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This study asks whether new CEOs care about innovation post-turnover. Using a large sample of Chinese listed firms between 2008 and 2019, our identification strategy relies on the exogenous variation in CEO turnovers. Our difference-in-difference estimates indicate that new CEOs improve R&D efficiency and generate more and higher quality patents. We further show that this positive effect is more pronounced when CEOs have longer career horizons and overseas experience. Overall, our findings indicate that CEO turnover represents an effective mechanism for fostering innovation and new CEOs indeed care about innovation. Our results could benefit several groups of stakeholders with respect to CEO selection process.

We examine the influence of corporate culture on innovation using a unique set of data from Chinese listed companies over the period 2008-2017. Using the Competing Value Framework, we quantify corporate culture using textual analysis of financial statements. We find a positive and significant impact of a creation culture on innovation measured by both patent applications and citations as well as innovation efficiency. We address endogeneity concerns and conduct a battery of robustness tests, including alternative proxies for both corporate innovation and culture and conclude that variations in culture have a significant impact on firm-level innovation. We also show that a strong creation culture is more likely to spur innovation for firms in more competitive product markets and firms that are subject to higher managerial career concerns. We provide empirical evidence that corporate culture is an important driver in enhancing innovation. Our results have clear implications for directors and shareholders.

Three-dimensional (3D) printing, also known as additive manufacturing, has unique advantages over traditional manufacturing technologies; thus, it has attracted widespread attention in the medical field. Especially in the context of the frequent occurrence of major public health events, where the medical industry’s demand for large-scale and customized production is increasing, traditional 3D printing production scheduling methods take a long time to handle large-scale customized medical 3D printing (M-3DP) production and have weak intelligent collaboration ability in the face of job-to-device matching under multimaterial printing. Given the problem caused by M-3DP large-scale customized production scheduling, an intelligent collaborative scheduling multiagent-based method is proposed in this study. First, a multiagent-based optimization model is established. On this basis, an improved genetic algorithm embedded with the product mix strategy and the intelligent matching mechanism is designed to optimize the completion time and load balance between devices. Finally, the effectiveness of the proposed method is evaluated using numerical simulation. The simulation results indicated that compared with the simple genetic algorithm, particle swarm optimization, and snake optimizer, the improved genetic algorithm could better reduce the M-3DP mass customization production scheduling time, optimize the load balance between devices, and promote the “intelligent manufacturing” process of M-3DP mass customization.

Deep Learning (DL) algorithms based on artificial neural networks have achieved remarkable success and are being extensively applied in a variety of application domains, ranging from image classification, automatic driving, natural language processing to medical diagnosis, credit risk assessment, intrusion detection. However, the privacy and security issues of DL have been revealed that the DL model can be stolen or reverse engineered, sensitive training data can be inferred, even a recognizable face image of the victim can be recovered. Besides, the recent works have found that the DL model is vulnerable to adversarial examples perturbed by imperceptible noised, which can lead the DL model to predict wrongly with high confidence. In this paper, we first briefly introduces the four types of attacks and privacy-preserving techniques in DL. We then review and summarize the attack and defense methods associated with DL privacy and security in recent years. To demonstrate that security threats really exist in the real world, we also reviewed the adversarial attacks under the physical condition. Finally, we discuss current challenges and open problems regarding privacy and security issues in DL. Published version

Our previous study reported that ADAM12 was highly expressed in small cell lung cancer (SCLC) and could be an effective marker for diagnosis and prognosis. Yet, the reason for the high expression of ADAM12 in SCLC requires further elucidation. Transcription factor E2F1 has been receiving increasing attention due to the complexity and diversity of its function in cancer. In the present study, the expression of ADAM12 was significantly decreased following silencing of E2F1 expression by siRNA, thus indicating that E2F1 may regulate the expression of ADAM12 at the level of transcription. Chromatin immunoprecipitation-to-sequence analysis identified three binding sites for E2F1 in the locus for ADAM12. They were Chr10: 128010444-128011026, located in the intron of ADAM12, named seq0; Chr10: 128076927‑128078127, located in the promoter of ADAM12, named seq1; and Chr10: 128086195‑128086876, located in the upstream 20 kb from the transcription start site of ADAM12, named: seq2. Dual‑luciferase reporter experiments revealed that seq1 not seq0 and seq2 was able to promote the expression of luciferase. Notably, co-transfection of E2F1 significantly increased the activity of seq1 not seq0 and seq2, but quantitative polymerase chain reaction results showed that seq0, seq1 and seq2 could recruit E2F1, indicating that the influence of E2F1 in regulating the expression of ADAM12 was complex. Sequence analysis clarified that seq1 was a part of the ADAM12 promoter, yet the functions of seq0 and seq2 were unknown. Fusion fragments containing seq0-seq1 or seq2-seq1 were analyzed in luciferase constructs. Compared with seq1 alone, the activities of these fusion fragments were non-significantly reduced. The activities of fusion fragments were significantly decreased following co-transfection with E2F1. Thus, the present findings support the conclusion that the E2F1 transcription factor regulates the expression of ADAM12 by binding differential cis-acting elements.

A meta-analysis was conducted to summarize evidence from prospective cohort studies about the association of fruit and vegetable consumption with the risk of lung cancer.Pertinent studies were identified by a search of Embase and PubMed databases to October 2014. A random-effects model was used to combine study-specific relative risks and 95% confidence interval [RR (95% CI)]. Dose-response relationship was assessed by restricted cubic spline.The RR (95% CI) of lung cancer for highest versus lowest category of fruit and vegetable (FV) consumption was 0.87 (0.79-0.95) (8 studies including 12,942 cases among 1,571,494 subjects), and the effect was 0.84 (0.79-0.90) for fruit (16 studies including 15,421 cases among 1,791,469 subjects) and 0.90 (0.84-0.96) for vegetable (19 studies including 16,422 cases among 1,877,375 subjects). The above-mentioned associations did not differed significantly in subgroup analysis by country, age, number of covariates adjusted, quality score, sex, smoking status and histological subtypes; however, studies with follow-up duration of ≥10 years and with FV assessed by interview showed a stronger association than those of10 years and by self-administrated food frequency questionnaires, respectively. The risk of lung cancer decreased by 3% (P=0.07), 5% (P0.01) and 3% (P=0.09) for every 1 serving/day increment in FV, fruit and vegetable consumption, respectively. There was a threshold around 2 servings/day of fruit and 2 servings/day of vegetable, respectively, after which the risk of lung cancer did not reduce further.Fruit and vegetable consumption are inversely associated with risk of lung cancer.

Background The role of tumor necrosis factor alpha (TNF-α) in cancer is complex with both apoptotic and anti-apoptotic roles proposed. However the mechanism is not clear. In the study, we designed to investigate the effect of TNF-α on the activation and expression of nuclear factor kappa B (NF-κB)/p65/SLUG/PUMA/Bcl-2 levels in human lung cancer A549 cell line, and in conditions of TNF-α-induced apoptosis. Methods We have engineered three A549 cell lines that were transiently transfected with PUMA siRNA, SLUG siRNA and Bcl-2 siRNA, respectively. We have measured the in vitro effects of siRNA on apoptosis, and sensitivity to 20 ng/ml of TNF-α treatment for 24–48 h. Results We found the NF-κB activity and PUMA mRNA/protein was significantly increased after treatment of TNF-α for 24 h in untreated A549 cells, and led to a significant increase in TNF-α-induced apoptosis, no significant increase of SLUG and Bcl-2 level was shown. However, after treatment of TNF-α for 48 h in untreated A549 cells, SLUG and Bcl-2 level was significant increased, and PUMA level was significant decreased, and TNF-α-induced apoptosis was significantly decreased compared to the apoptosis level after treatment of TNF-α for 24 h. Inhibition of the NF-κB activity could effectively decrease the PUMA level and increase the SLUG and Bcl-2 level. PUMA silencing by siRNA led to a significant decrease in TNF-α-induced apoptosis after treatment of TNF-α for 24 h. Bcl-2 and SLUG silencing by siRNA led to a significant increase in TNF-α-induced apoptosis for 48 h. Furthermore, SLUG silencing increased PUMA level and decreased Bcl-2 level. Conclusions The findings suggested that TNF-α treatment promoted apoptosis via the NF-κB-dependent PUMA pathway. The anti-apoptotic role of TNF-α was via NF-κB-dependent SLUG and Bcl-2 pathway at a later time.

Results from the recent meta-analysis suggested a favorable effect of green tea consumption and risk of lung cancer, while no significant association was found between black tea consumption and risk of lung cancer. Besides, a significantly positive association was found between coffee consumption and risk of lung cancer. However, the relationship of green tea and coffee consumption is unclear. Thus the dose-response relationship was assessed by restricted cubic spline model and multivariate random-effect meta-regression. Results suggested that a linear dose-response relationship exists between coffee consumption and risk of lung cancer, while the dose-response relationship is nonlinear between green tea consumption and risk of lung cancer.

Background The purpose of this study was to clarify the treatment value of zoledronic acid (ZA) and/or strontium-89 (Sr-89) in patients with non–small-cell lung cancer (NSCLC) with asymptomatic bone metastases (BMs). Patients and Methods Eligible patients were those with resectable NSCLC and asymptomatic BMs. These candidates were randomized into 4 groups: group A was treated with ZA and Sr-89 simultaneously, group B was treated with ZA, group C was treated with Sr-89, and group D was untreated. Patients were monitored and analyzed for the first skeletal-related event (SRE), overall survival (OS), and annual incidence of SREs. Results One hundred eighty patients were enrolled. Time to first SRE in group A was 15 months (95% confidence interval [CI], 14.0-16.0 months), in group B it was 12 months (95% CI, 11.1-13.0 months), in group C it was 9 months (95% CI, 8.5-9.5 months), and in group D it was 8 months (95% CI, 7.1-8.9 months) ( P = .000). The overall survival (OS) in group A was 17 months (95% CI, 16.0-18.1 months); in group B, it was 16 months (95% CI, 14.2-17.8 months); in group C, it was 12 months (95% CI, 11.1-12.9 months); and in group D, it was 12 months (95% CI, 10.8-13.2 months). The annual incidence of SREs in group A was 24.4%; in group B, it was 55.6%; in group C, it was 75.6%; in group D, it was 91.1% ( P = .000). Conclusions Treatment with ZA and/or Sr-89 significantly extended the time to first SRE as well as survival time and reduced the annual incidence of SREs. Treatment with the combined use of ZA and Sr-89 was safe and well tolerated and achieved the best effect on asymptomatic BMs of NSCLC.