Objective:To study the role of DDX3X/NF-κB pathway in early neuronal apoptosis in subarachnoid hemorrhage(SAH)mice.Methods:The mouse model of SAH was established by internal carotid artery puncture,and the neurological function score of the mice was evaluated.The DDX3X expression was knocked down using recombinant lentivirus expressing DDX3X targeted shRNA(Lv-shDDX3X),or the NF-κB pathway was inhibited by NF-κB-IN-1(IN-1).Western Blot was used to detect the expression of DDX3X and NF-κB(p65)in mouse cortex.TUNEL/NeuN staining was used to detect the apoptosis of cerebral cortex neurons.Results:Twenty-four hours after SAH operation,the neurological function of mice was significantly impaired(P＜0.05).While the expression of DDX3X was signifi-cantly increased and the expression of NF-κB(p65)was significantly decreased in the cortex(P＜0.05).When the DDX3X expression is knocked down firstly,then SAH surgery is performed.The neurological function of mice was sig-nificantly recovered,and the expression of NF-κB(p65)protein was significantly higher than that in SAH group(P＜0.05);If the NF-κB activity was inhibited by IN-1 while DDX3X knockdown,there is no significant recovery of neuro-logical function in SAH mice.TUNEL/NeuN staining showed that the number of TUNEL-positive neurons in the brain tissue after DDX3X knockdown was less than that in the SAH group(P＜0.05),while the number of TUNEL-positive neurons was not significantly reduced when IN-1 was used to inhibit NF-κB activity at the same time of DDX3X knock-down.Conclusion:DDX3X/NF-κB mediated cell death in mice with early brain injury after SAH.

Traumatic supraorbital fissure syndrome (TSOFS) is a symptom complex caused by nerve entrapment in the supraorbital fissure after skull base trauma. If the compressed cranial nerve in the supraorbital fissure is not decompressed surgically, ptosis, diplopia and eye movement disorder may exist for a long time and seriously affect the patients′ quality of life. Since its overall incidence is not high, it is not familiarized with the majority of neurosurgeons and some TSOFS may be complicated with skull base vascular injury. If the supraorbital fissure surgery is performed without treatment of vascular injury, it may cause massive hemorrhage, and disability and even life-threatening in severe cases. At present, there is no consensus or guideline on the diagnosis and treatment of TSOFS that can be referred to both domestically and internationally. To improve the understanding of TSOFS among clinical physicians and establish standardized diagnosis and treatment plans, the Skull Base Trauma Group of the Neurorepair Professional Committee of the Chinese Medical Doctor Association, Neurotrauma Group of the Neurosurgery Branch of the Chinese Medical Association, Neurotrauma Group of the Traumatology Branch of the Chinese Medical Association, and Editorial Committee of Chinese Journal of Trauma organized relevant experts to formulate Chinese expert consensus on the diagnosis and treatment of traumatic supraorbital fissure syndrome ( version 2024) based on evidence of evidence-based medicine and clinical experience of diagnosis and treatment. This consensus puts forward 12 recommendations on the diagnosis, classification, treatment, efficacy evaluation and follow-up of TSOFS, aiming to provide references for neurosurgeons from hospitals of all levels to standardize the diagnosis and treatment of TSOFS.

Objective:To conduct a bibliometric analysis of scientific publications on aneurysmal subarachnoid hemorrhage (aSAH) worldwide from 2012 to 2022 and to investigate the current research status and hotspots in this field.Methods:The Web of Science Core Collection was used as the data source. According to the set retrieval strategy, the CiteSpace bibliometric tools were used to analyze the published literature and explore the research hotspots and cutting-edge directions.Results:A total of 4 937 articles were included, and the number of publications increased year by year from 2012 to 2022. The United States is a leading country in this field, Harvard University is a leading institution in this field, and Rinkel Gabriel JE is the researcher with the most published articles in this field. The analysis of the keywords provided by the author showed that delayed cerebral ischemia, vasospasm, risk, intracranial aneurysms, endovascular treatment, risk factors, embolization, complications, Pipeline embolization device, coil embolization, hemodynamics, and wall shear stress were the main hotspots and cutting-edge directions of aSAH research.Conclusion:The results of bibliometric analysis help to grasp the current research status of aSAH and determine new directions for future research.

Objective:To investigate the effect of galectin-3 (gal-3) on microglia polarization after subarachnoid hemorrhage (SAH).Methods:C57BL/6 male adult mice were used to induce SAH or sham operation models. Gal-3 siRNA or negative control siRNA was injected into the lateral ventricle 48 h before the model was induced. After 24 h of model preparation, the SAH score, neurological function score, brain water content, and Evans blue exudate were measured. Western blot analysis was used to detect the expressions of M1 phenotypic markers (inducible nitric oxide synthase [iNOS], CD11b, tumor necrosis factor [TNF]-α) and M2 phenotype markers (CD206, YM1/2, arginase-1 [Arg1]).Results:After using Gal-3 siRNA to inhibit Gal-3, the neurological function score significantly increased, while the SAH score, brain water content, and Evans blue exudate significantly decreased ( P<0.001). Western blot analysis showed that the expressions of M1 phenotypic markers (iNOS, CD11b and TNF-α) in microglia were significantly decreased after Gal-3 inhibition, while the expressions of M2 phenotypic markers (CD206, YM1/2 and Arg1) were significantly increased ( P<0.001). Conclusion:Inhibition of Gal-3 expression can alleviate the early brain injury after SAH, and its mechanism may be associated with regulating the polarization of microglia from M1 to M2 phenotype.

Objective:To investigate the effect of Sirtuin 1 (SIRT1) on subarachnoid hemorrhage (SAH) and its possible mechanism.Methods:A mouse model of SAH was constructed by internal carotid artery puncture. The protein and mRNA expression levels of SIRT1 at 0, 3, 6, 12, 24, 48, and 72 h were detected by Western Blot and qRT-PCR. A Western Blot assay was used to examine SIRT1 and the expression levels of endoplasmic reticulum stress-related markers GRP78, p-PERK/PERK, p-eIF2α/eIF2α, and CHOP after administration of a SIRT1 inhibitor or SIRT1 si-RNA. At 24 h after SAH, subarachnoid hemorrhage volume, neurological function score, brain water content, and blood-brain barrier integrity were measured.Results:The highest expression of SIRT1 protein and mRNA was observed at 24 h compared with other time points, and the differences were statistically significant (all P < 0.001). Inhibition of SIRT1 expression leads to increased expression of endoplasmic reticulum stress-related proteins GRP78, p-PERK/PERK, p-eIF2α/eIF2α, and CHOP, exacerbating hemorrhage and brain water content, disrupting blood-brain barrier integrity, and significantly reducing neurological function scores. Conclusions:Inhibition of SIRT1 expression significantly increased the endoplasmic reticulum response to excitation and exacerbated early brain injury after SAH.

Ferroptosis is a new type of programmed cell death, which is different from apoptosis, pyrodeath, necrosis and autophagy. It is characterized by the imbalance of cell iron homeostasis, which leads to the accumulation of reactive oxygen species and lipid peroxides, which exceeds the antioxidant capacity of cells and eventually leads to oxidative death of cells. Studies have shown that ferroptosis plays an important role in acute renal injury induced by renal ischemia-reperfusion and inhibition of ferroptosis can effectively alleviate renal ischemia-reperfusion injury. It is of great significance to study the relationship and mechanism of ferroptosis and renal ischemia-reperfusion injury to prevent acute renal function injury caused by renal ischemia-reperfusion injury in clinical work .

Currently, the total ureteral avulsion are mainly secondary to ureteroscopy, and it is rarely caused by uterine evacuation clinically. This paper reported a case of total ureter avulsion after uterine evacuation, treating by ileal replacement for ureter under general anesthesia, and the surgical outcome was good. Uterine evacuation is a routine, less risky procedure, but it also can lead to serious complications such as total ureteral avulsion or bladder rupture. For potential high-risk patients with uterine evacuation, preventive measures such as accurate localization under B-ultrasound guidance or pre-operative ureteral stents indwelling are useful to avoid the occurrence of such serious complications. If total ureteral avulsion occurs, ileal replacement for ureter is a viable and effective treatment.

Objective:To investigate the effects of naringin on early brain injury in rats with subarachnoid hemorrhage and its possible mechanism of action.Methods:Rats were randomly divided into the sham operation group, the model group, and the naringin group. Each group had 8 rats. The SAH model was established by intravascular perforation, and then rats in the model group and the naringin group were administered 0.9% NaCl or naringin 40 mg/kg by intraperitoneal injection after 0.5 h. SAH score, neurological function score, cerebral edema, and blood-brain barrier permeability were detected. The level of NAD + and nflammatory factors were detected by ELISA. The expression of poly(ADP-ribose) polymerase-1 (PARP-1), apoptosis inducing factor (AIF), and protease-activated receptor (PAR) proteins was detected by Western Blot. The expression of PARP-1 mRNA was detected by quantitative real-time fluorescence PCR (qRT-PCR). Neuronal apoptosis was detected by an immunofluorescence assay. Results:Compared with the model group, naringin treatment improved neurological function ( P<0.01), reduced cerebral edema and Evans blue exudation (all P<0.01), increased the content of NAD + ( P<0.001), reduced IL-1β, IL-6 and TNF-α levels (all P<0.001), and reduced the expression of PARP-1/AIF pathway-related proteins in vivo (all P<0.001). In addition, naringin could inhibit neuronal apoptosis in early brain injury after SAH. Conclusions:Naringin can improve the early brain injury after SAH, which may be achieved by inhibiting the PARP-1/AIF pathway.

Objective:To investigate the efficacy and safety of distal transradial access for cerebral angiography and neurointervention.Methods:The literature about distal transradial access for cerebral angiography and neurointervention were searched in PubMed, EMbase, the Cochrane Library, CNKI, WanFang Data, and VIP database from January 2015 to September 2021. Two reviewers independently screened the literature and extracted data according to the inclusion and exclusion criteria, evaluated the literature quality according to the Newcastle-Ottawa scale. The R 4.0.5 software was used for meta-analysis.Results:A total of 12 articles with 987 patients were enrolled. All the studies were retrospective design and did not compare with the results of proximal transradial access and transfemoral access. A meta-analysis of the operation success rate and complication rate using a fixed effect model showed that the operation success rate of distal transradial access was 96% (95% confidence interval 95%-97%), and the incidence of minor complications was 3% (95% confidence interval 2%-4%). One patient had serious complications.Conclusion:The distal transradial access is a safe and effective alternative approach for cerebral angiography and neurointervention.

A recurrent misdiagnosed case of congenital left renal arteriovenous fistula (RAVF) with multiple left renal arteries and scoliosis was reported. The patient was admitted to hospital on 29 August 2020 due to repeated hematuria for one year. No abnormality was found in two flexible ureteroscope examinations, imaging and laboratory examinations after admission. It was found that the structure of blood vessels in the inferior pole of renal sinus was disordered, and the blood vessels were tortuous and clustered through careful reading of CT enhancement films. The dilated tortuous blood vessels were also seen around the renal pelvis, and hematuria was considered to be caused by renal vascular malformation. In order to confirm the etiology, digital subtraction angiography (DSA) of renal artery was performed. DSA showed a congenital left renal RAVF with three renal arteries, and the arteriovenous fistula of renal arteries was embolized. For patients presenting with severe gross hematuria, if tumor, stone, tuberculosis, or coagulation abnormalities were excluded by conventional imaging and/or laboratory examination the possibility of congenital renal vascular malformation should be suspected, and DSA examination should be performed. Endovascular embolization is an effective treatment for congenital RAVF.