Search

Abstract Background The new-onset postoperative atrial fibrillation (NOPAF) following pulmonary resection is a common clinical concern. The aim of this study was to construct a nomogram to intuitively predict the risk of NOPAF and offered protective treatments. Methods Patients who underwent pulmonary resection between January 2018 and December 2020 were consecutively enrolled. Forward stepwise multivariable logistic regression analyses were used to screen independent predictors, and a derived nomogram model was built. The model performance was evaluated in terms of calibration, discrimination and clinical utility and validated with bootstrap resampling. Results A total of 3583 patients who met the research criteria were recruited for this study. The incidence of NOPAF was 1.507% (54/3583). A nomogram, composed of five independent predictors, namely age, admission heart rate, extent of resection, laterality, percent maximum ventilation volume per minute (%MVV), was constructed. The concordance index (C-index) was 0.811. The nomogram showed substantial discriminative ability, with an area under the receiver operating characteristic curve of 0.811 (95% CI 0.758-0.864). Moreover, the model shows prominent calibration performance and higher net clinical benefits. Conclusion We developed a novel nomogram that can predict the risk of NOPAF following pulmonary resection, which may assist clinicians predict the individual probability of NOPAF and perform available prophylaxis. By using bootstrap resampling for validation, the optimal discrimination and calibration were demonstrated, indicating that the nomogram may have clinical practicality.

The authors present an intelligent metasurface system that uses a target detection algorithm combined with a depth camera, to automatically detect the position of moving targets and achieve real-time wireless communications. The system can operate for multiple targets in limited ambient light, outdoor and other realistic environments.

Abstract Inactivation of the p53 pathway is linked to a variety of human cancers. As a critical component of the p53 pathway, ubiquitin‐specific protease 7 (USP7) acts as a deubiquitinase for both p53 and its ubiquitin E3 ligase mouse double minute 2 homolog. Here, myeloid leukemia factor 2 (MLF2) is reported as a new negative regulator of p53. MLF2 interacts with both p53 and USP7. Via these interactions, MLF2 inhibits the binding of USP7 to p53 and antagonizes USP7‐mediated deubiquitination of p53, thereby leading to p53 destabilization. Functionally, MLF2 plays an oncogenic role in colorectal cancer, at least partially, via the negative regulation of p53. Clinically, MLF2 is elevated in colorectal cancer and its high expression is associated with poor prognosis in patients with colorectal cancer. In wild‐type‐p53‐containing colorectal cancer, MLF2 and p53 expressions are inversely correlated. These findings establish MLF2 as an important suppressor of p53 function. The study also reveals a critical role for the MLF2–p53 axis in promoting colorectal carcinogenesis.

ObjectiveIn order to solve the problem of time cooperative path planning for unmanned marine system (UMS) in complex environments, we propose a cooperative path planning method based on a differential evolution (DE) algorithm. MethodsFirst, natural environment and enemy threat models in the air, sea and underwater are established. The objective function of path planning with multiple constraints is constructed and a strategy proposed to solve the time coordination problem under the constraints of heterogeneous platforms starting at different times and places, but arriving at the same time and place. Next, a DE algorithm is used to optimize the solution, and the influence of the number of waypoints on the success rate of the planning is studied. ResultsBased on the reasonable selection of the number of waypoints, the DE algorithm can respectively plan the path that satisfies the time cooperative constraint for the UMS and find the shortest time to reaching the target in complex environments with multiple threats and obstacles. The results also show that either excessive or inadequate numbers of waypoints will result in success rate reduction of the path planning. ConclusionsThe results of this study show that the model and constraint conditions are reasonable, and the proposed algorithm can solve the problem of time coordination in the path planning of UMS, which has great practical application value.

BackgroundLung adenocarcinoma (LUAD) is a fatal malignancy in the world. Growing evidence demonstrated that autophagy-related genes regulated the immune cell infiltration and correlated with the prognosis of LUAD. However, the autophagy-based signature that can predict the prognosis and the efficiency of checkpoint immunotherapy in LUAD patients is yet to be discovered.MethodsWe used conventional autophagy-related genes to screen candidates for signature construction in TCGA cohort and 9 GEO datasets (tumor samples, n=2181; normal samples, n=419). An autophagy-based signature was constructed, its correlation with the prognosis and the immune infiltration of LUAD patients was explored. The prognostic value of the autophagy-based signature was validated in an independent cohort with 70 LUAD patients. Single-cell sequencing data was used to further characterize the various immunological patterns in tumors with different signature levels. Moreover, the predictive value of autophagy-based signature in PD-1 immunotherapy was explored in the IMvigor210 dataset. At last, the protective role of DRAM1 in LUAD was validated by in vitro experiments.ResultsAfter screening autophagy-related gene candidates, a signature composed by CCR2, ITGB1, and DRAM1 was established with the ATscore in each sample. Further analyses showed that the ATscore was significantly associated with immune cell infiltration and low ATscore indicated poor prognosis. Meanwhile, the prognostic value of ATscore was validated in our independent LUAD cohort. GSEA analyses and single-cell sequencing analyses revealed that ATscore was associated with the immunological status of LUAD tumors, and ATscore could predict the efficacy of PD-1 immunotherapy. Moreover, in vitro experiments demonstrated that the inhibition of DRAM1 suppressed the proliferation and migration capacity of LUAD cells.ConclusionOur study identified a new autophagy-based signature that can predict the prognosis of LUAD patients, and this ATscore has potential applicative value in the checkpoint therapy efficiency prediction.

IntroductionSegmentectomy is widely used for early-stage lung cancer presenting as single or multiple ground-glass opacities (GGOs). Precise segmentectomy is the recommended procedure in China. However, clinically, most routine segmentectomies are performed using only high-resolution computed tomography (CT). The aim of this study was to evaluate the effect of two segmentectomy approaches for GGOs in the lung.MethodsFrom January 2020 to September 2020, 55 precise segmentectomies performed with real-time guidance using 3D reconstruction and 343 routine segmentectomies for patients with single or multiple GGOs were performed as uniportal procedures. To reduce bias related to outcomes, preoperative clinical factors were used for propensity score matching (1:1); 55 precision and 55 routine segmentectomies were selected and further analyzed. Perioperative outcomes, namely operation time, blood loss, resection margins, number of removed lymph nodes, postoperative pulmonary function (1 month after surgery), length of postoperative stay, and postoperative complications were compared between the two groups.ResultsPatients constituted 43 men and 67 women, with an age range of 25–68 years (median: 53 years). No significant differences were seen between the groups regarding blood loss, complications, histological type, and postoperative pulmonary function, and there were no 30-day postoperative deaths in either group. The median operation time for the Precision group (74 min) was longer than in the Routine group (55 min) (p

IntroductionCancer progression is determined not only by the malignant behavior of tumors but also by the immune microenvironment. The tumor immune microenvironment also plays a pivotal role in determining the clinical response of non-small-cell lung cancer (NSCLC) to immunotherapies. To understand the possible mechanisms and explore new targets in lung cancer immunotherapy, we characterized the immune profiles in NSCLC patients.MethodsSeventy-one NSCLC patients who underwent radical resection were selected. The immune cell composition in paired tumor and adjacent normal lung tissues was tested by flow cytometry. The associations of tumor immune microenvironment characteristics with clinicopathological factors and overall survival were analyzed. Kaplan–Meier curves and Cox proportional hazards models were used to determine differences in survival.ResultsCompared with adjacent normal lung tissues, an increased proportion of CD45+ hematopoietic-derived cells, CD4+ T cell subtypes, Tregs and B cells was observed in tumor samples with a reduced frequency of myeloid cell populations. There was no significant increase in total CD8+ T cells, but both PD1+ and CD38+ CD8+ T cells were significantly enriched in tumor samples and statistically significantly associated with tumor size. In addition, positive CD38 expression was highly correlated with PD1 positivity. A high proportion of CD8+ T cells and a low percentage of PD1+ CD8+ T cells were statistically significantly associated with better survival in stage II and III patients, whereas a low frequency of CD38+ CD8+ T cells was statistically significantly associated with better survival in all patients and identified as an independent prognostic factor (p=0.049).ConclusionWe profiled the immune cells in the tumor tissues of NSCLC patients using flow cytometry. The results revealed significant enrichment of infiltrating immune cells. A strong correlation was identified between CD38 and PD-1 expression on CD8+ T cells in tumors. CD8+ T cells and their subtypes play a critical role in the prediction of prognosis.

ObjectiveThis study aimed to analyze the relationship between the number of examined lymph nodes (ELNs) at the N1 station and the postoperative clinicopathological features and prognosis of patients with pT1-3N0M0 non-small cell lung cancer (NSCLC).MethodsThe cut-off value of the number of ELNs at the N1 station was obtained using X-tile software analysis. Kaplan-Meier survival curve analysis and the Cox proportional hazard model were used to study the impact of the number of ELNs at the N1 station on the prognosis of postoperative patients with pT1-3N0M0 NSCLC.ResultsThe median survival time and 1-, 3- and 5-year survival rates of 0 ELNs at the N1 station were 28.0 months and 74.8%, 45.4%, and 21.2%, respectively. The median survival time and 1-, 3-, and 5-year survival rates of 1–4 ELNs at the N1 station were 45.0 months and 85.5%, 55.4%, and 39.1%, respectively. In the group with ≥ 5 ELNs at the N1 station, the median survival time and the 1-, 3- and 5-year survival rates were 59.0 months and 94.0%, 62.7%, and 48.2%, respectively. Both univariate and multivariate Cox regression analyses showed that the number of ELNs at the N1 station, T stage and operation type were independent factors affecting the prognosis of patients with pT1-3N0M0 NSCLC.ConclusionIncreasing the number of ELNs at the N1 station is positively correlated with the long-term survival rate of patients with T1-3N0M0 NSCLC. At least 5 LNs at the N1 station should be examined in pathological examination.

p53 plays a central role in tumor suppression. Emerging evidence suggests long noncoding RNA (lncRNA) as an important class of regulatory molecules that control the p53 signaling. Here, we report that the oncogenic lncRNA E2F1 messenger RNA (mRNA) stabilizing factor (EMS) and p53 mutually repress each other's expression. EMS is negatively regulated by p53. As a direct transcriptional repression target of p53, EMS is surprisingly shown to inhibit p53 expression. EMS associates with cytoplasmic polyadenylation element-binding protein 2 (CPEB2) and thus, disrupts the CPEB2-p53 mRNA interaction. This disassociation attenuates CPEB2-mediated p53 mRNA polyadenylation and suppresses p53 translation. Functionally, EMS is able to exert its oncogenic activities, at least partially, via the CPEB2-p53 axis. Together, these findings reveal a double-negative feedback loop between p53 and EMS, through which p53 is finely controlled. Our study also demonstrates a critical role for EMS in promoting tumorigenesis via the negative regulation of p53. [ABSTRACT FROM AUTHOR]

Deregulated expression of c-Myc is an important molecular hallmark of cancer. The oncogenic function of c-Myc has been largely attributed to its intrinsic nature as a master transcription factor. Here, we report the long noncoding RNA (lncRNA) E2F1 messenger RNA (mRNA) stabilizing factor (EMS) as a direct c-Myc transcriptional target. EMS functions as an oncogenic molecule by promoting G1/S cell cycle progression. Mechanistically, EMS cooperates with the RNA binding protein RALY to stabilize E2F1 mRNA, and thereby increases E2F1 expression. Furthermore, EMS is able to connect c-Myc to cell cycle control and tumorigenesis via modulating E2F1 mRNA stability. Together, these findings reveal a previously unappreciated mechanism through which c-Myc induces E2F1 expression and also implicate EMS as an important player in the regulation of c-Myc function. [ABSTRACT FROM AUTHOR]