考虑多层吸附诱导流的页岩微纳米孔道渗流分形模型

针对页岩气渗流过程模拟难度大的问题,运用分形理论描述页岩气储层微观结构,基于吸附层多层吸附现象,考虑了压力敏感效应和真实气体效应,推导了微纳米页岩气的质量流量表达式,建立了页岩气微纳米分形表观渗透率模型。通过数值模拟与昭通页岩气田A1井实际生产数据进行对比,验证了模型的准确性。结果表明:孔道表面吸附气层数对压力变化的敏感性较高,对温度变化的敏感性较低;受压力敏感效应的影响,页岩气扩散阻力随之增大,使得表观渗透率下降;随着气体压缩因子的增大,吸附层厚度增加,吸附区截面面积占比提高,同时,页岩孔道的压力敏感效应使得孔道直径减小,吸附气诱导流随之先减小后趋于平缓,使得页岩气整体表观渗透率减小。研究成果可为页岩气数值模拟提供部分理论基础,通过控制影响页岩气分形渗透的主控要素提高页岩气压裂开发采收率。

土壤中金属阳离子对Cl^-离子吸附的诱导效应

使用三种可变电荷土壤和一种恒电荷土壤 ,研究电解质溶液中金属阳离子对Cl-离子吸附的影响 .结果表明 ,在可变电荷土壤中 ,金属阳离子对Cl- 离子的吸附有明显的诱导效应 ,影响大小次序为 :AlCl3>CuCl2 >KCl>NaCl.

吸附诱导表面应力的分子动力学模拟

应用分子动力学方法结合镶嵌原子势,模拟研究了同质吸附Cu/Cu(100)和异质吸附Al/Ni(100)纳米薄膜中的吸附诱导表面应力.结果表明吸附原子对表面应力的影响主要源于两种原子间的相互作用;吸附原子和底物表面原子的结合将导致底物表面原子之间的化学键的强度减弱和平衡键长增加,从而导致表面压应力增加;吸附原子之间的相互作用也导致表面应力的变化,吸附原子间的吸引作用导致表面拉应力,而排斥作用导致表面压应力.这两种原子间相互作用所引起的表面应力与吸附原子的密度密切相关,吸附原子与底物表面原子的结合所引起的表面应力的大小与吸附原子的密度成线性关系,而吸附原子间的相互作用所引起的表面应力与吸附原子密度间呈非单调的依赖关系.

SnCl_(2)敏化的TiO_(2)表面对PbI_(2)粒子的诱导吸附

近年来,钙钛矿电池因其性能高、造价低且柔性好的优点而获得了极大的关注和发展,但其薄膜制备工艺还不够成熟.本工作主要关注两步法沉积钙钛矿时Pb I_(2)晶种层的沉积.受银镜反应中Sn Cl_(2)敏化思想的启发,本工作提出采用Sn Cl_(2)敏化层来增加Pb I_(2)粒子在TiO_(2)基底上的吸附能力.为验证其可行性,首先通过分子动力学模拟Sn Cl_(2)敏化的TiO_(2)表面对Pb I_(2)粒子的诱导吸附,分析了Sn Cl_(2)、Pb I_(2)、TiO_(2)三者的相互结合能.模拟结果表明,SnCl_(2)与TiO_(2)及Pb I_(2)粒子都有较大的结合能,因此可以很好地提高Pb I_(2)粒子在TiO_(2)基底上的吸附能力.最后,通过Pb I_(2)的溶液沉积实验和表征也验证了SnCl_(2)敏化层对PbI_(2)薄膜沉积质量具有较好的改善作用.

汽轮机润滑油乳化问题在线处理方法研究

陕西某电厂供热机组在供暖期内发生汽封漏气,导致汽轮机润滑油严重乳化,危害机组运行安全。为了不影响机组正常供暖,研究并验证了不同在线处理方法的处理效果。结果表明,采用极性诱导选择性吸附剂对运行油进行在线再生,可将油的破乳化度降至极限值,使乳化油在极短时间内破乳化,油与水在油箱中具有充足的分离时间,彻底解决了运行油乳化问题,为机组运行安全提供了保障。

光诱导原子解吸附实验中的光热效应研究

利用光诱导原子解吸附效应,无需加热就可实现碱金属原子浓度的调控,简易有效,故常被应用于光纤内碱金属原子的充载和磁光阱内单原子的捕获等.在使用460nm的发光二极管阵列进行原子解吸附时,发现铷原子池的温度上升,说明光解吸效应受到了光热效应的影响,但目前关于光解吸附实验中的光热效应研究鲜有报道.当解吸光功率密度较小时,光热效应的影响几乎可忽略.当增大解吸光功率密度时,光解吸效应以及光热效应的影响不断增大且对原子浓度增长的贡献趋于接近,在两种效应的共同作用下,原子浓度的增长幅度得到进一步提高.研究结论对光子芯片研究具有参考意义.

页岩储层纳米孔气体传输耦合模型新研究

页岩气在纳米孔隙的传输过程中受多种因素影响,包括孔隙尺寸和压力、孔隙壁面粗糙度、孔隙力学反应、吸附-诱导膨胀反应以及权重因子等。因此需要综合考虑以上因素以及吸附气分子在孔隙中所占空间对气体流动影响的条件下,厘清页岩气的不同运移机制(表面扩散、滑脱流、Knudsen扩散和黏性流动)在不同孔隙尺寸和压力下对纳米孔中总气体流量的贡献率。首先,对页岩气的不同运移方式进行了物理描述及数学表征,然后,在考虑孔隙壁面粗糙度、孔隙力学反应、吸附-诱导膨胀反应和权重因子等因素的条件下,建立页岩气在储层纳米孔中的气体传输耦合数学模型,模型可靠性通过格子Boltzmann方法计算结果验证。研究结果表明,当孔径小于10 nm时,纳米孔的总流量主要由表面扩散流量组成,孔径越小,表面扩散流量越大;当孔径为40～250 nm和低压条件下,滑脱流和Knudsen扩散对气体传输影响较大;当孔径大于10μm时,纳米孔的总流量主要为黏性流量。

金红石型TiO_2(011)晶面的表面化学研究进展

综述了采用高分辨扫描隧道显微镜(STM)等表面技术和密度泛函理论(DFT)计算等手段对TiO2(011)晶面的表面化学研究的进展,重点介绍了(011)面的表面结构组成、乙酸分子的吸附及诱导重构现象、水分子的吸附及产生的吸附氢原子的迁移和反应等方面的研究成果,揭示了TiO2表面结构与其化学性质的相互关系,为在原子尺度上理解TiO2催化材料的作用机理创造条件。

Gastric cancer cells induce human CD4^+ Foxp3^+ regulatory T cells through the production of TGF-β1

AIM: To elucidate the molecular and cellular features responsible for the increase of regulatory T cells (Tregs) in gastric cancer. METHODS: The frequencies of CD4 + Foxp3 + Tregs and the level of transforming growth factor-β1 (TGF-β1) were analyzed from 56 patients with gastric cancer byflow cytometry and enzyme-linked immunosorbent assay respectively. Foxp3 gene expression was analyzed by real-time polymerase chain reaction. The gastric cancer microenvironment was modeled by establishing the coculture of gastric cancer cell line, MGC-803, with sorting CD4 + T cells. The normal gastric mucosa cell line, GES-1, was used as the control. The production of TGF-β1 was detected in supernatant of MGC and GES-1. The carboxyfluorescein diacetatesuccinimidyl ester (CFSE) dilution assay was performed to evaluate the proliferation characteristics of induced Tregs. Neutralizing anti-TGF-β1 antibody was added to the co-culture system for neutralization experiments. RESULTS: The level of serum TGF-β1 in gastric cancer patients (15.1 ± 5.5 ng/mL) was significantly higher than that of the genderand age-matched healthy controls (10.3 ± 3.4 ng/mL) (P < 0.05). Furthermore, the higher TGF-β1 level correlated with the increased population of CD4 + Foxp3 + Tregs in advanced gastric cancer (r = 0.576, P < 0.05). A significant higher frequency of CD4 + Foxp3 + Tregs was observed in PBMCs cultured with the supernatant of MGC than GES-1 (10.6% ± 0.6% vs 8.7% ± 0.7%, P < 0.05). Moreover, using the purified CD4 + CD25 T cells, we confirmed that the increased Tregs were mainly induced from the conversation of CD4 + CD25 naive T cells, and induced Tregs were functional and able to suppress the proliferation of effector T cells. Finally, we demonstrated that gastric cancer cells induced the increased CD4 + Foxp3 + Tregs via producing TGF-β1. Gastric cancer cells upregulated the production of TGF-β1 and blockade of TGF-β1 partly abrogated Tregs phenotype. CONCLUSION: Gastric cancer cell can induce Tregs development via producing TGF-β1, by which the existence of cross-talk between the tumor and immune cells might regulate anti-tumor immune responses.

Exogenous carbon monoxide attenuates inflammatory responses in the small intestine of septic mice

AIM： To determine whether the carbon monoxide （CO）-releasing molecules （CORM）-Iiberated CO sup- press inflammatory responses in the small intestine of septic mice. METHODS： The C57BL/6 mice （male, n = 36; weight 20±2 g） were assigned to four groups in three re- spective experiments. Sepsis in mice was induced by cecal ligation and puncture （CLP） （24 h）. Tricarbonyl- dichlororuthenium （Ⅱ） dimer （CORM-2） （8 mg/kg, i. v.） was administrated immediately after induction of CLP. The levels of inflammatory cytokines [interleukin-1β （IL-1β） and tumor necrosis factor-α （TNF-α）] in tis- sue homogenates were measured with enzyme-linked immunosorbent assay. The levels of malondialdehyde （MDA） in the tissues were determined. The levels of nitric oxide （NO） in tissue homogenate were measured and the expression levels of intercellular adhesion mol- ecule 1 （ICAM-1） and inducible nitric oxide synthase （iNOS） in the small intestine were also assessed. NO and IL-8 levels in the supernatants were determined after the human adenocarcinoma cell line Caco-2 was stimulated by lipopolysaccharide （LPS） （10 g/mL） for 4 h in vitro. RESULTS： At 24 h after CLP, histological analysis showed that the ileum and jejunum from CLP mice in- duced severe edema and sloughing of the villous tips, as well as infiltration of inflammatory cells into the mu- cosa. Semi-quantitative analysis of histological samples of ileum and jejunum showed that granulocyte infil- tration in the septic mice was significantly increased compared to that in the sham group. Administration of CORM-2 significantly decreased granulocyte infiltration. At 24 h after CLP, the tissue MDA levels in the mid- ileum and mid-jejunum significantly increased com- pared to the sham animals （103.68 ± 23.88 nmol/ml vs 39.66 ± 8.23 nmol/mL, 89.66±9.98 nmol/mL vs 32.32 ± 7.43 nmol/mL, P 〈 0.01）. In vitro administra- tion of CORM-2, tissue MDA levels were significantly decreased （50.65±11.46 nmol/mL, 59.32 ± 6.62 nmol/mL, P 〈 0.05）. Meanwhile, the tissue IL-1β and TNF-α levels in the mid-ileum significantly increased compared to the sham animals （6.66±1.09 pg/mL vs 1.67±0.45 pg/mL, 19.34±3.99 pg/mL vs 3.98 ± 0.87 pg/mL, P 〈 0.01）. In vitro administration of CORM-2, tissue IL-1β and TNF-α levels were significantly de- creased （3.87 ± 1.08 pg/mL, 10.45±2.48 pg/mL, P 〈 0.05）. The levels of NO in mid-ileum and mid-jejunum tissue homogenate were also decreased （14.69 ± 2.45 nmol/mL vs 24.36 ± 2.97 nmol/mL, 18.47 ± 2.47 nmol/mL vs 27.33 ± 3.87 nmol/mL, P 〈 0.05）. The ex- pression of iNOS and ICAM-1 in the mid-ileum of septic mice at 24 h after CLP induction significantly increased compared to the sham animals. In vitro administration of CORM-2, expression of iNOS and ICAM-1 were sig- nificantly decreased. In parallel, the levels of NO and IL-8 in the supernatants of Caco-2 stimulated by LPS was markedly decreased in CORM-2-treated Caco-2 cells （2.22 ± 0.12 nmol/mL vs 6.25±1.69 nmol/mL, 24.97 ± 3.01 pg/mL vs 49.45± 5.11 pg/mL, P 〈 0.05）. CONCLUSION： CORM-released CO attenuates the inflammatory cytokine production （IL-1β and TNF-α）, and suppress the oxidative stress in the small intestine during sepsis by interfering with protein expression of ICAM-1 and iNOS.

Lipopolysaccharide induces and activates the Nalp3 inflammasome in the liver

AIM:To examine the activation of the Nalp3 inflammasome and its downstream targets following lipopolysaccharide(LPS) -induced stimulation in the liver. METHODS:Six-to-eight-week-old C57BL/6 chow fed mice were injected intraperitoneally with 0.5μg/g bodyweight LPS and sacrificed 2,4,6,18 or 24 h later. LPS-induced liver damage was confirmed by a biochemical assay to detect alanine aminotransferase(ALT) levels.To determine if LPS stimulation in the liver led to activation of the inflammasome,real-time quantitative polymerase chain reaction was used to evaluate the mRNA expression of components of the Nalp3 inflammasome.Enzyme-linked immunosorbent assays were used to determine the protein expression levels of several downstream targets of the Nalp3 inflammasome,including caspase-1 and two cytokine targets of caspase-1,interleukin(IL) -1βand IL-18. RESULTS:We found that LPS injection resulted in liver damage as indicated by elevated ALT levels.This was associated with a significant increase in both mRNA and protein levels of the proinflammatory cy-tokine tumor necrosis factor(TNF) -αin the liver,as well as increased levels of TNFs in serum.We showed that LPS stimulation led to upregulation of mRNA levels in the liver for all the receptor components of the inflammasome,including Nalp3,Nalp1,pannexin-1 and the adaptor molecule apoptosis-associated specklike,caspase recruitment domain-domain containing protein.We also found increased levels of mRNA and protein for caspase-1,a downstream target of the inflammasome.In addition,LPS challenge led to increased levels of both mRNA and protein in the liver for two cytokine targets of caspase-1,IL-1βand IL-18. Interestingly,substantial baseline expression of pre-IL1βand pre-IL-18 was found in the liver.Inflammasome and caspase-1 activation was indicated by the significant increase in the active forms of IL-1βand IL-18 after LPS stimulation. CONCLUSION:Our results show that the Nalp3 inflammasome is upregulated and activated in the liver in response to LPS stimulation.

Experimental and in silico studies on three hydrophobic charge-induction adsorbents for porcine immunoglobulin purification

Three hydrophobic charge-induction adsorbents with functional ligands of 4-mercapto-ethyl-pyridine, 2-mercapto-methyl-imidazole or 2-mercapto-benzimidazole were evaluated in the purification of porcine immunoglobulin from porcine blood. Adsorption isotherms were studied under different pH conditions. The adsorbent with 2-mercapto-methyl-imidazole as the ligand showed reasonable adsorption capacity(43.60 mg·g^(-1)gel)with great selectivity and it also showed the best elution performance in chromatographic studies. A multi-pH step elution process was proposed for the 2-mercapto-methyl-imidazole adsorbent, and the results showed that high immunoglobulin purity(94.3%) and a yield of 9.8 mg·(ml plasma)^(-1) could be achieved under the optimal condition of loading(pH 5.0)–pre-elution(pH 7.0)–elution(pH 3.8). Moreover, molecular simulation was employed to help in analyzing the binding mechanism between the ligands and immunoglobulin, and the results showed that both 2-mercapto-benzimidazole and 2-mercapto-methyl-imidazole ligands were docked on the same pocket(around TYR319 and LEU309) of the Fc fragment of immunoglobulin, with 2-mercaptobenzimidazole showing stronger binding interactions.

Irradiation-induced EMT is associated with activation of TGF-β and restriction of BMP signaling in esophageal cancer cells

Objective: Irradiation may enhance migration and/or invasiveness of cancer cells in vitro and in vivo, the mechanism of which may be associated with epithelial-mesenchymal transition (EMT). The present study explored the mechanisms of EMT induced by irradiation in esophageal cancer cells. Methods: Human esophageal cancer cell line EC109 was treated with increased doses of irradiation (0 Gy, 20 Gy, 40 Gy and 60 Gy). Cell morphology was observed. Expressions of E-cadherin and vimentin were determined by immunofluorescence assay or western blot. Secretion of transforming growth factor-β1 (TGF-β1) by cells was determined by enzyme-linked immunosorbent assay (ELISA), and the expressions of Smad2/3 and phosphorated Smad2 (p-Smad2) were also examined by Western blot. The mRNA expressions of BMP-4, a bone morphogenetic protein (BMP) ligand, and two secreted BMP antagonists (Chordin and Gremlin), were detected with reverse transcription-polymerase chain reaction (RT-PCR). Cell migratory capacity was evaluated. Results: Irradiation induced EMT in EC109 cells in a dose-dependent manner as evidenced by morphological changes, decreased expression of E-cadherin and increased expression of vimentin, and increased cell motility. The secretion of TGF-β1 and expression of p-Smad2 were gradually increased in an irradiation dose-dependent manner, but the Smad2/3 protein levels remained stable. The mRNA expression of BMP-4 was gradually down-regulated, but the expressions of Chordin and Gremlin were gradually up-regulated in cells treated with increased doses of irradiation. Conclusion: Irradiation can induce EMT in esophageal cancer cells in a dose-dependent manner, and the mechanism may be associated with activation of TGF-β and restriction of BMP signaling.

Docosahexaenoic acid suppresses arachidonic acid-induced proliferation of LS-174T human colon carcinoma cells

AIM： To investigate the impact of arachidonic acid （AA） and docosahexaenoic acid （DHA） and their combination on colon cancer cell growth. METHODS： The LS-174T colon cancer cell line was used to study the role of the prostaglandin precursor AA and the omega-3 polyunsaturated fatty acid DHA on cell growth. Cell viability was assessed in XTT assays. For analysis of cell cycle and cell death, flow cytometry and DAPI staining were applied. Expression of cyclooxygenase-2 （COX-2）, p21 and bcl-2 in ceils incubated with AA or DHA was examined by real-time RT-PCR. Prostaglandin E2 （PGE2） generation in the presence of AA and DHA was measured using a PGE2- ELISA. RESULTS： AA increased cell growth, whereas DHA reduced viability of LS 174T cells in a time- and dosedependent manner. Furthermore, DHA down- regulated mRNA of bcl-2 and up-regulated p21. Interestingly, DHA was able to suppress AA-induced cell proliferation and significantly lowered AA-derived PGE2 formation. DHA also down-regulated COX-2 expression. In addition to the effect on PGE2 formation, DHA directly reduced PGE2-induced cell proliferation in a dosedependent manner. CONCLUSION： These results suggest that DHA can inhibit the pro-proliferative effect of abundant AA or PGE2.

Inhibitive effect on phagocytosis of Candida albicans induced by pretreatment with quercetin via actin cytoskeleton interference

OBJECTIVE： To investigate the anti-inflammatory effect of pretreatment with quercetin on macro- phages after Candida albicans infection. METHODS： RAW 264.7 macrophages were used as a target cell line. Cell viability after treatment with quercetin at different time points was detected by Carboxyfluorescein diacetate, succinimidyl ester. Phagocytic function of macrophages was deter- mined by a fluorometric assay. Cytokine tumor ne- crosis factor a （TNF-a） production was measured by enzyme-linked immunosorbent assay. F-actin cy- toskeleton of L929 cells was stained by Alexa Fluor 488-phalloidin. RESULTS： Pretreatment with quercetin decreasedcell viability only at the highest concentration of 37 μg/mL 2, 24, and 48 h after the treatment. The phagocytic efficiency of macrophages pretreated with quercetin was significantly decreased in a time- and dose-dependent manner. F-actin label- ing showed that the actin cytoskeleton of the cells started to break down 2 h after treatment. More- over, it notably inhibited cytokine TNF-a produc- tion after Candida albicans infection. CONCLUSION： Pretreatment with quercetin in- duced an anti-inflammatory effect against Candida albicans infection in macrophages.

Isoflurane induces expression of vascular endothelial growth factor through activating protein kinase C in myocardial cells

Objective： Vascular endothelial growth factor （VEGF） plays important roles in establishing collateral circulation of ischemic myocardium. This study aimed to investigate the effect of isoflurane on VEGF expression and the potential intracellular signal transduction pathway in cultured rat myocardial cells in order to further reveal the molecular mechanism of myocardial preservation of isoflurane. Methods： Primary myocardial cells of Sprague-Dawley rats were isolated and cultured. They were divided randomly into control group, isoflurane group, protein kinase C （PKC） inhibitor group and PKC inhibitor＋isoflurane group where cells were respectively incubated without any treatment, treated by 0.5, 1.0 and 1.5 minimum alveolar concentration （MAC） of isoflurane for 6 hours, by PKC inhibitor calphostin C at a final concentration of 50 nmol/L and by 50 nmol/L calphosfin C＋ 1.0 MAC isoflurane for 6 hours. VEGF expression was detected by enzyme-linked immunosorbent assay （ELISA） and the expression levels of PKC isoforms were determined by Western immunoblotting method. Results： Isoflurane increased the VEGF expression in myocardial cells in a dose-dependent way. VEGF levels were significantly higher in 1.0 and 1.5 MAC isoflurane groups than in the control group （both P〈0.01）. The effect of isoflurane on upregulating VEGF expression was blocked by PKC inhibitor calphostin C （P〈0.01）, but calphostin C did not alter VEGF expression （P〉0.05）. Isoflurane induced the activation and translocation of PKC Immunoblotting analysis revealed that the immunoreactivity of PKC ε increased significantly in the membrane fractions and deceased significantly in the kytoplasm fractions for cells treated with 1.0 MAC isoflurane as compared with the untreated cells, but not of PKC a, PKCα and PKCζ （P〈0.01）. Conclusion： Isoflurane induces myocardial cells to release VEGF through activating PKCε from the endochylema to the cytomembrane, suggesting a possible novel mechanism of isoflurane protecting myocardial cells.