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.

Objective To explore the effect of PCSK9 inhibitor combined with atorvastatin on carotid atherosclerosis and its anti-inflammatory effect in patients with hypertension complicated with type 2 diabetes mellitus.Methods A total of 100 patients with hypertension complicated with type 2 diabetes mellitus who were treated in Nanchang Third Hospital from October 2022 to August 2023 were selected as the research subjects.They were divided into the control group and the study group by the random number table method,with 50 cases in each group.Both groups of patients received conventional antihypertensive,hypoglycemic,and antiplatelet therapy.The control group took 20 mg of atorvastatin calcium tablets orally,once a night.On the basis of the control group,the study group was additionally given 150 mg of evolocumab injection(a PCSK9 inhibitor)by subcutaneous injection,once every two weeks.Both groups of patients were followed up for 24 weeks.The levels of blood lipids,blood glucose,inflammatory cytokines,carotid intima-media thickness(IMT),atherosclerotic plaque score and adverse reactions of the patients in the two groups before and after treatment were detected and compared.Results The levels of TC,TG and LDL-C in the study group after treatment were lower than those before treatment and those in the control group at the same period,and the differences were statistically significant(P＜0.05).The levels of IL-1,IL-6,TNF-α,hs-CRP,as well as the ca-rotid IMT and atherosclerotic plaque score in the study group after treatment were lower than those before treatment and those in the control group at the same period,and the differences were statistically significant(P＜O.05).During the treatment period,there was no significant difference in the occurrence of adverse reac-tions between the two groups(P＞0.05).Conclusion The combination of PCSK9 inhibitor and atorvastatin can effectively regulate the blood lipid levels of patients with hypertension complicated and type 2 diabetes mellitus,alleviate the inflammatory response,and improve the degree of carotid atherosclerosis in these pa-tients.

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 assess the association of single nucleotide polymorphisms of rs700519 and rs4646 loci of cytochrome P450 19A1 ( CYP19A1) gene with risk of breast cancer. Methods:Two hundred patients with breast cancer treated at Xinxiang Central Hospital between January 2019 and January 2024 and 100 healthy individuals were enrolled as the study group and control group, respectively. The genotypes of the CYP19A1 gene at the rs700519 and rs4646 loci were determined by direct sequencing. The general data, distribution of CYP19A1 genotypes and alleles were compared between the two groups. This study has been approved by the Medical Ethics Committee of Xinxiang Central Hospital (Ethics No.2021-182). Results:No significant difference was found in age, body mass index, times of conception and proportion of menopause between the two groups ( P>0.05). The frequencies of AA genotype and A allele at the rs700519 locus, and the CC genotype and C allele at the rs4646 locus in the study group were significantly higher than those of the control group ( P<0.05). The frequencies of AA genotype at the rs700519 locus and CC genotype at the rs4646 locus in patients with breast cancer at stages Ⅲ-Ⅳ were significantly higher than those at stage Ⅰ-Ⅱ ( P<0.05). Conclusion:Polymorphisms of CYP19A1 gene at the rs700519 and rs4646 loci are associated with susceptibility of breast cancer. The AA and CC genotypes at the two loci may increase the risk for breast cancer.

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*

Objectives:To assess the situation of retained cardiac implantable electronic device(CIED)leads after cardiac transplantation,the associated factors,and their impact on long-term prognosis.Methods:A retrospective analysis was conducted on 1 096 patients who underwent cardiac transplantation at Fuwai Hospital of the Chinese Academy of Medical Sciences from January 1,2005 to January 1,2022.Among them,204 patients(18.6%)received CIED therapy before cardiac transplantation.Two physicians independently reviewed the pre-and post-transplant chest X-rays to determine the presence of retained CIED leads.Logistic multivariate regression analysis was used to assess factors associated with retained CIED leads,and Kaplan-Meier survival curves were plotted to analyze the impact of retained CIED leads on long-term prognosis.Results:Among the 204 patients who received CIED therapy before cardiac transplantation,the highest proportion were those treated with implantable cardioverter defibrillator(ICD)and cardiac resynchronization therapy-defibrillator(CRT-D),accounting for 47.5%(97/204)and 40.7%(83/204),respectively.The mean duration from CIED implantation to cardiac transplantation was(45.1±40.0)months,and 38 patients(18.6%)had retained CIED leads after cardiac transplantation.The results of the logistic multivariate regression analysis showed that the duration from CIED implantation to cardiac transplantation was the only factor associated with retained CIED leads after cardiac transplantation(OR=1.020,95%CI:1.011-1.030,P=0.000).Cumulative all-cause survival rates among patients without CIED implantation(n=892),those without retained CIED leads(n=166),and those with retained CIED leads(n=38)were 88.5%,93.3%and 84.2%,respectively.Kaplan-Meier survival curve analysis showed no significant difference in cumulative all-cause survival among the three groups(log-rank P=0.643).Conclusions:In patients who received CIED implantation before cardiac transplantation,18.6%had retained leads after surgery.The duration from CIED implantation to cardiac transplantation is the only factor associated with lead retained after cardiac transplantation,but retained leads does not affect the outcome post heart transplantation.

Objectives:To assess the situation of retained cardiac implantable electronic device(CIED)leads after cardiac transplantation,the associated factors,and their impact on long-term prognosis.Methods:A retrospective analysis was conducted on 1 096 patients who underwent cardiac transplantation at Fuwai Hospital of the Chinese Academy of Medical Sciences from January 1,2005 to January 1,2022.Among them,204 patients(18.6%)received CIED therapy before cardiac transplantation.Two physicians independently reviewed the pre-and post-transplant chest X-rays to determine the presence of retained CIED leads.Logistic multivariate regression analysis was used to assess factors associated with retained CIED leads,and Kaplan-Meier survival curves were plotted to analyze the impact of retained CIED leads on long-term prognosis.Results:Among the 204 patients who received CIED therapy before cardiac transplantation,the highest proportion were those treated with implantable cardioverter defibrillator(ICD)and cardiac resynchronization therapy-defibrillator(CRT-D),accounting for 47.5%(97/204)and 40.7%(83/204),respectively.The mean duration from CIED implantation to cardiac transplantation was(45.1±40.0)months,and 38 patients(18.6%)had retained CIED leads after cardiac transplantation.The results of the logistic multivariate regression analysis showed that the duration from CIED implantation to cardiac transplantation was the only factor associated with retained CIED leads after cardiac transplantation(OR=1.020,95%CI:1.011-1.030,P=0.000).Cumulative all-cause survival rates among patients without CIED implantation(n=892),those without retained CIED leads(n=166),and those with retained CIED leads(n=38)were 88.5%,93.3%and 84.2%,respectively.Kaplan-Meier survival curve analysis showed no significant difference in cumulative all-cause survival among the three groups(log-rank P=0.643).Conclusions:In patients who received CIED implantation before cardiac transplantation,18.6%had retained leads after surgery.The duration from CIED implantation to cardiac transplantation is the only factor associated with lead retained after cardiac transplantation,but retained leads does not affect the outcome post heart transplantation.

Oropharyngeal squamous cell carcinoma(OPSCC)is a malignant tumor originating from the squamous epithelium of the oro-pharyngeal mucosa,accounting for more than 90％of oropharyngeal malignancies.In recent years,human papillomavirus(HPV)infec-tion has become one of the primary etiological factors of oropharyngeal squamous carcinoma.The incidence of HPV-associated oropharyn-geal squamous carcinoma has been rising annually,with a noticeable trend toward younger populations,posing a significant threat to hu-man health.Due to the distinct biological behavior and clinical characteristics of HPV-associated oropharyngeal squamous carcinoma com-pared to its non-HPV-related counterpart,the diagnostic and treatment strategies for oropharyngeal squamous carcinoma have undergone substantial changes.Prevention and screening for oropharyngeal squamous carcinoma are of critical importance.The diagnostic and treat-ment process involves multi-disciplinary collaboration,including oral and maxillofacial surgery,otolaryngology,head and neck surgery,oncology,radiology and pathology.Based on evidence from clinical practice,a comprehensive,integrated diagnostic and therapeutic ap-proach has been established,centered around the concept of"prevention,screening,diagnosis,treatment,and rehabilitation",covering the entire patient lifecycle and providing a valuable reference for clinical practice.