For middle-aged and elderly patients with conditions such as spinal fractures and degenerative spinal diseases, spinal internal fixation is a core surgical procedure for reconstructing spinal stability, heavily relying on the biomechanical stability provided by pedicle screw systems. Whereas, these patients are often complicated by osteoporosis that can significantly compromise the stability of the bone-pedicle screw interface, leading to a marked increase in pedicle screw loosening and surgical failure rates. The bone cement-augmented pedicle screw technique, which involves injecting bone cement into the vertebral body or screw trajectory to optimize the mechanical properties of the bone-pedicle screw composite, has been proven to significantly enhance fixation strength and effectively prevent screw-related failures, thereby reducing the incidence of internal fixation failure in high-risk populations undergoing spinal fusion. However, the widespread clinical application of this technique has faced challenges such as inaccurate clinical decision-making (indication and contraindication selection), non-standardized operative practices, and insufficient awareness of complication prevention, resulting in considerable variability in clinical outcomes and even severe complications. To address this, Prof. Luo Fei from First Affiliated Hospital of Army Medical University initiated the project and the Chinese Association Orthopaedic Surgeons organized relevant experts to develop the Evidence-based clinical practice guideline for bone cement-augmented pedicle screw technique ( version 2025), based on current evidence. The guidelines put forward 8 recommendations regarding the clinical value, scope of application, and operational standards of the technique, aiming to provide evidence-based medical support and technical standardization for clinical decision-making.

Although myelin oligodendrocyte glycoprotein (MOG)-IgG is a biological marker for diagnosing MOG antibody-associated disease (MOGAD), the specificity of MOG-IgG in disease diagnosis remains controversial. In clinical practice, there is significant heterogeneity in MOGAD patients with low titer of MOG-IgG and low titer MOG-IgG can even be detected in asymptomatic populations. At the same time, MOG-IgG-positive individuals often combine with the positivity of other multiple autoimmune antibodies in the nervous system. Therefore, the relationship between MOG-IgG and MOGAD is complex, and the pathogenesis of MOGAD may involve immune factors other than MOG-IgG. This article reviews the research progress of MOGAD combined with other neuroimmune antibodies, assisting in the early identification and treatment of such diseases by clinical physicians in the future.

Objective:To explore the clinical symptoms, imaging characteristics, cerebrospinal fluid (CSF) features, as well as the treatment and prognosis of autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy.Methods:Sixty-one patients with anti-GFAP astrocyte antibody (GFAP-IgG) single-positive autoimmune encephalitis who were treated at the Third Affiliated Hospital, Sun Yat-sen University between January 2017 and September 2023 were retrospectively collected. The demographic characteristics (age at onset, sex), clinical symptoms (core symptoms, neurological deficits, psychiatric behavioral abnormalities, and autonomic dysfunction), imaging features [brain/spinal cord/optic nerve magnetic resonance imaging (MRI) lesion distribution and enhancement patterns], and CSF parameters were analyzed. Acute-phase treatments, including methylprednisolone pulse therapy, intravenous immunoglobulin (IVIG), etc, along with the follow-up outcomes [modified Rankin Scale (mRS) score] were recorded.Results:The onset age was 40 (30, 55) years, and 68.9% (42/61) of the patients were male. The most common clinical manifestations were fever (65.6%, 40/61), headache (60.7%, 37/61), and urinary/defecatory abnormalities (45.9%, 28/61). Brain MRI revealed lesions predominantly in the cerebral cortex and subcortical white matter (57.4%, 35/61), periventricular white matter (50.8%, 31/61), and basal ganglia (36.1%, 22/61). Periventricular linear-radiating enhancement was the predominant MRI enhancement pattern (55.7%, 34/61). Spinal MRI showed lesions mainly in the cervical (42.6%, 26/61) and thoracic spinal cord (32.8%, 30/61), with leptomeningeal enhancement (31.1%, 19/61) and scattered punctate/patchy enhancements (21.3%, 13/61). Optic neuropathy was observed in 6 cases (9.8%). CSF analysis demonstrated a pressure of 180 (133, 240) mmH 2O (1 mmH 2O=0.009 8 kPa), white blood cell count of 29 (4, 156)×10?/L, and protein level of 0.72 (0.40, 1.44) g/L. Nineteen patients (31.1%) experienced rapid progression of meningoencephalitis or myelitis within 3 days of admission. All patients received methylprednisolone pulse therapy, with 47.5% (29/61) additionally treated with IVIG. At a follow-up of 12 (3, 28) months, 12 cases (19.7%) relapsed, and 75.4% (46/61) had favorable outcomes (mRS score 0-2). Poor prognosis (mRS score>2) was observed in 4 cases, including 3 with cervical spinal cord involvement and status epilepticus, 1 elderly patient with lung cancer. Conclusions:GFAP astrocytopathy predominantly affects young adults, with a male predominance. Spinal cord involvement is common, manifesting as myelitis and myelopathy. Rapid progression of meningoencephalitis or myelitis may occur early in the disease course. Periventricular linear-radiating enhancement on brain MRI is a key diagnostic clue. Leukocyte and protein levels in the cerebrospinal fluid are generally mildly to moderately elevated. Most patients respond well to corticosteroids and immunotherapy, with favorable outcomes. However, advanced age and cervical spinal cord involvement are associated with poor prognosis.

For middle-aged and elderly patients with conditions such as spinal fractures and degenerative spinal diseases, spinal internal fixation is a core surgical procedure for reconstructing spinal stability, heavily relying on the biomechanical stability provided by pedicle screw systems. Whereas, these patients are often complicated by osteoporosis that can significantly compromise the stability of the bone-pedicle screw interface, leading to a marked increase in pedicle screw loosening and surgical failure rates. The bone cement-augmented pedicle screw technique, which involves injecting bone cement into the vertebral body or screw trajectory to optimize the mechanical properties of the bone-pedicle screw composite, has been proven to significantly enhance fixation strength and effectively prevent screw-related failures, thereby reducing the incidence of internal fixation failure in high-risk populations undergoing spinal fusion. However, the widespread clinical application of this technique has faced challenges such as inaccurate clinical decision-making (indication and contraindication selection), non-standardized operative practices, and insufficient awareness of complication prevention, resulting in considerable variability in clinical outcomes and even severe complications. To address this, Prof. Luo Fei from First Affiliated Hospital of Army Medical University initiated the project and the Chinese Association Orthopaedic Surgeons organized relevant experts to develop the Evidence-based clinical practice guideline for bone cement-augmented pedicle screw technique ( version 2025), based on current evidence. The guidelines put forward 8 recommendations regarding the clinical value, scope of application, and operational standards of the technique, aiming to provide evidence-based medical support and technical standardization for clinical decision-making.

Objective To observe the value of the integrated model of MR high-resolution vascular wall imaging(HR-VWI)and attention mechanism for predicting stroke recurrence in symptomatic intracranial atherosclerotic stenosis(sICAS)patients.Methods A total of 363 patients with sICAS who underwent HR-VWI were enrolled and stratified into training set(n=254)and validation set(n=109)according to their origins.Employing a radiomics model that utilized HR-VWI T1 and contrast-enhanced sequences for feature extraction,image data were captured from relevant plaques.Subsequently,a Trans model was developed by integrating the Transformer attention mechanism.The predictive performance and clinical utility of conventional radiomics models and Trans models for forecasting stroke recurrence among patients with sICAS were evaluated.Results In training set and validation set,the area under the curve of Trans model for predicting stroke recurrence in sICAS patients was 0.992 and 0.988,respectively,both superior to that of T1 model,T1 enhanced model and dual sequence model(all P＜0.05).The calibration curve and decision curve analysis showed that Trans model had good predictive probability and clinical practicality.Conclusion The obtained integrated model of HR-VWI radiomics combined with attention mechanism had certain value for predicting stroke recurrence in patients with sICAS.

Objective To observe the value of the integrated model of MR high-resolution vascular wall imaging(HR-VWI)and attention mechanism for predicting stroke recurrence in symptomatic intracranial atherosclerotic stenosis(sICAS)patients.Methods A total of 363 patients with sICAS who underwent HR-VWI were enrolled and stratified into training set(n=254)and validation set(n=109)according to their origins.Employing a radiomics model that utilized HR-VWI T1 and contrast-enhanced sequences for feature extraction,image data were captured from relevant plaques.Subsequently,a Trans model was developed by integrating the Transformer attention mechanism.The predictive performance and clinical utility of conventional radiomics models and Trans models for forecasting stroke recurrence among patients with sICAS were evaluated.Results In training set and validation set,the area under the curve of Trans model for predicting stroke recurrence in sICAS patients was 0.992 and 0.988,respectively,both superior to that of T1 model,T1 enhanced model and dual sequence model(all P＜0.05).The calibration curve and decision curve analysis showed that Trans model had good predictive probability and clinical practicality.Conclusion The obtained integrated model of HR-VWI radiomics combined with attention mechanism had certain value for predicting stroke recurrence in patients with sICAS.

Although myelin oligodendrocyte glycoprotein (MOG)-IgG is a biological marker for diagnosing MOG antibody-associated disease (MOGAD), the specificity of MOG-IgG in disease diagnosis remains controversial. In clinical practice, there is significant heterogeneity in MOGAD patients with low titer of MOG-IgG and low titer MOG-IgG can even be detected in asymptomatic populations. At the same time, MOG-IgG-positive individuals often combine with the positivity of other multiple autoimmune antibodies in the nervous system. Therefore, the relationship between MOG-IgG and MOGAD is complex, and the pathogenesis of MOGAD may involve immune factors other than MOG-IgG. This article reviews the research progress of MOGAD combined with other neuroimmune antibodies, assisting in the early identification and treatment of such diseases by clinical physicians in the future.

Objective:To explore the clinical symptoms, imaging characteristics, cerebrospinal fluid (CSF) features, as well as the treatment and prognosis of autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy.Methods:Sixty-one patients with anti-GFAP astrocyte antibody (GFAP-IgG) single-positive autoimmune encephalitis who were treated at the Third Affiliated Hospital, Sun Yat-sen University between January 2017 and September 2023 were retrospectively collected. The demographic characteristics (age at onset, sex), clinical symptoms (core symptoms, neurological deficits, psychiatric behavioral abnormalities, and autonomic dysfunction), imaging features [brain/spinal cord/optic nerve magnetic resonance imaging (MRI) lesion distribution and enhancement patterns], and CSF parameters were analyzed. Acute-phase treatments, including methylprednisolone pulse therapy, intravenous immunoglobulin (IVIG), etc, along with the follow-up outcomes [modified Rankin Scale (mRS) score] were recorded.Results:The onset age was 40 (30, 55) years, and 68.9% (42/61) of the patients were male. The most common clinical manifestations were fever (65.6%, 40/61), headache (60.7%, 37/61), and urinary/defecatory abnormalities (45.9%, 28/61). Brain MRI revealed lesions predominantly in the cerebral cortex and subcortical white matter (57.4%, 35/61), periventricular white matter (50.8%, 31/61), and basal ganglia (36.1%, 22/61). Periventricular linear-radiating enhancement was the predominant MRI enhancement pattern (55.7%, 34/61). Spinal MRI showed lesions mainly in the cervical (42.6%, 26/61) and thoracic spinal cord (32.8%, 30/61), with leptomeningeal enhancement (31.1%, 19/61) and scattered punctate/patchy enhancements (21.3%, 13/61). Optic neuropathy was observed in 6 cases (9.8%). CSF analysis demonstrated a pressure of 180 (133, 240) mmH 2O (1 mmH 2O=0.009 8 kPa), white blood cell count of 29 (4, 156)×10?/L, and protein level of 0.72 (0.40, 1.44) g/L. Nineteen patients (31.1%) experienced rapid progression of meningoencephalitis or myelitis within 3 days of admission. All patients received methylprednisolone pulse therapy, with 47.5% (29/61) additionally treated with IVIG. At a follow-up of 12 (3, 28) months, 12 cases (19.7%) relapsed, and 75.4% (46/61) had favorable outcomes (mRS score 0-2). Poor prognosis (mRS score>2) was observed in 4 cases, including 3 with cervical spinal cord involvement and status epilepticus, 1 elderly patient with lung cancer. Conclusions:GFAP astrocytopathy predominantly affects young adults, with a male predominance. Spinal cord involvement is common, manifesting as myelitis and myelopathy. Rapid progression of meningoencephalitis or myelitis may occur early in the disease course. Periventricular linear-radiating enhancement on brain MRI is a key diagnostic clue. Leukocyte and protein levels in the cerebrospinal fluid are generally mildly to moderately elevated. Most patients respond well to corticosteroids and immunotherapy, with favorable outcomes. However, advanced age and cervical spinal cord involvement are associated with poor prognosis.

Purpose: This study aimed to investigate the effect of the N6-methyladenosine (m6A) dependent ferroptosis on cisplatininduced Sertoli cell injury. Materials and Methods: A cisplatin exposure mouse model was established by intraperitoneal injection of cisplatin in our study. TM4 cell lines was used for in vitro study. Ferroptosis was detected according to metabolomic analysis and a series of assays, including malondialdehyde, glutathione, and glutathione disulfide concentration detection, 2′,7′-dichlorodihydrofluorescein diacetate and BODIPY 581/591 C11 probe detection, and transmission electron microscope imaging. Key ferroptosis-related genes were identified via transcriptomic analysis, western blot and immunohistochemistry. The m6A modification was demonstrated via m6A RNA immunoprecipitation and luciferase reporter assays. Immune cell infiltration was detected by mass cytometry, and verified by flow cytometry and immunofluorescence. Results: Ferroptosis, but not other types of programmed cell death, is a significant phenomenon in cisplatin-induced testis damage and Sertoli cell loss. Ferroptosis induced by cisplatin in Sertoli cell/TM4 cell is GPX4 independent but is regulated by SLC7A11 and ALOX12. Both SLC7A11 and ALOX12 are regulated via m6A dependent manner by METTL3. Furthermore, overexpressed ALOX12-12HETE pathway may result in macrophage polarization and inflammatory response in cisplatin exposure testis. Conclusions Cisplatin-induced Sertoli cell injury via ferroptosis and promoted ferroptosis in an m6A dependent manner. m6A modification of both SLC7A11 and ALOX12 mRNA could result in ferroptosis in our in vitro model. Further, overexpressed ALOX12 can cause more production of 12-HETE, which may be responsible for testis inflammation caused by cisplatin.

Purpose: This study aimed to investigate the effect of the N6-methyladenosine (m6A) dependent ferroptosis on cisplatininduced Sertoli cell injury. Materials and Methods: A cisplatin exposure mouse model was established by intraperitoneal injection of cisplatin in our study. TM4 cell lines was used for in vitro study. Ferroptosis was detected according to metabolomic analysis and a series of assays, including malondialdehyde, glutathione, and glutathione disulfide concentration detection, 2′,7′-dichlorodihydrofluorescein diacetate and BODIPY 581/591 C11 probe detection, and transmission electron microscope imaging. Key ferroptosis-related genes were identified via transcriptomic analysis, western blot and immunohistochemistry. The m6A modification was demonstrated via m6A RNA immunoprecipitation and luciferase reporter assays. Immune cell infiltration was detected by mass cytometry, and verified by flow cytometry and immunofluorescence. Results: Ferroptosis, but not other types of programmed cell death, is a significant phenomenon in cisplatin-induced testis damage and Sertoli cell loss. Ferroptosis induced by cisplatin in Sertoli cell/TM4 cell is GPX4 independent but is regulated by SLC7A11 and ALOX12. Both SLC7A11 and ALOX12 are regulated via m6A dependent manner by METTL3. Furthermore, overexpressed ALOX12-12HETE pathway may result in macrophage polarization and inflammatory response in cisplatin exposure testis. Conclusions Cisplatin-induced Sertoli cell injury via ferroptosis and promoted ferroptosis in an m6A dependent manner. m6A modification of both SLC7A11 and ALOX12 mRNA could result in ferroptosis in our in vitro model. Further, overexpressed ALOX12 can cause more production of 12-HETE, which may be responsible for testis inflammation caused by cisplatin.