Objective To establish the xenotransplanted tumor model of Craniopharyngioma in chick chorioallan?toic membrane (CAM) and detect the angiogenesis ability, microvessel density (MVD) and cell proliferation of the xeno?graft. Method Craniopharyngioma tissues from surgical craniopharyngioma patients were transplanted on the CAM. An?giogenesis assay was performed and the MVD and PCNA were evaluated using immunohistochemistry following the trans?plantation. Results The tumor formation rate of adamantinomatous craniopharyngioma (ACP) and squamous papillary cra?niopharyngioma (SPCP) was 47.14% and 43.33%, respectively. There was no significant difference in tumor formation rate between ACP and SPCP(χ2=0.123,P=0.726). The CAM angiogenesis, MVD and expression of PCNA were higher in ACP than in SPCP. The expression of PCNA was positively correlated with MVD (Pearson r=0.639,P<0.001) and CAM assay score (Spearman r=0.490,P=0.001 ) in CP. Conclusion The model of human craniopharyngioma can be es?tablished in the CAM. The angiogenesis of the xenograft in the CAM can be evaluated and the craniopharyngioma xeno?graft of CAM possesses a new blood circulation and cell proliferation ability.

ObjectiveTo compare the effects on left ventricular remodeling of bone marrow mononuclear cells transplantation one week and three months after acute myocardial infarction.MethodsAcute myocardial infarction models were successfully established in 15 swine,which were randomly divided into three groups:placebo group,early transplantation group and late trasplantation group.One week after model had been established,early transplantation group underwent bone marrow mononuclear cells transplantation,and then so did the late trasplantation group three months after acute myocardial infarction.B-ultrasound and single photon emission computed tomography (SPECT) examinations were performed to assess the left ventricular end diastolic dimension( LVd),left ventricular end diastolic volume(EDV) and left ventricular ejection fraction(EF) before and one week,three months,six months after acute myocardial infarction.ResultsThe LVd of late transplantation group [ (54.20:t:3.70) mm] was lower than placebo group [ (63.20 ±5.63)mm],but higher than early transplantation group [ (47.40 ± 1.14)mm].The EDV of late transplantation group [ ( 163.00 ±6.96)ml] was lower than placebo group [ (209.40 ± 18.69)ml],but higher than early transplantation group [ ( 135.40 ± 4.93 ) ml ].The EF of late transplantation group (0.25 ±0.02) was higher than placebo group (0.19 ±0.02),but lower than early transplantation group (0.37 ±0.02).ConclusionsBone marrow mononuclear cells transplantation can alleviate progressing ventricular remodeling,even it is performed three month after acute myocardial infarction,but its therapeutic effects are inferior to early transplantation's.

Objective To investigate the role of microRNA-192 (miR-192) in the regulation of epithelial mesenchymal transition induced by advanced glycation end products (AGEs) in human peritoneal mesothelial cells.Methods The human peritoneal mesothelial cells,the human peritoneal mesothelial cells transfected by miR-192 inhibitor and the human peritoneal mesothelial cells transfected by miR-192 inhibitor negative control were cultured for 72 hours in culture medium containing AGEs (80mM);M199 medium and medium with M199 medium containing 80mM BSA as negative control,the expression of miR-192 and mRNA was detected by real-time quantitative PCR,and the expression of miR-192 and mRNA was detected by Western blotting.Results AGEs significantly upregulated the expression of miR-192,Collagen Ⅰ mRNA,α-smooth muscle actin (α-SMA) mRNA and protein(P ＜ 0.05),while significantly downregulated the E-cadherin mRNA and protein expression(P ＜ 0.05).Compared with human peritoneal mesothelial cells transfected by miR-192 inhibitor,the expression of miR-192 and Collagen Ⅰ mRNA and α-SMA mRNA and protein was decreased (P ＜0.05),while E-cadherin mRNA and protein expression was significantly increased (P ＜ 0.05).Conclusion AGEs may induce EMT of human peritoneal mesothelial cells by upregulation of miR-192 expression.MiR-192 inhibitor may prevent AGEs-inducing EMT of human peritoneal mesothelial cells by down-regulation of miR-1 9 2 expression,and may play an important regulatory role in EMT of human peritoneal mesothelial cells induced by AGEs.

Objective To investigate the role of microRNA-192 (miR-192) in the regulation of epithelial mesenchymal transition induced by advanced glycation end products (AGEs) in human peritoneal mesothelial cells.Methods The human peritoneal mesothelial cells,the human peritoneal mesothelial cells transfected by miR-192 inhibitor and the human peritoneal mesothelial cells transfected by miR-192 inhibitor negative control were cultured for 72 hours in culture medium containing AGEs (80mM);M199 medium and medium with M199 medium containing 80mM BSA as negative control,the expression of miR-192 and mRNA was detected by real-time quantitative PCR,and the expression of miR-192 and mRNA was detected by Western blotting.Results AGEs significantly upregulated the expression of miR-192,Collagen Ⅰ mRNA,α-smooth muscle actin (α-SMA) mRNA and protein(P ＜ 0.05),while significantly downregulated the E-cadherin mRNA and protein expression(P ＜ 0.05).Compared with human peritoneal mesothelial cells transfected by miR-192 inhibitor,the expression of miR-192 and Collagen Ⅰ mRNA and α-SMA mRNA and protein was decreased (P ＜0.05),while E-cadherin mRNA and protein expression was significantly increased (P ＜ 0.05).Conclusion AGEs may induce EMT of human peritoneal mesothelial cells by upregulation of miR-192 expression.MiR-192 inhibitor may prevent AGEs-inducing EMT of human peritoneal mesothelial cells by down-regulation of miR-1 9 2 expression,and may play an important regulatory role in EMT of human peritoneal mesothelial cells induced by AGEs.

Objective: To analyze variants of PRRT2 gene in two children with paroxysmal kinesigenic dyskinesia. Methods: Genomic DNA of the two children and their parents was extracted from peripheral venous blood samples. All exons and their flanking regions of the PRRT2 gene were subjected to PCR and Sanger sequencing. Results: The two children were found to respectively harbor a c. 282dupA and a c. 715_716dupCC variant in exon 2 of the PRRT2 gene, which were both inherited from their mothers. Pooling together their frequencies in general population, genetic models, related literature and impact on protein function, the two novel variants were both predicted to be pathogenic. Conclusion The c. 282dupA and c. 715_716dupCC variants probably underlie the disease in the two children.

Objective:To investigate the electrophysiological features of patients with anti-neurofascin 155 (NF155) IgG4 antibodies positive chronic inflammatory demyelinating polyradiculoneuropathy (CIDP).Methods:The electrophysiological data of 6 anti-NF155 IgG4 antibodies positive CIDP patients in Beijing Tiantan Hospital, Capital Medical University from September 2018 to May 2021 were retrospectively analyzed. Parameters studies included standard motor and sensory nerve conduction studies, electromyography (EMG) and F waves studies. Correlation analysis was made to explore the relationships between clinical indicators and electrophysiological data.Results:There was statistically significant difference in the motor nerve conduction study on abnormal rate of tibial nerve (χ 2=11.08, P=0.011). Motor nerve conduction abnormalities were presented in a majority of patients with decreased motor conduction velocity (MCV) and prolonged distal motor latency (DML). There was no statistically significant difference in the overall abnormal rate between lower limbs and upper limbs (30/32, 93.8% vs 22/22, 100.0%; χ 2=1.43, P=0.508), sensory nerve conduction and motor nerve conduction (52/54, 96.3% vs 42/42, 100.0%; χ 2=1.59, P=0.503). There was statistically significant difference in the overall abnormal rate in median nerve, ulnar nerve and sural nerve (χ 2=14.96, P=0.001;χ 2=10.00, P=0.007; χ 2=9.95, P=0.008),and absent sensory nerve action potential was the most common abnormality in sensory nerve conduction abnormalities. The abnormal rate of EMG was 9/14, which was constituted by upper limbs (4/8) and lower limbs (5/6), and the spontaneous activity accompanied with prolonged duration and increased amplitude of motor unit action potential was common. Significant negative correlations were established between disease duration and compound muscle action potential (CMAP) amplitude and negative area of ulnar nerve ( r=-0.84, P=0.036; r =-0.76, P=0.011), and the correlations between age and MCV of median nerve and ulnar nerve were also found ( r=0.89, P=0.019; r=0.95, P=0.003). The DML of median nerve was negatively correlated with CMAP amplitude ( r=-0.63, P=0.049). Moreover, the correlation analysis revealed associations of the F wave latency with the DML, CMAP amplitude and MCV of tibial nerve ( r= 0.90, P=0.039; r=-0.96, P=0.012; r=-0.96, P=0.010). Conclusions:The motor nerve and sensory nerve, the myelin sheath and axon of peripheral nerves in anti-NF155 IgG4 CIDP patients were largely affected. The CMAP amplitude and negative area of ulnar nerve might be of certain clinical value in reflecting the disease duration.The younger the patients, the more severe the demyelination degree of the upper limbs. The F wave latency of tibial nerve not only reflected the abnormal proximal conduction, but also the distal damage degree of myelin sheath and axon.