Insufficient Radiofrequency Ablation Promotes Angiogenesis of Residual Hepatocellular Carcinoma Via HIF-1α/VEGFA

Background: The mechanism of rapid growth of the residual tumor after radiofrequency (RF) ablation is poorly understood. In this study, we investigated the effect of hyperthermia on HepG2 cells and generated a subline with enhanced viability and dys-regulated angiogenesis in vivo, which was used as a model to further determine the molecular mechanism of the rapid growth of residual HCC after RF ablation. Methodology/Principal Findings: Heat treatment was used to establish sublines of HepG2 cells. A subline (HepG2 k) with a relatively higher viability and significant heat tolerance was selected. The cellular protein levels of VEGFA, HIF-1α and p-Akt, VEGFA mRNA and secreted VEGFA were measured, and all of these were up-regulated in this subline compared to parental HepG2 cells. HIF-1α inhibitor YC-1 and VEGFA siRNA inhibited the high viability of the subline. The conditioned media from the subline exerted stronger pro-angiogenic effects. Bevacizumab, VEGFA siRNA and YC-1 inhibited proangiogenic effects of the conditioned media of HepG2 k cells and abolished the difference between parental HepG2 cells and HepG2 k cells. For in vivo studies, a nude mouse model was used, and the efficacy of bavacizumab was determined. HepG2 k tumor had stronger pro-angiogenic effects than parental HepG2 tumor. Bevacizumab could inhibit the tumor growth and angiogenesis, and also eliminate the difference in tumor growth and angiogenesis between parental HepG2 tumor and HepG2 k tumor in vivo. Conclusions/Significance: The angiogenesis induced by HIF1α/VEGFA produced by altered cells after hyperthermia treatment may play an important role in the rapid growth of residual HCC after RF ablation. Bevacizumab may be a good candidate drug for preventing and treating the process

Brief Communication Relationship of high CH50 level and interruption of cascade reaction of complement mRNA expression in acute venous thromboembolism patients

Abstract: In patients with pulmonary embolism (PE), forepart components of complements were activated. However there are interruption/decrease of cascade reaction and cytolytic effects in complement system. This study detected CRP, CH50, C3 and C4 levels in patients with venous thromboembolism (VTE) and compare with the imbalance of complement associated gene mRNA expression in PE patients. There was significant increase of CH50 in acute VTE patients. Even though CH50 increased significantly in acute VTE patients and had a relatively high sensitivity, cytolytic effects of complements might decrease, based on the genomics results of complement cascade reactions imbalance/interruption and increased total complements in VTE patients

Lightweight Intent Recognition Method Based on Diffusion Model

Abstract To address the challenges posed by imbalanced and limited battlefield data, which typically results in complex models prone to overfitting during training, we introduce a novel diffusion model grounded in Wasserstein distance (WDiffusion) tailored for the multi-categorical and multivariate characteristics inherent to intent recognition data. Subsequently, we propose a streamlined tactical intent recognition framework predicated on gate recurrent unit (GRU), designed to enhance model responsiveness, and train it on an innovative dataset. Comparative experimental analyses corroborate that the synthetic data generated via WDiffusion significantly outperforms other prevalent generation models. Furthermore, the WDiffusion-GRU model achieves a recognition accuracy of 97.09%, surpassing current aerial target intent recognition models by more than 1.07%. This advancement maintains high recognition precision while substantially curtailing model parameters, thereby amplifying the agility and reliability of battlefield commanders’ decision-making processes

Fourier transform infrared investigation on the interaction between CrCl3 and polyvinylpyrrolidone

Band shifting, splitting and widening of the amide I band of the CrCl3/poly(N-vinyl- pyrrolidone) system was studied by FTIR. Secondary derivative spectra show the band consists of several overlapping bands. It suggests Cr3+/amide group complexes of various coordinating and aggregating states co-exist in the system.EI

Hypochlorite-induced oxidative stress elevates the capability of HDL in promoting breast cancer metastasis

<p>Abstract</p> <p>Background</p> <p>Previous studies suggest that oxidative stress plays an important role in the development of breast cancer. There is a significant inverse relationship between HDL and the risk and mortality of breast cancer. However, it is well known that under conditions of oxidative stress, such as breast cancer, HDL can be oxidatively modifiedand these modifications may have an effect on the functions of HDL. The purpose of this study is to determine the different effects of normal and oxidized (caused by hypochlorite-induced oxidative stress) HDL on breast cancer cell metastasis.</p> <p>Methods</p> <p>Human breast cancer cell lines were treated with normal and hypochlorite-oxidized HDL, and then cell metastasis potency <it>in vivo </it>and the abilities of migration, invasion, adhesion to HUVEC and ECM <it>in vitro </it>were examined. Integrin expression and PKC activity were evaluated, and PKC inhibitor and PKC siRNA was applied.</p> <p>Results</p> <p>We found hypochlorite-oxidized HDL dramatically promotes breast cancer cell pulmonary metastasis (133.4% increase at <it>P </it>< 0.0 l for MDA-MB-231 by mammary fat pad injection; 164.3% increase at <it>P </it>< 0.01 for MCF7 by tail vein injection) and hepatic metastasis (420% increase at <it>P </it>< 0.0 l for MDA-MB-231 by mammary fat pad injection; 1840% fold increase at <it>P </it>< 0.001 for MCF7 by tail vein injection) in nude mice, and stimulates higher cell invasion (85.1% increase at <it>P </it>< 0.00 l for MDA-MB-231; 88.8% increase at <it>P </it>< 0.00 l for MCF7;), TC-HUVEC adhesion (43.4% increase at <it>P </it>< 0.00 l for MDA-MB-231; 35.2% increase at <it>P </it>< 0.00 l for MCF7), and TC-ECM attachment (41.0% increase at <it>P </it>< 0.00 l for MDA-MB-231; 26.7% increase at <it>P </it>< 0.05 for MCF7) <it>in vitro </it>compared with normal HDL. The data also shows that the PKC pathway is involved in the abnormal actions of hypochlorite-oxidized HDL.</p> <p>Conclusions</p> <p>Our study demonstrated that HDL under hypochlorite-induced oxidative stress stimulates breast cancer cell migration, invasion, adhesion to HUVEC and ECM, thereby promoting metastasis of breast cancer. These results suggest that HDL-based treatments should be considered for treatment of breast cancer patients.</p