[Application effects of nitrous oxide and oxygen mixed inhalation technology on analgesia and sedation during debridement and dressing change in children with moderate or severe burns].

Objective: To investigate the application effects of nitrous oxide and oxygen mixed inhalation technology on analgesia and sedation during debridement and dressing change in children with moderate or severe burns. Methods: A retrospective non-randomized contemporary controlled study was conducted. From December 2019 to November 2021, 140 burn children with moderate or severe burns, aged 1 to 3 years, who met the inclusion criteria were admitted to Central Hospital Affiliated to Shandong First Medical University. During debridement and dressing change 3 to 14 days after injury, 42 children, including 23 males and 19 females, who received nurse-centered pain management mode and analgesia and sedation with nitrous oxide and oxygen mixed inhalation technology were included in nitrous oxide group (the dressing change process using the above-mentioned technology for the first time was selected for the follow-up study). Another 42 children, including 24 males and 18 females, were included in non-nitrous oxide group from 98 children who did not apply analgesia or sedation treatment during dressing change with stratified random sampling (one dressing change process was randomly selected for the follow-up study). The face, legs, activity, cry, and consolability scale and Ramsay sedation scale were used to evaluate the pain intensity and degree of sedation, respectively, at 30 minutes before dressing change (hereinafter referred to as before dressing change), immediately after debridement, and at 30 minutes after finishing dressing change (hereinafter referred to as after dressing change). After dressing change, the self-made satisfaction scale was used to evaluate the satisfaction degree of dressing change surgeons and guardians of children for analgesic effects during dressing change. The duration of dressing change and the healing time of deep partial-thickness burn wounds were recorded. The heart rate and percutaneous arterial oxygen saturation (SpO2) before, during, and after dressing change and the occurrence of adverse events such as nausea and vomiting during dressing change were recorded. Data were statistically analyzed with Mann-Whitney U test, chi-square test, analysis of variance for repeated measurement, independent sample t test, and Bonferroni correction. Results: There were no significant differences in the score of pain intensity and score of sedation degree between children in two groups before and after dressing change (P>0.05). Immediately after debridement, the score of pain intensity of children in nitrous oxide group was 2.5±0.7, which was significantly lower than 7.6±1.0 in non-nitrous oxide group (t=-26.69, P<0.05); the score of sedation degree of children in nitrous oxide group was 1.83±0.38, which was significantly higher than 1.21±0.42 in non-nitrous oxide group (t=7.15, P<0.05). After dressing change, the satisfaction degree scores of dressing change surgeons and guardians of children for analgesic effects during dressing change of children in nitrous oxide group were significantly higher than those in non-nitrous oxide group (with t values of 10.53 and 2.24, respectively, P<0.05). The dressing change duration of children in nitrous oxide group was significantly shorter than that in non-nitrous oxide group (t=-5.33, P<0.05). The healing time of deep partial-thickness burn wounds in children between the two groups had no significant difference (P>0.05). The heart rate of children in nitrous oxide group was significantly lower than that in non-nitrous oxide group during dressing change (t=-12.40, P<0.05), while the SpO2 was significantly higher than that in non-nitrous oxide group (t=5.98, P<0.05). During dressing change, 2 children had nausea and 1 child had euphoria in nitrous oxide group, while heart rate of all children in non-nitrous oxide group continued to be higher than the normal range. Conclusions: In the process of debridement and dressing change in children with moderate or severe burns, the use of nurse-centered pain management mode and the standardized use of nitrous oxide and oxygen mixed inhalation technology can safely and effectively control pain and sedation.

LncRNA HOXA-AS2 accelerates the proliferation and migration and inhibits the apoptosis of vascular smooth muscle cells by absorbing miRNA-877-3p.

OBJECTIVE: The aim of this study was to clarify the role of long non-coding RNA (lncRNA) HOXA-AS2 in influencing the proliferative, migratory and apoptotic abilities of human aortic vascular smooth muscle cells (HA-VSMCs) by absorbing microRNA-877-3p (miRNA-877-3p). MATERIALS AND METHODS: HOXA-AS2 level in HA-VSMCs treated with different doses of oxidized low-density lipoprotein (ox-LDL) and for different time points was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). After transfection of si-HOXA-AS2 in HA-VSMCs undergoing ox-LDL treatment, the viability, apoptotic rate and migration of cells were detected, respectively. Meanwhile, the subcellular distribution of HOXA-AS2 was analyzed. The Dual-Luciferase reporter gene assay was applied to verify the binding relationship between HOXA-AS2 and miRNA-877-3p. MiRNA-877-3p level in HA-VSMCs treated with different doses of ox-LDL was determined as well. Furthermore, the regulatory effects of HOXA-AS2/miRNA-877-3p axis on cellular behaviors of HA-VSMCs were determined. RESULTS: HOXA-AS2 expression was upregulated by ox-LDL treatment in a time- and dose-dependent manner. After being treated with 100 mg/L ox-LDL for 48 h, the proliferative and migratory abilities of HA-VSMCs were significantly enhanced, while apoptosis was inhibited. Conversely, these changes were reversed by transfection of si-HOXA-AS2. HOXA-AS2 was mainly distributed in the nuclear fraction. Dual-Luciferase reporter gene assay confirmed the direct binding relationship between HOXA-AS2 and miRNA-877-3p. Moreover, miRNA-877-3p was markedly downregulated after transfection of si-HOXA-AS2. MiRNA-877-3p expression decreased gradually with an increased dose of ox-LDL. In addition, knockdown of miRNA-877-3p could reverse the regulatory effects of HOXA-AS2 on proliferative, migratory and apoptotic abilities of HA-VSMCs. CONCLUSIONS: HOXA-AS2 is upregulated after HA-VSMCs injury, which accelerates the proliferative and migratory abilities, and inhibits the apoptosis of vascular smooth muscle cells by absorbing miRNA-877-3p.

Expressions and significances of TTF-1 and PTEN in early endometrial cancer.

OBJECTIVE: To analyze the expressions and significances of TTF-1 (Thyroid transcription factor-1) and PTEN (Phosphatase and tensin homolog) in early endometrial cancer. PATIENTS AND METHODS: 41 patients with endometrial cancer, 38 patients with proliferative endometrium and 13 patients with normal endometrium, were selected. The fluorescence quantitative PCR (polymerase chain reaction) was used to detect the expression levels of TFF-1 and PTEN mRNAs (Messenger ribonucleic acids) in the above three endometria, and their relations with clinical pathological characteristics were analyzed. The RT-PCR (reverse transcription-polymerase chain reaction) was employed to detect the expression levels of miR-135b, miR-125b and Snail mRNAs in the three endometria, and their correlations with the expressions of TTF-1 and PTEN mRNAs, were analyzed. RESULTS: The expression levels of TFF-1 and PTEN mRNAs in endometrial cancer tissues were significantly lower than those in the other two groups, while those in normal endometrium tissues were the highest, and the differences were statistically significant (p < 0.05). There were no significant differences in the menstruation status and the expression levels of TFF-1 and PTEN mRNAs between adenocarcinoma and squamous carcinoma (p > 0.05). With the increase of FIGO (International Federation of Gynecology and Obstetrics) stage and depth of invasion, as well as the metastasis of pelvic lymph nodes, the expression levels of TFF-1 and PTEN mRNAs were significantly decreased, and the differences were statistically significant (p < 0.05). The expression level of miR-135b mRNA in endometrial cancer was significantly higher than that in the other two groups, while that in normal endometrium was the lowest. The expression levels of miR-125b and Snail mRNAs were significantly lower than those in the other two groups, while those in normal endometrium were the highest; the differences were statistically significant (p < 0.05). Expression levels of TTF-1 and PTEN mRNAs were negatively correlated with the expression level of miR-135b mRNA, and positively associated with the expression levels of miR-125b and Snail mRNAs (p < 0.05). The results from the ROC (Receiver Operating Characteristic) model showed that, for the diagnosis of endometrial cancer with TTF-1 mRNA, the sensitivity was 86.5%, the specificity was 84.2%, the accuracy (area under curve - AUC) was 0.823, 95% CI (confidence intervals) = 0.762-0.921, p = 0.012. For the diagnosis of endometrial cancer with PTEN mRNA, the sensitivity was 85.3%, the specificity was 83.6%, the accuracy was 0.842, 95% CI = 0.785-0.936, p = 0.010. CONCLUSIONS: TTF-1 and PTEN can be used as molecular markers for the early diagnosis of endometrial cancer, which are closely related to clinical features and may affect tumor progression by regulating the proliferation activity of tumor cells.

Chronic restraint stress decreases the repair potential from mesenchymal stem cells on liver injury by inhibiting TGF-ß1 generation.

Chronic psychological stress has been demonstrated to play an important role in several severe diseases, but whether it affects disease therapy or not remains unclear. Mesenchymal stem cells (MSCs) have been demonstrated to have therapeutic potentials in treating tissue injury based on their multidifferentiation potential toward various cell types. We investigated the effect of chronic restraint stress on therapeutic potential of MSCs on carbon tetrachloride (CCl4)-induced liver injury in mice. CCl4-induced mice were injected with enhanced green fluorescent protein-MSCs, which was followed by chronic restraint stress administration. Corticosterone and RU486, a glucocorticoid receptor (GR) antagonist, were employed in vivo and in vitro, too. In the present study, we illustrated that MSCs could repair liver injury by differentiating into myofibroblasts (MFs) which contribute to fibrosis, whereas stress repressed differentiation of MSCs into MFs displayed by reducing α-smooth muscle actin (α-SMA, a solid marker of MFs) expression. Whereas RU486 could maintain the liver injury reduction and liver fibrosis increases induced by MSCs in stressed mice and block the decrease of α-SMA expression induced by stress. Furthermore, chronic stress inhibited MFs differentiation from MSCs by inhibiting transforming growth factor-ß1 (TGF-ß1)/Smads signaling pathway which is essential for MFs differentiation. Chronic stress reduced autocrine TGF-ß1 of MSCs, but not blunted activation of Smads. All these data suggested that corticosterone triggered by chronic stress impaired liver injury repair by MSCs through inhibiting TGF-ß1 expression which results in reduced MFs differentiation of MSCs.