohort study. The patients' baseline characteristics and preoperative treatments were recorded.

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Anxiety disorders are the most common psychiatric diseases, and perioperative factors often increase the incidence of anxiety. However, the mechanism and treatment for perioperative anxiety, especially anesthesia/surgery-induced postoperative anxiety, are largely unknown. Sirtuin 3 (SIRT3) which located in the mitochondria is the NAD-dependent deacetylase protein.

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Neonates who receive repeated or prolonged general anesthesia before the age of 4 are at a significantly higher risk of developing cognitive dysfunction later in life. In this study, we investigated the effects of repeated neonatal propofol exposure on hippocampal synaptic plasticity, neuronal excitability, and cognitive function. Adeno-associated SIRT1 virus with CaMKIIɑ promotor and a viral vector carrying the photosensitive gene ChR2 with the CaMKIIɑ promotor, as well as their control vectors, were stereotaxically injected into the hippocampal CA1 region of postnatal day 5 (PND-5) rats.

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Article Synopsis
  • Postoperative cognitive dysfunction (POCD) is a frequent issue in elderly patients, and this study investigates the role of circular RNAs (circRNAs) in a POCD model using aged mice.
  • A circRNA microarray identified 124 differentially expressed circRNAs, which were further validated and analyzed for their involvement in various signaling pathways related to POCD.
  • The findings suggest that dysregulation of circRNAs in the hippocampus may play a contributing role in the development of POCD in older mice, highlighting the potential for circRNAs as targets for further research.
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The Notch signaling pathway plays an important role in the regulation of neurogenesis. The objective of this study was to investigate whether the Notch signaling pathway was involved in the neurogenesis impairment and long-term neurocognitive dysfunction caused by neonatal exposure to ketamine. On postnatal day 7 (PND-7), male Sprague-Dawley (SD) rats were intraperitoneally injected with 40 mg/kg ketamine four consecutive times (40 mg/kg × 4) at 1-h intervals.

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Comorbid chronic pain and depression are increasingly becoming a concerning public problem, but the underlying mechanisms remain unclear. Here, we demonstrate that pain-related depression-like behaviors are induced in a rat model of chronic constriction injury (CCI). Using this model, we found that chronic neuropathic pain decreased the activity and expression of sirtuin 1 (SIRT1, an NAD-dependent deacetylase) in the central nucleus of the amygdala (CeA).

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