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Glioma is diagnosed as the most common intracranial malignant tumor. cancer stem cells determine stemness and radioresistance, and may facilitate glioma recurrence. The present study aimed to investigate whether the long non-coding rna (lncrna) transmembrane phosphatase with tensin homology pseudogene 1 (TPTeP1) regulated cell stemness and radioresistance of glioma, and determine the underlying molecular mechanism of TPTeP1 in the modulation of glioma progression. cell and molecular biology techniques were applied for investigating the role of TPTeP1 in glioma cell lines, animal model, and clinical samples. The results demonstrated that TPTeP1 attenuated stemness and radioresistance of glioma both in vitro and in vivo. in addition, TPTeP1 augmented MaPK14 expression by competitively interacting with microrna (mir)-106a-5p, thus activating the P38 MaPK signaling pathway, and suppressing glioma stemness and radioresistance. TPTeP1 functionally bound to mir-106a-5p, which formed a reciprocal regulatory loop to stimulate the P38 MaPK signaling pathway. low TPTeP1 expression levels were detected in high-grade glioma tissues compared with low-grade glioma tissues, and were positively associated with poor prognosis of patients with glioma. Furthermore, analysis using data from The cancer Genome atlas database confirmed the molecular mechanism and biological significance of dysregulation of TPTEP1 in glioma progression. Taken together, the results of the present study suggest that TPTeP1 may be applied as a diagnostic and prognostic indicator for glioma, and may be an alternative target for the treatment of glioma.

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Objective: Lumbar sympathetic trunk (LST) injury is one of the major complications after oblique lumbar interbody fusion (OLIF). LST injury often manifests as unequal skin temperature in lower limbs after operation, and there may be a large number of missed diagnoses due to the lack of attention and different diagnostic methods. The study aimed to investigate the incidence and clinical characteristics of LST injury after OLIF. Methods:The data of patients with lumbar degenerative diseases who underwent OLIF in our hospital from April 2016 to October 2017 were retrospectively analyzed. Finally, a total of 54 patients were included. There were 10 males and 44 females, aged 58.4 AE 10.9 years. The skin temperature of lower limbs was measured before and a day after surgery. The patients were followed up at 1 week, 6 weeks, 6 months, and 2 years after the surgery. Likert five-point scale was used to evaluate the discomfort caused by LST injury. Injury severity score was introduced to grade injury degree according to the recovery time of postoperative symptoms. The chi-square test was used to analyze the association of incidence of lumbar sympathetic trunk (LST) injury with contributing factors, such as gender and number of surgical segments. Results:The unequal temperature was not found before surgery in all the patients. Postoperatively, 16 cases (29.6%) had difference of skin temperature more than 0.5 C and were diagnosed with LST injury. Eight patients (14.8%) had self-perception of skin temperature differences, and 12 patients (22.2%) had other symptoms, such as muscle pain, numbness, and weakness, which were not statistically different between patients with and without lumbar sympathetic trunk injury (p > 0.05). In the 16 patients with LST injury, the difference of skin temperature between the two legs was 0.6 AE 0.1 C on the first day, and the temperature difference lasted for 1.5-$12 months. According to Likert five-point scale, two cases (12.5%) were poor, and 14 cases (87.5%) were moderate immediately after surgery. Fifteen cases improved to some extent 6 weeks to 12 months after surgery. Conclusion:Postoperative LST injury is mainly manifested by different temperature of lower limbs. The incidence was higher in patients with multi-segment OLIF than in those with single-segment OLIF, and the subjective experience of most patients with LST injury was moderate discomfort.

Multifidus muscle dysfunction is associated with the multifidus muscle injury (MMI), which ultimately result in the low‐back pain. Increasing evidence shows that microRNAs (miRs) may be involved in multifidus muscle dysfunction. In this study, we tested the hypothesis that downregulation of let‐7b‐5p may inhibit the multifidus muscle dysfunction development and progression. The target prediction program and luciferase activity determination confirmed electron transfer flavoprotein alpha subunit (ETFA) as a direct target gene of let‐7b‐5p. To study the mechanisms and functions of let‐7b‐5p in relation to ETFA in MMI progression, we prepared rats with experimental MMI, and a lentivirus‐based packaging system was designed to upregulate expressions of let‐7b‐5p, and downregulate the expression of ETFA. ETFA was identified as a target gene of let‐7b‐5p. Older age, a longer duration of pain, and higher visual analog scale and Oswestry disability index scores for the patients with chronic low‐back pain were linked to a more severe degree of degenerative muscle atrophy and fatty infiltration. Increased expression of let‐7b‐5p and decreased expression of ETFA and vitamin D receptor (VDR) were positively correlated with multifidus muscle dysfunction. Downregulated let‐7b‐5p could inhibit infiltration of collagen fibers, reverse the ultrastructural changes of multifidus muscle, and induce the VDR expression, thereby repair the MMI. The results provided a potential basis for let‐7b‐5p that could support targeted intervention in multifidus muscle dysfunction. Collectively, this study confirmed that downregulation of let‐7b‐5p has a potential inhibitory effect on the development of the function of the musculus myocytes by upregulating ETFA.