An improved asymmetric t-tube model of the arterial system is proposed. The model consists of two viscoelastic tubes of differing lengths, each terminated in a modified windkessel with inductance as well as resistance and compliance. Equations for calculating the input impedance of this model are presented. Using typical data from the literature, the model predicts a more realistic impedance modulus and phase than previous models of the circulation. Parametric analysis shows that when peripheral compliances are altered, sharp peaks in the very low frequency portions of the impedance spectra are produced, whereas alterations of either the characteristic impedances or inductances of the terminations have little effect on input impedance. Alteration of the elasticity or relative lengths of the tubes results in shifts in the positions of the maxima and minima akin to those observed experimentally. Change in the viscosity of the walls or of the blood only affects the fluctuations of the impedance spectra without affecting the positions of the maxima and minima. Thus, with this still simple model, very realistic impedance spectra are obtainable. The model provides more insight than previously proposed models into the individual influence of various parameters of the proximal and peripheral vasculature on central hemodynamics.
New semiconductor electric film has many advantages, such as the uniform film surface, long life, no inductance, high thermal efficiency, etc. Especially its wide voltage range, AC and DC characteristics of efficient use of available,can be direct coupling with solar, wind and other energy.Thereby reducing the use of sustainable energys cost here.In this paper, we design a new type of energy-saving electrothermal furnace which take a semiconductor electric film as the electric heating element,and well try to explore the application of this new type of electric materials.
Purpose Recent studies have shown that G protein-regulated inducer of neurite outgrowth 1 (GPRIN1) regulates cancer proliferation and migration. However, there is limited research regarding its role in gallbladder cancer (GBC). We aimed to investigate the mechanism by which GPRIN1 promotes GBC cell proliferation and migration. Methods Immunohistochemistry was performed to visualize in situ GPRIN1 expression in 65 human GBC tissues and 59 corresponding normal tissues. The Kaplan–Meier method was used to analyze the correlation between GPRIN1 and overall survival. Cell proliferation (Celigo and MTT), apoptosis (FACS), and cell migration and invasion assays and a subcutaneous xenograft tumor model were used to define the effects of GPRIN1 downregulation in GBC cells in vitro and in vivo. Coimmunoprecipitation assays, mass spectrometry and Western blotting were performed to identify GPRIN1-interacting proteins. Cell proliferation, MTT and Transwell assays were performed to verify the functional recovery effect of cyclin-dependent protein kinase 1 (CDK1) on GPRIN1. Proteomic analysis of differentially expressed proteins and/or phosphorylated peptides was performed. Results GPRIN1 is upregulated in GBC tumor tissues and high GPRIN1 expression is positively correlated with a poor prognosis in GBC patients. High GPRIN1 expression reinforced the proliferative and invasive capacities of GBC in vitro and in vivo. Coimmunoprecipitation assays, mass spectrometry and Western blotting validated the direct interaction between GPRIN1 and CDK1. Cell proliferation, MTT and Transwell assays suggested that CDK1 exerts a functional recovery effect on GPRIN1. Proteomic analysis revealed the involvement of CDK1 in many biological processes and cellular pathways. Conclusions GPRIN1 promotes the invasion and metastasis of GBC cells via CDK1 pathway activation.
e23532 Background: Ewing sarcoma is a highly aggressive round cell mesenchymal tumor that commonly occurs in children and young adults. It is molecularly characterized by chromosomal translocations, most commonly t (11;22), resulting in the abnormal EWSR1-FLI1 fusion. In addition to EWSR1-FLI1, patients may have other genomic variants that can be used for risk stratification. In the present study, we retrospectively investigated the association between co-variant genes and prognosis in patients with Ewing sarcoma. Methods: From 2019 to 2021, 10 patients with Ewing sarcoma were enrolled in the study, and their standard first-line treatment consisted of five-drug regimen chemotherapy including vincristine, doxorubicin (Adriamycin) and cyclophosphamide, alternating with ifosfamide and etoposide (VAC/IE). We carried out whole-exome sequencing on collected tumor samples and matched leukocyte DNA from these patients. Mutations, indels, gene deletions, and amplifications were identified, and survival analysis was performed. Results: In general, median progression-free survival (PFS) of the 10 confirmed Ewing sarcoma (with EWSR1-FLI1 fusion) patients was 10.5 months. We found that 60%, 30%, and 30% of patients had genetic variants (including mutation and copy number variation) in the three signaling pathways of cell cycle, WNT, and NOTCH, respectively. Their PFS was shorter than patients without these variants (log-rank test, p = 0.0345, 0.0053, and 0.0053, respectively). Median PFS was 7 vs 17 months in cell cycle pathway (the former with variants and the latter without variants), 5 vs 14 months in WNT pathway, and 5 vs 14 months in NOTCH pathway. However, there was no difference in PFS between patients with and without variants in other pathways (including TP53, RTK-RAS, MYC, DDR, PI3K) (log-rank test, p>0.05). Conclusions: We found that the variants in cell cycle, WNT and NOTCH signaling pathway were associated with poor prognosis of Ewing sarcoma. This study provides important molecular markers for risk stratification in patients with Ewing sarcoma, which may provide insights into later clinical trials.
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