Analgesic effects of pectoserratus plane block and intermediate cervical plexus block for transaxillary endoscopic thyroidectomy: a prospective randomized controlled trial.

BACKGROUND: Transaxillary endoscopic thyroidectomy (TAET) is favored for its favorable cosmetic outcomes and the preservation of anterior cervical function. Despite these benefits, postoperative analgesia has traditionally relied on pharmacological interventions, and regional anesthetic procedures may be an alternative method. This study aimed to evaluate the efficacy of an ultrasound-guided pectoserratus plane block (PSPB) combined with an intermediate cervical plexus block (ICPB) for TAET. METHODS: Forty patients undergoing TAET were randomized into two groups: the nerve block group (N.=20) received ultrasound guided PSPB with 20 ml of 0.375% ropivacaine and ICPB with 8 mL of 0.3% ropivacaine, while the control group (N.=20) received no block. The primary outcome was the Visual Analog Scale (VAS) scores for postoperative neck and axillary pain at different time points (1, 6, 12, 24 h) during rest and movement post-TAET. The secondary outcomes included intraoperative remifentanil consumption, incidence of postoperative nausea and vomiting (PONV), number of remedial analgesic requirements, and patient satisfaction postoperatively. RESULTS: Compared to the control group, patients in the nerve block had significantly lower VAS scores of the neck and axilla whether at rest or movement, and 1, 6, 12, and 24 h postoperatively (P<0.0125). The nerve block group showed higher patient satisfaction (P<0.001). No difference was observed in intraoperative remifentanil consumption, need for rescue analgesics, or other adverse effects 48 h postoperatively. CONCLUSIONS: Ultrasound-guided PSPB with ICPB significantly alleviated postoperative pain and improved patient satisfaction with TAET.

A blockade of microRNA-155 signal pathway has a beneficial effect on neural injury after intracerebral haemorrhage via reduction in neuroinflammation and oxidative stress.

MicroRNAs (miRNAs) have important contributions to multiple pathophysiological processes for cellular response to stress and are considered as promising therapeutic targets with respect to drug development due to their small size, relative ease of delivery, and sequence specificity. Thus, in the current report, we examined the effects of inhibiting miRNA-155 (miR-155) on the levels of pro-inflammatory cytokines (PICs), oxidative stress products as well as vascular endothelial growth factor (VEGF) in the parietal cortex and hippocampus of rats following intracerebral haemorrhage (ICH). Real time PCR was used to examine the levels of miR-155 in the parietal cortex and hippocampus of rats; and ELISA to measure IL-1ß, IL-6 and TNF-α, oxidative 8-iso PGF2α and 8-OHdG, and VEGF. Additionally, modified neurological Severity Score (mNSS) was examined to indicate neurological function in animals. In results, with induction of ICH, the levels of miR-155 were amplified in the parietal cortex and hippocampus and this was accompanied with increases of IL-1ß, IL-6 and TNF-α; and 8-iso PGF2α and 8-OHdG. Intracerebroventricular infusion of miR-155 inhibitor attenuated the elevation of PICs and amplification of oxidative stress products. Interestingly, miR-155 inhibitor promoted VEGF levels. Furthermore, inhibition of miR-155 led to improvement of neurological deficits in ICH rats. In conclusion, miR-155 signal in the parietal cortex and hippocampus is engaged in the processes of neural injury during ICH and blocking central miR-155 pathway plays a beneficial role in regulating neurological function via reduction in PICs and products of oxidative stress; and enhancement of VEGF. This has implications to target miR-155 and its downstream signal pathway for neuronal dysfunction and vulnerability related to ICH.

High CTSL2 expression predicts poor prognosis in patients with lung adenocarcinoma.

Cathepsin like 2 (CTSL2) is a lysosomal cysteine protease, and may be associated with tumor metastasis. However, CTSL2 has not been reported as a biomarker in lung adenocarcinoma (LUAD). In this study, bioinformatics analysis using data from The Cancer Genome Atlas was performed. Wilcoxon rank-sum test and chi-square test were carried out. Kaplan-Meier and Cox regression were performed to evaluate the effect of CTSL2 expression in the overall survival. Our results indicated that CTSL2 in tumor was significantly higher than that in normal tissue (P < 0.001). High CTSL2 expression was significantly associated with age (P = 0.02), vital status (P < 0.001), and T classification (P = 0.03), and correlated with poor overall survival (HR = 1.62, 95% CI = 1.21-2.18, P = 0.001). CTSL2 expression was an independent risk factor for overall survival in patients with LUAD (HR = 1.52, 95% CI = 1.12-2.05, P = 0.006). A nomogram was plotted for illustration of CTSL2 expression on the risk of LUAD. Furthermore, in vitro cell experiments showed the CTSL2 promoted the proliferation and migration of A549 cells. In summary, high CTSL2 expression predicts poor prognosis in patients with LUAD.

Successful surgical treatment of Cronkhite-Canada Syndrome with bilateral flail chest: a case report.

BACKGROUND: Development of multiple rib fractures leading to bilateral flail chest in Cronkhite-Canada Syndrome (CCS) has not been reported. CASE PRESENTATION: A 59-year-old man presented with complaints of fatigue, chest pain, respiratory distress and orthopnea requiring ventilatory support to maintain oxygenation. CCS with bilateral anterior and posterior flail chest due to multiple rib fractures (2nd-10th on the right side and 2nd-11th on the left side). He underwent open reduction and anterior and posterior internal fixation using a titanium alloy fixator and a nickel-titanium memory alloy embracing fixator for chest wall reconstruction. He recovered gradually from the ventilator and showed improvement in his symptoms. He gained about 20 kg of weight in the follow up period (6 months after discharge from the hospital). CONCLUSION: CCS is a rare, complex disease that increases the risk of developing multiple rib fractures, which can be successfully treated with open reduction and internal fixation.

Inhibition of microRNA-155 Reduces Neuropathic Pain During Chemotherapeutic Bortezomib via Engagement of Neuroinflammation.

As a chemotherapeutic agent, bortezomib (BTZ) is used for the treatment of multiple myeloma with adverse effect of painful peripheral neuropathy. Our current study was to determine the inhibitory effects of blocking microRNA-155 (miR-155) signal on BTZ-induced neuropathic pain and the underlying mechanisms. We employed real time RT-PCR and western blot analysis to examine the miR-155 and expression of pro-inflammatory tumor necrosis factor-α receptor (TNFR1) in the dorsal horn of the spinal cord. Its downstream signals p38-MAPK and JNK and transient receptor potential ankyrin 1 (TRPA1) were also determined. Mechanical pain and cold sensitivity were assessed by behavioral test. In result, inhibition of miR-155 significantly attenuated mechanical allodynia and thermal hyperalgesia in BTZ rats, which was accompanied with decreasing expression of TNFR1, p38-MAPK, JNK, and TRPA1. In contrast, miRNA-155 mimics amplified TNFR1-TRPA1 pathway and augmented mechanical pain and cold sensitivity. In addition, mechanical and thermal hypersensitivity induced by miRNA-155 mimics were attenuated after blocking TNFR1, p38-MAPK, JNK, and TRPA1. Overall, we show the key role of miR-155 in modifying BTZ-induced neuropathic pain through TNFR1-TRPA1 pathway, suggesting that miR-155 is a potential target in preventing neuropathic pain development during intervention of BTZ.

Anesthetic effect of propofol combined with remifentanil or sevoflurane anesthesia on patients undergoing radical gastrectomy.

Anesthetic effect of propofol combined with remifentanil or sevoflurane intravenous anesthesia on patients undergoing radical gastrectomy was evaluated. The clinical data of 516 cancer patients who received radical gastrectomy in the First Bethune Hospital of Jilin University between January 2011 and December 2017 were retrospectively analyzed. In total 203 patients with propofol combined with remifentanil anesthesia were used as group A, and 313 patients with propofol combined with sevoflurane anesthesia as group B. The changes of respiration and circulation were analyzed at the time of entering the operating room (t0), the beginning of the operation (t1), 10 min after the beginning of the operation (t2) and 10 min after operation (t3). The onset time of anesthesia, the total time of operation, the time of waking up after operation and the time of leaving the operating room were analyzed. The effects of sedation and amnesia were evaluated, and the occurrence of adverse reactions were recorded. The inhibition of circulation and respiration was more obvious at t1 and t2 in group A when compared to group B (P<0.05), and the respiration and circulation in group B was more stable than that in group A (P<0.001). Patients' sedation scores in group A were lower than those in group B, and the difference was statistically significant (P<0.05); there were 56 (27.59%) patients and 30 (9.58%) patients with postoperative pain in group A and group B, respectively (P<0.001). The application of propofol combined with sevoflurane in the anesthesia of patients undergoing radical gastrectomy can make the respiration and circulation more stable, and reduce the incidence of postoperative pain and adverse reactions.

Blocking Mammalian Target of Rapamycin (mTOR) Alleviates Neuropathic Pain Induced by Chemotherapeutic Bortezomib.

BACKGROUND/AIMS: Bortezomib (BTZ) is largely used as a chemotherapeutic agent for the treatment of cancer. However, one of the significant limiting complications of BTZ is painful peripheral neuropathy during BTZ therapy. Drugs preventing and/or treating the painful symptoms induced by BTZ are lacking since the underlying mechanisms leading to neuropathic pain remain largely unclear. The purposes of this study were to examine 1) the effects of blocking mammalian target of rapamycin (mTOR) on mechanical pain and cold hypersensitivity evoked by BTZ and 2) the underlying mechanisms responsible for the role of mTOR in regulating BTZ-induced neuropathic pain. METHODS: Behavioral test was performed to determine mechanical pain and cold sensitivity in a rat model. Western blot analysis and ELISA were used to examine expression of mTOR and phosphatidylinositide 3-kinase (p-PI3K) signals, and the levels of substance P and calcitonin gene-related peptide (CGRP). RESULTS: Systemic injection of BTZ significantly increased mechanical pain and cold sensitivity as compared with control animals (P< 0.05 vs. control rats). The expression of p-mTOR, mTOR-mediated phosphorylation of p70 ribosomal S6 protein kinase 1 (p-S6K1), 4E-binding protein 4 (p-4E-BP1) as well as p-PI3K was amplified in the dorsal horn of spinal cord of BTZ rats as compared with control rats. Blocking mTOR by intrathecal infusion of rapamycin attenuated mechanical pain and cold hypersensitivity. Blocking PI3K signal also attenuated activities of mTOR, which was accompanied with decreasing neuropathic pain. Inhibition of either mTOR or PI3K blunted enhancement of the spinal substance P and CGRP in BTZ rats. CONCLUSIONS: The data for the first time revealed specific signaling pathways leading to BTZ-induced peripheral neuropathic pain, including the activation of mTOR and PI3K. Inhibition of these signal pathways alleviates pain. Targeting one or more of these signaling molecules may present new opportunities for treatment and management of peripheral painful neuropathy observed during chemotherapeutic application of BTZ.

Mechanism of gastrodin in cell apoptosis in rat hippocampus tissue induced by desflurane.

This study investigated the protective effect ofgastrodin on cell apoptosis in rats hippocampus tissues induced by desflurane to explore its mechanism. A total of 36 rats were randomly divided into three groups: Blank control group (C group, n=12), desflurane anesthesia group (DF group, n=12) and gastrodin treatment group (GT group, n=12). Rats in DF group were treated with anesthesia using desflurane. Rats in GT group were treated with gavage using gastrodin and the same treatment as DF group. After the experiment, novel object recognition test and water maze test were performed. The hippocampus tissues were taken from the rat after the behavioral experiment; then the number of apoptotic cells was detected using the terminal deoxynucleotidyltransferase-mediated dUTP nick end labelling (TUNEL) kit, and the mRNA and protein expression levels of p38 and interleukin-1 (IL-1) were detected via semi-quantitative polymerase chain reaction (PCR) and western blot analysis. After the desflurane anesthesia, novel object recognition showed that compared with that in DF group, the exploration capacity of novel objects in GT group was increased (P<0.01). The water maze test showed that the escape latencies in DF group, T1 in GT group was significantly shortened, but T2 was significantly prolonged (P<0.01). TUNEL assay showed that the number of apoptotic cells in hippocampus tissues in GT group was significantly fewer than that in group DF (P<0.01). Semi-quantitative PCR and western blot analysis showed that the expression levels of p38 and IL-1ß in GT group were lower than those in DF group (P<0.01). The results show that gastrodin has a protective effect on the apoptosis of hippocampus cells of rats induced by desflurane. Its protection mechanism may be realized through decreasing the increased p38 and IL-1ß expression levels induced by desflurane, thus blocking the p38 mitogen-activated protein kinase (p38 MAPK) pathway.

Involvement of pro-inflammation signal pathway in inhibitory effects of rapamycin on oxaliplatin-induced neuropathic pain.

Background Oxaliplatin is a third-generation chemotherapeutic agent that is commonly used to treat metastatic digestive tumors; however, one of the main limiting complications of oxaliplatin is painful peripheral neuropathy. The purpose of this study was to examine the underlying mechanisms by which mammalian target of rapamycin (mTOR) and its signal are responsible for oxaliplatin-evoked neuropathic pain. Methods Neuropathic pain was induced by intraperitoneal injection of oxaliplatin in rats. ELISA and Western blot analysis were used to examine the levels of pro-inflammatory cytokines (including interleukin (IL)-1ß, IL-6, and tumor necrosis factor (TNF)-α) and the expression of mTOR signal pathway. Results Oxaliplatin increased mechanical and cold sensitivity as compared with control animals ( P < 0.05 vs. control rats). Oxaliplatin also amplified the expression of p-mTOR and mTOR-mediated phosphorylation of p70 ribosomal S6 protein kinase 1 and 4E-binding protein 1 in the lumbar dorsal root ganglion. Blocking mTOR using rapamycin attenuated peripheral painful neuropathy observed in oxaliplatin rats ( P < 0.05 vs. vehicle control). This inhibitory effect was accompanied with decreases of IL-1ß, IL-6, and TNF-α. In addition, inhibition of phosphatidylinositide 3-kinase (p-PI3K) attenuated the expression of p-mTOR and the levels of pro-inflammatory cytokines in oxaliplatin rats, and this further attenuated mechanical and cold hypersensitivity. Conclusions The data revealed specific signaling pathways leading to oxaliplatin-induced peripheral neuropathic pain, including the activation of PI3K-mTOR and pro-inflammatory cytokine signal. Inhibition of these pathways alleviates neuropathic pain. Targeting one or more of these molecular mediators may present new opportunities for treatment and management of neuropathic pain observed during chemotherapeutic application of oxaliplatin.