PURPOSE:To evaluate the safety and efficacy of debulking with drug-coated balloon angioplasty (DCB) for femoropopliteal in-stent restenosis (FP-ISR) treatment. METHODS:Embase, PubMed, and the Cochrane Library were searched from January 2004 to August 2025 for studies evaluating debulking with DCB treatment of FP-ISR. A meta-analysis was performed to assess the technical success, bailout stenting, postoperative embolization, amputation, 6- and 12-month primary patency rates, and 12-month target lesion revascularization (TLR). RESULTS:Seven studies (three randomized controlled trials and four retrospective cohort studies) involving 584 patients were included; 281 underwent debulking with DCB and 303 underwent DCB alone. The technical success, bailout stenting, postoperative embolization, and 6- and 12-month primary patency rates did not differ between groups. However, debulking with DCB was associated with a lower amputation rate than that with DCB alone ([RR] 0.37, 95% CI 0.18-0.75, P = 0.006) and reduced TLR risk at 12 months ([RR] 0.58, 95% CI 0.38-0.88, P = 0.01). Subgroup analysis indicated that the combined treatment was associated with improved 12-month primary patency ([RR] 1.66, 95% CI 1.19-2.34, P = 0.003) and reduced TLR ([RR] 0.35, 95% CI 0.18-0.69, P = 0.002) for lesion length >20 cm or Tosaka type III lesions. CONCLUSION:Debulking with DCB reduces amputation risk and 12-month TLR in patients with FP-ISR, particularly those with long lesions (>20 cm) or occlusive lesions (Tosaka type III), in whom it may improve 12-month primary patency. However, the advantages require further confirmation because of the limited number of studies.

Digital subtraction angiography (DSA) devices guide procedures across numerous diseases, performed on more than 100,000 patients daily worldwide. However, these procedures expose patients and healthcare providers to radiation, increasing the risk of health issues. Despite many low-dose DSA imaging methods proposed, none have been prospectively clinically validated. In this study, 46,829 patients (over 5 million DSA images) from 70 centers were used to iterate our previously developed generative artificial intelligence system (named GenDSA-V2). A total of 1,068 patients (533 in intervention arm and 535 in control arm), with suspected cerebral aneurysms (n = 435), lung cancer (n = 417) or advanced liver cancer (n = 216), meeting surgical criteria, were enrolled to validate the GenDSA-V2. The primary outcome was radiation dose, while secondary outcomes included efficiency, operation time and intraoperative complications. Group assignments were blinded to patients, surgeons and investigators, while technicians were aware but not involved in data collection or analysis. The GenDSA-V2 group showed substantially reduced radiation exposure, with an air kerma (AK) of 151.3 ± 125.1 mGy compared to 457.4 ± 407.4 mGy in the standard clinical protocols (SCP) group (mean difference = -306.1 mGy, 95% confidence interval (CI) = -342.3 to -269.9, P < 0.001 for superiority) and a dose-area product (DAP) of 4009.7 ± 2767.9 μGy m2 versus 12531.6 ± 9145.9 μGy m2 (mean difference = -8521.9 μGy m2, 95% CI = -9333.1 to -7710.7, P < 0.001 for superiority). Mean operation time was 33.1 ± 10.8 min in the SCP group and 34.8 ± 11.8 min in the GenDSA-V2 group (mean difference = 1.7 min, 95% CI = 0.3 to 3.1, P < 0.001 for noninferiority). Complication rates were similar (SCP = 8.1%, GenDSA-V2 = 7.5%, mean difference = -0.6%, 95% CI = -3.8% to 2.6%, P < 0.001 for noninferiority). The GenDSA system reduces radiation exposure to both physicians and patients by approximately two-thirds during DSA-guided procedures, demonstrating substantial clinical and translational value. Chinese Clinical Trial Registry: ChiCTR2400084789 .

Atherosclerosis is a disorder of lipid metabolism, but its pathogenesis has not yet been fully elucidated. This study aimed to clarify the roles of homeodomain interacting protein kinase 2 (HIPK2) in atherosclerosis. Atherosclerotic model was constructed by feeding apolipoprotein E knockout (ApoE-/-) mice with a high-fat diet. Human THP-1 macrophages and mouse RAW 264.7 macrophages were stimulated with IFN-gamma to establish an in vitro model. We showed an upregulation of HIPK2 in the aorta of atherosclerotic mice. HIPK2 knockdown reduced macrophage infiltration, M1 polarization, and attenuates atherosclerosis development. Downregulation of HIPK2 in macrophages led to a significant suppression in the expression of pro-inflammatory factors, which was accompanied by an enhancement in the phosphorylation and degradation of (3-catenin, as well as the activation of the signal transducer and activator of transcription 1 (STAT1) signaling pathway. Silencing of HIPK2 alone in THP-1 macrophages resulted in anti-inflammatory effects and suppression of M1 macrophage polarization. However, simultaneous silencing of HIPK2 and (3-catenin (CTNNB1) reversed these effects, counteracting the outcomes observed with HIPK2 silencing alone. We validated that small ubiquitin-like modifier (SUMO)-specific peptidase 1 (SENP1) regulated HIPK2 function by affecting the SUMOylation of HIPK2 at the K32 site. SENP1 knockdown promoted HIPK2 SUMOylation, impairing its protein stability. In the rescue experiments, IFN-gamma-induced inflammation and M1 polarization were resumed upon restoration of HIPK2 expression in SENP1-silenced macrophages. Our work demonstrated that HIPK2 accelerated the progression of atherosclerosis by regulating (3-catenin/STAT1 signaling cascade to promote macrophage infiltration and M1 polarization. HIPK2 was regulated by SENP1-mediated de-SUMOylation.

Atherosclerosis is a disorder of lipid metabolism, but its pathogenesis has not yet been fully elucidated. This study aimed to clarify the roles of homeodomain interacting protein kinase 2 (HIPK2) in atherosclerosis. Atherosclerotic model was constructed by feeding apolipoprotein E knockout (ApoE-/-) mice with a high-fat diet. Human THP-1 macrophages and mouse RAW 264.7 macrophages were stimulated with IFN-γ to establish an in vitro model. We showed an upregulation of HIPK2 in the aorta of atherosclerotic mice. HIPK2 knockdown reduced macrophage infiltration, M1 polarization, and attenuates atherosclerosis development. Downregulation of HIPK2 in macrophages led to a significant suppression in the expression of pro-inflammatory factors, which was accompanied by an enhancement in the phosphorylation and degradation of β-catenin, as well as the activation of the signal transducer and activator of transcription 1 (STAT1) signaling pathway. Silencing of HIPK2 alone in THP-1 macrophages resulted in anti-inflammatory effects and suppression of M1 macrophage polarization. However, simultaneous silencing of HIPK2 and β-catenin (CTNNB1) reversed these effects, counteracting the outcomes observed with HIPK2 silencing alone. We validated that small ubiquitin-like modifier (SUMO)-specific peptidase 1 (SENP1) regulated HIPK2 function by affecting the SUMOylation of HIPK2 at the K32 site. SENP1 knockdown promoted HIPK2 SUMOylation, impairing its protein stability. In the rescue experiments, IFN-γ-induced inflammation and M1 polarization were resumed upon restoration of HIPK2 expression in SENP1-silenced macrophages. Our work demonstrated that HIPK2 accelerated the progression of atherosclerosis by regulating β-catenin/STAT1 signaling cascade to promote macrophage infiltration and M1 polarization. HIPK2 was regulated by SENP1-mediated de-SUMOylation.

Pyroptosis, a novel form of programmed cell death, has been implicated in neurodegeneration diseases. However, its role in status epilepticus (SE)—a condition characterized by prolonged or repeated seizures—remains inadequately understood. SE were induced by intraperitoneal injection of pilocarpine (PILO). Neuronal excitability was assessed through electroencephalogram (EEG) recordings and patch clamp. Chromatin immunoprecipitation (ChIP) assay was applied to verify the interaction of phosphorylated signal transducer and activator of transcription 3 (p-STAT3) protein with the promoters of Nlrp3 (the gene encoding NOD-like receptor family pyrin domain containing 3) and Trpm7 (transient receptor potential melastatin 7). To further investigate the role of TRPM7 in SE, AAV-sh-TRPM7-EGFP transfected mice and TRPM7 conditional knockout (TRPM7-CKO) mice were utilized. Our findings revealed elevated levels of IL-18 and IL-1β levels in primary epilepsy patients, along with increased expression level of the TRPM7 in SE models. Knockdown of TRPM7 alleviated neuronal damage and pyroptosis, reversing PILO-treated neuronal hyperexcitability. We demonstrated that p-STAT3 binds to the promoters of both Trpm7 and Nlrp3, modulating their transcriptions in SE. Importantly, inhibition of TRPM7 with NS8593, and inflammasome inhibition with MCC950, alleviated neuronal hyperexcitability and pyroptosis in SE. A new compound, SDUY-225, formulated based on the structure of NS8593 mitigated neuronal damage, pyroptosis, and hyperexcitability. TRPM7 contributes to pyroptosis in SE, establishing a positive feedback loop involving the p-STAT3/TRPM7/Zn2+/p-STAT3 signaling pathway. Findings in this study raise the possibility that targeting TRPM7 and NLRP3 represents a promising therapeutic approach for SE.

Hepatocellular carcinoma (HCC) is the prevailing subtype of hepatocellular malignancy. While previous investigations have evidenced a robust link with programmed cell death (PCD) and tumorigenesis, a comprehensive inquiry targeting the relationship between multiple PCDs and HCC remains scant. Our aim was to develop a predictive model for different PCD patterns in order to investigate their impact on survival rates, prognosis and drug response rates in HCC patients. We performed functional annotation and pathway analysis on identified PCD-related genes (PCDRGs) using multiple bioinformatics tools. The prognostic value of these PCDRGs was verified through a dataset obtained from GEO. Consensus clustering analysis was utilized to elucidate the correlation between diverse PCD clusters and pertinent clinical characteristics. To comprehensively uncover the distinct PCD regulatory patterns, our analysis integrated gene expression profiling, immune cell infiltration and enrichment analysis. To predict survival differences in HCC patients, we established a PCD model. To enhance the clinical applicability for the model, we developed a highly accurate nomogram. To address the treatment of HCC, we identified several promising chemotherapeutic agents and novel targeted drugs. These drugs may be effective in treating HCC and could improve patient outcomes. To develop a cell death feature for HCC patients, we conducted an analysis of 12 different PCD mechanisms using eligible data obtained from public databases. Through this analysis, we were able to identify 1254 PCDRGs likely to contribute to cell death on HCC. Further analysis of 1254 PCDRGs identified 37 genes with prognostic value in HCC patients. These genes were then categorized into two PCD clusters A and B. The categorization was based on the expression patterns of the genes in the different clusters. Patients in PCD cluster B had better survival probabilities. This suggests that PCD mechanisms, as represented by the genes in cluster B, may have a protective effect against HCC progression. Furthermore, the expression of PCDRGs was significantly higher in PCD cluster A, indicating that this cluster may be more closely associated with PCD mechanisms. Furthermore, our observations indicate that patients exhibiting elevated tumour mutation burden (TMB) are at an augmented risk of mortality, in comparison to those displaying low TMB and low-risk statuses, who are more likely to experience prolonged survival. In addition, we have investigated the potential distinctions in the susceptibility of diverse risk cohorts towards emerging targeted therapies, designed for the treatment of HCC. Moreover, our investigation has shown that AZD2014, SB505124, LJI308 and OSI-207 show a greater efficacy in patients in the low-risk category. Conversely, for the high-risk group patients, PD173074, ZM447439 and CZC24832 exhibit a stronger response. Our findings suggest that the identification of risk groups and personalized treatment selection could lead to better clinical outcomes for patients with HCC. Furthermore, significant heterogeneity in clinical response to ICI therapy was observed among HCC patients with varying PCD expression patterns. This novel discovery underscores the prospective usefulness of these expression patterns as prognostic indicators for HCC patients and may aid in tailoring targeted treatment for those of distinct risk strata. Our investigation introduces a novel prognostic model for HCC that integrates diverse PCD expression patterns. This innovative model provides a novel approach for forecasting prognosis and assessing drug sensitivity in HCC patients, driving a more personalized and efficacious treatment paradigm, elevating clinical outcomes. Nonetheless, additional research endeavours are required to confirm the model's precision and assess its potential to inform clinical decision-making for HCC patients.

Background and aims: Atherosclerosis (AS), an arterial vasculature disease, is characterized by abnormal lipid accumulation and inflammatory response. ADP ribosylation factor like GTPase 11 (ARL11) is linked to multifarious processes in cells. This study aims to clarify the underlying mechanism of ARL11 in AS. Methods: ApoE(-/-) mice fed with high-fat diet were used as mouse model of AS. Gene expression in AS was determined by mRNA-sequencing. ARL11 expression was detected by real-time PCR, Western blot and immunofluorescence. M1 polarization of macrophages was indicated by TNF-alpha and IL-6 levels as detected with ELISA, and iNOS expression determined by real-time PCR and Western blot. The role of ARL11 during AS was explored through loss-of-function analysis. Results: There were 1301 upregulated and 1110 downregulated genes during AS. These differentially expressed genes (DEGs) were mainly enriched in pathways and terms which are involved in inflammation. Moreover, Arl11 was highly expressed in AS models. Downregulation of Arl11 decreased lipid deposition and atherosclerotic plaques in the aortas of AS mice, and declined inflammatory cytokines and M1 polarization of macrophages induced by IFN-gamma. Furthermore, ARL11 interacted with JAK2 and p-JAK2 and modulated their degradation, thus inhibiting the activation of JAK2/STAT1 pathway. Conclusions: ARL11 promoted the development of AS via interacting with JAK2 and activating JAK2/STAT1 pathway. Thus, silencing ARL11 may prevent the process of AS and be a novel way to treat AS.

Atherosclerosis (AS), a metabolic disorder, is usually caused by chronic inflammation. LETM1 Domain-Containing Protein 1 (LETMD1) is a mitochondrial outer membrane protein required for mitochondrial structure. This study aims to evaluate the functional role of LETMD1 in endothelial pathogenesis of AS. Oxidized low-density lipoprotein (ox-LDL)-induced human umbilical vein endothelial cells (HUVECs) and high-fat diet apolipoprotein E-deficient (ApoE−/−) mice were used to establish in vitro and in vivo models, respectively. Recombinant adenovirus vectors were constructed to investigate the role of LETMD1 in AS. mRNA sequencing was used to explore the effect of LETMD1 overexpression on gene expression in ox-LDL-induced HUVECs. A dual-luciferase reporting assay and chromatin immunoprecipitation (ChIP)-PCR were further conducted to verify the relationship between KLF4 and LETMD1. Results showed that LETMD1 was highly expressed in the aortas of atherosclerotic animals. LETMD1 overexpression reduced the expression of inflammatory factors, pyroptosis, ROS production, and NF-κB activation in ox-LDL-induced HUVECs, whereas LETMD1 knockdown had the opposite impact. LETMD1 overexpression was involved in regulating gene expression in ox-LDL-induced HUVECs. Overexpression of LETMD1 in mice reduced serum lipid levels as well as atherosclerotic lesions in the aortic roots. Furthermore, LETMD1 overexpression suppressed inflammatory reactions, cell pyroptosis, nuclear p65 protein level, cell apoptosis, and ROS generation in the aortas of AS mice. KLF4 (Krüppel-like factor 4) was found to be the transcriptional regulator of LETMD1. In conclusion, LETMD1, a target of KLF4, hinders endothelial inflammation and pyroptosis, which is a mechanism inhibiting the development of atherosclerosis.

Hepatocellular carcinoma (HCC) is one of the most common gastrointestinal malignancies, characterized by insidious onset and high propensity for metastasis and recurrence. Apart from surgical resection, there are no effective curative methods for HCC in recent years, due to resistance to radiotherapy and chemotherapy. Heat shock proteins (HSP) play a crucial role in maintaining cellular homeostasis and normal organism development as molecular chaperones for intracellular proteins. Both basic research and clinical data have shown that HSPs are crucial participants in the HCC microenvironment, as well as the occurrence, development, metastasis, and resistance to radiotherapy and chemotherapy in various malignancies, particularly liver cancer. This review aims to discuss the molecular mechanisms and potential clinical value of HSPs in HCC, which may provide new insights for HSP-based therapeutic interventions for HCC.

Atherosclerosis (AS), characterized by a maladaptive inflammatory response, is one of the most common causes of death among the elderly. Karyopherin subunit alpha 2 (KPNA2), a member of the nuclear transport protein family, has been reported to play a pro-inflammatory role in various pathological processes by regulating the nuclear translocation of pro-inflammatory transcription factors. However, the function of KPNA2 in AS remains unknown. ApoE −/− mice were fed high-fat diets for 12 weeks to establish an AS mice model. Human umbilical vein endothelial cells (HUVECs) were treated with lipopolysaccharide (LPS) to establish an AS cell model. We found that KPNA2 was upregulated in the aortic roots of atherosclerotic mice and LPS-stimulated cells. KPNA2 knockdown inhibited LPS-induced secretion of pro-inflammatory factors and monocyte-endothelial adhesion in HUVECs, whereas KPNA2 overexpression exerted the opposite effects. p65 and interferon regulatory factor 3 (IRF3), the transcription factors known to regulate the transcription of pro-inflammatory genes, interacted with KPNA2, and their nuclear translocations were blocked following KPNA2 silencing. Furthermore, we found that KPNA2 protein level was decreased by E3 ubiquitin ligase F-box and WD repeat domain containing 7 (FBXW7), which was downregulated in the atherosclerotic mice. FBXW7 overexpression induced ubiquitination with subsequent proteasomal degradation of KPNA2. Meanwhile, the effects of KPNA2 deficiency on atherosclerotic lesions were further confirmed by in vivo experiments. Taken together, our study indicates that KPNA2 downregulation, regulated by FBXW7, may alleviate endothelial dysfunction and related inflammation in the progression of AS by suppressing the nuclear translocation of p65 and IRF3.

PurposeLiver abscess is a rare and serious complication after transarterial chemoembolization (TACE) for liver cancer; however, its impact on the prognosis is unclear. This retrospective study examined the outcomes of patients with liver abscess formation following TACE for malignant liver tumors to elucidate the impact of liver abscess formation on the prognosis of these patients.MethodsFrom January 2017 to January 2022, 1,387 patients with malignant tumors underwent 3,341 sessions of TACE at our hospital. Clinical characteristics of patients at baseline and follow-up were examined, including treatment and outcome of liver abscess, tumor response to the TACE leading to liver abscess, and overall survival time.ResultsOf 1,387 patients, 15 (1.1%) patients with liver abscess complications after TACE resulted in a total of 16 (0.5%) cases of liver abscess after 3,341 TACE sessions (including one patient with two events). After antibiotic or percutaneous catheter drainage (PCD) treatment, all the infections associated with liver abscesses were controlled. In the PCD group, eight patients died before drainage tube removal, one retained the drainage tube until the end of follow-up, and five underwent drainage tube removal; the mean drainage tube removal time was 149.17 ± 134.19 days. The efficacy of TACE leading to liver abscess was evaluated as partial response (18.75%), stable disease (37.5%), and progressive disease (43.75%). Eleven patients died during the follow-up period owing to causes unrelated to infections caused by liver abscesses. The survival rates at 3 months, 6 months, 1 year, and 5 years were 86.7%, 50.9%, 25.5%, and 17%, respectively.ConclusionPatients with liver abscess formation following TACE for malignant liver tumors experienced prolonged drainage tube removal time after PCD; while this condition did not directly cause death, it indirectly contributed to a poor prognosis in these patients.

The deployment of covered stent grafts has been considered as a less invasive alternative to surgery in emergency settings for rupture of femoropopliteal arteries caused by infection. Limited case reports show good short- and medium-term results ( 1 Wang S. Wang Q. Liu H. et al. Endovascular treatment of thoracic aortic pseudoaneurysm due to brucellosis: a rare case report. BMC Infect Dis. 2017; 17: 387 Crossref PubMed Scopus (4) Google Scholar , 2 Siani A. Flaishman I. Siani L.M. et al. Spontaneous rupture of the superficial femoral artery treated via an endovascular approach. Texas Heart Inst J. 2008; 35: 66-68 PubMed Google Scholar ). The present publication reports a case of a covered stent graft spontaneously migrating out of the blood vessel 15 months after placement. This retrospective case was approved by the local ethics committee (2020PS572K), and the patient provided informed consent.

目的:评价经导管动脉栓塞术(Transcatheter arterial embolization,TAE)在儿童外伤性肝破裂中的应用价值.方法:回顾性分析我院在2012年12月-2018年7月期间收治的7例采用TAE治疗外伤性肝破裂的患儿临床资料,男4例,女3例,平均年龄5.9岁,均经增强CT确诊为肝破裂.2例急诊行TAE,4例保守治疗无效采用TAE;1例肝破裂修补术后2月复发出血行TAE治疗.结果:7例患者均成功止血,其中5例血管造影均表现为局部造影剂外溢,采用明胶海绵颗粒进行栓塞;2例表现为假性动脉瘤形成,采用弹簧圈进行栓塞.术后7例患者出现不同程度的转氨酶升高,6例出现发热,1例出现肝区疼痛,经对症治疗后均缓解.结论:TAE具有微创、安全、有效且并发症发生率低等优点,为小儿创伤性肝破裂提供一种有效的治疗方法.

Objective The aims of this study were to evaluate image quality of virtual monoenergetic images (VMIs) compared with conventional images (CIs) from spectral detector CT (SDCT) and to explore the optimal energy level in run-off computed tomography angiography (CTA). Methods The data sets of 35 patients who received run-off CTA on the SDCT were collected in this retrospective study. Conventional images were generated via iterative reconstruction algorithm and VMI series from 40 to 120 keV were generated via spectral reconstruction algorithm. The objective indices including vascular attenuation, noise, signal-to-noise ratio, and contrast-to-noise ratio were compared. Two readers performed subjective evaluation using a 5-point scale. Results The attenuation showed higher values compared with CIs at 40 to 60 keV (P < 0.001). The noise was similar in 60- to 80-keV VMIs and significantly decreased in 90- to 120-keV VMIs (P < 0.001) in comparison with CIs. The signal-to-noise ratio and contrast-to-noise ratio were improved in 40- to 60-keV VMIs compared with CIs (P < 0.05). The score of subjective assessment was higher than that of CIs in 50- to 70-keV VMIs (P < 0.001). Conclusions Virtual monoenergetic images can provide improved image quality compared with CIs from SDCT in run-off CTA, and VMIs at 60 keV may be the best choice in evaluating lower extremity arteries.

PURPOSE:The present meta-analysis evaluated the role of drug-coated balloon (DCB) angioplasty for in-stent restenosis (ISR) in femoropopliteal artery disease. MATERIALS AND METHODS:Cochrane Library, Embase, and PubMed were searched without language restrictions from inception to May 10, 2020. The endpoints included target lesion revascularization (TLR), recurrent ISR, clinical improvement, ankle-brachial index (ABI), and death. There were 5 randomized controlled trials with 425 patients (218 with DCB angioplasty and 207 with plain old balloon angioplasty [POBA]) were included in the meta-analysis. RESULTS:Compared with POBA, DCB angioplasty was associated with lower risk of TLR (odds ratio [OR], 0.21; 95% confidence interval [CI]: 0.09-0.49, P < .001 at 6 months and OR, 0.15; 95% CI, 0.08-0.30; P < .001 at 12 months) and recurrent ISR (OR, 0.22; 95% CI, 0.13-0.38; P < .001 at 6 months and OR, 0.31; 95% CI, 0.16-0.61; P < .001 at 12 months), and superior clinical improvement (OR, 1.98; 95% CI, 1.07-3.65; P = .03 at 6 months and OR, 2.84; 95% CI: 1.50-5.35; P = .001 at 12 months). There were no significant differences between groups in ABI and death. Subgroup analysis for patients with DCB angioplasty showed similar rates of TLR, recurrent ISR, clinical improvement, and death between the short lesion (<15 cm) and long lesion group (≥15 cm) (P > .05). CONCLUSIONS:The current meta-analysis suggests that DCB angioplasty is an improvement over POBA for femoropopliteal ISR. Future studies about the effect of lesion length on DCB performance are still needed.

动脉循环中的炎症被认为是动脉粥样硬化斑块发展的一个因素.过去几十年中,通过测量血清生化标志物来量化持续炎症程度的尝试一直在进行.中性粒细胞/淋巴细胞比值作为下肢动脉硬化闭塞症(ASO)有效的炎症预测因子已得到越来越多学者的关注,在下肢ASO患者中适当使用生物标志物可能有助于早期诊断,增强对疾病发展过程的了解,并改进现有疗法和开发新疗法.

Background The aim of the present study was to assess the feasibility of applying low-dose contrast media (CM), and to explore the optimal virtual monoenergetic images (VMIs) in run-off computed tomography (CT) angiography (CTA) on dual-layer spectral detector CT (SDCT). Methods Forty patients were randomly assigned into a control group using routine volume CM (group A) and an experimental group using half-volume CM (group B). In groups A and B, 120 kVp polychromatic conventional images were generated via hybrid iterative reconstruction algorithm defined as A1 and B1, respectively. Additionally, in group B, VMIs (range, 40-120 keV) were reconstructed via a spectral reconstruction algorithm defined as B2-B10. Vascular attenuation, noise, signal-to-noise ratio (SNR), contrast-to-noise ratio (CNR), and radiation dose were evaluated. Subjective evaluation was performed using a 5-point scale. Results The patient demographics and radiation dose demonstrated no significant difference between groups A and B [dose length product (DLP): 1,823.45±512.68 vs. 2,014.40±453.25 mGy·cm, P=0.229; volume CT dose index: 14.92±3.40 vs. 16.26±2.85 mGy, P=0.208; the effective dose (ED): 10.82±3.02 vs. 11.88±2.67 mSv, P=0.229]. The mean vascular attenuation was higher in group B2 (40 keV) and was lower in group B3 (50 keV) in comparison with that in group A1 (487.07±154.21 vs. 414.35±71.66 HU, 329.90±100.25 vs. 414.35±71.66 HU, P>0.05). Compared with group A1, the mean noise was similar in group B2 (40 keV) and was lower in group B1 and groups B3-B10 (50-120 keV) (14.81±5.67 vs. 17.29±4.70 HU, P>0.05; 6.75±1.23-11.26±3.24 vs. 17.29±4.70 HU, P<0.05). The mean SNR and CNR in group B2 (40 keV), as well as the mean SNR in group B3 (50 keV), were significantly higher than those of group A1 (38.21±7.52 vs. 28.25±7.20, 32.70±7.79 vs. 24.54±6.60, 32.85±7.10 vs. 28.25±7.20, P<0.05), and the mean CNR in group B3 (50 keV) was similar to that in group A1 (26.66±7.32 vs. 24.54±6.60, P>0.05). Scores of subjective image quality (IQ) in group B2 (40 keV) and B3 (50 keV) were similar to those in group A1 {5 [4.25, 5] vs. 5 [4, 5], 5 [5, 5] vs. 5 [4, 5], P>0.05}, and showed a declining trend in group B4 (60 keV) {4 [4, 5] vs. 5 [4, 5], P>0.05}. Conclusions It is feasible to perform run-off CTA using low-dose CM with VMI on SDCT. The VMIs at 40-50 keV were the optimal choice and did not compromise IQ.

BACKGROUND:This study aimed to assess the impact of pre-existing pulmonary interstitial lesions (PIL) on the efficacy and prognosis of patients with epidermal growth factor receptor (EGFR) mutant non-small cell lung cancer (NSCLC) treated with EGFR tyrosine kinase inhibitor (TKI). METHODS:Patients with advanced NSCLC harboring EGFR exon 19 deletion (E19 del) or exon 21 (E21) L858R were enrolled in this study. All patients underwent high resolution computed tomography (HRCT) chest scans prior to EGFR-TKI treatment. Pre-existing PIL was graded according to HRCT imaging (PIL 0, 1, 2, and 3). Cox proportional-hazards regression models were used to identify the prognostic factors for progression-free survival (PFS). RESULTS:A total of 134 eligible patients were enrolled. The overall objective response rate (ORR) and median PFS were 73.1% and 10.0 months (95% CI: 7.51-12.49), respectively. There were 62 (46.3%), 25 (18.7%), 28 (20.9%), and 19 (14.1%) cases of PIL grade 0, 1, 2, and 3, respectively, with median PFS and ORR of 12.9 months and 80.6%, 11.0 months and 72.0%, 10.0 months and 71.4%, and 7.0 months and 52.6%, respectively. Multivariate analysis showed that squamous cell carcinoma (vs. adenocarcinoma, HR =4.33), E21 L858R (vs. E19 del, HR =1.57), and PIL grade 3 (vs. grade 0-2, HR =1.60-2.48) were poor prognostic factors for PFS (P<0.05 for all). CONCLUSIONS:Pre-existing PIL grade is an independent prognostic factor for predicting resistance to EGFR-TKIs in patients with EGFR-mutant advanced NSCLC. Higher PIL grade suggests higher risk of early progression.

双层光谱探测器CT从探测器角度进行技术革新,实现同时、同源、同向和同步能量分离扫描,可降低噪声、优化图像质量,提高病灶检出率,抑制伪影,具有定量定性分析物质、降低辐射剂量和减少对比剂用量等优势,临床应用前景广阔.本文对双层光谱探测器CT临床应用与研究进展进行综述.

Objective:To explore the value of 70 keV virtual monoenergetic images(VMI) on dual-layer spectral detector CT in improving abdominal arterial phase images quality.Methods:The arterial phase images of patients who underwent abdominal enhanced scan on the Philips IQon dual-layer spectral detector CT in Shengjing Hospital of China Medical University from January to May 2019 were retrospectively analyzed. Fifty patients (12 males, 38 females) were included with age of 26-74 （53±12） years. Objective and subjective evaluation was performed in 120 kVp polychromatic conventional images (group CI) which derived from iterative reconstruction algorithm and group 70 keV VMI which derived from spectral reconstruction algorithm. The attenuation, noise, signal to noise ratio and contrast to noise ratio of abdominal aorta, celiac trunk, superior mesenteric artery, left kidney artery, right kidney artery, liver, spleen, pancreas, left and right kidney were compared between group 70 keV VMI and CI by using paired t test. Image quality of group 70 keV VMI and CI was evaluated by two radiologists independently with a 5-point scale and compared by Wilcoxon rank test. The inter-agreement of subjective scoring between the two radiologists was evaluated by Kappa test. Results:Except for pancreas, the attenuation of abdominal arteries and solid organs in group 70 keV VMI were higher than that of group CI and the difference was statistically significant ( Pall<0.05). The attenuation of pancreas was lower than that of group CI ( t=-3.097， P=0.003). The noise of abdominal arteries and solid organs in group 70 keV VMI showed lower values compared to group CI and the difference was statistically significant ( Pall<0.001). The signal to noise ratio as well as contrast to noise ratio of abdominal arteries and solid organs in group 70 keV VMI was higher than that of group CI and the difference was statistically significant ( Pall<0.001). Subjective image quality scores in group 70 keV VMI were higher than that of group CI and scores of group 70 keV VMI and CI were 5 (4,5) and 4 (4,5), respectively. The difference was statistically significant ( Z=-4.131, P<0.001). There was a good consistency of subjective image quality scores between two radiologists, which Kappa values of group 70 keV VMI and CI were 0.79 and 0.69, respectively. Conclusions:Compared to CI, 70 keV VMI derived from dual-layer spectral detector CT can optimize abdominal arterial phase image quality by decreasing the noise, improving the signal to noise ratio and contrast to noise ratio.