Artificial intelligent patient-controlled intravenous analgesia improves the outcomes of older patients with laparoscopic radical resection for colorectal cancer.

METHODS: Patients undergoing elective laparoscopic radical resection of colorectal cancer from July 2019 to May 2021 were selected. The patients were assigned to Ai-PCIA group and control group. Ai-PCIA group received postoperative analgesia management and effect evaluation through intelligent wireless analgesia system + postoperative follow-up twice a day, while control group received analgesia management and effect evaluation through ward physician feedback + postoperative follow-up twice a day. The pain numerical score (NRS), Richards-Campbell Sleep Scale (RCSQ), and adverse outcomes were collected and compared. RESULTS: A total of 60 patients (20 females and 40 males with average (78.26 ± 6.42) years old) were included. The NRS scores at rest and during activity of the Ai-PCA group at 8, 12, and 24 h after the operation were significantly lower than that of the control group (all P < 0.05). The RCSQ score of Ai-PCA group was significantly higher than that of control group on the 1st and 2nd days after operation (all P < 0.05). There were no significant differences in the incidence of dizziness and nausea, vomiting, and myocardial ischemia (all P > 0.05). CONCLUSIONS: Ai-PCIA can improve the analgesic effect and sleep quality of older patients after laparoscopic radical resection, which may be promoted in clinical analgesia practice.

Butorphanol inhibits angiogenesis and migration of hepatocellular carcinoma and regulates MAPK pathway.

Butorphanol, a synthetic opioid, exerts analgesic and anti-inflammatory effects against pathogenic diseases. Butorphanol repressed malignant behaviors of tumor cells. In this study, the role of butorphanol in hepatocellular carcinoma was evaluated. Firstly, hepatocellular carcinoma cells were treated with butorphanol. The results showed that butorphanol decreased cell viability of hepatocellular carcinoma cells. Cell proliferation and metastasis of hepatocellular carcinoma cells were inhibited by butorphanol. Secondly, butorphanol suppressed angiogenesis, and reduced phosphorylation levels of p38 and JNK in hepatocellular carcinoma cells. Thirdly, butorphanol reduced in vivo tumor growth of hepatocellular carcinoma in nude mice. Butorphanol reduced tumor micro-vascular density (MVD) and repressed lung metastasis. In conclusion, butorphanol exerted anti-angiogenic and anti-metastatic effects on hepatocellular carcinoma and induced inactivation of MAPKs signaling.

The protective effects of butorphanol tartrate against homocysteine-induced blood-brain barrier dysfunction.

A high concentration of homocysteine (Hcy) has been recently reported to be closely associated with the development of stroke, which is related to the Hcy-induced blood-brain barrier (BBB) dysfunction. Butorphanol tartrate is a promising analgesic agent that targets the opiate receptor and shows promising protective effects on ischemia/reperfusion injury. The present research proposes to investigate the protective effect of butorphanol tartrate on Hcy-induced BBB disruption to explore the potential application of butorphanol tartrate in treating Hcy-induced stroke. Hcy was utilized to establish both an in vivo animal model and in vitro human brain vascular endothelial cells (HBVECs) injury model. We found that the increased diffusion of sodium fluorescein and Evan's blue, declined expression of Claudin-5, and increased production of interleukin- 6 (IL-6) and tumor necrosis factor-α (TNF-α) were observed in Hcy-treated mice, which were all significantly reversed by butorphanol tartrate. In Hcy-stimulated HBVECs, increased endothelial permeability and reduced expression levels of Claudin-5 and Krüppel-like factor 5 (KLF5) were observed, all of which were dramatically rescued by 2 and 5 µM butorphanol tartrate. Lastly, the protective function of butorphanol tartrate in Hcy-stimulated HBVECs was dramatically abolished by the knockdown of KLF5. Collectively, butorphanol tartrate showed protective effects on Hcy-induced BBB disruption by upregulating the KLF5/Claudin-5 axis.

Immune changes in peripheral blood and hematoma of patients with intracerebral hemorrhage.

Immunologic changes in the hematoma of patients with intracerebral hemorrhage (ICH) and the contribution of these changes to prognosis are unknown. We collected the blood samples and hematoma fluid from 35 patients with acute ICH (<30 hours from symptom onset) and 55 age-matched healthy controls. Using flow cytometry and ELISA, we found that the percentages of granulocytes, regulatory T cells, helper T (Th) 17 cells, and dendritic cells were higher in the peripheral blood of patients with ICH than in healthy controls, whereas the percentages of lymphocytes, M1-like macrophages, and M2-like macrophages were lower. Levels of IL-6, IL-17, IL-23, TNF-α, IL-4, IL-10, and TGF-ß were higher in the peripheral blood of patients with ICH. The absolute counts of white blood cells, lymphocytes, monocytes, and granulocytes in the hematoma tended to be greater at 12-30 hours than they were within 12 hours after ICH, but the percentage of Th cells decreased in peripheral blood. Increased levels of IL-10 in the serum and hematoma, and a reduction in M1-like macrophages in hematoma were independently associated with favorable outcome on day 90. These results indicate that immunocytes present in the hematoma may participate in the acute-phase inflammatory response after ICH.

Anesthetic postconditioning plus hypothermia following cardiopulmonary resuscitation protects the myocardial ultrastructure by modulating inflammatory events in rabbits.

Myocardial ischemia/reperfusion (I/R) injury is usually caused by resuscitation following cardiac arrest. The aim of the present study was to investigate the influence of sevoflurane postconditioning on the myocardial ultrastructure induced by cardiac arrest and successful resuscitation in mature rabbits. A total of 32 rabbits were randomly and equally divided into an I/R group (I/R group), a hypothermia group (H group), a sevoflurane postconditioning group (S group), and hypothermia plus sevoflurane postconditioning group (H + S group). Interleukin (IL)-8 and IL-10 levels in blood were evaluated at four different time points (1 h pre-ischemia: T1; 1, 2 and 3 h after reperfusion: T2, T3 and T4, respectively). The myocardial ultrastructure was evaluated by microscope after the rabbits were scarified. Plasma levels of IL-8 and IL-10 increased in all of the groups from T2. However, compared with the I/R group from T3 and T4, downregulation of IL-8 was significant in the S and H + S groups (P<0.05), and the result of intra-group comparison demonstrated that the level of serum IL-8 was the lowest in the H + S group (P<0.05). By contrast, upregulation of IL-10 was significantly higher in the S and H + S groups (P<0.05), particularly in the H + S group. Notably, ultrastructure damage of the myocardium was significantly lighter, and the structural integrity of the myocardium in the H + S group was better when compared with that of the S group. Thus, sevoflurane postconditioning plus hypothermia protected the myocardial ultrastructure following cardiopulmonary resuscitation by suppressing inflammatory effects.

Expression of RUNX2 and MDM21 in rats with periodontitis under chronic intermittent hypoxia.

OBJECTIVE: To discuss the expression of RUNX2 and MDM21 in rats with periodontitis under the chronic intermittent hypoxia. METHODS: A total of 32 SD healthy rats were randomly divided into four groups, with 8 rats in each group. The molecular biological techniques of immunohistochemistry, RT-PCR and Western blotting were employed to detect the effect of different hypoxia time (0, 6, 12, 24 and 48 h) and different concentrations of hypoxia (0.000, 0.001, 0.010, 0.060 and 0.100 ppm) on the expression of RUNX2 and MDM21 in rats of four groups. RESULTS: The expression of RUNX2 and MDM21 in each group was significantly higher than the one at other concentrations when the concentration was 0.010 ppm, with the statistical difference (P < 0.05). The expression of RUNX2 and MDM21 was that normoxic control group > normoxic periodontitis group > hypoxia control group > hypoxia periodontitis group under the action with the concentration of 0.010 ppm for 12 h, but there was no significant difference for the comparison among groups (P > 0.05). CONCLUSIONS: The condition of chronic intermittent hypoxia can reduce the expression of RUNX2 and MDM21 in rats with periodontitis and aggravate the damage of periodontal bone.

Renoprotective effects of propofol on the expression of iNOS protein in rats with ischemia reperfusion injury.

AIMS: This study aims to explore the pathogenesis of myocardial ischemia-reperfusion injury and the treatment method. METHODS: Myocardial Ischemia-reperfusion rat model was established in this study. They were divided into three groups: sham operation (SO) group, IRI control (C) group and IRI with propofol (A) group (n = 9). Myocardial infarct size was compared with HE staining method. TUNEL assay was used to detect cell apoptosis. Changes in the expression of iNOS were detected using real-time PCR and Western blotting methods. RESULTS: Myocardial infarct size of control group and propofol group was 53.03 ± 8.90% and 34.73 ± 7.20% respectively, there were significant differences between them (P < 0.01). Apoptotic index of two groups was 0.21 ± 0.02 and 0.31 ± 0.05, with statistical significance (P < 0.05). The expression levels of iNOS in propofol group reduced significantly (P < 0.05). CONCLUSION: The levels of iNOS increase in IRI rats, suggesting that the severity of myocardial failure may be correlated with iNOS; propofol can specifically inhibit iNOS and thus protect the myocardial function.