Publications by authors named "Zhouya Xue"

Aims: This study aimed to test the hypothesis that nuclear factor of activated T cells 1 (NFAT1) signaling contributes to bone cancer pain by regulating interleukin (IL)-18 expression in spinal microglia.

Methods: This study was performed on male mice using a Lewis lung carcinoma-induced bone cancer pain model. Nociceptive behaviors were evaluated by measuring mechanical allodynia, thermal hyperalgesia, and spontaneous pain.

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Introduction: Prone positioning with head rotation can influence cerebral haemodynamics, potentially affecting cerebral perfusion and oxygenation. Elderly patients with impaired brain perfusion and oxygenation are at an increased risk of developing postoperative delirium (POD). Despite this, few studies have explored whether head orientation during prone positioning contributes to POD in older adults, an aspect often overlooked by clinicians.

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Background: OFA (Opioid-free anesthesia) has the potential to reduce the occurrence of opioid-related adverse events and enhance postoperative recovery. Our research aimed to investigate whether OFA, combining esketamine and dexmedetomidine, could serve as an alternative protocol to traditional OBA (opioid-based anesthesia) in shoulder arthroscopy, particularly in terms of reducing PONV (postoperative nausea and vomiting).

Methods: A total of 60 patients treated with shoulder arthroscopy from September 2021 to September 2022 were recruited.

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Chronic inflammatory pain caused by neuronal hyperactivity is a common and refractory disease. Kv3.1, a member of the Kv3 family of voltage-dependent K channels, is a major determinant of the ability of neurons to generate high-frequency action potentials.

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To explore the risk factors affecting the length of hospital stay (LOS) as well as to examine the relationship between preoperative serum albumin levels and LOS following non-cardiac, non-obstetric surgery in patients with pulmonary hypertension (PHTN). This study represents a secondary retrospective analysis based on 287 non-cardiac, non-obstetric procedures performed on 195 PTHN patients at a single institution in the USA between 2007 and 2013. The primary outcome was the LOS.

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Introduction: Serum neurofilament light chain (sNfL) is an emerging biomarker of neuronal damage in several neurological disorders. Its association with cognitive function in the general US population aged 60 years and above is unknown. The aim of this study was to investigate the correlation between sNfL and cognitive function in the general US population aged 60 and above.

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Nerve injury-induced aberrant changes in gene expression in spinal dorsal horn neurons are critical for the genesis of neuropathic pain. N6-methyladenine (m 6 A) modification of DNA represents an additional layer of gene regulation. Here, we report that peripheral nerve injury significantly decreased the level of m 6 A-specific DNA methyltransferase 1 ( N6amt1 ) in dorsal horn neurons.

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Aims: Nerve injury-induced maladaptive changes in gene expression in the spinal neurons are essential for neuropathic pain genesis. Circular RNAs (ciRNA) are emerging as key regulators of gene expression. Here, we identified a nervous-system-tissues-specific ciRNA-Kat6 with conservation in humans and mice.

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Circular RNAs (ciRNAs) are emerging as new players in the regulation of gene expression. However, how ciRNAs are involved in neuropathic pain is poorly understood. Here, we identify the nervous-tissue-specific ciRNA-Fmn1 and report that changes in ciRNA-Fmn1 expression in spinal cord dorsal horn neurons play a key role in neuropathic pain after nerve injury.

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Article Synopsis
  • RNA N4-acetylcytidine (ac4C) modification is significant for gene regulation, but its role in pain regulation is unexplored; this study identifies NAT10 as a key player in neuropathic pain.
  • After peripheral nerve injury, NAT10 expression increases due to USF1 activation, leading to elevated ac4C levels in dorsal root ganglia (DRGs).
  • Silencing or deleting NAT10 reduces pain sensitivity in nerve-injured mice, while its upregulation without injury induces pain behaviors, indicating that NAT10-targeted ac4C could be a therapeutic target for neuropathic pain treatment.
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Chronic inflammatory pain seriously affects patients' quality of life because of a paucity of effective clinical treatments caused, at least in part, by lack of full understanding of the underlying mechanisms. miRNAs are known to be involved in inflammatory pain via silencing or degrading of target mRNA in the cytoplasm. The present study provides a novel mechanism by which miRNA-22 positively regulates metal-regulatory transcription factor 1 () in the nuclei of neurons in the dorsal horn of the spinal cord.

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The methyltransferase-like 3 (Mettl3) is a key component of the large N6-adenosine-methyltransferase complex in mammalian responsible for RNA N6-methyladenosine (m6A) modification, which plays an important role in gene post-transcription modulation. Although RNA m6A is enriched in mammalian neurons, its regulatory function in nociceptive information processing remains elusive. Here, we reported that Complete Freund's Adjuvant (CFA)-induced inflammatory pain significantly decreased global m6A level and m6A writer Mettl3 in the spinal cord.

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Introduction: Routine anesthesia modality for modified radical mastectomy (MRM) includes general anesthesia (GA), epidural blockade-combined GA and nerve blockade-combined GA. However, GA has been associated with postoperative adverse effects such as vertigo, postoperative nausea and vomiting and requirement for postoperative analgesia, which hinders recovery and prognosis. Moreover, combined blockade of thoracic paravertebral nerves or intercostal nerves and adjuvant basic sedation for massive lumpectomy provided perfect anesthesia and reduced opioid consumption, whereas the excision coverage did not attain the target of MRM.

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Dysfunctions of gene transcription and translation in the nociceptive pathways play the critical role in development and maintenance of chronic pain. Circular RNAs (circRNAs) are emerging as new players in regulation of gene expression, but whether and how circRNAs are involved in chronic pain remain elusive. We showed here that complete Freund's adjuvant-induced chronic inflammation pain significantly increased circRNA-Filip1l (filamin A interacting protein 1-like) expression in spinal neurons of mice.

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Aim And Methods: Chronic pain associated with inflammation is a common clinical problem, and the underlying mechanisms yet are incompletely defined. DNA methylation has been implicated in the pathogenesis of chronic pain. However, the specific genes regulated by DNA methylation under inflammatory pain condition remain largely unknown.

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Purpose: The current study aims at investigating the downstream targets of spinal Annexin A10 in modulating neuropathic pain.

Materials And Methods: Paw withdrawal latency and paw withdrawal threshold were measured to evaluate the pain-associated behaviour in rats. The expression of spinal Annexin A10, phosphorylated-extracellular regulated kinase 1/2 and extracellular regulated kinase were detected by western blotting.

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Background: Ten-eleven translocation methylcytosine dioxygenase converts 5-methylcytosine in DNA to 5-hydroxymethylcytosine, which plays an important role in gene transcription. Although 5-hydroxymethylcytosine is enriched in mammalian neurons, its regulatory function in nociceptive information processing is unknown.

Methods: The global levels of 5-hydroxymethylcytosine and ten-eleven translocation methylcytosine dioxygenase were measured in spinal cords in mice treated with complete Freund's adjuvant.

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Unlabelled: DNA 5-hydroxylmethylcytosine (5hmC) catalyzed by ten-eleven translocation methylcytosine dioxygenase (TET) occurs abundantly in neurons of mammals. However, the in vivo causal link between TET dysregulation and nociceptive modulation has not been established. Here, we found that spinal TET1 and TET3 were significantly increased in the model of formalin-induced acute inflammatory pain, which was accompanied with the augment of genome-wide 5hmC content in spinal cord.

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Article Synopsis
  • Recent research indicates that microRNA (miRNA) plays a role in chronic pain, but how it works is still unclear.
  • In a study, mice with chronic inflammation showed lower levels of miR-219 in their spinal neurons, and higher levels of CaMKIIγ, a target of miR-219.
  • Boosting miR-219 levels helped reduce pain sensitivity and reverse changes in spinal neuron behavior, suggesting that changes in miR-219 due to DNA methylation influence chronic pain management through CaMKIIγ regulation.
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