Objective To investigate the effect of propofol and isoflurane anesthesia on serum heat shock protein 70 ( HSP70 ) of perioperative patients with brain injury and compare the anesthetic effect of the two narcotic drugs. Methods 30 patients with medium or severe traumatic brain injury,treated by hematoma evacuation operation,were randomly divided into propofol ( n = 15 ) and isoflurane group ( n = 15 ). After anesthesia induction,propofol (target effect concentration of 3 ～ 4 μg/ml ) was intravenously injected and 1.2% isoflurane was inhalated into the patients of the 2 groups,respectively. In addition,vecuronium and fentany were intermittent intravenously injected into patients to maintain the depth of anesthesia. HSP70 in blood of patients were detected before anesthesia induction, 1 h after the dura was opened and 24 h after the operation by ELISA method. Recovery and tracheal extubation time of patients were recorded. Results HSP70 levels in blood of patients in the 2 groups were significantly increased compared with the former time point(P＜0.05 ). HSP70 content in propofol group was significantlyhigher at 1 h after the dura was opened( ( 2.00 ± 0. 24 ) ng/ml, ( 2.19 ± 0.26 ) ng/ml, t = 2. 080, P = 0.047 ) and 24 h after the operation( t=2.086, P=0.046) ,and recovery and tracheal extubation time was shorter compared with the isoflurane group(P＜0. 05). Conclusion Perioperative moderate stress,and early postoperative recovery and extubation can be maintained in patients with traumatic brain injury with profol anesthesia.

ObjectiveTo investigate the pathogenesy and operation method in patients with ossification of thoracic ligamentum flavum.MethodsThe imaging and clinical data of 56 patients who underwent laminectomy combined with posterolateral fusion were studied retrospectively.The method of laminectomy included enbloc laminectomy and decomposed laminectomy.Postoperative outcomes were evaluated according to a recovery scale in terms of JOA score.ResultsThe patients were followed up for 18-70 (25.00 ± 11.56) months.There were a total of 237 ossified segments in this series,57.4％(136/237)located in lower thoracic segments.According to the configuration of ossification on CT scans,lateral type occurred in 6 patients,diffuse type in 17 patients and thickened nodular type in 33 patients.All patients with lateral type and majority of patients with diffuse type were treated with enbloc laminectomy,and the rate of fineness of postoperative outcome was 83.3％ (5/6),82.4％ ( 14/17 ) respectively.Most of the patients with thickened nodular type were treated with decomposed laminectomy,and the rate of fineness of postoperative outcome was 78.8％ (26/33).Four patients withthickened nodular type were performed with enbloc laminectomy,2 of them resulted in deteriorated myelopathy.Twenty-nine patients with thickened nodular type were performed with decomposed laminectomy,however,only 2 of them resulted in worse outcomes.ConclusionsThe pathogenesis of ossification of thoracic ligamentum flavum is mainly due to the localizedmechanical stress.Laminectomy combining with lateral fusion may be the ideal method for the treatment ofthis condition.Furthermore,enbloc laminectomy is suitable for the patients in lateral type and diffuse type according to the configuration of ossifications.For the thickened nodular type,decomposed laminectomy is favorable.

Carbon monoxide has been proved to be an important signal molecule in body. Transition metal carbonyl compounds are solidified form of carbon monoxide. Numerous studies have shown that Ruthenium carbonyl carbon monoxide releasing molecules have a strong pharmacological activity. In this paper, five Ruthenium (II) carbonyl CORMs 1-5 were synthesized and their toxicology, tissue distribution and interaction with blood endogenous substances were investigated. The results showed CORMs' IC50 to fibroblasts are ranged from 212.9 to 2089.2 micromol x L(-1). Their oral LD50 to mouse is between 800 to 1600 mg x kg(-1). After repeated administration, CORMs 1 and CORMs 5 haven't shown an obvious influence to rats' liver and kidney function, but caused the injury to liver and kidney cells. The in vivo distribution result revealed the majority of CORMs were distributed in blood, liver and kidney, only a small part of CORMs distributed in lung, heart and spleen. They could scarcely cross the blood-brain barrier and distribute to brain. The non-CO ligands in structure have an obvious relevance to their in vivo absorption and distribution. Interestingly, CORMs could enhance the fluorescence of bovine serum albumin, and this enhancement was in direct proportion with the concentration of CORMs. Under different conditions, interaction of CORMs with glutathione got different type of products, one is Ruthenium (II) tricarbonyl complexes, and Ruthenium (II) dicarbonyl complexes.

Objective To analyze the correlation between emphysema extent measured by high resolution computed tomography (HRCT) and pulmonary function tests, symptom score in patients with chronic obstructive pulmonary disease ( COPD ) , and to study the value of HRCT in the emphysema quantification in the clinical evaluation of COPD patients. Methods 78 patients with stable COPD were recruited to take the HRCT scan , and emphysema extent was qualified by measuring the proportion of low attenuation area in the whole lung (LAA%). Correlations between LAA% and indices of pulmonary function test, bronchial dilation test, mMRC scale, CAT score and six minutes walking distance (6MWD) were assessed. Results LAA% was negatively correlated with FEV1/FVC and DLCO%pred, and the correlation coefficients were -0.759 and -0.589 (P <0.01), respectively. LAA% was positively related to mMRC score (r = 0.342, P < 0.01), and negatively asso-ciated with 6MWD (r = -0.365,P< 0.01). There was no association between LAA% and indices of bronchodila-tion test (⊿FVC, ⊿FVC%, ⊿FEV1, ⊿FEV1%) (P > 0.05). Conclusions The severity of emphysema measured by HRCT is well correlated with the clinical symptoms , pulmonary function tests and exercise capacity in COPD patients. It can be used to diagnose emphysema early and to evaluate the severity of the disease com-prehensively. Thus, the risk factors of COPD can be controlled and the prognosis of the patients can be im-proved.

BACKGROUND:Transformation growth factor-β(TGF-β) and brain-derived neurotrophic factor (BDNF) are the main regulatory factors in the process of spinal cord injury. There are many researches for TGF-βand BDNF pathogenesis in the spinal cord injury, but the regulation of Ginsenoside Rg1 intervention on TGF-βand BDNF in the spinal cord injury is rarely reported.
OBJECTIVE:To observe the effect of Ginsenoside Rg1 intervention on TGF-βand BDNF expression at themolecular protein levels, and to study the protection effect of Ginsenoside Rg1 on the spinal cord and nerve function after spinal cord injury.
METHODS:Experimental rats were randomly divided into blank control group, model group and Ginsenoside Rg1 group. In the model and Ginsenoside Rg1 groups, spinal cord injury model was established with the impact method in rats. In the Ginsenoside Rg1 group, rats were intraperitoneal y injected with 10 mg/kg Ginsenoside Rg1 24 hours after modeling, once per day, for 14 days. Rats in the blank control and model groups were injected with equal saline.
RESULTS AND CONCLUSION:Compared with the control group, serum malondialdehyde levels increased, the content of superoxide dismutase decreased, TGF-βexpression levels in spinal cord tissue increased, and BDNF expression levels decreased in the model and Ginsenoside Rg1 groups. Compared with the model group, serum malondialdehyde levels decreased, the content of superoxide dismutase increased, TGF-βexpression levels in spinal cord tissue decreased, and BDNF expression levels increased in the Ginsenoside Rg1 group. Ginsenoside Rg1 can protect the injury spinal cord in rats after spinal cord injury.

BACKGROUND:Chinese herb extracts can restore and protect the nervous system of rats through intervention of neural stem cels. OBJECTIVE:To explore the role of ginsenosides Rg1 in the proliferation and protection of neural stem cels. METHOD:Sprague-Dawley rats at pregnant 19 days were dissected to take out fetal rats, and then the hippocampal tissues from fetal rats were isolated to extract neural stem cels. Neural stem cels were co-cultured with DMEM/F12 medium containing 50 g/L ginsenosides Rg1 as intervention group, with DMEM/F12 medium as blank control group, and with DMEM/F12 containing 0.64% phenol as positive control group, respectively. MTT assay was used to detect the proliferation of neural stem cels in each group, and western blot method to detect the protein expression of brain-derived neurotrophic factor and transforming growth factor-β in neural stem cels. RESULTS AND CONCLUSION:Rat neural stem cels were round single cels with clear border at early period after isolation but at 2 days after inoculation, the cels were adherent and aggregated into smal cel spheres. Compared with the blank control group, the proliferative rate of neural stem cels was significantly increased in the ginsenosides Rg1 group (P < 0.05), but decreased in the positive control group (P < 0.05). Compared with the blank control group, in the ginsenosides Rg1 group, the expression of brain-derived neurotrophic factor was elevated, and the expression of transforming growth factor-β was reduced, indicating ginsenosides Rg1 has a certain effect to promote the proliferation of neural stem cels as wel as to protect the neural stem cels.

Background: The present investigation explored the therapeutic actions of oleuropein along with the possible signaling pathway involved in attenuating neuropathic pain in chronic constriction injury (CCI) and vincristine-induced neuropathic pain in male rats. Methods: Four loose ligatures were placed around the sciatic nerve to induce CCI, and vincristine (50 μg/kg) was injected for 10 days to develop neuropathic pain.The development of cold allodynia, mechanical allodynia, and mechanical hyperalgesia was assessed using different pain-related behavioral tests. The levels of H2S, cystathionine-γ-lyase (CSE), cystathionine-β-synthase (CBS), orexin, and nuclear factor erythroid-2-related factor 2 (Nrf2) were measured in the sciatic nerve. Results: Treatment with oleuropein for 14 days led to significant amelioration of behavioral manifestations of neuropathic pain in two pain models. Moreover, oleuropein restored both CCI and vincristine-induced decreases in H2S, CSE, CBS, orexin, and Nrf2 levels. Co-administration of suvorexant, an orexin receptor antagonist, significantly counteracted the pain-attenuating actions of oleuropein and Nrf2 levels without modulating H2S, CSE and CBS. Conclusions Oleuropein has therapeutic potential to attenuate the pain manifestations in CCI and vincristine-induced neuropathic pain, possibly by restoring the CSE, CBS, and H2S, which may subsequently increase the expression of orexin and Nrf2 to ameliorate behavioral manifestations of pain.

Background: The present investigation explored the therapeutic actions of oleuropein along with the possible signaling pathway involved in attenuating neuropathic pain in chronic constriction injury (CCI) and vincristine-induced neuropathic pain in male rats. Methods: Four loose ligatures were placed around the sciatic nerve to induce CCI, and vincristine (50 μg/kg) was injected for 10 days to develop neuropathic pain.The development of cold allodynia, mechanical allodynia, and mechanical hyperalgesia was assessed using different pain-related behavioral tests. The levels of H2S, cystathionine-γ-lyase (CSE), cystathionine-β-synthase (CBS), orexin, and nuclear factor erythroid-2-related factor 2 (Nrf2) were measured in the sciatic nerve. Results: Treatment with oleuropein for 14 days led to significant amelioration of behavioral manifestations of neuropathic pain in two pain models. Moreover, oleuropein restored both CCI and vincristine-induced decreases in H2S, CSE, CBS, orexin, and Nrf2 levels. Co-administration of suvorexant, an orexin receptor antagonist, significantly counteracted the pain-attenuating actions of oleuropein and Nrf2 levels without modulating H2S, CSE and CBS. Conclusions Oleuropein has therapeutic potential to attenuate the pain manifestations in CCI and vincristine-induced neuropathic pain, possibly by restoring the CSE, CBS, and H2S, which may subsequently increase the expression of orexin and Nrf2 to ameliorate behavioral manifestations of pain.

Objective To evaluate the application effect of telemedicine robot on the postoperative follow-up of liver transplantation recipients from donation after cardiac death (DCD). Methods A total of 100 recipients undergoing liver transplantation from DCD in the First Affiliated Hospital of Xi 'an Jiaotong University from January 2014 to December 2017 were recruited in this investigation. According to differnt follow-up patterns, all recipients were divided into the research group (n=50, follow-up by telemedicine robot) and control group (n=50, follow-up by traditional telephone). The compliance (medication compliance, self-monitoring, life compliance and follow-up compliance), follow-up time and follow-up satisfaction at postoperative 3 months of all DCD liver transplantation recipients were analyzed and statistically compared between research group and control group. Results The scores of medication compliance, self-monitoring, life compliance, follow-up compliance and the total score of compliance in the research group were significantly higher than those in the control group (all P < 0.05). The each follow-up time of liver transplantation recipients in the research group was (9±4) min, significantly shorter than (13±4) min in the control group (t=-4.452, P < 0.001). The score of satisfaction during postoperative follow-up in the research group was 19.8±2.6, significantly higher than 16.2±3.1 in the control group (t=6.234, P < 0.001). Conclusions The application effect of telemedicine robot on the postoperative follow-up of liver transplantation recipients from DCD is satisfactory, deserves widespread application in clinical practice. It is expected to become an indispensable part of the postoperative follow-up of liver transplantation recipients from DCD.

Objective:To investigate the central mechanism of moxibustion in treating chronic inflammatory visceral pain(CIVP)and its analgesic effect from the perspective of the p38 mitogen-activated protein kinase(MAPK)/Ets-like transcription factor 1(ELK1)signaling pathway in the spinal cord. Methods:Clean-grade male Sprague-Dawley rats were randomly divided into a normal group,a model group,a herb-partitioned moxibustion(HPM)group,a sham-HPM group,a p38 MAPK inhibitor group,and a dimethyl sulfoxide(DMSO)group.CIVP rat models were prepared using an enema mixture of 2,4,6-trinitrobenzene sulfonic acid solution and 50%ethanol.The HPM group was treated with HPM;the sham-HPM group was treated the same as the HPM group,but the moxa cones were not ignited;rats in the p38 MAPK inhibitor group received L5-L6 intrathecal injection of p38 MAPK inhibitor(SB203580);rats in the DMSO group received L5-L6 intrathecal injection of 2%DMSO.Abdominal withdrawal reflex(AWR),mechanical withdrawal threshold(MWT),and thermal withdrawal latency(TWL)were used to observe pain-related behaviors in each group.Hematoxylin-eosin staining was used to observe the morphological changes in rat colon tissue.Western blotting and real-time quantitative reverse-transcription polymerase chain reaction were used to detect the phosphorylated protein and mRNA expression of apoptosis signal-regulating kinase 1(ASK1),MAPK kinase(MKK)3/6,p38 MAPK,ELK1,and mitogen and stress-activated protein kinase 1(MSK1)in the spinal cord. Results:Compared with the normal group,CIVP rats had severe colonic inflammatory injuries,and the pathological injury scores increased significantly,along with increased AWR scores under different colorectal distension(CRD)stimulation pressures and decreased MWT and TWL;the mRNA and phosphorylated protein expression of p38 MAPK,ELK1,MSK1,ASK1,MKK3,and MKK6 all increased in the spinal cord(P<0.01).After HPM treatment,the colon injuries were repaired,and the pathological injury scores decreased;under different CRD stimulation pressures,the AWR scores decreased,and the MWT and TWL increased;the mRNA and phosphorylated protein expression of p38 MAPK,ELK1,ASK1,and MKK3 in the spinal cord also decreased,with statistically significant differences compared with the model group and the sham-HPM group(P<0.01).There were no significant differences in the above indicators between the HPM group and the p38 MAPK inhibitor group(P>0.05),and the same was true regarding the comparisons between the model group and the DMSO group. Conclusion:HPM exerted analgesic effects via downregulating the mRNA and phosphorylated protein expression of ASK1,MKK3,p38 MAPK,and ELK1 in the spinal cord of CIVP rats.The inhibition of spinal p38 MAPK/ELK1 signaling pathway activation may be one of the mechanisms by which HPM relieves pain in CIVP.