Increased protein and mRNA expression of endostatin in the ischemic brain tissue of rabbits after middle cerebral artery occlusion

Objective To explore the changes of endostatin （a strong anti-angiogenesis factor） and vascular endothelial growth factor （VEGF） in the brain tissues of rabbits following cerebral ischemia induced by middle cerebral artery occlusion （MCAO）. Methods Twenty-four New Zealand white rabbits were randomly divided into 5 groups： control （n = 5）, sham-operation （n = 4）, 2-hour ischemia （n = 5）, 24-hour ischemia （n = 5）, and 48-hour ischemia （n = 5）. The expression of VEGF and endostatin were measured by enzyme-linked immunosorbent assay （ELISA） and immunohistochemistry, respectively. In situ hybridization was used to characterize the expression of mRNA for the endostatin. Results Both the protein （at least 50%, P 〈 0.01） and mRNA （at least 70%, P 〈 0.05） of endostatin increased significantly in the ischemic brain tissues after MCAO compared with the control group. VEGF increased at least 270% in the brain after cerebral ischemia （P 〈 0.05）. Conclusion Cerebral ischemia leads to an up-regulation of endostatin in the brain, which is not associated with the increase of VEGF in the brain. The increase of endostatin may serve as a deleterious mechanism for ischemic injury through blocking angiogenesis.

Effect of NF-κB inhibitor PDTC on VEGF and endostatin expression of mice with Lewis lung cancer

Objective:To investigate the effects of NF-κB inhibitor pyrrolidine dithiocarbamate hydrochloride(PDTC) on vascular endothelial growth factor(VEGF) and endostatin expression in mice with Lewis lung cance;and its mechanism.Methods:Mice survival rate and anti-tumor effects were observed in different concentrations of NF-κB inhibitor PDTC after the Lewis lung cancer mice model was established.VEGF and endostatin expressions were detected by immunohistochemical assay.Results:Lewis lung cancer was be inhibited by 0.5 mg/kg.1.5 mg/kg and 3.0 mg/kg of NF-κB inhibitor PDTC(P<0.05).Microvessel density(MVD) in 0.5 mg/kg.1.5 mg/kg and 3.0 mg/kg NF-κB inhibitor PDTC groups were significantly lower than the control group(P<0.05).Immunohistochemical assay results showed that VEGF and endostatin expressions in the 0.5 mg/kg.1.5 mg/kg and 3.0 mg/kg NF-κB inhibitor PDTC groups were significantly lower than the control group(P<0.05).Western blot results also showed that NF-κB inhibitor PDTC could inhibit VEGF and endostatin expressions in tumor tissues.Conclusions:NF-κB inhibitor PDTC can inhibit tumor formation and reduce tumor angiogenesis in mice with Lewis lung cancer;and its mechanism maybe associated to VEGF and endostatin down-regulation.

Enhanced Effects of TRAIL-endostatin-based Double-gene-radiotherapy on Suppressing Growth, Promoting Apoptosis and Inducing Cell Cycle Arrest in Vascular Endothelial Cells

This study examined the effects of TRAIL-endostatin-based gene-radiotherapy on cellu-lar growth, apoptosis and cell cycle progression in human vascular endothelial cells ECV304 in vitro. The expression of TRAIL and endostatin protein in ECV304 cells was detected by ELISA after the transfection of recombinant plasmid pshuttle-Egr1-shTRAIL-shES and X-ray irradiation. Then MTT assay was used for determining the cellular proliferation, and flow cytometry (FCM) plus Annexin V and propidium iodide (PI) double-staining or PI single-staining were employed for the detection of apoptosis and cell cycle progression. The results showed that expression of TRAIL and endostatin protein exhibited a time- and dose-dependent change in ECV304 cells after pshut-tle-Egr1-shTRAIL-shES transfection in conjunction with irradiation. In the TRAIL-endostatin-based single- or double-gene-radiotherapy, the cell viability declined in a time- and dose-dependent manner, the percentage of cells at G2/M phase and apoptotic rate was increased, and the percentage of cells at G0/G1 phase was lowered as compared with those receiving radiotherapy alone. Moreover, TRAIL-endostatin-based double-gene-radiotherapy demonstrated better effects on growth inhibition, promotion of apoptosis and induction of cell cycle arrest in ECV304 cells than single-gene-radiotherapy.

Effect of recombinant human endostatin onradiotherapy for esophagus cancer

Objective:To investigate the effect of radiotherapy plus recombinant human endostatin（RHendostatin） on esophageal cancer and its mechanism.Methods:A total of SO nudemice were equally randomized into control group,radiotherapy group,and combined therapy group Ⅰ,Ⅱ,and Ⅲ after inoculating with Ecal09 cell suspension（1×107 cells/mL）.On the day of grouping,control group and radiotherapy group were injected normal saline,while radiotherapy group and 3 combined therapy groups received radiotherapy;besides,combined therapy group Ⅰ,Ⅱ,and Ⅲ was injected RH-endostatin of 2.5,5,10 mg/kg respectively.After 3-week therapy,the tumors of each group were collected and microvessel density and VEGF expression in tumors were determined.In vitro,Eca109 cells were divided into control group,radiotherapy group,and combined therapy group.Forty-eight hours after treatment cell cycle distribution and apoptosis rate were detected,and the activity of VEGF signal paths was semiquantitatively analyzed.Results:Since the 6th day of treatment,the relative tumor proliferation rate of combined therapy group Ⅱ was lower than radiotherapy group（P<0.05） and 40%since the 15 th day.Average microvessel density and EGFR expression in combined therapy group Ⅱ were lower than radiotherapy group（P<0.05）.In vitro,the cell percentage in S and G2/M phase of combined therapy group cells was lower than that in radiotherapy group cells,while the apoptosis rate and the expression of VEGF,AKT,p-AKT,ERK1/2 and p-ERKl/2 in combined group were higher than that in radiotherapy group（P<0.05）.Conclusions:RH-endostatin promotes the efficacy of radiotherapy on esophageal cancer,which may be partly realized by inhibiting the activity of VEGF related signal paths.

Endostatin enhances antitumor effect of tumor antigen-pulsed dendritic cell therapy in mouse xenograft model of lung carcinoma

Objective： To investigate the antitumor effect of endostatin combined with tumor antigen-pulsed dendritic cell （DC）-T cell therapy on lung cancer. Methods： Transplanted Lewis lung cancer （LLC） models of C57BL/6 mice were established by subcutaneous injection of LLC cells in left extremity axillary. Tumor antigen-pulsed DC-T cells from spleen cells and bone of mice were cultured in vitro. Tumor-bearing mice were randomly divided into three groups, including DC- T＋endostatin group, DC-T group, and phosphate-buffered saline （PBS） control group. Microvessel density （MVD） of tumor tissue in tumor-bearing mice was determined by immunohistochemistry （IHC）. The expressions of vascular endothelial growth factor （VEGF） and hypoxia-inducible factor-1α （HIF-1α） were determined by Western blotting and IHC staining. The proportions of CD8＋ T cells, mature dendritic cells （mDC）, tumor-associated macrophages [TAM （M1/M2）], and myeloid-derived suppressor cells （MDSC） in suspended cells of tumor tissue were determined by flow cytometry. The expressions of inter｜eukin （IL）-6, IL-10, IL-17, transforming growth factor-β（TGF-β） and interferon-γ （IFN-γ） in suspended cells of tumor tissue were detected by enzyme-linked immune sorbent assay （ELISA）. Results： DC-T cells combined with endostatin remarkably suppressed tumor growth. MVD of mice in DC- T＋endostatin group was significantly lower than that of the control group and DC-T monotherapy group. The expressions of VEGF, IL-6 and IL-17 in tumors were markedly decreased, but IFN-γ, and HIF-1α increased after treating with DC-T cells combined with endostatin, compared to control group and DC-T group. In the DC- T＋endostatin group, the proportions of MDSC and TAM （M2 type） were significantly decreased, mDC and TAM （Nil type） were up-regulated, and CD8＋ T cells were recruited to infiltrate tumors, in contrast to PBS control and DC-T monotherapy. DC-T cells combined with endostatin potently reduced the expressions of IL-6, IL-10, TGF-β and IL-17 in tumor tissue, and enhanced the expression of IFN-γ. Conclusions： The study indicated the synergic antitumor effects between endostatin and tumor antigen-pulsed DC-T cells, which may be a prospective therapy strategy to achieve potent antitumor effects on lung cancer.

Inhibitory Effect of Recombinant Endostatin on Angiogenesis and Tumor Growth of Hepatoma

To study the influence of recombinant endostatin on angiogenesis and tumor growth of mice H22 hepatoma, tumor models were constructed by injecting H22 hepatoma cells into the leg muscle of mice Recombinant endostatin was produced by gene engineering in E coli The recombinant protein was injected subcutaneously to treat transplanted hepatoma faraway The weight of tumors was measured, and the changes of necrosis of tumor cells and vessel density were observed by immunohistochemistry The results suggested that the growth of hepatoma models transplanted in the muscle of legs was suppressed by recombinant endostatin The density of vacularity was decreased, but the necrosis of tumor cells increased The inhibitory effect of recombinant endostatin on angiogenesis and tumor growth of hepatoma was not affected after chemotherapy

Comparisons of biophysical properties and bioactivities of mono-PEGylated endostatin and an endostatin analog

Background:Endostatin(ES) is a well-established potent endogenous antiangiogenic factor.An ES variant,called zinc-binding protein-ES(ZBP-ES),is clinically available;however,its use is limited by rapid renal clearance and short residence time.PEGylation has been exploited to overcome these shortcomings,and mono-PEGylated ES(called M_2ES) as well as mono-PEGylated ZBP-ES(MZBP-ES) are developed in our study.This study aimed to compare the biophysical properties and biological effects of M_2ES and MZBP-ES to evaluate their druggability.Methods:Circular dichroism and tryptophan emission fluorescence were used to monitor the conformational changes of M_2ES and MZBP-ES.Their resistance to trypsin digestion and guanidinium chloride(GdmCl)-induced unfolding was examined by Coomassie staining and tryptophan emission fluorescence,respectively.The biological effects of M_2ES and MZBP-ES on endothelial cell migration were evaluated using Transwell migration and wound healing assays,and the uptake of M_2ES and MZBP-ES in endothelial cells was also compared by Western blotting and immunofluorescence.Results:Structural analyses revealed that M_2ES has a more compact tertiary structure than MZBP-ES.Moreover,M_2ES was more resistant to trypsin digestion and GdmCI-induced unfolding compared with MZBP-ES.In addition,although M_2ES and MZBP-ES showed comparable levels of inhibiting transwell migration and wound healing of endothelial cells,M_2ES displayed an increased ability to enter cells compared with MZBP-ES,possibly caused by the enhanced interaction with nucleolin.Conclusions:M_2ES has a more compact tertiary structure,is more stable for trypsin digestion and GdmCI-induced unfolding,exhibits increased cellular uptake and shows equivalent inhibitory effects on cell migration relative to MZBP-ES,indicating that M_2ES is a more promising candidate for anticancer drug development compared with MZBP-ES.

Chinese medicinal compound delisheng has satisfactory anti-tumor activity,and is associated with up-regulation of endostatin in human hepatocellular carcinoma cell line HepG2 in three-dimensional culture

AIM： TO investigate the multicellular resistance of human hepatocellular carcinoma HepG2 cells in three-dimensional culture to delisheng, 5-fluorouracil and adriamycin, and the possible molecular mechanisms of delisheng. METHODS： Human hepatocellular carcinoma HepG2 cells were cultured with a liquid overlay technique. After the formation of multicellular spheroids, morphology was analyzed by phase contrast microscopy, scanning electron microscopy and transmission electron microscopy. Sensitivity of HepG2 cells to delisheng, 5-fluorouracil and adriamycin was investigated by Ml-I- assay in multicelluar spheroids and monolayers. Vascular endothelial growth factor （VEGF） and endostatin expression were analyzed in multicellular spheroids treated with delisheng, 5-fluorouracil, adriamycin and negative control PBS, with immunohistochemical staining. RESULTS： Multicellular spheroids exhibited structural characteristics somewhat different to those in monolayers. The cells in three-dimensional cell culture turned out to be less sensitive to delisheng, 5-fluorouracil and adriamycin than the cells cultured in monolayer. This showed that delisheng had a satisfactory cells inhibition ratio compared to 5-fluorouracil and adriamycin. Immunohistochemical staining showed that VEGF and endostatin expression was positive during growth as multicellular spheroids, and endostatin expression in spheroids with treatment of delisheng was higher than that with 5-fluorouracil, adriamycin and PBS （139.35 ± 7.83, 159.23 ± 10.34, 162.83 ± 3.47 and 148.48 ± 11.06, P 〈 0.05）.CONCLUSION： Chinese medicine compound delisheng has satisfactory anti-tumor activity in HepG2 cells in three-dimensional culture, and the effects are associated with up-regulation of endostatin.

基于扭曲混合Copula函数的均值-ES模型的构建与应用

考虑到金融资产间的极端尾部相依结构对投资组合风险优化的影响,构建基于扭曲混合Copula函数的均值-ES模型,通过扭曲函数来刻画金融资产间的极端尾部特征,获得一定预期收益下的投资组合优化策略。首先,将均值-ES模型中用于刻画相依结构的协方差矩阵扩展为可以描述极端尾部相依结构的扭曲混合Copula函数,构建了基于扭曲混合Copula函数的均值-ES模型;其次,提出了基于该模型的ES估计算法;最后,通过数值模拟和实证研究说明了该模型用于刻画极端尾部相依结构特征并进行投资组合优化的效果。数值模拟的结果表明,基于扭曲混合Copula函数的均值-ES模型适用于具有极端尾部相依结构特征的数据集;利用该模型进行投资组合优化后收益明显提升,风险显著降低。实证研究的结果表明,该模型能显著提升最优投资组合的样本外策略表现,同时返回检验的结果也验证了使用该模型对投资组合优化进行风险预测的准确性。因此,基于扭曲混合Copula函数的均值-ES模型弥补了传统投资组合风险优化模型中忽略极端尾部风险的不足,推动了扭曲混合Copula函数在投资组合风险优化中的应用研究。

Epidermal growth factor receptor antibody plus recombinant human endostatin in treatment of hepatic metastases after remnant gastric cancer resection

We report a 55-year-old male who developed advanced hepatic metastasis and peritoneal carcinomatosis after resection of remnant gastric cancer resection 3 mo ago. The patient only received epidermal growth factor (EGF) receptor antibody (Cetuximab) plus recombinant human endostatin (Endostar). Anti-tumor activity was assessed by 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography/computer tomography (PET/CT) at baseline and then every 4 wk. The case illustrates that 18FDG-PET/CT could make an early prediction of the response to Cetuximab plus Endostar in such clinical situations. 18FDG-PET/CT is a useful molecular imaging modality to evaluate the biological response advanced hepatic metastasis and peritoneal carcinomatosis to Cetuximab plus Endostar in patients after remnant gastric cancer resection.

Endostatin promotes the anabolic program of rabbit chondrocyte

Endostatin is a natural occurred angiogenesis inhibitor derived from collagenXVIII. So far its function during the angiogenesis process of bone formation and arthropathy has not been well studied yet. The present study addresses the function of endostatin in rabbit articular chondrocytes (RAC). We found that endostatin can promote RAC adhesion and spreading as well as its proliferation. In monolayer cultured RAC, CollagenII, TIMP1 and collagenXVIII transcription were up regulated by endostatin while collagenI and MMP9 were down regulated. Moreover collagenXVIII and endostatin antigens are present at synovial fluid. These findings indicate new function of endostatin as a homeostatic factor in cartilage metabolism.

117 cases of advanced malignancies treated with recombinant human endostatin plus chemotherapy

Objective: The aim of this study was to evaluate the recent efficacy and adverse reactions of recombinant human endostatin (Endostar) plus chemotherapy in the treatment of advanced malignancies. Methods: One hundred and seventeen cases of advanced malignancies were diagnosed and confirmed by histopathological examination, patients were treated with Endostar combined with chemotherapeutic drugs with no cross-resistance. Evaluate the efficacy and adverse reactions after finished two cycles of combination therapy. Results: All the 117 cases of patients were evaluated according to relevant standards, and there were 12 cases of complete remission (CR), 30 cases of partial remission (PR), 58 cases of stable disease (SD), 17 cases of progressive disease (PD). The response rate (RR) was 35.8%, disease control rate (DCR) was 85.4%. Conclusion: The protocol of Endostar combined with chemotherapy could improve the quality of life of patients with malignances, it also has the advantage of low toxicity. Considering the time span of the study, the long-term efficacy remains to be observed.

Inhibitory effect of endostatin expressed by human liver carcinoma SMMC7721 on endothelial cell proliferation in vitro

AIM: To construct a stable transfectant of human liver carcinoma cell line SMMC7721 that could secret human endostatin and to explore the effect of human endostatin expressed by the transfectant on endothelial cell proliferation. METHODS: Recombinant retroviral plasmid pLncx-Endo containing the cDNA for human endostatin gene together with rat albumin signal peptide was engineered and transferred into SMMC7721 cell by lipofectamine. After selection with G418, endostatin-transfected SMMC7721 cells were chosen and expanded. Immunohistochemical staining and Western blot were used to detect the expression of human endostatin in transfected SMMC7721 cells and its medium. The conditioned medium of endostatin-transfected and control SMMC7721 cells were collected to cultivate with human umbilical vein endothelial cells for 72 hours. The inhibitory effect of endostatin, expressed by transfected SMMC7721 cells, on endothelial proliferation in vitro was observed by using MTT assay. RESULTS: A 550 bp specific fragment of endostatin gene was detected from the PCR product of endostatin-transfected SMMC7721 cells. Immunohistochemistry and Western blot analysis confirmed the expression and secretion of foreign human endostatin protein by endostatin-transfected SMMC7721 cells. In vitro endothelial proliferation assay showed that 72 hours after cultivation with human umbilical vein endothelial cells, the optical density (OD) in group using the medium from endostatin-transfected SMMC7721 cells was 0.51 +/- 0.06, lower than that from RPMI 1640 group (0.98 +/- 0.09) or that from control plasmid pLncx-transfected SMMC7721 cells (0.88 +/- 0.11). The inhibitory rate for medium from endostatin-transfected SMMC7721 cells was 48%, significantly higher than that from empty plasmid pLncx-transfected SMMC7721 cells (10.2%, P【0.01). CONCLUSION: Human endostatin can be stably expressed by SMMC7721 cell transferred with human endostatin gene and its product can significantly inhibit the proliferation of human umbilical vein endothelial cell in vitro.

Perioperative rh-endostatin with chemotherapy improves the survival of conventional osteosarcoma patients: a prospective non-randomized controlled study

Objective: Anti-angiogenic drugs are an emerging treatment option against malignant tumors. The aim of this study was to determine whether the addition of perioperative rh-endostatin to chemotherapy could improve the probability of distant metastasis-free survival(DMFS) and overall survival(OS) in patients newly diagnosed with non-metastatic conventional osteosarcoma.Methods: This was a controlled non-randomized clinical study that included 388 patients without clinically detectable metastatic disease enrolled from January 2008 to April 2012. The control treatment group had 272 patients; 180 were male and 92, female,with a median age of 17 years. The treatment group had 58 patients; 36 were male and 22, female, with a median age of 16 years.The control group received preoperative chemotherapy followed by surgery and postoperative chemotherapy. The treatment group received 4 cycles of rh-endostatin perioperatively in addition to chemotherapy as per the control group. Patients were followed up from 6-101 months with a median follow-up period of 50.2 months.Results: The 5-year DMFS of the control group(61%) was significantly lower than that of the rh-endostatin group(79%)(P = 0.013). The 5-year OS of the control group(74%) was significantly lower than that of the rh-endostatin treatment group(87%)(P = 0.029). No difference in adverse drug reactions was found between these 2 groups.Conclusions: The addition of perioperative rh-endostatin to chemotherapy could significantly improve the DMFS and OS of patients with non-metastatic osteosarcoma.

Study progression of recombinant human endostatin (Endostar) for the treatment of malignant serous effusion

Since recombinant human endostatin (rh-endostatin;Endostar) has been listed 5 years,clinicians have combined it with chemotherapy for the treatment of lung cancers and other malignant tumors,and proved its effect and safety.A number of scholars have explored the application of Endostar alone or in combination with chemotherapy for treatment of malignant serous effusion,finding its high efficiency and low toxicity;and that hydrops controlling is stronger,and that it can significantly improve patients' quality of life.It is worthy of conducting prospective,randomized and multi-center clinical studies and basic researches to clarify the mechanism.

PP/ES短纤高强土工非织造布的制备及其抗老化性能研究

为降低紫外线对聚丙烯(Polyethylene,PP)非织造土工布的影响,选择ES(Ethylene-Propylene Side By Side)纤维和含有抗老化母粒的PP纤维为原料,TiO_(2)浸轧处理为后整理工序,采用针刺加固和热黏合加固技术制备了具有抗紫外老化功能的PP/ES高强非织造土工布。研究了抗老化工艺对PP/ES土工布力学性能和抗紫外老化性能的影响。结果表明:添加抗老化母粒和TiO_(2)浸轧后整理的PP/ES土工布力学性能少许上升;该土工布紫外老化后的羰基吸收峰强度最弱,T 5%仅下降4.73℃,纵向和横向的断裂强度保留率仅下降26.55%和26.76%,表现出最佳的抗紫外老化性能。

Effects of endostatin on expression of vascular endothelial growth factor and its receptors and neovascularization in colonic carcinoma implanted in nude mice

AIM:To investigate the antiangiogenic effects of endostatin on colonic carcinoma cell line implanted in nude mice and its mechanism. METHODS:Nude mice underwent subcutaneous injection with LS-174t colonic carcinoma cell line to generate carcinoma and were randomly separated into two groups.Mice received injection of vehicle or endostatin every day for two weeks. After the tumor was harvested,the tumor volumes were determined,and the expressions of CD34,VEGF and FIk-1 were examined by immunohistochemical method. RESULTS:Tumor volume was significantly inhibited in the endostatin group(84.17%)and tumor weight was significantly inhibited in the endostatin group(0.197±0.049) compared to the control group(1.198±0.105)(F=22.56, P=0.001),microvessel density(MVD)was significantly decreased in the treated group(31.857±3.515)compared to the control group(100.143±4.290)(F=151.62,P<0.001). Furthermore,the expression of FIk-1 was significantly inhibited in the treated group(34.29%) ompared to the control group(8.57%)(X^2=13.745,P=0.001).However no significant decrease was observed in the expression of vascular endothelial growth factor(VEGF)between these two groups(X^2=0.119,P=0.730). CONCLUSION:Endostatin can inhibit tumor growth and angiogenesis by blocking Vegf/FIk-1 pathway.This experiment provides the theory basis for developing a new anti-carcinoma drug through studying the properties of anti-angiogenesis inhibitors.

Clinical Study of Recombinant Human Endostatin Combined with Iressa in Targeted Treatment of Patients with Lung Adenocarcinoma with Pleural Metastasis

Objective:To evaluate and comprehensively analyze the clinical efficacy of recombinant human endostatin combined with Iressa targeted therapy in patients with pleural metastasis of lung adenocarcinoma.Methods:The interval of the selected study period span was from January 2017 to April 2021.The sample source of the study was 42 patients with lung adenocarcinoma admitted to hospital.The random number table method was used for study grouping,and they were further divided into study groups(n=21,14 cases with pleural metastasis)and control group(n=21,13 cases with pleural metastasis),all patients received systemic chemotherapy with pemetrexed and cisplatin.Patients with pleural metastases in the control group were injected with 60 mg cisplatin into the thoracic cavity.Patients in the study group were treated with Iressa(gefitinib)targeted therapy if genetic testing showed epidermal growth factor receptor(EGRF)mutations,and patients with pleural metastases were treated with pleural metastasis with Endo(recombinant human endostatin YH-16)to control pleural effusion.Two sets of related indicators were compared and analyzed.Results:Comparing the short-term disease control rate,treatment effectiveness and long-term survival rate between the two groups shows that the study group has more advantages(P<0.05).In the comparison between the two groups of serum markers and related indicators,the study group has more advantages(P<0.05),whereas in the comparison between the two groups in the incidence of adverse reactions,there is no significant difference(P>0.05).Based on statistics of the recurrence rate of pleural fluid in the two groups,the study group is significantly lower than the control group(P<0.05).Conclusion:Recombinant human endostatin combined with Iressa targeted therapy for patients with lung adenocarcinoma with pleural metastasis has significant short-term and long-term effects without serious adverse reactions.It can be fully promoted in medical institutions at all levels.

ES/棉热粘合混纺纱的制备及性能

为了开发一种热粘合混纺纱,研究热粘合纤维的混入对纱线结构和性能的影响,采用ES纤维和棉纤维进行混纺,制备出不同混纺比(40/60、50/50、60/40、70/30、100/0)、不同细度(30tex、24tex、18tex)的ES纤维/棉混纺纱,研究了不同热粘合处理条件下(加热温度、加热时间)纱线断裂强力、毛羽指数和芯吸性能等变化。结果表明,热粘合处理后混纺纱的断裂强力有较大的提升,随着热粘合温度的升高、热粘合时间的增加,纱线的毛羽指数明显减小,但芯吸性能有所下降。

一种评价新思维:ESE评价理论与方法——城市轨道交通可持续发展状态评价

目前城市轨道交通可持续发展评价体系,采用简单的分层加权汇总方法,未考虑同层指标间的相互影响以及下层指标对上层指标的一对多影响,不能系统、全面、准确地反映实际可持续发展情况。针对这一问题,本文提出了一种评价新思维——ESE评价理论与方法,即通过数据具有ESE(经济-社会-环境)三性影响这一新认识,构建了一个ESE空间直角坐标系,并以此表征城市轨道交通所有业务场景。在此ESE三维立体空间中,城市轨道交通的可持续发展状态被分成“八种四类”,同时对可持续发展程度进行了量化计算,并实现了立体的可视化表达。