Photon-counting CT (PCCT) uses semiconductor detectors to directly convert X-ray photons to electrical signals, the intensity of which is directly proportional to the energy of the individual photons. PCCT offers several advantages in cardiovascular imaging, including ultra-high-resolution (UHR) imaging, improved multi-energy capabilities, reduced noise and artifacts, and improved iodine signal and radiation dose efficiencies. UHR imaging enhances the assessment of small vessels, dense calcifications, and stents. Multienergy mode enhances the iodine signal, reduces artifacts, and allows for material separation and lesion characterization. In this article, we review PCCT technology, highlight the benefits of PCCT in cardiovascular imaging using case examples, and discuss its challenges.

Objective To design an outpatient intelligent service platform based on medical insurance electronic vouchers(MIEVs)to enhance treatment efficiency and insured patients'experience.Methods The platform with a 4-tier architecture realized electronic medical insurance service by building a medical insurance service middleware,adopted direct payment mode for transaction,and implemented embedded application of the MIEV-based whole process of outpatient diagnosis and treatment by transforming the links of diagnosis and treatment and the hospital information system.The medical insurance service middleware was designed with ASP.NET WebAPI and developed with C# language,which provided unified standard interfaces to the outside world with the mode how hypertext transfer protocol secure(HTTPS)called JavaScript object notation(JSON)data.There were three functional modules for appointment,consultation registration and electronic medical insurance settlement involved in the platform.Results The platform provided insured patients with a two-way medical care mode of real-name authentication,online registration,offline consultation and mobile medical insurance payment,realizing the integration of online and offline medical insurance services and improving the operational efficiency of hospitals.Conclusion The platform enhances the outpatient efficiency and promotes smart hospital services.[Chinese Medical Equipment Journal,2024,45(12):45-49]

Objective To design an outpatient intelligent service platform based on medical insurance electronic vouchers(MIEVs)to enhance treatment efficiency and insured patients'experience.Methods The platform with a 4-tier architecture realized electronic medical insurance service by building a medical insurance service middleware,adopted direct payment mode for transaction,and implemented embedded application of the MIEV-based whole process of outpatient diagnosis and treatment by transforming the links of diagnosis and treatment and the hospital information system.The medical insurance service middleware was designed with ASP.NET WebAPI and developed with C# language,which provided unified standard interfaces to the outside world with the mode how hypertext transfer protocol secure(HTTPS)called JavaScript object notation(JSON)data.There were three functional modules for appointment,consultation registration and electronic medical insurance settlement involved in the platform.Results The platform provided insured patients with a two-way medical care mode of real-name authentication,online registration,offline consultation and mobile medical insurance payment,realizing the integration of online and offline medical insurance services and improving the operational efficiency of hospitals.Conclusion The platform enhances the outpatient efficiency and promotes smart hospital services.[Chinese Medical Equipment Journal,2024,45(12):45-49]

BACKGROUND: There is still uncertainty regarding whether diabetes mellitus (DM) can adversely affect patients undergoing carotid endarterectomy (CEA) for carotid stenosis. The aim of the study was to assess the adverse impact of DM on patients with carotid stenosis treated by CEA. METHODS: Eligible studies published between 1 January 2000 and 30 March 2023 were selected from the PubMed, EMBASE, Web of Science, CENTRAL, and ClinicalTrials databases. The short-term and long-term outcomes of major adverse events (MAEs), death, stroke, the composite outcomes of death/stroke, and myocardial infarction (MI) were collected to calculate the pooled effect sizes (ESs), 95% confidence intervals (CIs), and prevalence of adverse outcomes. Subgroup analysis by asymptomatic/symptomatic carotid stenosis and insulin/noninsulin-dependent DM was performed. RESULTS: A total of 19 studies (n = 122,003) were included. Regarding the short-term outcomes, DM was associated with increased risks of MAEs (ES = 1.52, 95% CI: [1.15-2.01], prevalence = 5.1%), death/stroke (ES = 1.61, 95% CI: [1.13-2.28], prevalence = 2.3%), stroke (ES = 1.55, 95% CI: [1.16-1.55], prevalence = 3.5%), death (ES = 1.70, 95% CI: [1.25-2.31], prevalence =1.2%), and MI (ES = 1.52, 95% CI: [1.15-2.01], prevalence = 1.4%). DM was associated with increased risks of long-term MAEs (ES = 1.24, 95% CI: [1.04-1.49], prevalence = 12.2%). In the subgroup analysis, DM was associated with an increased risk of short-term MAEs, death/stroke, stroke, and MI in asymptomatic patients undergoing CEA and with only short-term MAEs in the symptomatic patients. Both insulin- and noninsulin-dependent DM patients had an increased risk of short-term and long-term MAEs, and insulin-dependent DM was also associated with the short-term risk of death/stroke, death, and MI. CONCLUSIONS In patients with carotid stenosis treated by CEA, DM is associated with short-term and long-term MAEs. DM may have a greater impact on adverse outcomes in asymptomatic patients after CEA. Insulin-dependent DM may have a more significant impact on post-CEA adverse outcomes than noninsulin-dependent DM. Whether DM management could reduce the risk of adverse outcomes after CEA requires further investigation.
Humans ; Endarterectomy, Carotid/adverse effects* ; Carotid Stenosis/surgery* ; Risk Factors ; Treatment Outcome ; Time Factors ; Stents/adverse effects* ; Diabetes Mellitus, Type 2/complications* ; Diabetes Mellitus, Type 1 ; Stroke/complications* ; Insulin/therapeutic use* ; Myocardial Infarction/complications* ; Risk Assessment

Muscle, Smooth, Vascular ; RNA, Long Noncoding/genetics* ; Cell Proliferation/genetics* ; Myocytes, Smooth Muscle ; Cells, Cultured

Photon-counting detector (PCD) CT is a new CT technology utilizing a direct conversion X-ray detector, where incident X-ray photon energies are directly recorded as electronical signals. The design of the photon-counting detector itself facilitates improvements in spatial resolution (via smaller detector pixel design) and iodine signal (via count weighting) while still permitting multi-energy imaging. PCD-CT can eliminate electronic noise and reduce artifacts due to the use of energy thresholds. Improved dose efficiency is important for low dose CT and pediatric imaging. The ultra-high spatial resolution of PCD-CT design permits lower dose scanning for all body regions and is particularly helpful in identifying important imaging findings in thoracic and musculoskeletal CT. Improved iodine signal may be helpful for low contrast tasks in abdominal imaging. Virtual monoenergetic images and material classification will assist with numerous diagnostic tasks in abdominal, musculoskeletal, and cardiovascular imaging. Dual-source PCD-CT permits multi-energy CT images of the heart and coronary arteries at high temporal resolution. In this special review article, we review the clinical benefits of this technology across a wide variety of radiological subspecialties.

Objective:To investigate the role of CUL4B-RING E3 ubiquitin ligase (CRL4B) complex in pancreatic tumorigenesis and the molecular mechanism.Methods:Pancreatic cells were divided into control group (transfected with negative control lentivirus), shCUL4B group (transfected with CUL4B lentivirus), shDDB1 group [transfected with DNA damage binding protein 1 (DDB1) lentivirus], and shCUL4B+ siSFRP1 group (transfected with CUL4B lentivirus and SFRP1-siRNA). RNA-seq was performed in pancreatic cancer cell lines with CUL4B and DDB1 knocked down respectively, to identify the target genes regulated by CRL4B complex. Real-time fluorescent quantitative polymerase chain reaction (qRT-PCR) was used to detect the mRNA expression levels of target genes. Chromatin immunoprecipitation (ChIP) assay was used to identify the target genes directly regulated by CUL4B and DDB1. Western blot was used to detect the protein expression levels of the epithelial-mesenchymal transition (EMT) markers. The EdU cell proliferation test was used to detect cell proliferation ability. The scratch repair test and Transwell cell invasion test were used to detect cell migration and invasion ability. Finally, the sequencing data of pancreatic cancer-related tumor samples and normal samples in GEO, TCGA and GTEx databases were used to analyze the expression correlations of CUL4B, DDB1 and their downstream target genes.Results:RNA-seq results showed that target genes regulated by CRL4B complex involved in a number of malignant tumor-related signaling pathways. qRT-PCR results verified that the mRNA expression levels of the target genes of CUL4B or DDB1 knockdown groups were higher than those of the control group, and the difference was statistically significant ( P<0.05). ChIP-PCR results showed that CRL4B complex directly bound to the promoter regions of the target genes, NME1 and SFRP1, and the enrichment of monoubiquitination of lysine at 119 of histone H2A (H2AK119ub1) in the promoter region of target gene was reduced after CUL4B knockdown. The proliferation rate in PANC-1 cell line of the control group was (32.10±3.58)%, higher than (13.95±1.66)% in the shCUL4B group and (22.38±0.77)% in the shCUL4B+ siSFRP1 group ( P<0.05). The proliferation rate in AsPC-1 cell line of the control group was (35.47±7.80)%, higher than (19.60±3.58)% in the shCUL4B group and (30.09±0.81)% in the shCUL4B+ siSFRP1 group ( P<0.05). The scratch repair experiment showed that the migration rate of PANC-1 cell line control group was (53.18±3.70)%, higher than that (17.46±2.62)% in the shCUL4B group and (44.99±9.18)% in the shCUL4B + siSFRP1 group ( P<0.05). Western blot showed the expression levels of epithelial markers including α-catenin and γ-catenin in the control group were 1.00±0.03 and 1.01±0.11, respectively, lower than 1.44±0.01 and 1.21±0.06 in the shCUL4B group ( P<0.05). The expression levels of mesenchymal markers including fibronectin and vimentin in the control group were 1.01±0.14 and 1.02±0.18, respectively, higher than 1.53±0.13 and 1.22±0.07 in the shCUL4B+ siSFRP1 group ( P<0.05). The cell metastasis rate of the control group was (100.00±3.96)%, higher than the (35.49±0.34)% in the shCUL4B group and (107.06±2.77)% in the shCUL4B+ siSFRP1 group, the difference was statistically significant ( P<0.05). The expressions of CUL4B and DDB1 were significantly upregulated in the pancreatic cancer tissues, and were negatively correlated with the expression of SFRP1 ( r=-0.342 and r=-0.264, respectively). Conclusions:CRL4B complex inhibits the transcription of target gene SFRP1 and promotes the development of pancreatic cancer. Moreover, CRL4B complex is upregulated in pancreatic cancer, which provide a potential of therapeutic target for pancreatic cancer.

In the past,treatment of acute ilio-femoral deep vein thrombosis (IFDVT) was mainly based on anticoagulation alone,but 30%-50% of patients will develop post-thrombotic syndrome,causing a serious medical burden.Thrombus removal technology such as catheter-directed thrombolysis and percutaneous mechanical thrombectomy can effectively remove blood clots and compensate for the deficiencies of simple anticoagulation,which is expected to improve the prognosis of such disease,but the current evidence is insufficient,and other treatments such as filter implantation and compression therapy are also controversial.This article summarizes the treatment strategies and the latest progress of acute IFDVT,hoping to help the treatment of this type of disease.

Objective:To investigate the role of CUL4B-RING E3 ubiquitin ligase (CRL4B) complex in pancreatic tumorigenesis and the molecular mechanism.Methods:Pancreatic cells were divided into control group (transfected with negative control lentivirus), shCUL4B group (transfected with CUL4B lentivirus), shDDB1 group [transfected with DNA damage binding protein 1 (DDB1) lentivirus], and shCUL4B+ siSFRP1 group (transfected with CUL4B lentivirus and SFRP1-siRNA). RNA-seq was performed in pancreatic cancer cell lines with CUL4B and DDB1 knocked down respectively, to identify the target genes regulated by CRL4B complex. Real-time fluorescent quantitative polymerase chain reaction (qRT-PCR) was used to detect the mRNA expression levels of target genes. Chromatin immunoprecipitation (ChIP) assay was used to identify the target genes directly regulated by CUL4B and DDB1. Western blot was used to detect the protein expression levels of the epithelial-mesenchymal transition (EMT) markers. The EdU cell proliferation test was used to detect cell proliferation ability. The scratch repair test and Transwell cell invasion test were used to detect cell migration and invasion ability. Finally, the sequencing data of pancreatic cancer-related tumor samples and normal samples in GEO, TCGA and GTEx databases were used to analyze the expression correlations of CUL4B, DDB1 and their downstream target genes.Results:RNA-seq results showed that target genes regulated by CRL4B complex involved in a number of malignant tumor-related signaling pathways. qRT-PCR results verified that the mRNA expression levels of the target genes of CUL4B or DDB1 knockdown groups were higher than those of the control group, and the difference was statistically significant ( P<0.05). ChIP-PCR results showed that CRL4B complex directly bound to the promoter regions of the target genes, NME1 and SFRP1, and the enrichment of monoubiquitination of lysine at 119 of histone H2A (H2AK119ub1) in the promoter region of target gene was reduced after CUL4B knockdown. The proliferation rate in PANC-1 cell line of the control group was (32.10±3.58)%, higher than (13.95±1.66)% in the shCUL4B group and (22.38±0.77)% in the shCUL4B+ siSFRP1 group ( P<0.05). The proliferation rate in AsPC-1 cell line of the control group was (35.47±7.80)%, higher than (19.60±3.58)% in the shCUL4B group and (30.09±0.81)% in the shCUL4B+ siSFRP1 group ( P<0.05). The scratch repair experiment showed that the migration rate of PANC-1 cell line control group was (53.18±3.70)%, higher than that (17.46±2.62)% in the shCUL4B group and (44.99±9.18)% in the shCUL4B + siSFRP1 group ( P<0.05). Western blot showed the expression levels of epithelial markers including α-catenin and γ-catenin in the control group were 1.00±0.03 and 1.01±0.11, respectively, lower than 1.44±0.01 and 1.21±0.06 in the shCUL4B group ( P<0.05). The expression levels of mesenchymal markers including fibronectin and vimentin in the control group were 1.01±0.14 and 1.02±0.18, respectively, higher than 1.53±0.13 and 1.22±0.07 in the shCUL4B+ siSFRP1 group ( P<0.05). The cell metastasis rate of the control group was (100.00±3.96)%, higher than the (35.49±0.34)% in the shCUL4B group and (107.06±2.77)% in the shCUL4B+ siSFRP1 group, the difference was statistically significant ( P<0.05). The expressions of CUL4B and DDB1 were significantly upregulated in the pancreatic cancer tissues, and were negatively correlated with the expression of SFRP1 ( r=-0.342 and r=-0.264, respectively). Conclusions:CRL4B complex inhibits the transcription of target gene SFRP1 and promotes the development of pancreatic cancer. Moreover, CRL4B complex is upregulated in pancreatic cancer, which provide a potential of therapeutic target for pancreatic cancer.

In the past,treatment of acute ilio-femoral deep vein thrombosis (IFDVT) was mainly based on anticoagulation alone,but 30%-50% of patients will develop post-thrombotic syndrome,causing a serious medical burden.Thrombus removal technology such as catheter-directed thrombolysis and percutaneous mechanical thrombectomy can effectively remove blood clots and compensate for the deficiencies of simple anticoagulation,which is expected to improve the prognosis of such disease,but the current evidence is insufficient,and other treatments such as filter implantation and compression therapy are also controversial.This article summarizes the treatment strategies and the latest progress of acute IFDVT,hoping to help the treatment of this type of disease.