Background: Mesenchymal Stem Cells (MSCs) are pivotal in immunomodulation, hematopoiesis, and tissue repair. The interplay between MSCs and the pathological microenvironment influences their proliferation and differentiation. Transforming Growth Factor-Beta 1 (TGF- β1) serves as a key cytokine in the MSC microenvironment. This study aimed to scrutinize the impact of TGF-β1 on human placenta-derived MSCs of fetal origin (fPMSCs) and elucidate its underlying mechanism. Methods: fPMSCs were isolated, and surface markers were identified by flow cytometry. Cell proliferation in fPMSCs was assessed using Cell Counting Kit-8 (CCK-8) and 5-Ethynyl-2’-Deoxy Uridine (EdU). Apoptosis was detected via Annexin V/PI staining, and apoptosis-related proteins were detected by western blot. Endoplasmic reticulum (ER) stress-related proteins were detected by western blot, and Flou-4 AM staining was utilized to assess intracellular Ca2+ levels under TGF-β1 exposure. The impact of 4-PBA treatment on ER stress and apoptosis was assessed by western blot and Annexin V/PI staining. Additionally, the PERK and p-PERK expressions were evaluated via Western blot. Results: CCK-8 and EdU assays revealed inhibited proliferation of fPMSCs under TGF-β1 exposure. Annexin V/PI staining demonstrated a significant induction of apoptosis in fPMSCs following TGF-β1 treatment. Furthermore, TGF-β1 treatment significantly elevated intracellular Ca2+ levels and the expressions of GRP78, p-eIF2α, and CHOP. Interruption of ER stress with 4-PBA mitigated TGF-β1-induced apoptosis in fPMSCs. Moreover, TGF-β1 increased p-PERK expression. Inhibition of PERK autophosphorylation with GSK2606414 suppressed TGF-β1-induced apoptosis and ER stress in fPMSCs. Conclusion: Our findings indicated that TGF-β1 induced ER stress-dependent apoptosis in fPMSCs through the PERK signaling pathway. These results offer insights into enhancing the therapeutic efficacy of fPMSCs by modulating TGF-β1-induced apoptosis.

Objective To investigate the molecular mechanism of IL-6 regulating the expression of secretory phosphoprotein 1 (SPP1) in human placental-derived mesenchymal stem cells (hfPMSCs) and influencing the polarization of macrophages. Methods hfPMSCs were prepared by enzymatic digestion and cultured in a defined, serum-free medium. The morphology of hfPMSCs was observed under a microscope, and the expression of surface markers CD14, CD34, CD45, CD73, CD90, CD105, and human leukocyte antigen DR (HLA-DR) was detected by flow cytometry. hfPMSCs were treated with IL-6 at the final dosage of 100 ng/mL for 24 hours. ELISA, Western blot, and real-time quantitative PCR were used to detect the expression of SPP1 at the protein and mRNA levels; after being treated with IL-6, hfPMSCs infected with SPP1 interference lentivirus were co-cultured with activated macrophage THP-1 cells induced by 100 ng/mL lipopolysaccharide (LPS) and 80 ng/mL phorbol 12-myristate 13-acetate (PMA), and flow cytometry was used to detect the proportion of CD11c and CD206 positive cells in THP-1 cells; hfPMSCs were treated with IL-6 and/or specific inhibitors of nuclear factor kappa B p65 (NF-κB p65), SC75741, and Western blot was used to detect the expression of genes in the NF-κB signaling pathway and SPP1. Results IL-6 significantly upregulates the expression of SPP1 in protein and mRNA levels in hfPMSCs; interference of SPP1 significantly downregulates the expression of SPP1 in hfPMSCs and significantly reduces the positive cell ratio of CD206 in co-cultured macrophages; IL-6 significantly upregulates the expression of p-p65 in hfPMSCs, activating the NF-κB signaling pathway; SC75741 significantly downregulates the expression of p-p65 and SPP1 in hfPMSCs treated with IL-6. Conclusion IL-6 upregulates the expression of SPP1 through the NF-κB signaling pathway in hfPMSCs, which enhances the capability to induce macrophages to polarize towards the M2 phenotype.

Objective To investigate the regulation of IL-1β on the expression of CD200 in human umbilical cord mesenchymal stem cells (hUC-MSCs), its role in macrophage polarization and the underlying mechanism. Methods hUC-MSCs were isolated and cultured in serum-free medium. Morphological observation and the expressions of CD73, CD90, CD105, CD14, CD34, CD45 and HLA-DR were detected by flow cytometry to confirm the properties of mesenchymal stem cells. hUC-MSCs were treated with IL-1β at the final concentration of 20 ng/mL for 24 hours. The proportion of CD200 positive cells was measured by flow cytometry. Real-time quantitative PCR and Western blot analysis were used to detect CD200 mRNA and protein expression levels. hUC-MSCs infected with CD200 overexpression (OE-CD200) and its negative control (OE-NC) lectin virus were treated with IL-1β and co-cultured with PMA-activated THP-1 macrophages. The proportion of CD11c and CD206 positive cells was measured by flow cytometry. hUC-MSCs were treated with IL-1β in combination with PD98059, and the expression of MAPK signaling pathway-related proteins and its effect on CD200 expression were detected by Western blot analysis. Results IL-1β significantly down-regulated the expression of CD200 protein and the proportion of CD200 positive cells. Overexpression of CD200 significantly up-regulated the expression of CD200 in hUC-MSCs, and increased the proportion of CD206-positive macrophages. IL-1β activated the ERK1/2 signaling pathway in hUC-MSCs, and PD98059 up-regulated the expression of CD200 protein in hUC-MSCs treated with IL-1β. Conclusion IL-1β inhibits the expression of CD200 by activating ERK1/2 signaling pathway, and reduces the immunosuppressive effect of hUC-MSCs on regulating the M2-type polarization of macrophages.

Background: Mesenchymal stem cells (MSCs) are promising remedies for various inflammatory disease including pulmonary fibrosis (PF). However, the properties of MSCs in PF pathological microenvironment remain unclear. In this study, the efficacy of autophagy in placental mesenchymal stem cells of fetal origin (fPMSCs) in either IL-1 beta treatment or BLM induced pulmonary fibrosis mice model was examined. Methods: The characteristic of fPMSCs was identified by morphological observation, flow cytometry and dif-ferentiation potential. In vitro experiments, fPMSCs were stimulated with IL-1 beta, to mimic inflammatory microenvironment of pulmonary fibrosis. The immunosuppressive properties and autophagic function in fPMSCs treated with IL-1 beta were evaluated by both macrophage cells THP-1 activation and the expression of CD200 situation, autophagy marker and MAPK signaling pathway. The in vivo anti-fibrotic activity of fPMSCs inter-fering autophagy was evaluated by using BLM induced pulmonary fibrosis mice model. Results: fPMSCs belonged to CD73+CD90+CD105+/CD14- CD34-CD45-HLA-DR- cells, and capable differentiation to adipogenic, osteogenic and chondrogenic cells. In addition, immunoinhibitory activity of fPMSCs for macrophage was restrained by IL-1 beta treatment in CD200 dependent manner. Suppression of autophagy by sh-Atg5 lentivirus increased the expression of CD200 and ratio of CD200 positive fPMSCs, and enhanced fPMSCs immunosuppression for THP-1 activation. Mechanistically, IL-1 beta induced autophagy regulated by p38 signaling cascade. In vivo, autophagy inhibition induced by Atg5 knockdown in fPMSCs resulted in strengthening anti -fibrotic effects on PF mice model. Conclusions: Collectively, autophagy derived from inflammatory microenvironment hampered the immu-noinhibitory properties of MSCs. Based on this, adjustment of autophagy may be a valid approach to facilitate their immunomodulatory and anti-fibrotic efficacy. Superscript/Subscript Available

通过全面预算绩效管理,生态建设一定程度上实现了财政资金的科学使用和自然资源的合理配置,但生态预算面临的各自为政问题日益凸显.基于生态建设的系统性和复杂性,介绍生态建设中"碎片化"治理和多元生态要素交叉影响的客观现状和绩效评价困境,提出运用行政合作手段开展预算绩效管理工作.本研究从跨区域和跨部门两方面的行政合作入手,建立生态全面预算绩效评价指标体系,并以流域生态系统治理的空间难题和"山水林田湖草"生态项目多元生态要素共生发展的问题为例探讨其应用价值.

Objective To investigate the mechanism of formononetin regulating the heat production of brown adipocytes via decoupling protein 1 (UCP1). Methods The brown preadipocytes was isolated from wild-type (WT) C57BL/6J mice and differentiated into mature fat cells in vitro. Moreover, the mRNA levels of fatty acid binding protein 4 (FABP4) and adiponectin were detected by real-time quantitative PCR (RT-qPCR). To confirm formononetin could induce the expression of thermogenic genes, we first prepared WT mature brown adipocytes and treated them with DMSO and formononetin separately. The mRNA and protein levels of thermogenic genes, such as peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), peroxisome proliferators-activated receptor γ (PPARγ), UCP1 and iodothyronine deiodinase 2 (Dio2), were detected by RT-qPCR and Western blot analysis. To investigate the role of UCP1 in mediating differentiation of brown preadipocytes, Fabp4 and adiponectin mRNA levels were analyzed by RT-qPCR in WT and UCP1 mutation differentiated brown adipocytes. To determine cellular oxygen consumption, isolated WT and UCP1 mutation brown preadipocytes were plated in an XF24-well microplate and differentiated into mature brown adipocytes treated with formononetin or DMSO, followed by oxygen consumption rate (OCR) measurement using XF24 analyser. Results Both WT and UCP1 KO brown preadipocytes could be differentiated into adipocyte. The expression of thermogenic genes, including PGC-1α, Dio2, PPARγ and UCP1, induced by formononetin was similar in UCP1 KO adipocytes and WT cells. But the ability of formononetin to increase cellular respiration was inhibited in Ucp1 KO cells. Conclusion Formononetin mediated stimulation of thermogenesis and oxygen consumption via UCP1 in brown fat cells.

Objective To investigate the protective function of paracrine hepatocyte growth factor (HGF) derived from human placental mesenchymal stem cells of fetal origin (hfPMSCs) cultured in serum-free medium against endothelial cell injury induced by lipopolysaccharide (LPS). Methods The hfPMSCs were cultured in serum-free medium and surface antigen CD73, CD90, CD105, CD14, CD34, CD45 and HLA-DR were analyzed by flow cytometry. Using TranswellTM co-culture system [human pulmonary microvascular endothelial cell (HPMECs) were added into the upper chambers of TranswellTM inserts, and hfPMSCs were added into the lower chambers of TranswellTM inserts], the influence of hfPMSCs paracrine HGF on the permeability of HPMECs in LPS condition was identified. Then four different co-culture conditions were used as follows: 100 ng/mL LPS treatment group; hfPMSCs co-culture group; HGF neutralization group; HPMECs normal control. After 100 μg FITC-dextran was added into the upper chambers of TranswellTM inserts, the effect of stain permeability was detected by fluorescence microplate reader. The expression of VE-cadherin, caveolin-1 and cleaved caspase-3, cleaved PARP-1 in HPMECs were measured by Western blot analysis. Results The hfPMSCs showed the classic morphology of mesenchymal stem cells and expressed the surface markers CD73, CD90 and CD105, but did not express CD14, CD34, CD45 and HLA-DR. Compared with LPS treatment group, the co-culture with hfPMSCs dramatically inhibited the permeability of HPMECs, significantly up-regulated the expression of VE-cadherin, and reduced the expression of caveolin-1, cleaved caspase-3, cleaved PARP1. In contrast, neutralizing HGF with anti-HGF antibody reversed the above effects of hfPMSCs-HPMECs co-culture. Conclusion Owing to paracrine HGF, hfPMSCs possess the capability to availably inhibit the permeability of HPMECs induced by LPS.

输电线路杆塔基础在长期服役过程中,开裂是其最常见的破坏形式.造成此现象的原因有:(1)施工控制不严格,因离析现象导致混凝土力学性能发展不良,诱发开裂现象;(2)基于硫酸盐侵蚀生成的膨胀性产物水化硫铝酸钙和钙钒石会进一步加剧开裂行为,最终导致结构整体开裂.

The oxidative stresses are a major insult in pulmonary injury such as acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), two clinical manifestations of acute respiratory failure with substantially high morbidity and mortality. Mesenchymal stem cells (MSCs) hold a promise in treatments of many human diseases, mainly owing to their capacities of immunoregulation and antioxidative activity. The strong immunoregulatory role of human placental MSCs of fetal origin (hfPMSCs) has been previously demonstrated; their antioxidant activity, however, has yet been interrogated. In this report, we examined the antioxidative activity of hfPMSCs by accessing the ability to scavenge oxidants and radicals and to protect alveolar epithelial cells from antioxidative injury using both a cell coculture model and a conditioned culture medium (CM) of hfPMSCs. Results showed a comparable antioxidative capacity of the CM with 100 μ M of vitamin C (VC) in terms of the total antioxidant capacity (T-AOC), scavenging abilities of free radicals DPPH, hydroxyl radical (·OH), and superoxide anion radical (O 2 - ), as well as activities of antioxidant enzymes of SOD and GSH-PX. Importantly, both of the CM alone and cocultures of hfPMSCs displayed a protection of A549 alveolar epithelial cells from oxidative injury of 600 μ M hydrogen peroxide (H 2 O 2 ) exposure, as determined in monolayer and transwell coculture models, respectively. Mechanistically, hfPMSCs and their CM could significantly reduce the apoptotic cell fraction of alveolar epithelial A549 cells exposed to H 2 O 2 , accompanied with an increased expression of antiapoptotic proteins Bcl-2, Mcl-1, Nrf-2, and HO-1 and decreased proapoptotic proteins Bax, caspase 3, and Keap1, in comparison with naïve controls. Furthermore, hfPMSCs-CM (passage 3) collected from cultures exposed an inhibition of the Nrf2/Keap1/ARE signaling pathway which led to a significant reduction in caspase 3 expression in A549 cells, although the addition of Nrf2 inhibitor ML385 had no effect on the antioxidative activity of hfPMSCs-CM. These data clearly suggested that hfPMSCs protected the H 2 O 2 -induced cell oxidative injury at least in part by regulating the Nrf2-Keap1-ARE signaling-mediated cell apoptosis. Our study thus provided a new insight into the antioxidative mechanism and novel functions of hfPMSCs as antioxidants in disease treatments, which is warranted for further investigations.

Background and objective Tumor recurrence and drug resistance are the main causes of death in tumor patients. The family of acetaldehyde dehydrogenase (ALDH) is closely related to the proliferation, migration, invasion and resistance of tumor cells, and different ALDH subtypes are expressed in different tumor cells. The aim of this study is to elucidate the ALDH subtype in human lung adenocarcinoma HCC-827/GR cells, which resistant to the gefitinib. Methods The human lung adenocarcinoma HCC-827 cells were used to generate the gefitinib-resistant HCC-827/GR cells; the expression of ALDH subtype in either HCC-827 or HCC-827/GR was detected by flow cy-tometry; The proliferative capacity and sensitivity to gefitinib of hcc-827/GR cells were analyzed by MTT assay before and after treatment with 100 μmol/L diethyllaminaldehyde (DEAB); Real-time quantitative PCR was used to detect the expression of ALDH subtypes at mRNA levels in hcc-827 cells and hcc-827/GR cells. Results Compared with HCC-827 cells, the positive rate of ALDH in HCC-827/GR cells increased. The proliferation ability of HCC-827/GR cells decreased after treatment with 100 μmol/L DEAB. Compared with HCC-827 cells, the expression of ALDH1A1 and ALDH1L1 mRNA was increased in hcc-827/GR cells, but the ALDH3B2 expression was decreased. Conclusion ALDH might be used as a molecular biomarker to test the gefitinib-resistant to lung adenocarcinoma cancer cells, and the ALDH1A1 may play a role in gefitinib resistance in lung cancer.

近些年来自然灾害、地质灾害呈现频发趋势,输电设备受损后需要快速抢修,现浇基础无法在短时间内满足抢修需求.通过研究装配式基础发展现状以及技术特点,分析现浇混凝土结构基础弊端,对装配式基础和现浇基础的经济性、工期、人员等方面进行了比较,建议在今后电力输电线路紧急抢修中采用装配式基础.

The objective of this study was to analyze the effect of the expression of WWOX and p53 on the growth of MG-63 osteosarcoma cells and to explore the correlation between osteosarcoma and the expression of WWOX and p53. WWOX and p53-overexpressing MG-63 osteosarcoma cell lines were established by transfection and named the MW and MP cell lines, respectively. Untransfected MG-63 cells (blank control) were used as control. Quantitative polymerase chain reaction (qPCR) and western blot analysis were used to detect the expression of WWOX and wild-type p53 mRNA and protein, respectively. The effects of WWOX and p53 (wild-type) on the activity of MG-63 cells were determined by MTT assay and flow cytometry. The expression of mutant p53 protein in 65 cases of osteosarcoma was detected by immunohistochemistry to analyze the correlation between p53 and the development of osteosarcoma. qPCR showed that WWOX and p53 mRNA was overexpressed in MW and MP cells, respectively. Western blot analysis showed that the levels of WWOX and p53 protein in MW and MP cells were higher than in the blank control group. MTT assay showed that the cell proliferation ability of MW and MP cells was significantly lower than in the blank control group. Flow cytometry showed that 78.49% of MW and 66.76% of MP cells were arrested in the G0/G1 phase. Immunohistochemistry showed that mutant p53 was highly expressed in osteosarcoma, with a positive expression rate of 47.7%. The expression rate was positively correlated with the pathological grade of cancer. In conclusion, WWOX can affect the cell cycle of MG-63 osteo-sarcoma cells to inhibit cell proliferation, which provides new insights into gene therapy for osteosarcoma. The two types of the p53 gene have different functions in the development of osteosarcoma. Wild-type p53 acts as a tumor suppressor, while mutant p53, which is overexpressed in malignant osteosarcoma, has a carcinogenic effect associated with the degree of osteosarcoma.

超导磁体是超导磁储能系统(SMES)的核心部件,其优化设计可以提高SMES的经济性和运行性能。提出了一种考虑磁体动态特性的高温超导磁储能磁体设计方法,该方法以有限元方法为基础,选取遗传算法作为优化工具,对高温超导磁体的内径、单饼匝数和双饼个数进行了优化。该方法将超导磁体的优化分为了两个部分,一次优化以磁体的用线量为优化目标,二次优化将交流损耗低为优化目标。最后用此方法对储能容量为150 k J的高温超导磁储能磁体进行了优化设计,经过两次优化后的150 k J磁体方案兼具低用线量和低交流损耗的优点。

阐述了在现场进行特高压换流变压器空载试验的主要困难,分析了通常用于大型变压器现场空载试验的电容补偿法的缺陷,给出了实例.

Objective To investigate the therapeutic effect and mechanism of human placental mesenchymal stem cells of fetal origin (hfPMSCs) cultured in serum-free medium on mouse pulmonary fibrosis induced by bleomycin treatment. Methods Human hfPMSCs were cultured and identified by flow cytometry. Fifteen 6-week-old male SPF C57BL/6J mice were divided into 3 groups: bleomycin treatment group, hfPMSCs transplantation group and negative control group. Pulmonary fibrosis model was induced in the mice of bleomycin treatment group and hfPMSCs transplantation group with bleomycin (1 μg/L, 50 μL) via intratracheal instillation. The mice in negative control group were instilled with PBS (50 μL) through the same manner of the other two groups. Three days post-modelling, 200 μL containing 5×105 hfPMSCs were injected into hfPMSCs transplantation group via tail vein. All the mice were sacrificed at day 21 after modeling in batch. Lung tissues were collected for analyzing the pathological changes by HE staining and Masson staining as well as detecting collagen content. The total protein of lung tissues was extracted for observing the expressions of myeloid differentiation factor 88 (MyD88) and transforming growth factor-β (TGF-β); the level of TGF-β in sera was determined by Western blotting. Results The hfPMSCs possessed the morphology of mesenchymal stem cells and expressed the surface markers CD73, CD90 and CD105, but did not express CD14, CD34 and CD45. HE and Masson staining showed that hfPMSCs transplantation significantly reduced the degree of pulmonary fibrosis compared with bleomycin treatment group. The collagen content and the expression levels of MyD88 and TGF-β in bleomycin treatment group were obviously higher than those in hfPMSCs transplantation group and negative control group. Conclusion hfPMSCs possess the capability of alleviating pulmonary fibrosis by down-regulating the expressions of MyD88 and TGF-β.

In this paper, the internal fuse of shunt capacitor which was BAM6.56-556-1W used in AC UHV project had been designed and calculated.Combined with the method of energy calculation and fuse current density, and the internal fuse model withΦ0.42 ×160mm was chosen.In order to test the performance of the internal fuse, based on the improvement of the internal fuse parameter, the test sample capacitor was designed and tested according to experi-mental plan which was stricter than GB/T 11024.1-2010, GB/T 11024.1-2001, DL/T840-2003, et al.The result indicated that the revised-design internal fuse which was used in BAM6.56-556-1W sample capacitor had passed all verification test items.Compared with the requirement of standard, the short-circuit discharging voltage was increasing by 30%, the upper limit voltage of fuse insulating test was increasing by 30%, the range of lower limit voltage was in-creasing 10%, and the withstanding voltage of the fuse fracture was increasing 30%.The internal fuse which was ver-ified by test was helpful for the safe and reliable operation of the shunt capacitor installation used in AC UHV project.

司法鉴定是一个高风险活动,电力司法鉴定机构需要在鉴定执业活动中控制各类风险,实现规范运作.本文运用风险控制管理理论,以问题为导向,探索如何实现规范管理,提出了广义的司法鉴定风险概念,主张控制司法鉴定风险是司法机构规范管理的核心目标.实践中要咨询专家,调研兄弟电力司法鉴定机构,借鉴先进管理经验,寻找防范鉴定风险的措施和途径.确定了规范管理的六个重点环节,建立并逐步完善工作流程和制度体系.

A 600-V/150-kJ/100-kW conduction-cooled high-temperature superconducting (HTS) magnetic energy storage (SMES) system is developed. In this paper, the configuration of the HTS SMES is introduced. The magnet is a solenoid type, which uses two kinds of HTS tapes, and cooled to about 20 K. A series of laboratory experiments and field tests are carried out to evaluate the performance of the SMES system, including the current-carrying ability of a magnet, the active and reactive power exchange capability between the SMES and an alternating-current power system, power oscillation damping, the improving electrical energy quality, etc. The results show that the SMES system meets the design requirements and can maintain a long-term stable operation in a power system.

The current flowing through a SMES is subjected to variations at a rate ranging from 0.1 A/s to 300 A/s under the influence of the power grid. The duration of power exchange varies from milliseconds to minutes, even to hours. When operating, the impact of AC losses in HTS tapes on the cryogenic cooling system should be considered. If the cryogenic cooling system fails to take away the generated heat effectively, this may lead to the temperature rise of the magnet and its possible damage. Therefore, it is essential to evaluate the technical and economical characteristic of cryogenic cooling system. Thus, a 5 MJ SMES model is built to calculate the temperature characteristic. A new factor 5 is defined to assess the technological and economical validity of the chosen cryogenic scheme. The suitable capacity of the cryogenic cooling system is evaluated for different applications. The effect of the operating temperature on the technical and economical factor is also discussed. (C) 2015 Elsevier Ltd. All rights reserved.

Due to the high JC of the superconductor, the volume and the weight of the generator can be significantly reduced if the superconducting coils are used. This paper has designed a 40-pole racetrack excitation winding for the 12MW offshore wind turbines generator. The excitation winding are wound by Nb-Ti superconductor, running at the temperature of 4.2K. In order to ensure the stability and reliability of the magnetic field, some optimizers for the design of the excitation winding are adopted. As a result, the fundamental magnetic field at the air-gap center of the armature winding could reach 2.1T, thereby the 12MW power generation could be achieved.