Identification and validation of anoikis-related genes to clarify the prognosis and immune mechanisms of patients with low-grade glioma.

BACKGROUND: Low-grade glioma (LGG) has an extremely poor prognosis, and the mechanism leading to malignant development has not been determined. The aim of our study was to clarify the function and mechanism of anoikis and TIMP1 in the malignant progression of LGG. METHODS: We screened 7 anoikis-related genes from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases to construct a prognostic-predicting model. The study assessed the clinical prognosis, pathological characteristics, and immune cell infiltration in both high- and low-risk groups. Additionally, the potential modulatory effects of TIMP1 on proliferation, migration, and anoikis in LGG were investigated both in vivo and in vitro. RESULTS: In this study, we identified seven critical genes, namely, PTGS2, CCND1, TIMP1, PDK4, LGALS3, CDKN1A, and CDKN2A. Kaplan‒Meier (K‒M) curves demonstrated a significant correlation between clinical features and overall survival (OS), and single-cell analysis and mutation examination emphasized the heterogeneity and pivotal role of hub gene expression imbalances in LGG development. Immune cell infiltration and microenvironment analysis further elucidated the relationships between key genes and immune cells. In addition, TIMP1 promoted the malignant progression of LGG in both in vitro and in vivo models. CONCLUSIONS: This study confirmed that TIMP1 promoted the malignant progression of LGG by inhibiting anoikis, providing insights into LGG pathogenesis and potential therapeutic targets.

Analysis of risk factors for contralateral symptomatic foraminal stenosis after unilateral transforaminal lumbar interbody fusion.

PURPOSE: To analyze the risk factors of contralateral symptomatic foraminal stenosis (FS) after unilateral transforaminal lumbar interbody fusion (TLIF) and to guide and standardize the operation process of unilateral TLIF to reduce the occurrence of contralateral symptomatic FS. METHODS: A retrospective study was undertaken on 487 patients with lumbar degeneration who underwent unilateral TLIF in the Department of Spinal Surgery of Ningbo Sixth Hospital between January 2017 and January 2021, comprising 269 males and 218 females, with a mean age of 57.1 years (range, 48-77 years). Cases of intraoperative improper operations, such as screw deviation, postoperative hematoma, and contralateral disc herniation, were excluded, and cases of nerve root symptoms caused by contralateral FS were analyzed. Post-surgery, 23 patients with nerve root symptoms caused by contralateral FS were categorized as group A, and 60 patients without nerve root symptoms were randomly selected as group B during the same period. The general data (gender, age, body mass index (BMI), bone mineral density (BMD), and diagnosis) and imaging parameters before and after operation (including contralateral foramen area (CFA), lumbar lordosis angle (LL), segmental lordosis angle (SL), disc height (DH), foramen height (FH), foramen width (FW), fusion cage position, and the difference between postoperative and preoperative) were compared between the two groups. Univariate analysis was performed, and multivariate analysis was undertaken through logistics analysis to determine the independent risk factors. Additionally, the clinical outcomes of the two groups were compared immediately before surgery and one year after surgery, using the visual analogue scale (VAS) score and the Japanese Orthopaedic Association (JOA) score for evaluation. RESULTS: The patients in this study were followed up for a period of 19-25 (22.8atien months. Among them, 23 cases (4.72% incidence) were diagnosed with contralaterally symptomatic FS after the surgery. Univariate analysis indicated significant differences between the two groups in CFA, SL, FW, and cage coronal position. Logistic regression analysis identified preoperative contralateral foramen area (OR = 1.176, 95% CI (1.012, 1.367)), small segmental lordosis angle (OR = 2.225, 95% CI (1.124, 4.406)), small intervertebral foramen width (OR = 2.706, 95% CI (1.028, 7.118)), and cage coronal position not crossing the midline (OR = 1.567, 95% CI (1.142, 2.149)) as independent risk factors for contralateral symptomatic FS after unilateral TLIF. However, there was no statistically significant difference in the pain VAS score between the two groups one year after the operation. In contrast, there was a significant difference in the JOA score between the two groups. CONCLUSION: The identified risk factors for contralateral symptomatic FS after TLIF include preoperative contralateral intervertebral foramen stenosis, a small segmental lordosis angle, a small intervertebral foramen width, and the coronal position of the cage not crossing the midline. For patients with these risk factors, it is recommended to carefully lock the screw rod during the recovery of lumbar lordosis and ensure that the coronal position of the fusion cage is implanted beyond the midline. If necessary, preventive decompression should also be considered. However, this study did not quantify the imaging data for each risk factor, and further research is needed to improve our understanding of the topic.

Intracranial drainage versus extracranial shunt in the treatment of intracranial arachnoid cysts: a meta-analysis.

OBJECTIVE: To review the literature and analyze the efficacy and safety of two surgery procedures, intracranial drainage and extracranial shunt, for intracranial arachnoid cysts. METHODS: We searched the online Medlars, PubMed, and Cochrane Central electronic databases and collected studies of patients with intracranial arachnoid cysts treated with two surgical methods. RESULTS: The meta-analysis results shows that there were not statistically significant in clinical symptoms improvement, cyst reduction, the improvement of epilepsy, epidural hematoma, cerebrospinal fluid leak, and recurrence rate (P > 0.05, with RR values are 0.99, 0.94, 1.00, 0.94, 1.21, and 0.75 respectively). There was statistically significant in the occurrence rate of intracranial infection (P = 0.0004, RR = 0.28). The intracranial drainage group was lower than extracranial shunt group. CONCLUSION: The results indicated that the efficacy and safety of two surgery procedures are similar in the treatment of intracranial arachnoid cysts, but the intracranial drainage was better than extracranial shunt in reducing the risk of intracranial infection.

Reliability and repeatability of a modified thoracolumbar spine injury classification scoring system.

Purpose: On the basis of the Thoracolumbar Injury Classification and Severity Score (TLICS), an modified TLICS classification system was presented, its reliability and repeatability were assessed, and the factors influencing classification consistency were examined. Methods: Five spinal surgeons were chosen at random. The clinical data of 120 patients with thoracolumbar fractures admitted to the Department of Spine Surgery, Ningbo Sixth Hospital from December 2019 to June 2021 were categorized using the modified TLICS system. After 6 weeks, disrupt the order of data again. Using unweighted Cohen's kappa coefficients, the consistency of the modified TLICS system was assessed in five aspects: neurofunctional status, disc injury status, fracture morphology, posterior ligament complex (PLC) integrity, and treatment plan. Results: In terms of reliability, the average kappa values for the subclasses of the modified TLICS system (neurofunctional status and disc injury status) were 0.920 and 0.815, respectively, reaching the category of complete confidence. Fracture morphology and treatment plan had average kappa values of 0.670 and 0.660, respectively, which were basically reliable. The average kappa value of PLC integrity was 0.453, which belonged to the category of moderate confidence. The average kappa coefficients of each subcategory (neurological status, disc injury status) had excellent consistency, and the kappa values were 0.936 and 0.879, respectively, which belonged to the completely credible category. The kappa values of fracture morphology and treatment plan repeatability were 0.772 and 0.749, respectively, reaching the basic credibility category. PLC integrity repeatability kappa value is low, 0.561, to moderate credibility category. Conclusion: The modified TLICS system is intuitive and straightforward to understand. The examination of thoracolumbar fracture injuries is more exhaustive and precise, with excellent reliability and repeatability. The examination of neurological status and disc injury status is quite reliable and consistent. The consistency of fracture morphology is slightly poor, which is basically credible; the PLC integrity consistency is poor, reaching a reliability level of moderate, which may be associated with the subjectivity of clinical evaluation of PLC.

Nitric oxide inhibits ghrelin-induced cell proliferation and ERK1/2 activation in GH3 cells.

Ghrelin stimulates growth hormone release and cell proliferation, which strongly supports a significant role for this peptide in the control of growth hormone-releasing adenomas function and growth. Nitric oxide can influence the stimulatory effects of ghrelin on growth hormone secretion in growth hormone-releasing adenomas. However, the effect of nitric oxide (NO) on ghrelin-induced cell proliferation and the mechanism of this effect in the adenoma were not clarified. In this study, we observed that ghrelin, at a concentration of 10⁻9 to 10⁻6 M, significantly increased BrdU incorporation into rat GH3 cells. A NO donor, S-nitroso-N-acetylpenicillamine (SNAP), blunted basal, and ghrelin-induced cell proliferation. A blocker of NO synthase, Nw-nitro-L-arginine methyl ester hydrochloride (NAME), had no influence on these actions. The activation of extracellular signal-regulated kinase (ERK) 1/2 was examined by western blotting. The results showed that SNAP reduced ghrelin-stimulated ERK1/2 activation but NAME had no influence on this activation. Together, this study indicates that NO inhibited ghrelin-induced cell proliferation by blocking ERK1/2 activation in GH3 cells.