Objective. The safety and efficacy of three‐dimensional‐ (3D‐) printed hydroxyapatite/polylactic acid (HA‐PLA) composites in repairing cranial defects were evaluated in a rabbit experimental model. Methods. Twelve New Zealand rabbits were selected as experimental subjects. Two holes (A and B), each with a diameter of approximately 1 cm, were made in the cranium of each rabbit. Hole A served as the experimental manipulation, and hole B served as the control manipulation. A 3D‐printed HA‐PLA composite was used for placement onto hole A, whereas autologous bone powder was used for placement onto hole B. Samples from the experimental holes and the control holes were collected at 30 and 90 days after surgery. The obtained materials were examined in terms of their morphologies and histopathologies and were also subjected to simultaneous hardness tests. Results. Both the 3D‐printed HA‐PLA composite and autologous bone powder were able to repair and fill the cranial defects at 30 days and 90 days after surgery. At 30 days after surgery, the microhardness of the area repaired by the HA‐PLA composite was lower than that of the area repaired by autogenous bone powder (p < 0.01), but neither of these treatments reached the hardness of normal bone at this time (p < 0.01). At 90 days after surgery, there was no statistically significant difference in the microhardness of the repaired area from the 3D‐printed HA‐PLA composite compared with that of the repaired area from autologous bone powder (p > 0.05), and there was no statistically significant difference in the hardness of the two repaired areas compared with that of the normal bone (p > 0.05). Hematoxylin‐eosin staining showed that bone cells in the HA‐PLA material in the experimental group grew and were arranged in an orderly manner. Bone trabeculae and marrow cavities were formed on the pore surface and inside of the HA‐PLA scaffold, and the arrangement of bone trabeculae was regular. Conclusion. 3D‐printed HA‐PLA composites can induce bone regeneration, are biocompatible, have the same strength as autologous bone powder, are able to degrade, and are ultimately safe and effective for repairing cranial defects in rabbits. However, further research is needed to determine the feasibility of 3D‐printed HA‐PLA composites in human cranioplasty.

Spinal cord injury (SCI) is a severe condition that often leads to permanent functional impairments. The current treatment options are limited and there is a need for more effective treatments. Human umbilical cord mesenchymal stem cells (hUCMSCs) have shown promise in promoting neuroregeneration and modulating immune response. In addition, miR‑124‑3p has been identified as a potential biomarker for monitoring the progress of neural repair, making it a focus of the present study, which used a rat model of SCI to evaluate the effects of intrathecal hUCMSC transplantation. The present study included three groups: A sham‑operated group, an SCI model group receiving PBS and an SCI group receiving hUCMSCs. Neurological function was assessed using the Basso, Beattie and Bresnahan locomotor rating scale and Rivlin inclined plane test on days 1, 3, 7, 14 and 21 post‑injury. Histological analysis included hematoxylin and eosin staining to assess tissue morphology, Nissl staining to evaluate neuron survival and immunofluorescence to detect bromodeoxyuridine (BrdU)+/neuron‑specific enolase (NSE)+ cells, which indicate neurogenesis. Detection of brain‑derived neurotrophic factor (BDNF) protein expression at various time points in rats with spinal cord injury using western blotting. miR‑124‑3p expression was quantified using reverse transcription‑quantitative (RT‑q)PCR to assess its potential as a biomarker for SCI recovery. The hUCMSC group showed significant improvements in motor function compared with the control group, particularly on days 7 and 14 post‑injury. Histological analysis revealed reduced scar tissue formation and increased neuron survival in the hUCMSC group. Immunofluorescence analysis showed a higher number of BrdU+/NSE+ cells in the hUCMSC group, indicating enhanced neurogenesis. The expression of the neurorepair‑related protein BDNF was markedly higher in the hUCMSCs group compared with the control group. Furthermore, RT‑qPCR analysis demonstrated a marked upregulation of miR‑124‑3p in the hUCMSC group, which was correlated with improved functional recovery. The present study demonstrated that intrathecal transplantation of hUCMSCs notably enhanced recovery following SCI, probably by promoting neurogenesis and modulating miR‑124‑3p expression. miR‑124‑3p upregulation in the hUCMSC group highlighted its potential as a biomarker for tracking the progress of SCI recovery. These findings provided a foundation for the future clinical applications of hUCMSCs in SCI treatment and the use of miR‑124‑3p as a monitoring tool.

Dural injuries often result in severe complications such as cerebrospinal fluid (CSF) leakage, intracranial infections, and brain herniation, which significantly impact patient recovery and quality of life. Conventional dural repair materials, which rely on suturing to peripheral tissues, fail to promote tissue regeneration and provide sufficient CSF leakage prevention, leading to suboptimal outcomes. To address these limitations, we developed a Janus adhesive bio-patch with both antibacterial and pro-angiogenic properties to enhance dura mater repair. This bio-patch consisted of a polyacrylic acid (PAA) adhesive gel layer loaded with vancomycin and magnesium carbonate (MgCO₃), integrated onto a small intestinal submucosa (SIS) extracellular matrix. It exhibited a burst strength of 20.50±2.89kPa, effectively sealing CSF leaks, while demonstrating excellent antibacterial efficacy (∼99%) and significant enhanced angiogenesis (3.47-fold higher than the control). In rat, rabbit, and dog dural injury models, the bio-patch adhered seamlessly to the injury site, successfully preventing leaks and promoting tissue regeneration. These results highlighted the Janus adhesive bio-patch as a promising solution for improving dural repair in neurosurgery, offering a safer and more effective alternative to conventional suturing techniques.

To study the differences in VASH2 expression in pediatric medulloblastoma (MB) tumor tissues of different molecular subtypes, to analyze the correlation between VASH2 and the molecular subtypes of medulloblastoma, clinicopathological data, and prognosis, and to explore the specific mechanism of VASH2’s role in SHH medulloblastoma cell lines DAOY. We analyzed 47 pediatric medulloblastoma cases admitted to the Department of Pediatric Neurosurgery of the First Affiliated Hospital of Xinjiang Medical University from January 2011 to December 2019, and the expression levels of YAP1 and GAB1 in these tumor tissues were detected by immunohistochemistry (IHC) and molecularly typed (WNT-type, SHH-type, and non-WNT/SHH-type). The correlation between VASH2 and molecular typing of medulloblastoma was analyzed. We also analyzed the medulloblastoma dataset in the GEO database (GSE30074 and GSE202043) to explore the correlation between VASH2 and the prognosis of medulloblastoma patients, as well as performed a comprehensive GO enrichment analysis specifically for the VASH2 gene to reveal the underlying biological pathways of its complex molecular profile. We used vasopressin 2 (VASH2) as a research target and overexpressed and knocked down VASH2 in SHH medulloblastoma cell lines DAOY by lentiviral vectors in vitro, respectively, to investigate its role in SHH medulloblastoma cell lines DAOY cell proliferation, apoptosis, migration, invasion and biological roles in the cell cycle. (1) Among 47 pediatric medulloblastoma cases, 8 were WNT type, 29 were SHH type, and 10 were non-WNT/SHH type. the positive rate of VASH2 was highest in the SHH type with a 68.97% positive rate, followed by non-WNT/SHH and lowest in the WNT type. The results of the multifactorial analysis showed that positive expression of VASH2 was associated with medulloblastoma molecular subtype (SHH type), site of tumor development (four ventricles), and gender (male), P < 0.05. (2) The results of cellular experiments showed that overexpression of VASH2 increased the invasion and migration ability of medulloblast Daoy, while knockdown of VASH2 inhibited the invasion and Overexpression of VASH2 upregulated the expression of Smad2 + 3, Smad4, Mmp2 and the apoptotic indicators Bcl-2 and Caspase3, while knockdown of VASH2 suppressed the expression of Smad2 + 3 and Mmp2, and silenced the expression of Smad4 and the apoptotic indicators Bcl2, Caspase3 expression. Flow cytometric cycle analysis showed that VASH2 overexpression increased the S phase in the Daoy cell cycle, while VASH2 knockdown decreased the S phase in the SHH medulloblastoma cell lines DAOY cell cycle. Bioinformatics analysis showed that there was no statistically significant difference between the expression of VASH2 genes in the GSE30074 and GSE202043 datasets and the prognosis of the patients, but the results of this dataset analysis suggested that we need to continue to expand the sample size of the study in the future. The results of the GO enrichment analysis showed that the angiogenic pathway was the most significantly enriched, and the PPI interactions network of VASH2 was obtained from the STRING database. Using the STRING database, we obtained the PPI interaction network of VASH2, and the KEGG enrichment analysis of VASH2-related genes showed that VASH2-related genes were related to the apoptosis pathway, and therefore it was inferred that VASH2 also affects the development of tumors through apoptosis. We found for the first time that the positive expression rate of VASH2 was closely associated with SHH-type pediatric medulloblastoma and that VASH2 was involved in the invasion, migration, cell cycle, and apoptotic capacity of SHH medulloblastoma cell lines DAOY by affecting downstream indicators of the TGF-β pathway. This suggests that it is involved in the progression of pediatric medulloblastoma, and VASH2 is expected to be a diagnostic and therapeutic target for SHH-type pediatric medulloblastoma.

Purpose: Spontaneous intracerebral hemorrhage (ICH) cases caused by hypertension often have poor prognoses. The use of dehydrant agents, such as mannitol, is common to reduce intracranial pressure and alleviate cerebral edema, but they may also pose a risk of worsening kidney function. This study aimed to investigate the impact of impaired kidney function on the outcomes of surgically treated hypertensive ICH patients. Methods: We conducted a retrospective analysis of a consecutive cohort of patients who underwent surgical intervention due to hypertension-related ICH at our institute between December 1, 2017, and January 31, 2022. Demographic, clinical, radiological, and prognostic data were collected. Patients were categorized into two groups based on 90-day mortality: group A [overall survival (OS) ≤3 months] and group B (OS >3 months). Survival analysis was performed to identify factors associated with poor outcomes. Results: Among the 232 eligible patients, group A exhibited significantly impaired kidney function, as indicated by mean estimated glomerular filtration rate (eGFR) at admission, postoperative, 3-day postoperative, and 7-day postoperative time points (91.9, 82.5, 73.5, 75.2 ml/min/1.73 m²). In contrast, group B did not show significant changes in kidney function (mean eGFR for the corresponding time points: 108.1, 106.5, 111.5, 109.6 ml/min/1.73 m²). The 3-day postoperative eGFR showed the strongest predictive ability for assessing prognosis [areas under the curve (AUC): 0.617, 0.675, 0.737, 0.730]. Univariate and multivariate analyses identified low Glasgow Coma Scale (GCS) score (3–8), ventricle intrusion of hematomas, cardiac failure, larger hematoma volume, infection, and lower 3-day postoperative eGFR as adverse factors for survival. Conclusions: Preserving kidney function is crucial for achieving favorable outcomes in hypertensive ICH cases. Impaired 3-day postoperative eGFR emerged as an independent risk factor for overall survival. Patients with cardiac failure, infection, and larger hematoma volume should receive careful management to improve outcomes.

Background. VASH1 is a novel angiogenic regulatory factor, that participates in the process of carcinogenesis and the development of diverse tumors. Our study aimed to investigate the expression and prognostic value of the VASH1 in Lower-Grade Glioma (LGG), to explore its functional network in LGG and its effects on biological behaviors. Methods. LGG transcriptome data, somatic mutation profiles and clinical features analyzed in the present study were obtained from the TCGA, GTEx, CCLE, CGGA, UALCAN, and GEPIA2 databases, as well as clinical data and tissue sections of 83 LGG patients in our hospital. The expression characteristics of VASH1 in LGG were investigated by univariate, multivariate, immunohistochemistry, qRT-PCR, and western-blot. Subsequently, we analyzed the prognostic significance of VASH1 in LGG patients by survival analysis, subject operation characteristic curve, correlation analysis, external validation, independent prognostic significance analysis, and clinical stratification, and confirmed its biological effect on glioma cell lines in vitro. Finally, we performed GO, KEGG, and GSEA to clarify biological functions and related pathways. CIBERSORT and ESTIMATE algorithms were used to calculate the proportion of immune cells and immune microenvironment fraction in LGG. Result. We found that VASH1 is highly expressed in LGG tissues and is associated with poor prognosis, WHO grade, IDH1 wild-type, and progressive disease ( ). Multivariate and the Nomogram model showed that high VASH1 expression was an independent risk factor for glioma prognosis and had better prognostic prediction efficacy in different LGG Patient cohorts (HR = 4.753 and ). In vitro experiments showed that knockdown of VASH1 expression in glioma cell lines caused increased glioma cell proliferation, invasion, and migration capacity. The mechanism may be related to VASH1 promoting microtubule formation and remodeling of immune microenvironment. Conclusion. Our study firstly found that high VASH1 expression was associated with poor prognosis. In addition, We identified the possible mechanism by which VASH1 functioned in LGG. VASH1 inhibits the invasion and migration of tumor cells by affecting microtubule formation and immune infiltration in the tumor microenvironment. May be an important endogenous anti-tumor factor for LGG and provide a potential biomarker for individualized treatment of LGG.