14 results on '"Yu, W.-g."'
Search Results
2. First Report of Tomato yellow leaf curl virus Infecting Common Bean in China
- Author
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Ji, Y. H., primary, Cai, Z. D., additional, Zhou, X. W., additional, Liu, Y. M., additional, Xiong, R. Y., additional, Zhao, T. M., additional, Yu, W. G., additional, Tao, X. R., additional, and Zhou, Y. J., additional
- Published
- 2012
- Full Text
- View/download PDF
3. Modeling of Novel Modulated Helix Induction MEMS Switch on Time-Domain
- Author
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Yu, W G, primary, Zhou, K Q, additional, and Yang, T H, additional
- Published
- 2006
- Full Text
- View/download PDF
4. Differential IL-12 responsiveness of T cells but not of NK cells from tumor-bearing mice in IL-12-responsive versus -unresponsive tumor models
- Author
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Iwasaki, M., Yu, W-G., Uekusa, Y., Nakajima, C., Yang, Y-F., Gao, P., Wijesuriya, R., Fujiwara, H., and Hamaoka, T.
- Abstract
While IL-12 administration induces tumor regression through stimulating T cells in tumor-bearing mice, this IL-12 effect is observed in some but not all tumor models. The present study aimed to compare IL-12 responsiveness of T cells from tumor-bearing mice in IL-12-responsive (CSA1M and OV-HM) and -unresponsive (Meth A) tumor models. Tumor regression in IL-12-responsive tumor models required the participation of T cells, but not of NK1.1+ cells. Because a NK1.1+ cell population was the major producer of IFN-γ, comparable levels of IFN-γ production were induced in IL-12-responsive and -unresponsive tumor-bearing mice. This indicates that the amount of IFN-γ produced in tumor-bearing individuals does not correlate with the anti-tumor efficacy of IL-12. In contrast, IL-12 responsiveness of T cells differed between the responsive and unresponsive models: purified T cells from CSA1M/OV-HM-bearing or Meth A-bearing mice exhibited high or low IL-12 responsiveness respectively, when evaluated by the amounts of IFN-γ produced in response to IL-12. T cells from CSA1M- or OV-HM-bearing but not from Meth A-bearing mice exhibited enhanced levels of mRNA for the IL-12 receptor (IL-12R). These results indicate that a fundamental difference exists in IL-12 responsiveness of T cells between IL-12-responsive and -unresponsive tumor models, and that such a difference is associated with the expression of IL-12R on T cells.
- Published
- 2000
5. Molecular mechanisms underlying IFN-gamma-mediated tumor growth inhibition induced during tumor immunotherapy with rIL-12.
- Author
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Yu, W G, Yamamoto, N, Takenaka, H, Mu, J, Tai, X G, Zou, J P, Ogawa, M, Tsutsui, T, Wijesuriya, R, Yoshida, R, Herrmann, S, Fujiwara, H, and Hamaoka, T
- Abstract
The present study investigates the molecular mechanisms by which IFN-gamma produced as a result of in vivo IL-12 administration exerts its anti-tumor effects. rIL-12 was administered three or five times into mice bearing CSA1M fibrosarcoma, OV-HM ovarian carcinoma or MCH-1-A1 fibrosarcoma. This regimen induced complete regression of CSA1M and OV-HM tumors but only transient growth inhibition of MCH-1-A1 tumors. The anti-tumor effects of IL-12 were associated with enhanced induction of IFN-gamma because these effects were abrogated by pretreatment of hosts with anti-IFN-gamma antibody. Exposure in vitro of the three types of tumor cells to rRFN-gamma resulted in moderate to potent inhibition of tumor cell growth. IFN-gamma stimulated the expression of mRNAs for an inducible type of NO synthase (iNOS) in CSA1M cells and indoleamine 2,3-dioxygenase (IDO), an enzyme capable of degrading tryptophan, in OH-HM cells, but induced only marginal levels of these mRNAs in MCH-1-A1 cells. In association with iNOS gene expression, IFN-gamma-stimulated CSA1M cells produced a large amount of NO which functioned to inhibit their own growth in vitro. Although OV-HM and MCH-1A1 cells did not produce NO, they also exhibited NO susceptibility. Whereas the tumor masses from IL-12-treated CSA1M-bearing or OV-HM-bearing mice induced higher levels of iNOS (for CSA1M) or IDO and iNOS (for OV-HM) mRNAs, the MCH-1-A1 tumor mass expressed lower levels of iNOS mRNA alone. Moreover, massive infiltration of CD4(+) and CD8(+) T cells and Mac-1(+) cells was seen only in the CSA1M and OV-HM tumors. Thus, these results indicate that IFN-gamma produced after IL-12 treatment induces the expression of various genes with potential to modulate tumor cell growth by acting directly on tumor cells or stimulating tumor-infiltrating lymphoid cells and that the effectiveness of IL-12 therapy is associated with the operation of these mechanisms.
- Published
- 1996
- Full Text
- View/download PDF
6. [The effect on bleeding volume and postoperative recovery of regional cerebral oxygen saturation guides controlled hypotension in elderly patients with hypertension undergoing spinal surgery].
- Author
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Wang L, Li XZ, Yu WG, Dong R, Wang MS, Bi YL, Chu HC, Wang SD, and Li JZ
- Subjects
- Aged, Humans, Oxygen, Postoperative Period, Sevoflurane, Hypertension, Hypotension, Controlled
- Abstract
Objective: To evaluate the effect on bleeding volume and postoperative recovery of regional cerebral oxygen saturation (rSO(2)) guides controlled hypotension in elderly patients with hypertension undergoing spinal surgery. Methods: One hundred and twenty elderly patients who underwent spinal surgery in the department of anesthesiology of Qingdao Municipal Hospital and the Affiliated Hospital of Qingdao University from January 2017 to December 2019 were selected and divided into 2 groups according to the random number table method ( n= 60): rSO(2) guides the controlled hypotension group (group A) and control group (group C). Both groups were performed with endotracheal intubation for general anesthesia, maintain anesthesia with sevoflurane and remifentanil, rSO(2) were monitored throughout the procedure. If necessary, sodium nitroprusside or esmolol were used to control blood pressure. In group A, the goal of controlled hypotension was that rSO(2) decreased ≤ 10% of the basic value or maintained at 64±3 and the moderate operative field bleeding. Group C underwent routine anesthesia management. Intraoperative blood loss and urine output, the incidence of hypothermia after operation, postoperative delirium, chills, nausea and vomiting, the PACU residence time, postoperative drainage volume, eating time, postoperative hospital stay were compared between the two groups. Results: Compared with group C, the blood loss [(589±157) vs (764±213) ml] and urine output [(778±121) vs (1 079±239) ml] of group A were decreased ( t= -5.120, -8.712, all P< 0.05). The rates of hypothermia after operation (26.7% vs 45.0%), postoperative delirium (18.3% vs 36.7%), chills (10.0% vs 25.0%), nausea and vomiting (21.7% vs 40.0%) of group A were decreased (χ(2)=4.385, 5.057, 4.675, 4.728, all P< 0.05) . The PACU residence time [(56±9) vs (63±11) min], postoperative drainage volume [(217±66) vs (289±81) ml], eating time [(17.8±2.8) vs (22.3±4.1) h] and numbers of days in hospital [(7.2±2.7) vs (8.2±2.9) d] were decreased of group A ( t= -3.399, -5.334, -7.000, -2.031, all P< 0.05). Conclusion: The guidance of controlled hypotension with rSO(2) monitoring can reduce the blood loss and infusion volume during spinal surgery in elderly patients with hypertension, reduce postoperative related complications and enhance recovery after surgery.
- Published
- 2020
- Full Text
- View/download PDF
7. A critical role for a peritumoral stromal reaction in the induction of T-cell migration responsible for interleukin-12-induced tumor regression.
- Author
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Ogawa M, Umehara K, Yu WG, Uekusa Y, Nakajima C, Tsujimura T, Kubo T, Fujiwara H, and Hamaoka T
- Subjects
- Animals, Cell Movement, Female, Intercellular Adhesion Molecule-1 analysis, Male, Mice, Mice, Inbred BALB C, Mice, Inbred C3H, Mice, Inbred C57BL, Neoplasms, Experimental immunology, Neoplasms, Experimental therapy, Tumor Cells, Cultured, Vascular Cell Adhesion Molecule-1 analysis, Interleukin-12 therapeutic use, Neoplasms, Experimental blood supply, T-Lymphocytes physiology
- Abstract
Interleukin (IL) 12 has been shown to elicit tumor regression when this cytokine induces the migration of T cells to tumor sites. The present study investigates the role of a peritumoral stromal reaction in IL-12-induced T-cell migration. In the CSA1M and OV-HM tumor models, IL-12 treatment induced tumor regression that is associated with T-cell migration. Neither T-cell migration nor tumor regression was observed in the Meth A and MCH-1-A1 models. Stromal tissue containing neovascular blood vessels developed at the peritumoral area of the former two IL-12-responsive tumors but not at the peritumoral area of the latter two IL-12-unresponsive tumors. The significance of stroma development was investigated using a pair of tumor models (CSA1M and a subline derived from CSA1M designated the CSA1M variant), both of which exhibit the same tumor immunogenicity. In contrast to the parental CSA1M cell line, the variant cell line was not responsive to IL-12, and neither stroma development nor T-cell migration was observed, even after IL-12 treatment. Histological analyses revealed that the parental cell line had peritumoral stroma with intrastromal vessels but only a few vessels in tumor parenchyma, whereas the variant cell line showed no stroma but had abundant vasculature in the tumor parenchyma. Most importantly, only stromal vessels in the parental tumors expressed detectable and enhanced levels of vascular cell adhesion molecule 1 (VCAM-1)/ intercellular adhesion molecule 1 (ICAM-1) before and after IL-12 treatment, respectively. In contrast, parenchymal vasculature in the variant cell line failed to express VCAM-1/ICAM-1 even after IL-12 treatment. When transferred into recipient tumor-bearing mice, IL-12-stimulated T cells from the parental CSA1M-bearing or the variant CSA1M-bearing mice migrated into the parental but not into the variant tumor mass. Together with our previous finding that T-cell migration depends on the VCAM-1/ICAM-1 adhesive interactions, the present results indicate a critical role for peritumoral stroma/stromal vasculature in the acceptance of tumor-infiltrating T cells that is a prerequisite for IL-12-induced tumor regression.
- Published
- 1999
8. Multiple roles of interferon-gamma in the mediation of interleukin 12-induced tumor regression.
- Author
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Ogawa M, Yu WG, Umehara K, Iwasaki M, Wijesuriya R, Tsujimura T, Kubo T, Fujiwara H, and Hamaoka T
- Subjects
- Animals, Antibodies, Monoclonal, Cell Movement drug effects, Down-Regulation, Female, Fibrosarcoma blood supply, Fibrosarcoma drug therapy, Fibrosarcoma pathology, Intercellular Adhesion Molecule-1 biosynthesis, Male, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Neoplasms, Experimental blood supply, Neoplasms, Experimental pathology, Neovascularization, Pathologic, Ovarian Neoplasms blood supply, Ovarian Neoplasms drug therapy, Ovarian Neoplasms pathology, Rats, Remission Induction, T-Lymphocytes drug effects, Tumor Cells, Cultured, Vascular Cell Adhesion Molecule-1 biosynthesis, Antineoplastic Agents therapeutic use, Interferon-gamma physiology, Interleukin-12 therapeutic use, Neoplasms, Experimental drug therapy
- Abstract
Administration of recombinant interleukin 12 (IL-12) induces tumor regression that is associated with T-cell infiltration in the OV-HM ovarian carcinoma and CSA1M fibrosarcoma models. After confirming the blocking of regression by injection of anti-IFN-gamma monoclonal antibody (mAb), we investigated the mechanisms underlying the requirement of IFN-gamma in T-cell migration and tumor regression. T-cell migration was inhibited by injection of anti-IFN-gamma mAb to OV-HM tumor-bearing mice prior to IL-12 treatment. We examined, using the lymphoid cell migration assay, whether IFN-gamma is required for enhancing the migratory capacity of T cells or the T cell-accepting potential of tumor masses during IL-12 treatment. Spleen cells from IL-12-treated or untreated OV-HM-bearing mice were stained in vitro with a fluorescein chemical and transferred i.v. into OV-HM-bearing mice that were not treated with IL-12. Migration of donor cells was quantitated by counting the number of fluorescent cells on cryostat sections of tumor masses from recipient mice. Compared to spleen cells from OV-HM-bearing mice that were not treated with IL-12, enhanced migration was observed for cells from IL-12-treated OV-HM-bearing mice. Anti-IFN-gamma pretreatment of donor mice before IL-12 treatment did not reduce the migratory capacity of T cells, whereas migration was markedly inhibited in recipient mice injected with anti-IFN-gamma. Anti-IFN-gamma pretreatment decreased vascular cell adhesion molecule-1 (VCAM-1)-/intercellular adhesion molecule-1 (ICAM-1)-positive blood vessels at tumor sites. Consistent with this, migration was also inhibited by treatment of recipient mice with either anti-VCAM-1 or anti-ICAM-1 mAb. In contrast to the OV-HM model, T-cell migration was not affected in the CSA1M model following preinjection of anti-IFN-gamma mAb. In this model, VCAM-1-/ICAM-1-positive blood vessels existed even after anti-IFN-gamma treatment, although tumor regression was completely inhibited. These results indicate that IFN-gamma plays two distinct roles in expressing the antitumor efficacy of IL-12: one is to support the T-cell acceptability of tumor masses, and the other is to mediate the antitumor effects of migrated T cells.
- Published
- 1998
9. Hypotonically induced whole-cell currents in A6 cells: relationship with cell volume and cytoplasmic Ca2+.
- Author
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Yu WG and Sokabe M
- Subjects
- Animals, Cell Line, Chloride Channels antagonists & inhibitors, Cytoplasm drug effects, Osmolar Concentration, Patch-Clamp Techniques, Potassium Channel Blockers, Xenopus laevis, Calcium metabolism, Calcium Channel Blockers pharmacology, Cell Size drug effects, Cytoplasm metabolism, Hypotonic Solutions pharmacology
- Abstract
We investigated changes in whole-cell currents, cell volume, and intracellular calcium concentration ([Ca2+]i) during hypotonic stimulation in whole-cell clamped cultured amphibian renal cells (A6 cells). Upon being exposed to hypotonic solution (80% osmolality), the A6 cells swelled and peaked in the first 5 min, which was followed by a progressive decrease in cell volume termed regulatory volume decrease (RVD). Following the cell swelling, there were large increases in both outward- and inward-currents, which seemed to be carried by K+ efflux and Cl- efflux, respectively. A K+ channel blocker (TEA or quinine) or a Cl- channel blocker (NPPB or SITS) significantly inhibited both currents and RVD, suggesting that the inward- and outward-currents are highly correlated with each other and essential to RVD. Hypotonic stimulation also induced a transient [Ca2+]i increase, of which the time course was essentially similar to that of the currents. When internal and external Ca2+ were deprived to eliminate the Ca2+ transient increase, whole-cell currents and RVD were strongly inhibited. On the other hand, channel blockers TEA and NPPB, which inhibited whole-cell currents and RVD, did not inhibit the [Ca2+]i increase. It is concluded that hypotonic stimulation to A6 cells first induces cell swelling, which is followed by [Ca2+]i increase that leads to the coactivation of K+ and Cl- channels. This coactivation may accelerate K+ and Cl- effluxes, resulting in RVD.
- Published
- 1997
- Full Text
- View/download PDF
10. IL-12-induced tumor regression correlates with in situ activity of IFN-gamma produced by tumor-infiltrating cells and its secondary induction of anti-tumor pathways.
- Author
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Yu WG, Ogawa M, Mu J, Umehara K, Tsujimura T, Fujiwara H, and Hamaoka T
- Subjects
- Animals, Chemokine CXCL10, Chemokines biosynthesis, DNA Probes, DNA, Complementary, Fibrosarcoma pathology, Lymphocytes, Tumor-Infiltrating pathology, Male, Mice, Mice, Inbred BALB C, Neutralization Tests, Nitric Oxide Synthase biosynthesis, Polymerase Chain Reaction, RNA, Messenger biosynthesis, Recombinant Proteins therapeutic use, Antibodies, Monoclonal pharmacology, Chemokines, CXC, Fibrosarcoma immunology, Fibrosarcoma therapy, Interferon-gamma biosynthesis, Interferon-gamma immunology, Interleukin-12 therapeutic use, Lymphocytes, Tumor-Infiltrating immunology, Transcription, Genetic drug effects
- Abstract
Administration of recombinant interleukin-12 (rIL-12) into CSA1M fibrosarcoma-bearing mice results in complete regression of growing tumors. This tumor regression is associated with massive lymphoid cell infiltration to tumor sites and is completely blocked by injection of anti-interferon-gamma (IFN-gamma) monoclonal antibody (mAb). We investigated whether anti-IFN-gamma mAb exerts its suppressive effect on tumor regression by blocking the IL-12-induced lymphoid cell migration to tumor sites or by inhibiting the secondary effects of IFN-gamma produced by infiltrating cells. Injection of anti-IFN-gamma mAb to CSA1M-bearing mice before IL-12 treatment prevented the induction of tumor regression, whereas this treatment affected only marginally the infiltration of lymphoid cells to tumor masses. In accordance with this, IFN-gamma mRNA was expressed inside tumor masses by infiltrating cells after IL-12 therapy irrespective of whether anti-IFN-gamma mAb was injected. However, anti-IFN-gamma mAb treatment almost completely abrogated the in situ expression of inducible nitric oxide synthase (iNOS) as well as IFN-inducible protein-10 (IP-10) genes as examples of IFN-gamma-inducible genes. Immunohistochemical analyses also revealed that the expression of iNOS protein was completely inhibited by anti-IFN-gamma injection. These results suggest that the implementation of in situ IFN-gamma activity and its secondary induction of anti-tumor pathways such as iNOS and IP-10 expression are important processes in the IL-12-induced tumor regression.
- Published
- 1997
- Full Text
- View/download PDF
11. Enhanced induction of very late antigen 4/lymphocyte function-associated antigen 1-dependent T-cell migration to tumor sites following administration of interleukin 12.
- Author
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Ogawa M, Tsutsui T, Zou JP, Mu J, Wijesuriya R, Yu WG, Herrmann S, Kubo T, Fujiwara H, and Hamaoka T
- Subjects
- Animals, Antibodies, Blocking immunology, Antibodies, Monoclonal immunology, CD4 Antigens immunology, CD8 Antigens immunology, Cell Movement immunology, Female, Immunohistochemistry, Integrin alpha4beta1, Integrins immunology, Intercellular Adhesion Molecule-1 immunology, Lymphocyte Function-Associated Antigen-1 immunology, Male, Mice, Mice, Inbred BALB C, Mice, Inbred C3H, Mice, Inbred Strains, Neoplasm Transplantation, Receptors, Lymphocyte Homing immunology, Spleen cytology, Spleen transplantation, T-Lymphocyte Subsets immunology, Tumor Cells, Cultured, Vascular Cell Adhesion Molecule-1 immunology, Interleukin-12 pharmacology, Lymphocytes, Tumor-Infiltrating drug effects, Neoplasms, Experimental immunology, T-Lymphocytes drug effects
- Abstract
Administration of interleukin 12 (IL-12) into mice bearing CSA1M, OV-HM, Meth A, or MCH-1-A1 tumor induced complete regression of CSA1M and OV-HM tumors but induced only a slight growth inhibition of Meth A and MCH-1-A1 tumors. These effects of IL-12 were associated with high and only marginal levels of T-cell infiltration into CSA1M/OV-HM and Meth A/MCH-1-A1 tumor masses, respectively. Here, we investigated the role of IL-12 in the induction of T-cell migration. Spleen cells from untreated or IL-12-treated CSA1M-bearing mice were stained in vitro with a fluorescein chemical and transferred i.v. into IL-12-untreated CSA1M-bearing mice. Migration of donor cells was quantitated by counting the number of fluorescent cells on cryostat sections of tumor masses. Although only a slight migration was detected for spleen cells from IL-12-untreated CSA1M-bearing as well as IL-12-treated or untreated normal mice, enhanced migration was observed for cells from IL-12-treated CSA1M-bearing mice. A similar enhanced migration was observed for the OV-HM model. In contrast, such an enhancement was only marginal in the Meth A and MCH-1-A1 models. Immunohistochemical studies of tumors from IL-12-treated mice revealed that the predominant T-cell subset was CD4+ in CSA1M and CD8+ in OV-HM tumor masses. Consistent with this observation, the dominant subset of migrating T cells was found to be CD4+ in the CSA1M and CD8+ in the OV-HM models. T-cell migration was inhibited by pretreatment of recipients with either combination of anti-very late antigen 4 + anti-vascular cell adhesion molecule 1 or anti-lymphocyte function-associated antigen 1 + anti-intercellular adhesion molecule 1 monoclonal antibody. These results indicate that IL-12 can confer T cells with a capacity to migrate to tumor sites through very late antigen 4/lymphocyte function-associated antigen 1 adhesion pathways and that the in vivo acquisition of such a capacity following IL-12 treatment correlates with the induction of tumor regression.
- Published
- 1997
12. Establishment of an IL-12-responsive T cell clone: its characterization and utilization in the quantitation of IL-12 activity.
- Author
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Maruo S, Ahn HJ, Yu WG, Tomura M, Wysocka M, Yamamoto N, Kobayashi M, Hamaoka T, Trinchieri G, and Fuijiwara H
- Subjects
- Animals, Biological Assay, Cell Aggregation, Cell Division, Cell Line, Cytokines metabolism, Interleukin-12 metabolism, Mice, Mice, Inbred C57BL, Phenotype, Receptors, Interleukin-12, Th1 Cells cytology, Th1 Cells metabolism, Interleukin-12 pharmacology, Receptors, Interleukin metabolism, Th1 Cells drug effects
- Abstract
We previously demonstrated that proliferation of terminally differentiated Th1 clones depends primarily on an interleukin-12 (IL-12)-paracrine mechanism mediated by their interactions with antigen-presenting cells (APC) rather than on an IL-2-autocrine mechanism. Such a Th1 clone (4-86, C57BL/6 origin) was cultured with recombinant IL-12 (rIL-12) in the absence of either antigen or APC. Some cells survived for several passages of culture with only rIL-12, and by limiting dilution, several clones highly reactive to rIL-12 alone were obtained. One of these clones, designated 2D6, was found to proliferate strongly in response to less than 1 pg/mL of rIL-12. This clone exhibited the following surface phenotypes: CD3+, T cell receptor (TCR) alpha beta+, Vbeta11+, NK-1.1-; CD4-CD8-; LFA-1+, ICAM-1+; and CD28+, CD80+, CD86+, CTLA-4-. In accordance with high responsiveness to IL-12, 2D6 cells were also found to express IL-12 receptor (IL-12R) as detected by incubation with rIL-12 and then staining with anti-IL-12 monoclonal antibody (mAb). Stimulation of 2D6 with rIL-12 resulted in the expression of interferon-gamma (IFN-gamma) and IL-10 mRNAs and production of these cytokines. The 2D6 clone responded to IL-2 (vigorously), IL-7 (moderately), and IL-4 (mildly) in addition to IL-12. However, the Ab capture assay using anti-IL-12 mAb enabled us to quantify IL-12-specific activity contained in a given sample. Thus, this study describes the unique features of the IL-12-responsive T cell clone and demonstrates the utilization of this clone in the quantitation of a specific IL-12 activity.
- Published
- 1997
- Full Text
- View/download PDF
13. Formation of monohydroxy derivatives of arachidonic acid, linoleic acid, and oleic acid during oxidation of low density lipoprotein by copper ions and endothelial cells.
- Author
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Wang T, Yu WG, and Powell WS
- Subjects
- Cells, Cultured, Chromatography, High Pressure Liquid, Fatty Acids metabolism, Gas Chromatography-Mass Spectrometry, Humans, Kinetics, Linoleic Acid, Lipid Peroxidation, Male, Oleic Acid, Oxidation-Reduction, Spectrophotometry, Ultraviolet, Arachidonic Acids metabolism, Copper metabolism, Endothelium, Vascular metabolism, Linoleic Acids metabolism, Lipoproteins, LDL metabolism, Oleic Acids metabolism
- Abstract
An important event in the formation of atherosclerotic lesions is the uptake of modified low density lipoprotein (LDL) by macrophages via scavenger receptors. Modification of LDL, which results in its recognition by these receptors, can be initiated by peroxidation of LDL lipids. The first step in this process is the formation of monohydroperoxy derivatives of fatty acids, which are subsequently degraded to the corresponding monohydroxy compounds, or to a variety of secondary oxidation products. In order to understand this process more completely, we have developed a mass spectrometric procedure to measure the amounts of specific hydroperoxy/hydroxy fatty acids formed by oxidation of the major unsaturated fatty acids in human LDL, oleic acid, linoleic acid, and arachidonic acid. Oxidation of human LDL in the presence of a relatively strong stimulus (20 microM CuSO4) resulted in very large increases in the amounts of the major monohydroxy derivatives of linoleic acid (9- and 13-hydroxy derivatives) and arachidonic acid (5-, 8-, 9-, 11-, 12-, and 15-hydroxy derivatives) in LDL lipids in the early stages of the reaction. After 20 h, the amounts of these products declined due to substrate depletion, but large amounts of monohydroxy derivatives of oleic acid (8-, 10-, and 11-hydroxy derivatives) were detected. Although thiobarbituric acid-reactive substances clearly increased under these conditions, the changes were not nearly so dramatic as those observed for monohydroxy fatty acids. Oxidation of LDL in the presence of endothelial cells, a much milder stimulus, resulted in 2.5- to 3-fold increases in the amounts of monohydroxy derivatives of linoleic and arachidonic acids, as well as thiobarbituric acid-reactive substances, with more modest increases in the amounts of hydroxylated derivatives of oleic acid. There was little positional specificity in the oxidation of the above fatty acids in the presence of either stimulus, suggesting that the formation of these products proceeds primarily by lipid peroxidation, rather than by catalysis by lipoxygenases. However, an important role for lipoxygenases in the initiation of these reactions cannot be excluded. In conclusion, oxidation of LDL in the presence of copper ions or endothelial cells results in the formation of a large number of monohydroxy derivatives of oleic, linoleic, and arachidonic acids. The relative amounts of products formed from each of these fatty acids depends on the strength of the stimulus as well as the incubation time.
- Published
- 1992
14. Intestinal polyposis of 13 cases.
- Author
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Zhang SQ and Yu WG
- Subjects
- Adolescent, Adult, Child, Female, Humans, Infant, Intestinal Neoplasms genetics, Intestinal Neoplasms surgery, Intestinal Polyps genetics, Intestinal Polyps surgery, Male, Middle Aged, Intestinal Neoplasms pathology, Intestinal Polyps pathology
- Published
- 1983
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