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991.
Aleksey I. Kovalev Kazuhiko Takeuchi Alexander V. Barzykin Michihiko Asai Mitsuru Ueda Alexander L. Rusanov 《Macromolecular chemistry and physics.》2005,206(20):2112-2121
Summary: The polycondensation of 1‐ethynyl‐2,5‐dihexyl‐4‐iodobenzene in the presence of 1‐ethynyl‐2,5‐dihexyl‐4‐(2‐phenylethynyl)benzene proceeds according to the mechanism of initiated chain growth polycondensation. It has allowed the synthesis of oligomers with a desired molecular weight and a narrow molecular weight distribution. The reasons for the side reaction leading to the formation of diyne compounds are revealed and the presumed mechanism is given. This opens prospects for the preparation of defectless poly(p‐phenyleneethynylene)s with required molecular weights and narrow molecular weight distributions.
992.
Oksala NK Oksala A Paavonen T Alhava E Paimela H 《APMIS : acta pathologica, microbiologica, et immunologica Scandinavica》2003,111(4):497-506
AIM: In restitution after superficial injury of the gastric mucosa, the epithelial continuity is restored by cellular migration. We have shown that heat shock preconditioning inhibits restitution after superficial injury. This study investigates the effect of heat shock preconditioning on tissue proliferation and apoptosis. EXPERIMENTAL DESIGN: Paired guinea pig gastric mucosae were mounted and perfused in Ussing chambers (37 degrees C). After heat shock preconditioning (42 degrees C) (30 min) and normothermic recovery (37 degrees C) (150 min) or normothermic perfusion, a superficial injury was induced by luminal exposure to 1.25 mol/L NaCl (5 min) followed by a 3 h restitution. During perfusion, the mucosa was exposed to 30 micromol/L arachidonic acid (AA) to enhance heat shock response, to 50 micromol/L quercetin (Q) to inhibit the metabolism of arachidonic acid via lipoxygenases, to 50 micromol/L indomethacin (In) to inhibit the metabolism of arachidonic acid via cyclo-oxygenases, or to 150 micromol/L cycloheximide (CHX) to inhibit de novo protein synthesis. After the experiment the mucosa was prepared for immunohistochemical analysis of the expression of Mib-1 proliferation antigen and pro-apoptotic protein Bax. RESULTS: Heat shock decreased Mib-1/Bax ratio and this effect was maintained after superficial injury and exposure to Q, to AA+CHX or to In+CHX. Exposure to CHX, to AA, to In+Q, to In+AA, In+AA+Q or to In+AA+CHX, however, blocked the effect of heat shock preconditioning. The decreasing effect of heat shock preconditioning on Mib-1/Bax ratio could be reversed by exposure to AA+Q or to In. CONCLUSION: The heat-preconditioning-induced effects on the mucosa are reversible and sensitive to exogenous pharmacological modulation. Heat shock preconditioning inhibits proliferation of superficially injured isolated gastric mucosa by a mechanism involving eicosanoid pathways and de novo protein synthesis. 相似文献
993.
This special issue of the Journal of Immunological Methods brings together articles from some of the leaders in labelling antigen-specific T and NKT cells, describing recent technical advances and their impact on the study of immunology. Although tetramers, or tetrameric MHC class I/peptide complexes, are the best known reagents in the field, various forms of oligomeric complexes are now being successfully used to detect antigen-specific T cells, including cytotoxic T lymphocytes, MHC class II-restricted CD4+ T cells, and glycolipid-specific T cells restricted by CD1 isoforms. The articles presented here detail the breadth of the oligomeric structures being used to probe T, NK and NKT cell function, and cover both the technical and practical aspects of their use, as well as the new biology revealed. In addition to providing a summary of the current state of the art, these contributions also provide clear pointers to strategies likely to succeed in the future. In this introductory chapter, we summarise the work presented in the other articles of this issue, and provide an overarching view of this rapidly evolving field. We also provide a summary of the MHC class I molecules successfully refolded to date, and provide references to other relevant sources of technical information. 相似文献
994.
树突状细胞在黏膜免疫模型小鼠中的分布及E-cadherin和ICAM-1表达的研究 总被引:1,自引:0,他引:1
目的通过研究小鼠树突状细胞在黏膜免疫模型小鼠中分布特征及上皮型钙黏附分子(E-cadherin)和细胞间黏附分子-1(ICAM-1)的表达,以探讨E-cadherin和ICAM-1在树突状细胞迁移过程中的调控作用.方法采用光镜和免疫组织化学染色方法,观察黏膜免疫模型小鼠中树突状细胞的分布特征;分析E-cadherin和ICAM-1的表达情况.结果体内的树突状细胞在黏膜免疫模型小鼠中,主要分布于肠系膜淋巴结、回肠集合淋巴小结、胃和空回肠黏膜及黏膜下层,与对照组相比有显著差异,其ICAM-1表达明显增高,E-cadherin表达下调,分别与对照组数密度和面密度比较有显著差异.结论在树突状细胞迁移运动过程中,E-cadherin和ICAM-1黏附分子可能起着关键性的调控作用. 相似文献
995.
Nae Yu Kim Jung-Soo Pyo Dong-Wook Kang Seung-Min Yoo 《Pathology, research and practice》2019,215(3):580-585
Objective
The aim of this study was to elucidate the clinicopathological significance and prognostic role of loss of claudin-1 in colorectal cancer (CRC).Methods
The correlations between claudin-1 expression and clinicopathological characteristics, including survival rates, were assessed using immunohistochemistry on 260 archival, paraffin-embedded CRC tissues. In addition, the correlations between cludin-1 and nuclear factor-kappa B (NF-κB), epithelial-mesenchymal transition markers and tumor-infiltrating lymphocytes were investigated.Results
Claudin-1 expression was markedly lost in 42.7% of the 260 CRCs analyzed. Loss of claudin-1 expression significantly correlated with larger tumor size, vascular invasion, higher pT stage, and high metastatic lymph node ratio. In addition, loss of claudin-1 expression significantly correlated with NF-κB activation (P?<?0.001), high SNAI (P?<?0.001), and low E-cadherin (P?<?0.001) expressions. Patients with high immunoscores showed significantly lower rates of claudin-1 expression loss (P?=?0.020). In detail, loss of claudin-1 expression were frequently found in CRCs low CD3- and CD8-positive lymphocytes. There were significant correlations between claudin-1 expression loss and poor overall and recurrence-free survivals (P?<?0.001 and P?<?0.001, respectively).Conclusion
Taken together, our results suggest that the loss of claudin-1 expression significantly correlates with aggressive tumor behaviors, high SNAI expression, lower immunoscore, and poor prognoses. 相似文献996.
IMMUNOHISTOCHEMICAL DISTRIBUTION OF CANNABINOID CB 1 RECEPTOR IN THE RAT CENTRAL NERVOUS SYSTEM@邹冈 相似文献
997.
Susceptibility to clinically manifest cyclosporine A (CsA)-induced autoimmune disease is associated with interferon-gamma (IFN-γ)-producing CD45RC+RT6− T helper cells 下载免费PDF全文
L J J BEIJLEVELD H GROEN C P M BROEREN F A KLATTER J KAMPINGA J G M C DAMOISEAUX P J C VAN BREDA VRIESMAN 《Clinical and experimental immunology》1996,105(3):486-496
Lethally irradiated Lewis (LEW) rats reconstituted with syngeneic bone marrow and given CsA for a 4-week period, develop, upon withdrawal of CsA, a graft-versus-host-like disease, so-called CsA-induced autoimmunity (CsA-AI). This T cell-mediated autoimmune disease is thymus-dependent; it is generally held that this disease is a consequence of aberrant T cell recovery brought about by CsA. In this study we determined mononuclear cell subsets phenotypically by tri-colour flow cytometry. A strong decrease in recent thymic emigrants (Thy1.1+, TCR αβ+) was observed as a consequence of CsA treatment, eventually resulting in decreased absolute peripheral T cell numbers. In these rats no altered CD4:CD8 T cell ratio was observed before onset of CsA-AI; CD4+ and CD8+ cells consisted predominantly of monocytes (CD4dim+, TCR αβ−) and natural killer cells (CD8+, TCR αβ−), respectively. LEW rats, x-irradiated, syngeneic bone marrow-reconstituted and treated with CsA, showed a marked and persistent, relative expansion of mature CD45RC+, RT6− Th cells. In contrast, Brown-Norway rats treated in a similar fashion, or LEW rats subjected to either CsA treatment or x-irradiation, did not show a comparable expansion of mature CD45RC+, RT6− Th cells, nor did these animals develop CsA-AI. The CD45RC+, RT6− Th cells produced IL-2, and moreover constituted the only Th subset producing IFN-γ upon stimulation, and therefore were considered as Th1-like effector cells. These results are consistent with the view that a persistent preponderance of Th1 cells and not the mere presence of autoreactive cells determines whether or not clinically manifest CsA-AI will occur. 相似文献
998.
Brooks TD Slomp J Quax PH De Bart AC Spencer MT Verheijen JH Charlton PA 《Clinical & experimental metastasis》2000,18(6):445-453
Recent reports suggest that elevated levels of plasminogen activator inhibitor-1 (PAI-1) may contribute to tumour progression.
The studies reported here were designed to help elucidate PAI-1's contribution to the invasive and migratory phenotype. Antibodies
to PAI-1 dose-dependently, and significantly, inhibited the invasive and migratory potential of human HT1080 fibrosarcoma
cells, as did an antibody to uPA and the plasmin inhibitor aprotinin. Invasion of the human melanoma cell line, BLM, was also
attenuated by the anti-PAI-1 monoclonal antibody MAI-12. The non-invasive human melanoma cell line, IF6, which does not express
uPA, provided further confirmation of PAI-1 and uPA's role as, upon transfection with uPA, this cell line attained an invasive
phenotype, which was again attenuated by MAI- 12. Although antibodies to PAI-1 did not affect the adhesion of HT1080 cells
to vitronectin, the antibody to uPA reduced their attachment. Addition of exogenous PAI-1, however, prevented HT1080 cell
adhesion (IC50 180nM) and promoted cell detachment from vitronectin. Furthermore melanoma cells transfected with a uPA variant, which had
an impaired interaction with PAI-1, were not invasive and had impaired binding to vitronectin. These data highlight the importance
of a balanced proteolysis and suggest an additional role for PAI-1 distinct from its role in proteolysis. These data also
suggest that uPA and PAI-1 may co-operate in the migratory process by respectively facilitating the attachment to, and subsequent
detachment from, vitronectin in the extracellular matrix. These results support the clinical findings and indicate that modulation
of PAI-1 activity may be of therapeutic benefit for the treatment of cancer.
This revised version was published online in July 2006 with corrections to the Cover Date. 相似文献
999.
1000.
以体外培养的猪主动脉内皮细胞(EC)为模型研究Ilopost对EC抗血栓功能的影响。用放免法、发色底物法测定培养液中6-酮-PGF1α(6-keto-PGF1α),血栓素B2(TXB2)含量,纤溶酶原激活物(PA),纤溶酶原激活物抑制物(PAI)活性及EC环磷酸腺苷(cAMP)含量。结果表明:Iloprost中以使EC生成6-keto-PGF1α,cAMP含量显著增多,TXB2含量显著减少,并使P 相似文献