Predicting the brain age of children with cerebral palsy using a two-dimensional convolutional neural networks prediction model without gray and white matter segmentation.

Background: Abnormal brain development is common in children with cerebral palsy (CP), but there are no recent reports on the actual brain age of children with CP. Objective: Our objective is to use the brain age prediction model to explore the law of brain development in children with CP. Methods: A two-dimensional convolutional neural networks brain age prediction model was designed without segmenting the white and gray matter. Training and testing brain age prediction model using magnetic resonance images of healthy people in a public database. The brain age of children with CP aged 5-27 years old was predicted. Results: The training dataset mean absolute error (MAE) = 1.85, r = 0.99; test dataset MAE = 3.98, r = 0.95. The brain age gap estimation (BrainAGE) of the 5- to 27-year-old patients with CP was generally higher than that of healthy peers (p < 0.0001). The BrainAGE of male patients with CP was higher than that of female patients (p < 0.05). The BrainAGE of patients with bilateral spastic CP was higher than those with unilateral spastic CP (p < 0.05). Conclusion: A two-dimensional convolutional neural networks brain age prediction model allows for brain age prediction using routine hospital T1-weighted head MRI without segmenting the white and gray matter of the brain. At the same time, these findings suggest that brain aging occurs in patients with CP after brain damage. Female patients with CP are more likely to return to their original brain development trajectory than male patients after brain injury. In patients with spastic CP, brain aging is more serious in those with bilateral cerebral hemisphere injury than in those with unilateral cerebral hemisphere injury.

Micro-RNA29b enhances the sensitivity of glioblastoma multiforme cells to temozolomide by promoting autophagy.

To explore whether or not aberrant expression of miR-29b in glioblastoma multiforme (GBM) cells was associated with temozolomide (TMZ) resistance and to elucidate potential underlying mechanisms. Upregulation of miR-29 in GBM cells was achieved by transfecting miR-29b mimics. Changes in cell viability were measured by using CCK-8 assays. Flow cytometry and TUNEL assays were used to quantify the number of apoptotic cells. The expression levels of apoptosis-related proteins as well as autophagy-associated proteins, and the expression levels of both apoptotic and autophagic genes were determined by Western blotting. Autophagy flux was monitored by transfecting mRFP-GFP-LC3 adenovirus. We halted autophagy by introducing Atg 5-specific siRNA or the autophagy inhibitor Bafilomycin A1 (Baf-A1). We also employed a GBM xenograft mice model to confirm the role of miR-29b in vivo. miR-29b overexpression induced inhibition of cell viability, and also induced apoptosis and autophagy in U251 and U87MG cells. Furthermore, upregulation of miR-29b was able to potentiate the level of antitumor activity of TMZ against tested cells. We also found that autophagy induced by miR-29b, at least partially, contributed to the increase of TMZ sensitivity in GBM cells. As was evidenced by blockade of autophagy, the application of Atg 5 siRNA or Baf-A1 was able to significantly reverse these effects. Consistent with observations in vitro, findings of in vivo assessment also confirmed that overexpression of miR-29b was able to effectively halt tumor growth and enhance the antitumor activity of TMZ. miR-29b potentiates TMZ sensitivity against GBM cells by inducing autophagy and the combined use of miR-29 mimic and TMZ might represent a potential therapeutic strategy for GBM patients.

Microsurgery with or without Neuroendoscopy in Petroclival Meningiomas.

AIM: This study aimed to investigate the operative procedure for neuroendoscope-assisted microscopic resection of petroclival meningioma to improve prognosis. MATERIAL AND METHODS: Twelve patients with petroclival meningioma who had undergone neuroendoscope-assisted microscopic resection at the Department of Neurosurgery, First Affiliated Hospital of Xinjiang Medical University were selected. In addition, 12 patients with petroclival meningioma who had undergone microscopic surgery were used as control. Clinical data from the 24 cases of petroclival meningioma were analyzed. RESULTS: For the neuroendoscope-assisted group, six, five, and one cases were respectively subjected to total resection, subtotal resection, and most resection. For the microscopic surgery group, two, three, and seven cases were respectively subjected to total resection, subtotal resection, and most resection. Both the total and subtotal resection rates of petroclival meningioma in the neuroendoscope-assisted group were significantly higher than those in the microscopic surgery group (p < 0.05). No difference was observed for short-term and long-term complications (p > 0.05) between the two groups. CONCLUSION: Neuroendoscope-assisted microscopic resection for petroclival meningioma can improve the total and subtotal resection rates of the tumor. Moreover, this method does not increase postoperative short-term and long-term complications.