Spatiotemporal distribution of migraine in China: analyses based on baidu index.

BACKGROUND: In recent years, innovative approaches utilizing Internet data have emerged in the field of syndromic surveillance. These novel methods aim to aid in the early prediction of epidemics across various scenarios and diseases. It has been observed that these systems demonstrate remarkable accuracy in monitoring outbreaks even before they become apparent in the general population. Therefore, they serve as valuable complementary tools to augment existing methodologies. In this study, we aimed to investigate the spatiotemporal distribution of migraine in China by leveraging Baidu Index (BI) data. METHODS: Migraine-related BI data from January 2014 to December 2022 were leveraged, covering 301 city-level areas from 31 provincial-level regions by using the keyword "migraine ()". Prevalence data from the Global Burden of Disease study (GBD) were attracted to ensure the reliability of utilizing migraine-related BI data for research. Comprehensive analytical methods were then followed to investigate migraine's spatiotemporal distribution. The Seasonal-Trend decomposition procedure based on Loess (STL) was used to identify the temporal distribution. Spatial distribution was explored using the Getis-Ord Gi* statistic, standard deviation ellipse analysis, Moran's Index, and Ordinary Kriging. The top eight migraine-related search terms were analyzed through the Demand Graph feature in the Baidu Index platform to understand the public's concerns related to migraine. RESULTS: A strong association was observed between migraine-related BI and the prevalence data of migraine from GBD with a Spearman correlation coefficient of 0.983 (P = 4.96 × 10- 5). The overall trend of migraine-related BI showed a gradual upward trend over the years with a sharp increase from 2017 to 2019. Seasonality was observed and the peak period occurred in spring nationwide. The middle-lower reaches of the Yangtze River were found to be hotspots, while the eastern coastal areas had the highest concentration of migraine-related BI, with a gradual decrease towards the west. The most common search term related to migraine was "How to treat migraine quickly and effectively ()". CONCLUSIONS: This study reveals important findings on migraine distribution in China, underscoring the urgent need for effective prevention and management strategies.

A Sound and Vibration Fusion Method for Fault Diagnosis of Rolling Bearings under Speed-Varying Conditions.

The fault diagnosis of rolling bearings is critical for the reliability assurance of mechanical systems. The operating speeds of the rolling bearings in industrial applications are usually time-varying, and the monitoring data available are difficult to cover all the speeds. Though deep learning techniques have been well developed, the generalization capacity under different working speeds is still challenging. In this paper, a sound and vibration fusion method, named the fusion multiscale convolutional neural network (F-MSCNN), was developed with strong adaptation performance under speed-varying conditions. The F-MSCNN works directly on raw sound and vibration signals. A fusion layer and a multiscale convolutional layer were added at the beginning of the model. With comprehensive information, such as the input, multiscale features are learned for subsequent classification. An experiment on the rolling bearing test bed was carried out, and six datasets under various working speeds were constructed. The results show that the proposed F-MSCNN can achieve high accuracy with stable performance when the speeds of the testing set are the same as or different from the training set. A comparison with other methods on the same datasets also proves the superiority of F-MSCNN in speed generalization. The diagnosis accuracy improves by sound and vibration fusion and multiscale feature learning.

Morphine Promotes the Angiogenesis of Postoperative Recurrent Tumors and Metastasis of Dormant Breast Cancer Cells.

BACKGROUND: Surgery plays a significant role in the comprehensive treatment of breast cancer, and opioids are often the first-choice analgesics in the perioperative period. However, recent studies showed that opioids may enhance the angiogenesis of breast cancer and the recurrence and metastasis of tumor cells. OBJECTIVES: We aim to investigate the influence of opioids on recurrence and metastasis of breast cancer in nude mice. METHODS: Forty female nude mice with breast tumor were randomly divided into 4 groups (n = 10). They were treated with (i) normal saline (10 mL/kg), (ii) morphine (10 mg/kg), (iii) morphine plus naloxone (10 + 4 mg/kg), and (iv) naloxone (4 mg/kg) for 2 weeks. Four groups of MDA-MB-231 cells were administered (i) Dulbecco's Modified Eagle's Medium, (ii) morphine (10 µmol/mL), (iii) morphine plus naloxone (10 + 10 µmol/mL), and (iv) naloxone (10 µmol/mL). The influence of morphine in each treated group was evaluated by immunocytochemistry and Western blotting. RESULTS: Mice in the morphine group had higher rates of Ki67-positive cells, lower rates of apoptotic index, and a significant increase in the microvessels density of the tumor as evidenced by CD31 staining (p < 0.05). Furthermore, the MDA-MB-231 cells in the morphine group showed an increase in p-Akt, c-Myc, and thrombosponin-1 expression. CONCLUSION: In the current study, we found that morphine promotes the angiogenesis of the recurrent postoperative tumors of nude mice with breast cancer and the proliferation of tumor cells and such promotion may be related to the PI3K-c-Myc signaling pathway.

Astrocyte-derived exosomes-transported miRNA-26a-5p ameliorates sevoflurane-induced cognitive dysfunction in aged mice.

Prolonged sevoflurane anesthesia is the primary factor contributing to the development of perioperative neurocognitive disorders (PND). Recent studies have highlighted neuronal apoptosis and abnormal dendritic structures as crucial features of PND. Astrocytes-derived exosomes (ADEs) have been identified as carriers of microRNAs (miRNAs), playing a vital role in cell-to-cell communication through transmitting genetic material. Nevertheless, the specific mechanisms by which miRNAs in ADEs contribute to sevoflurane-induced cognitive deficit are currently unknown. Through a series of in vivo and in vitro experiments, we demonstrated that ADEs contributed to improved neurocognitive outcomes by reducing neuronal apoptosis and promoting dendritic development. Our miRNA microarray analysis revealed a significant increase in the expression level of miR-26a-5p within ADEs. Furthermore, we identified NCAM as the downstream target gene of miR-26a-5p. Subsequent gain- and loss-of-function experiments were conducted to validate the role of the miR-26a-5p/NCAM axis. Finally, we found that the AKT/GSK3-ß/CRMP2 signaling pathway was involved in regulating neurons through exosomal miR-26a-5p. Taken together, our findings suggest that the treatment with miR-26a-5p in ADEs can improve neurocognitive outcomes induced by long-term sevoflurane anesthesia, suggesting a promising approach for retarding the progress of PND.

THE EFFECTS OF EARLY-PHASE FUROSEMIDE USE ON THE PROGRESSION OF OLIGURIC ACUTE KIDNEY INJURY ACROSS DIFFERENT CENTRAL VENOUS PRESSURE: A RETROSPECTIVE ANALYSIS.

ABSTRACT: Background: Furosemide is a commonly used loop diuretic in critical care. However, its effect on the progression of oliguric acute kidney injury across different central venous pressure (CVP) remains unknown. This study therefore aims to investigate the association between furosemide 6-12h (defined as the use of furosemide within 6 h after the diagnosis of AKI according to the urine output [UO] criteria set by the Kidney Disease: Improving Global Outcomes [KDIGO] guidelines) and the progression of AKI across different CVP 6-12h (defined as CVP within 6 h after the diagnosis of AKI by the KDIGO UO criteria) levels. Methods: Patients involved in this study were identified from the Medical Information Mart for Intensive Care IV database with the following criteria: (i) adults with UO <0.5 mL/kg per hour for the first 6 h upon admission to the intensive care unit (ICU) (meeting stage 1 AKI by UO) and (ii) CVP 6-12h ranging from 0 to 30 mm Hg. From there on, the target primary outcome would be progression to stage 3 AKI by UO among these chosen patients. The secondary outcome was 28-d mortality since ICU admission. The risks of severe-stage AKI progression and 28-d mortality were respectively examined against furosemide 6-12h (vs. without furosemide 6-12h ) within the full cohort and across different subgroups of CVP 6-12h , using multivariate adjusted logistic regression and inverse probability treatment weighting (IPTW). Sensitivity analyses were performed to assess the robustness of our findings. Results: One thousand one hundred eighty patients were ultimately selected for this study, of whom 643 (54.5%) progressed to stage 3 AKI from stage 1 based on the UO criteria by KDIGO. Multivariate analysis showed that furosemide 6-12h is significantly associated with this severe-stage progression within the full cohort (odds ratio [OR] was 0.62 at 95% confidence interval [CI] of 0.43-0.90, P = 0.011). After dividing the patients into CVP 6-12h subgroups according to their CVP during the early phases, lower risk of AKI progression was observed only in furosemide 6-12h application at CVP 6-12h of ≥12 mm Hg (adjusted OR was 0.40 at 95% CI of 0.25-0.65, P < 0.001), as confirmed by the IPTW analysis (OR was 0.47 at 95% CI of 0.29-0.76, P = 0.002). The robustness of these findings was confirmed by sensitivity analyses. In addition, for patients with CVP 6-12h ≥12 mm Hg, furosemide 6-12h is also significantly associated with lower risk of 28-d mortality (adjusted OR was 0.47 at 95% CI of 0.25-0.92, P = 0.026) in the multivariate logistic regression analysis, and there was a similar trend in the IPTW analysis (adjusted OR was 0.55 at 95% CI of 0.28-1.10, P = 0.092). Conclusions: Among the identified early-stage AKI patients in critical care, the use of furosemide was associated only with lower risk of oliguric AKI progression and 28-d mortality within the high CVP group. These findings suggest the potential of CVP as a guidance or reference point in the usage of furosemide among early-stage oliguric AKI patients in the ICU.

Modified intraoperative temperature management prevents prolonged length of stay after head and neck surgery with free flap reconstruction.

The present study aimed to investigate the association between intraoperative body temperature and prolonged length of stay (PLOS) after free flap reconstruction. A total of 753 patients who underwent head and neck surgery with free flap reconstruction were collected and randomly assigned into primary and validation cohorts. In the primary cohort, univariable and multivariable analyses were conducted to evaluate associations between intraoperative time-weighted (TW) temperature (TW average [TWA] temperature, TW hypothermia and TW hyperthermia) and PLOS. Nomograms were developed with and without intraoperative TW temperature, and validated in the validation cohort. Severe intraoperative TW hypothermia (OR = 1.004; 95% CI: 1.000, 1.007; p = 0.032) was identified as an independent risk factor for PLOS. Intraoperative TWA temperature and TW hypothermia showed linear related predictive effect for PLOS. The nomogram incorporating intraoperative TW temperature showed higher C-index (0.652, 95% CI: 0.591, 0.713) and improved net reclassification improvement for non-event (0.277, 95% CI: 0.118, 0.435; p < 0.001). Lower TWA temperature with mild TW hypothermia had a preventive effect on PLOS with a linear association, which may provide a modified range for intraoperative temperature management. The proposed nomogram incorporating intraoperative TW temperature could be used to develop personalized preventive strategies for PLOS after free flap reconstruction. IRB NUMBER: SYSEC-KY-KS-2022-037. CLINICAL TRIAL REGISTRATION NUMBER: Not applicable.

Value of Evoked Potential Changes Associated with Neck Extension Prior to Cervical Spine Surgery.

Background: Multimodal intraoperative monitoring (MIOM) is a useful tool to warn surgeons to intervene for intraoperative spinal cord injury in cervical spine surgery. However, the value of MIOM remains controversial before cervical spine surgery. Objective: To explore the value of MIOM in early detecting spinal cord injury associated with neck extension before cervical spine surgery. Methods and Materials: Data of 191 patients receiving cervical spine surgery with the MIOM were enrolled from June 2014 to June 2020. The subjects were divided into a group of evoked potentials (EP) changes and a group of no EP changes for analysis according to the monitoring alerts or not. Results: Five (2.62%) patients showed EP changes associated with neck extension during intubation or positioning. After early different interventions, such as repositioning and timely surgical decompression, none or transient postoperative neurological deficits were observed in four cases, and only one case was with permanent neurological deficits. The average preoperative Japanese Orthopaedic Association (JOA) scores of the group with EP changes were lower than those of the group with no EP changes (P = 0.037 < 0.05). There was no statistical significance in gender, average age, mean Pavlov ratio, and the minimum Palov ratio between the two groups (P > 0.05). Conclusions: The MIOM could identify spinal cord injury associated with neck extension before cervical spine surgery. Active and effective interventions could prevent or reduce permanent postoperative neurological deficits. Severe spinal cord compression might be a risk factor for EP changes.

Early-Phase Urine Output and Severe-Stage Progression of Oliguric Acute Kidney Injury in Critical Care.

Background: The relationship between urine output (UO) and severe-stage progression in the early phase of acute kidney injury (AKI) remains unclear. This study aimed to investigate the relationship between early-phase UO6-12h [UO within 6 h after diagnosis of stage 1 AKI by Kidney Disease: Improving Global Outcomes (KDIGO) UO criteria] and severe-stage progression of AKI and to identify a reference value of early-phase UO6-12h for guiding initial therapy in critical care. Methods: Adult patients with UO < 0.5 ml/kg/h for the first 6 h after intensive care unit (ICU) admission (meeting stage 1 AKI by UO) and UO6-12h ≥ 0.5 ml/kg/h were identified from the Medical Information Mart for Intensive Care (MIMIC) III database. The primary outcome was progression to stage 2/3 AKI by UO. After other variables were adjusted through multivariate analysis, generalized additive model (GAM) was used to visualize the relationship between early-phase UO6-12h and progression to stage 2/3 AKI by UO. A two-piecewise linear regression model was employed to identify the inflection point of early-phase UO6-12h above which progression risk significantly leveled off. Sensitivity and subgroup analyses were performed to assess the robustness of our findings. Results: Of 2,984 individuals, 1,870 (62.7%) with KDIGO stage 1 UO criteria progressed to stage 2/3 AKI. In the multivariate analysis, early-phase UO6-12h showed a significant association with progression to stage 2/3 AKI by UO (odds ratio, 0.40; 95% confidence interval, 0.34-0.46; p < 0.001). There was a non-linear relationship between early-phase UO6-12h and progression of AKI. Early-phase UO6-12h of 1.1 ml/kg/h was identified as the inflection point, above which progression risk significantly leveled off (p = 0.780). Patients with early-phase UO6-12h ≥ 1.1 ml/kg/h had significantly shorter length of ICU stay (3.82 vs. 4.17 days, p < 0.001) and hospital stay (9.28 vs. 10.43 days, p < 0.001) and lower 30-day mortality (11.05 vs. 18.42%, p < 0.001). The robustness of our findings was confirmed by sensitivity and subgroup analyses. Conclusions: Among early-stage AKI patients in critical care, there was a non-linear relationship between early-phase UO6-12h and progression of AKI. Early-phase UO6-12h of 1.1 ml/kg/h was the inflection point above which progression risk significantly leveled off.

Nomogram for predicting mandatory ICU admission after gastrectomy for gastric cancer.

BACKGROUND: This study aimed to identify risk factors that were associated with mandatory intensive care unit (ICU) admission after gastrectomy for gastric cancer. We then employed these risk factors to construct and validate a nomogram for predicting mandatory ICU admission after gastrectomy, which may identify those who require ICU indeed and improve ICU utilization. METHODS: A number of 999 gastric cancer patients undergoing gastrectomy from January 2010 to June 2019 were included in the retrospective study. Forty-three patients were classified into mandatory ICU admission groups, and the remaining 956 patients were allocated into the no need for ICU admission group. The candidate variables, including patient demographic characteristics, preoperative laboratory tests and surgical variables, were compared between the two groups. We then carried out univariate and multivariate logistic regression analyses to find out risk factors for mandatory ICU admission. In order to develop the predictive model, we used Akaike information criterion (AIC) to select risk factors via a step-down backward process from the multivariate regression model. RESULTS: A number of risk factors for mandatory ICU admission were identified and subsequently used to build the nomogram: age [odds ratio (OR), 1.03; 95% CI, 1.00-1.07; P=0.031], ASA status (III-IV vs. I-II: OR,1.74; 95% CI, 0.88-3.46; P=0.114), tumor size (OR, 1.28; 95% CI, 1.08-1.51; P=0.004), estimated blood loss (OR, 1.001; 95% CI, 1.000-1.001; P=0.082) as well as intraoperative transfusion (Yes vs. No: OR, 3.82; 95% CI, 1.87-7.82; P<0.001). C-index of the nomogram was 0.800, indicating good discrimination. Both Calibration curve and Hosmer-Lemeshow goodness-of-fit tests (P=0.128) showed that there was a high degree of agreement between the prediction and actual outcome. CONCLUSIONS: A nomogram to predict mandatory ICU admission after gastrectomy for gastric cancer was constructed and validated. Clinicians could apply this predictive model to improve usage of limited ICU resources effectively.

LncRNA THOR promotes tongue squamous cell carcinomas by stabilizing IGF2BP1 downstream targets.

THOR, a highly conserved lncRNA, is potentially involved in various cancer development. However, its involvement in tongue squamous cell carcinoma (TSCC) remains unclear. The present study aims to explore the biological function and molecular mechanism of THOR in TSCC progression. The expressions of THOR and IGF2BP1 in TSCC tissues and adjacent non-cancerous tongue tissues (ANT) were examined through qRT-PCR. THOR levels were manipulated in TSCC cells to explore its function in cancer progression in vitro and in vivo, which were subsequently evaluated by CCK8, colony formation assay, flow cytometry, xenograft tumor assays. In situ hybridization, RIP and Western blot assay were performed to explore the underlying molecular mechanisms. We discovered that THOR and IGF2BP1 were dramatically upregulated in TSCC tissues. The expression of THOR is positively correlated with IGF2BP1 mRNA level. THOR mediated IGF2 expression via interacting with IGF2BP1, and affected the downstream MEK-ERK signaling pathway to regulate TSCC cells proliferation. THOR/IGF2BP1/IGF2-MEK-ERK axis regulated the proliferation of TSCC cells, implying that THOR would be a promising therapeutic target for TSCC patients.

Influence of sevoflurane exposure on mitogen-activated protein kinases and Akt/GSK-3ß/CRMP-2 signaling pathways in the developing rat brain.

Prolonged exposure to volatile anesthetics causes neurodegeneration in developing animal brains. However, their underlying mechanisms of action remain unclear. The current study investigated the expression of proteins associated with the mitogen-activated protein kinases (MAPK) and protein kinase B (Akt)/glycogen synthase kinase-3ß (GSK-3ß)/collapsin response mediator protein 2 (CRMP-2) signaling pathways in the cortices of neonatal mice following exposure to sevoflurane. Seven-day-old (P7) neonatal C57BL/6 mice were randomly divided into 2 groups and either exposed to 2.6% sevoflurane or air for 6 h. Terminal deoxyribonucleotide transferase mediated dUTP nick end labeling (TUNEL) staining, as well as the expression of activated caspase-3 and α-fodrin, was used to detect neuronal apoptosis in the cortices of mice. MAPK signaling pathways were investigated by detecting the expression of phosphorylated (p-) extracellular signal-regulated kinase 1/2 (ERK1/2), p-cyclic adenosine monophosphate response element-binding protein (CREB), p-p38, p-nuclear factor (NF-κB) and p-c-Jun N-terminal kinase (p-JNK). Akt/GSK-3ß/CRMP-2 signaling pathways were assessed by detecting the expression of p-Akt, p-GSK-3ß and p-CRMP-2 in the cortices of P7 mice 2 h following exposure to sevoflurane. The results demonstrated that sevoflurane significantly increased the apoptosis of cells in the retrosplenial cortex (RS), frontal cortex (FC) and parietal association cortex (PtA), increased the expression of cleaved caspase-3 expression and promoted the formation of 145 kDa and 120 kDa fragments from α-fodrin. Sevoflurane inhibited the phosphorylation of ERK1/2 and CREB, stimulated the phosphorylation of p38 and NF-κB, but did not significantly affect the phosphorylation of JNK. Furthermore, sevoflurane inhibited the phosphorylation of Akt, decreased the phosphorylation of GSK-3ß at ser9 and increased the phosphorylation of CRMP2 at Thr514. These results suggest that multiple signaling pathways, including ERK1/2, P38 and Akt/GSK-3ß/CRMP-2 may be involved in sevoflurane-induced neuroapoptosis in the developing brain.

Efficacy of 2-(1-hexyloxyethyl)-2-devinyl pyropheophorbide-a in photodynamic therapy of human esophageal squamous cancer cells.

The present study investigated the effects of 2-(1-hexyloxyethyl)-2-devinylpyro pheophorbide-a (HPPH)-mediated photodynamic therapy (PDT) on in vitro cell survival and in vivo tumor growth derived from human esophageal squamous cancer cells (Eca109). A cell counting kit 8 (CCK8) assay was used to assess the phototoxicity of HPPH-mediated PDT in cultured Eca109 cells. The inhibition of tumor growth was determined by the changes in the relative tumor volume (RTV) and tumor weight. The results revealed that HPPH, in the range of 0.005-1 µg/ml, exhibited no cytotoxicity in the Eca109 cells without light exposure and that the in vitro efficiency of HPPH-mediated PDT was higher compared with that of Photofrin®-mediated PDT. The in vivo results indicated that graded doses of HPPH-mediated PDT significantly inhibited the xenograft tumor growth derived from the Eca109 cells in a dose-dependent manner. The inhibition efficacy of 0.6 and 1.0 mg/kg HPPH-mediated PDT was similar to that of 10 mg/kg Photofrin-mediated PDT. Furthermore, HPPH possessed a lower toxicity than Photofrin at the dose that achieved the same efficacy in mice bearing Eca109 subcutaneous tumors. The histopathological findings indicated that the tumor tissues in the photosensitizer (PS)-treated mice demonstrated varying degrees of necrosis. HPPH and Photofrin exhibited vascular cytotoxicity on the treated tumors. In conclusion, the present study demonstrated that the phototoxicity of HPPH-mediated PDT is higher than that of Photofrin-mediated PDT of the same dose. HPPH possessed lower toxicity than Photofrin at the dose that achieved the same efficacy. Therefore, HPPH may be a promising agent for treating human esophageal squamous cell cancer (ESCC).

Effects of the altered activity of δ-opioid receptor on the expression of glutamate transporter type 3 induced by chronic exposure to morphine.

Altered δ-opioid receptor (DOR) activity can affect the activity and function of excitatory amino acid transporter 3 (EAAT3), but the effects of DOR on EAAT3 expression in morphine relapse remain unknown. In this study, a C6δ cell line and SD rats in a conditioned place preference (CPP) reinstatement model were used. Here, we show that EAAT3 protein levels in C6δ cells decreased significantly after chronic exposure to morphine (10 µM) for 48 h and returned to normal 12 h after drug withdrawal. When C6δ cells were re-exposed to 5 µM morphine for 4 h, EAAT3 protein levels again decreased significantly. The selective µ opioid receptor (MOR) specific agonist DAMGO had a similar effect as morphine, and CTOP, a specific MOR blocker, reversed the declined expression of EAAT3 protein triggered by morphine exposure. The selective DOR agonist [d-pen2, 5] enkephalin (DPDPE) significantly increased EAAT3 expression in C6δ cells and even reversed the decreased EAAT3 expression caused by chronic morphine exposure. The non specific antagonist naloxone, but not the DOR inhibitor Naltrindole (NTI), reversed the decreased EAAT3 expression in C6δ cells caused by chronic morphine exposure. In vivo, EAAT3 levels in the prefrontal cortex of rats with morphine-induced CPP reinstatement significantly decreased. Naloxone completely suppressed reinstatement and reversed the decrease in EAAT3 expression induced by morphine re-exposure. In contrast, NTI only weakened CPP reinstatement and exerted no influence on EAAT3 expression. These findings suggest that DOR can affect the expression of EAAT3. However, the morphine-induced down-regulation of EAAT3 in C6δ cells and in the prefrontal cortex of rats may not be mediated by DOR.

Simvastatin-induced up-regulation of gap junctions composed of connexin 43 sensitize Leydig tumor cells to etoposide: an involvement of PKC pathway.

Some of lipophilic statins have been reported to enhance toxicities induced by antineoplastic agents but the underling mechanism is unclear. The authors investigated the involvement of Cx43-mediated gap junction intercellular communication (GJIC) in the effect of simvastatin on the cellular toxicity induced by etoposide in this study. The results showed that a major component of the cytotoxicity of therapeutic levels of etoposide is mediated by gap junctions composed of connexin 43(Cx43) and simvastatin at the dosage which does not induce cytotoxicity enhances etoposide toxicity by increasing gap junction coupling. The augmentative effect of simvastatin on GJIC was related to the inhibition of PKC-mediated Cx43 phosphorylation at ser368 and subsequent enhancement of Cx43 membrane location induced by the agent. The present study suggests the possibility that upregulation of gap junctions may be utilized to increase the efficacy of anticancer chemotherapies.

Inhibition by dexmedetomidine of the activation of spinal dorsal horn glias and the intracellular ERK signaling pathway induced by nerve injury.

Activation of glial cells and the intracellular ERK signaling pathway plays an important role in the development and maintenance of neuropathic pain. As well as neurons, glial cell membranes also express α2-adrenergic receptors, but the effects of selective activation of these receptors on glial cell activation induced by neuropathic pain have yet to be clarified. We investigated the effects of intraperitoneal (IP) injections of tolerable doses of dexmedetomidine (DEX), a highly selective agonist of α2-adrenergic receptors, on activation of spinal dorsal root glial cells and the intracellular ERK signaling pathway induced by neuropathic pain. Adult rats that underwent partial sciatic nerve ligation (PNSL) were treated with repeated IP injections of DEX 20 µg/kg or 40 µg/kg, and their thermal and mechanical hyperalgesia thresholds were measured. The distribution and morphological changes of microglias and astrocytes were observed by immunofluorescence. Western blot was used to detect changes of glial fibrillary acid protein (GFAP) and pERK expression. Repeated IP injections of DEX 40 µg/kg for 7 or 14 days markedly reduced the thermal and mechanical hyperalgesia induced by PSNL. In addition, DEX 20 µg/kg for 14 days and 40 µg/kg for 7 days also significantly inhibited PSNL-induced activation of pERK in the spinal dorsal horn. Thus, repeated IP injections of DEX can markedly relieve the hyperalgesia of neuropathic pain in rats. The analgesic effect of DEX may be attributed to its inhibition of glial cell hypertrophy in the spinal dorsal horn and activation of the intracellular ERK signaling pathway.