Objective To explore the MRI appearances of tuberculosis of myelon and spinal meninges,and to study the value of MRI in diagnosis of this disease.Methods The imaging appearances of tuberculosis of myelon and spinal meninges tuberculosis in 8 cases were reviewed.All cases underwent plain MRI and contrast-enhanced MRI examinations.Results In 8 cases,there were myelonic tuberculosis in 3,myelonic tuberculosis accompanied with spinal meninges tuberculosis in 2 and spinal meninges tuberculosis in 3.Myelonic tuberculosis appeared as intramedullary tuberculous granuloma in 2,granulitis in 1 and tuberculous myelitis in 2.The appearances of MRI were spinal cord swelling,low signal intensity on T1WI and high signal intensity on T2WI.On contrast-enhanced MRI,the lesions were circular enhancement,military nodules or non-enhancement.The typical MRI appearances of spinal meningeal tuberculosis showed spinal meninges generally thickened,narrowing or closing of subarachnoid cavity,on contrast-enhanced MRI,the lesions were tubiform enhancement of sagittal images or circular enhancement of axial images.All cases had active tuberculosis in neighbourhood organ or tissue.Conclusion The MRI appearances of tuberculosis of myelon and spinal meninges are representative,the definite diagnosis of which can be made when the MRI appearances in combination with the history of the patients and the active tuberculosis of neighbourhood organ or tissue.

Objective:To investigate whether astaxanthin (AST) down-regulates dynamin-related protein 1 (Drp1) through activating the silent mating type information regulation 2 homolog-1 (SIRT1) signaling pathway, thereby attenuating contrast-induced acute kidney injury.Methods:Forty adult male Sprague-Dawley rats weighing 160-180 g were randomly divided into five groups: sham surgery group (Sham group), contrast medium injury group (CM group), astaxanthin-intervention group (AST+CM group), SIRT1 inhibitor Ex527 intervention group (Ex527+CM group), and astaxanthin combined with Ex527 intervention group (AST+Ex527+CM group). After 72 hours of modeling, heart blood was removed and kidney tissues were collected for follow-up testing. Serum creatinine (Scr), blood urea nitrogen (BUN), and oxidative stress-related indexes total superoxide dismutase (T-SOD) and malondialdehyde (MDA) were measured by biochemistry; hematoxylin and eosin staining was performed to observe the pathological changes in the kidney; mitochondrial morphology and number were observed by transmission electron microscopy; reactive oxygen species (ROS) levels were detected by ROS staining in frozen sections; TUNEL staining was performed to detect apoptosis level. The expression levels of SIRT1, p53, peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), Drp1 and apoptosis-related proteins Bcl-2 and Bax were detected by Western blotting.Results:(1) Compared with the CM group, Scr and BUN level were significantly lower, T-SOD level was higher and MDA level was lower in the AST+CM group, while T-SOD level decreased and MDA level increased after the combination of Ex527 (all P<0.05). (2) ROS expression was lower in the AST+CM group compared to the CM group and higher after the combination of Ex527 (both P<0.05). (3) The number of apoptotic cells was significantly reduced in the AST+CM group compared to the CM group and increased after the combination of Ex527 (both P<0.05). (4) The protein expression levels of SIRT1, PGC-1α and Bcl-2 were increased and the protein expression levels of p53, Drp1 and Bax were decreased (all P<0.05) in the AST+CM group compared with the CM group, and the protein expression levels of SIRT1, PGC-1α and Bcl-2 were decreased and the protein expression levels of p53, Drp1 and Bax were increased when Ex527 was combined (all P<0.05). Conclusion:Astaxanthin can inhibit Drp1-mediated mitochondrial fission by activating the SIRT1 pathway, thereby reducing contrast-induced acute kidney injury in rats.

Objective To explore the effect of open reading frame 66(C12ORF66)located at chromosome 12 on the viability of MYCN amplified NB cell lines.Methods DDatasets GSE16476 and GSE49710 in R2 database were analyzed for expression level of C12ORF66 in MYCN amplified and MYCN non-amplified NB cells and its potential correlation with the prognosis of pediatric patients.C12ORF66 mRNA expression level in normal tissue immortalized cell lines,MYCN amplified and MYCN non-amplified cell lines were detected by RT-qRCR.Transient or stable knockdown of C12ORF66 cell lines were constructed to compare the difference in real time cellular analysis(RTCA),colony formation,Ki67 positive cells between the control group and the C12ORF66 knockdown group.Results By analyzing R2 datasets,C12ORF66 level in MYCN amplified samples was significantly higher than that in MYCN non-amplified samples,and the expression of C12ORF66 was negatively correlated with the prognosis of pediatric patients(P＜0.05).C12ORF66 highly expressed in MYCN-amplified BE(2)-C and SK-N-BE(2)cell lines than in MYCN non-amplified CHLA-255 and SH-SY5Y cell lines(P＜0.001).Transient or stable knockdown of C12ORF66 resulted in significant slow down of proliferation of MYCN amplified NB cells(P＜0.001),the colony formation ability was significantly reduced(P＜0.001),and the proportion of Ki67 positive cells was significantly decreased(P＜0.05).Conclusions C12ORF66 was highly expressed in MYCN amplified clinical NB samples and cell lines which is believed to be correlated with poor prognosis of pediatric patients.C12ORF66 knockdown signifi-cantly inhibits cell viability of NB cells.

Objective:To investigate the function and underlying mechanism of cysteine and glycine-rich protein 2(CSRP2)in neuroblastoma(NB).Methods:The correlation between the expression level of CSRP2 mRNA and the prognosis of NB children in NB clinical samples was analyzed in R2 Genomics Analysis and Visualization Platform.The small interfering RNA(siRNA)targeting CSRP2 or CSRP2 plasmid were transfected to NB cell lines SK-N-BE(2)and SH-SY5Y.Cell proliferation was observed by crystal violet staining and real-time cellular analysis.The ability of colony formation of NB cells was ob-served by colony-forming unit assay.Immunofluorescence assay was used to detect the expression of the proliferation marker Ki-67.Flow cytometry analysis for cell cycle proportion was used with cells stained by propidium iodide(PI).Annexin V/7AAD was used to stain cells and analyze the percentage of cell apoptosis.The ability of cell migration was determined by cell wound-healing assay.The level of protein and mRNA expression of CSRP2 in NB primary tumor and NB cell lines were detected by Western blot and quantitative real-time PCR(RT-qPCR).Results:By analyzing the NB clinical sample databases,it was found that the expression levels of CSRP2 in high-risk NB with 3/4 stages in international neuroblas-toma staging system(INSS)were significantly higher than that in low-risk NB with 1/2 INSS stages.The NB patients with high expression levels of CSRP2 were shown lower overall survival rate than those with low expression levels of CSRP2.We detected the protein levels of CSRP2 in the NB samples by Western blot,and found that the protein level of CSRP2 in 3/4 INSS stages was significantly higher than that in 1/2 INSS stages.Knockdown of CSRP2 inhibited cell viability and proliferation of NB cells.Overexpression of CSRP2 increased the proliferation of NB cells.Flow cytometry showed that the proportion of sub-G1,G0/G1 and S phase cells and Annexin V positive cells were increased after CSRP2 deficiency.In the cell wound-healing assay,the healing rate of NB cells was significantly attenuated after knockdown of CSRP2.Further mechanism studies showed that the proportion of the proliferation marker Ki-67 and the phospho-rylation levels of extracellular signal-regulated kinases 1/2(ERK1/2)were significantly decreased after CSRP2 knockdown.Conclusion:CSRP2 is highly expressed in high-risk NB with 3/4 INSS stages,and the expression levels of CSRP2 are negatively correlated with the overall survival of NB patients.CSRP2 significantly increased the proliferation and cell migration of NB cells and inhibited cell apoptosis via the activation of ERK1/2.All these results indicate that CSRP2 promotes the progression of NB by activating ERK1/2,and this study will provide a potential target for high-risk NB therapy.