ObjectiveGliomas in the motor functional area can damage the corticospinal tract (CST), leading to motor dysfunction. Currently, there is a lack of unified methods for evaluating the extent of CST damage, especially in patients with high surgical risk where the minimum distance from the lesion to the CST is less than 10 mm. This study aims to further clarify the classification method and clinical significance of CST morphological changes in these patients. MethodsThis retrospective study analyzed 109 high-risk functional area glioma patients who underwent neurosurgical treatment with preoperative diffusion tensor imaging (DTI) imaging and intraoperative neurostimulation guidance between 2014 and 2024. All patients had a lesion-to-tract distance (LTD) of less than 10 mm between the CST and the lesion. Preoperative DTI evaluation of CST involvement-induced morphological changes were reviewed. Patients were divided into 3 groups: 17 cases (15.6%) with symmetric CST morphology compared to the healthy side (CST symmetry), 48 cases (44.0%) with significant CST morphology changes compared to the healthy side (CST deformation), and 44 cases (40.4%) with CST overlap with the tumor (CST overlap). Then we classified patients according to preoperative assessment of tumor-induced morphological changes, and analyze postoperative motor function for each category. ResultsPostoperative pathology showed a significantly higher proportion of high-grade gliomas (HGG) in the CST overlap group compared to the other two groups (P=0.001). Logistic regression analysis showed that CST overlap was a predictor of HGG (P=0.000). The rate of total tumor resection in the CST deformation group and overlap group was lower than in the CST symmetric group (P=0.008). There was a total of 41 postoperative hemiplegic patients, with 4 cases (23.5%) in the CST symmetric group, 11 cases (22.9%) in the CST deformation group, and 26 cases (59.1%) in the CST overlap group. CST overlap with the tumor predicted postoperative hemiplegia (P=0.016). Two-way ANOVA analysis of the affected/healthy side and CST morphology groups showed significant main effects of CST grouping and healthy-affected side (P=0.017 and P=0.010), with no significant interaction (P=0.31). The fractional anisotropy (FA) value in the CST overlap group and the affected side was lower. A decrease in the FA value on the affected side predicted postoperative hemiplegia (sensitivity 69.2%, specificity 71.9%). ConclusionWe have established a method to predict postoperative hemiplegia in high-risk motor functional area glioma patients based on preoperative CST morphological changes. CST overlap leads to a decrease in CST FA values. This method can be used for precise patient management and aid in accurate preoperative surgical planning.

Objective To observe the correlation between cortical thickness and pathological deposition of β-amyloid(Aβ)in patients with Alzheimer disease(AD)induced mild cognitive impairment(MCI)or dementia.Methods Totally 22 AD patients were prospectively enrolled and divided into dementia group(n=12)and MCI group(n=10)based on the degree of cognitive impairment,while 17 healthy individuals without cognitive impairment were recruited as control group.MR examination and 18F-florbutaben(18F-FBB)PET imaging were performed,the cortical thickness and Aβ deposition value(Centiloid[CL]value)were calculated and compared among 3 groups and between each 2 groups,then the correlation between the above two indexes was analyzed.Results The cortical thickness in dementia group,MCI group and control group was(2.18±0.14),(2.35±0.08)and(2.36±0.09)mm,respectively,with significant difference among 3 groups(P＜0.05).The cortical thickness in dementia group was significantly thinner than that in MCI group and control group(both P＜0.05).CL value in dementia group,MCI group and control group was 77.97(63.07,95.55),65.51(54.54,90.50)and-1.17(-9.66,4.88),respectively,with significant difference among 3 groups(P＜0.05).CL value in dementia group and MCI group were significantly higher than in control group(both P＜0.05).The cortical thickness was moderately negatively correlated with CL value in MCI group(r=-0.580,P=0.048)but not in the other 2 groups(both P＞0.05).Conclusion The cortical thickness was moderately negatively correlated with abnormal deposition of Aβ in patients with AD induced MCI,but was not during dementia.

Purpose To investigate the cortical thickness features in Parkinson's disease(PD)patients at various stages and their association with dopamine transporter(DAT)levels in the putamen.Materials and Methods We retrospectively enrolled 30 PD patients and 15 healthy subject who underwent 11C-CFT PET and T1 MRI scans at the Department of Nuclear Medicine/PET Center of Huashan Hospital from August 2016 to October 2020.DAT average radioactivity in the anterior and posterior putamen was analysis using SPM12 software,with the occipital lobe as the reference region.Cortical segmentation and reconstruction were performed on T1 images using Freesurfer v7.2.The differences in cortical thinning between the groups were compared using a general linear model.Additionally,the relationship between cortical thickness in various brain regions and DAT uptake in the putamen were assessed.Results Compared to healthy subjects,significant cortical thinning was observed in the left inferior parietal lobule and the right and left inferior middle frontal gyrus of PD patients(all P<0.05).There was a significant positive correlation between the cortical thickness of the left inferior parietal lobule and right inferior middle frontal gyrus and DAT uptake in the corresponding anterior/posterior parts of the putamen(r=0.30-0.47,all P<0.05).Furthermore,the DAT uptake in the right precentral gyrus was positively correlated with the ipsilateral posterior putamen,exhibiting a stronger correlation than on the contralateral side(r=0.32,P=0.029).Conclusion The results show that the thickness of the thinning cortex area in the PD patients correlates significantly positively with DAT levels in the putamen,highlighting the importance of the basal ganglia cortical circuit and providing a basis for further research into the neural mechanisms of PD.

Purpose To investigate the cortical thickness features in Parkinson's disease(PD)patients at various stages and their association with dopamine transporter(DAT)levels in the putamen.Materials and Methods We retrospectively enrolled 30 PD patients and 15 healthy subject who underwent 11C-CFT PET and T1 MRI scans at the Department of Nuclear Medicine/PET Center of Huashan Hospital from August 2016 to October 2020.DAT average radioactivity in the anterior and posterior putamen was analysis using SPM12 software,with the occipital lobe as the reference region.Cortical segmentation and reconstruction were performed on T1 images using Freesurfer v7.2.The differences in cortical thinning between the groups were compared using a general linear model.Additionally,the relationship between cortical thickness in various brain regions and DAT uptake in the putamen were assessed.Results Compared to healthy subjects,significant cortical thinning was observed in the left inferior parietal lobule and the right and left inferior middle frontal gyrus of PD patients(all P<0.05).There was a significant positive correlation between the cortical thickness of the left inferior parietal lobule and right inferior middle frontal gyrus and DAT uptake in the corresponding anterior/posterior parts of the putamen(r=0.30-0.47,all P<0.05).Furthermore,the DAT uptake in the right precentral gyrus was positively correlated with the ipsilateral posterior putamen,exhibiting a stronger correlation than on the contralateral side(r=0.32,P=0.029).Conclusion The results show that the thickness of the thinning cortex area in the PD patients correlates significantly positively with DAT levels in the putamen,highlighting the importance of the basal ganglia cortical circuit and providing a basis for further research into the neural mechanisms of PD.

Objective To observe the correlation between cortical thickness and pathological deposition of β-amyloid(Aβ)in patients with Alzheimer disease(AD)induced mild cognitive impairment(MCI)or dementia.Methods Totally 22 AD patients were prospectively enrolled and divided into dementia group(n=12)and MCI group(n=10)based on the degree of cognitive impairment,while 17 healthy individuals without cognitive impairment were recruited as control group.MR examination and 18F-florbutaben(18F-FBB)PET imaging were performed,the cortical thickness and Aβ deposition value(Centiloid[CL]value)were calculated and compared among 3 groups and between each 2 groups,then the correlation between the above two indexes was analyzed.Results The cortical thickness in dementia group,MCI group and control group was(2.18±0.14),(2.35±0.08)and(2.36±0.09)mm,respectively,with significant difference among 3 groups(P＜0.05).The cortical thickness in dementia group was significantly thinner than that in MCI group and control group(both P＜0.05).CL value in dementia group,MCI group and control group was 77.97(63.07,95.55),65.51(54.54,90.50)and-1.17(-9.66,4.88),respectively,with significant difference among 3 groups(P＜0.05).CL value in dementia group and MCI group were significantly higher than in control group(both P＜0.05).The cortical thickness was moderately negatively correlated with CL value in MCI group(r=-0.580,P=0.048)but not in the other 2 groups(both P＞0.05).Conclusion The cortical thickness was moderately negatively correlated with abnormal deposition of Aβ in patients with AD induced MCI,but was not during dementia.

Objective To investigate the influencing factors for stroke-associated pneumonia(SAP)in acute ischemic stroke(AIS)patients after endovascular treatment(EVT).Methods A retrospective case-control trial was conducted on 426 AIS patients with large vessel occlusion(LVO)in anterior circulation admitted in the neurological departments from First Affiliated Hospital of Army Medical University and Zigong Third People's Hospital during January 2017 and April 2021.Based on SAP occurrence or not,they were divided into an SAP group and a non-SAP group.Demographic information(gender and age),TOAST stroke subtypes(large artery atherosclerosis type,cardiac embolism type,others),vascular risk factors(hypertension,hyperlipidemia,diabetes,atrial fibrillation,smoking,prior stroke history,smoking),and post-onset clinical data[dysphagia,LDL cholesterol,white blood cells,neutrophils,baseline and postoperative NIHSS scores,endovascular outcomes(mTICI grade 2b or 3),90-day good prognosis(mRS 0-1)]were collected and compared between the 2 groups.Multivariate logistic regression analysis was performed using the parameters with P<0.1 in univariate analysis as independent variables to investigate factors influencing SAP occurrence after EVT in AIS patients.Results Among the 426 participants,SAP occurred in 194 cases(45.5%).Multivariate logistic regression analysis revealed that admission white blood cell count(OR=1.125,95%CI:1.043～1.213,P=0.000 2),postoperative NIHSS score(OR=1.019,95%CI:1.001～1.037,P=0.041),and male(OR=1.687,95%CI:1.078～2.638,P=0.022)were associated with SAP occurrence after EVT in AIS patients.Conclusion Higher admission white blood cell count,elevated postoperative NIHSS score,and male gender are risk factors for SAP in AIS patients after EVT.These risk factors should be focused on clinical practice to control SAP incidence.

The study explores the traditional Chinese medicine （TCM） diagnostic and treatment approach to coronary microvascular disease （CMVD） from the perspective of "disharmony of blood collaterals and dysfunction of qi transformation". It is proposed that the core pathogenesis of CMVD lies in these two mechanisms. From an integrative medicine perspective， different CMVD types are analyzed based on their specific pathogenesis. Through clinical practice， four targeted treatment methods， i.e. warming， unblocking， tonifying， and activating， are formulated. CMVD caused by atherosclerosis is primarily associated with myocardial ischemia， myocardial infarction， and coronary revascularization， with corresponding pathological mechanisms of latent pathogenic obstruction， toxic accumulation in the collaterals， and deficiency with collateral stasis. The disease progression exhibits characteristics of correlation， staging， and transformation. Accordingly， treatment principles include warming to assist qi transformation， unblocking obstruction and dispelling turbidity， activating to disperse toxic stasis and invigorate collaterals， and tonifying to eliminate stasis and nourish collaterals. For CMVD unrelated to atherosclerosis， attention should be paid to the underlying disease， analyzing the main syndromes of blood and collateral disharmony. An approach combining disease-syndrome differentiation with blood and collateral regulation is emphasized for precise treatment.

Neuropathic pain, a debilitating condition caused by dysfunction of the somatosensory nervous system, remains difficult to treat due to limited understanding of its molecular mechanisms. Bioinformatics analysis identified cerebellin 2 (CBLN2) as highly enriched in human and murine proprioceptive and nociceptive neurons. We found that CBLN2 expression is persistently upregulated in dorsal root ganglia (DRG) following spinal nerve ligation (SNL) in mice. In addition, transcription factor SOX11 binds to 12 cis-regulatory elements within the Cbln2 promoter to enhance its transcription. SNL also induced SOX11 upregulation, with SOX11 and CBLN2 co-localized in nociceptive neurons. The siRNA-mediated knockdown of Sox11 or Cbln2 attenuated SNL-induced mechanical allodynia and thermal hyperalgesia. High-throughput sequencing of DRG following intrathecal injection of CBLN2 revealed widespread gene expression changes, including upregulation of numerous NF-κB downstream targets. Consistently, CBLN2 activated NF-κB signaling, and inhibition with pyrrolidine dithiocarbamate reduced CBLN2-induced pain hypersensitivity, proinflammatory cytokines and chemokines production, and neuronal hyperexcitability. Together, these findings identified the SOX11/CBLN2/NF-κB axis as a critical mediator of neuropathic pain and a promising target for therapeutic intervention.
Animals ; Neuralgia/metabolism* ; Ganglia, Spinal/metabolism* ; Up-Regulation ; Mice ; NF-kappa B/metabolism* ; SOXC Transcription Factors/genetics* ; Male ; Neuroinflammatory Diseases/metabolism* ; Mice, Inbred C57BL ; Nerve Tissue Proteins/genetics* ; Hyperalgesia/metabolism* ; Signal Transduction ; Spinal Nerves

Objective:To investigate the potential value of cerebral glucose metabolism characteristics in anti-leucine-rich glioma-inactivated protein 1 (LGI1) antibody-related encephalitic patients during acute phase as the clinical indicator of disease outcomes.Methods:From October 2019 to December 2023, 28 patients (18 males, 10 females; age (56.6±11.9) year) with anti-LGI1 antibody-related encephalitis diagnosed at Huashan Hospital, Fudan University were prospectively enrolled. All patients received baseline brain 18F-FDG PET imaging and were divided into different subgroups according to the prognosis (good prognosis and poor prognosis groups) and recurrence (recurrence and non-recurrence groups) after follow-up. The difference of Montreal Cognitive Assessment (MoCA) score between the two groups was compared by Mann-Whitney U test. Statistical parametric mapping (SPM) analysis was used to analyze the PET images of different groups by independent-sample t test, and the characteristics of cerebral glucose metabolism of patients with different outcomes were obtained. Results:MoCA scores between the recurrence group ( n=6) and the non-recurrence group ( n=22; 14.0(9.8, 20.5) vs 22.0(18.0, 24.0); Z=2.17, P=0.030), and between the poor prognosis group ( n=13) and the good prognosis group ( n=15; 14.0(10.0, 22.0) vs 22.0(19.8, 25.3); Z=2.47, P=0.013) were significantly different. Compared with the good prognosis group, the cerebral glucose metabolism in the poor prognosis group was decreased in the bilateral frontal lobe, lateral temporal lobe, inferior parietal lobule and cingulate gyrus, but increased in the brainstem, bilateral lentiform nucleus and bilateral paracentral lobule/postcentral gyrus (all t=1.71, all P<0.05). Compared with the non-recurrence group, the metabolism of bilateral medial frontal gyrus, anterior cingulate gyrus, bilateral insula, superior temporal gyrus and thalamus decreased in the recurrence group, while the metabolism of bilateral precentral gyrus, inferior frontal gyrus and bilateral lentiform nucleus increased (all t=1.71, all P<0.05). Conclusion:18F-FDG PET imaging reveals the differences in brain metabolism of anti-LGI1 antibody-related encephalitic patients at baseline with different outcomes (prognosis, recurrence or not), which can provide a new perspective for the clinical evaluation of the disease at baseline.

ObjectiveTo investigate the mechanism of Huangqin Tang （HQT） in regulating metabolic reprogramming during the inflammation-cancer transformation in colitis-associated colorectal cancer （CAC）. MethodsCAC mouse model was established using the carcinogen azoxymethane （AOM） combined with the inflammatory agent dextran sulfate sodium （DSS）. HQT treatment was adopted. Serum metabolomics analysis was performed at three stages （inflammation， proliferation， and tumor formation） using liquid chromatography-tandem mass spectrometry （LC-MS/MS） untargeted metabolomics coupled with multivariate statistical analysis to explore the mechanism of HQT intervention in metabolism in CAC. ResultsThe results revealed that HQT significantly reversed the disturbance of key metabolites in CAC mice. A total of 52， 67， and 45 differential metabolites were identified in the model group， compared to the normal group， during inflammation， proliferation， and tumor stages， respectively. Lactate， linoleic acid， oleic acid， elaidic acid， and betaine were characteristic metabolites persistently enriched throughout colitis-cancer transformation. Pathway enrichment analysis of differential metabolites showed that linoleic acid metabolism and arachidonic acid metabolism were the most significantly disturbed in CAC pathogenesis. The proliferation stage featured expanded amino acid metabolic networks， while the tumor stage uniquely exhibited two new pathways of nicotinate and nicotinamide metabolism and phosphoinositide metabolism. HQT exerted stage-specific regulatory effects： targeting arachidonic acid metabolism in the inflammation stage， correcting the dysregulation of choline-carnitine metabolism in the proliferation stage， and rescuing nicotinamide and tryptophan metabolic collapse in the tumor stage. ConclusionHQT exerts regulatory effects on metabolic disorders at various stages of the colitis-cancer transformation process， thereby effectively slowing the progression from colitis to cancer. The study also reveals the dynamic metabolic characteristics of colorectal "inflammation-cancer transformation，"providing new insights for research on the targeted mechanisms of traditional Chinese medicine in anti-tumor therapy based on metabolic reprogramming.