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Background and objective Lung cancer is the leading cause of cancer-related death, and small cell lung cancer (SCLC) has a poor prognosis in all types of lung cancer. This study evaluated the relationship between pretreatment serum apolipoprotein levels and prognosis in patients with SCLC, seeks a new index can guide diagnosis and treatment of SCLC. Methods This study retrospectively analyzed the clinical data of 122 patients with SCLC. The clinical results of patients with serum apolipoprotein levels within 2 weeks before treatment were collected, including apolipoprotein AI (ApoA-I), apolipoprotein B (ApoB), and the ratio of apolipoprotein B to apolipoprotein AI (ApoB/ApoA-I). Patients' progression-free survival (PFS) and overall survival (OS) are the main outcome indicators. The best critical to determine the index's value by X-tile tool. For survival analysis, Kaplan-Meier method was used for analysis, and Cox regression analysis method was used for single factor analysis and multifactor analysis. Results Compared with patients with low ApoA-I levels, patients with high ApoA-I levels (ApoA-I>1.12 g/L) had better OS (21.5 mon vs 12.3 mon, P=0.007) and PFS (7.3 mon vs 5.5 mon, P=0.017). In contrast, patients with higher ApoB/ApoA-I levels had worse median OS than patients with lower ApoB/ApoA-I levels (13.4 mon vs 20.7 mon, P=0.012). Multivariate Cox regression analysis showed that ApoA-I was an independent prognostic factor affecting PFS in SCLC patients (HR=0.67, 95%CI: 0.45-0.99, P=0.043). ApoB/ApoA-I is an independent risk factor for OS in patients with SCLC (HR=1.98, 95%CI: 1.21-3.23, P=0.007). Conclusion Serum ApoA-I level and ApoB/ApoA-I level before treatment can be important prognostic factors for SCLC, which is helpful to judge the prognosis of patients.

In recent years, lung cancer has become the leading cause of cancer-related deaths. There is increasing evidence that many lipids and lipid analogs are key regulators of tumorigenesis, and factors that affect blood lipid levels such as smoking, diet, and obesity may be associated with cancer risk. With the deepening of research on the relationship between lipids and tumorigenesis, exploring the correlation between blood lipids and lung cancer risk and prognosis has become a research hotspot. This article reviews the research progress of the relationship between blood lipid levels and the risk of lung cancer, blood lipid levels and the prognosis of lung cancer patients, and the adjustment of blood lipid drugs and the prevention and treatment of lung cancer.

The relentless debate on postoperative adjuvant radiotherapy in gastric adenocarcinoma (GA) has been lasting for decades. In this study, a new biomarker, named promoter methylation burden of DNA repair genes (RPMB), was established to identify the subgroup of patients who might benefit from adjuvant radiotherapy. Methylation profiles of 397 GA tumor samples were downloaded from The Cancer Genome Atlas (TCGA). RPMB for a patient was defined as the ratio of methylated DNA repair genes to the number of all DNA repair genes. Subgroup analyses in term of overall survival (OS) and disease-free survival (DFS) indicated that most of the subgroups favored the high-RMPB group. Kaplan-Meier analysis showed that overall the patients with high RPMB after R0 resection had a significantly better clinical outcome regarding DFS (hazard ratio [HR] = 0.013, p = 0.042). Additionally, high-RPMB patients, who underwent adjuvant radiotherapy with both ≥T2 tumor and positive lymph nodes, showed superior DFS in comparison with the low-RPMB group (HR = 5.35 × 10−10, n = 26, p = 0.010). RPMB might be considered as a promising biomarker for decision-making with regard to postoperative adjuvant radiotherapy for GA patients.

Abstract Hole drilling or contour milling for the large and complex workpieces such as automobile panels and aircraft fuselages makes a high combined demand on machining accuracy, stiffness and workspace of machining equipment. Therefore, a 5-DOF (degrees of freedom) parallel kinematic machine (PKM) with redundant constraints is proposed. Based on the kinematics analysis of the parallel mechanism using intermediate variables, the kinematics problems of the PKM are solved through equivalent kinematics model. The structural stiffness matrix method is adopted to model the stiffness of the parallel mechanism of the PKM, where the stiffness of each joint and branch component is obtained by stiffness formula and finite element analysis. And the stiffness model of the parallel mechanism is improved by correction coefficient matrix, each element of which is constructed as a polynomial function of three independent end variables of the parallel mechanism. The terminal stiffness matrices obtained by simulation result are used to determine the coefficients of polynomial function by least square fitting to describe the correction coefficient over the workspace of the parallel mechanism quantitatively. The experiment results prove that the modification method can greatly improve the stiffness model of the parallel mechanism. To enhance the machining accuracy of the PKM, the proposed kinematics model and the improved stiffness model are utilized to optimize the working stiffness of parallel machine by searching the best relative position of parallel machine and workpiece. A plate workpiece taken as example is examined in the case study section, which demonstrates the effectiveness of optimization method.

GSDME is a newly recognized executor of cellular pyroptosis, and has been recently implicated in tumor growth and immunity. However, knowledge about the molecular regulators underlying GSDME abundance remains limited. Here, we performed integrative bioinformatics analyses and identified that epithelial-mesenchymal transition (EMT) gene signatures exhibited positive correlation with GSDME levels across human cancers. A causal role was supported by the observation that EMT dictated GSDME reversible upregulation in multiple experimental models. Mechanistically, transcriptional activation of GSDME was directly driven by core EMT-activating transcription factors ZEB1/2, which bound to the GSDME promoter region. Of functional importance, elevated GSDME in mesenchymally transdifferentiated derivatives underwent proteolytic cleavage upon antineoplastic drug exposure, leading to pyroptotic cell death and consequent cytokine release. Taken together, our findings pinpointed a key transcriptional machinery controlling GSDME expression and indicated potential therapeutic avenues to exploit GSDME-mediated inflammatory pyroptosis for the treatment of mesenchymal malignancies.

C23H39ClN2O4, triclinic, P1‾$P‾{1}$ (no. 2), a = 9.0752(19) Å, b = 9.542(2) Å, c = 16.049(3) Å, α = 99.088(4)°, β = 94.422(4)°, γ = 107.146(4)°, V = 1300.0(5) Å3, Z = 2, Rgt(F) = 0.0646, wRref(F2) = 0.2298, T = 293.0 K.

C24H34N6Cl2Zn, monoclinic, P21/c (no. 14), a = 9.513(3) Å, b = 9.546(3) Å, c = 30.956(10) Å, β = 101.228(9)°, V = 2757.3(15) Å3, Z = 4, Rgt(F) = 0.0452, wRref(F2) = 0.1299, T = 293 K.