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Relevant bibliographies by topics / Inhibit

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Academic literature on the topic 'Inhibit'

Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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Journal articles on the topic "Inhibit"

1

Katiyar, Santosh K. "Hsp90 Inhibitor Can Inhibit UV Carcinogenesis." Journal of Investigative Dermatology 135, no. 4 (April 2015): 945–47. http://dx.doi.org/10.1038/jid.2014.504.

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Ferrarelli, L. K. "Inhibit PIM to inhibit PI3K." Science Signaling 9, no. 449 (October 11, 2016): ec237-ec237. http://dx.doi.org/10.1126/scisignal.aal1638.

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Balasubramanian, Sujata, Meiyun Fan, Angela F. Messmer-Blust, Chuan H. Yang, Jill A. Trendel, Jonathan A. Jeyaratnam, Lawrence M. Pfeffer, and Deborah J. Vestal. "The Interferon-γ-induced GTPase, mGBP-2, Inhibits Tumor Necrosis Factor α (TNF-α) Induction of Matrix Metalloproteinase-9 (MMP-9) by Inhibiting NF-κB and Rac Protein." Journal of Biological Chemistry 286, no. 22 (April 18, 2011): 20054–64. http://dx.doi.org/10.1074/jbc.m111.249326.

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Matrix metalloproteinase-9 (MMP-9) is important in numerous normal and pathological processes, including the angiogenic switch during tumor development and tumor metastasis. Whereas TNF-α and other cytokines up-regulate MMP-9 expression, interferons (IFNs) inhibit MMP-9 expression. We found that IFN-γ treatment or forced expression of the IFN-induced GTPase, mGBP-2, inhibit TNF-α-induced MMP-9 expression in NIH 3T3 fibroblasts, by inhibiting MMP-9 transcription. The NF-κB transcription factor is required for full induction of MMP-9 by TNF-α. Both IFN-γ and mGBP-2 inhibit the transcription of a NF-κB-dependent reporter construct, suggesting that mGBP-2 inhibits MMP-9 induction via inhibition of NF-κB-mediated transcription. Interestingly, mGBP-2 does not inhibit TNF-α-induced degradation of IκBα or p65/RelA translocation into the nucleus. However, mGBP-2 inhibits p65 binding to a κB oligonucleotide probe in gel shift assays and to the MMP-9 promoter in chromatin immunoprecipitation assays. In addition, TNF-α activation of NF-κB in NIH 3T3 cells is dependent on Rac activation, as evidenced by the inhibition of TNF-α induction of NF-κB-mediated transcription by a dominant inhibitory form of Rac1. A role for Rac in the inhibitory action of mGBP-2 on NF-κB is further shown by the findings that mGBP-2 inhibits TNF-α activation of endogenous Rac and constitutively activate Rac can restore NF-κB transcription in the presence of mGBP-2. This is a novel mechanism by which IFNs can inhibit the cytokine induction of MMP-9 expression.

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&NA;. "Inhibit pancreatic tumour growth with PKD inhibitor." Oncology Times UK 6, no. 5 (May 2009): 4. http://dx.doi.org/10.1097/01434893-200905000-00003.

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Xu, W., C. Gatto, and M. A. Milanick. "Positive charge modifications alter the ability of XIP to inhibit the plasma membrane calcium pump." American Journal of Physiology-Cell Physiology 271, no. 3 (September 1, 1996): C736—C741. http://dx.doi.org/10.1152/ajpcell.1996.271.3.c736.

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Exchange inhibitory peptide (XIP; RRLLFYKYVYKRYRAGKQRG) is the shortest peptide that inhibits the plasma membrane Ca pump at high Ca (A. Enyedi, T. Vorherr, P. James, D. J. McCormick, A. G. Filoteo, E. Carafoli, and J. T. Penniston, J. Biol. Chem. 264: 12313-12321, 1989). Sulfosuccinimidyl acetate (SNA)-modified XIP does not inhibit the Ca pump; SNA neutralizes the positive charge on Lys at positions 7, 11, and 17. Peptide 2CK-XIP (RRLLFYRYVYRCYCAGRQKG) inhibits the pump, but the iodoacetamido-modified peptide does not inhibit. Three peptide analogues, in which 7, 11, and 17 were Ala, Cys, or Lys, inhibited about as well as XIP. SNA modification of these analogues (each with 1 Lys) did not inhibit. SNA modification of 2CK-XIP results in a peptide that does not inhibit; thus position 19 is important. Our results suggest that it is critical that position 19 be positively charged, that positions 7, 11, and 17 are important contact points between XIP and the Ca pump (with at least one positively charged), and that, whereas it is not essential that residues 12 and 14 be positive, they cannot be negative.

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Yan, Huifang, Xiwei Peng, Hao Xu, Jiahuan Zhu, and Changqing Deng. "Inhibition of Aortic Intimal Hyperplasia and Vascular Smooth Muscle Proliferation and Extracellular Matrix Protein Expressions by Astragalus–Angelica Combination." Evidence-Based Complementary and Alternative Medicine 2018 (August 13, 2018): 1–15. http://dx.doi.org/10.1155/2018/1508637.

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VSMC proliferation and ECM deposition always resulted in intimal hyperplasia. Astragalus–Angelica combination has a protective effect on the cardiovascular system. The inhibition effect of different Astragalus–Angelica combination on the hyperplastic intima after vascular balloon injury in rats was investigated in this study. Astragalus–Angelica combination can inhibit the intima hyperplasia after balloon injury, in which a 1:1 ratio shows excellent results. Astragalus–Angelica combination can enhance the expression of smooth muscleα-actin (SMа-actin) and inhibit the expression of proliferating cell nuclear antigen (PCNA), cyclin D1, cyclin E, collagen I (Col-I), fibronectin (FN), and matrix metallopeptidase-9 (MMP-9) in hyperplastic intima, suggesting that Astragalus–Angelica combination can inhibit the intimal hyperplasia of blood vessels in rats. The mechanism is related to the inhibition of PI3K/Akt signaling pathway activation and thereby inhibits the phenotypic transformation and cell proliferation of VSMCs and thus inhibits the extracellular matrix (ECM) deposition of vascular wall during intimal hyperplasia.

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BISWAS, Swati, Manju RAY, Sanjoy MISRA, D. P. DUTTA, and Subhankar RAY. "Selective inhibition of mitochondrial respiration and glycolysis in human leukaemic leucocytes by methylglyoxal." Biochemical Journal 323, no. 2 (April 15, 1997): 343–48. http://dx.doi.org/10.1042/bj3230343.

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The effect of methylglyoxal on the oxygen consumption of mitochondria of both normal and leukaemic leucocytes was tested by using different respiratory substrates and complex specific artificial electron donors and inhibitors. The results indicate that methylglyoxal strongly inhibits mitochondrial respiration in leukaemic leucocytes, whereas, at a much higher concentration, methylglyoxal fails to inhibit mitochondrial respiration in normal leucocytes. Methylglyoxal strongly inhibits ADP-stimulated α-oxoglutarate and malate plus NAD+-dependent respiration, whereas, at a higher concentration, methylglyoxal fails to inhibit succinate and α-glycerophosphate-dependent respiration. Methylglyoxal also fails to inhibit respiration which is initiated by duroquinone and cannot inhibit oxygen consumption when the N,N,N´,N´-tetramethyl-p-phenylenediamine by-pass is used. NADH oxidation by sub-mitochondrial particles of leukaemic leucocytes is also inhibited by methylglyoxal. Lactaldehyde, a catabolite of methylglyoxal, can exert a protective effect on the inhibition of leukaemic leucocyte mitochondrial respiration by methylglyoxal. Methylglyoxal also inhibits l-lactic acid formation by intact leukaemic leucocytes and critically reduces the ATP level of these cells, whereas methylglyoxal has no effect on normal leucocytes. We conclude that methylglyoxal inhibits glycolysis and the electron flow through mitochondrial complex I of leukaemic leucocytes. This is strikingly similar to our previous studies on mitochondrial respiration, glycolysis and ATP levels in Ehrlich ascites carcinoma cells [Ray, Dutta, Halder and Ray (1994) Biochem. J. 303, 69–72; Halder, Ray and Ray (1993) Int. J. Cancer 54, 443–449], which strongly suggests that the inhibition of electron flow through complex I of the mitochondrial respiratory chain and inhibition of glycolysis by methylglyoxal may be common characteristics of all malignant cells.

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King, Frank W., and Emma Shtivelman. "Inhibition of Nuclear Import by the Proapoptotic Protein CC3." Molecular and Cellular Biology 24, no. 16 (August 15, 2004): 7091–101. http://dx.doi.org/10.1128/mcb.24.16.7091-7101.2004.

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ABSTRACT We report here that the normal cellular protein CC3/TIP30, when in excess, inhibits nuclear import in vitro and in vivo. CC3 binds directly to the karyopherins of the importin β family in a RanGTP-insensitive manner and associates with nucleoporins in vivo. CC3 inhibits the nuclear import of proteins possessing either the classical nuclear localization signal or the M9 signal recognized by transportin. CC3 also inhibits nuclear translocation of transportin itself. Cells modified to express higher levels of CC3 have a slower rate of nuclear import and, as described earlier, show an increased sensitivity to death signals. A mutant CC3 protein lacking proapoptotic activity has a lower affinity for transportin, is displaced from it by RanGTP, and fails to inhibit nuclear import in vitro and in vivo. Together, our results support a correlation between the ability of CC3 to form a RanGTP-resistant complex with importins, inhibit nuclear import, and induce apoptosis. Significantly, a dominant-negative form of importin β1 shown previously to inhibit multiple transport pathways induces rapid cell death, strongly indicating that inhibition of nuclear transport serves as a potent apoptotic signal.

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Sicher, S. C., M. A. Vazquez, and C. Y. Lu. "Inhibition of macrophage Ia expression by nitric oxide." Journal of Immunology 153, no. 3 (August 1, 1994): 1293–300. http://dx.doi.org/10.4049/jimmunol.153.3.1293.

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Abstract Bacterial LPS inhibits the expression of Ia by macrophages stimulated by IFN-gamma. We now present the following observations that suggest a causal relationship between nitric oxide (NO) and this inhibition of Ia expression: 1) NO production precedes inhibition of Ia, 2) the ability of LPS to inhibit Ia expression by IFN-gamma stimulated macrophages is correlated in a dose-dependent fashion with NO production, 3) Ia expression is restored if NO production is inhibited by NG-monomethyl-L-arginine or culturing the macrophages in L-arginine-free medium, and 4) exogenous NO inhibits IFN-gamma-stimulated Ia expression. Taken together these experiments indicate that NO inhibits macrophage expression of Ia. Furthermore, the following studies showed that inhibition of Ia by NO was not due to macrophage death: trypan blue exclusion, macrophage adhesion, conversion of the tetrazolium dye (MTT) to its formazan by a functioning electron transport system, and phagocytosis of IgG opsonized SRBCs. By inhibiting Ia expression, NO may inhibit Ag-presentation to T cells, secretion of IFN-gamma by these T cells, and ultimately inhibit the IFN-gamma-dependent production of NO synthetase. This inhibitory mechanism may prevent excessive NO formation and tissue injury.

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Gilbert, R. L., C. J. Blunt, D. R. Harper, D. J. Jeffries, and R. A. J. Mcllhinney. "Effect of Inhibitors of Protein Myristoylation on Varicella-Zoster Virus Replication." Antiviral Chemistry and Chemotherapy 5, no. 3 (June 1994): 182–86. http://dx.doi.org/10.1177/095632029400500307.

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Inhibitors of N-myristoyltransferase (NMT) have been shown to inhibit retrovirus replication, notably that of the human immunodeficiency virus (HIV), where the absence of protein myristoylation inhibits viral replication. The authors have assayed 14 compounds derived from myristic acid for activity against varicella-zoster virus (human herpesvirus 3; VZV) by plaque reduction assay. Seven showed cytotoxicity and of the others, two failed to inhibit VZV replication. One of these was N-myristoylglycinaldiethylacetal (GoA), which has been reported to be active against HIV. 12-(methoxy) dodecanoic acid (13-oxamyristic acid), which has also been reported to inhibit HIV replication, was found to inhibit VZV replication but was cytotoxic at high concentrations. The greatest inhibitory effect without apparent toxicity was induced by 2-hydroxytetradecanoic acid and its enantiomers. The results of these assays provide further evidence that inhibitors of NMT have potential as antiviral agents against the many viruses with myristoylated proteins.

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Dissertations / Theses on the topic "Inhibit"

1

Songjang, Khemika. "Peptides to inhibit crop predation." Thesis, University of Reading, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.428155.

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Chen, Shao Ru. "Andrographolide analogues inhibit acute inflammation." Thesis, University of Macau, 2018. http://umaclib3.umac.mo/record=b3953265.

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Subramanian, Gayatri. "TDRD7, a Novel Viral Restriction Factor, Inhibits Cellular AMP-dependent Kinase to Inhibit Virus Replication." University of Toledo Health Science Campus / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=mco1596574176173965.

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Starks, Kenneth Maurice. "Novel pyridinium salts which inhibit acetylcholinesterase." Thesis, Georgia Institute of Technology, 1994. http://hdl.handle.net/1853/26950.

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Hasan, Jurjees. "Heparin oligosaccharides inhibit angiogenesis in vivo." Thesis, University of Manchester, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.488657.

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The prototypic heparan sulfate (HS)-dependent angiogenic cytokine is FGF-2. Here we present the first in vivo study of size fractionated heparin oligosaccharides in 3 models of angiogenesis that are progressively less dependent on FGF-2. We developed the modified hollow fibre assay, a novel model for quantifying angiogenesis in vivo. We tested the ability of size defined oligosaccharides (dp 6-14) to inhibit FGF-2 in a sponge model of angiogenesis, where the process can be driven by a defined angiogenic molecule. Sponges were implanted subcutaneously and injected with FGF2 100 ng/day and oligosaccharides (20 mglkg/day). After 14 days the sponges were excised and the microvessel density (MVD) measured. Octasaccharides were the most potent species, reducing MVD to levels below those observed in saline treated implants. In a second experiment HEC-FGF2 human endometrial cancer cells that over-express FGF-2 were implanted in a hollow fibre placed subcutaneously in vivo. Oligosaccharides were administered at 20 mglkg/day for 2 weeks and the data again showed that octasaccharides significantly reduced MVD around the fiber. In a more complex model, where angiogenesis was induced by a broad spectrum of growth factors including VEGF, we implanted H460 lung carcinoma cells in hollow fibers and treated the animals with oligosaccharides at 20mglkg/day over three weeks. The data showed that octasaccharides were able to reduce the microvessel density to the level of angiogenesis present in empty hollow fibres. Preliminary investigation of 6-0-desulfated heparins showed that these also had anti-angiogenic activity. In summary, we have shown that heparin octasaccharides have antiangiogenic activity in vivo in several models of variable dependence on FGF-2. We have now embarked on a synthetic programme to produce and investigate oligosaccharides with predefined sulfation patterns and cytokine specificities as FGF inhibitors.

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Yuceer, Buse, Devin Narwani, and Sean Fox. "Does Alcaligenes inhibit other Staphylococcal species?" Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/157.

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Members of the Staphylococcus genus are a major health issue in the clinical environment and can cause a wide range of disease in humans. However, this genus is also found as a part of the normal flora in humans, usually on the skin, nasal cavities, or on the linings of the throat. Normal flora members of the Staphylococcus genus become an opportunistic infection when there is breach in the physical barriers or the immune status of the human host. Another challenge with the Staphylococcus genus is the increase in drug resistant strains, such as Methicillin resistant Staphylococcus aureus (MRSA), making simple infections difficult to treat and leading to severe toxic shock or even death. Recently, there have been numerous studies demonstrating normal flora bacterial interactions inhibiting bacteria that are potentially harmful to humans. Our research lab has previously demonstrated that the benign bacterium Alcaligenes faecalis has inhibitory effects against Staphylococcus aureus. In the present study, we wanted to explore: 1) if the inhibitory effect of A. faecalis would translate to other Staphylococcus species (S. capitis, S. saprophyticus, and S. epidermidis); 2) if this inhibitory effect was found in other Alcaligenes species (A. viscolactis). To determine this possible interactions, two parallel experimental projects were undertaken. A. faecalis and A. viscolactis were tested for their interactions with Staphylococcus species on both agar and liquid medium. For agar medium analysis, Staphylococcus lawns were grown on agar plates and either Alcaligenes cells, heat killed Alcaligenes, or Alcaligenes cell free supernatant were spotted onto the lawns and observed and scored for zones of inhibition (ZOI). It was demonstrated live cells of both A. faecalis and A. viscolactis were needed to produce ZOI on Staphylococcus lawns and that all Staphylococcus species were inhibited. For liquid medium analysis, Staphylococcus species were either inoculated alone (control) or in a co-culture with Alcaligenes, serially diluted, and colony forming units (CFU) were enumerated. Both A. faecalis and A. viscolactis inhibited all Staphylococcus species in liquid culture. Based on the results from these experiments, it is our conclusion that: 1) Alcaligenes faecalis and Alcaligenes viscolactis both possess the ability to inhibit Staphylococcus growth; 2) all Staphylococcus species are inhibited by Alcaligenes, but at varying levels. The exact mechanism of how Alcaligenes can inhibit Staphylococcus species is unknown, which will require further studies to analyze and understand the exact mechanism in order to create effective therapeutic targets to combat these increasingly resistant strains of Staphylococcus.

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Podugu, Sireesha P. Ferrari Michael B. "Long duration calcium transients inhibit sarcomere assembly." Diss., UMK access, 2006.

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Thesis (M.S.)--School of Biological Sciences. University of Missouri--Kansas City, 2006.
"A thesis in cellular and molecular biology." Typescript. Advisor: Michael B. Ferrari. Title from "catalog record" of the print edition Description based on contents viewed Nov. 1, 2007. Includes bibliographical references (leaves 48-52). Online version of the print edition.

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Gopakumar, Bhaskaran Nair. "Molecular strategies to inhibit vein graft disease." Thesis, University of Leeds, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426787.

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Hofmann, Ronald. "Using ammonia to inhibit bromate formation during ozonation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0019/NQ53686.pdf.

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Pridham, Kevin James. "Investigating Novel Targets to Inhibit Cancer Cell Survival." Diss., Virginia Tech, 2004. http://hdl.handle.net/10919/82855.

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Cancer remains the second leading cause of death in the United States and the world, despite years of research and the development of different treatments. One reason for this is cancer cells are able to survive through adaptation to their environment and aberrantly activated growth signaling. As such, developing new therapies that overcome these hurdles are necessary to combat cancer. Previous work in our laboratory using RNA interference screening identified genes that regulate the survival of glioblastoma (GBM) or autophagy in chronic myelogenous leukemia (CML) cancer cells. One screen identified Phosphatidylinositol-4,5-bisophosphate 3-kinase catalytic subunit beta (PIK3CB) in the family of Phosphatidylinositol 3-kinases (PI3K) as a survival kinase gene in GBM. Work contained in this dissertation set out to study PIK3CB mediated GBM cell survival. We report that only PIK3CB, in its family of other PI3K genes, is a biomarker for GBM recurrence and is selectively important for GBM cell survival. Another screen identified the long non-coding RNA, Linc00467, as a gene that regulates autophagy in CML. Autophagy is a dynamic survival process used by all cells, benign and cancerous, where cellular components are broken down and re-assimilated to sustain survival. Work contained in this dissertation set out to characterize the role that Linc00467 serves in regulating autophagy in a myriad of cancers. Collectively our data have showed Linc00467 to actively repress levels of autophagy in cancer cells. Further, our data revealed an important role for Linc00467 in regulating the stability of the autophagy regulating protein serine-threonine kinase 11 (STK11). Because of the unique role that Linc00467 serves in regulating autophagy we renamed it as, autophagy regulating long intergenic noncoding RNA or ARLINC. Taken together the work in this dissertation unveils the inner-workings of two important cancer cell survival pathways and shows their potential for development into therapeutic targets to treat cancer.
Ph. D.

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Books on the topic "Inhibit"

1

Coleman, Michael C. The major factors that inhibit better policing. Dublin: University College Dublin, 1989.

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Norgrove, Heather. Professional tribalism: Does it inhibit collaborative working? : differing stakeholder perceptions which inhibit collaborative working across organizational boundaries. [s.l.]: typescript, 1999.

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Quantifying competitive ability of perennial grasses to inhibit scotch broom. Portland, OR: U.S. Department of Agriculture, Pacific Northwest Research Station, 2011.

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Kibble, Karen-Jane. Growing pains: An analysis of the factors that inhibit growth in micro enterprises. Oxford: Oxford Brookes University, 2000.

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Abraham, Katharine G. Does employment protection inhibit labor market flexibility?: Lessons from Germany, France and Belgium. Cambridge, MA: National Bureau of Economic Research, 1993.

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Peter, Chalk, ed. Terrorism & development: Using social and economic development to inhibit a resurgence of terrorism. Santa Monica, CA: Rand, 2003.

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Hollyoak, Ken. Does the inconsistent application of visibility standards inhibit the development of brownfield sites. Oxford: Oxford Brookes University, 2000.

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Clements, Harold William. An analysis of stress absorbing membrane interlayers used to inhibit tensile fatigue reflective cracking. [s.l: The Author], 2001.

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Cowey, Lisa. University spinout companies: An investigation of the factors perceived to inhibit sucessful technology transfer. Oxford: Oxford Brookes University, 2004.

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Huisken, Ronald. Globalising the INF treaty: The best way to inhibit the proliferation of long-range missiles? Canberra: Strategic and Defence Studies Centre, The Australian National University, 2008.

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Book chapters on the topic "Inhibit"

1

Weik, Martin H. "inhibit." In Computer Science and Communications Dictionary, 782. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/1-4020-0613-6_8995.

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Weik, Martin H. "write inhibit." In Computer Science and Communications Dictionary, 1935. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/1-4020-0613-6_21255.

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Torino, Francesco, Roberta Sarmiento, Raffaelle Longo, and Giampietro Gasparini. "Therapeutic Agents That Inhibit Angiogenesis." In The Molecular Basis of Human Cancer, 757–69. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-59745-458-2_39.

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Buddeberg, C. "Does Marriage Inhibit Sexual Desire?" In Sexology, 172–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73794-7_25.

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Bhattacharjee, Mrinal K. "Antibiotics That Inhibit Protein Synthesis." In Chemistry of Antibiotics and Related Drugs, 129–51. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-40746-3_6.

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Pauletto, P., and G. Scannapieco. "Do calcium antagonists inhibit atherogenesis?" In Atherosclerosis and Cardiovascular Disease, 347–53. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-0731-7_45.

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Bhattacharjee, Mrinal K. "Antibiotics That Inhibit Protein Synthesis." In Chemistry of Antibiotics and Related Drugs, 149–77. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-07582-7_6.

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Deng, Jun, Yang Xiao, Qing-Wei Li, and Hao Zhang. "Technologies to Inhibit Coal Fires." In Bow Ties in Process Safety and Environmental Management, 45–68. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9781003140382-4.

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Fairholm, Gilbert W. "Work Factors That Inhibit Doing Leadership." In Management for Professionals, 29–36. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17154-8_3.

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Bhattacharjee, Mrinal K. "Antibiotics That Inhibit Cell Wall Synthesis." In Chemistry of Antibiotics and Related Drugs, 49–94. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-40746-3_3.

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Conference papers on the topic "Inhibit"

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Akbar, Huzoor, David Wallace, and Khursheed Anwer. "HUMAN PLATELET ACTIVATION BY BACTERIAL PHOSPHOLIPASE C: MECHANISM OF INHIBITION BY FLURAZEPAM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643442.

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We have shown earlier that flurazepam inhibits human platelet aggregation and serotonin secretion induced by bacterial phospholipase C (BPLC, Thromb. Res. 38, 361-374, 1985). This study was conducted to examine the mechanism(s) of inhibitory action of flurazepam. Only 15 uM and 11 uM flurazepam were required to inhibit platelet aggregation and serotonin secretion by 50%. In a platelet free system, BPLC hydrolyzed 14C-phosphatidylcholine (14C-PC> in a time- and concentration-dependent manner in the presence of calcium ions. Flurazepam had no effect on BPLC-induced hydrolysis of 14C-PC. Incubation of 14C-arachidonic acid labelled platelets with BPLC produced diacylglycerol(DAG) in a time- and concentration-dependent manner. Flurazepam did not inhibit DAG production by BPLC. However, prostaglandin E1 and paranitrophenolphosphorylcholine inhibited DAG production by 20% and 75% respectively. Platelet cytosolic fraction,containing phosphatidylinositol-specific PLC (PI-PLC), hydrolyzed 3H -phosphatidylinositol (3H-PI) in a concentration-dependent manner. Flurazepam did not inhibit hydrolysis:of 3H-PI by PI-PLC. BPLC caused phosphorylation of 47,000 Dalton protein (P47) in 32P-labelled platelets. Flurazepam did not inhibit phosphorylation of P47 in the first five minutes of incubation. However, flurazapam completely blocked phosphorylation of P47 by seven minutes. In Other experiments, flurazepam inhibited platelet aggregation induced by ionomycion, a calcium ionophore, in a concentration-dependent manner. These data lead us to suggest that flurazapam does not inhibit BPLC-ihduced platelet activation by inhibiting the action of BPLC or PI-PLC on platelet phospholipids or DAG production. However, the ability of flurazepam to inhibit ionomycin-induced platelet aggregation indicates that it may be blocking BPLC-induced platelet aggreagtion by interfering with the influx, of calcium ions into platelets. (Supported in part by the American Osteopathic Association, The Baker Award from Ohio University and the OUCOM).

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Kowalska, M. A., A. K. Rao, and J. Disa. "HIGH CONCENTRATIONS OF EXOGENOUS ARACHIDONATE INHIBIT CALCIUM MOBILIZATION IN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644675.

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Exogenous arachidonic acid (AA) induces platelet aggregation and secretion which are inhibited at higher AA concentrations.To define the mechanisms for platelet inhibition at high AA,we studied the effect of itS2$odium salt on cytoplasmic ionized calcium concentration [Ca ]i, a key modulator of several platelet responses. In platelets suspended in Hepes buffer containing no albumin, peak aggregation and secretion occurred at 2-5 pM AA with partial inhibition above 10-15 pM AA and complete inhj^ition around 25-50 pM AA. In platelets ^aded with quin2, [Ca+2 ]i rose, in presence of 1 mM external Ca , from basal levels of 70-80 nM to peak of 300-500 nM at 2-5 μM AA; this was followed by inhibition to basal levels at 25-50 μM AA. At these AA concentrations there was no cell lysis. Thromboxane B. production, measured using a radioimmunoassay, was not inhibited even at 25 pM AA. Elevated celjlar levels of cAMP inhibit platelet responses including Ca2+ signals and were therefore measured using a radioimmunoassay. Platelet cAMP levels rose, in the presence of theophylline (7mM), from basal levels of 3.4 pmol/102+ plat to 5.5 at 5 μM AA and to 6.8 pmol/108 plat at 50 pM AA; Ca signals, aggregation, and secretion were inhibited with doubling of cAMP levels. On incubation of platelets with adenylate cyclase inhibitor, 2'5' dideoxgdenosine (DDA, 200 μM, 2 min) there was enhancement of peak [Ca +2]and aggregation noted with 15 pM AA; at 25 μM AA peak [Ca2+ ]i rose from 126 nM to 205 nM and aggregation was restored. Incubation with SQ 22,536 (500 μM, 5min), another adenylate cyclase inhibitor, also attenuated the inhibition by high AA levels. Treatment of platelets with aspirin or_BW 755C, a combined lipooxygenase/cyclooxygenase inhibitor, did not pryent the inhibition by high AA levels of aggregation and Ca responses induced by thromboxane analog, U46619 In conclusion, high AA concentrations inhibit cytoplasmic Ca+2 mobilization in platelets which is related to elevation of platelet cAMP through stimulation of adenylate cyclase. We propose that high AA levels inhibit aggravation and secretion by modulating cytoplasmic levels of Ca2+ and cAMP, two major messenger molecules in platelets.

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3

Saeki, T., K. HARADA, T. Youshimura, Y. Nakamura, T. Fujimori, K. E. Katayama, Y. Yamagish, I. Yamastu, and I. Ikeda. "MODE OF ACTION OF A NOVEL ANTI-PLATELET AGENT (E-5510)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643427.

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A novel anti-platelet agent, 4-cyano-5,5-bis(4-methoxy-phenyl)-4-pentenoic acid(E-5510), has been shown to inhibit platelet aggregation and secretion induced by thrombin as well as by other inducers such as ADP, collagen and PAF. Although E-5510 can act as a cyclooxygenase inhibitor,inhibition of cyclooxygenase may not be the primary mode of action since this compound effectively inhibits thrombin-induced platelet activation. In this paper, effects^of E-5510 on arachidonic acid (AA) metabolism, intracellular Ca++ and cAMP in human platelets are examined.(1) Effect on AA metabolism. Platelets prelabeled with [14 C]-AA were stimulated with thrombin. E-5510 inhibited not only thromboxane A2 and HHT generation but also 12-HETE generation in a dose-dependent fashion. The total AA released was also reduced by E-5510. An almost 50% reduction was obtained by 10 uM of this compound. On the other hand, a cyclooxygenase inhibitor such as U-53059 increased 12-HETE generation in a dose-dependent fashion. In addition to the inhibition of AA metabolism, E-5510 exerted inhibitory effects on phosphatidic acidgeneration, which suggests the possible inhibition of phospholipase C activity by this compound.(2) Effect on intracellular Ca++ and protein phosphorylation. Intracellular Ca++ mobilization was examined using Fura-2 loaded human platelet suspension. The increase in intracellular Ca induced by thrombin was inhibited by E-5510 and the increase in phosphorylation of 40 K protein was also suppressed by this compound after the stimulation of human platelets by thrombin.(3) Effect on cAMP. Platelets were incubated with 10-100 uM of E-5510 and the cAMP content in human platelets was measured. E-5510 increased the cAMP content in a dose-dependent fashion. In platelet homogenate, E-5510 inhibited phosphodiesterase activity with an IC50 of 10 uM.These results suggest that E-5510 may inhibit platelet aggregation and secretion through the multiple modes of action, such as inhibition of phospholipase C, phosphodiesterase and cyclooxygenase, in the process of platelet activation.

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4

Tans, G., T. Janssen-Claessen, J. Rosing, and J. H. Griffin. "APPLICATION OF SPECIFIC SERINE PROTEASE INHIBITORS IN ASSAYS FOR ACTIVATED CONTACT FACTORS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643301.

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We developed amidolytic assays to determine human Factor Xlla, Factor XIa and plasma kallikrein in mixtures containing variable amounts of each enzyme. The commercially available chromogenic substrates pro-phe-arg-pNA (S2302 or chromozym PK), glu-pro-arg-pNA (S2366), ile-glu-(piperidyl)-gly-arg-pNA (S2337), and ile-glu-gly-arg-pNA (S2222) were tested for their suitability as substrates in these assays. 8-Factor Xlla, Factor XIa and plasma kallikrein each exhibit considerable activity towards a number of these substrates. This precludes direct quantitation of the individual enzymes when large amounts of other activated contact factors are present. Several serine protease inhibitors were tested on their ability to selectively inhibit those contact factors that may interfere with the factor tested for. Soybean trypsin inhibitor efficiently inhibits kallikrein, inhibits Factor XIa at moderate concentrations, but did not affect the amidolytic activity of Factor Xlla. Therefore, this inhibitor can be used to abolish a kallikrein and Factor XIa contribution in a Factor Xlla assay. We also report the rate constants of inhibition of contact activation factors by three different chloromethylketones. D-phe-pro-arg-CH 2 Cl was moderately active against contact factors (k - 2271 M-ls-1 at pH 8.3) but showed no differences in specif ity. D-phe-phe-arg-CH2 Cl was a very efficient inhibitor of kallikrein (k = 118,000 M-ls-1 at pH 8.3) whereas it slowly inhibited Factor Xlla (k = 1389 M-ls-1) and Factor XIa (k = 110 M-ls-1). Also dansyl-glu-gly-arg-CH2Cl was more reactive towards kallikrein (k 15,662 M-ls-1) than towards Factor Xlla (k = 462 M-ls-1) and Factor XIa (k = 63 M-ls-1). Since phe-phe-arg-CH2Cl is highly specific for kallikrein it can be used in a Factor XIa assay to selectively inhibit kallikrein. Based on the catalytic efficiencies of chromogenic substrate conversion and the inhibition characteristics of serine protease inhibitors and chloromethyl ketones we were able to develop quantitative assays for Factor Xlla, Factor XIa and kallikrein in mixtures of contact activation factors.

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5

de Groot, Philip G., Jan A. van Mourik, and Jan J. Sixma. "PRIMARY BINDING SITE OF VON WILLEBRAND FACTOR IN THE SUBENDOTHELIUM WHICH MEDIATES PLATELET ADHESION IS NOT COLLAGEN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643587.

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We have studies the binding of von Willebrand factor (vWF) to extracellular matrices of endothelial cells and smooth muscle cells and to the vessel wall of human umbilical arteries in relation to its function in supporting platelet adhesion at high shear rates. CLB-RAg 38, a monoclonal antibody directed against vWF inhibits the binding of 125I-vWF extracellular matrices completely. The binding of 125I-vWF to subendothelium is not inhibited, because there are many different binding sites. CLB-RAg 38 inhibits platelet adhesion to extracellular matrices and subendothelium, in sofar as it is dependent on plasma vWF. CLB-RAg 38 has no effect on adhesion depending on vWF already bound to the matrix or subendothelium. CLB-RAg 38 does not inhibit binding of vWF to collagen type I and type III. Another monoclonal antibody against vWF, CLB-RAg 201, completely inhibits binding of vWF to collagen type I and type III. CLB-RAg 201 does not inhibit binding of 125I-vWF ot the extracellular matrices. CLB-RAg 201 partly inhibits platelet adhesion but this inhibition is also present when the adhesion depends on vWF already present in matrix or subendothelium, indicating that CLB-RAg 201 also inhibits the adhesion of platelets directly, this in contrast to CLB-RAg 38. The epitopes for CLB-RAg 201 and 38 were found on different tryptic fragments of vWF. These data indicate that vWF binds to subendothelium and to matrices of cultured cells by mechanism that is different from binding to collagen.

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6

Beretz, A., F. Lanza, A. Stierlé, and J.-P. Cazenave. "CYCLIC NUCLEOTIDE PHOSPHODIESTERASE INHIBITORS PREVENT AGGREGATION AND SECRETION OF HUMAN PLATELETS BY RAISING CYCLIC AMP AND REDUCING CYTOPLASMIC FREE CALCIUM MOBILIZATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643586.

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Drugs that raise platelet cyclic AMP (cAMP) are potent inhibitors of platelet activation. We have studied the effects of 5 inhibitors of cyclic nucleotide phosphodiesterase (PDE) of different chemical structures (quercetin, Ro 15-2041, HL-725, cilostamide and MY-5445), which are all potent inhibitors of platelet function. The concentrations that inhibit by 50 % crude cAMP-PDE activity (IC50) from human platelets are: 0.06 μM(HL-725), 0.15 μM(Ro 15-2041 ), 0.23 μM(cilostamide), 6.9 μM(MY-5445) and 44.4 μM(quercetin). We measured on the same preparation of washed human platelets loaded with quin2, the aggregation and the increase in intracellular Ca2+ ([Ca2+]i) induced by 5 μM ADP alone or in the presence of PDE inhibitors.PGE1 (2 nM) potentiates significantly (1.6 to 3.3 fold) the inhibitory effects of PDE inhibitors on [Ca2+]i rises and platelet aggregation. Adrenaline, an inhibitor of adenylate cylase, prevents the effect of PDE inhibitors on ADP-induced [Ca2+]i rise and platelet aggregation. These results suggest that these compounds inhibit [Ca2+]i mobilization and subsequent ADP-induced aggregation through a rise in cAMP, because both effects are potentiated by PGE1 and inhibited by adrenaline. The inhibitor concentrations which potentiate the action of PGE1, on [ Ca2+]i levels also potentiate the rise in platelet cAMP induced by PGE-<. These results suggest that PDE inhibitors inhibit platelet aggregation Ly raising cAMP levels and subsequently inhibiting [Ca2+]i mobilization.

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7

Steinert, Bruce W., James M. Onoda, Bonnie F. Sloane, John D. Taylor, and Kenneth V. Honn. "CYCLOOXYGENASE AND LIPOXYGENASE PRODUCTS SYNERGISTICALLY MODULATE TUMOR CELL INDUCED PLATELET AGGREGATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644668.

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There has been considerable controversy surrounding the ability of inhibitors of arachidonic acid metabolism to concomitantly inhibit tumor cell induced platelet aggregation (TCIPA). Reconciliation of this controversy has been difficult due to the wide variability of experimental conditions (e.g., inhibitor concentration, strength of the inducing agonist).In the present study, we examined the effects of several cyclooxygenaseand lipoxygenase inhibitors on the induction of platelet aggregation by Walker 256 carcinosarcoma (W256) cells. We have previously demonstrated that aggregation of platelet rich plasma (PRP), induced by W256 cells, was initiated via a thrombin dependent mechanism. Platelet aggregation was induced by the addition of W256 cells (75,000-J500,000 cells/cuvette) to rat PRP preincubated with inhibitor(s) or diluent. The strength of the inducing stimulus affected both the degree of aggregation and the production of thromboxane A2 (TXA2) in a dose dependent manner. A weak stimulus (low concentration of W256 cells) produced only a low level of aggregation and low TXA2 production, whereas aggregation induced by a strong stimulus (high concentration of W256 cells) resulted in significant aggregation and increased TXA2 production. Preincubation (5 min., 37°C) of rat PRP with cyclooxygenase inhibitors (e.g., aspirin, indomethacin, ibuprofen) resulted in complete inhibition of platelet aggregation at low agonist concentration (75,000 W256 cells), whereas when a high agonist concentration (500,000 W256 cells) was used to induce aggregation, the inhibitors failed to inhibit TCIPA. The addition of fewer than 50,000W256 cells failed to induce any measurable platelet aggregation in the presence or absence of inhibitors. TCIPA was not affected by lipoxygenaseinhibitors (e.g.,quercetin) alone regardless of agonist concentration. Both cyclooxygenase and lipoxygenase inhibitors, however, were required to significantly inhibit TCIPA induced by high agonist concentration. Compounds which inhibited both the cycloogygenase and lipoxygenase pathways (e.g.,hydroquinone, BW755c) inhibited TCIPA at all agonist concentrations. Nafazatrom failed to inhibit TCIPA consistant with a lack of effect on platelet cyclooxygenase and lipoxygenase. Therefore, we conclude cyclooxygenase (e.g., TXA2) and lipoxygenase (e.g., 12-HETE) products of platelet arachidonic acid metabolism and the strength of the inducingagonist are important criteria in TCIPA. This study may help to clarify the current controversy regarding the inhibition of TCIPA by inhibitors of arachidonic acid metabolism.

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8

Cheung, A., and K. F. Hebert. "A TUMOR SERINE PROTEASE INHIBITOR WHICH MAY FUNCTION AS A TISSUE PLASMINOGEN ACTIVATOR INHIBITOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644448.

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A protease inhibitor has been isolated from human colorectal adenocarcinomas by extraction with a low ionic strength-buffer and a combination of concanavalin A-Sepharose, Sephadex G-200, DEAE cellulose and chromatofocusing steps. The preparation appeared to be homogeneous upon gel exclusion chromatography and SDS polyacrylamide gel electrophoresis. It had an apparent Mr of ~66,000 and its isoelectric point was 4.6-4.7. The inhibitor was able to bind and inhibit urokinase, plasmin, trypsin, tissue plasminogen activator and thrombin. The bindings appeared to be stoichiometric and relative fast and diisopropylfluorophoshphate interfered with the bindings. However tPA was the only enzyme that was inhibited in a linear concentration-dependent manner.The inhibitor crossreacted with antiserum against al-antitrypsin but not with antisera against β2-macroglobulin, α2-antiplasmin, antithrombin III, or Cl-inhibitor. Whereas αl-antitrypsin completely inhibited the amidolytic activity of elastase, the tumor inhibitor had no effect on elastase under the same conditions.

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9

Rodzynek, J. J., C. Van Rissenghem, P. Leautaud, and A. Delcourt. "STUDY OF THE PROCOAGULANT ACTIVITY OF ASCITIC FLUID." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643060.

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The aims of the study were to determine the nature of the procoagulant activity present in the ascitic fluid and the means to inhibit the thrombotic complications appearing after peritoneovenous shunting. In a prospective study, 10 ascitic fluids (5 exsudates, 5 transsudates) were studied. The procoagulant activity was defined as the capacity of ascitic fluid to shorten the recalcification time of a control plasma.Our results showed :1. All the ascitic fluids exhibited a procoagulant activity.2. The procoagulant activity of the cellular fraction was related to the presence of platelet factor 3 (PF3) and polymorphonuclear elastase and may be inhibited by the combination of inhibitors of PF3 (phospholipase A inhibitor calbio-chem) and elastase antibody.3. The procoagulant activity of the free cellular fraction was related to the presence of thrombin, factor Xa, PF3 and tissular thromboplastin, and may be inhibited by a combination of Antithrombin III, phospholipase A and Diisopropyl-fluorophosphate.Conclusion :1. The important procoagulant activity of ascitic fluid is present in both cellular and acellular fractions and is related to the presence of different coagulation activators (PF3, elastase, Xa, thrombin, tissular thromboplastin).2. The administration of a combination of AT III and phospholipase A in the ascitic fluid before the contact with the whole blood allows to inhibit the procoagulant activity of ascitic fluid and could prevent the thrombotic complications appearing after peritoneovenous shunt.

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10

Sheehan, S. J., A. B. Latif, S. R. Bibby, R. C. Kester, and S. M. Rajah. "THE RECOVERY OF ENDOTHELIAL CELL AND PLATELET PROSTAGLANDIN SYNTHESES AFTER ADMINISTRATION OF ASPIRIN AND INDOBUFEN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643389.

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Suppression of endothelial prostacyclin (PGI2) by cyclooxygenase inhibition may contribute to the formation of neointimal hyperplasia. While aspirin (ASA) inhibits platelet function for several days, it returns to normal within 24 hours after indobufen (IDB), a reversible cyclooxygenase inhibitor, suggesting that prostacyclin may recover at an even faster rate. In a randomised, controlled study, recovery of platelet and endothelial cell prostaglandin synthesis was compared in 49 New Zealand white rabbits following indobufen (3.5 mg/kg) or aspirin (5 mg/kg). Prostacyclin in arterial incubates and platelet thromboxane A2 (TXA2) production in serum were measured by radioimmunoassay of their meta-bolities, 6Keto PGF1 and thromboxane B2. Platelet prostaglandin synthesis was also monitored by changes in serum malondiealdehyde (MDA).At one hour, both ASA and IDB significantly inhibited PGI2 (p<0.005). TXA2 (p<0.005), and MDA (p<0.02). After IDB, TXA2 and MDA levels returned to normal by 24 hours while inhibition continued in the ASA group (p<0.01). PGI2 synthesis following IDB recovered at 8 hours against 24 hours in the ASA group. We conclude that while both drugs inhibit platelet and endothelial prostaglandins, the earlier recovery of prostacyclin synthesis following indobufen may allow the endothelium to resume its physiological function.

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Reports on the topic "Inhibit"

1

Sato, J. D. Receptor Monoclonal Antibodies that Inhibit Tumor Angiogenesis. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada398146.

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2

Eugene J Fine, Eugene J. Fine. Can low carbohydrate ketogenic diets inhibit cancers? Experiment, January 2015. http://dx.doi.org/10.18258/4496.

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3

Sato, J. D. Receptor Monoclonal Antibodies that Inhibit Tumor Angiogenesis. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada383129.

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4

Eugene J Fine, Eugene J. Fine. Part 2: Can low carbohydrate ketogenic diets inhibit cancers? Experiment, July 2016. http://dx.doi.org/10.18258/7344.

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5

Harrington, Timothy. Quantifying competitive ability of perennial grasses to inhibit Scotch broom. Portland, OR: U.S. Department of Agriculture, Forest Service, Pacific Northwest Research Station, 2011. http://dx.doi.org/10.2737/pnw-rp-587.

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6

Apidianakis, Georgios. Identification of Human Intestinal Bacteria that Promote or Inhibit Inflammation. Fort Belvoir, VA: Defense Technical Information Center, November 2012. http://dx.doi.org/10.21236/ada607490.

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7

Gilroy, Jill M. Overexpression of IL-4 Signaling Pathway to Inhibit Breast Tumor Growth. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada403390.

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8

Douglas, Joanne T. A Novel Strategy to Inhibit Osteolytic Bone Metastases of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2002. http://dx.doi.org/10.21236/ada405259.

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9

Gooch, Jennifer L. Overexpression of IL-4 Signaling Pathway to Inhibit Breast Tumor Growth. Fort Belvoir, VA: Defense Technical Information Center, July 1999. http://dx.doi.org/10.21236/ada390684.

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10

Gooch, Jennifer. Overexpression of IL-4 Signaling Pathway to Inhibit Breast Tumor Growth. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada384372.

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