Background: Neurological deficits following subarachnoid hemorrhage (SAH) are caused by early or delayed brain injuries. Our previous studies have demonstrated that hyperglycemia induces profound neuronal apoptosis of the cerebral cortex. Morphologically, we found that hyperglycemia exacerbated late vasospasm following SAH. Thus, our previous studies strongly suggest that post-SAH hyperglycemia is not only a response to primary insult, but also an aggravating factor for brain injuries. In addition, mitochondrial fusion and fission are vital to maintaining cellular functions. Current evidence also shows that the suppression of mitochondrial fission alleviates brain injuries after experimental SAH. Hence, this study aimed to determine the effects of mitochondrial dynamic modulation in hyperglycemia-related worse SAH neurological prognosis. Materials and methods: In vitro, we employed an enzyme-linked immunosorbent assay (ELISA) to detect the effect of mitochondrial division inhibitor-1 (Mdivi-1) on lipopolysaccharide (LPS)-induced BV-2 cells releasing inflammatory factors. In vivo, we produced hyperglycemic rats via intraperitoneal streptozotocin (STZ) injections. Hyperglycemia was confirmed using blood-glucose measurements (>300 mg/dL) 7 days after the STZ injection. The rodent model of SAH, in which fresh blood was instilled into the craniocervical junction, was used 7 days after STZ administration. We investigated the mechanism and effect of Mdivi-1, a selective inhibitor of dynamin-related protein (Drp1) to downregulate mitochondrial fission, on SAH-induced apoptosis in a hyperglycemic state, and evaluated the results in a dose–response manner. The rats were divided into the following five groups: (1) control, (2) SAH only, (3) Diabetes mellitus (DM) + SAH, (4) Mdivi-1 (0.24 mg/kg) + DM + SAH, and (5) Mdivi-1 (1.2 mg/kg) + DM + SAH. Results: In vitro, ELISA revealed that Mdivi-1 inhibited microglia from releasing inflammatory factors, such as tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6. In vivo, neurological outcomes in the high-dose (1.2 mg/kg) Mdivi-1 treatment group were significantly reduced compared with the SAH and DM + SAH groups. Furthermore, immunofluorescence staining and ELISA revealed that a high dose of Mdivi-1 had attenuated inflammation and neuron cell apoptosis by inhibiting Hyperglycemia-aggravated activation, as well as microglia and astrocyte proliferation, following SAH. Conclusion: Mdivi-1, a Drp-1 inhibitor, attenuates cerebral vasospasm, poor neurological outcomes, inflammation, and neuron cell apoptosis following SAH + hyperglycemia.

Rationale: Cranioplasty is a surgical procedure used to repair cranial defects for both cosmetic and functional reasons. The complication rate of cranioplasty is between 10% and 50%. The failure of cranioplasty is associated with various factors, including etiologies, types of material, and the timing of cranioplasty. In this study, a case series of managing cranioplasty complications at a single institution. Patient concerns: Eighteen patients were identified who underwent craniofacial defect reconstruction due to the failure of their initial cranioplasty between January 2010 and May 2020. Five men (27.78%) and thirteen women (72.22%) were included. The mean age was 39.61 years old. The average follow-up duration was 5.94 years. Diagnoses: The indication for initial cranioplasty included previous decompressive craniectomy (77.78%, n = 14), traumatic cranial defects (16.67%, n = 3), and congenital cranial deformity (5.56%, n = 1). The reported complications were infection (50%, n = 9), implant exposure (50%, n = 9), wound dehiscence (22.22%, n = 4) and cranial deformity (11.11%, n = 2). Interventions: More than half of the materials used for initial cranioplasty were synthetic [titanium mesh: 44.44%, n = 8; polymethyl metacrylate: 5.56%, n = 1; titanium mesh and polymethyl metacrylate: 5.56%, n = 1], while 44.44% of the patients received autologous bone graft. Outcomes: Of all reconstructive procedures for cranioplasty failure, 55.56% was local flap with or without skin graft (n = 10), 16.67% was free flap (n = 3), 11.11% was skin graft only (n = 2), 5.56% was regional flap (n = 1). The free flap survival rate was 100% (3/3), and implant removal with sebsquent second cranioplasty was performed on 27.78% (n = 5) of the patients. Lessons: Management of cranioplasty failure can be challenging due to infection, refractory implant exposure, and wound dehiscence. The principles of management are based on adequate infection control and reconstructive ladder. Meanwhile, collaboration with plastic surgery and neurosurgery should be strengthened in order to achieve the best clinical outcomes.

Glioblastoma (GBM) is the most common primary brain malignancy in adults. Despite multimodal treatment that involves maximal safe resection, concurrent chemoradiotherapy, and tumour treatment for supratentorial lesions, the prognosis remains poor. The current median overall survival is only <2 years, and the 5-year survival is only 7.2%. Thioredoxin domain-containing protein 11 (TXNDC11), also known as EF-hand binding protein 1, was reported as an endoplasmic reticulum stress-induced protein. The present study aimed to elucidate the prognostic role of TXNDC11 in GBM. We evaluated the clinical parameters and TXNDC11 scores in gliomas from hospitals. Additionally, proliferation, invasion, migration assays, apoptosis, and temozolomide (TMZ)-sensitivity assays of GBM cells were conducted to evaluate the effects of short interfering RNA (siRNA) on these processes. In addition, these cells were subjected to Western blotting to detect the expression levels of N-cadherin, E-cadherin, and Cyclin D1. High levels of TXNDC11 protein expression were significantly associated with World Health Organization (WHO) high-grade tumour classification and poor prognosis. Multivariate analysis revealed that in addition to the WHO grade, TXNDC11 protein expression was also an independent prognostic factor of glioma. In addition, TXNDC11 silencing inhibited proliferation, migration, and invasion and led to apoptosis of GBM cells. However, over-expression of TXNDC11 enhanced proliferation, migration, and invasion. Further, TXNDC11 knockdown downregulated N-cadherin and cyclin D1 expression and upregulated E-cadherin expression in GBM cells. Knock-in TXNDC11 return these. Finally, in vivo, orthotopic xenotransplantation of TXNDC11-silenced GBM cells into nude rats promoted slower tumour growth and prolonged survival time. TXNDC11 is a potential oncogene in GBMs and may be an emerging therapeutic target.