Excess non-COVID-19-related mortality among inflammatory bowel disease decedents during the COVID-19 pandemic.

BACKGROUND: The coronavirus disease 2019 (COVID-19) pandemic disrupted healthcare in the United States. AIM: To investigate COVID-19-related and non-COVID-19-related death and characteristics associated with excess death among inflammatory bowel disease (IBD) decedents. METHODS: We performed a register-based study using data from the National Vital Statistics System, which reports death data from over 99% of the United States population, from January 1, 2006 through December 31, 2021. IBD-related deaths among adults 25 years and older were stratified by age, sex, race/ethnicity, place of death, and primary cause of death. Predicted and actual age-standardized mortality rates (ASMRs) per 100000 persons were compared. RESULTS: 49782 IBD-related deaths occurred during the study period. Non-COVID-19-related deaths increased by 13.14% in 2020 and 18.12% in 2021 [2020 ASMR: 1.55 actual vs 1.37 predicted, 95% confidence interval (CI): 1.26-1.49; 2021 ASMR: 1.63 actual vs 1.38 predicted, 95%CI: 1.26-1.49]. In 2020, non-COVID-19-related mortality increased by 17.65% in ulcerative colitis (UC) patients between the ages of 25 and 65 and 36.36% in non-Hispanic black (NHB) Crohn's disease (CD) patients. During the pandemic, deaths at home or on arrival and at medical facilities as well as deaths due to neoplasms also increased. CONCLUSION: IBD patients suffered excess non-COVID-19-related death during the pandemic. Excess death was associated with younger age among UC patients, and with NHB race among CD patients. Increased death at home or on arrival and due to neoplasms suggests that delayed presentation and difficulty accessing healthcare may have led to increased IBD mortality.

Unlocking the NIR-II AIEgen for High Brightness through Intramolecular Electrostatic Locking.

Fluorescent imaging and biosensing in the near-infrared-II (NIR-II) window holds great promise for non-invasive, radiation-free, and rapid-response clinical diagnosis. However, it's still challenging to develop bright NIR-II fluorophores. In this study, we report a new strategy to enhance the brightness of NIR-II aggregation-induced emission (AIE) fluorophores through intramolecular electrostatic locking. By introducing sulfur atoms into the side chains of the thiophene bridge in TSEH molecule, the molecular motion of the conjugated backbone can be locked through intramolecular interactions between the sulfur and nitrogen atoms. This leads to enhanced NIR-II fluorescent emission of TSEH in both solution and aggregation states. Notably, the encapsulated nanoparticles (NPs) of TSEH show enhanced brightness, which is 2.6-fold higher than TEH NPs with alkyl side chains. The in vivo experiments reveal the feasibility of TSEH NPs in vascular and tumor imaging with a high signal-to-background ratio and precise resection for tiny tumors. In addition, polystyrene nanospheres encapsulated with TSEH are utilized for antigen detection in lateral flow assays, showing a signal-to-noise ratio 1.9-fold higher than the TEH counterpart in detecting low-concentration antigens. This work highlights the potential for developing bright NIR-II fluorophores through intramolecular electrostatic locking and their potential applications in clinical diagnosis and biomedical research.

Carnosic acid nanocluster-based framework combined with PD-1 inhibitors impeded tumorigenesis and enhanced immunotherapy in hepatocellular carcinoma.

Clinically, the immune checkpoint inhibitor anti-PD-1 antibody has shown a certain effect in the treatment of hepatocellular carcinoma (HCC), which is limited to a small number of patients with HCC. This study aims to reveal whether carnosic acid nanocluster-based framework (CA-NBF) has a sensitization effect on anti-PD-1 antibody in the treatment of HCC at the cellular and animal levels. MHCC97H cells were treated with CA-NBF, anti-PD-1 and their combination. The effects of CA-NBF and anti-PD-1 on cell proliferation, cell cycle, apoptosis, invasion, and migration were evaluated by MTT assay, flow cytometry, and scratch test. The effects of CA-NBF and anti-PD-1 on Wnt/ß-catenin signaling pathway in MHCC97H cells were detected. A BALB/C nude mouse model of hepatocellular carcinoma was established, and the tumor growth was observed at different time points. The expression of cytotoxic T lymphocyte and helper T lymphocyte markers CD8 and CD4 in tumor tissues was detected by immunohistochemistry. Western blotting was used to detect the Wnt/ß-catenin signaling pathway proteins (Wnt-3a, ß-catenin, and GSK-3ß) level in tumor tissues after CA-NBF and anti-PD-1 treatment. CA-NBF activity was significantly higher than CA, which could prominently reduce the proliferation, migration and invasion of MHCC97H cells and enhance apoptosis by inactivating Wnt/ß-catenin signaling pathway. CA-NBF combined with anti-PD-1 antibody further enhanced cell proliferation, migration, invasion and pro-apoptosis but had no significant effect on Wnt/ß-catenin signaling pathway. CA-NBF in vivo improved the tumor response to PD1 immune checkpoint blockade in HCC, manifested by reducing tumor size and weight, promoting CD4 and CD8 expression. CA-NBF combined with anti-PD-1 have stronger immunomodulatory and anticancer effects without increasing biological toxicity.

Clinical study of melodic intonation therapy combined with transcranial direct current stimulation for post-stroke aphasia: a single-blind, randomized controlled trial.

Background: Globally, more than 10 million new stroke cases occur annually, of which aphasia accounts for about one-third. Aphasia has become an independent predictor of functional dependence and death for the stroke population. The closed-loop rehabilitation of combining behavioral therapy with central nerve stimulation seems to be the research trend of post-stroke aphasia (PSA) due to its advantages in improving linguistic deficits. Objective: To verify the clinical efficacy of a closed-loop rehabilitation program combining melodic intonation therapy (MIT) with transcranial direct current stimulation (tDCS) for PSA. Methods: This was a single-center, assessor-blinded, randomized controlled clinical trial, which screened 179 patients and included 39 PSA subjects, with the registration number ChiCTR2200056393 in China. Demographic and clinical data were documented. The primary outcome was the Western Aphasia Battery (WAB) used to assess language function, and the secondary outcomes included Montreal Cognitive Assessment (MoCA), Fugl-Meyer Assessment (FMA), and Barthel Index (BI) for evaluating cognition, motor, and activities of daily living, respectively. With the computer-generated randomization sequence, subjects were randomly divided into the conventional group (CG), MIT combined with sham stimulation group (SG), and MIT combined with tDCS group (TG). After the three-week intervention, the functional changes in each group were analyzed by the paired sample T-test, and the functional difference between the three groups was analyzed by ANOVA. Results: There was no statistical difference on the baseline. After the intervention, the WAB's aphasia quotient (WAB-AQ), MoCA, FMA, and BI were statistically different in SG and TG, including all the sub-items in WAB and FMA, while only listening comprehension, FMA, and BI were statistically different in CG. The differences of WAB-AQ, MoCA, and FMA were statistically different among the three groups, but BI was not. The post hoc test results revealed that the changes of WAB-AQ and MoCA in TG were more significant than the others. Conclusion: MIT combined with tDCS can augment the positive effect on language and cognitive recovery in PSA.

Site-Specific Incorporation of Sulfotyrosine into Proteins in Mammalian Cells.

Protein tyrosine O-sulfation (PTS) plays a crucial role in numerous extracellular protein-protein interactions. It is involved in diverse physiological processes and the development of human diseases, including AIDS and cancer. To facilitate the study of PTS in live mammalian cells, an approach for the site-specific synthesis of tyrosine-sulfated proteins (sulfoproteins) was developed. This approach takes advantage of an evolved Escherichia coli tyrosyl-tRNA synthetase to genetically encode sulfotyrosine (sTyr) into any proteins of interest (POI) in response to a UAG stop codon. Here, we give a step-by-step account of the incorporation of sTyr in HEK293T cells using the enhanced green fluorescent protein as an example. This method can be widely applied to incorporating sTyr into any POI to investigate the biological functions of PTS in mammalian cells.

Excess psoriasis and psoriatic arthritis mortality during the COVID-19 pandemic in the United States: A nationwide population-based study from 2010 to 2021.

BACKGROUND: Little is known about mortality trends among patients with psoriasis (PsO) and psoriatic arthritis (PsA) in the United States. OBJECTIVES: To ascertain mortality trends of PsO and PsA between 2010 and 2021, focusing on the effects of the COVID-19 pandemic. METHODS: We collected data from the National Vital Statistic System and calculated age-standardized mortality rates (ASMR) and cause-specific mortality for PsO/PsA. We evaluated observed versus predicted mortality for 2020-2021 based on trends from 2010 to 2019 with joinpoint and prediction modelling analysis. RESULTS: Among 5810 and 2150 PsO- and PsA-related deaths between 2010 and 2021, ASMR for PsO dramatically increased between 2010-2019 and 2020-2021 (annual percentage change [APC] 2.07% vs. 15.26%; p < 0.01), leading to a higher observed ASMR (per 100,000 persons) than predicted for 2020 (0.27 vs. 0.22) and 2021 (0.31 vs. 0.23). The excess mortality of PsO was 22.7% and 34.8% higher than that in the general population in 2020 (16.4%, 95% CI: 14.9%-17.9%) and 2021 (19.8%, 95% CI: 18.0%-21.6%) respectively. Notably, the ASMR rise for PsO was most pronounced in the female (APC: 26.86% vs. 12.19% in males) and the middle-aged group (APC: 17.67% vs. 12.47% in the old-age group). ASMR, APC and excess mortality for PsA were similar to PsO. SARS-CoV-2 infection contributed to more than 60% of the excess mortality for PsO and PsA. CONCLUSIONS: Individuals living with PsO and PsA were disproportionately affected during the COVID-19 pandemic. Both ASMRs increased at an alarming rate, with the most pronounced disparities among the female and middle-aged groups.

Effectiveness and tolerability of camrelizumab combined with molecular targeted therapy for patients with unresectable or advanced HCC.

There is a lack of effective programmed cell death protein 1 (PD-1)-targeted immunotherapy with good tolerability in patients with advanced hepatocellular carcinoma (HCC) and severely compromised liver function. We assessed patient outcomes after combined camrelizumab and molecular targeted therapy in a multicenter cohort study in China. The study included 99 patients with advanced HCC (58 Child-Pugh A and 41 Child-Pugh B), 84 of them received camrelizumab combined with molecular targeted therapy from January 10, 2019, to March 31, 2021. Overall survival (OS), progression-free survival (PFS), objective response rate (ORR), disease control rate (DCR), and adverse events (AEs) were assessed. The median follow-up was 12.1 months. For patients with Child-Pugh B, the OS probability at 12-months, ORR and DCR were 49.7%, 31.7% and 65.9%, respectively, and the median PFS was 5.1 months [95% confidence interval (CI) 3.0-7.1], which were comparable with Child-Pugh A patients, although median OS was shorter in Child-Pugh B patients (20.5 vs.13.4 months, P = 0.12). In multivariate analysis, macrovascular infiltration (MVI), but not sex, age, hepatitis B virus etiology, extrahepatic metastasis, Child-Pugh B, or AFP > 400 ng/ml, was associated with 12-months OS [hazard ratio (HR) 2.970, 95% CI 1.276-6.917, P = 0.012] and ORR (HR 2.906, 95% CI 1.18-7.16, P = 0.020). Grade 3/4 immune-related AEs occurred in 26.8% of Child-Pugh B patients, including one potentially treatment-related death. In both groups, the most common AEs were immune thrombocytopenia and hepatotoxicity. Camrelizumab combined with targeted therapy showed favorable effectiveness and tolerability with manageable toxicities in Chinese HCC patients, regardless of Child-Pugh A/B liver function. MVI was associated with suboptimal immunotherapy response and poor prognosis.

Comparison of three cognitive assessment methods in post-stroke aphasia patients.

Background: The cognitive level of post-stroke aphasia (PSA) patients is generally lower than non-aphasia patients, and cognitive impairment (CI) affects the outcome of stroke. However, for different types of PSA, what kind of cognitive assessment methods to choose is not completely clear. We investigated the Montreal Cognitive Assessment (MoCA), the Mini-Mental State Examination (MMSE), and the Non-language-based Cognitive Assessment (NLCA) to observe the evaluation effect of CI in patients with fluent aphasia (FA) and non-fluent aphasia (NFA). Methods: 92 stroke patients were included in this study. Demographic and clinical data of the stroke group were documented. The language and cognition were evaluated by Western Aphasia Battery (WAB), MoCA, MMSE, and NLCA. PSA were divided into FA and NFA according to the Chinese aphasia fluency characteristic scale. Pearson's product-moment correlation coefficient test and multiple linear regression analysis were performed to explore the relationship between the sub-items of WAB and cognitive scores. The classification rate of CI was tested by Pearson's Chi-square test or Fisher's exact test. Results: The scores of aphasia quotient (AQ), MoCA, MMSE, and NLCA in NFA were lower than FA. AQ was positively correlated with MoCA, MMSE, and NLCA scores. Stepwise multiple linear regression analysis suggested that naming explained 70.7% of variance of MoCA and 79.9% of variance of MMSE; comprehension explained 46.7% of variance of NLCA. In the same type of PSA, there was no significant difference in the classification rate. The classification rate of CI in NFA by MoCA and MMSE was higher than that in FA. There was no significant difference in the classification rate of CI between FA and NFA by NLCA. Conclusion: MoCA, MMSE, and NLCA can be applied in FA. NLCA is recommended for NFA.

Determining levels of linguistic deficit by applying cluster analysis to the aphasia quotient of Western Aphasia Battery in post-stroke aphasia.

The aphasia quotient of Western Aphasia Battery (WAB-AQ) has been used as an inclusion criterion and as an outcome measure in clinical, research, or community settings. The WAB-AQ is also commonly used to measure recovery. This study aimed to quantitatively determine levels of the linguistic deficit by using a cluster analysis of the WAB-AQ in post-stroke aphasia (PSA). 308 patients were extracted from the database. Cutoff scores are defined by mean overlap WAB-AQ scores of clusters by systematic cluster analysis, the method of which is the farthest neighbor element, and the metrics are square Euclidean distance and Pearson correlation, performed on the full sample of WAB-AQ individual subitem scores. A 1-way analysis of variance, with post hoc comparisons conducted, was used to determine whether clusters had significant differences. Three clusters were identified. The scores for severe, moderate, and mild linguistic deficit levels ranged from 0 to 30, 30.1 to 50.3, and 50.4 to 93.7, respectively. For PSA, the cluster analysis of WAB-AQ supports a 3-impairment level classification scheme.

Assembling p53 Activating Peptide With CeO2 Nanoparticle to Construct a Metallo-Organic Supermolecule Toward the Synergistic Ferroptosis of Tumor.

Inducing lipid peroxidation and subsequent ferroptosis in cancer cells provides a potential approach for anticancer therapy. However, the clinical translation of such therapeutic agents is often hampered by ferroptosis resistance and acquired drug tolerance in host cells. Emerging nanoplatform-based cascade engineering and ferroptosis sensitization by p53 provides a viable rescue strategy. Herein, a metallo-organic supramolecular (Nano-PMI@CeO2) toward p53 restoration and subsequent synergistic ferroptosis is constructed, in which the radical generating module-CeO2 nanoparticles act as the core, and p53-activator peptide (PMI)-gold precursor polymer is in situ reduced and assembled on the CeO2 surface as the shell. As expected, Nano-PMI@CeO2 effectively reactivated the p53 signaling pathway in vitro and in vivo, thereby downregulating its downstream gene GPX4. As a result, Nano-PMI@CeO2 significantly inhibited tumor progression in the lung cancer allograft model through p53 restoration and sensitized ferroptosis, while maintaining favorable biosafety. Collectively, this work develops a tumor therapeutic with dual functions of inducing ferroptosis and activating p53, demonstrating a potentially viable therapeutic paradigm for sensitizing ferroptosis via p53 activation. It also suggests that metallo-organic supramolecule holds great promise in transforming nanomedicine and treating human diseases.

NCAPD3 enhances Warburg effect through c-myc and E2F1 and promotes the occurrence and progression of colorectal cancer.

BACKGROUND: NCAPD3 is one of the three non-SMC subunits of condensin II complex, which plays an important role in the chromosome condensation and segregation during mitosis. Notably, elevated levels of NCAPD3 are found in many somatic cancers. However, the clinical role, biological functions of NCAPD3 in cancers especially in colorectal cancer (CRC) and the underlying molecular mechanisms remain poorly elucidated. METHODS: Clinical CRC and adjacent normal tissues were used to confirm the expression of NCAPD3. The association of NCAPD3 expression with clinicopathological characteristics and patient outcomes were analyzed by using online database. In vivo subcutaneous tumor xenograft model, NCAPD3 gene knockout following azoxymethane (AOM)/dextran sodium sulfate (DSS)-induced tumor mouse model, Co-IP, western blot, qRT-PCR, IHC, ChIP assays and cell functional assays were used to investigate the biological functions of NCAPD3 in CRC and the underlying molecular mechanisms. RESULTS: NCAPD3 was overexpressed in CRC tissues and positively correlated with poor prognosis of CRC patients. NCAPD3 knockout suppressed CRC development in AOM/DSS induced and xenograft mice models. Moreover, we found that NCAPD3 promoted aerobic glycolysis in CRC. Mechanistically, NCAPD3 up-regulated the level of c-Myc and interacted with c-Myc to recruit more c-Myc to the gene promoter of its downstream glycolytic regulators GLUT1, HK2, ENO1, PKM2 and LDHA, and finally enhanced cellular aerobic glycolysis. Also, NCAPD3 increased the level of E2F1 and interacted with E2F1 to recruit more E2F1 to the promoter regions of PDK1 and PDK3 genes, which resulted in the inhibition of PDH activity and TCA cycle. CONCLUSIONS: Our data demonstrated that NCAPD3 promoted glucose metabolism reprogramming and enhanced Warburg effect in colorectal tumorigenesis and CRC progression. These findings reveal a novel mechanism underlying NCAPD3 mediated CRC cell growth and provide new targets for CRC treatment.

Regulatory mechanism of androgen receptor on NCAPD3 gene expression in prostate cancer.

BACKGROUND: Androgen receptor (AR) is an essential transcriptional factor that contributes to the development and progression of prostate cancer (PCa). NCAPD3 is a component of the condensin II complex and plays a critical role in cell mitosis by regulating chromosome condensation; however, the relationship between NCAPD3 and AR remains unknown. METHODS: Transcriptome sequencing assay is carried out to analyze the expression of the NCAP family in clinic samples. Chromatin immunoprecipitation (ChIP) sequencing, ChIP assay, and dual-luciferase assay are used to identify the androgen-responsive element in NCAPD3 enhancer. Immunohistochemistry, quantitative reverse transcription-polymerase chain reaction, and western-blot assay are employed to check the expression of genes in PCa tissues and in PCa cells. Confocal immunofluorescence microscopy analysis is used for identifying the regulation of AR on NCAPD3-mediated chromosome condensation. Colony formation, cell cycle assay, wound healing assay, and transwell experiments are used to explore the regulation of AR on the functions of NCAPD3. In vivo experiment is employed to identify in vitro experimental results. RESULTS: NCAPD3 is an androgen/AR axis-targeted gene and is involved in AR-induced PCa cell proliferation, migration, and invasion in vitro and in vivo. Androgen treatment and AR overexpression increase the expression of NCAPD3 in PCa cell lines. The canonical exist in the enhancer region of NCAPD3. Androgen/AR axis regulates NCAPD3-invovled chromosome condensation during cell mitosis. CONCLUSIONS: Our report demonstrated that NCAPD3 is an androgen-responsive gene and upregulated by androgen/AR axis and involved in AR-promoted progression of PCa, suggesting a potential role of NCAPD3 in the PCa development.

NCAPD2 inhibits autophagy by regulating Ca2+/CAMKK2/AMPK/mTORC1 pathway and PARP-1/SIRT1 axis to promote colorectal cancer.

Non-SMC condensin I complex subunit D2 (NCAPD2) is one of the three non-SMC subunits in condensin I. Previous studies have shown that NCAPD2 plays an important role in the chromosome condensation and segregation. However, its role in the development of colorectal cancer (CRC) and specific molecular mechanisms still need to be further studied. Here we show that NCAPD2 inhibits autophagy and blocks autophagic flux via Ca2+/CAMKK/AMPK/mTORC1 pathway and PARP-1/SIRT1 axis. NCAPD2 acts as a tumor promoter both in vitro and in vivo. NCAPD2 knockout suppresses colorectal cancer development in AOM/DSS induced mice model. Therefore, our findings support a role for NCAPD2 in autophagy to promote CRC development and highlight NCAPD2 as a potential target for CRC therapy.

Facile and Sensitive Method for Protein Kinase A Activity Assay Based on Fluorescent Off-On PolyU-peptide Assembly.

Phosphorylation mediated by protein kinases plays a pivotal role in metabolic and cell-signaling processes, and the dysfunction of protein kinases such as protein kinase A (PKA) may induce several human diseases. Therefore, it is of great significance to develop a facile and effective method for PKA activity assay and high-throughput screening of inhibitors. Herein, we develop a new fluorescent off-on method for PKA assay based on the assembly of anionic polyuridylic acid (polyU) and cationic fluorescent peptide. The phosphorylation of the peptide disrupts its electrostatic binding with polyU, suppresses the concentration quenching effect of polyU, and thus causes fluorescence recovery. The recovered fluorescence intensity at 585 nm is directly proportional to the PKA activity in the range of 0.1-3.2 U/mL with a detection limit of 0.05 U/mL. Using our method, the PKA activity in HeLa cell lysate is determined to be 58.2 ± 5.1 U/mg protein. The method has also been employed to evaluate the inhibitory effect of PKA inhibitors with satisfactory results and may be expected to be a promising candidate for facile and cost-effective assay of kinase activity and high-throughput inhibitor screening.

In vivo imaging of leucine aminopeptidase activity in drug-induced liver injury and liver cancer via a near-infrared fluorescent probe.

The liver, a main detoxification organ, has evolved a complex enzymatic system to respond to multiple pathological conditions, in which leucine aminopeptidase (LAP) has been reported to participate in detoxifying cisplatin in hepatoma cells and contribute to the intrinsic drug resistance. In vivo imaging of LAP activity in liver disease models is thus helpful to further understand the function of LAP in detoxification and medicine, but such an imaging approach is still lacking. Herein, we develop a selective and sensitive near-infrared fluorescent probe (HCAL) for this purpose. Using the probe, combined with confocal fluorescence imaging, we disclose the upregulations of LAP in acetaminophen-induced liver injury and tumor-bearing mice models. Supplementary acetylcysteine can suppress this upregulation, revealing that the LAP increase may be connected with a deficiency in biothiols. Moreover, HCAL has been used to image LAP in hepatoma cells, tumor tissues and xenograft tumor mice models successfully. These results demonstrate that HCAL may be a promising tool for studying the function of LAP in LAP-associated liver diseases.

Ultrasensitive Detection of Aminopeptidase N Activity in Urine and Cells with a Ratiometric Fluorescence Probe.

An ultrasensitive ratiometric fluorescent probe (CVN) has been designed and synthesized by incorporating alanine into the cresyl violet fluorophore. The probe shows ratiometric fluorescence response toward aminopeptidase N (APN) through the increase of fluorescent intensity ratio of 626/575 nm. The sensitivity of the probe is ultrahigh with a detection limit of 33 pg/mL, which can quantify the contents of APN in 500-fold diluted human urine samples. Furthermore, by using ratiometric fluorescence imaging, the probe reveals significantly higher contents of APN in HepG2 cells than those in LO2 cells, which has been further used to distinguish these two types of cells in mixed cocultures. The probe could be of great importance for the APN-related disease diagnosis and pathophysiology elucidation.

Comparison of N-acetylcysteine and cysteine in their ability to replenish intracellular cysteine by a specific fluorescent probe.

A specific fluorescent probe, designed by a substitution-rearrangement mechanism, can discriminate cysteine from other thiols. Using this probe, N-acetylcysteine is revealed to be superior to cysteine to replenish intracellular cysteine in cells.

A cresyl violet-based fluorescent off-on probe for the detection and imaging of hypoxia and nitroreductase in living organisms.

A new cresyl violet-based fluorescent off-on probe has been developed through a one-step synthesis for the detection of nitroreductase (NTR) and hypoxia. The detection mechanism is based on the NTR-catalyzed reduction of the probe to cresyl violet, accompanied with a large fluorescence enhancement at a long wavelength of 625 nm. The probe can detect NTR in aqueous solution with high selectivity and sensitivity, and the detection limit is 1 ng mL(-1) NTR. Most importantly, the probe has been successfully used to image not only NTR and hypoxia in living cells, but also the distribution of NTR in zebrafish in vivo.

[Correlation between computed tomographic vascular convergence sign and enhancement value in patients with pulmonary nodules].

OBJECTIVE: To explore the correlation between computed tomographic (CT) vascular convergence sign and enhancement value in patients with pulmonary nodules. METHODS: A total of 708 consecutive patients with pulmonary nodule received dual-source CT scan from January 2010 to January 2012. They were divided into vascular convergence sign group (including 4 subgroups) and non-vascular convergence sign group. Then the correlation between CT vascular convergence sign and enhancement values was analyzed. RESULTS: The enhancement values in vascular convergence sign group were significantly higher than those in non-vascular convergence sign group ((27.6 ± 10.5) vs (3.2 ± 2.8) HU, P = 0.000). The CT enhancement values in lesions tended to increase with the number of connecting blood vessels. However, no significant differences existed among the subgroups (P > 0.05). The accuracy of vascular convergence sign for detection of pulmonary malignant nodules was 84.9%, 70.6% and 60.3% according to the standards of CT enhancement values ≥ 15, 20, 25 HU respectively. The sensibility, specificity and accuracy of determining pulmonary malignant nodules were 97.2%, 68.8% and 93.7% according to the standard of vascular convergence sign. The accuracy of determining pulmonary nodules' CT enhancement values ≥ 15 HU was 88.1% according to the standard of vascular convergence sign. CONCLUSION: Vascular convergence sign may be used to indicate the enhancement of pulmonary nodules when CT enhancement images are not available.