Objective To investigate the effects of muscle relaxants on motor evoked potentials (MEPs) monitoring during intracranial surgery. Methods 62 patients with neurological tumor were divided into 2 groups: muscle relaxant group (n=21) and non-muscle relaxant group (n=41). The incidence of successful MEPs monitoring was investigated. Results The incidence of successful MEPs monitoring was 76.2% in the muscle relaxant group and 41.5% in the non-muscle relaxant group (P<0.05). Conclusion Muscle relaxants can affect the MEP monitoring, which would not be administered as possible during anesthesia for intracranial surgery in functional area.

ObjectiveTo evaluate the effect of lornoxicam used for craniotomy. Methods60 neurosugical patients, ASA physical I～II, were randomly allocated into three groups to receive normal saline in controlled group (GroupⅠ), lornoxicam 8 mg (Group Ⅱ) and lornoxicam 24 mg (Group Ⅲ) intravenously 10～15 min before anesthesia. The end-tidal concentration of isoflurane was measured. The volumes of bleeding, transfusion, fluid infusion and urine were recorded. The time of consciousness, psychomotor and cognitive recoveries from general anesthesia were observed. The VAS scores of pain were evaluated 48 h after operation.ResultsThe concentrations of end-tidal isoflurane in the controlled group were significantly higher than other groups (P<0.01). There was no difference among the three groups in the volume of bleeding, transfusion, infusion and urine. The recovery time of conscious, psychomotor and cognitive from general anesthesia were shorter in group Ⅱ and Ⅲ (P<0.01). The total dose of tramadol and VAS score after the operation were no difference among the three groups.ConclusionThe preoperative application of lornoxicam can reduce the concentrations of end-tidal isoflurane significantly, smooth the recovery from anesthesia.

Objective To explore the function and mechanisms of Wnt7a in bone msenchymal stem cells (BMSCs) osteogenic differentiation.Methods BMSCs were isolated and cultured.After transfection of siRNA-Wnt7a and mock in BMSCs and induction by osteogenic medium for 3 d,Western Blot were employed to detect the silencing effect of siRNA-Wnt7a.Then the effect of silencing Wnt7a on the expression of osteocyte marker osteocalcin and osteogenesis regulator protein Runx2 were detected by Western Blot after culture by osteogenic medium for 10 d.Finally,Alizarin S Red staining was used to detect the effect of silencing siRNA-Wnt7a on osteogenesis after culture by osteogenic medium for 2 weeks.Results The silencing effect of siRNA-Wnt7a was confirmed by Western Blot after transfection of oligocleotides siRNA-Wnt7a and mock into mesechymal stem cells.The silencing Wnt7a decreased the expression of osteocalcin and Runx2 after culture by osteogenic medium for 10 d.Alizarin S red staining results showed that silencing Wnt7a blocked bone differentiation.Conclusions The results demonstrated that Wnt7a could promot osteocyte marker osteocalcin expression by upregulating osteogenesis regulator protein Runx2 expression,which played a key role in BMSCs osteogenic differentiation.

BACKGROUND: Quiet a number of researches has reported the morphological changes of global ischemic reperfusion model. However, there are few reports on the ultrastructural changes of cortex in early reperfusion, especially the change of blood brain barrier.OBJECTIVE: To explore the changes of brain cortex neurons, glial cells and blood brain barrier in order to provide reliable evidence for clinical treatment.DESIGN: A randomized and controlled trial.SETTING: Department of Neurosurgery, Departnent of Anesthesia and Electron Microscope Room of Beijing Tiantan Hospital.MATERIALS: The experiment was conducted to 6 Wistar rats in Beijing Neurological Surgery Research Institute of Capital University of Medical Sciences during February 2003 to February 2004. The rats were randomly divided into two groups with one of ischemia-reperfusion group and sham operation group with 3 rats in each group.INTERVENTIONS: To prepare global ischemic reperfusion model of rats. Brain was removed from ischemic group in one hour of reperfusion and from sham operation group one hour after the operation. Electronic microscope technique was used to observe the ultrastructural changes of cortex.MAIN OUTCOME MEASURES: Ultrastructural changes of cortex.RESULTS: The neurons of cortex shrank to certain degree in the early stage of ischemic reperfusion(1 hour) . The glial cells were swollen with dissolved chromosome in nucleus and unclear nuclear membrane. The foot protrusions around blood vessel slightly swelled and separated from basement membrane. Mircro-tubes were partially dissolved.CONCLUSION: In early stage of reperfusion injury, the cortex neurons, glial cells, cellular framework and blood brain barrier already changed which suggested that the protective treatment such as reducing brain edema, protecting blood brain barrier should start as early as possible.

Objective To explore the feasibility and safety of dexmedetomidine sedation in interventional neuroradiology operations.Methods Eighty-five cases ASA grade Ⅱ-Ⅲ grade patients undergoing cerebral angiography according to age divided into two groups:old group(more than 60 years old,35 cases) and young group (18-59 years old,50 cases).The loading dose of dexmedetomidine were dexmedetomidine 0.5 μ g/kg in old group and 1.0 μ g/kg in young group,respectively.The loading dose was administered for 10 min followed by continuous infusion dexmedetomidine 0.5 μ g/ (kg· h).Blood pressure,heart rate (HR),peripheral oxygen saturation (SpO2) and respiratory rate (RR),Ramsay score and bispectral index(BIS) were monitored and recorded during the study.Results The BIS,Ramsay score after administration 10,15,30,45 min in two groups was significantly longer than that before administration [old group:84 ±22,83 ±22,85 ± 15,75 ±23 vs.94 ±5; (2.0 ±0.4),(2.3 ±0.6),(2.8 ±0.7),(3.0 ±0.7)scores vs.(1.7 ± 0.5) scores; young group:91 ± 8,89 ± 11,86 ± 12,81 ± 13 vs.96 ± 2; (1.9 ± 0.6),(2.3 ±0.7),(2.7 ± 0.9),(3.0 ± 0.9) scores vs.(1.6 ± 0.5) scores,P ＜ 0.05].The systolic blood pressure,diastolic blood pressure,mean arterial pressure (MAP) after administration 10,15,30,45 min in two groups was significantly longer than that before administration [old group:(152 ± 23),(144 ± 23),(140 ± 21),(135 ±21) mm Hg(1 mm Hg =0.133 kPa) vs.(165 ± 25) mm Hg; (87 ± 11),(83 ± 11),(78 ± 8),(75 ± 8) mm Hg vs.(89± 13)mm Hg;(106±14),(100±13),(99±12),(95±12)mm Hg vs.(113±16)mm Hg;young group:(131 ± 24),(127 ± 23),(124 ± 25),(124 ± 26) mm Hg vs.(142 ± 23) mm Hg; (81 ± 13),(79±13),(77±13),(76±13)mmHgvs.(86± 14) mmHg;(97±16),(94±16),(91±19),(92±20) mm Hg vs.(104 ± 19) mm Hg,P ＜0.05],but the decreases in blood pressure were ＜20％ from baseline.The HR,RR and SpO2 was no significant difference (P ＞ 0.05).Conclusions Continuous infusion of dexmedetomidine sedation during cerebral angiography has little effect on hemodynamics,no significant respiratory depression,is safe and effective.

Objective:To analyze the clinical features and genetic factors of neonatal 17β-hydroxysteroid dehydrogenase type10 (HSD10) deficiency.Methods:The clinical characteristics and genetic test results of a child with HSD10 deficiency coming from Children′s Hospital of Nanjing Medical University in April 2019 were retrospectively analyzed.The keywords" 17β-hydroxysteroid dehydrogenase type 10 deficiency" or " 2-Methyl3-Hydroxybutyryl-CoA dehydrogenase deficiency" or " HSD10" , etc.were searched in various databases, including CNKI, Wanfang, Weipu, Embase and PubMed to review the cases collected from all published data until May 31, 2020.Results:The patient was a newborn male who developed symptoms on the first day after birth.The main signs were metabolic acidosis, increased blood ammonia and lactate, and hypotonia.Trio whole exom sequencing in the patient and his parents identified hemizygous NM001037811: c.650G>A, p.R217Q in the HSD17B10 gene that is inherited from the mother.Since the child died on the third day after birth, no further central nervous system examination was performed.The mother of the child has intellectual disability, the sibling sister is normal and the HSD17B10 locus is wild type.By lite-rature reviewing, 5 newborn cases with clear medical records and genetic test results were listed.All patients were male, and had onset of HSD10 deficiency within 1 week after birth.The main phenotypes include metabolic acidosis (increased blood ammonia and lactate), hypoglycemia, hypotonia, and convulsions.All 6 children died in early infancy.The corresponsive HSD17B10 variants were c. 740A>G/p.N247S, c.677G>A/p.R226Q, c.257A>G/p.D86G and c. 650G>A/p.R217Q, which did not indicate the hot spots of mutation. Conclusions:HSD10 deficiency in the neonatal period is relatively rare.The clinical diagnosis is difficult due to the serious condition and short course of the disease.Severe metabolic acidosis, hypotonia, and convulsions in neonatal patients are the main reasons for the poor prognosis, which can be attributed to the hemizygous variation and heterogeneity of the mutation site in male patients.c.650G>A may be closely associated with severe neonatal HSD10 deficiency, but the molecular biological mechanism needs to be further clarified.HSD10 deficiency has a poor prognosis and lacks effective treatment.

OBJECTIVETo study the effect of sophoridine against bone cancer pain in bone cancer pain model rats induced by W256 tumor cells and its mechanism.

METHODThe rat model of bone cancer pain was reproduced by injecting W256 tumor cells into the rat marrow cavity. Ten days after the model establishment, 36 rats were selected and randomly divided into the model control group and the sophoridine treated group. At the same time, other 10 rats with sham-operation were selected to be the normal control group. Since the 15th day after the operation, rats in the treated group had been given sophoridine (25 mg x kg(-1)) for 10 days. The mechanical withdrawal threshold and the thermal withdrawal latency of each group were measured before and after the treatment. After the last treatment, the radiological and histopathological observation shall be conducted for sick legs of all rats. The expressions of cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF) in tumor tissues were detected by mmunohistochemistry.

RESULTSophoridine could significantly increase the mechanical withdrawal threshold and the thermal withdrawal latency (P < 0.05, P < 0.01), significantly relief the bone injury caused by W256 tumor cells (P < 0.05), and notably down-regulate the COX-2 and VEGF expressions in tumor tissues (P < 0.05).

CONCLUSIONSSophoridine has the effect in relieving pain and inhibiting tumor progression in bone cancer pain rats induced by W256 tumor cells. Its mechanism may be related to the down-regulated expressions of COX-2 and VEGF.

Alkaloids ; pharmacology ; therapeutic use ; Animals ; Bone Neoplasms ; complications ; Cell Line, Tumor ; Cyclooxygenase 2 ; metabolism ; Female ; Gene Expression Regulation, Neoplastic ; drug effects ; Hyperalgesia ; complications ; drug therapy ; Pain ; complications ; diagnostic imaging ; drug therapy ; metabolism ; Quinolizines ; pharmacology ; therapeutic use ; Rats ; Rats, Sprague-Dawley ; Tomography, X-Ray Computed ; Vascular Endothelial Growth Factor A ; metabolism

Objective To investigate the role of prenatal single-dose administration of dexamethasone and ambroxol on the expression of Toll-like receptor 4 (TLR4) of fetal and neonatal rats. Methods Fifty-four pregnant rats were randomly divided into three groups with eighteen rats in each group:rats treated with 0.2 mg/kg dexamethasone (group 1),0.2 mg/kg dexamethasone and 100 mg/kg ambroxol (group 2),or saline(controls) on the 17th day of gestation.The lung tissues of the offsprings were harvest independently on the 19th day of gestation,the postnatal 3 days and 7 days.The expressions of TLR4 in fetal/neonatal rat lungs of each pregnant rat were analyzed by reverse transcription-polymerase chain reaction(RT-PCR),immunohistochemistry stain,and Western blot. ANOVA and two independent samples t-test were applied. Results On the 19th day of pregnancy,TLR4 mRNA expression was up-regulated in lungs of the two treatment groups compared with controls(controls:0.26 ± 0.18,group 1:0.39 ± 0.21,t =5.866,P＜ 0.05 ; control:0.27 ± 0.22,group 2:0.46 ± 0.13,t =9.572,P＜ 0.01 ).TLR4 mRNA expression was up-regulated in group 2 compared with controls on the postnatal 3 days and 7 days(postnatal 3 d:0.59 ± 0.23 and 0.47 ±0.24,t=2.295,P＜0.05;postnatal 7 d:0.52±0.12 and 0.35±0.17,t=4.219,P＜0.05),while no significant difference was found in group 1 compared with the controls(postnatal 3 d:0.45±0.22 and 0.44±0.14,t=0.128,P＞0.05; postnatal 7 d:0.40±0.16 and 0.36 ±0.12,t=1.365,P＞0.05).Results of the immunohistochemistry demonstrated that on the 19th day of pregnancy,the protein expression of TLR4 was significantly increased in the two treatment groups (controls:0.20 ± 0.29,group 1:0.35±0.32,t=7.179,P＜0.05 ;controls:0.20±0.29,group 2:0.39±0.25,t=10.764,P＜0.01).The protein expression of TLR4 was significantly increased in group 2 on the postnatal 3 days and 7 days(postnatal 3 d:0.55±0.32 and 0.37±0.18,t=7.121,P＜0.05;postnatal 7 d:0.41±0.29and 0.25±0.24,t=6.355,P＜0.05),while no notable difference was found between group 1 and the control (postnatal 3 d:0.40±0.21 and 0.37±0.18,t=0.683,P＞0.05 ;postnatal 7 d:0.28±0.31 and 0.25±0.24,t=0.462,P＞0.05).Results of the Western blot demonstrated that on the 19th day of pregnancy,the protein expression of TLR4 was significantly increased in the two treatment groups (controls:0.15 ± 0.12,group 1:0.27± 0.20,t =7.835,P＜0.05; controls:0.16 ± 0.18,group 2:0.34±0.16,t=10.470,P＜0.01).The protein expression of TLR4 was significantly increased in lungs of the combination administration group on the postnatal 3 days and 7 days(postnatal 3 d:group 2:0.37±0.20 and 0.25±0.22,t=6.379,P＜0.05; postnatal 7 d:0.35±0.15 and 0.24±0.13,t=5.152,P＜0.05),while no notable difference could be found between group 1 and the control (postnatal3 d:0.32±0.26 and 0.25±0.16,t=1.167,P＞0.05; postnatal 7 d:0.29±0.19 and 0.24±0.10,t =1.248,P ＞ 0.05 ). Conclusions Prenatal single-dose administration of dexamethasone may up-regulate the expression of TLR4 in the rat fetal lung.The up-regulation of TLR4 might be one of the critical factors for glucocorticoid-induced maturity of fetal lung.Prenatal single-dose administration of dexamethasone and ambroxol may have effects on the regulation of TLR4 not only in fetal rats,but also in neonatal rats.

Objective To clarify the effects of Xinfukang containing-serum on stromal cell-derived factor-1α (SDF-1α) translation and protein secretion of bone marrow stem cells (BMSCs).Methods BMSCs were isolated and amplified using bone marrow culture method,and were identified by flow cytometry.mRNA and protein secretion of SDF-1α were detected by quantitative PCR (q-PCR) and enzyme linked immunosorbent assay (ELISA),respectively.Results The expression of SDF-1α mRNA were significantly increased after 72 h in drug-containing serum,and SDF-1α mRNA in the experimental group was approximately 200 times as that in the control group (P＜0.05).Secretion of SDF-1 α in the experimental group (277.561 1 ± 15.651 8) pg/ml was nearly doubled compared with that in the control group (153.107 1±14.765 1) pg/ml (P＜0.05).Conclusions BMSCs from whole bone marrow adherent culture have high purity,and drug-containing serum can promote BMSCs to express SDF-1 α mRNA and secretion of SDF-1 α.

Objective To compare the effects of antenatal ambroxol and 3-day dexamethasone and 1-day dexamethasone on rats′ fetal lung morphogenesis.Methods Twelve pregnant rats were divided into 4 groups randomly:3-day ambroxol group,3-day dexamethasone group,1-day dexamethasone group and control group,every group had 3 rats.On gestational day 19,cesareans were carried out and the histologic structures of 6 fetal rats lungs of each pregnant rats were observed with light microscope,electronic microscope and image analysis.Results 1.Under the light microscope,compared with control group,fetal rats lung in three treatment groups had more alveolar numbers,larger alveolar space,and thinner alveolar septum(Pa