Global research trends in labor analgesia: A bibliometric analysis from 2013 to 2023.

Objective: In the past decade, thousands of original articles focus on labor analgesia have published. However, little has been published in the literature that includes a bibliometric analysis of labor analgesia. Therefore, this study is designed to analyze the current status of research on labor analgesia over the past ten years and explore potential directions for the future. Methods: We retrieved the Web of Science Core Collection (WOSCC) for labor analgesia articles published from 2013 to 2023 and extracted the data from the literature. To perform the bibliometric analysis, we used CiteSpace (6.2. R5) and VOS viewer (1.6.19) as our primary analysis tools. Results: A total of 2406 articles were included, and the number of publications has increased steadily in the last ten years. The United States was the leading contributor to the area, and Harvard University was the most productive institution. The American Journal of Obstetrics and Gynecology was the most cited and influential journal. The most co-cited reference was "Epidural versus non-epidural or no analgesia for pain management in labour". The labels of the co-citation cluster have identified the characteristics of 5major clusters, such as "postpartum depression", "programmed intermittent epidural bolus", "childbirth experience" "intrapartum maternal fever" and "dural puncture", which play important roles in this field. Keywords co-occurrence and keywords burst detection showed that "vaginal birth", "postpartum depression", "maternal fever", "inflammation", "systematic review", "guidelines", "decreased risk" and "scale" were the most recent and most prominent topics of labor analgesia. Discussion: This study provided a global review of labor analgesia using bibliometric and visual techniques to provide an intuitive understanding of this topic and identify hotspots and research trends. Notably, intrapartum fever and postpartum depression have emerged as hotpots and trends in labor analgesia research, reflecting the current research landscape.

Hydrogen Attenuated Inflammation Response and Oxidative in Hypoxic Ischemic Encephalopathy via Nrf2 Mediated the Inhibition of NLRP3 and NF-κB.

Hypoxia and ischemia cause neonatal encephalopathy and brain injury and can further result in cerebral palsy, cognitive impairment, growth restriction, and epilepsy. Induction of neuroprotection is a crucial therapeutic strategy for the treatment of perinatal hypoxic-ischaemic encephalopathy (HIE). Hydrogen has neuroprotective effects against brain-related diseases. Inflammation and oxidative stress are the two main pathophysiological mechanisms in neonatal hypoxic-ischaemic injury. Nuclear factor erythroid 2-related factor 2 (Nrf2) is an endogenous redox-sensitive transcription factor that participates in the antioxidant defence system through its effects on inflammation and oxidative stress. Herein, the research focuses on the mechanisms by which Nrf2 participates in the protection of hydrogen against HIE. The model of HIE was established by ligation of the right carotid artery and hypoxia in wild-type (WT) and Nrf2-/- mice. First, Nrf2 pathway activity was detected after hypoxia-ischaemia (HI) followed or not by hydrogen treatment. Brain injury, apoptosis, the inflammatory response, oxidative stress injury, and learning and memory function were assayed. We found that HI induced Nrf2 expression and signalling activation. Hydrogen alleviated the infarction volume, brain water content, neurological scores, apoptosis and long-term learning and memory functions after HI in WT mice but not in Nrf2-/- mice. Moreover, the oxidative products reactive oxygen species (ROS) and malondialdehyde (MDA) and the cytokines tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6) and High mobility group box 1 (HMGB1) were reduced and the antioxidant enzymes Superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) were upregulated by hydrogen treatment after HI in WT mice, but not in Nrf2-/- mice. In addition, the absence of Nrf2 abolished the suppressive effect of hydrogen on the expression of Nacht, Lrr, and Pyd domains-containing protein 3 (NLRP3) pathway members and p65 NF-κB after HI. Taken together, our findings showed that hydrogen alleviated cellular injury and apoptosis, neurobehavioural deficits, the inflammatory response and oxidative stress via the Nrf2-mediated NLRP3 and NF-κB pathways.

Effect of Scalp Nerve Block with Ropivacaine on Postoperative Pain in Patients Undergoing Craniotomy: A Randomized, Double Blinded Study.

Scalp nerve block with ropivacaine has been shown to provide perioperative analgesia. However, the best concentration of ropivacaine is still unknown for optimal analgesic effects. We performed a prospective study to evaluate the effects of scalp nerve block with varied concentration of ropivacaine on postoperative pain and intraoperative hemodynamic variables in patients undergoing craniotomy under general anesthesia. Eighty-five patients were randomly assigned to receive scalp block with either 0.2% ropivacaine, 0.33% ropivacaine, 0.5% ropivacaine, or normal saline. Intraoperative hemodynamics and post-operative pain scores at 2, 4, 6, 24 hours postoperatively were recorded. We found that scalp blockage with 0.2% and 0.33% ropivacaine provided adequate postoperative pain relief up to 2 h, while administration of 0.5% ropivacaine had a longer duration of action (up to 4 hour after craniotomy). Scalp nerve block with varied concentration of ropivacaine blunted the increase of mean arterial pressure in response to noxious stimuli during incision, drilling, and sawing skull bone. 0.2% and 0.5% ropivacaine decreased heart rate response to incision and drilling. We concluded that scalp block using 0.5% ropivacaine obtain preferable postoperative analgesia compared to lower concentrations. And scalp block with ropivacaine also reduced hemodynamic fluctuations in craniotomy operations.

Effect of autophagy on allodynia, hyperalgesia and astrocyte activation in a rat model of neuropathic pain.

Primary damage or dysfunction of the nervous system may cause or initiate neuropathic pain. However, it has been difficult to establish an effective treatment for neuropathic pain, as the mechanisms responsible for its pathology remain largely unknown. Autophagy is closely associated with the pathological process of neurodegenerative diseases, neuropathic injury and cancer, among others. The aim of the present study was to examine the changes in the autophagy­lysosomal pathway and discuss the effects of autophagy on allodynia, hyperalgesia and astrocyte activation in neuropathic pain. A neuropathic pain model was induced by chronic constriction injury (CCI) in rats. Inducers and inhibitors of autophagy and lysosomes were used to assess autophagy, allodynia, hyperalgesia and astrocyte activity. Neuropathic pain was found to induce an increase in the levels of the autophagy­related proteins, LC3II and Beclin 1 and, and in those of the lysosomal proteins, lysosomal­associated membrane protein type 2 (LAMP2) and Ras­related protein Rab­7a (RAB7), whereas p62 levels were found to decrease from day 1 to 14 following CCI. The autophagy inducer, rapamycin, further increased the LC3II, Beclin 1, lysosomal­associated membrane protein 2 (LAMP2) and Ras­related protein Rab­7a (RAB7) expression levels, and decreased the p62 expression levels, which were accompanied by alleviation of allodynia, hyperalgesia and astrocyte activation in the rats subjected to CCI; the autophagy inhibitor, 3­methyladenine, reversed these effects. The use of the lysosomal inhibitors, bafilomycin and chloroquine, resulted in the accumulation of LC3II and Beclin 1, a decrease in the levels of LAMP2 and RAB7, and the exacerbation of allodynia, hyperalgesia and astrocyte activation in rats with neuropathic pain. On the whole, the findings of this study indicate that neuropathic pain activates autophagy, which alleviates mechanical and thermal hyperalgesia and suppresses astrocyte activity. Therefore, neuropathic pain induced by CCI in rats appears to be mediated via the autophagy­lysosomal pathway.

An Integrated In Silico Method to Discover Novel Rock1 Inhibitors: Multi- Complex-Based Pharmacophore, Molecular Dynamics Simulation and Hybrid Protocol Virtual Screening.

Rho-associated, coiled-coil containing protein kinase 1 (ROCK1) is an important regulator of focal adhesion, actomyosin contraction and cell motility. In this manuscript, a combination of the multi-complex-based pharmacophore (MCBP), molecular dynamics simulation and a hybrid protocol of a virtual screening method, comprised of multipharmacophore- based virtual screening (PBVS) and ensemble docking-based virtual screening (DBVS) methods were used for retrieving novel ROCK1 inhibitors from the natural products database embedded in the ZINC database. Ten hit compounds were selected from the hit compounds, and five compounds were tested experimentally. Thus, these results may provide valuable information for further discovery of more novel ROCK1 inhibitors.

[Behavioral and ultrastructural changes of intrathecal administered ropivacaine in spinal cord of rats].

OBJECTIVE: To investigate the behavioral and ultrastructural changes of intrathecal administration of different concentrations of ropivacaine for 12 h. METHODS: Thirty male SD rats were randomly divided into 5 groups (6 rats in each group):group N (control), group A (ropivacaine 0.25%), group B (ropivacaine 0.5%), group C (ropivacaine 0.75%),and group D (ropivacaine 1.0%). A polyurethane microcatheter was inserted into the lumbar subarachnoid space 8 cm according to Yakshos intrathecal administration. The rats in group N received saline 0.12 mL/kg for 8 times at 1.5 h interval through the catheter, and the rats in the other groups received different concentrations of ropivacaine in the same way as in group N. The poster paw withdrawal latency to heat (PWHL) and mechanical stimulation (von Fray filament) (PWML) were measured the day before the intrathecal administration and 12 hours after the first intrathecal administration of ropivacaine. Motor function (MF) was measured after the last intrathecal administration. After the behavior test, the rats were sacrificed and the lumber segments of the spinal cord were immediately removed for electron microscopic examination. RESULTS: A total hind limb paralysis was seen at 30 seconds and intramuscular strain gradually came back 10~60 minutes after the intrathecal administration of ropivacaine in group A, B, C, and D, but not in group N. The recovery time of motor block of group A was the shortest (P<0.05), that of group D was the longest,and that of group B and C was between group A and D. Intrathecal administration of different concentrations of ropivacaine did not affect the percent maximum possible effect (%MPE) of PWHL and PWML. Electron microscopic examination showed that the spinal cords were normal in group N and A, slight edema of mitochondria and endoplasmic reticulum (ER) in group B, loosened fibrous layers in medullary sheath, edema and local degeneration of neuraxis in group C,and shrinkage of nuclear membrane, serious edema of ER, vacuolus change of mitochondria and local demyelination in group D. CONCLUSION: Ropivacaine (0.5%, 0.75%, and 1.0%) administered intrathecally for 12 hours causes different degrees of ultrastructural changes in the spinal cord depending on concentrations.