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Nerve injury induces changes in gene transcription in dorsal root ganglion (DRG) neurons, which may contribute to nerve injury-induced neuropathic pain. DNA methylation represses gene expression. Here, we report that peripheral nerve injury increases expression of the DNA methyltransferase DNMT3a in the injured DRG neurons via the activation of the transcription factor octamer transcription factor 1. Blocking this increase prevents nerve injury-induced methylation of the voltage-dependent potassium (Kv) channel subunit Kcna2 promoter region and rescues Kcna2 expression in the injured DRG and attenuates neuropathic pain. Conversely, in the absence of nerve injury, mimicking this increase reduces the Kcna2 promoter activity, diminishes Kcna2 expression, decreases Kv current, increases excitability in DRG neurons and leads to spinal cord central sensitization and neuropathic pain symptoms. These findings suggest that DNMT3a may contribute to neuropathic pain by repressing Kcna2 expression in the DRG. Transcriptional changes occur in the dorsal root ganglion in response to nerve injury and may contribute to neuropathic pain. Here the authors show that the DNA methyltransferase DNMT3a is upregulated in rodents following nerve injury, and may contribute to pain-like behaviour by decreasing expression of the voltage-gated potassium channel Kv1.2.

A plethora of evidence has suggested that gut microbiota is involved in the occurrence and development of postmenopausal osteoporosis (PMO). It has been suggested that neuropeptide Y (NPY) modulates the bone metabolism through Y1 receptor (Y1R), and might be associated with gut microbiota. The present study aims to evaluate the anti-osteoporotic effects of Y1R antagonist and to investigate the potential mechanism by which Y1R antagonist regulates gut microbiota. In this study, eighteen female rats were randomly divided into three groups: the sham surgery (SHAM) group, the ovariectomized (OVX) group, and OVX+BIBO3304 group. After 6 weeks following surgery, Y1R antagonist BIBO3304 was administered to the rats in OVX+BIBO3304 group for 7 days. The bone microstructure and serum biochemical parameters were measured at 12 weeks after operation. The differences in the gut microbiota were analyzed by 16S rDNA gene sequencing. Heat-map and Spearman’s correlation analyses were constructed to investigate the correlations between microbiota and bone metabolism-related parameters. The results indicated that OVX+BIBO3304 group showed significantly higher BMD, BV/TV, Tb.Th, Tb.N, Conn.D, and serum Ca 2+ level than those in OVX group. Additionally, Y1R antagonist changed the gut microbiota composition with lower Firmicutes / Bacteroidetes ratio and higher proportions of some probiotics, including Lactobacillus . The correlation analysis showed that the changes of gut microbiota were closely associated with bone microstructure and serum Ca 2+ levels. Our results suggested that Y1R antagonist played an anti-osteoporotic effect and regulated gut microbiota in OVX rats, indicating the potential to utilize Y1R antagonist as a novel treatment for PMO.

Reference data analysis and visualization methods were applied to identify current knowledge mapping methods in the neuroimmune modulation research field. A comprehensive search of publications within the field of neuroimmune modulation in the Web of Science Core Collection database and PubMed from 2005-2024 was conducted. The reference type was restricted to articles and reviews in the WOSCC database and clinical trials in PubMed. The data were visualized and analyzed via visualization and bibliometric tools, including CiteSpace and VOSviewer. A total of 5,280 publications were included in the field of neuroimmune modulation. The United States ranked first as the most influential country in terms of both publication number and academic influence. Harvard University had the greatest impact on institutions. The leading scientists in the neuroimmune modulation field have focused on the mechanism at both the peripheral and central levels. Citation analysis and cocitation analysis revealed that acute kidney injury, neuropathic pain, and neuronal regulation are key focal points in neuroimmune research. Furthermore, keyword analysis revealed that \"inflammation\", \"neuroinflammation\", \"microglia\", \"cytokines\", \"cholinergic anti-inflammatory pathway\" and \"neuroimmune\" had more than 200 co-occurrences and represented research hotspots in this field. A total of 73 clinical trials were identified that targeted neuroimmune modulation to treat diseases. These studies highlighted the central role of the neuroimmune network in diseases, with a particular emphasis on innovative therapies that regulate inflammation through the cholinergic system. Further exploration is needed to develop precise intervention strategies targeting specific cytokines. This analysis provides comprehensive knowledge mapping in the current research field of neuroimmune modulation. The trends in the field include mechanism studies combined with neuronal regulation. Neuroimmune crosstalk might provide new therapeutic targets for treating nervous system diseases.

We utilized bibliometric and data visualization techniques to discern the primary research domains and emerging frontiers in the field of adult hippocampal neurogenesis (AHN). We systematically searched the Web of Science database for AHN-related articles published between 2004 and 2023. The retrieved articles were filtered based on publication types (articles and reviews) and language (English). We employed CiteSpace, VOSviewer, and the online bibliometric platform (bibliometric.com) to visualize and analyze the collected data. In total, 1,590 AHN-related publications were discovered, exhibiting a steady increase in yearly publications over time. The United States emerged as the leading contributor in AHN research in terms of both publication quantity and national influence. Among all research institutions in the field of AHN, the University of California System exhibited the highest impact. Kempermann, Gerd was the most active author. The publications of the top three active authors primarily focused on the functions of AHN, and reversing hippocampal damage and cognitive impairment by improving AHN. An analysis of reference co-citation clustering revealed 8 distinct research clusters, and the notable ones included \"adult hippocampal neurogenesis,\" \"neurogenesis,\" \"hippocampus,\" \"dentate gyrus,\" \"neural stem cell,\" and \"depression.\" Additionally, a burst keyword detection indicated that 'anxiety' is a current research hotspot in the field of AHN. This in-depth bibliographic assessment of AHN offers a deeper insight into the present research hotspots in the field. The association between AHN and cognitive diseases, such as Alzheimer's disease (AD) and anxiety, has emerged as a prominent research hotspot.

To explore the potential therapeutic strategies of different types of neuropathic pain (NP) and to summarize the cutting-edge novel approaches for NP treatment based on the clinical trials registered on ClinicalTrials.gov. The relevant clinical trials were searched using ClinicalTrials.gov Dec 08, 2022. NP is defined as a painful condition caused by neurological lesions or diseases. All data were obtained and reviewed by the investigators to confirm whether they were related to the current topic. A total of 914 trials were included in this study. They were divided into painful diabetic neuropathy (PDN), postherpetic neuralgia (PHN), sciatica (SC), peripheral nerve injury-related NP (PNI), trigeminal neuralgia (TN), chemotherapy-induced NP (CINP), general peripheral NP (GPNP) and spinal cord injury NP (SCI-NP). Potential novel therapeutic strategies, such as novel drug targets and physical means, were discussed for each type of NP. NP treatment is mainly dominated by drug therapy, and physical means have become increasingly popular. It is worth noting that novel drug targets, new implications of conventional medicine, and novel physical means can serve as promising strategies for the treatment of NP. However, more attention needs to be paid to the challenges of translating research findings into clinical practice.

Aims To visualize the trends and hotspots in the scientific research related to vascular cognitive impairment (VCI) quantitatively and qualitatively. Methods Cross‐sectional bibliometric analysis of publications that related to VCI was conducted. Publications were found by searching in the Web of Science Core Collection database (WoSCC) – Edition: Science Citation Index Expanded (SCI‐Expanded) from January 2000 to December 2021. Publication type was restricted to article and review in the English language. The downloaded data were screened and analyzed in January 2022. Results In total, 16,264 publications were identified, with a steady increase in annual publications. The United States was the leading country in VCI research regarding publication numbers and national influence. National Institute of Aging had the highest influence among all the institutes in the field of VCI. Philip Scheltens was the most active author. The top five active authors' publications focused on pathobiology, neuroimaging standards, risk factors, prevention, and the standard diagnosis of vascular dementia (VaD). A co‐cited publication clustering resulted in 19 main clusters, and the prevention, blood–brain barrier, cholesterol, cerebral amyloid angiopathy, and VaD were the top 5 clusters. Moreover, burst keywords detection revealed that the “small vessel disease” is the current hotspot in the field of VCI. Conclusions This bibliometric analysis mapped the overall research structure of VCI and analyzed the current research trends and hotspots for future studies orientation. Neuroimaging, risk factors detection, and pathobiology are the current trends in VCI research. Small vessel disease and its mechanisms are the current hotspots of VCI research. This bibliometric analysis mapped the overall research structure of VCI and analyzed the current research trends and hotspots for future studies orientation.

Bibliometric and data visualization methods were used to identify the current status, key areas, and emerging frontiers in ropivacaine research. We conducted a comprehensive search of the Web of Science database for publications related to ropivacaine published from 2000 to 2023. The publication types were limited to original articles and reviews. We utilized CiteSpace, VOSviewer, and the online bibliometric platform to visualize and analyze the collected data. A total of 4,147 publications related to ropivacaine were identified, with a consistent growth in annual publications over time. The United States emerged as the most influential country in the field of ropivacaine research, and ranked first in the annual number of publications until 2014. China surpassed the United States in the number of publications for the first time in 2015 and has remained in first place ever since. Of all the research institutions in the field of ropivacaine, University of Copenhagen in Denmark exhibited the highest impact. Brian M. Ilfeld and Casati A were identified as the most influential authors. The leading researchers in this field primarily focused their publications on continuous nerve blocks for postoperative analgesia and ultrasound-guided nerve block techniques. An analysis of reference co-citation clustering revealed 18 distinct research clusters, with current hotspots including erector spinae plane block, dexmedetomidine, quadratus lumborum block, labor analgesia, and mitochondrial respiration. Additionally, keywords analysis indicated that \"dexmedetomidine as an adjuvant in nerve blocks\" currently represents a research hotspot in the field of ropivacaine. This bibliometric analysis provides a comprehensive overview of the research landscape in ropivacaine. It reveals research trends in this field and emerging areas for future investigations. Notably, the application of ropivacaine in nerve blocks is a prominent focus in current research, with a particular emphasis on its combination with dexmedetomidine.

Osteoporosis is characterized by diminished bone density and quality, compromised bone microstructure, and increased bone fragility, culminating in a heightened risk of fracture. Relatively few attempts have been made to survey the breadth of osteoporosis research using bibliometric approaches. This study aims to delineate the current landscape of osteoporosis research, offering clarity and visualization, while also identifying potential future directions for investigation. We retrieved and filtered articles and reviews pertaining to osteoporosis from the Web of Science Core Collection database, specifically the Science Citation Index Expanded (SCI-E) edition, spanning the years 2014 to 2023. Informatics tools such as CiteSpace and VOSviewer were employed to dissect the intellectual framework, discern trends, and pinpoint focal points of interest within osteoporosis research. Our dataset comprised 33,928 osteoporosis-related publications, with a notable surge in annual publication numbers throughout the last decade. China and the United States lead in terms of research output. The University of California System contributed substantially to this body of work, with Amgen demonstrating the highest degree of centrality within the network. Cooper Cyrus emerged as a pivotal figure in the field. An analysis of highly-cited studies, co-citation networks, and keyword co-occurrence revealed that recent years have predominantly concentrated on elucidating mechanisms underlying osteoporosis, as well as its diagnosis, prevention, and treatment strategies. Burst detection analyses of citations and keywords highlighted osteoblasts, sarcopenia, gut microbiota, and denosumab as contemporary hotspots within osteoporosis research. This bibliometric analysis has provided a visual representation of the fundamental knowledge structure, prevailing trends, and key focal areas within osteoporosis research. The identification of osteoblasts, sarcopenia, gut microbiota, and denosumab as current hotspots may guide future research endeavors. Continued efforts directed at understanding the mechanisms, fracture outcomes, diagnostics, and therapeutics related to osteoporosis are anticipated to deepen our comprehension of this complex disease.

Background: Although major joint replacement surgery has a high overall success rate, postoperative cognitive dysfunction (POCD) is a common complication after anesthesia and surgery, increasing morbidity and mortality. Identifying POCD risk factors would be helpful to prevent and decrease the occurrence of POCD. We hypothesized that preoperative chronic pain increases the risk of POCD. Methods: A single-center, observational, prospective cohort study was conducted from January 2018 to March 2020. All consecutive elderly patients (>65 years) who underwent elective total hip arthroplasty or hemiarthroplasty with general anesthesia by the same surgeon were enrolled. The patients underwent neuropsychological testing preoperatively and at 7 days and 2 months after surgery. To determine POCD, a nonsurgical control group was recruited from the general community. Results: Of the 141 patients who finished the neuropsychological testing 7 days after surgery, 61 (43.2%) had preoperative chronic pain. Of the 61 patients, 17 (27.9%) developed POCD; of the 79 patients with no chronic pain, 10 (12.7%) had developed POCD by 7 days after surgery. Multivariate logistic regression analysis identified preoperative chronic pain as a risk factor of POCD assessed 7 days after surgery (odds ratio 6.527; P = 0.009). There was no significant difference in the POCD incidence 2 months after surgery between patients with and without preoperative chronic pain. Conclusion: Preoperative chronic pain was a risk factor of developing POCD within 7 days after surgery in elderly patients following hip joint replacement surgery. Clinical Trial Registration: [ www.ClinicalTrials.gov ], identifier [NCT03393676].

Neuropathic pain, a distressing and debilitating disorder, is still poorly managed in clinic. Opioids, like morphine, remain the mainstay of prescribed medications in the treatment of this disorder, but their analgesic effects are highly unsatisfactory in part due to nerve injury-induced reduction of opioid receptors in the first-order sensory neurons of dorsal root ganglia. G9a is a repressor of gene expression. We found that nerve injury-induced increases in G9a and its catalyzed repressive marker H3K9m2 are responsible for epigenetic silencing of Oprm1, Oprk1, and Oprd1 genes in the injured dorsal root ganglia. Blocking these increases rescued dorsal root ganglia Oprm1, Oprk1, and Oprd1 gene expression and morphine or loperamide analgesia and prevented the development of morphine or loperamide-induced analgesic tolerance under neuropathic pain conditions. Conversely, mimicking these increases reduced the expression of three opioid receptors and promoted the mu opioid receptor-gated release of primary afferent neurotransmitters. Mechanistically, nerve injury-induced increases in the binding activity of G9a and H3K9me2 to the Oprm1 gene were associated with the reduced binding of cyclic AMP response element binding protein to the Oprm1 gene. These findings suggest that G9a participates in the nerve injury-induced reduction of the Oprm1 gene likely through G9a-triggered blockage in the access of cyclic AMP response element binding protein to this gene.