Time Characteristics of Shoulder Pain after Laparoscopic Surgery.

OBJECTIVE: To explore the time characteristics of shoulder pain after laparoscopic gynecological operation. METHODS: We conducted prospective clinical observations and literature review. We studied 442 cases of laparoscopic gynecological surgery. We used a visual analogue scale to evaluate the pain of patients at different time points after operation. We searched the English literature of shoulder pain after gynecological laparoscopic surgery. The observation time points of these studies included 12-24 hours or the first day after surgery, and at least one time point before this time point. RESULTS: The total incidence of shoulder pain was 68%. More than 90% of patients begin to feel shoulder pain on the first day after surgery, not on the day of surgery. 26 articles observed the severity of postlaparoscopic shoulder pain (PLSP) at different time points, of which 17 articles found that the intensity of the shoulder pain peaked at 12-24 hours or the first day after operation. DISCUSSION: The occurrence of PLSP presents obvious time characteristics. The incidence and severity of PLSP peaked on the first day or 12-24 hours after operation. To prevent and treat PLSP better, clinicians should make a more in-depth study according to the time characteristics of PLSP.

Effects of sevoflurane exposure during different stages of pregnancy on the brain development of rat offspring.

OBJECTIVE: This study explored the effects of sevoflurane exposure during different stages of pregnancy on the brain development of offspring. METHODS: Thirty-six pregnant SD rats were randomly divided into 4 groups: control, sevoflurane exposure in early (S1) pregnancy, sevoflurane exposure in middle (S2) pregnancy, and sevoflurane exposure in late (S3) pregnancy. After natural birth, the learning and memory capacity of offspring rats was analyzed using the Morris water maze experiment. The hippocampi of offspring rats were collected. The levels of interleukin (IL)-1ß, IL-6, and tumor necrosis factor (TNF)-α in the hippocampus were measured by ELISA. Additionally, the Nissl bodies in the hippocampus were analyzed using Nissl staining. Immunohistochemistry was used to examine the expression of BDNF and CPEB2 in the hippocampus of offspring. Proteins related to the NR4A1/NF-κB pathway were analyzed using western blotting. RESULTS: The memory and learning capacity of offspring rats was significantly reduced in the S1 and S2 groups compared to the control group (p < 0.05), while there was no obvious difference between the control and S3 groups (p > 0.05). The level of IL-1ß was significantly increased (p < 0.05) in the S1 group compared with the control group. Sevoflurane anesthesia received in early and middle pregnancy could significantly affect the formation of Nissl bodies in the hippocampi of offspring rats. In addition, the expression of BDNF and CPEB2 in the hippocampi of offspring rats was greatly decreased in the S1 group compared with the control group (p < 0.05). The expression of NR4A1 in the hippocampi of rat offspring was significantly decreased in the S1 and S2 groups compared with the control group (p < 0.05). The expression of proteins related to the NF-κB pathway was increased in the S1 group compared to the control group (p < 0.05). CONCLUSIONS: The neurotoxic effect of maternal sevoflurane anesthesia on the brain development of offspring is higher when the exposure occurs in early pregnancy than in late pregnancy, and its mechanism might involve the NR4A1/NF-κB pathway to increase the secretion of inflammatory cytokines.

YY1 promotes SOCS3 expression to inhibit STAT3­mediated neuroinflammation and neuropathic pain.

Neuropathic pain is induced by primary injury and dysfunction of the nervous system, and is accompanied by the activation of inflammation signaling pathways. Yin Yang 1 (YY1) is reported to be involved in inflammation; however, its role in the development of neuropathic pain is still unclear. In the present study, a neuropathic pain model was established using the bilateral chronic constriction injury (bCCI) method in rats. The indexes of neuropathic pain were detected, including paw mechanical withdrawal threshold (MWT), paw thermal withdrawal latency (PTWL) and paw frequency in response to cold stimulus, characterizing the symptoms of mechanical allodynia, thermal hyperalgesia and cold hyperalgesia, respectively. YY1 mRNA expression was significantly decreased in the spinal cord cells of bCCI rats. In addition, YY1 was overexpressed in the bCCI rats by intrathecally injecting different doses of the pcDNA­YY1. YY1 reduced rat mechanical allodynia, thermal hyperalgesia and cold hyperalgesia in a dose­dependent manner. Furthermore, YY1 increased the expression of suppressor of cytokine signaling 3 (SOCS3) and suppressed signal transducer and activator of transcription 3 (STAT3)­mediated production of inflammatory factors in a dose­dependent manner. Finally, YY1 were respectively overexpressed and knocked down in primary spinal cord cells. The results revealed that YY1 overexpression promoted SOCS3 expression, increased cell proliferation and suppressed cell apoptosis, and reduced the activation of STAT3 and STAT3­mediated production of inflammatory factors. YY1 knockdown induced the opposite effect to that observed following YY1 overexpression. Furthermore, blockade of SOCS3 by SOCS3­antibody abrogated the effect of YY1 overexpression on the suppression of SOCS3­mediated STAT3 activation and inflammation. In conclusion, YY1 alleviated neuropathic pain by inhibiting the STAT3 signaling pathway, which may be due to the upregulation of SOCS3 expression.

Corrigendum: Lipoxin A4 Inhibits NLRP3 Inflammasome Activation in Rats With Non-compressive Disc Herniation Through the JNK1/Beclin-1/PI3KC3 Pathway.

[This corrects the article DOI: 10.3389/fnins.2020.00799.].

Lipoxin A4 Inhibits NLRP3 Inflammasome Activation in Rats With Non-compressive Disc Herniation Through the JNK1/Beclin-1/PI3KC3 Pathway.

BACKGROUND: Non-compressive disc herniation is induced by an inflammatory response from the nucleus pulposus tissue and nerve roots. Lipoxins (LXs) are important endogenous anti-inflammatory mediators in the body, helping to inhibit neutrophil recruitment and stimulate autophagy in monocytes and macrophages. Here, we investigated the molecular mechanisms underlying the effects of exogenous lipoxin administration on rats with non-compressive disc herniation. METHOD: A non-compressive disc herniation model was established in rats. Fifty rats were randomly divided into: sham group, model group, PI3K inhibitor (LY294002) group, lipoxin A4 group (LXA4), and PI3K inhibitor and lipoxin A4 group (LY294002 + LXA4). Similar groupings were established for rat spinal neurons. Changes in the mechanical pain threshold and thermal pain threshold were monitored at different times. The expression of proinflammatory and anti-inflammatory mediators was assessed by ELISA, while immunohistochemistry was employed to measure the expression levels of NLRP3 and p-JNK1. The expression levels of autophagy-related proteins were measured by western blot. RESULTS: In vivo, the pain threshold was markedly decreased in the model group at each time point examined compared with that in sham group. LY294002 treatment further reduced the pain threshold. After LXA4 injection, the pain threshold was significantly increased, and the effect of LY294002 was significantly weakened (p < 0.05). The levels of proinflammatory cytokines were increased in rats with non-compressive disc herniation, and these levels were further increased by LY294002 treatment (p < 0.05). However, treatment with LXA4 significantly reduced the levels of these proinflammatory cytokines in the model group (p < 0.05). The opposite effect was observed for anti-inflammatory mediators. The expression of NLRP3 was largely increased in the model group compared with that in the sham group (p < 0.05). Treatment with LY294002 also increased the NLRP3 expression level, while the administration of LXA4 elicited the opposite effect. Furthermore, western blot analysis showed that the expression of autophagy-related proteins was greatly decreased in the model group, whereas it was significantly increased in the LXA4 group (p < 0.05). The in vitro results were consistent with the outcomes observed in vivo. CONCLUSIONS: These data suggested that LXA4 inhibited NLRP3 activation in rats with non-compressive disc herniation by regulating the JNK1/beclin-1/PI3KC3 pathway.

Sevoflurane attenuates brain damage through inhibiting autophagy and apoptosis in cerebral ischemia­reperfusion rats.

The present study aimed to investigate the effects of sevoflurane post­conditioning in a rat brain cerebral ischemia­reperfusion (I/R) model and examine its possible mechanism. Rats were randomly divided into six groups: Sham control group (Sham), I/R group, sevoflurane group (Se), Toll­like receptor­4 (TLR4) inhibitor group (Tak­242), nuclear factor (NF)­κB inhibitor group (QNZ) and Sevoflurane post­conditioning combined with TLR4­NF­κB signaling pathway inhibitor group (Se + Tak­242). Morris water maze test and tetrazolium chloride staining were used to investigate the I/R injury. The nerve cell apoptosis and autophagy in cortical tissue were detected by TUNEL and transmission electron microscopy, respectively. The expression of TLR4 protein in cortical tissue was observed by immunohistochemical staining. The expression of autophagy and apoptotic associated proteins in cortical tissues and the activity of TLR4­NF­κB signaling pathway were assayed by western blot analysis. Sevoflurane post­conditioning improved the learning and memory dysfunction caused by cerebral I/R injury. The cerebral infarction area, nerve cell apoptosis and formation of autophagic vacuoles were reduced after sevoflurane administration. The expression of light chain 3II/I, Beclin­1, Bad and Cleaved­Caspase­3 proteins were inhibited and the expression of Bcl­2 protein was upregulated after sevoflurane administration. Sevoflurane post­conditioning also inhibited the TLR4 protein and NF­κB phosphorylation, and increased inhibitor of kBα phosphorylation. The treatment effect of Tak­242 and QNZ groups were not significantly different compared with the Se group (P>0.05), and the Se + Tak­242 group had the best results. The present study demonstrated that sevoflurane post­conditioning could protect middle cerebral artery occlusion­induced brain injury rats by inhibiting autophagy and apoptosis, and that its mechanism is related to the TLR4­NF­κB signaling pathway.

Erythropoietin protects propofol induced neuronal injury in developing rats by regulating TLR4/NF-κB signaling pathway abstract.

OBJECTIVE: To explore the protective effect of erythropoietin on propofol induced neuronal injury in developing rats by regulating TLR4/NF-κB signaling pathway. METHOD: Rats were divided into normal control group (Control), propofol group (PPF), erythropoietin group (EPO), propofol + erythropoietin group (P + E), propofol + TAK-242 group (P + T), and propofol + EPO + LPS group (P + E+L) (n = 12). The pathology of hippocampal neurons was observed. The inflammatory factors were detected by ELISA. The expression of TLR4/NF-κB pathway-related proteins were detected by Western blot. RESULTS: Compared with the PPF group, the percentage of apoptotic cells in the hippocampal CA1 area of the erythropoietin treatment groups were greatly decreased while the percentage of positive cells in the hippocampus were remarkably increased(p < 0.05). The production of inflammatory factors and the expressions of TLR4/NF-κB pathway-related proteins were greatly improved in treatment groups (p < 0.05). Compared with P + E group, the percentage of apoptotic cells in CA1 area of the P + E+L group was significantly increased and the percentage of positive cells was remarkably reduced(p < 0.05), the levels of interleukin-1ß(IL-1ß), interleukin-6(IL-6), interleukin-8(IL-8) and tumor necrosis factor-α(TNF-α) were significantly increased and interleukin-4(IL-4) and interleukin-10(IL-10) was notably reduced(p < 0.05). The protein expression of TLR4 and p-P65 was significantly increased, while the protein expression of p-IκBαwas significantly decreased (p < 0.05). CONCLUSION: Erythropoietin has a protective effect on propofol induced neuropathic injury propofol in rats, and its mechanism is relevant to the regulation of TLR4/NF-κB signaling pathway.

Effect of Remifentanil Combined Anesthesia on Cytokines and Oxidative Stress in Patients undergoing Laparoscopic Surgery for Colon Cancer.

OBJECTIVE: To investigate the effect of remifentanil combined anesthesia on serum cytokines and oxidative stress indices in patients undergoing laparoscopic surgery for colon cancer. STUDY DESIGN: Experimental study. PLACE AND DURATION OF STUDY: Department of Anesthesiology, Yuhuangding Hospital Affiliated to Qingdao University, Yantai, China, from May 2016 to March 2018. METHODOLOGY: A total of 154 patients undergoing laparoscopic surgery for colon cancer were randomly divided into control group and observation group, with 77 cases in each group. Control group received fentanyl combined anesthesia, and observation group received remifentanil combined anesthesia. Levels of serum cytokines IL-8, IL-6, CRP, TNF- α and the levels of oxidative stress indices SOD, MDA, CAT, and GSH on the first day after operation were compared. Occurrence of adverse reactions during anesthesia recovery was observed and recorded in both groups. RESULTS: On the first day after surgery, levels of serum cytokines IL-8, IL-6, CRP, TNF- α and MDA in the observation group were lower than those in the control group (all p<0.001); levels of serum SOD, GSH, and CAT in the observation group were higher than those in the control group (all p<0.001). The frequency of adverse reactions such as nausea and vomiting, chills, restlessness, cough, and tachycardia in the observation group was lower than that in the control group (p=0.029, 0.016, 0.009, 0.025, and 0.003, respectively). CONCLUSION: Compared with fentanyl combined anesthesia, the remifentanil combined anesthesia can significantly reduce serum levels of cytokines IL-8, IL-6, CRP, TNF- α and oxidative stress level, and is, therefore, more secure for patients undergoing laparoscopic surgery for colon cancer.

miR-34a Inhibitor May Effectively Protect against Sevoflurane-Induced Hippocampal Apoptosis through the Wnt/ß-Catenin Pathway by Targeting Wnt1.

PURPOSE: Research has shown that sevoflurane-induced toxicity causes neurodegeneration in the developing brain. miR-34a has been found to negatively regulate ketamine-induced hippocampal apoptosis and memory impairment. However, the role of miR-34a in sevoflurane-induced hippocampal neurodegeneration remains largely unclear. MATERIALS AND METHODS: C57/BL6 mice (7-day-old) inhaled 2.3% sevoflurane for 2 h/day over 3 consecutive days. miR-34a expression was reduced through intracerebroventricular injection with miR-34a interference lentivirus vector (LV-anti-miR-34a) into mouse hippocampus after anesthesia on the first day of exposure. Hippocampal apoptosis was detected by TUNEL assay and flow cytometry analysis. Spatial memory ability was evaluated by the Morris water maze test. The interaction between miR-34a and Wnt1 was confirmed by luciferase reporter assay, RNA immunoprecipitation, Western blot, and immunofluorescence staining. The effects of miR-34a on protein levels of B-cell lymphoma 2 (Bcl-2), bcl-2-like protein 4 (Bax), and Wnt/ß-catenin pathway-related proteins were evaluated using Western blot analysis. RESULTS: Sevoflurane upregulated hippocampal miR-34a, and miR-34a inhibitor attenuated sevoflurane-induced hippocampal apoptosis and memory impairment. miR-34a negatively regulated Wnt1 expression by targeting miR-34a in hippocampal neurons. Moreover, forced expression of Wnt1 markedly undermined miR-34a-mediated enhancement of sevoflurane-induced apoptosis of hippocampal neurons, while Wnt1 silencing greatly restored anti-miR-34a-mediated repression of sevoflurane-induced apoptosis of hippocampal neurons. Increased expression of miR-34a inhibited the Wnt/ß-catenin pathway in hippocampal neurons exposed to sevoflurane, while anti-miR-34a exerted the opposite effects. CONCLUSION: miR-34a inhibitor may effectively protect against sevoflurane-induced hippocampal apoptosis via activation of the Wnt/ß-catenin pathway by targeting Wnt1.

Andrographolide protects mouse astrocytes against hypoxia injury by promoting autophagy and S100B expression.

Andrographolide (ANDRO) has been studied for its immunomodulation, anti-inflammatory, and neuroprotection effects. Because brain hypoxia is the most common factor of secondary brain injury after traumatic brain injury, we studied the role and possible mechanism of ANDRO in this process using hypoxia-injured astrocytes. Mouse cortical astrocytes C8-D1A (astrocyte type I clone from C57/BL6 strains) were subjected to 3 and 21% of O2 for various times (0-12 h) to establish an astrocyte hypoxia injury model in vitro. After hypoxia and ANDRO administration, the changes in cell viability and apoptosis were assessed using CCK-8 and flow cytometry. Expression changes in apoptosis-related proteins, autophagy-related proteins, main factors of JNK pathway, ATG5, and S100B were determined by western blot. Hypoxia remarkably damaged C8-D1A cells evidenced by reduction of cell viability and induction of apoptosis. Hypoxia also induced autophagy and overproduction of S100B. ANDRO reduced cell apoptosis and promoted cell autophagy and S100B expression. After ANDRO administration, autophagy-related proteins, S-100B, JNK pathway proteins, and ATG5 were all upregulated, while autophagy-related proteins and s100b were downregulated when the jnk pathway was inhibited or ATG5 was knocked down. ANDRO conferred a survival advantage to hypoxia-injured astrocytes by reducing cell apoptosis and promoting autophagy and s100b expression. Furthermore, the promotion of autophagy and s100b expression by ANDRO was via activation of jnk pathway and regulation of ATG5.

Andrographolide protects mouse astrocytes against hypoxia injury by promoting autophagy and S100B expression

Andrographolide (ANDRO) has been studied for its immunomodulation, anti-inflammatory, and neuroprotection effects. Because brain hypoxia is the most common factor of secondary brain injury after traumatic brain injury, we studied the role and possible mechanism of ANDRO in this process using hypoxia-injured astrocytes. Mouse cortical astrocytes C8-D1A (astrocyte type I clone from C57/BL6 strains) were subjected to 3 and 21% of O2 for various times (0-12 h) to establish an astrocyte hypoxia injury model in vitro. After hypoxia and ANDRO administration, the changes in cell viability and apoptosis were assessed using CCK-8 and flow cytometry. Expression changes in apoptosis-related proteins, autophagy-related proteins, main factors of JNK pathway, ATG5, and S100B were determined by western blot. Hypoxia remarkably damaged C8-D1A cells evidenced by reduction of cell viability and induction of apoptosis. Hypoxia also induced autophagy and overproduction of S100B. ANDRO reduced cell apoptosis and promoted cell autophagy and S100B expression. After ANDRO administration, autophagy-related proteins, S-100B, JNK pathway proteins, and ATG5 were all upregulated, while autophagy-related proteins and s100b were downregulated when the jnk pathway was inhibited or ATG5 was knocked down. ANDRO conferred a survival advantage to hypoxia-injured astrocytes by reducing cell apoptosis and promoting autophagy and s100b expression. Furthermore, the promotion of autophagy and s100b expression by ANDRO was via activation of jnk pathway and regulation of ATG5.

Intraoperative use of dexmedetomidine promotes postoperative sleep and recovery following radical mastectomy under general anesthesia.

Postoperative sleep disturbance and fatigue following radical mastectomy were high risks for prolonged convalescence in patients with breast cancer. The present study was designed to observe the effect of intraoperative use of dexmedetomidine on postoperative sleep, fatigue and recovery following radical mastectomy under general anesthesia. Forty-seven patients were randomized into two groups that were maintained with propofol/remifentanil/Ringer's solution (Control group), or propofol/remifentanil/Dexmedetomidine (DEX group) for surgery under general anesthesia. During the first night following surgery, patients receiving dexmedetomine spent more time sleeping when compared with those form the Control group. During the first week following operation, when compared with the Control group, patients from the DEX group had a higher score of global 40-item recovery questionnaire on day 3 following operation, and lower 9-question fatigue severity scores on day 3 and day 7 following operation. In conclusion, intraoperative use of dexmedetomidine is sufficient to improve postoperative sleep disorder, promote postoperative recovery. The adverse effect of dexmedetomidine on sleep disturbance might be contributed to its recovery-promoting effect.

Effects of andrographolide on postoperative cognitive dysfunction and the association with NF-κB/MAPK pathway.

The present study investigated the effects of andrographolide on postoperative cognitive dysfunction (POCD) in aged rats to gain insight of the underlying mechanism, which may provide theoretical basis for the clinical application of andrographolide to prevent POCD in older patients. Thirty aged male rats were randomly assigned to 3 groups: Control, model and andrographolide groups. The Morris water maze test was used to examine the spatial memory and learning ability of the rats postoperatively. The histological alterations of neuronal cells in the hippocampus were visualized by H&E staining. The serum levels of neuron-specific enolase (NSE), human soluble protein-100ß (S-100ß) and the inflammation factors of interluekin (IL)-1ß, IL-6 and TNF-α involved in the nuclear factor κB (NF-κB)/mitogen-activated protein kinase (MAPK) signaling pathway were detected by ELISA. The NF-κB/MAPK signaling pathway-associated proteins in rat serum were detected by western blotting. Following andrographolide treatment, the rats significantly gained learning ability after surgery. Is it ameliorated hippocampal neuronal injury in rats following surgery. Andrographolide decreased NSE, S-100ß, and the inflammation factors, IL-6, IL-1ß and TNF-α in serum. Andrographolide reduced NF-κB/MAPK pathway-associated protein expression. Andrographolide ameliorated POCD in aged rats following surgery. The underlying mechanism may be associated with the downregulation the inflammatory factors and NF-κB/MAPK-associated protein expression.

Effects of docosahexaenoic acid on learning and memory impairment induced by repeated propofol anesthesia in young rats.

The aim of the present study was to investigate the effects of docosahexaenoic acid (DHA) on the learning and memory ability of young rats exposed to propofol, and its underlying mechanisms. Sprague Dawley rats (n=60) were randomly divided into six groups: Control group (group A); solvent control group (group B); propofol group (group C); low-dose DHA + propofol group (group D); medium dose DHA + propofol group (group E); and high-dose DHA + propofol group (group F). The Morris water maze (MWM) test was performed to evaluate the rats' learning and memory ability, and tissue samples from the hippocampi of the rats were obtained for biochemical analysis. The results of the MWM test revealed that DHA supplementation administered to young rats led to an evident decrease in the latency to find the maze platform, and a significant increase in the number of platform crossings in groups E and F compared with group C (P<0.05). High-performance liquid chromatography indicated that glutamate concentration levels were significantly lower and γ-aminobutyric acid concentration levels were significantly higher in the hippocampi of group E and F rats treated with DHA compared with group C rats (P<0.05). Furthermore, DHA treatment alleviated the decrease in brain-derived neurotrophic factor levels (P<0.05), and superoxide dismutase (P<0.05) and glutathione peroxidase (P<0.05) activities induced by the administration of propofol. Additionally, DHA treatment decreased malondialdehyde levels in the hippocampi of rats (P<0.05). The aforementioned findings demonstrate that DHA was able to effectively improve learning and memory dysfunction induced by repeated propofol-induced anesthesia in young rats. This data suggests that DHA may be a potential candidate for further preclinical studies aimed at treating postoperative cognitive dysfunction.

THE INVESTIGATION OF EFFECT OF FLURBIPROFEN AXETIL ON THE TISSUE GROWTH AND THE CONTENT OF PGE2 IN CERVICAL CANCER.

The aim of this study was to investigate whether flurbiprofen axetil can inhibit the tissue growth and the content of PGE2 in cervical cancer or not. Fifty female BALB/c nude mice were randomly divided into control group (C), tumor + saline group (T), tumor + flurbiprofen axetil 10 mg/kg (Cfl0) group, tumor + flurbiprofen axetil 25 mg/kg (Cf25) group, tumor + flurbiprofen axetil tumor 50 mg/kg (Cf50), so that each group had 10 animals. Then, the animal model of human cervical carcinoma was established, and the relative tumor volume (RTV), relative tumor proliferation rate (T/C) and tumor inhibition rate were measured. The content of PGE2 in tumor tissue was determined by using enzyme-linked immunosorbent assay. There was no tumor formation in group C, and the time of tumor growth in other groups was non-statistically different. The RVT in Cf50 group was lower than in other groups. It was evident from the curve of tumor growth that the tumor weight in T group was evidently higher than that of administration groups (p < 0.01). The tumor inhibition rates of Cf10, Cf25 and Cf50 groups were 16.8, 19.6 and 36%, respectively, and the relative tumor proliferation rate were 85, 91 and 72%, respectively. The PGE, level of Cf50 was statistically (p < 0.01) lower than that of Cfl0 and Cf25 groups. Flurbiprofen axetil can inhibit the growth of cervical cancer transplanted tumor in nude mice and this inhibitory effect was maximal in Cf50 group. Flurbiprofen axetil can inhibit the production of PGE2 in tumor tissue of cervical carcinoma in nude mice.

Effect of preemptive analgesia with parecoxib sodium in patients undergoing radical resection of lung cancer.

OBJECTIVE: To discuss the effect of preemptive analgesia with parecoxib sodium in patients undergoing radical resection of lung cancer. METHODS: 115 cases of lung cancer patients with American society of anesthesiologists class (ASA) grade I~II who received selective operation were randomly divided into the research group and the control group. The research group patients were given preoperative parecoxib sodium 40 mg plus postoperative normal saline 2 ml, while the control group patients were treated with preoperative normal saline 2 ml plus postoperative parecoxib sodium 40 mg. The pain condition at postoperative 1, 2, 4, 8, 12, 24 and 48 h were evaluated by visual analogue scale (VAS), and emergence agitation was tested by agitation score. RESULTS: Finally there were 56 cases and 57 cases can be used for evaluation in the research group and control group. The VAS scores after 1, 2, 4, 8, 12, 24 and 48 h in the research group and control group were [2.23±0.45, 2.35±0.48, 2.51±0.51, 2.41±0.45, 2.28±0.42, 2.16±0.39, 2.11±0.40] and [3.80±0.62, 4.01±0.64, 4.31±0.67, 4.10±0.64, 3.65±0.70, 3.12±0.66, 2.46±0.53], respectively. The research group were obviously lower than the control group, the difference were statistically significant (P<0.05). The rate of agitation was 24.44% (11/56) in the research group, significantly lower than the control group of 59.65% (34/57) (P<0.05). CONCLUSION: Preemptive analgesia with parecoxib sodium can obviously relieve acute pain using in patients undergoing radical resection of lung cancer, and is helpful to reduce the incidence of emergence agitation.

Clinical application of a novel developed pressure bladder indicator in lumbar epidural puncture.

STUDY OBJECTIVE: A novel pressure bladder indicator was developed, and this study aimed to evaluate the clinical application of the pressure bladder indicator by measuring the epidural space pressure and bladder working pressure on patients undergoing lumbar epidural puncture. DESIGN: Randomized, prospective, double-blinded study PATIENTS: 130 patients SETTING: The Second Hospital of Shandong University INTERVENTIONS: In this study, 60 patients undergoing surgical procedures under lumbar epidural anesthesia were enrolled to detect epidural pressure, and other 70 patients who were undergoing lumbar epidural anesthesia or combined spinal-epidural anesthesia were enrolled to evaluate the pressure bladder indicator. MEASUREMENTS: After successful breakthrough of ligamentum flavum by traditional methods, a pressure transducer was connected to an epidural needle tail and a monitor to measure the epidural pressure at L1-L5 in 60 patients. The working pressure of the bladder was also measured by a transducer. Then lumbar epidural puncture was performed with the pressure bladder indicator in other 70 patients. MAIN RESULTS: The lumbar epidural pressure of the 60 patients was 9.8 ± 4.3 mm Hg, and the bladder working pressure of the pressure bladder indicator was 122 ± 15 mm Hg. All these 70 patients were confirmed with successful bladder indication and lumbar epidural puncture. Thus, the coincidence ratio was 100%. CONCLUSIONS: The novel developed pressure bladder indicator was a reliable and useful technique to conduct successful lumbar epidural puncture.

[Distribution characteristics of soil nematodes in reclaimed land of copper-mine-tailings in different plant associations].

A survey was carried out to investigate soil nematode communities in the plant associations of gramineae (Arthraxon lanceolatus, AL; Imperata cylindrica, IC) and leguminosae (Glycine soja, GS) in reclaimed land of copper-mine-tailings and in the plant associations of gramineae (Digitaria chrysoblephara, DC-CK) of peripheral control in Fenghuang Mountain, Tongling City. A total of 1277 nematodes were extracted and sorted into 51 genera. The average individual density of the nematodes was 590 individuals · 100 g(-1) dry soil. In order to analyze the distribution character- istics of soil nematode communities in reclaimed land of copper-mine-tailings, Shannon community diversity index and soil food web structure indices were applied in the research. The results showed that the total number of nematode genus and the Shannon community diversity index of soil nematode in the three plant associations of AL, IC and GS were less than that in the plant associations of DC-CK. Compared with the ecological indices of soil nematode communities among the different plant associations in reclaimed land of copper-mine-tailings and peripheral natural habitat, we found that the structure of soil food web in the plant associations of GS was more mature, with bacterial decomposition being dominant in the soil organic matter decomposition, and that the soil ecosystem in the plant associations of GS was not stable with low interference. This indicated that the soil food web in the plant associations of leguminosae had a greater development potential to improve the ecological stability of the reclaimed land of copper-mine-tailings. On the other hand, the structure of soil food web in the plant associations of AL and IC were relatively stable in a structured state with fungal decomposition being dominant in the decomposition of soil organic matter. This indicated that the soil food web in the plant associations of gramineae was at a poor development level.

The impact of anesthetic techniques on survival for patients with colorectal cancer: evidence based on six studies.

BACKGROUND/AIMS: Epidural-supplemented general anesthesia is perceived as a more beneficial method over general anesthesia since it reduces incidence of side effects, provides better postoperative pain relief and lowers the possibility to use immunosuppressive anesthetics. However, previous prospective and retrospective studies reported conflicting results in the effects of epidural anesthesia on post-operative outcomes of colorectal cancer surgery. Therefore, this study aims to pool available evidence to assess the association between epidural anesthesia and the post- operative outcomes in this group of patients. METHODOLOGY: Relevant studies were searched in databases and a meta-analysis was performed to estimate the association between epidural anesthesia and overall survival and recurrence free survival. RESULTS: Compared with the anesthetic choice without epidural anesthesia, epidural-supplemented anesthesia is associated with significantly longer overall survival (HR: 0.72, 95% CI: 0.55-0.94, p = 0.01) but not with prolonged recurrence free survival (HR: 1.06, 95% CI: 0.96-1.16, p = 0.23). These results showed a highlevel of robustness in sensitive test. CONCLUSION: Although epidural anesthesia might not lead to improved recurrence free survival, it had significant benefit in improving overall survival and reducing all-cause of death. It might be a useful anesthetic technique for colorectal cancer patients undergoing surgery. However, prospective studies are required to confirm whether this benefit is causative with epidural anesthesia.