The safety and efficacy of the fissure-first approach in lung segmentectomy for patients with incomplete fissures.

Background: Lung segmentectomy has gained much more attention as an important surgical method for treating early-stage lung cancer. However, incomplete fissures increase the difficulty of lung segmentectomy. The aim of this study was to analyze the safety and efficacy of the fissure-first approach in precision resection of lung segments for patients with incomplete fissures. Methods: The clinical data of patients with incomplete fissures who underwent lung segmentectomy were retrospectively analyzed. Date was divided into fissure-first approach in lung segmentectomy group (group A) and fissure-last approach in lung segmentectomy group (group B). The general linear data, operation times, intraoperative adverse events, postoperative recovery dates and complications were compared. Results: A total of 122 patients with complete clinical data were included. Patients in group B had more COPD (p < 0.05), and the lesions in group A were more closely related to the hilum of the lung (p < 0.05). Compared to Group B, Group A achieved better surgical outcomes, such as operation time, postoperative hospital stays, intraoperative bleeding, number of intrapulmonary lymph nodes sampled, counts of resected subsegments (except the upper lobe of the right lung), and rate of conversion to thoracotomy (all p < 0.05). Conclusion: The fissure-first approach is a safe and effective surgical approach in lung segmentectomy for patients with incomplete fissures. This approach can reduce the counts of resected subsegments and improve techniques in lung segmentectomy for patients with lung incomplete fissures.

Clinical Analysis of Superficial Temporal Artery-Middle Cerebral Artery Bypass Combined with Brain-Temporal Muscle Sticking in the Treatment of Chronic Internal Carotid Artery Occlusion.

Objective: NHISS score, MMSE scale, craniocerebral CTA or DSA, and craniocerebral magnetic resonance 3D-ASL were used to evaluate the efficacy and safety of superficial temporal artery-middle cerebral artery (STA-MCA) shunt combined with cranial-muscular-merging (EMS) in the treatment of symptomatic chronic internal carotid artery occlusion. Methods: The purpose of this study was to retrospectively analyze the clinical data of 15 patients with symptomatic chronic internal carotid artery occlusion who received STA-MCA shunt combined with EMS treatment at Weifang Brain Hospital and Weifang Traditional Chinese Medicine Hospital from July 2016 to December 2020. The patients' neurological and cognitive functions were evaluated by NHISS score and MMSE examination before surgery and 6 months after surgery. Adverse reactions after surgery were observed, and preoperative and postoperative cerebral hemodynamics, the patency of the shunt anastomosis, and the compensation of collateral circulation were evaluated by cranial CTA or DSA and cranial MRI 3D-ASL. Results: All 15 patients underwent successful surgery. One patient experienced transient mild cerebral hyperperfusion syndrome postoperatively. Six months after surgery, the NHISS score was significantly improved compared with that before surgery (P = .0001), and the MMSE score was also significantly improved compared with before surgery (P = .0124). No adverse events of poor scalp healing, intracranial infection, subcutaneous fluid accumulation, subdural hematoma, or cerebral hemorrhage were observed postoperatively. Imaging examination showed that the shunt vessels were unobstructed, the middle cerebral artery was dilated, collateral circulation in the surgical area was increased, and cerebral blood flow increased. Conclusion: STA-MCA shunt combined with EMS treatment is safe and effective for symptomatic chronic internal carotid artery occlusion. It has the potential to improve cerebral blood flow and reduce clinical symptoms.

Performance of the 2019 ESC pre-test probability model in predicting obstructive coronary artery disease in a Chinese population using coronary computed tomography angiography outcomes.

BACKGROUND: The 2019 European Society of Cardiology (ESC) guidelines proposed a pre-test probability (PTP) model to determine the likelihood of coronary artery disease (CAD). However, the prediction accuracy of this model has not yet been evaluated in Chinese populations. This study aimed to validate the 2019 ESC-PTP model in predicting CAD using coronary computed tomography angiography (CCTA) outcomes in a Chinese population. METHODS: A total of 26,346 consecutive patients with suspected CAD who underwent CCTA were included. The 2019 ESC-PTP model and 2013 ESC-PTP model were calculated for each patient, considering age, sex, and the symptom of chest pain, and the patients were categorized into low-, intermediate-, and high-risk groups. The predictive performance of the 2019 ESC-PTP model was evaluated by comparing it with the 2013 ESC-PTP model and the observed prevalence of CAD from CCTA. RESULTS: Among the 11,234 patients analyzed in the study, 1896 (16.9%) patients were found to have obstructive CAD from CCTA. The 2019 ESC-PTP model had better calibration compared to the 2013 ESC-PTP model. After categorization, 80.9% of patients (67.9% in men and 94.4% in women) were in the same risk category as in the 2019 ESC-PTP model, but the risks of younger patients (7.5% versus 2.5%; P â€‹< â€‹0.001) and patients with non-anginal chest pain (13.7% versus 8.2%; P â€‹< â€‹0.001) were underestimated in the 2019 ESC-PTP model. CONCLUSION: The 2019 ESC-PTP model demonstrated a good calibration in predicting CAD in a Chinese population who underwent CCTA, but it exhibited an underestimation of CAD probability in younger patients and patients with non-anginal chest pain.

New concepts drive the development of delivery tools for sustainable treatment of diabetic complications.

Diabetic complications, especially diabetic retinopathy, diabetic nephropathy and painful diabetic neuropathy, account for a large portion of patients with diabetes and display rising global prevalence. They are the leading causes of blindness, kidney failure and hypersensitivity to pain caused by diabetes. Current approved therapeutics against the diabetic complications are few and exhibit limited efficacy. The enhanced cell-specificity, stability, biocompatibility, and loading capacity of drugs are essential for the mitigation of diabetic complications. In the article, we have critically discussed the recent studies over the past two years in material sciences and biochemistry. The insightful concepts in these studies drive the development of novel nanoparticles and mesenchymal stem cells-derived extracellular vesicles to meet the need for treatment of diabetic complications. Their underlying biochemical principles, advantages and limitations have been in-depth analyzed. The nanoparticles discussed in the article include double-headed nanodelivery system, nanozyme, ESC-HCM-B system, soft polymer nanostars, tetrahedral DNA nanostructures and hydrogels. They ameliorate the diabetic complication through attenuation of inflammation, apoptosis and restoration of metabolic homeostasis. Moreover, mesenchymal stem cell-derived extracellular vesicles efficiently deliver therapeutic proteins to the retinal cells to suppress the angiogenesis, inflammation, apoptosis and oxidative stress to reverse diabetic retinopathy. Collectively, we provide a critical discussion on the concept, mechanism and therapeutic applicability of new delivery tools to treat these three devastating diabetic complications.

Direct degradation and stabilization of proteins: New horizons in treatment of nonalcoholic steatohepatitis.

Nonalcoholic fatty liver disease (NAFLD) is featured with excessive hepatic lipid accumulation and its global prevalence is soaring. Nonalcoholic steatohepatitis (NASH), the severe systemic inflammatory subtype of NAFLD, is tightly associated with metabolic comorbidities, and the hepatocytes manifest severe inflammation and ballooning. Currently the therapeutic options for treating NASH are limited. Potent small molecules specifically intervene with the signaling pathways that promote pathogenesis of NASH. Nevertheless they have obvious adverse effects and show long-term ineffectiveness in clinical trials. It poses the fundamental question to efficiently and safely inhibit the pathogenic processes. Targeted protein degradation (TPD) belongs to the direct degradation strategies and is a burgeoning strategy. It utilizes the small molecules to bind to the target proteins and recruit the endogenous proteasome, lysosome and autophagosome-mediated degradation machineries. They effectively and specifically degrade the target proteins. It has exhibited promising therapeutic effects in treatment of cancer, neurodegenerative diseases and other diseases in a catalytic manner at low doses. We critically discuss the principles of multiple direct degradation strategies, especially PROTAC and ATTEC. We extensively analyze their emerging application in degradation of excessive pathogenic proteins and lipid droplets, which promote the progression of NASH. Moreover, we discuss the opposite strategy that utilizes the small molecules to recruit deubiquinases to stabilize the NASH/MASH-suppressing proteins. Their advantages, limitations, as well as the solutions to address the limitations have been analyzed. In summary, the innovative direct degradation strategies provide new insights into design of next-generation therapeutics to combat NASH with optimal safety paradigm and efficiency.

Large-scale and cost-efficient agrivoltaics system by spectral separation.

Agrivoltaics (AV) offers a promising solution to address both food and energy crises. However, crop growth under photovoltaic (PV) conditions faces substantial challenges due to insufficient light transmission. We propose a large-scale and cost-effective spectral separated concentrated agricultural photovoltaic (SCAPV) system. The system utilizes concentrator modules, cell components, and dual-axis tracking systems to enhance power conversion efficiency (PCE), achieving a maximum PCE of 11.6%. After three years of successful operation, a 10 kWp power plant achieved an average annual electricity generation exceeding 107 MWh/ha. The results showed higher yields of various crops, including ginger and sweet potatoes, and significant improvements in soil moisture retention compared to open air. The improvements in PCE and microclimate validate the scalability of the SCAPV, which provides better plant conditions and cost-effectiveness, with an estimated cost reduction of 18.8% compared to conventional PV power plant. This study provides valuable insights and directions for improvement in AV.

Ion channels regulate energy homeostasis and the progression of metabolic disorders: Novel mechanisms and pharmacology of their modulators.

The progression of metabolic diseases, featured by dysregulated metabolic signaling pathways, is orchestrated by numerous signaling networks. Among the regulators, ion channels transport ions across the membranes and trigger downstream signaling transduction. They critically regulate energy homeostasis and pathogenesis of metabolic diseases and are potential therapeutic targets for treating metabolic disorders. Ion channel blockers have been used to treat diabetes for decades by stimulating insulin secretion, yet with hypoglycemia and other adverse effects. It calls for deeper understanding of the largely elusive regulatory mechanisms, which facilitates the identification of new therapeutic targets and safe drugs against ion channels. In the article, we critically assess the two principal regulatory mechanisms, protein-channel interaction and post-translational modification on the activities of ion channels to modulate energy homeostasis and metabolic disorders through multiple novel mechanisms. Moreover, we discuss the multidisciplinary methods that provide the tools for elucidation of the regulatory mechanisms mediating metabolic disorders by ion channels. In terms of translational perspective, the mechanistic analysis of recently validated ion channels that regulate insulin resistance, body weight control, and adverse effects of current ion channel antagonists are discussed in details. Their small molecule modulators serve as promising new drug candidates to combat metabolic disorders.

Effects of intensive lipid lowering compared with moderate-intensity lipid lowering on coronary atherosclerotic plaque phenotype and major adverse cardiovascular events in adults with low to intermediate 10-year ASCVD risk (ILLUMINATION study): protocol for a multicentre, open-label, blinded-endpoint, randomised controlled trial.

INTRODUCTION: Current guidelines recommend moderate-intensity lipid lowering (low-density lipoprotein cholesterol, LDL-C of <2.6 mmol/L or 30%-49% reduction from the baseline) for patients with intermediate 10-year atherosclerotic cardiovascular disease (ASCVD) risk. The effects of intensive lipid lowering (LDL-C of <1.8 mmol/L) on coronary atherosclerotic plaque phenotype and major adverse cardiovascular events (MACE) in adults with both non-obstructive coronary artery disease (CAD) and low to intermediate 10-year ASCVD risk remain uncertain. METHODS AND ANALYSIS: Intensive Lipid-lowering for Plaque and Major Adverse Cardiovascular Events in Low to Intermediate 10-year ASCVD Risk Population is a multicentre, randomised, open-label, blinded endpoint clinical trial. Inclusion criteria are as follows: (1) patients with the age of 40-75 years within 1 month of coronary CT angiography (CCTA) and coronary artery calcium score (CACS) evaluation; (2) population with low to intermediate 10-year ASCVD risk (<20%) and (3) patients with non-obstructive CAD (stenosis <50%) using CCTA. 2900 patients will be randomly assigned to the intensive lipid lowering (LDL-C of <1.8 mmol/L or ≥50% reduction from the baseline) or the moderate-intensity lipid lowering (LDL-C of<2.6 mmol/L or 30%-49% reduction from the baseline) group in a 1:1 ratio. The primary endpoint is MACE (composite of all-cause death, non-fatal MI, non-fatal stroke, any revascularisation and hospitalisation for angina) within 3 years after enrolment. The secondary endpoints are changes in coronary total plaque volume (mm3), plaque burden (%), plaque composition (mm3, %), high-risk plaque characteristics detected using CCTA and CACS determined using CT. ETHICS AND DISSEMINATION: Ethics committee approval for this study was obtained from the review boards of Fuwai Hospital (No.2022-1787) and all other study sites. Written informed consent will be obtained from all participants. The results of this study will be published in peer-reviewed journals and reported at international conferences. TRIAL REGISTRATION NUMBER: NCT05462262.

KMT2D Deficiency Promotes Myeloid Leukemias which Is Vulnerable to Ribosome Biogenesis Inhibition.

KMT2C and KMT2D are the most frequently mutated epigenetic genes in human cancers. While KMT2C is identified as a tumor suppressor in acute myeloid leukemia (AML), the role of KMT2D remains unclear in this disease, though its loss promotes B cell lymphoma and various solid cancers. Here, it is reported that KMT2D is downregulated or mutated in AML and its deficiency, through shRNA knockdown or CRISPR/Cas9 editing, accelerates leukemogenesis in mice. Hematopoietic stem and progenitor cells and AML cells with Kmt2d loss have significantly enhanced ribosome biogenesis and consistently, enlarged nucleolus, increased rRNA and protein synthesis rates. Mechanistically, it is found that KMT2D deficiency leads to the activation of the mTOR pathway in both mouse and human AML cells. Kmt2d directly regulates the expression of Ddit4, a negative regulator of the mTOR pathway. Consistent with the abnormal ribosome biogenesis, it is shown that CX-5461, an inhibitor of RNA polymerase I, significantly restrains the growth of AML with Kmt2d loss in vivo and extends the survival of leukemic mice. These studies validate KMT2D as a de facto tumor suppressor in AML and reveal an unprecedented vulnerability to ribosome biogenesis inhibition.

DNMT3AR882H accelerates angioimmunoblastic T-cell lymphoma in mice.

DNA methylation-related genes, including TET2, IDH2, and DNMT3A are highly frequently mutated in angioimmunoblastic T-cell lymphoma (AITL), an aggressive malignancy of T follicular helper (Tfh) cells associated with aberrant immune features. It has been shown that TET2 loss cooperates with RHOAG17V to promote AITL in mice but the functional role of DNMT3A mutations in AITL remains unclear. Here, we report that DNMT3AR882H, the most common mutation of DNMT3A in AITL, accelerates the development of Tet2-/-; RHOAG17V AITL in mice, indicated by the expansion of malignant Tfh cells and aberrant B cells, skin rash, and significantly shortened disease-free survival. To understand the underlying cellular and molecular mechanisms, we performed single-cell transcriptome analyses of lymph nodes of mice transplanted with Tet2-/-, Tet2-/-; RHOAG17V or DNMT3AR882H; Tet2-/-; RHOAG17V hematopoietic stem and progenitor cells. These single-cell landscapes reveal that DNMT3A mutation further activates Tfh cells and leads to rapid and terminal differentiation of B cells, probably through enhancing the interacting PD1/PD-L1, ICOS/ICOSL, CD28/CD86, and ICAM1/ITGAL pairs. Our study establishes the functional roles of DNMT3A mutation in AITL and sheds light on the molecular mechanisms of this disease.

Pulsed-lighting LED luminaire for agriculture with a geometrical optical solution.

Light-emitting diodes (LEDs) are the 4th plant supplemental lighting source. Pulsed lighting is benefit to increase energy utilization efficiency in greenhouse production. A pulsed-lighting LED luminaire with geometrical optical solution is proposed to overcome the shortcoming with pulse width modulation (PWM) solution. In addition, this luminaire also achieves uniform lighting by designing optical surfaces. In the illumination area, the lighting frequency is 117.6 Hz and the illuminance uniformity is 0.789, which is better than 0.75 (+/- 12.5%). In an actual planting experiment of Brassica chinensis, the average fresh weight of the plants under the pulsed-lighting LED luminaire was 33.1% higher than that under the conventional LED luminaire. The results showed that the energy utilization efficiency of the pulsed-lighting LED luminaire is 22.9% higher than that of the conventional LED luminaire.

Fractal analysis on CO2 hydrate-bearing sands during formation and dissociation processes with NMR.

Injecting CO2 into submarine sediments to form hydrates is one of the potential methods of CO2 sequestration. The transition behavior of CO2 hydrates in porous media is of great practical significance. In this work, CO2 hydrate formation/dissociation in porous media was monitored in real time by a low-field magnetic resonance (MR) system, and a series of dynamic fractal dimensions of the pore space occupied by converted water during the hydrate formation/dissociation process were obtained based on the transverse relaxation time (T2) distributions. In general, the dimension of the converted water space increases with hydrate formation and decreases with the hydrate dissociation progress. A smaller particle size of porous media and a lower initial water saturation can promote hydrate formation, and the corresponding fractal dimension is higher during the hydrate formation process. There is a special status of the fractal period observed during the hydrate formation/dissociation process, and it is considered the temporally and spatially uniform distribution of hydrate crystal formation/dissociation inside the porous media. These results also indicate the relationships between the hydrate transition progress and the dynamic fractal dimension, which are useful for future works on pore-scale hydrate-bearing transitions during hydrate-based CO2 sequestration.

Exceptional terrestrial warmth around 4200-2800 years ago in Northwest China.

One of the Holocene abrupt events around 4200 years ago, lasting for âˆ¼ 200 years, is thought to have caused cultural disruptions, yet terrestrial climatic status right after the cold/dry event remains poorly defined and is often presumed that a generally cool condition prevailed during the Bronze Age (∼ 4000-2200 years ago). Here we report an alkenone-based summer temperature record over the past âˆ¼ 12,000 years, in addition to two updated alkenone records, from Northwest China, providing new insights into the climatic status right after the event. Our results indicate that exceptional terrestrial warmth, up to âˆ¼ 6 °C, occurred around 4200-2800 years ago during the Bronze Age, superimposed on the long-term Holocene cooling trend. The exceptional warmth in Northwest China, together with other climate anomalies elsewhere, suggests an unusual large-scale climatic reorganization at 4200-2800 years ago when solar activity remained high, with important implications to the climate background for cultural developments during the Bronze Age.

Dissecting the genetic and microenvironmental factors of gastric tumorigenesis in mice.

Gastric cancer (GC) is one of the most frequent and lethal malignancies in the world. However, our understanding of the mechanisms underlying its initiation and progression is limited. Here, we generate a series of primary GC models in mice with genome-edited gastric organoids, which elucidate the genetic drivers for sequential transformation from dysplasia to well-differentiated and poorly differentiated GC. Further, we find that the orthotopic GC, but not the subcutaneous GC even with the same genetic drivers, display remote metastasis, suggesting critical roles of the microenvironment in GC metastasis. Through single-cell RNA-seq analyses and functional studies, we show that the interaction between fibronectin 1 on stomach-specific macrophages and integrin a6ß4 on GC cells promotes remote metastases. Taken together, our studies propose a strategy to model GC and dissect the genetic and microenvironmental factors driving the full-range gastric tumorigenesis.

Acquired semi-squamatization during chemotherapy suggests differentiation as a therapeutic strategy for bladder cancer.

Cisplatin-based chemotherapy remains the primary treatment for unresectable and metastatic muscle-invasive bladder cancers (MIBCs). However, tumors frequently develop chemoresistance. Here, we established a primary and orthotopic MIBC mouse model with gene-edited organoids to recapitulate the full course of chemotherapy in patients. We found that partial squamous differentiation, called semi-squamatization, is associated with acquired chemoresistance in both mice and human MIBCs. Multi-omics analyses showed that cathepsin H (CTSH) is correlated with chemoresistance and semi-squamatization. Cathepsin inhibition by E64 treatment induces full squamous differentiation and pyroptosis, and thus specifically restrains chemoresistant MIBCs. Mechanistically, E64 treatment activates the tumor necrosis factor pathway, which is required for the terminal differentiation and pyroptosis of chemoresistant MIBC cells. Our study revealed that semi-squamatization is a type of lineage plasticity associated with chemoresistance, suggesting that differentiation via targeting of CTSH is a potential therapeutic strategy for the treatment of chemoresistant MIBCs.

Simultaneous determination of oxalate and citrate in urine and serum of calcium oxalate kidney stone rats by IP-RP LC-MS/MS.

Oxalate and citrate in 24 h urine and serum are considered to be associated with the incidence and recurrence risk of calcium oxalate kidney stones. The quantification of oxalate and citrate contributes to understand the pathological metabolism of kidney stones and guide the early diagnosis and recurrence monitoring. Although simultaneous quantification of oxalate and citrate in urine using liquid chromatography tandem mass spectrometry (LC-MS/MS) have been reported, the optimization of chromatographic column, mobile phase and mass spectrometry (MS) parameters has not been performed. In addition, these is a lack of suitable method for simultaneous detection of oxalate and citrate both in serum and urine. Therefore, we developed a method for the simultaneous determination of oxalate and citrate in urine and serum based on ion-pairing reversed-phase (IP-RP) LC-MS/MS. Herein, five ion-pair reagents, namely, triethanolamine, dimethylbutyl amine, diisopropenyl amine, N,N-dimethylcyclohexylamine and tripropylamine, and three ion-pairing reagent (IPR) buffers, namely, acetic acid, hexafluoro-2-isopropanol, and hexafluoro-2-methyl-2-propanol, were compared in regard to their chromatographic peak abundance and separation of oxalate and citrate. Moreover, MS parameters and the multiple reaction monitoring (MRM) conditions were also evaluated and optimized to obtain the maximum peak abundance. After that, the method was validated in the linear range of 0.25-1000 µM, and the correlation coefficient was ≥ 0.99. The precision and accuracy were < 14.70% and < 19.73%, respectively. The extraction recovery was 80.53-108.79%, and the matrix effect was < 8.79%. The quality control samples were stable at room temperature for 4 h, 4 °C for 24 h, and for 3 freeze-thaw cycles. Finally, this method was applied to the determination of oxalate and citrate in the serum and urine of rats with calcium oxalate kidney stones. The establishment of a stable and effective oxalate and citrate detection method is conducive to the diagnosis and monitoring of kidney stones.

KMT2C deficiency promotes small cell lung cancer metastasis through DNMT3A-mediated epigenetic reprogramming.

Small cell lung cancer (SCLC) is notorious for its early and frequent metastases, which contribute to it as a recalcitrant malignancy. To understand the molecular mechanisms underlying SCLC metastasis, we generated SCLC mouse models with orthotopically transplanted genome-edited lung organoids and performed multiomics analyses. We found that a deficiency of KMT2C, a histone H3 lysine 4 methyltransferase frequently mutated in extensive-stage SCLC, promoted multiple-organ metastases in mice. Metastatic and KMT2C-deficient SCLC displayed both histone and DNA hypomethylation. Mechanistically, KMT2C directly regulated the expression of DNMT3A, a de novo DNA methyltransferase, through histone methylation. Forced DNMT3A expression restrained metastasis of KMT2C-deficient SCLC through repressing metastasis-promoting MEIS/HOX genes. Further, S-(5'-adenosyl)-L-methionine, the common cofactor of histone and DNA methyltransferases, inhibited SCLC metastasis. Thus, our study revealed a concerted epigenetic reprogramming of KMT2C- and DNMT3A-mediated histone and DNA hypomethylation underlying SCLC metastasis, which suggested a potential epigenetic therapeutic vulnerability.

Combined metabolomics with transcriptomics reveals potential plasma biomarkers correlated with non-small-cell lung cancer proliferation through the Akt pathway.

BACKGROUND: Non-small-cell lung cancer (NSCLC) is one of the main types of lung cancer. Due to lack of effective biomarkers for early detection of NSCLC, the therapeutic effect is not ideal. This study aims to reveal potential biomarkers for clinical diagnosis. METHODS: The plasma metabolic profiles of the patients were characterized by liquid chromatography-mass spectrometry (LC-MS). Differential metabolites were screened by p less than 0.05 and VIP greater than 1. Multivariate statistical analysis was used to search for potential biomarkers. Receiver operating characteristic (ROC) curve was used to evaluate the predictors of potential biomarkers. Pathway enrichment analysis was performed on metabolomics data by Ingenuity Pathway Analysis (IPA) and transcriptomics data from GEO were used for validation. RESULTS: A plasma metabolite biomarker panel including 13(S)-hydroxyoctadecadienoic acid (13(S)-HODE) and arachidonic acid was chose. The area under the ROC curve were 0.917, 0.900 and 0.867 for the panel in the different algorithm like Partial Least Squares Discrimination Analysis (PLS-DA), Support Vector Machine (SVM), Random Forest (RF). The candidate biomarkers were associated with the Akt pathway. Genes involved in the biological pathway had significant changes in the expression levels. CONCLUSION: 13(S)-HODE and arachidonic acid may be potential biomarkers of NSCLC. The Akt pathway was associated with this biomarker panel in NSCLC. Further studies are needed to clarify the mechanisms of disruption in this pathway.