MiR-152 and lncRNA H19 have been frequently implicated in various cellular process including cell proliferation, invasion, angiogenesis and apoptosis. However, the interaction between miR-152 and H19 in glioma has never been reported. qRT PCR was used to examine the expression of miR 152 and H19 in human glioma cell lines and normal human astrocytes (NHAs) cells The interaction between miR 152 and lncRNA H19 were assessed by dual luciferase reporter assay. MTT assay and transwell invasion assay were used to determine the proliferation and invasion of U251 and U87 cells. Xenograft tumor experiment was performed to confirm the role of H19 in vivo. The results showed that H19 expression was upregulated and miR 152 expression was downregulated in human glioma cell lines. H19 downregulation or miR-152 upregulation suppressed glioma cell proliferation and invasion in vitro. Moreover, H19 and miR-152 directly regulated each other. Furthermore, decreased miR-152 expression alleviated si-H19-induced inhibitory effects on proliferation and invasion in glioma cells. As expected, H19 silencing hindered glioma growth in vivo. Taken together, H19 promoted glioma cell proliferation and invasion by negatively regulating miR-152 expression, providing evidence for the potential application of H19 as a biomarker and therapy target for glioma.
Netrin‐1 ( NTN ‐1) is a novel drug to alleviate early brain injury following subarachnoid haemorrhage ( SAH ). However the molecular mechanism of NTN ‐1‐mediated protection against early brain injury following SAH remains largely elusive. This study aims to evaluate the effects and mechanisms of NTN ‐1 in protecting SAH ‐induced early brain injury. The endovascular perforation SAH model was constructed using male C57 BL /6J mice, and recombinant NTN ‐1 was administrated intravenously. Mortality rates, SAH grade, brain water content, neurological score and neuronal apoptosis were evaluated. The expression of PPAR γ, Bcl‐2, Bax and nuclear factor‐kappa B ( NF ‐κB) were detected by Western blot. Small interfering RNA specific to NTN ‐1 receptor, UNC 5B, and a selective PPAR γ antagonist, bisphenol A diglycidyl ether ( BADGE ), were applied in combination with NTN ‐1. The results suggested that NTN ‐1 improved the neurological deficits, reduced the brain water content and alleviated neuronal apoptosis. In addition, NTN ‐1 enhanced PPAR γ and Bcl‐2 expression and decreased the levels of Bax and NF ‐κB. However, the neuroprotection of NTN ‐1 was abolished by UNC 5B and BADGE . In conclusion, our results demonstrated that NTN ‐1 attenuates early brain injury following SAH via the UNC 5B PPAR γ/ NF ‐κB signalling pathway.
Anterior cranial fossa intra-and extracranial tumors arise from the anterior cranial fossa and invade the orbit and nose. Anterior cranial fossa tumor resection and skull base reconstruction are challenging for neurosurgeons due to the complex anatomy, leakage of cerebrospinal fluid, and critical neurovasculature involvement. The authors report a case series of cranio-orbital communicating tumors and cranionasal-orbital communicating tumors. All patients underwent a modified Derome approach or transfrontal basal approach, and all tumor resections were satisfactory. Skull base reconstruction for small defects (<1.5 cm) can be performed with autogenous fascia, muscle, and fat. Large defects (!1.5 cm) require autogenous fascia, muscle, and fat combined with osseous reconstruction (autogenous bone, titanium mesh, and polyetheretherketone). The techniques and treatments were successful, and only 1 patient experienced mild cerebrospinal fluid leak but no intracranial infection, pneumocrania or intracranial hemorrhage. Additionally, long-term follow-up demonstrated that the outcomes remain favorable. According to a literature review, this technique might be an alternative strategy for treating anterior cranial fossa intra-and extracranial tumors, and better skull base reconstruction can prevent many postoperative complications.
Epidermoid cysts are rare benign tumors that account for 0.3% to 1.8% of all intracranial space-occupying lesions. They are usually congenital in origin and are thought to derived from ectodermal cell inclusions occurring during closure of the neural tube around third to fifth week of gestation. They are most commonly located in the cerebellopontine angle and the parasellar area, and their location in the diploic space is very rare. In this article, a case of giant epidermoid cyst located in the orbital roof intradiploic space is presented with clinical, radiologic features and surgical treatment.
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