Objective To explore mechnism and effect of fentanyl on proliferation of gastric cancer SGC-7901 cell.Methods Gastric cancer SGC-7901 cell was cultured with fentanyl of 0 (negative control), 0.5, 5 and 50 nmol/L, MTT method was used to detect the effect of fentanyl on SGC-7901 viability.The effect of fentanyl on SGC-7901 cell cycle was measured by flow cytometry.The level of cell related protein,cell cycle protein cyclin D1, Bcl-2.Results Compared with control group, fentanyl (0.5, 5, 50 nmol/L) could inhibit SGC-7901 cell viability, and the inhibitory rate was highest at 48 h.0.5, 5, 50 nmol/L fentanyl made cell cycle arrested in G1 phase.Compared with control group, fentanyl can significantly inhibit cyclinD1 and Bcl-2 expression with drug concentration increasing(P<0.05).Conclusion These results suggeste fentanyl inhibit proliferation of gastric cancer SGC-7901 cell.

Aim To investigate the effects of midazolam on porcine isolated coronary artery rings pre-contracted by potassium chloride(KCl)and the possible mechanism.Methods The vessel tension recorder system was used.Isotonic tension of porcine isolated coronary artery rings precontracted by KCl(30 mmol·L-1)was recorded.The vasorelaxing action of midazolam and effects of various drugs were observed in the rings.Results Midazolam(3×10-6～1×10-4 mol·L-1)respectively concentration-dependently reduced the contraction induced by KCl,and there was significant difference between the rings with intact and denude endothelium(P<0.05).On KCl-induced precontraction,midazolam′s relaxation was depressed by L-NAME and the blend of L-NAME and L-Arg(P<0.05),but was not affected by Indo,L-Arg and 1400W.The contraction was not prevented by pretreatment with the inhibitor of Na+/Ca2+ exchanger(KB-R7943).The inhibitor of KATP(Gli)restrained the diastolic function of midazolam(P<0.05),while the inhibitor of BKCa(TEA),Kir(BaCl2),KV(4-AP)had no obvious effect.Conclusions Midazolam produces remarkable vasodilatation on KCl pre-contracted porcine isolated coronary artery rings.Its relaxtion effect is via concentration-dependent and endothelium-dependent mechanisms and relevant to the production of NO.Na+/Ca2+ exchanger is not involved midazolam′s vasodilatation on KCl pre-contracted porcine coronary artery rings.The relaxant mechanism of midazolam may be concerned with KATP.The Kir,BKCa and KV may be not involved.

Objective To explore the relations of clinical phenotypes of type Ⅰ-ⅣV spinal muscular atrophy (SMA) with neural electrophysiological features and survival motor neuron (SMN)gene.Methods A total of 85 patients with SMA,including 46 with infantile form in which 19 of type Ⅰ and 27 of type Ⅱ,24 with juvenile form (type Ⅲ),and 15 with adult form (type ⅣV),were involved in this clinical study.Their clinical data were analyzed.The neural conduction,needle electromyography (EMG)and SMN1 gene deletion were analyzed.Results There existed different clinical features among patients who suffered from type Ⅰ to type ⅣV SMA.However,the major clinical features of SMA were displayed by progressively aggravating of flaccid paralysis in muscles of the four limbs,and the younger of the patients,the more serious of the clinical manifestations.EMG exhibited neurogenic lesion in all 43 SMA patients,33 patients presented generalized neurogenic lesions,and the abnormal degree of muscles in lower limbs was more severe than that of upper limbs,and the proximal muscles was more severe than that of the distal ones.The abnormal rate of spontaneous potential,weak contraction with raise potential and amplitude of compound motor active potential in adult and juvenile SMA were significantly lower than those in infantile SMA.SMN1 gene exon 7 and 8 were detected in all 85 patients with SMA.A total of 61 patients were found with deletion of exon 7 and/or 8 in SMN1 gene.Infantile SMA patients enjoyed 95.7％ (44/46) detection rate,juvenile SMA patients enjoyed 70.8％ (17/24) detection rate;no adult SMA patients were found with deletion ofexon 7 and/or 8 in SMN1 gene.Conclusions The more serious of clinical manifestations in SMA patients,the higher abnormality rote in electrophysiological tests.The exons deletion in SMN1 gene could result in alterations of SMA phenotypes,but it has nothing to do with the severity of SMA.Gene deletion analysis of SMN1 gene can be considered as the preferred fimal diagnosis method for infantile SMA patients.But as for juvenile form,its diagnosis depending on gene deletion analysis of SMN1 gene will be analyzed with precaution.While as for adult form of SMA,the incidence of SMA may be independent with SMN1 gene deletion.Therefore,generally,SMN1 gene assay is not taken as the routine diagnose method for adult form SMA.

Patient participation in patient safety serves as one of the objectives in patient safety management, and as a priority research area in patient safety, bearing critical importance in ensuring patient safety, and reducing or avoiding medical adverse events. Children′s Hospital of Fudan University has made active explorations to promote patients in patient safety by inviting patient participation. The measures taken include empowering the child patient families and encouraging their proactive awareness and involvement, especially in establishing an advisory council of child patient parents as a platform for patient participation in patient safety. The research found that as a doctor-patient communication and collaboration platform, the council proves highly effective. It can optimally integrate child patient families, medical institutions, and third-party supervisors, making worthy contributions to discovering patient safety hazards, improving patient safety issues, and promoting patient participation in patient safety.From patient perspectives, the council plays an important role in awareness advocating, suggestions, and communication assistance. At the same time, the three-level participation of the council provides new horizons for encouraging participation awareness of patients, broaden channels of participation and capabilities of patient participation.

African swine fever virus (ASFV) infection leads to a mortality rate of up to 100%, causing devastating disasters to the pig industry. Understanding the ASFV infection and replication is therefore of great importance. ASFV has more than 150 open reading frames, among which the inner coat protein p17 encoded by the D117L gene is involved in the formation of the icosahedral structure of the virus. However, little is known about the mechanism how p17 regulates host cell function. In this study, the potential host proteins interacting with ASFV p17 were screened by immunoprecipitation technique combined with protein profiling analysis. The interactions of p17 with mitochondrial membrane protein TOMM70 and heat shock protein HSPA8 were confirmed by co-immunoprecipitation technique and laser confocal experiments. This study provides important information for further exploring the function of p17 during ASFV infection.
African Swine Fever ; African Swine Fever Virus/metabolism* ; Animals ; Open Reading Frames ; Swine ; Viral Proteins/metabolism*