The aim of this study was to compare the effects of preoperative intranasal dexmedetomidine and oral midazolam on preoperative sedation and postoperative agitation in pediatric dentistry. A total of 60 children (ASA grade I, aged 3–6 years) scheduled for elective pediatric dental treatment were randomly divided into the dexmedetomidine (DEX) and midazolam (MID) groups. Ramsay sedation score, parental separation anxiety scale, mask acceptance scale, pediatric anesthesia emergence delirium scale, and hemodynamic parameters were recorded. The Ramsay sedation scale and hemodynamic parameters of the children were observed and recorded immediately before administration and 10, 20, and 30 min after administration. A satisfactory mask acceptance scale rate was 93.33% in both MID and DEX groups, and there was no significant difference between the two groups (p>0.05). The proportions of children that “successfully separated from their parents” were 93.33% (MID) and 96.67% (DEX). No significant difference was found between the two groups (p>0.05). The incidence of agitation was 20% in the MID group and 0% in the DEX group, and the difference was statistically significant (p<0.05). Intranasal dexmedetomidine and oral midazolam provided satisfactory sedation. No significant difference between the two groups was found in terms of parental separation anxiety and mask acceptance (p>0.05). The incidence of postoperative pediatrics emergence delirium was significantly lower in the DEX group (p<0.05).

Dexmedetomidine refers to an α2-adrenergic receptor agonist causing potent sedative, analgesic, and minimal respiratory depression compared with alternative drugs. The present study was aimed at comparing the efficaciousness and safety of midazolam and dexmedetomidine as sedatives for dental implantation. We recruited 60 patients belonging to group I or II of the American Society of Anesthesiologists (ASA) and treated them with either midazolam or dexmedetomidine in a random manner. Patients’ duration of analgesia after surgery, surgeon and patient degrees of satisfaction, Observer’s Assessment of Alertness/Sedation Scale (OAAS) scores after drug administration, visual analogue scale (VAS) pain scores, and vital signs were recorded variables. Patients administered dexmedetomidine had significantly lower OAAS scores than those administered midazolam (p<0.05). Patients administrated dexmedetomidine had a significantly longer analgesia duration after the surgical procedure than those administered midazolam, and the difference was statistically significant (p<0.05). Dexmedetomidine had a significantly larger number of surgeons satisfied with the level of sedation/analgesia than midazolam (p<0.05). Accordingly, it is considered that dexmedetomidine can achieve better postoperative analgesia, surgeon satisfaction, and sedation than midazolam.

Many studies have verified that microRNAs contribute a lot to neuropathic pain progression. Furthermore, nerve‐related inflammatory cytokines play vital roles in neuropathic pain progression. miR‐183 has been identified to have a common relationship with multiple pathological diseases. However, the potential effects of miR‐183 in the process of neuropathic pain remain undetermined. Therefore, we performed the current study with the purpose of finding the functions of miR‐183 in neuropathic pain progression using a chronic sciatic nerve injury (CCI) rat model. We demonstrated that miR‐183 expression levels were evidently reduced in CCI rats in contrast with the control group. Overexpression of miR‐183 produced significant relief of mechanical hyperalgesia, as well as thermal hyperalgesia in CCI rats. Furthermore, neuropathic pain‐correlated inflammatory cytokine expression levels containing interleukin‐6 (IL‐6) and interleukin‐1β (IL‐1β), cyclooxygenase‐2 (COX‐2) were obviously inhibited by upregulation of miR‐183. Meanwhile, dual‐luciferase reporter assays showed MAP3K4 was a direct downstream gene of miR‐183. The expression levels of MAP3K4 were modulated by the increased miR‐183 negatively, which lead to the downregulation of IL‐6, IL‐1β, and COX‐2, and then reduced neuropathic pain progression, respectively. Overall, our study pointed out that miR‐183 was a part of the negative regulator which could relieve neuropathic pain by targeting MAP3K4. Thus it may provide a new clinical treatment for neuropathic pain patients clinical therapy.

The dysfunction of the nervous system contributes to neuropathic pain.Long noncoding RNAs are reported to participate in neuropathic pain. Recently, Linc00052 is implicated to be closely associated with multiple diseases.Nevertheless, the mechanisms of Linc00052 remain barely explored in neuropathic pain development. Currently, spinal nerve ligation (SNL) triggered neuropathic pain was employed in our investigation. Here, we assessed the function of Linc00052 in SNL rat models. Interestingly, we reported Linc00052 was significantly elevated in SNL rats. Loss of Linc00052 could reduce neuropathic pain progression via regulating the behaviors of neuropathic pain. Additionally, knockdown of Linc00052 repressed the processes of neuroinflammation. Interleukin (IL)-6 and tumor necrosis factor α level were inhibited while IL-10 was induced by the silence of Linc00052. Moreover, we predicted miR-448 can serve as a target of Linc00052. miR-448 exerts a crucial power in several diseases. Currently, we exhibited miR-448 was remarkably downregulated in SNL rats. RNA immunoprecipitation experiments validated the association between miR-448 and Linc00052. Inhibition of Linc00052 could reverse the roles of miR-448 on neuropathic pain development. Furthermore, Janus kinase 1 (JAK1) was displayed as the putative target of miR-448 in the present investigation. It was showed that JAK1 was induced in SNL rats. Loss of miR-448 could dramatically induce the expression of JAK1, which was rescued by knockdown of Linc00052. Taken these together, our study implied that Linc00052 functioned as a novel target of neuropathic pain via sponging miR-448 and regulating JAK1.

The aim of the investigation is to clarify the beneficial sedative effects for patients with postoperative intubation in the intensive care unit (ICU) after oral and maxillofacial surgery. Forty patients with postoperative intubation were divided into two groups in method of random number table: midazolam group and dexmedetomidine group. The Ramsay score, the behavioral pain scale (BPS) score, SpO 2 , HR, MAP, and RR were recorded before sedation (T0), 30 minutes (T1), 1 hour (T2), 2 hours (T3), 6 hours (T4), and 12 hours (T5) after dexmedetomidine or midazolam initiation in intensive care unit, and 10 minutes after extubation (T6). The rate of incidences of side effects was calculated. Sedation with midazolam was as good as standard sedation with dexmedetomidine in maintaining target sedation level. The BPS score in the midazolam group was higher than that in the dexmedetomidine group. The time of tracheal catheter extraction in the dexmedetomidine group was shorter than that in the midazolam group (p ≤ 0:001). The incidence of bradycardia in the dexmedetomidine group was higher than that in the midazolam group (p = 0:028). There was no statistically significant difference in the incidence of hypotension between the two groups (p = 0:732). The incidence of respiratory depression of group midazolam was higher than that of group dexmedetomidine (p = 0:018). The incidence of delirium in the dexmedetomidine group was significantly lower than that in the midazolam group, and the difference was statistically significant (p = 0:003). Dexmedetomidine and midazolam can meet the needs for sedation in ICU patients. And dexmedetomidine can improve patients' ability to communicate pain compared with midazolam.