Background: and Purpose Guillain–Barré syndrome (GBS) is an autoimmune-mediated disorder characterized by demyelinating or axonal injury of the peripheral nerve. Our aim is to determine whether serum amyloid A (SAA) is a biomarker of demyelinating injury and disease severity in patients with GBS. Methods: This study retrospectively enrolled 40 patients with either the demyelinating or axonal GBS and sex- and age-matched controls with other neurological diseases as well as healthy subjects. The demographic and clinical features at entry were collected. The serum levels of the SAA isoforms SAA1, SAA2, and SAA4 were determined in the patients with GBS and the controls using the enzyme-linked immunosorbent assay and analyzed for the associations between levels of different SAA isoforms and the clinical features of the patients. Results: The levels of SAA2 and SAA4 were significantly higher in patients with GBS than in both the other neurological disease controls and the healthy subjects (p<0.05 for all). The level of SAA1 did not differ between patients with GBS and the controls. The level of SAA2 was considerably higher in GBS patients with antecedent infection than in those without infection (p=0.020). The levels of different SAA isoforms were not associated with the disease severity or other clinical features of patients with GBS (p>0.05 for all). Conclusions Increased levels of SAA2 and SAA4 may only represent the acute inflammatory status and so cannot be utilized as biomarkers of the disease severity or demyelinating injury in patients with GBS.

Background: and Purpose Guillain–Barré syndrome (GBS) is an autoimmune-mediated disorder characterized by demyelinating or axonal injury of the peripheral nerve. Our aim is to determine whether serum amyloid A (SAA) is a biomarker of demyelinating injury and disease severity in patients with GBS. Methods: This study retrospectively enrolled 40 patients with either the demyelinating or axonal GBS and sex- and age-matched controls with other neurological diseases as well as healthy subjects. The demographic and clinical features at entry were collected. The serum levels of the SAA isoforms SAA1, SAA2, and SAA4 were determined in the patients with GBS and the controls using the enzyme-linked immunosorbent assay and analyzed for the associations between levels of different SAA isoforms and the clinical features of the patients. Results: The levels of SAA2 and SAA4 were significantly higher in patients with GBS than in both the other neurological disease controls and the healthy subjects (p<0.05 for all). The level of SAA1 did not differ between patients with GBS and the controls. The level of SAA2 was considerably higher in GBS patients with antecedent infection than in those without infection (p=0.020). The levels of different SAA isoforms were not associated with the disease severity or other clinical features of patients with GBS (p>0.05 for all). Conclusions Increased levels of SAA2 and SAA4 may only represent the acute inflammatory status and so cannot be utilized as biomarkers of the disease severity or demyelinating injury in patients with GBS.

Background: and Purpose Guillain–Barré syndrome (GBS) is an autoimmune-mediated disorder characterized by demyelinating or axonal injury of the peripheral nerve. Our aim is to determine whether serum amyloid A (SAA) is a biomarker of demyelinating injury and disease severity in patients with GBS. Methods: This study retrospectively enrolled 40 patients with either the demyelinating or axonal GBS and sex- and age-matched controls with other neurological diseases as well as healthy subjects. The demographic and clinical features at entry were collected. The serum levels of the SAA isoforms SAA1, SAA2, and SAA4 were determined in the patients with GBS and the controls using the enzyme-linked immunosorbent assay and analyzed for the associations between levels of different SAA isoforms and the clinical features of the patients. Results: The levels of SAA2 and SAA4 were significantly higher in patients with GBS than in both the other neurological disease controls and the healthy subjects (p<0.05 for all). The level of SAA1 did not differ between patients with GBS and the controls. The level of SAA2 was considerably higher in GBS patients with antecedent infection than in those without infection (p=0.020). The levels of different SAA isoforms were not associated with the disease severity or other clinical features of patients with GBS (p>0.05 for all). Conclusions Increased levels of SAA2 and SAA4 may only represent the acute inflammatory status and so cannot be utilized as biomarkers of the disease severity or demyelinating injury in patients with GBS.

OBJECTIVE: To evaluate the effect of biodegradable magnesium alloy materials in promoting tendon-bone healing during rotator cuff tear repair and to investigate their potential underlying biological mechanisms. METHODS: Forty-eight 8-week-old Sprague Dawley rats were taken and randomly divided into groups A, B, and C. Rotator cuff tear models were created and repaired using magnesium alloy sutures in group A and Vicryl Plus 4-0 absorbable sutures in group B, while only subcutaneous incisions and sutures were performed in group C. Organ samples of groups A and B were taken for HE staining at 1 and 2 weeks after operation to evaluate the safety of magnesium alloy, and specimens from the supraspinatus tendon and proximal humerus were harvested at 2, 4, 8, and 12 weeks after operation. The specimens were observed macroscopically at 4 and 12 weeks after operation. Biomechanical tests were performed at 4, 8, and 12 weeks to test the ultimate load and stiffness of the healing sites in groups A and B. At 2, 4, and 12 weeks, the specimens were subjected to the following tests: Micro-CT to evaluate the formation of bone tunnels in groups A and B, HE staining and Masson staining to observe the regeneration of fibrocartilage at the tendon-bone interface after decalcification and sectioning, and Goldner trichrome staining to evaluate the calcification. Immunohistochemical staining was performed to detect the expressions of angiogenic factors, including vascular endothelial growth factor (VEGF) and bone morphogenetic protein 2 (BMP-2), as well as osteogenic factors at the tendon-bone interface. Additionally, immunofluorescence staining was used to examine the expressions of Arginase 1 and Integrin beta-2 to assess M1 and M2 macrophage polarization at the tendon-bone interface. The role of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway in tendon-bone healing was further analyzed using real-time fluorescence quantitative PCR. RESULTS: Analysis of visceral sections revealed that magnesium ions released during the degradation of magnesium alloys did not cause significant toxic effects on organs such as the heart, liver, spleen, lungs, and kidneys, indicating good biosafety. Histological analysis further demonstrated that fibrocartilage regeneration at the tendon-bone interface in group A occurred earlier, and the amount of fibrocartilage was significantly greater compared to group B, suggesting a positive effect of magnesium alloy material on tendon-bone interface repair. Additionally, Micro-CT analysis results revealed that bone tunnel formation occurred more rapidly in group A compared to group B, further supporting the beneficial effect of magnesium alloy on bone healing. Biomechanical testing showed that the ultimate load in group A was consistently higher than in group B, and the stiffness of group A was also greater than that of group B at 4 weeks, indicating stronger tissue-carrying capacity following tendon-bone interface repair and highlighting the potential of magnesium alloy in enhancing tendon-bone healing. Immunohistochemical staining results indicated that the expressions of VEGF and BMP-2 were significantly upregulated during the early stages of healing, suggesting that magnesium alloy effectively promoted angiogenesis and bone formation, thereby accelerating the tendon-bone healing process. Immunofluorescence staining further revealed that magnesium ions exerted significant anti-inflammatory effects by regulating macrophage polarization, promoting their shift toward the M2 phenotype. Real-time fluorescence quantitative PCR results demonstrated that magnesium ions could facilitate tendon-bone healing by modulating the PI3K/AKT signaling pathway. CONCLUSION Biodegradable magnesium alloy material accelerated fibrocartilage regeneration and calcification at the tendon-bone interface in rat rotator cuff tear repair by regulating the PI3K/AKT signaling pathway, thereby significantly enhancing tendon-bone healing.
Animals ; Rotator Cuff Injuries/metabolism* ; Rats, Sprague-Dawley ; Signal Transduction ; Wound Healing/drug effects* ; Alloys/pharmacology* ; Rats ; Proto-Oncogene Proteins c-akt/metabolism* ; Rotator Cuff/metabolism* ; Macrophages/metabolism* ; Magnesium/pharmacology* ; Phosphatidylinositol 3-Kinases/metabolism* ; Vascular Endothelial Growth Factor A/metabolism* ; Male ; Biocompatible Materials ; Bone Morphogenetic Protein 2/metabolism*

Objective: To evaluate the clinical value of combining low-dose energy spectrum CT with virtual un-enhanced(VUE) scanning and deep-learning image reconstruction(DLIR) in aortic CT angiography(CTA). Methods : In a prospective study, 94 patients scheduled for aortic CTA were randomized into two groups: a low-dose energy spectrum group and a standard 100 kVp enhancement group, with 47 patients in each. All patients initially underwent a true un-enhanced(TUE) scan at 120 kVp using adaptive statistical iterative reconstruction-V(ASIR-V) at 40% for image reconstruction. The low-dose group received enhanced scans using gemstone spectral imaging(GSI) mode with DLIR-H, producing 60 keV virtual monoenergetic images(VMIs) and VUE images. The standard group was scanned at 100 kVp, with images reconstructed using ASIR-V at 50%. Parameters were measured including CT values, noise(SD), signal-to-noise ratio(SNR), and contrast-to-noise ratio(CNR) for key vascular and muscular areas, alongside the effective radiation dose(ED). Two radiologists evaluated the image quality using a 5-point scale. Results : The low-dose group exhibited significantly higher SNR and CNR values in the ascending aorta, descending aorta, abdominal aorta, and common iliac artery compared to the standard group(P<0.05), with comparable subjective quality scores. The VUE images also demonstrated superior SNR values in the abdominal aorta, common iliac artery, and psoas major muscle, and CNR value in the ascending aorta compared to TUE images, with similar subjective quality. Importantly, the ED in the low-dose group was about 40% lower than that of the standard group. Conclusion Low-dose energy spectrum CT with DLIR in aortic CTA can significantly enhance SNR and CNR, while approximating the image quality of traditional TUE scans, thereby substantially reducing radiation exposure.

Combining with molecular imaging,nuclear medicine gradually utilized radiopharmaceuticals with targeted radionuclide therapy for accurate diagnosis and individualized treatment of diseases,hence advancing the progresses of theranostics.The clinical research progresses of radiotheranostics in diagnosis and therapy of diseases were reviewed in this article.

【Objective】 To analyze the expression of lncRNA SNHG25 in prostate cancer and its significance, so as to explore the biomarkers and potential therapeutic targets for the diagnosis and prognosis of this disease. 【Methods】 Based on the TCGA database, differential, survival, and clinical correlation analyses of SNHG25 were performed.SNHG25 expression in prostate cancer was analyzed in the UALCAN database to determine its relationship with the clinical and pathological characteristics.The lncRNA-miRNA-mRNA correlation analysis was performed.The relevant ceRNA regulatory network was constructed.Prostate cancer samples were divided into high and low SNHG25 expression groups, and differential SNHG25 related genes were filtered and then enriched. 【Results】 SNHG25 expression was significantly upregulated in prostate cancer specimens compared to normal prostate specimens (P<0.001), and the progression-free survival of the low SNHG25 expression group was significantly longer than that of the high SNHG25 expression group (P<0.001).There were no significant differences in age, T-stage and N-stage between the two groups, and there was no significant correlation between the expression of SNHG25 and Gleason score (P>0.05).Regulatory networks of SNHG25/miR-330-3p/DLX1 and RPL22L1 were constructed. 【Conclusion】 SNHG25 is highly expressed in prostate cancer tissues and correlated with poor prognosis.SNHG25 expression does not significantly correlate with age, T-stage, N-stage, and Gleason score.SNHG25/miR-330-3p/DLX1 and RPL22L1 regulatory networks may play an important role in the development of prostate cancer.SNHG25 may become a biomarker and potential therapeutic target for prostate cancer.

AIM:To investigate the impact of celastrol intervention on excitatory amino acid transporter 2(EAAT2)and its neuroprotective role in subarachnoid hemorrhage(SAH).METHODS:Western blot analysis was uti-lized to assess the EAAT2 expression level within 72 h after SAH,while glutamate concentration in cortical brain tissues was measured.Computational simulation was employed to explore the binding of celastrol with EAAT2.Seventy SD rats were randomly assigned to sham,model,model+GT949(an EAAT2 agonist),model+dihydrokainic acid(DHK;an EAAT2 inhibitor),and model+celastrol groups.Glutamate concentration in cortical brain tissues was quantified,and brain edema was assessed by dry-wet weight method.Western blot analysis was conducted to evaluate the expression of EAAT2,aquaporin 4 and apoptosis-related proteins(Bax,Bcl-2,caspase-3 and caspase-9),and TUNEL staining was employed to assess the apoptotic cell count in each group.RESULTS:(1)EAAT2 level decreased while glutamate con-centration increased.(2)Celastrol was found to directly bind to EAAT2,enhancing EAAT2 expression and reducing glu-tamate concentration after SAH.(3)Celastrol demonstrated the ability to inhibit brain edema after SAH.(4)Celastrol was effective in reducing neuronal apoptosis after SAH.CONCLUSION:Celastrol has the potential to up-regulate EAAT2 expression,lower glutamate level,mitigate brain edema,and decrease neuronal apoptosis after SAH.

Chemical cleaning and disinfection are crucial steps for eliminating infection in root canal treatment.However,irrigant selection or irrigation procedures are far from clear.The vapor lock effect in the apical region has yet to be solved,impeding irrigation efficacy and resulting in residual infections and compromised treatment outcomes.Additionally,ambiguous clinical indications for root canal medication and non-standardized dressing protocols must be clarified.Inappropriate intracanal medication may present side effects and jeopardize the therapeutic outcomes.Indeed,clinicians have been aware of these concerns for years.Based on the current evidence of studies,this article reviews the properties of various irrigants and intracanal medicaments and elucidates their effectiveness and interactions.The evolution of different kinetic irrigation methods,their effects,limitations,the paradigm shift,current indications,and effective operational procedures regarding intracanal medication are also discussed.This expert consensus aims to establish the clinical operation guidelines for root canal irrigation and a position statement on intracanal medication,thus facilitating a better understanding of infection control,standardizing clinical practice,and ultimately improving the success of endodontic therapy.

Objective:To investigate associations of cerebral perfusion impairment with early neurological deterioration (END) and poor outcome in patients with acute small subcortical infarction (SSI).Methods:Patients with SSI in the perforator artery region admitted to the Department of Neurology, Zhengzhou People's Hospital between January 2020 and November 2022 were prospectively included. END was defined as an increase of ≥2 in the total score of the National Institutes of Health Stroke Scale (NIHSS) or an increase of ≥1 in the motor function score within 72 h after admission. Poor outcome was defined as the modified Rankin Scale score of 2 at 90 d after onset. Cerebral perfusion impairment was defined according to MRI perfusion-weighted imaging parameters. The demographic, baseline clinical and imaging data were collected. Multivariate logistic regression analysis was used to determine associations of cerebral perfusion impairment and END and poor outcome in patients with SSI. Results:A total of 100 patients with SSI were enrolled, including 56 males (56.0%), and aged 69.2±5.8 years. Among them, 19 patients (19.0%) developed END, 27 (27.0%) had poor outcome, and 51 (51.0%) had significant cerebral perfusion impairment. There were statistically significant differences in high sensitivity C-reactive protein, white matter hyperintensities (WMHs) in the basal ganglia, enlarged perivascular space (EPVS) in the basal ganglia, deep cerebral microbleeds (CMBs), and cerebral perfusion impairment between the END group and the non-END group (all P<0.05). Multivariate logistic regression analysis showed that higher diastolic blood pressure (odds ratio [ OR] 1.070, 95% confidence interval [ CI] 1.003-1.141); P=0.040], deep WMHs ( OR 2.271, 95% CI 1.135-4.544; P=0.020), deep CMBs ( OR 5.047, 95% CI 1.240-20.549; P=0.024), and cerebral perfusion impairment ( OR 6.083, 95% CI 1.318-28.080; P=0.021) were independent risk factors for END in patients with SSI. There were statistically significant differences in hypersensitive C-reactive protein, NIHSS score at END, basal ganglia EPVS, END, and cerebral perfusion impairment between the poor outcome group and the good outcome group ( P<0.05). Multivariate logistic regression analysis showed that NIHSS score at END ( OR 1.485, 95% CI 1.034-2.133; P=0.032), basal ganglia EPVS ( OR 3.005, 95% CI 1.224-7.378; P=0.016), and cerebral perfusion impairment ( OR 9.234, 95% CI 1.994-42.765; P=0.004) were independent risk factors for the poor outcome at 90 d in patients with SSI, while anterior circulation infarction ( OR 0.066, 95% CI 0.013-0.334; P=0.001) was independently negatively correlated with the poor outcomes at 90 d after onset. Conclusion:Cerebral perfusion impairment is an independent risk factor for END and poor outcome at 90 d after onset in patients with SSI.