Objective　To explore the clinical manifestations,pathological characteristics and therapeutic responses of lipid storage myopathy (LSM).Methods　The clinical information of 22 LSM patients were collected and analyzed retrospectively.Results　Proximal limb muscle weakness and motor intolerance were observed in all patients.The concentrations of creatine kinase in blood were found increased to various degrees in 20 cases.EMG examinations showed myogenic damage in 18 cases.Muscle pathology examination of 22 cases showed increased lipid droplets in the muscle fibers.Follow-up data was available for 20 of all the patients after treatment.Nineteen cases were treated with low-doses prednisone,18 cases with riboflavin and 6 cases with L-Carnitine.All patients showed distinct degree of improvement of clinical symptoms within a month.After treatment for 3 months,8/22 patients were recovered except for 2 patients who were relapsed.And repeated treatment was effective.Conclusions　LSM is a curable disease.It is recommended to avoid fever,fatigue and other triggering factors.In the absence of genetic testing,riboflavin,L-carnitine,and prednisone should be used empirically.In the presence of genetic testing,targeted therapy should be performed based on gene mutations.

Objective : o explore the effects of long non⁃coding RNA LINC00092 on the proliferation , migration and invasion of glioma. Methods : Using the cancer genome atlas(TCGA) and genotype⁃tissue expression (GTEx) databases , this study analyzed the expression of LINC00092 in pan⁃carcinoma and its effect on the prognosis of glioma. In addition , LINC00092 overexpression plasmid was constructed to detect the effects of LINC00092 on proliferation , migration , invasion and apoptosis of glioma cells by cell function experiments , including CCK⁃8 assay , Transwell assay and flow cytometry. Finally , qRT⁃PCR and Western blot were used to detect the effect of overexpression of LINC00092 on the expression level of IGF2BP1 . Results : The analysis of public databases revealed a widespread downregulation of LINC00092 in tumors , and its association with the development of glioblastoma multiforme (GBM) and low⁃grade glioma (LGG) . In vitro experiments demonstrated that overexpression of LINC00092 significantly reduced the proliferation , migration and invasion of glioma cells , while promoting apoptosis. Moreover, overexpression of LINC00092 led to a decrease in the expression levels of IGF2BP1 . Conclusion LINC00092 may inhibit glioma proliferation , migration and invasion by targeting IGF2BP1 , and promote glioma cell apoptosis.

Objective : To explore the effect of LncRNA MEG3 in temozolomide (TMZ) resistance of glioma cells. Methods : TMZ⁃resistant glioma cells U87(U87/TMZ) were constructed,qRT⁃PCR was used to detect the LncRNA MEG3 expression level, and MTT was used to detect the cell proliferation ability. The LncRNA MEG3 in U87/TMZ was overexpressed by liposome method (pcDNA⁃MEG3 group), the empty vector was transfected as the empty vector group ( pcDNA group), and the conventionally cultured U87/TMZ was used as the blank group ( Control group),then treated with 10 μg/ml TMZ. The plasmid transfection effect was analyzed by qRT⁃PCR. The expression of LncRNA MEG3⁃related protein was confirmed by Western blot. The cell cloning experiment detects the effect of LncRNA MEG3 on cell proliferation. The effect of LncRNA MEG3 on cell invasion was tested by Transwell. The effect of LncRNA MEG3 on cell apoptosis was detected by flow cytometry. And mouse transplant tumoranimal model was constructed for in vivo experiments. Results : Compared with U87, the expression level of Ln cRNA MEG3 in U87/TMZ was lower (P < 0. 01), and the cell viability of U87/TMZ was higher than that of U87 (P < 0. 01) . After overexpression of MEG3 combined with TMZ, compared with the Control group and the pcDNA group, the pcDNA⁃MEG3 group up⁃regulated the expression of MEG3 mRNA and p53 protein, and down⁃regulated the expression of MDM2 protein, and the proliferation and invasion ability of the pcDNA⁃MEG3 group decreased while the apoptosis ability increased (P < 0. 01) . The construction of mouse transplant tumor animal model showed that the tumor volume and mass of the pcDNA⁃MEG3 group were reduced compared with the pcDNA group (P < 0. 01) . Conclusion Overexpression of LncRNA MEG3 can attenuate the drug resistance of TMZ⁃resistant glioma cells.