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Article ; Online: RACK1 promotes autophagy via the PERK signaling pathway to protect against traumatic brain injury in rats.

Ni, Haibo / Kan, Xugang / Rui, Qin / Zhang, Yang / Zhai, Weiwei / Zhang, Baole / Yu, Zhengquan

2024 Volume 30, Issue 3, Page(s) e14691

Abstract: Aims: Neuronal cell death is a primary factor that determines the outcome after traumatic brain injury (TBI). We previously revealed the importance of receptor for activated C kinase (RACK1), a multifunctional scaffold protein, in maintaining neuronal ... ...

Abstract	Aims: Neuronal cell death is a primary factor that determines the outcome after traumatic brain injury (TBI). We previously revealed the importance of receptor for activated C kinase (RACK1), a multifunctional scaffold protein, in maintaining neuronal survival after TBI, but the specific mechanism remains unclear. The aim of this study was to explore the mechanism underlying RACK1-mediated neuroprotection in TBI. Methods: TBI model was established using controlled cortical impact injury in Sprague-Dawley rats. Genetic intervention and pharmacological inhibition of RACK1 and PERK-autophagy signaling were administrated by intracerebroventricular injection. Western blotting, coimmunoprecipitation, transmission electron microscopy, real-time PCR, immunofluorescence, TUNEL staining, Nissl staining, neurobehavioral tests, and contusion volume assessment were performed. Results: Endogenous RACK1 was upregulated and correlated with autophagy induction after TBI. RACK1 knockdown markedly inhibited TBI-induced autophagy, whereas RACK1 overexpression exerted the opposite effects. Moreover, RACK1 overexpression ameliorated neuronal apoptosis, neurological deficits, and cortical tissue loss after TBI, and these effects were abrogated by the autophagy inhibitor 3-methyladenine or siRNAs targeting Beclin1 and Atg5. Mechanistically, RACK1 interacted with PERK and activated PERK signaling. Pharmacological and genetic inhibition of the PERK pathway abolished RACK1-induced autophagy after TBI. Conclusion: Our findings indicate that RACK1 protected against TBI-induced neuronal damage partly through autophagy induction by regulating the PERK signaling pathway.
MeSH term(s)	Rats ; Animals ; Rats, Sprague-Dawley ; Signal Transduction ; Brain Injuries, Traumatic/metabolism ; Neuroprotection ; Apoptosis ; Autophagy ; Receptors for Activated C Kinase
Chemical Substances	RACK1 protein, rat ; Receptors for Activated C Kinase
Language	English
Publishing date	2024-03-26
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2423461-8
ISSN	1755-5949 ; 1755-5930
ISSN (online)	1755-5949
ISSN	1755-5930
DOI	10.1111/cns.14691
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Zs.A 4537: Show issues

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Article: miRNA-323a-3p promoted intracranial, aneurysm-induced inflammation via AMPK/NF-κB signaling pathway by AdipoR1.

Sun, Bing / Liu, Zehao / Yu, Zhengquan

Advances in clinical and experimental medicine : official organ Wroclaw Medical University

2022 Volume 31, Issue 11, Page(s) 1243–1254

Abstract: Background: An intracranial arterial wall which locally protrudes outward, typically in the capsule and fusiform, is called an intracranial aneurysm (IA). Among these aneurysms, 1-2% might spontaneously rupture before treatment. Anterior and posterior ... ...

Abstract	Background: An intracranial arterial wall which locally protrudes outward, typically in the capsule and fusiform, is called an intracranial aneurysm (IA). Among these aneurysms, 1-2% might spontaneously rupture before treatment. Anterior and posterior communicating aneurysms are more likely to rupture than other aneurysms, and an anterior communicating aneurysm is more likely to rupture than a posterior communicating aneurysm. Objectives: To identify the effects of miRNA-323a-3p expression in intracranial aneurysms and its potential regulatory mechanism. Material and methods: Patients with IA and healthy volunteers were enrolled, and their serum samples were extracted for the detection of tumor necrosis factor alpha (TNF-α), interleukin 1β (IL-1β), IL-6, IL-18, and miRNA-323a-3p. Then, the regulatory effects of miRNA-323a-3p on the above inflammatory factors and AdipoR1/AMPK/NF-kb signaling were also detected in vitro. Results: The downregulation of miRNA-323a-3p reduced the expression of inflammatory factors (TNF-α, IL-1β, IL-6, and IL-18) in an in vitro model in comparison with the control group. The overexpression of miRNA-323a-3p suppressed the protein expression of adiponectin receptor R1 (AdipoR1) and p-AMPK, and induced NF-κB-p65 protein expression in an in vitro model. Conclusions: We showed that AdipoR1 plasmid, AMPK activator 1 or si-NF-κB reduced the pro-inflammatory effects of miRNA-323a-3p in an in vitro model. The miRNA-323a-3p exacerbated the inflammatory reaction in IA through AMPK/NF-κB signaling by AdipoR1. Our findings suggest that miRNA-323a-3p targeting AdipoR1 is promising in further anti-inflammatory treatment of IAs.
MeSH term(s)	Humans ; AMP-Activated Protein Kinases/metabolism ; AMP-Activated Protein Kinases/pharmacology ; Inflammation/genetics ; Inflammation/metabolism ; Interleukin-18 ; Interleukin-6 ; Intracranial Aneurysm/genetics ; MicroRNAs/genetics ; MicroRNAs/metabolism ; NF-kappa B/metabolism ; Receptors, Adiponectin/genetics ; Signal Transduction ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	ADIPOR1 protein, human ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Interleukin-18 ; Interleukin-6 ; MicroRNAs ; NF-kappa B ; Receptors, Adiponectin ; Tumor Necrosis Factor-alpha ; MIRN323 microRNA, human
Language	English
Publishing date	2022-09-14
Publishing country	Poland
Document type	Journal Article
ZDB-ID	2270257-X
ISSN	1899-5276 ; 1230-025X
ISSN	1899-5276 ; 1230-025X
DOI	10.17219/acem/151053
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Zs.A 6489: Show issues

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Article ; Online: WDR34 affects PI3K/Akt and Wnt/β-catenin pathways to regulates malignant biological behaviors of glioma cells.

Zuo, Jiandong / Liu, Chun / Ni, Hongzao / Yu, Zhengquan

Journal of neuro-oncology

2022 Volume 156, Issue 2, Page(s) 281–293

Abstract: Purpose: Glioma is the most prevalent primary intracranial tumor globally. WDR34, a member of the WDR superfamily with five WD40 repeats, is involved in the pathogenesis of several tumors. However, the role of WDR34 in glioma progression is unknown.: ... ...

Abstract	Purpose: Glioma is the most prevalent primary intracranial tumor globally. WDR34, a member of the WDR superfamily with five WD40 repeats, is involved in the pathogenesis of several tumors. However, the role of WDR34 in glioma progression is unknown. Methods: The expression and prognostic significance of WDR34 in glioma patients were analyzed using GEPIA. WDR34 expression was detected by qRT-PCR. Western blot was employed to determine the expression of Ki67, proliferating cell nuclear antigen (PCNA), matrix metallopeptidase (MMP)2, MMP9, phosphatase and tensin homolog, protein kinase B (Akt), phosphorylated Akt, β-catenin, and c-Myc. CCK-8, BrdU incorporation assay, Transwell invasion assay, flow cytometry analysis, and measurement of caspase-3 and caspase-9 activities were conducted to examine the effects of WDR34 knockdown on glioma cells. Results: WDR34 was upregulated in glioma, which predicted a poor prognosis in glioma patients. WDR34 knockdown inhibited cell proliferation and reduced the expression of Ki67 and PCNA in glioma cells. WDR34 knockdown repressed the invasive ability of glioma cells by decreasing MMP-2 and MMP-9 expression. WDR34 knockdown increased the apoptotic rate and caspase-3 and caspase-9 activities in glioma cells. The PI3K/Akt and Wnt/β-catenin pathways were inhibited after WDR34 knockdown in glioma cells. Moreover, overexpression of Akt or β-catenin reversed the function of WDR34 knockdown on proliferation, invasion, and apoptosis. WDR34 knockdown reduced tumor growth in vivo. Conclusions: WDR34 knockdown inhibited malignant biological behaviors of glioma cells by inactivating the PI3K/Akt and Wnt/β-catenin signaling cascades.
MeSH term(s)	Brain Neoplasms/genetics ; Brain Neoplasms/pathology ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Gene Expression Regulation, Neoplastic ; Glioma/genetics ; Glioma/pathology ; Humans ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Wnt Signaling Pathway ; beta Catenin/metabolism
Chemical Substances	Carrier Proteins ; WDR34 protein, human ; beta Catenin ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2022-01-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	604875-4
ISSN	1573-7373 ; 0167-594X
ISSN (online)	1573-7373
ISSN	0167-594X
DOI	10.1007/s11060-021-03932-2
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Zs.A 1825: Show issues

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Article ; Online: Corrigendum to "RIP3 participates in early brain injury after experimental subarachnoid hemorrhage in rats by inducing necroptosis" [Neurobiology of Disease 129(2019) 144-158].

Yuan, Shuai / Yu, Zhengquan / Zhang, Zhuwei / Zhang, Juyi / Zhang, Peng / Li, Xiang / Li, Haiying / Shen, Haitao / Chen, Gang

Neurobiology of disease

2024 , Page(s) 106507

Language	English
Publishing date	2024-04-30
Publishing country	United States
Document type	Published Erratum
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2024.106507
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Zs.A 4444: Show issues

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Article ; Online: Dysregulation of LINC00324 promotes poor prognosis in patients with glioma.

Jin, Xin / Zhu, Jiandong / Yu, Haoyun / Shi, Shengjun / Shen, Kecheng / Gu, Jingyu / Yin, Ziqian / Yu, Zhengquan / Wu, Jiang

PloS one

2024 Volume 19, Issue 3, Page(s) e0298055

Abstract: Background: LINC00324 is a long-stranded non-coding RNA, which is aberrantly expressed in various cancers and is associated with poor prognosis and clinical features. It involves multiple oncogenic molecular pathways affecting cell proliferation, ... ...

Abstract	Background: LINC00324 is a long-stranded non-coding RNA, which is aberrantly expressed in various cancers and is associated with poor prognosis and clinical features. It involves multiple oncogenic molecular pathways affecting cell proliferation, migration, invasion, and apoptosis. However, the expression, function, and mechanism of LINC00324 in glioma have not been reported. Material and methods: We assessed the expression of LINC00324 of LINC00324 in glioma patients based on data from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) to identify pathways involved in LINC00324-related glioma pathogenesis. Results: Based on our findings, we observed differential expression of LINC00324 between tumor and normal tissues in glioma patients. Our analysis of overall survival (OS) and disease-specific survival (DSS) indicated that glioma patients with high LINC00324 expression had a poorer prognosis compared to those with low LINC00324 expression. By integrating clinical data and genetic signatures from TCGA patients, we developed a nomogram to predict OS and DSS in glioma patients. Gene set enrichment analysis (GSEA) revealed that several pathways, including JAK/STAT3 signaling, epithelial-mesenchymal transition, STAT5 signaling, NF-κB activation, and apoptosis, were differentially enriched in glioma samples with high LINC00324 expression. Furthermore, we observed significant correlations between LINC00324 expression, immune infiltration levels, and expression of immune checkpoint-related genes (HAVCR2: r = 0.627, P = 1.54e-77; CD40: r = 0.604, P = 1.36e-70; ITGB2: r = 0.612, P = 6.33e-7; CX3CL1: r = -0.307, P = 9.24e-17). These findings highlight the potential significance of LINC00324 in glioma progression and suggest avenues for further research and potential therapeutic targets. Conclusion: Indeed, our results confirm that the LINC00324 signature holds promise as a prognostic predictor in glioma patients. This finding opens up new possibilities for understanding the disease and may offer valuable insights for the development of targeted therapies.
MeSH term(s)	Humans ; Apoptosis ; CD18 Antigens ; CD40 Antigens ; Cell Proliferation ; Glioma ; Prognosis ; RNA, Untranslated/genetics
Chemical Substances	CD18 Antigens ; CD40 Antigens ; RNA, Untranslated
Language	English
Publishing date	2024-03-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0298055
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Article ; Online: Cathepsin B as a key regulator of ferroptosis in microglia following intracerebral hemorrhage.

Lu, Jinxin / Li, Haiying / Yu, Zhengquan / Cao, Chang / Xu, Zhongmou / Peng, Lu / Zhang, John H / Chen, Gang

Neurobiology of disease

2024 Volume 194, Page(s) 106468

Abstract: Intracerebral hemorrhage (ICH) is a subtype of stroke marked by elevated mortality and disability rates. Recently, mounting evidence suggests a significant role of ferroptosis in the pathogenesis of ICH. Through a combination of bioinformatics analysis ... ...

Abstract	Intracerebral hemorrhage (ICH) is a subtype of stroke marked by elevated mortality and disability rates. Recently, mounting evidence suggests a significant role of ferroptosis in the pathogenesis of ICH. Through a combination of bioinformatics analysis and basic experiments, our goal is to identify the primary cell types and key molecules implicated in ferroptosis post-ICH. This aims to propel the advancement of ferroptosis research, offering potential therapeutic targets for ICH treatment. Our study reveals pronounced ferroptosis in microglia and identifies the target gene, cathepsin B (Ctsb), by analyzing differentially expressed genes following ICH. Ctsb, a cysteine protease primarily located in lysosomes, becomes a focal point in our investigation. Utilizing in vitro and in vivo models, we explore the correlation between Ctsb and ferroptosis in microglia post-ICH. Results demonstrate that ICH and hemin-induced ferroptosis in microglia coincide with elevated levels and activity of Ctsb protein. Effective alleviation of ferroptosis in microglia after ICH is achieved through the inhibition of Ctsb protease activity and protein levels using inhibitors and shRNA. Additionally, a notable increase in m6A methylation levels of Ctsb mRNA post-ICH is observed, suggesting a pivotal role of m6A methylation in regulating Ctsb translation. These research insights deepen our comprehension of the molecular pathways involved in ferroptosis after ICH, underscoring the potential of Ctsb as a promising target for mitigating brain damage resulting from ICH.
MeSH term(s)	Humans ; Brain Injuries/metabolism ; Cathepsin B/genetics ; Cathepsin B/metabolism ; Cerebral Hemorrhage/pathology ; Ferroptosis ; Microglia/metabolism ; Animals ; Mice
Chemical Substances	Cathepsin B (EC 3.4.22.1) ; Ctsb protein, mouse (EC 3.4.22.1)
Language	English
Publishing date	2024-03-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2024.106468
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Article ; Online: ERBB1 alleviates secondary brain injury induced by experimental intracerebral hemorrhage in rats by modulating neuronal death via PLC-γ/PKC pathway.

Li, Bing / Wu, Jiang / Cao, Demao / Cao, Cheng / Zhang, Juyi / Li, Xiang / Li, Haiying / Shen, Haitao / Yu, Zhengquan

CNS neuroscience & therapeutics

2024 Volume 30, Issue 3, Page(s) e14679

Abstract: Aims: Intracerebral hemorrhage (ICH) is a disease with high rates of disability and mortality. The role of epidermal growth factor receptor 1 (ERBB1) in ICH was elucidated in this study.: Methods: ICH model was constructed by injecting autologous ... ...

Abstract	Aims: Intracerebral hemorrhage (ICH) is a disease with high rates of disability and mortality. The role of epidermal growth factor receptor 1 (ERBB1) in ICH was elucidated in this study. Methods: ICH model was constructed by injecting autologous arterial blood into the right basal ganglia. The protein level of ERBB1 was detected by western blot analysis. To up- and downregulation of ERBB1 in rats, intraventricular injection of a lentivirus overexpression vector of ERBB1 and AG1478 (a specific inhibitor of ERBB1) was used. The cell apoptosis, neuronal loss, and pro-inflammatory cytokines were assessed by TUNEL, Nissl staining, and ELISA. Meanwhile, behavioral cognitive impairment of ICH rats was evaluated after ERBB1-targeted interventions. Results: ERBB1 increased significantly in brain tissue of ICH rats. Overexpression of ERBB1 remarkably reduced cell apoptosis and neuronal loss induced by ICH, as well as pro-inflammatory cytokines and oxidative stress. Meanwhile, the behavioral and cognitive impairment of ICH rats were alleviated after upregulation of ERBB1; however, the secondary brain injury (SBI) was aggravated by AG1478 treatment. Furthermore, the upregulation of PLC-γ and PKC in ICH rats was reversed by AG1478 treatment. Conclusions: ERBB1 can improve SBI and has a neuroprotective effect in experimental ICH rats via PLC-γ/PKC pathway.
MeSH term(s)	Animals ; Rats ; Apoptosis ; Brain Injuries/metabolism ; Cerebral Hemorrhage/complications ; Cerebral Hemorrhage/metabolism ; Cytokines/metabolism ; Phospholipase C gamma/metabolism ; Quinazolines ; Rats, Sprague-Dawley ; Tyrphostins ; ErbB Receptors/metabolism ; Protein Kinase C/metabolism
Chemical Substances	Cytokines ; Phospholipase C gamma (EC 3.1.4.3) ; Quinazolines ; RTKI cpd (170449-18-0) ; Tyrphostins ; ErbB Receptors (EC 2.7.10.1) ; Protein Kinase C (EC 2.7.11.13)
Language	English
Publishing date	2024-03-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2423461-8
ISSN	1755-5949 ; 1755-5930
ISSN (online)	1755-5949
ISSN	1755-5930
DOI	10.1111/cns.14679
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Zs.A 4537: Show issues

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Article: Non-Angry Superficial Draining Veins: A New Technique in Identifying the Extent of Nidus Excision during Cerebral Arteriovenous Malformation Surgery.

Zhu, Jiandong / Chen, Zhouqing / Zhai, Weiwei / Wang, Zhong / Wu, Jiang / Yu, Zhengquan / Chen, Gang

Brain sciences

2023 Volume 13, Issue 2

Abstract: Background: As essential techniques, intraoperative indocyanine green video angiography (ICG-VA) and FLOW 800 have been widely used in microsurgery for arteriovenous malformations (AVMs). In the present report, we introduced a supplementary technical ... ...

Abstract	Background: As essential techniques, intraoperative indocyanine green video angiography (ICG-VA) and FLOW 800 have been widely used in microsurgery for arteriovenous malformations (AVMs). In the present report, we introduced a supplementary technical trick for judging the degree of lesion resection when there were superficial drainage veins. FLOW 800 analysis is used to verify our conjecture. Methods: A retrospective analysis of a 33 case cohort treated surgically from June 2020 to September 2022 was conducted and their lesions were removed by superficial drainage veins as a supplementary technical trick and analyzed with FLOW800. Results: In our 33 AVMs, the feeding artery was visualized earlier than the draining vein. Intraoperatively, the T1/2 peak and slope of the draining vein were significantly higher than that of the lesion. However, the maximum fluorescence intensity (MFI) of the draining vein decreased as the procedure progressed ( Conclusions: ICG-VA integrated with FLOW 800 is an available method for determining the velocity of superficial drainage veins. Whether the color of the superficial drainage veins on the cortical surface returns to normal can determine whether the lesion is completely resected and can reduce the possibility of residual postoperative lesions.
Language	English
Publishing date	2023-02-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2651993-8
ISSN	2076-3425
ISSN	2076-3425
DOI	10.3390/brainsci13020366
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Article ; Online: Efficacy and Safety of PRC-063 for Attention-Deficit/Hyperactivity Disorder: A Systematic Review and Meta-analysis From Randomized Controlled Trials.

Zhu, Shixin / Wang, Tianyi / Wang, Jiahe / Yang, Siyuan / Yu, Zhengquan / Gao, Heng / Chen, Gang

Journal of attention disorders

2023 Volume 27, Issue 5, Page(s) 470–487

Abstract: Objective: A new formulation of extended-release methylphenidate (PRC-063) was approved to treat ADHD. This meta-analysis was conducted to study the efficacy and safety of PRC-063 for ADHD.: Method: We searched for published trials to October 2022 in ...

Abstract	Objective: A new formulation of extended-release methylphenidate (PRC-063) was approved to treat ADHD. This meta-analysis was conducted to study the efficacy and safety of PRC-063 for ADHD. Method: We searched for published trials to October 2022 in several databases. Results: A total of 1,215 patients from 5 RCTs were included. We observed significant improvement for PRC-063 in ADHD Rating Scale (ADHD-RS; MD = -6.73, 95% CI [-10.34, -3.12]) compared with placebo. The effect of PRC-063 on the sleep problems due to ADHD was not statistically different from placebo. Six subscales of Pittsburg Sleep Quality Index (PSQI) showed no statistical significance between PRC-063 and placebo. The result showed no significant difference comparing PRC-063 with placebo in serious treatment-emergent adverse events (TEAEs) (RR = 0.80, 95% CI [0.03, 19.34]). In subgroup analysis according to age, PRC-063 was more efficacious in minors compare to adults. Conclusion: PRC-063 is an efficacious and safe treatment for ADHD, especially in children and adolescents.
MeSH term(s)	Child ; Adult ; Adolescent ; Humans ; Attention Deficit Disorder with Hyperactivity/drug therapy ; Attention Deficit Disorder with Hyperactivity/chemically induced ; Central Nervous System Stimulants/adverse effects ; Randomized Controlled Trials as Topic ; Methylphenidate/adverse effects ; Data Management ; Treatment Outcome ; Double-Blind Method ; Dose-Response Relationship, Drug
Chemical Substances	Central Nervous System Stimulants ; Methylphenidate (207ZZ9QZ49)
Language	English
Publishing date	2023-02-16
Publishing country	United States
Document type	Meta-Analysis ; Systematic Review ; Journal Article
ZDB-ID	2004350-8
ISSN	1557-1246 ; 1087-0547
ISSN (online)	1557-1246
ISSN	1087-0547
DOI	10.1177/10870547231153941
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Zs.A 5196: Show issues

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Article ; Online: Microscopic with Endoscopic Surgery via Subtemporal Approach for Cavernous Sinus Cholesteatomas.

Bu, Jiyuan / Hu, Yukun / Sun, Song / Jin, Xin / Zhu, Jiandong / Yu, Zhengquan / Wu, Jiang

World neurosurgery

2023 Volume 180, Page(s) e624–e630

Abstract: Objective: The aim of this study was to retrospectively analyze the clinical data of 16 patients with cavernous sinus cholesteatomas, explore the surgical outcomes, and summarize the surgical experience.: Methods: Patients with cavernous sinus ... ...

Abstract	Objective: The aim of this study was to retrospectively analyze the clinical data of 16 patients with cavernous sinus cholesteatomas, explore the surgical outcomes, and summarize the surgical experience. Methods: Patients with cavernous sinus cholesteatomas underwent surgery between June 2016 and June 2022 at the Department of Neurosurgery at the First Affiliated Hospital of Soochow University. Clinical data were obtained from all patients for analysis. Results: Common preoperative symptoms included headache, dizziness, diplopia, ptosis, and facial numbness. There were 7 patients with 2 or more symptoms. There were 13 patients with total resection and 3 patients with subtotal resection. There were 5 patients with improved postoperative symptoms, 10 patients with no significant change, and 1 patient with worse symptoms. New postoperative cranial nerve defects occurred in 4 patients. During the follow-up, all patients had favorable prognosis without progression. Conclusions: Using "double-scope" technique, the subtemporal approach, a surgical strategy for cavernous sinus cholesteatomas, was sufficient to completely resect the tumors.
MeSH term(s)	Humans ; Cavernous Sinus/diagnostic imaging ; Cavernous Sinus/surgery ; Cavernous Sinus/pathology ; Retrospective Studies ; Endoscopy ; Neurosurgical Procedures/methods ; Cranial Nerves ; Treatment Outcome
Language	English
Publishing date	2023-10-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	2534351-8
ISSN	1878-8769 ; 1878-8750
ISSN (online)	1878-8769
ISSN	1878-8750
DOI	10.1016/j.wneu.2023.09.124
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