Objective:To compare the diagnostic value of contrast-enhanced ultrasound(CEUS)combined with conventional ultrasound and magnetic resonance imaging(MRI)in distinguishing benign and malignant non-mass lesions of breast.Methods:A retrospective analysis was conducted on 131 patients with non-mass lesions of breast(76 benign cases,55 malignant cases),who were pathologically confirmed at The 910th Hospital of People's Liberation Army Joint Service Support Force from January 2019 to January 2024.The CEUS and MRI characteristics between benign and malignant non-mass lesions of breast were compared.Using pathological results as the gold standard,the receiver operating characteristic(ROC)curve were employed to compare the area under curve(AUC)value,sensitivity and specificity of CEUS+conventional ultrasound and MRI in diagnosing malignant non-mass lesions of breast.The diagnostic performances of them on non-mass lesions with different sizes(maximum diameter<10 mm,10-20 mm,and>20 mm)were further explored.Results:Conventional ultrasound identified 131 non-mass lesions of breast,whereas MRI identified 79 non-mass lesions(60.31%),40 cases with mass-like lesions(30.53%),and 12 normal breast(9.16%).The overall consistency between conventional ultrasound and MRI was higher(Kappa=0.603).After CEUS combined with conventional ultrasound,38 lesions that were classified as BI-RADS 4 by conventional ultrasound downgraded to BI-RADS 3.In the 131 patients,the specificity(71.1%)of CEUS combined with conventional ultrasound was significantly higher than that(55.3%)of MRI,with a statistically significant difference(x2=5.775,P=0.016).For all patients,the AUC value(0.828)of CEUS combined with conventional ultrasound in diagnosing malignant non-mass lesions of breast was higher than that(0.776)of MRI(Z=3.246,P=0.006).Among of them,the diagnostic AUC value of CEUS combined with ultrasound was 0.842 for the patients whose size of the non-mass lesions of breast was between 10-20 mm,which was significantly larger than that(0.758)of MRI(Z=4.856,P<0.001).Conclusions:The diagnostic specificity of CEUS+conventional ultrasound is higher than that of MRI for malignant non-mass lesions of breast,which has a certain of advantage.

Background and Objectives: SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms. Methods: Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes. Results: The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes. Conclusions This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.

Background and Objectives: SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms. Methods: Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes. Results: The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes. Conclusions This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.

Background and Objectives: SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms. Methods: Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes. Results: The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes. Conclusions This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.

Background and Objectives: SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms. Methods: Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes. Results: The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes. Conclusions This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.

Objective:To compare the diagnostic value of contrast-enhanced ultrasound(CEUS)combined with conventional ultrasound and magnetic resonance imaging(MRI)in distinguishing benign and malignant non-mass lesions of breast.Methods:A retrospective analysis was conducted on 131 patients with non-mass lesions of breast(76 benign cases,55 malignant cases),who were pathologically confirmed at The 910th Hospital of People's Liberation Army Joint Service Support Force from January 2019 to January 2024.The CEUS and MRI characteristics between benign and malignant non-mass lesions of breast were compared.Using pathological results as the gold standard,the receiver operating characteristic(ROC)curve were employed to compare the area under curve(AUC)value,sensitivity and specificity of CEUS+conventional ultrasound and MRI in diagnosing malignant non-mass lesions of breast.The diagnostic performances of them on non-mass lesions with different sizes(maximum diameter<10 mm,10-20 mm,and>20 mm)were further explored.Results:Conventional ultrasound identified 131 non-mass lesions of breast,whereas MRI identified 79 non-mass lesions(60.31%),40 cases with mass-like lesions(30.53%),and 12 normal breast(9.16%).The overall consistency between conventional ultrasound and MRI was higher(Kappa=0.603).After CEUS combined with conventional ultrasound,38 lesions that were classified as BI-RADS 4 by conventional ultrasound downgraded to BI-RADS 3.In the 131 patients,the specificity(71.1%)of CEUS combined with conventional ultrasound was significantly higher than that(55.3%)of MRI,with a statistically significant difference(x2=5.775,P=0.016).For all patients,the AUC value(0.828)of CEUS combined with conventional ultrasound in diagnosing malignant non-mass lesions of breast was higher than that(0.776)of MRI(Z=3.246,P=0.006).Among of them,the diagnostic AUC value of CEUS combined with ultrasound was 0.842 for the patients whose size of the non-mass lesions of breast was between 10-20 mm,which was significantly larger than that(0.758)of MRI(Z=4.856,P<0.001).Conclusions:The diagnostic specificity of CEUS+conventional ultrasound is higher than that of MRI for malignant non-mass lesions of breast,which has a certain of advantage.

The Qa-1 in mice is homologous to human leukocyte antigen E(HLA-E), and both of them belong to the non-classical major histocompatibility complex I b(MHC-I b) molecules. Qa-1 is capable of presenting self or exogenous antigen peptides to interact with two distinct receptors, namely T cell receptor (TCR) and natural killer cell group 2 member A (or C) (NKG2A/C), thus playing an important role in immune response and regulation. Qa-1-restricted regulatory CD8⁺ T cell (CD8⁺ Treg) is one of the most studied CD8⁺ Treg subgroups, which can maintain immune homeostasis and autoimmune tolerance by exerting immunosuppressive effects. Consequently, Qa-1-restricted CD8⁺Treg cells are closely associated with the occurrence and development of various clinical diseases, such as tumors, infections, autoimmune diseases, and transplant rejections. This paper provides a comprehensive review of the phenotypic characteristics, functional effects, regulatory mechanisms of Qa-1-restricted CD8⁺ Treg cells, as well as the latest research progresses of Qa-1-restricted CD8⁺ Treg cells involved in the pathogenesis of infectious diseases.
Humans ; Animals ; T-Lymphocytes, Regulatory/immunology* ; Histocompatibility Antigens Class I/immunology* ; CD8-Positive T-Lymphocytes/immunology* ; Communicable Diseases/immunology*

Objective To investigate the relationship between disease courses and severity and monocyte subsets distribution and surface CD31 intensity in patients of hemorrhagic fever with renal syndrome (HFRS). Methods Peripheral blood samples from 29 HFRS patients and 13 normal controls were collected. The dynamic changes of classical monocyte subsets (CD14⁺⁺CD16^-), intermediated monocyte subsets (CD14⁺⁺CD16⁺) and non-classical monocyte subsets (CD14⁺CD16⁺⁺) and the mean fluorescent intensity (MFI) of CD31 on monocyte subsets were detected by multiple-immunofluorescent staining and flow cytometry. Results In acute phase of HFRS, the ratio of classical monocyte subsets to total monocytes was dramatically decreased compared to convalescent phase and normal control. It was still much lower in convalescent phase compared to normal controls. The ratio of classical monocyte subsets to total monocytes were decreased in HFRS patients compared to that in normal control, whereas there was no difference between severe/critical groups and mild/moderate groups. On the contrary, the ratio of intermediate monocyte subsets to total monocytes in acute phase of HFRS was significantly increased compared to convalescent phase and normal control. The ratio of intermediate monocyte subsets to total monocytes were increased in HFRS patients compared to that in normal control, whereas no difference was found between severe/critical groups and mild/moderate groups. Phases or severity groups had no difference in ratio of non-classical monocyte subsets to total monocytes. Additionally, the ratio of classical monocyte subsets had a tendency to decline and that of intermediate monocyte subsets showed an increase both to total monocytes between the acute and convalescent phases in 11 HFRS patients with paired-samples. Moreover, in acute phase of HFRS, the mean fluorescent intensity (MFI) of CD31 on three monocyte subsets all decreased, specifically classical monocyte subsets showed the highest MFI of CD31 while the normal control reported the highest MFI of CD31 in non-classical monocyte subsets. In convalescent phase, the MFI of CD31 on classical and intermediated monocyte subsets were both lower than that of normal control, while MFI of CD31 was still significantly lower than normal control on non-classical monocyte subsets. Finally, MFI of CD31 on classical and intermediated monocyte subsets in severe/critical group were both lower than those in mild/moderate group, showing no statistical difference in MFI of CD31 on non-classical monocyte subset across groups of different disease severity. Conclusion The ratio of classical and intermediated monocyte subsets to total monocytes are correlated with the course of HFRS, and so are the surface intensity of CD31 on these monocyte subsets with the disease course and severity. The surface intensity of CD31 on non-classical monocyte subsets, however, is correlated only with the course of the disease. Together, the underlying mechanisms for the observed changes in monocyte subsets in HFRS patients should be further investigated.
Humans ; Monocytes ; Lipopolysaccharide Receptors ; Hemorrhagic Fever with Renal Syndrome ; Receptors, IgG ; Disease Progression

The concept of "ntigen"is a relative one. The narrow concept of it condenses the process of activation of adaptive immune response and re-recognition of the same antigen, revealing the protective mechanism of vaccines with great significance for research and development of vaccines. However, the narrow concept involves adaptive immune system members: B cells, T cells and their effector products, which is difficult for beginners to understand the inherent meaning. Meanwhile, antigen classification fully summarizes the immune response process, so a variety of classification approach increases the difficulty in learning. Our teaching team analyzes the difficulties of this chapter in depth, and we implements the strategy that takes antibody structure and function as the breakthrough point and simplified adaptive immune response process as the core in teaching. A mind map that includes the main contents of this chapter is made during the process, which promotes the effectiveness of classroom teaching greatly.
Learning ; Vaccines ; Antibodies

Objective To evaluate the diagnostic value of contrast-enhanced ultrasound(CEUS) in regenerative nodules(RNs)and small hepatocellular carcinoma(sHCC).Methods Thirty-four cases of liver cirrhosis with small nodule were examined by CEUS.Among these cases,18 cases with 20 lesions were diagnosed s HCC,16 cases with 18 lesions were diagnosed RN eventually,all the diagnoses were confirmed by pathology.Perfusion characteristic and quantitative difference of RNs and sHCC were summarized.Results ①The majority of sHCC showed hyper-enhancement during the arterial phase,iso-enhancement or hypo-enhancement during the portal phase,hypo-enhancement during the late phase.The enhanced phase and degree of RNs were diverse,most of RNs showed iso enhancement during the three phases.The enhanced phase of two groups had significant difference(P ＜0.05).②The enhancement type of RNs and sHCC had no significant difference (P ＞ 0.05).③ 11 of 20 sHCC lesions showed contrast-enhancement pattern of fast-in and slow-out,9 lesions were fast-in and fast-out;among 18 RNs,1 lesion enhanced during the portal phase and the late phase,it didn't enhanced during the arterial phase,3 lesions started to enhanced at the late arterial phase,14 lesions were iso-enhancement during the three phases.④Comparison of parameters of RNs and the adjacent liver parenchyma had no significant difference(P ＞0.05).Compared with the adjacent liver parenchyma or RNs,the arrival time and peak time were shorter,the peak intensity and the curve sharpness were higher in sHCC (P ＜ 0.05).Conclusions CEUS is a useful method to distinguish RNs and sHCC in liver cirrhosis.