Jiangbing Li's research while affiliated with Henan Provincial People’s Hospital and other places

This study was to develop a radiomics nomogram mainly using wavelet features for identifying malignant and benign early-stage lung nodules for high-risk screening. A total of 116 patients with early-stage solitary pulmonary nodules (SPNs) (≤ 3 cm) were divided into a training set (N = 70) and a validation set (N = 46). Radiomics features were extracted from plain LDCT images of each patient. A radiomics signature was then constructed with the LASSO with the training set. Combined with independent risk factors, a radiomics nomogram was built with a multivariate logistic regression model. This radiomics signature, consisting of one original and nine wavelet features, achieved favorable predictive efficacy than Mayo Clinic Model. The radiomics nomogram with radiomics signature and age also showed good calibration and discrimination in the training set (AUC 0.9406; 95% CI 0.8831–0.9982) and the validation set (AUC 0.8454; 95% CI 0.7196–0.9712). The decision curve indicated the clinical usefulness of our nomogram. The presented radiomics nomogram shows favorable predictive accuracy for identifying malignant and benign lung nodules in early-stage patients and is much better than the Mayo Clinic Model.

Background The association between low‐density lipoprotein cholesterol, high‐density lipoprotein cholesterol, and triglycerides with cardiovascular disease ( CVD ) has been well studied. No previous studies considered trajectory of these lipids jointly. This study aims to characterize longitudinal trajectories of lipid profile jointly and examine its impact on incident CVD . Methods and Results A total of 9726 participants (6102 men), aged from 20 to 58 years who had lipids repeatedly measured 3 to 9 times, were included in the study. Three distinct trajectories were identified using the multivariate latent class growth mixture model: inverse U‐shape (18.72%; n=1821), progressing (66.03%; n=6422), and U‐shape (15.25%; n=1483). Compared with the U‐shape class, the adjusted hazard ratio and 95% CI were 1.33 (1.05–1.68) and 1.49 (1.14–1.95) for the progressing and inverse U‐shape class, respectively. The area under the curve was calculated using the integral of the model parameters. In the adjusted model, total and incremental area under the curve of lipid profile were significantly associated with CVD risk. Furthermore, the model‐estimated levels and linear slopes of lipids were calculated at each age point according to the latent class growth mixture model model parameters and their first derivatives, respectively. After adjusting for covariates, standardized odds ratio of slope increases gradually from 1.11 (1.02, 1.21) to 1.21 (1.12, 1.31) at 20 to 40 years and then decreased to 1.02 (0.94, 1.11) until 60 years. Conclusions These results indicate that the lipids profile trajectory has a significant impact on CVD risk. Age between 20 and 42 years is a crucial period for incident CVD , which has implications for early lipids intervention.

Background: Studies have demonstrated that high or low haemoglobin increases the risk of stroke. Previous studies, however, performed only a limited number of haemoglobin measurements, while there are dynamic haemoglobin changes over the course of a lifetime. This longitudinal cohort study aimed to classify the long-term trajectory of haemoglobin and examine its association with stroke incidence. Methods: The cohort consisted of 11,431 participants (6549 men) aged 20 to 50 years whose haemoglobin was repeatedly measured 3-9 times during 2004-2015. A latent class growth mixture model (LCGMM) was used to classify the long-term trajectory of haemoglobin concentrations, and hazard ratios (HRs) and 95% confidence intervals (95% CI) according to the Cox proportional hazard model were used to investigate the association of haemoglobin trajectory types with the risk of stroke. Results: Three distinct trajectory types, high-stable (n = 5395), normal-stable (n = 5310), and decreasing (n = 726), were identified, with stroke incidence rates of 2.7, 1.9 and 3.2 per 1000 person-years, respectively. Compared to the normal-stable group, after adjusting for the baseline covariates, the decreasing group had a 2.94-fold (95% CI 1.22 to 7.06) increased risk of developing stroke. Strong evidence was observed in men, with an HR (95% CI) of 4.12 (1.50, 11.28), but not in women (HR = 1.66, 95% CI 0.34, 8.19). Individuals in the high-stable group had increased values of baseline covariates, but the adjusted HR (95% CI), at 1.23 (0.77, 1.97), was not significant for the study cohort or for men and women separately. Conclusions: This study revealed that a decreasing haemoglobin trajectory was associated with an increased risk of stroke in men. These findings suggest that long-term decreasing haemoglobin levels might increase the risk of stroke.

Atherosclerosis is a chronic inflammatory disease of the vasculature. Exosomes derived from mesenchymal stem cells (MSCs) exert immunomodulatory and immunosuppressive effects; however, the MSCs-exosomes administration on atherosclerosis was unknown. Here, our ApoE −/- mice were fed a high-fat diet and received intravenous injections of exosomes from MSCs for 12 weeks. After tail-vein injection, MSCs-exosomes were capable of migrating to atherosclerotic plaque and selectively taking up residence near macrophages. MSCs-exosomes treatment decreased the atherosclerotic plaque area of ApoE −/- mice and greatly reduced the infiltration of macrophages in the plaque, associating induced macrophage polarization towards M2. In vitro, MSCs-exosomes treatment markedly inhibited LPS-induced M1 markers expression, while increased M2 markers expression in macrophages. Moreover, miR-let7 family was found to be highly enriched in MSCs-exosomes. Endogenous miR-let7 expression was found in the aortic root of ApoE −/- mice, and MSCs-exosomes treatment further up-regulated miR-let7 levels. In addition, inhibition of miR-let7 in U937 cells significantly inhibited the migration and M2 polarization via IGF2BP1 and HMGA2 pathway respectively in vitro. Our study demonstrates that MSCs-exosomes ameliorated atherosclerosis in ApoE −/- and promoted M2 macrophage polarization in the plaque through miR-let7/HMGA2/NF-κB pathway. In addition, MSCs-exosomes suppressed macrophage infiltration via miR-let7/IGF2BP1/PTEN pathway in the plaque. This finding extends our knowledge on MSCs-exosomes affect inflammation in atherosclerosis plaque and provides a potential method to prevent the atherosclerosis. Exosomes from MSCs hold promise as therapeutic agents to reduce the residual risk of coronary artery diseases.

Hypoxia induces protective autophagy in advanced glioblastoma cells, and targeting this process may improve the outcome for glioblastoma patients. Recent studies have suggested that the autophagic process is upregulated in glioblastoma cells in response to extensive hypoxia. Here, we describe a novel tumor suppressor in glioblastoma cells, whereby hypoxia downregulated CREBRF expression and acts as a potent inhibitor of autophagy in glioblastoma cells via the CREB3/ATG5 pathway. Our results demonstrate that CREBRF expression negatively correlates with autophagic and HIF-1α levels in different grade gliomas. Given that CREBRF is a negative regulator of CREB3, CREB3 knockdown also repressed hypoxia-induced autophagy in glioblastoma cells in vitro. Collectively, our findings provide new insight into the molecular mechanisms underlying hypoxia-induced glioblastoma cell autophagy and indicate that the hypoxia/CREBRF/CREB3/ATG5 pathway plays a central role in malignant glioma progression.

Highlighted the spectrum of coronary atherosclerosis in asymptomatic population by Computed Tomography Angiography (CTA) and developed a surrogation of expensive CTA to early detect coronary atherosclerosis. Three hundred and seven self-referred urban Han Chinese asymptomatic individuals underwent coronary CTA were consecutively enrolled. Total plaque score (TPS), Segment stenosis score (SSS) and Coronary Artery Disease severity (CADS) were used to measure and illustrate the spectrum of atherosclerosis burden by mapping their incidence and proportion onto coronary artery tree. Logistic regression model was further used to explore the association between lipid biomarkers and TPS (SSS) for developing a surrogation of CTA to early detect coronary atherosclerosis. We found that the incidence of TPS, SSS and CADS were up to 71.34%, 68.08%, and 71.34%; and high-risk individuals reached up to 11.07%, 15.31% and 16.29% respectively. All TPS, SSS and CADS were much higher in male than female, and have trend of increasing with age. The most lesion segment emerged on proximal LAD, followed by proximal RCA, mid LAD, proximal LCX, and mid RCA with mixed plaque as dominant. HDL-C was a predictor to both TPS [OR: 0.12 (0.02-0.82)] and SSS [OR: 0.15 (0.03-0.76)], and could identify the serious atherosclerosis subjects of TPS or SSS score >5 (AUC 0.73 and 0.70). The atherosclerosis plaque burden was about one in ten as high-risk individuals in this specific urban Han Chinese population. As potential surrogation of CTA, HDL-C was recognized as a significant predictor to atherosclerosis burden and revealed a good performance for identifying high-risk individuals.