Artificial intelligence in lung cancer screening: Detection, classification, prediction, and prognosis.

BACKGROUND: The exceptional capabilities of artificial intelligence (AI) in extracting image information and processing complex models have led to its recognition across various medical fields. With the continuous evolution of AI technologies based on deep learning, particularly the advent of convolutional neural networks (CNNs), AI presents an expanded horizon of applications in lung cancer screening, including lung segmentation, nodule detection, false-positive reduction, nodule classification, and prognosis. METHODOLOGY: This review initially analyzes the current status of AI technologies. It then explores the applications of AI in lung cancer screening, including lung segmentation, nodule detection, and classification, and assesses the potential of AI in enhancing the sensitivity of nodule detection and reducing false-positive rates. Finally, it addresses the challenges and future directions of AI in lung cancer screening. RESULTS: AI holds substantial prospects in lung cancer screening. It demonstrates significant potential in improving nodule detection sensitivity, reducing false-positive rates, and classifying nodules, while also showing value in predicting nodule growth and pathological/genetic typing. CONCLUSIONS: AI offers a promising supportive approach to lung cancer screening, presenting considerable potential in enhancing nodule detection sensitivity, reducing false-positive rates, and classifying nodules. However, the universality and interpretability of AI results need further enhancement. Future research should focus on the large-scale validation of new deep learning-based algorithms and multi-center studies to improve the efficacy of AI in lung cancer screening.

Application of computer-aided detection for NCCN-based follow-up recommendation in subsolid nodules: Effect on inter-observer agreement.

RATIONALE AND OBJECTIVES: Computer-aided detection (CAD) of pulmonary nodules reduces the impact of observer variability, improving the reliability and reproducibility of nodule assessments in clinical practice. Therefore, this study aimed to assess the impact of CAD on inter-observer agreement in the follow-up management of subsolid nodules. MATERIALS AND METHODS: A dataset comprising 60 subsolid nodule cases was constructed based on the National Cancer Center lung cancer screening data. Five observers independently assessed all low-dose computed tomography scans and assigned follow-up management strategies to each case according to the National Comprehensive Cancer Network (NCCN) guidelines, using both manual measurements and CAD assistance. The linearly weighted Cohen's kappa test was used to measure agreement between paired observers. Agreement among multiple observers was evaluated using the Fleiss kappa statistic. RESULTS: The agreement of the five observers for NCCN follow-up management categorization was moderate when measured manually, with a Fleiss kappa score of 0.437. Utilizing CAD led to a notable enhancement in agreement, achieving a substantial consensus with a Fleiss kappa value of 0.623. After using CAD, the proportion of major and substantial management discrepancies decreased from 27.5% to 15.8% and 4.8% to 1.5%, respectively (p < 0.01). In 23 lung cancer cases presenting as part-solid nodules, CAD significantly elevates the average sensitivity in detecting lung cancer cases presenting as part-solid nodules (overall sensitivity, 82.6% vs. 92.2%; p < 0.05). CONCLUSION: The application of CAD significantly improves inter-observer agreement in the follow-up management strategy for subsolid nodules. It also demonstrates the potential to reduce substantial management discrepancies and increase detection sensitivity in lung cancer cases presenting as part-solid nodules.

Efficacy and safety assessment on herbs invigorating spleen and removing dampness, blood stasis and toxin combined with chemotherapy in the treatment of advanced colorectal cancer / 肿瘤研究与临床

Objective To evaluate systematically whether or not the treatment of herbs invigorating spleen and removing dampness,blood stasis and toxin with chemotherapy is better than chemotherapy alone for advanced colorectal cancer.Methods The randomized controlled trails (RCT) involving combined treatment of herbs with chemotherapy,published from January 2000 to October 2015,were searched in CBM,CNKI,Wanfang Data,VIP,PubMed,Embase databases.Stata 14.0 software was used to analyze the data.Results 19 RCT containing 941 patients were included in this reta-analysis.Compared with chemotherapy alone,the combined treatment of Chinese herbal medicine and chemotherapy was obviously better in 1-year survival rate (RR =1.28,95 ％ CI 1.14-1.45),2-year survival rate (RR =1.52,95 ％ CI 1.05-2.18),3-year survival rate (RR =2.76,95 ％ CI 1.56-4.88),objective response (RR =1.11,95 ％ CI 1.04-1.19),Karnofsky score (RR =1.46,95 ％ CI 1.27-1.68) and traditional chinese medicine (TCM) symptom score (RR =1.58,95 ％ CI 1.33-1.75).The adverse effect rate was statistically reduced in the combined treatment group:leukopenia (RR =0.59,95 ％ CI 0.40-0.8),nausea and vomiting (RR =0.68,95 ％ CI 0.59-0.79),diarrhea (RR =0.67,95 ％ CI 0.53-0.85),neurotoxicity (RR =0.79,95 ％ CI 0.65-0.96).Conclusion Compared with chemotherapy alone,the treatment of herbs invigorating spleen and removing dampness,blood stasis and toxin combined with chemotherapy for advanced colorectal cancer can significantly increase survival rate and objective response rate,improve the quality of life,and meanwhile decrease the adverse effect rate.

IL-25 promotes Th2 immunity responses in airway inflammation of asthmatic mice via activation of dendritic cells.

Allergic asthma occurs as a consequence of inappropriate immunologic inflammation to allergens and characterized by Th2 adaptive immune response. Recent studies indicated that interleukin (IL)-25, a member of the IL-17 cytokine family, had been implicated in inducing Th2 cell-dependent inflammation in airway epithelium and IL-25-deficient mice exhibit impaired Th2 immunity responses; however, how these cytokines influence innate immune responses remains poorly understood. In this study, we used ovalbumin (OVA) sensitization and challenge to induce the murine asthmatic model and confirmed by histological analysis of lung tissues and serum levels of total and OVA-specific immunoglobulin (Ig)-E. The expression of IL-25 was detected by quantitative real-time PCR and immunohistochemistry, respectively, and the dendritic cells (DCs) activation was detected by levels of CD80 and CD86 in bronchoalveolar lavage fluid (BALF) by flow cytometry. The mice sensitized and challenged with OVA showed high expression of IL-25 in both mRNA and protein levels in lungs. We detected the expression of CD80 and CD86 in BALF was also increased. A tight correlation between IL-25 mRNA and other Th2 cells producing cytokines such as IL-4, IL-5, and IL-13 in BALF was identified. Furthermore, when the asthmatic mice were treated with inhaled corticosteroids, the inflammatory cells infiltration and the inflammatory cytokines secretion were significantly decreased. In this study, we show that IL-25 promoted the accumulation of co-stimulatory molecules of CD80 and CD86 on DCs and then induced the differentiation of prime naive CD4(+) T cells to become proinflammatory Th2 cells and promoted Th2 cytokine responses in OVA-induced airway inflammation. The ability of IL-25 to promote the activation and differentiation of DCs population was identified as a link between the IL-17 cytokine family and the innate immune response and suggested a previously unrecognized innate immune pathway that promotes Th2 cytokine responses in asthmatic airway inflammation. Inhaled corticosteroids might be capable of inhibiting the promotion of IL-25 and present a promising strategy for the treatment of asthma.

Effects of Tanshinone ⅡA on proliferation and apoptosis of myeloblastic leukemia cell lines / 白血病·淋巴瘤

Objective To investigate effects of Tanshinone Ⅱ A (Tan Ⅱ) on proliferation and apoptosis of myeloblastic leukemia cell lines.Methods NB4,K562 and THP-1 cells were incubated with TanⅡA for 24,48 and 72 hours.Ddaunorubicin was used as a positive control.Cell proliferation was monitored by MTT assay.Cell apoptosis and cell cycle were determined by Annexin Ⅴ-FITC/PI flow cytometry.Expression of Caspase-3 was quantified by spectrophotometry.Results After incubation with various leukemia cells for 24,48 and 72 hours,Tan Ⅱ inhibited proliferation of NB4 cells with IC50 of 24.11,9.60 and 7.28 μmol/L,inhibited K562 cells with IC50 of 31.75,11.88 and 6.81 μmol/L and inhibited THP-1 cells with IC50 of 111.10,32.82 and 11.82,respectively.After treatment with Tan Ⅱ for 48 hours,cell apoptosis,the number of G1 phase cells and the expression of Caspase-3 in all three leukemia cell lines were increased significantly comparing with the blank control group (P ＜ 0.05).Conclusions Tan Ⅱ A has proliferation inhibitory effect on myeloblastic leukemia cell lines by the order of effect NB4＞K562＞THP-1.Tan ⅡA displays anti-leukemia activity possibly through arresting leukemia cells in G1 phase and inducing apoptosis by increasing Caspase-3 expression.

Overexpression of glucosylceramide synthase and its significance in the clinical outcome of non-small cell lung cancer / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Glucosylceramide synthase (GCS), an enzyme responsible for ceramide glycosylation, plays an important role in multidrug resistance (MDR) in some tumors in vitro; however, its expression and clinicopathological significance in non-small cell lung cancer (NSCLC) remains unclear.</p><p><b>METHODS</b>We evaluated GCS expression in 116 paired tumor and adjacent non-cancerous tissues and 50 frozen tissues from patients with NSCLC using immunohistochemistry and western blotting, and explored the correlation between GCS and NSCLC clinicopathological characteristics and prognosis. We observed the association between GCS and the MDR proteins P-glycoprotein (P-gp) and lung resistance-related protein (LRP) to determine the link between GCS and MDR at the histological level.</p><p><b>RESULTS</b>GCS expression was significantly upregulated in NSCLC tumors compared with non-cancerous tissue. There was high GCS expression in 75/116 tumor specimens (64.7%) and 16/116 non-cancerous specimens (13.8%). High GCS expression was significantly associated with poor differentiation (P = 0.01), lymph node metastasis (P = 0.004), recurrence/distant metastasis (P = 0.006), and chemotherapy resistance (P = 0.025). Multivariate analysis demonstrated that GCS immunopositivity was an independent risk factor for survival (P = 0.018). P-gp was expressed in 80/116 tumors (69.0%) and in 12/116 non-cancerous tissue specimens (10.3%; P = 0.001); LRP was expressed in 85/116 tumors (73.3%) and 19/116 non-cancerous tissue specimens (16.4%; P = 0.001). Importantly, the results demonstrated that increased GCS expression in NSCLC cancer specimens correlated with increased expression of P-gp and LRP, molecules known to stimulate cancer cell MDR (r = 0.612 and 0.503, P = 0.01 and 0.035, respectively).</p><p><b>CONCLUSION</b>GCS upregulation might contribute to the development of NSCLC and could be a useful prognostic indicator and chemoresistance predictor for NSCLC patients.</p>

Expression and significance of interleukin-25 level in airway inflammation of asthmatics / 中华全科医师杂志

A total of 59 untreated asthmatics and 47 healthy control subjects were recruited from Qianfoshan Hospital of Shandong Province from May 2011 to April 2012.Compared with healthy control subjects,the levels of IL-25 in induced sputum and eosinophils,IgE,interleukin-4 (IL-4) and interleukin25 (IL-25) in serum samples of asthmatics were significantly higher while the level of interferon-gamma (IFN-γ) were much lower.However,after inhaled glucocorticoid treatment,the levels of eosinophils,IL-4 and IL-25 decreased and IFN-γ significantly increased,while the level of IgE showed no significant changes.It was also found the expression of IL-25 was markedly positively correlated with the levels of eosinophils and IL-4 in serum and markedly negatively correlated with the levels of IFN-γ and had no relatio.

House dust mite regulate the lung inflammation of asthmatic mice through TLR4 pathway in airway epithelial cells.

Aberrant innate and adaptive immune responsed to allergens and environmental pollutants lead to respiratory allergic disease such as asthma. In this study, we focused on toll-like receptor-4 (TLR4) expressed on airway epithelium to identify house dust mite (HDM)-regulated allergic inflammation via TLR4 signaling pathway and the triggering to alveolar macrophages (AM)-driven adaptive immune response. The authors found that mouse exposed to HDM showed more eosinophils, neutrophils, monocytes, lymphocytes as well as total cells in bronchoalveolar lavage fluid (BALF) confirmed by flow cytometry. Besides, the expression of TLR4 in airway epithelial cells was significantly increased in both mRNA and protein levels in mice treated with HDM and the expression of CD40 and CD86 in AM was also increased in mice exposed to HDM. Tight correlation between TLR4 protein and CD40, CD86 in AM was identified. This study demonstrates that TLR4 expression on airway epithelium played an essential role in HDM-induced activation of AM in immune responses and allergic inflammation. The airway epithelial TLR4 signaling pathway revealed tight connection between endotoxin exposure and asthma prevalence in the clinic.

TSLP promotes lung Inflammation via activating dendritic cells in OVA-induced mice asthmatic model / 中华微生物学和免疫学杂志

Objective To study the expression of thymic stromal lymphopoietin(TSLP) and the activation of DCs in OVA-induced murine asthma model, and investigate the effects and underlying mecha-nisms of TSLP on lung inflammation. Methods Thirty BALB/c mice were randomly divided into control group, OVA group and TSLP neutralizing antibody treated group. The asthma model was evaluated by airway responsiveness and histological analysis of lung tissues ; The levels of TSLP mRNA in lungs were determined by quantitative real-time PCR; The expression of TSLP in lungs were determined by immunohistochemistry and Western blot; The expression of CD40, CD80, CD86 in BALF was detected by FACS. Results Both the histological analysis of lung tissues and the airway responsiveness were all consistent with the characteris-tic of murine asthma model. The expression of TSLP and TSLP mRNA in the OVA group was significantly in-creased compared with blank group. The expression of CD40, CD80, CD86 in BALF from OVA group was increased significantly compared with the control group. Furthermore, treating mice with TSLP neutralizing antibody reduced the expression of CD40, CD80, CD86 on dendritic cells, and IL-4, IL-5, IL-13 in the OVA group. Conclusion Our study indicate that TSLP was highly expressed in the bronchial epithelia of murine asthma model, via upregulation of CD40, CD80, CD86, induce DCs to active CD4~+ T cells and pro-duce type 2 responses, so that aggravating the lung inflammation of asthma. Blocking TSLP is capable of in-hibiting the production of Th2 cytokines, thus presents a promising strategy for the treatment of asthma.