Background: Glioma, the most frequent central nervous system malignancy, is often promoted by the overexpression of Fos-like antigen 1 (FOSL1). However, the regulation of FOSL1 remains unexplored. The present study aimed to investigate the regulatory mechanism of FOSL1 to identify potential therapeutic targets for glioblastoma. Methods: This study's initial investigation utilized dual-luciferase reporter gene assays and quantitative polymerase chain reaction (qPCR) assays to establish that Kruppel-like factor 14 (KLF14) inhibits the transcription of FOSL1. Subsequent immunohistochemistry and western blotting (WB) assays on glioma tissues confirmed a negative association between FOSL1 and KLF14. This study generated KLF14 knockdown cells and double knockdown cells of KLF14 and FOSL1 and further assessed cell growth through various experimental methods. The impact of KLF14 on tumor cell migration via FOSL1 was determined using qPCR and WB assays. A xenograft tumor model was utilized to verify tumor growth suppression by KLF14. Results: The present study demonstrated that KLF14 restrains FOSL1 transcription and is inversely correlated with FOSL1 in glioma tissues. KLF14 overexpression was found to counteract FOSL1's effect on cell migration and epithelial-to-mesenchymal transition in glioma cells, which coincided with decreased Snail2 and cluster of differentiation 44 (CD44) expressions. Further, KLF14 overexpression was shown to hinder tumor progression in vivo. Conclusion: This study highlights that FOSL1 is negatively regulated by KLF14 in glioblastoma and suggests that KLF14 overexpression can mitigate tumor growth by inhibiting FOSL1, thus identifying KLF14 as a novel molecular target for treating glioblastoma. Further research into the interplay and regulatory dynamics between KLF14 and FOSL1 under varying stress conditions can enhance the precision of glioblastoma treatment.

Temozolomide (TMZ)-based chemotherapy is a standard strategy for gliomas, although chemoresistance remains a major therapeutic challenge. The chemical mechanism by which TMZ induces cell death is DNA methylation, leading to double-stranded breaks (DSBs) and thus to apoptosis. However, TMZ-induced N6-meG sites are efficiently repaired and mediated by the DNA repair protein O6-methylguanine-DNA methyl-transferase (MGMT), leading to TMZ resistance. KLF15, a member of the Kruppel-like factors family, mainly functions as transcription factor and potential suppressor gene by inhibiting proliferation, migration, and inducing apoptosis. However, the roles and regulatory mechanisms of KLF15 in glioma tumorigenesis and chemoresistance are poorly understood. In this study, KLF15 expression was upregulated in glioma tissues and cell lines upon TMZ treatment. Knockdown of KLF15 amplified TMZ-induced repression of cell proliferation, while KLF15 overexpression reversed this process. Mechanistically, KLF15 functioned as a transcriptional activator of MGMT. Moreover, KLF15 knockdown sensitized tumors to TMZ treatment in vivo. Taken together, these results suggested that KLF15 up-regulated MGMT through direct binding to the promoter of MGMT, which plays an important role in glioma resistance to TMZ, and which may be a potential target for cancer diagnosis and treatment.

Objective:To study the risk factors for ipsilateral severe hearing impairment in patients with hemifacial spasm (HFS) after microvascular decompression (MVD).Methods:MVD was performed in 3700 patients with HFS, admitted to our hospital from October 2007 to August 2020; according to the existence of ipsilateral severe hearing impairment, these patients were divided into severe hearing impairment group and non-severe hearing impairment group. The clinical data of these patients were compared. Multivariate linear regression analysis was used to determine the independent influencing factors for ipsilateral severe hearing impairment.Results:Forty-five patients (1.2%) had ipsilateral severe hearing impairment after MVD; no one got recovery of hearing impairment during the follow-up period (0.6-11.8 years, 6.3 years in average). As compared with those in the non-severe hearing impairment group, patients in the severe hearing impairment group had significantly older age, significantly higher percentages of male patients, and patients with left HFS, hypertension, and diabetes mellitus, statistically higher percentage of patients having small posterior fossa volume, arachnoid thickening and adhesion, and vertebral artery compression, significantly lower percentage of patients with anterior inferior cerebellar artery compression, significantly higher percentage of patients with arteriosclerosis of offending arteries and difficult decompression ( P<0.05). Multivariate linear regression analysis revealed that hypertension, vertebral artery compression, arteriosclerosis of offending artery and difficult decompression were independent risk factors for severe hearing impairment in patients with HFS after MVD. Conclusion:It's difficult to get recovery for severe hearing impairment in patients with HFS after MVD; this complication is much common in patients with hypertension, vertebral artery compression, arteriosclerosis of offending artery or difficult decompression.

Background Thyroid cancer (TC) is an endocrine disease, and its progression is regulated by many factors, including circular RNAs (circRNAs). However, as a new circRNA, the role of circ_0058124 in TC is worth further exploration. Methods The expression levels of circ_0058124, microRNA-940 (miR-940) and mitogen-activated protein kinase 1 (MAPK1) were assessed by quantitative polymerase chain reaction (q-PCR). The circular characteristic of circ_0058124 was identified by oligo (dT)18 primers, Ribonuclease R (RNase R) and Actinomycin D (ActD), and its localization was determined by nuclear-cytoplasmic separation assay. Also, cell proliferation was detected by colony formation assay, and cell migration and invasion were assessed by transwell assay. Further, Seahorse XF Extracellular Flux Analyzer was used to measure the oxygen consumption rate (OCR) of cells. Besides, dual-luciferase reporter, RNA immunoprecipitation (RIP) and RNA pull-down assays were used to identify the mechanism of circ_0058124. Western blot (WB) analysis was used to test the MAPK1 protein level. In addition, mice xenograft models were constructed to test the effect of circ_0058124 on TC tumor growth in vivo. Results Circ_0058124 was highly expressed in TC and is a stable cyclic transcript, mainly located in the cytoplasm. Circ_0058124 knockdown suppressed proliferation, migration, invasion and metabolic abilities in TC cells. MiR-940 could be absorbed by circ_0058124, and the inhibition effect of its overexpression on TC progression could be reversed by overexpressed-circ_0058124. MAPK1 was a target of miR-940, and the suppression effect of its silencing on TC progression could be inverted by miR-940 inhibitor. Besides, MAPK1 expression was regulated by circ_0058124 and miR-940. Interference of circ_0058124 also reduced TC tumor growth in vivo. Conclusion Circ_0058124 might play a carcinogenic role in TC progression by regulating the miR-940/MAPK1 axis, which might provide a new idea for the treatment of TC.

Objective To study the surgical outcome and safety of combined selective peripheral neurotomy (SPN) for treatment of spasticity in lower limbs of cerebral palsy patients.Methods A total of 109 cerebral palsy patients with lower limb spasticity (218 limbs) were treated with combined SPN on bilateral obturator nerve,tibial nerves and sciatic nerves from March 2007 to March 2017 at Department of Neurosurgery,Linyi Traditional Chinese Medicine Hospital.The modified Asworth scale (mAS) was used for the evaluation of the patients' spasticity and their movement ability was assessed by the gross motor function classification system (GMFCS).Results The mean follow-up period was 73.6 ± 16.7 months (range:12-132 months).The spasticity was alleviated in 209 (95.9％) lower limbs immediately post surgery,and the rate of alleviation was 90.8％ (198 limbs) at the last follow-up.The mAS scores of adductor muscle of hip and ankle metatarsal flexor muscle were 2.66 ± 0.49 and 3.36 ± 0.52 respectively prior to surgery and 1.52 ± 0.46 and 1.57 ± 0.56 respectively at last follow-up.Those differences were statistically significant (P ＜0.01).At the last follow-up,95 of 109 (87.2％) had improvement on motor function.There was significant improvement on motor function indicated by elevated GMFCS scales (P ＜ 0.05).The sensory disorder of limb was found in 51 (23.4％) lower limbs,decreased muscle strength occurred in 39 (17.9％) lower limbs during hospitalization,and both complications were improved during the follow-up period.Conclusions Combined SPN on bilateral obturator nerve,tibial nerves and sciatic nerves was an effective and safe method for the treatment of lower limb spasticity and improvement of lower limb movement in cerebral palsy patients who cannot undergo selective posterior rhizotomy (SPR) due to various reasons or those whose spasticity cannot be completely relieved after SPR.

目的 观察大承气汤加减联合西医常规治疗动脉瘤性蛛网膜下腔出血后延迟性缺血性神经功能障碍的临床疗效.方法 将92例动脉瘤性蛛网膜下腔出血后延迟性缺血性神经功能障碍患者随机分为治疗组和对照组,各46例.对照组予西医常规治疗,治疗组在对照组治疗方法的基础上给予颗粒剂型的大承气汤加减方,治疗28 d后比较2组的临床疗效.结果 治疗组总有效率为93.48％,对照组为82.61％,2组比较差异有统计学意义(P＜0.05),表明治疗组临床疗效显著优于对照组.结论 大承气汤加减联合西医常规治疗动脉瘤性蛛网膜下腔出血后延迟性缺血性神经功能障碍具有较好的疗效,能显著改善患者的神经功能缺损程度,降低病残率,改善预后.

目的:观察中西医结合治疗脑外伤后综合征的临床疗效.方法:选符合纳入标准的脑外伤后综合征患者100例,随机分为治疗组60例,对照组40例.治疗组予参芪五味子片和脑复新治疗,对照组仅予脑复新.治疗2个疗程(4周).结果:治疗组痊愈32例,有效25例,无效3例,总有效率为95.0%(95%CI=85.8%～98.9%);对照组痊愈16例,有效13例,无效11例,总有效率为72.5%(95%CI=58.7%～86.3%);两组综合疗效比较,有明显差异(u=1.9652,P=0.0494).结论:参芪五味子片和脑复新治疗脑外伤后综合征的综合疗效优于脑复新,其收益为OR=0.14(95%CI=0.03～0.54);NNT=4(95%CI=2.75～11.60).