Combined use of transversus abdominis plane block and laryngeal mask airway during implementing ERAS programs for patients with primary liver cancer: a randomized controlled trial.

The incidence and mortality of primary liver cancer are very high and resection of tumor is the most crucial treatment for it. We aimed to assess the efficacy and safety of combined use of transversus abdominis plane (TAP) block and laryngeal mask airway (LMA) during implementing Enhanced Recovery After Surgery (ERAS) programs for patients with primary liver cancer. This was a prospective, evaluator-blinded, randomized, controlled parallel-arm trial. A total of 96 patients were enrolled (48 in each group). Patients in the control group received general anesthesia with endotracheal intubation, while patients in the TAP + LMA group received general anesthesia with LMA and an ultrasound-guided subcostal TAP block. The primary end-point was postoperative time of readiness for discharge. The secondary end-points were postoperative pain intensity, time to first flatus, quality of recovery (QoR), complications and overall medical cost. Postoperative time of readiness for discharge in the TAP + LMA group [7 (5-11) days] was shorter than that of the control group [8 (5-13) days, P = 0.004]. The postoperative apioid requirement and time to first flatus was lower in the TAP + LMA group [(102.8 ± 12.4) µg, (32.7 ± 5.8) h, respectively] than the control group [(135.7 ± 20.1) µg, P = 0.000; (47.2 ± 7.6) h, P = 0.000; respectively]. The QoR scores were significantly higher in the TAP + LMA group than the control group. The total cost for treatment in the TAP + LMA group [(66,608.4 ± 6,268.4) CNY] was lower than that of the control group [(84,434.0 ± 9,436.2) CNY, P = 0.000]. There was no difference in complications between these two groups. The combined usage of a TAP block and LMA is a simple, safe anesthesia method during implementing ERAS programs for patients with primary liver cancer. It can alleviate surgical stress, accelerate recovery and reduce medical cost.

Impact of different analgesic depths and abdominal trauma of different severities on stress and recovery of rats undergoing total intravenous anesthesia.

A number of animal models have been developed to examine the pathophysiological consequences of surgical procedures, but anesthetic methods, monitoring, and management measures in these models are very different from those used in humans. This study was designed to create a rat model of abdominal surgery using anesthetic methods and perioperative treatment similar to those used in the clinic and to investigate the effects of different injury severities and depths of anesthesia and analgesia on surgical stress and postoperative recovery. Abdominal skin/muscle incision was compared with exploratory laparotomy in rats under propofol intravenous anesthesia, accompanied by perioperative measures such as oxygen inhalation, fluid infusion, warmth, blood gas analysis, and infection prevention. Stress indices (mean arterial pressure, heart rate, blood glucose, and plasma corticosterone) were monitored during anesthesia and surgery, and recovery indicators (body weight, food consumption, and pain) were measured after surgery. In addition, animals undergoing laparotomy were subjected to low and high dosages of propofol and sufentanil, in order to examine the relationship between anesthetic and analgesic depth and stress on recovery. Exploratory laparotomy induced a greater stress response and caused slower postoperative recovery as measured than somatic injury. High-dose sufentanil downregulated plasma corticosterone and improved postoperative recovery more effectively than high-dose propofol (P<0.05). Taken together, a rat model of abdominal surgery using anesthetic methods and perioperative treatment similar to those used in the clinic was successfully developed. It showed a positive correlation between severity of surgical trauma and stress response and postoperative recovery and a significant role of adequate analgesia in reducing surgical stress and improving postoperative recovery.

The application of color Doppler flow imaging in the diagnosis and therapeutic effect evaluation of erectile dysfunction.

We aim to investigate the correlations between hemodynamic parameters, penile rigidity grading, and the therapeutic effects of phosphodiesterase type 5 inhibitors using color Doppler flow imaging after intracavernosal injection in patients with erectile dysfunction. This study involved 164 patients. After intracavernosal injection with a mixture of papaverine (60 mg), prostaglandin E 1 (10 mg), and lidocaine (2%, 0.5-1 ml), the penile vessels were assessed using color Doppler flow imaging. Penile rigidity was classified based on the Erection Hardness Score system as Grades 4, 3, 2 or 1 (corresponding to Schramek Grades V to II). Then, the patients were given oral sildenafil (50-100 mg) and scored according to the International Index of Erectile Function (IIEF-5) questionnaire. The number of patients with penile rigidities of Schramek Grades II to V was 14, 18, 21, and 111, respectively. The IIEF-5 score was positively correlated with the refilling index of the penile cavernosal artery (r = 0.79, P< 0.05), the peak systolic velocity (r = 0.45, P< 0.05), and penile rigidity (r = 0.75, P< 0.05), and was negatively correlated with the end diastolic velocity (r = -0.74, P< 0.05). For patients with erectile dysfunction, both the IIEF-5 score after sildenafil administration, which is correlated with penile rigidity, and the hemodynamic parameters detected using color Doppler flow imaging may predict the effects of phosphodiesterase type 5 inhibitor treatment and could provide a reasonable model for the targeted-treatment of erectile dysfunction.

MicroRNA-155 promotes bladder cancer growth by repressing the tumor suppressor DMTF1.

MicroRNA-155 (miR-155) is dysregulated in human cancers. In this study, we reported that miR-155 was over-expressed in bladder cancer tissues. We found that miR-155 promoted cell proliferation in vitro and tumorigenesis in vivo. MiR-155 directly reduced the expression of the tumor suppressor DMTF1. The expression of DMTF1 was decreased in bladder cancer tissues. Similar to the restoring miR-155 expression, knockdown of DMTF1 promoted cell growth and cell cycle progression, whereas DMTF1 over-expression rescued the effect of miR-155. Moreover, we investigated DMTF1-Arf-p53 pathway and found that DMTF1 worked in both p53-dependent and p53-independent manners. Taken together, our findings suggested that miR-155 functions as a tumor promoter in bladder cancer, which is partially through repressing DMTF1 expression. The identification of miR-155 and its novel target DMTF1 will be valuable in developing diagnostic markers and therapeutic applications for bladder cancer.

Kidney cancer cells secrete IL-8 to activate Akt and promote migration of mesenchymal stem cells.

BACKGROUND: Mesenchymal stem cells (MSCs) are multipotent adult stem cells that have the capability of homing to cancer cells. Thus, MSCs play an important role in the development, metastasis, and drug resistance of cancers. The mechanisms underlying the homing of MSCs in kidney cancer are still poorly understood. METHODS: In the present study, enzyme-linked immunosorbent assay was used to measure the level of IL-8 in patients with kidney cancer and in the culture medium of kidney cancer cells. Immunofluorescence staining and reverse transcription polymerase chain reaction were utilized to explore the main receptor for IL-8 in MSCs. Transwell migration assay was performed to measure the migration ability of MSCs and Western blot test was performed to test the activation of signaling pathways. RESULTS: The serum level of IL-8 was markedly increased in patients with kidney cancer, and 2 kidney cancer cell lines were found to secrete IL-8. MSCs had high expression of the IL-8 receptor (CXCR2). Blocking IL-8 or CXCR2 could decrease the migration ability of MSCs. IL-8 could significantly increase Akt phosphorylation in MSCs. CONCLUSIONS: Kidney cancer cells secrete IL-8 to activate the Akt signaling pathway via CXCR2 on MSCs, inducing the migration of MSCs, which may be one of the important mechanisms underlying the homing of MSCs in kidney cancer.