Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)Liability, Legal: Accountability and responsibility to another, enforceable by civil or criminal sanctions.Malpractice: Failure of a professional person, a physician or lawyer, to render proper services through reprehensible ignorance or negligence or through criminal intent, especially when injury or loss follows. (Random House Unabridged Dictionary, 2d ed)MedlinePlus: NATIONAL LIBRARY OF MEDICINE service for health professionals and consumers. It links extensive information from the National Institutes of Health and other reviewed sources of information on specific diseases and conditions.Judicial Role: The kind of action or activity proper to the judiciary, particularly its responsibility for decision making.Harvey murine sarcoma virus: A replication-defective mouse sarcoma virus (SARCOMA VIRUSES, MURINE) first described by J.J. Harvey in 1964.Jurisprudence: The science or philosophy of law. Also, the application of the principles of law and justice to health and medicine.Glycosylation: The chemical or biochemical addition of carbohydrate or glycosyl groups to other chemicals, especially peptides or proteins. Glycosyl transferases are used in this biochemical reaction.Cyclooxygenase 2: An inducibly-expressed subtype of prostaglandin-endoperoxide synthase. It plays an important role in many cellular processes and INFLAMMATION. It is the target of COX2 INHIBITORS.Oligosaccharides: Carbohydrates consisting of between two (DISACCHARIDES) and ten MONOSACCHARIDES connected by either an alpha- or beta-glycosidic link. They are found throughout nature in both the free and bound form.Prostaglandin-Endoperoxide Synthases: Enzyme complexes that catalyze the formation of PROSTAGLANDINS from the appropriate unsaturated FATTY ACIDS, molecular OXYGEN, and a reduced acceptor.Prostaglandins: A group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway. They are extremely potent mediators of a diverse group of physiological processes.Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.GermanyArthropod Proteins: Proteins synthesized by organisms belonging to the phylum ARTHROPODA. Included in this heading are proteins from the subdivisions ARACHNIDA; CRUSTACEA; and HORSESHOE CRABS. Note that a separate heading for INSECT PROTEINS is listed under this heading.Antigens, Dermatophagoides: Antigens from the house dust mites (DERMATOPHAGOIDES), mainly D. farinae and D. pteronyssinus. They are proteins, found in mite feces or mite extracts, that can cause ASTHMA and other allergic diseases such as perennial rhinitis (RHINITIS, ALLERGIC, PERENNIAL) and atopic dermatitis (DERMATITIS, ATOPIC). More than 11 groups of Dermatophagoides ALLERGENS have been defined. Group I allergens, such as Der f I and Der p I from the above two species, are among the strongest mite immunogens in humans.1,4-alpha-Glucan Branching Enzyme: In glycogen or amylopectin synthesis, the enzyme that catalyzes the transfer of a segment of a 1,4-alpha-glucan chain to a primary hydroxy group in a similar glucan chain. EC 2.4.1.18.War: Hostile conflict between organized groups of people.Halobacteriales: An order of extremely halophilic archaea, in the kingdom EURYARCHAEOTA. They occur ubiquitously in nature where the salt concentration is high, and are chemoorganotrophic, using amino acids or carbohydrates as a carbon source.Carcinogens: Substances that increase the risk of NEOPLASMS in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included.9,10-Dimethyl-1,2-benzanthracene: 7,12-Dimethylbenzanthracene. Polycyclic aromatic hydrocarbon found in tobacco smoke that is a potent carcinogen.Papilloma: A circumscribed benign epithelial tumor projecting from the surrounding surface; more precisely, a benign epithelial neoplasm consisting of villous or arborescent outgrowths of fibrovascular stroma covered by neoplastic cells. (Stedman, 25th ed)Skin Neoplasms: Tumors or cancer of the SKIN.Skin: The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.Keratinocytes: Epidermal cells which synthesize keratin and undergo characteristic changes as they move upward from the basal layers of the epidermis to the cornified (horny) layer of the skin. Successive stages of differentiation of the keratinocytes forming the epidermal layers are basal cell, spinous or prickle cell, and the granular cell.Mice, Inbred SENCAR: Mice selectively bred for hypersusceptibility to two-stage chemical skin carcinogenesis. They are also hypersusceptible to UV radiation tumorigenesis with single high-dose, but not chronic low-dose, exposures. SENCAR (SENsitive to CARcinogenesis) mice are used in research as an animal model for tumor production.Sheep: Any of the ruminant mammals with curved horns in the genus Ovis, family Bovidae. They possess lachrymal grooves and interdigital glands, which are absent in GOATS.Scrapie: A fatal disease of the nervous system in sheep and goats, characterized by pruritus, debility, and locomotor incoordination. It is caused by proteinaceous infectious particles called PRIONS.PrPSc Proteins: Abnormal isoform of prion proteins (PRIONS) resulting from a posttranslational modification of the cellular prion protein (PRPC PROTEINS). PrPSc are disease-specific proteins seen in certain human and animal neurodegenerative diseases (PRION DISEASES).Cyclooxygenase 1: A constitutively-expressed subtype of prostaglandin-endoperoxide synthase. It plays an important role in many cellular processes.Cyclooxygenase Inhibitors: Compounds or agents that combine with cyclooxygenase (PROSTAGLANDIN-ENDOPEROXIDE SYNTHASES) and thereby prevent its substrate-enzyme combination with arachidonic acid and the formation of eicosanoids, prostaglandins, and thromboxanes.Cyclooxygenase 2 Inhibitors: A subclass of cyclooxygenase inhibitors with specificity for CYCLOOXYGENASE-2.Anti-Inflammatory Agents, Non-Steroidal: Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions.They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects.Pyrazoles: Azoles of two nitrogens at the 1,2 positions, next to each other, in contrast with IMIDAZOLES in which they are at the 1,3 positions.Sulfonamides: A group of compounds that contain the structure SO2NH2.Lactones: Cyclic esters of hydroxy carboxylic acids, containing a 1-oxacycloalkan-2-one structure. Large cyclic lactones of over a dozen atoms are MACROLIDES.Anti-Inflammatory Agents: Substances that reduce or suppress INFLAMMATION.Fibrinolytic Agents: Fibrinolysin or agents that convert plasminogen to FIBRINOLYSIN.Naproxen: An anti-inflammatory agent with analgesic and antipyretic properties. Both the acid and its sodium salt are used in the treatment of rheumatoid arthritis and other rheumatic or musculoskeletal disorders, dysmenorrhea, and acute gout.Spinal Cord Injuries: Penetrating and non-penetrating injuries to the spinal cord resulting from traumatic external forces (e.g., WOUNDS, GUNSHOT; WHIPLASH INJURIES; etc.).PubMed: A bibliographic database that includes MEDLINE as its primary subset. It is produced by the National Center for Biotechnology Information (NCBI), part of the NATIONAL LIBRARY OF MEDICINE. PubMed, which is searchable through NLM's Web site, also includes access to additional citations to selected life sciences journals not in MEDLINE, and links to other resources such as the full-text of articles at participating publishers' Web sites, NCBI's molecular biology databases, and PubMed Central.Spinal Cord: A cylindrical column of tissue that lies within the vertebral canal. It is composed of WHITE MATTER and GRAY MATTER.Quadriplegia: Severe or complete loss of motor function in all four limbs which may result from BRAIN DISEASES; SPINAL CORD DISEASES; PERIPHERAL NERVOUS SYSTEM DISEASES; NEUROMUSCULAR DISEASES; or rarely MUSCULAR DISEASES. The locked-in syndrome is characterized by quadriplegia in combination with cranial muscle paralysis. Consciousness is spared and the only retained voluntary motor activity may be limited eye movements. This condition is usually caused by a lesion in the upper BRAIN STEM which injures the descending cortico-spinal and cortico-bulbar tracts.Periodicals as Topic: A publication issued at stated, more or less regular, intervals.Bones of Lower Extremity: The bones of the upper and lower LEG. They include the PELVIC BONES.Paraplegia: Severe or complete loss of motor function in the lower extremities and lower portions of the trunk. This condition is most often associated with SPINAL CORD DISEASES, although BRAIN DISEASES; PERIPHERAL NERVOUS SYSTEM DISEASES; NEUROMUSCULAR DISEASES; and MUSCULAR DISEASES may also cause bilateral leg weakness.Thromboxanes: Physiologically active compounds found in many organs of the body. They are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase.Arachidonic AcidsTobacco Smoke Pollution: Contamination of the air by tobacco smoke.SmokeTobacco: A plant genus of the family SOLANACEAE. Members contain NICOTINE and other biologically active chemicals; its dried leaves are used for SMOKING.Smoking: Inhaling and exhaling the smoke of burning TOBACCO.Tobacco Industry: The aggregate business enterprise of agriculture, manufacture, and distribution related to tobacco and tobacco-derived products.Cotinine: The N-glucuronide conjugate of cotinine is a major urinary metabolite of NICOTINE. It thus serves as a biomarker of exposure to tobacco SMOKING. It has CNS stimulating properties.Tobacco, Smokeless: Powdered or cut pieces of leaves of NICOTIANA TABACUM which are inhaled through the nose, chewed, or stored in cheek pouches. It includes any product of tobacco that is not smoked.

Transformation of intestinal epithelial cells by chronic TGF-beta1 treatment results in downregulation of the type II TGF-beta receptor and induction of cyclooxygenase-2. (1/6133)

The precise role of TGF-beta in colorectal carcinogenesis is not clear. The purpose of this study was to determine the phenotypic alterations caused by chronic exposure to TGF-beta in non-transformed intestinal epithelial (RIE-1) cells. Growth of RIE-1 cells was inhibited by >75% following TGF-beta1 treatment for 7 days, after which the cells resumed a normal growth despite the presence of TGF-beta1. These 'TGF-beta-resistant' cells (RIE-Tr) were continuously exposed to TGF-beta for >50 days. Unlike the parental RIE cells, RIE-Tr cells lost contact inhibition, formed foci in culture, grew in soft agarose. RIE-Tr cells demonstrated TGF-beta-dependent invasive potential in an in vitro assay and were resistant to Matrigel and Na-butyrate-induced apoptosis. The RIE-Tr cells were also tumorigenic in nude mice. The transformed phenotype of RIE-Tr cells was associated with a 95% decrease in the level of the type II TGF-beta receptor (TbetaRII) protein, a 40-fold increase in cyclooxygenase-2 (COX-2) protein, and 5.9-fold increase in the production of prostacyclin. Most RIE-Tr subclones that expressed low levels of TbetaRII and high levels of COX-2 were tumorigenic. Those subclones that express abundant TbetaRII and low levels of COX-2 were not tumorigenic in nude mice. A selective COX-2 inhibitor inhibited RIE-Tr cell growth in culture and tumor growth in nude mice. The reduced expression of TbetaRII, increased expression of COX-2, and the ability to form colonies in Matrigel were all reversible upon withdrawal of exogenous TGF-beta1 for the RIE-Tr cells.  (+info)

Down-regulation of oxytocin-induced cyclooxygenase-2 and prostaglandin F synthase expression by interferon-tau in bovine endometrial cells. (2/6133)

Oxytocin (OT) is responsible for the episodic release of luteolytic prostaglandin (PG) F2alpha from the uterus in ruminants. The attenuation of OT-stimulated uterine PGF2alpha secretion by interferon-tau (IFN-tau) is essential for prevention of luteolysis during pregnancy in cows. To better understand the mechanisms involved, the effect of recombinant bovine IFN-tau (rbIFN-tau) on OT-induced PG production and cyclooxygenase-2 (COX-2) and PGF synthase (PGFS) expression in cultured endometrial epithelial cells was investigated. Cells were obtained from cows at Days 1-3 of the estrous cycle and cultured to confluence in RPMI medium supplemented with 5% steroid-free fetal calf serum. The cells were then incubated in the presence or absence of either 100 ng/ml OT or OT+100 ng/ml rbIFN-tau for 3, 6, 12, and 24 h. OT significantly increased PGF2alpha and PGE2 secretion at all time points (p < 0.01), while rbIFN-tau inhibited the OT-induced PG production and reduced OT receptor binding in a time-dependent manner. OT increased the steady-state level of COX-2 mRNA, measured by Northern blot, which was maximal at 3 h (9-fold increase) and then decreased with time (p < 0.01). OT also caused an increase in COX-2 protein, which peaked at 12 h (11-fold increase), as measured by Western blot. Addition of rbIFN-tau suppressed the induction of COX-2 mRNA (89%, p < 0.01) and COX-2 protein (50%, p < 0.01) by OT. OT also increased PGFS mRNA, and this stimulation was attenuated by rbIFN-tau (p < 0.01). To ensure that the decrease in COX-2 was not solely due to down-regulation of the OT receptor, cells were stimulated with a phorbol ester (phorbol 12-myristate 13-acetate; PMA) in the presence and absence of rbIFN-tau. The results showed that rbIFN-tau also decreased PMA-stimulated PG production and COX-2 protein. It can be concluded that rbIFN-tau inhibition of OT-stimulated PG production is due to down-regulation of OT receptor, COX-2, and PGFS.  (+info)

Mechanisms of prostaglandin E2 release by intact cells expressing cyclooxygenase-2: evidence for a 'two-component' model. (3/6133)

Prostaglandin (PG) release in cells expressing constitutive cyclooxygenase-1 is known to be regulated by liberation of arachidonic acid by phospholipase A2 followed by metabolism by cyclooxygenase. However, the relative contribution of phospholipase A2 to the release of PGs in cells expressing cyclooxygenase-2 is not clear. We addressed this question by using radioimmunoassay to measure PGE2 release by human cells (A549) induced to express cyclooxygenase-2 (measured by Western blot analysis) by interleukin-1beta. Cells were either unstimulated or stimulated with agents known to activate phospholipase A2 (bradykinin, Des-Arg10-kallidin, or the calcium ionophore A23187) or treated with exogenous arachidonic acid. When cells were treated to express cyclooxygenase-2, the levels of PGE2 released over 15 min were undetectable; however, in the same cells stimulated with bradykinin, A23187, or arachidonic acid, large amounts of prostanoid were produced. Using selective inhibitors/antagonists, we found that the effects of bradykinin were mediated by B2 receptor activation and that prostanoid release was due to cyclooxygenase-2, and not cyclooxygenase-1, activity. In addition, we show that the release of PGE2 stimulated by either bradykinin, A23187, or arachidonic acid was inhibited by the phospholipase A2 inhibitor arachidonate trifluoromethyl ketone. Hence, we have demonstrated that PGE2 is released by two components: induction of cyclooxygenase-2 and supply of substrate, probably via activation of phospholipase A2. This is illustrated in A549 cells by a clear synergy between the cytokine interleukin-1beta and the kinin bradykinin.  (+info)

Inhibition of prostaglandin synthesis up-regulates cyclooxygenase-2 induced by lipopolysaccharide and peroxisomal proliferators. (4/6133)

Primary cultures of fetal hepatocytes expressed cyclooxygenase-2 (COX-2) upon stimulation with bacterial lipopolysaccharide (LPS) or peroxisomal proliferators. This enzyme was active and a good correlation between the mRNA levels, the amount of protein, and the synthesis of prostaglandin E2 was observed. However, when cells were incubated in the presence of indomethacin or the COX-2-specific inhibitor NS398, the amount of COX-2 protein increased 5-fold after activation with LPS and 2-fold after treatment with clofibrate. This up-regulation of COX-2 was not observed at the mRNA level. The mechanism of protein accumulation might involve either a direct stabilization of the enzyme by the inhibitors or the absence of prostaglandins involved in the regulation of its turnover. Among the prostaglandins assayed, only 15-deoxy-Prostaglandin J2 exerted a statistically significant decrease in the COX-2 levels in cells stimulated with LPS or LPS plus NS398. The accumulation of COX-2 in the presence of inhibitors was also observed in peritoneal macrophages treated under identical conditions. These results indicate that COX-2 protein accumulates after enzyme inhibition, and because removal of the inhibitors restored the enzyme activity, suppression of treatment with reversible COX-2 inhibitors may cause a transient overproduction of prostaglandins.  (+info)

Characterization of the analgesic and anti-inflammatory activities of ketorolac and its enantiomers in the rat. (5/6133)

The marked analgesic efficacy of ketorolac in humans, relative to other nonsteroidal anti-inflammatory drugs (NSAIDs), has lead to speculation as to whether additional non-NSAID mechanism(s) contribute to its analgesic actions. To evaluate this possibility, we characterized (R,S)-ketorolac's pharmacological properties in vivo and in vitro using the nonselective cyclooxygenase (COX) inhibitors [indomethacin (INDO) and diclofenac sodium (DS)] as well as the selective COX-2 inhibitor, celecoxib, as references. The potency of racemic (R,S)-ketorolac was similar in tests of acetic acid-induced writhing, carrageenan-induced paw hyperalgesia, and carrageenan-induced edema formation in rats; ID50 values = 0.24, 0. 29, and 0.08 mg/kg, respectively. (R,S)-ketorolac's actions were stereospecific, with (S)-ketorolac possessing the biological activity of the racemate in the above tests. The analgesic potencies for (R,S)-, (S)-, and (R)-ketorolac, INDO, and DS were highly correlated with their anti-inflammatory potencies, suggesting a common mechanism. (R,S)-ketorolac was significantly more potent than INDO or DS in vivo. Neither difference in relative potency of COX inhibition for (R,S)-ketorolac over INDO and DS nor activity of (S)-ketorolac at a number of other enzymes, channels, or receptors could account for the differences in observed potency. The distribution coefficient for (R,S)-ketorolac was approximately 30-fold less than for DS or INDO, indicating that (R,S)-ketorolac is much less lipophilic than these NSAIDs. Therefore, the physicochemical and pharmacokinetics properties of (R,S)-ketorolac may optimize the concentrations of (S)-ketorolac at its biological target(s), resulting in greater efficacy and potency in vivo.  (+info)

Oxidative bioactivation of the lactol prodrug of a lactone cyclooxygenase-2 inhibitor. (6/6133)

The lactol derivative of a lactone cyclooxygenase-2 inhibitor (DFU) was evaluated in vivo and in vitro for its potential suitability as a prodrug. DFU-lactol was found to be 10 to 20 times more soluble than DFU in a variety of aqueous vehicles. After administration of DFU-lactol at 20 mg kg-1 p.o. in rats, a Cmax of 7.5 microM DFU was reached in the plasma. After oral administration, the ED50s of DFU-lactol in the carrageenan-induced paw edema and lipopolysaccharide-induced pyresis assays in rats are comparable with the ED50s observed when dosing with DFU. Incubations of DFU-lactol with rat and human hepatocytes demonstrated that the oxidation of DFU-lactol can be mediated by liver enzymes and that a competing pathway is direct glucuronidation of the DFU-lactol hydroxyl group. Assays with subcellular fractions from rat liver indicated that most of the oxidation of DFU-lactol occurs in the cytosolic fraction and requires NAD(P)+. Human liver cytosol can also support the oxidation of DFU-lactol to DFU when NAD(P)+ is added to the incubations. Fractionation of human liver cytosolic proteins showed that at least three enzymes are capable of efficiently effecting the oxidation of DFU-lactol to DFU. Incubations with commercially available dehydrogenases suggest that alcohol and hydroxysteroid dehydrogenases are involved in this oxidative process. These data together suggest that lactols may represent useful prodrugs for lactone-containing drugs.  (+info)

Arachidonic acid in platelet microparticles up-regulates cyclooxygenase-2-dependent prostaglandin formation via a protein kinase C/mitogen-activated protein kinase-dependent pathway. (7/6133)

Activation of platelets results in shedding of membrane microparticles (MP) with potentially bioactive properties. Platelet MP modulate platelet, monocyte, and vascular endothelial cell function, both by direct effects of MP arachidonic acid (AA) and by its metabolism to bioactive prostanoids. We have previously reported that platelet MP induce expression of cyclooxygenase (COX)-2 and prostacyclin production in monocytes and endothelial cells. To elucidate further the molecular mechanisms that underlie MP-induced up-regulation of COX-2 expression, we investigated the response of a human monocytoid (U-937) cell line to platelet MP stimulation. In U-937 cells, MP-induced COX-2 expression and eicosanoid formation is prevented by pharmacological inhibitors of protein kinase C (PKC), PI 3-kinase, mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase, and p38 kinase. Treatment with the PI 3-kinase inhibitors wortmannin and LY294002 also blocked MP-induced p42/p44 MAPK, p38, and JNK1 phosphorylation. Conversely, platelet MP stimulation of U-937 cells results in direct activation of PKC, p42/p44 MAPK, p38 kinase, and c-Jun N-terminal kinase (JNK) as well as activation of the transcription factors c-Jun and Elk-1. However, MP failed to activate the cAMP response element. Activation of U-937 cells by MP induces translocation of classical (PKCbeta), novel (PKCdelta) and atypical (PKCzeta and PKClambda) isozymes of PKC from the cytosol to the membrane, with concomitant activation of downstream MAPK. While MP-induced activation of p42/p44 MAPK and p38 kinase is transient, a sustained activation of JNK1 was observed. Although PKC activation is required for MP-induced p42/p44 MAPK, activation of the stress kinases p38 and JNK1 was PKC-independent. The fatty acid fraction of the MP accounted for these effects, which were mimicked by MP AA. Rather than acting directly via nuclear receptors, MP AA activates COX-2-dependent prostaglandin production by a PKC/p42/p44 MAPK/p38 kinase-sensitive pathway in which PI 3-kinase plays a significant role. MP AA also stimulates transcriptional activation of COX-2 as well as c-Jun and Elk-1.  (+info)

Coordinate regulation of cyclooxygenase-2 and TGF-beta1 in replication error-positive colon cancer and azoxymethane-induced rat colonic tumors. (8/6133)

Evidence is accumulating which indicates that cyclooxygenase-2 (COX-2) is involved in the pathogenesis of colorectal cancer. We evaluated the expression of COX-2 in replication error-positive (RER) colon cancers, colon cancers metastatic to liver and azoxymethane (AOM)-induced rat colonic tumors. Immunohistochemistry showed that COX-2 was low to undetectable in normal human mucosa, but abundant in the RER adenocarcinomas we examined. COX-2 immunoreactivity in metastatic colon cancers was less abundant, but clearly detectable. In the colon of AOM-treated rats, COX-2 protein was not detectable in normal mucosa, but present in most of the epithelial cells comprising the tumors. The TGF-beta1 staining pattern in these human and rat tumors was similar to that observed for COX-2. The role of TGF-beta in RER adenocarcinomas is complex because of the increased mutation rate of TGF-beta type II receptors. Northern analysis showed abundant TGF-beta1 mRNA in AOM-induced tumors, but not in paired mucosa. TGF-beta1 induced the expression of COX-2 mRNA and protein in intestinal epithelial cells (IEC-6). Chronic TGF-beta1 treatment caused a TGF-beta-dependent overexpression of COX-2 in rat intestinal epithelial cells (RIE-1). TGF-beta1 may regulate COX-2 expression during the colonic adenoma to carcinoma sequence.  (+info)

*Maluku sectarian conflict

Cox, Caroline; Catherine Butcher (2006). Cox's book of modern saints and martyrs. Continuum. pp. 6-8. Retrieved 1 April 2011. ... This account has been reprinted in Cox's 2006 book and on Christian blogs, a photo purported to be of Roy exists online. " ... Retrieved 2 April 2011. Workers of Open Doors, a Christian organisation, claim to have interviewed a friend of Roy Pontoh who ... Retrieved 2 April 2011. van Klinken 2007, p. 179 Littik, Semmy. "The Battle of Waai and the Ambon Demo". Sala Foundation Waku ...

*Hamilton Mausoleum

Cox, T., 2014. Sonic wonderland: A scientific odyssey of sound. Random House. Hamilton Mausoleum Chatelerhaut Country Park and ...

*Largest organisms

Cox, C. B.; Hutchinson, P. (1991). "Fishes and amphibians from the Late Permian Pedrado Fogo Formation of northern Brazil" (PDF ... 2 (3): 1-14. Benson, R. B. J.; Campione, N. S. E.; Carrano, M. T.; Mannion, P. D.; Sullivan, C.; Upchurch, P.; Evans, D. C. ( ... One of these flukes can be up to 7.5 cm (3.0 in) long and 2 cm (0.79 in) thick. Tapeworms (Cestoda) The largest known species ... 63 (2): 131-155. doi:10.1093/mollus/63.2.131. Gumboot Chiton. alaska.gov Kauffman, E. G.; Harries, P. J.; Meyer, C.; Villamil, ...

*JMP (statistical software)

Ian Cox; Marie A. Gaudard; Philip J. Ramsey; Mia L. Stephens; Leo Wright (21 December 2009). Visual Six Sigma: Making Data ... Version 2 was twice the size as the original, though it was still delivered on a floppy disk. It required 2 MB of memory and ... 32 (2): 174-175. doi:10.1021/ci00006a600. ISSN 1549-9596. John P. Sall, Northern Illinois University, archived from the ... 392-. ISBN 978-1-60764-301-2. Retrieved 13 December 2012. Hayes Weier, Mary (June 25, 2007). "Scientists use BI Software and ...

*Eugene Gelfand

Cox, Harold (November 3, 2004). "Pennsylvania House of Representatives - 1973-1974" (PDF). Wilkes University Election ... Cox, Harold. "House Members G". Wilkes University Election Statistics Project. Wilkes University. ...

*Resolvin

COX-2 modified in activity by aspirin or atorvastatin or, alternatively, a microbial or possibly mammalian cytochrome P450 ... cyclooxygenase-2 (i.e. COX-2), and certain Cytochrome P450 monooxygenases. While only one of these enzymes may form certain Rvs ... COX-2 modified in activity by aspirin or atorvastatin (a statin-type drug) or, alternatively, a microbial or possibly mammalian ... re made by the initial conversion of DHA by aspirin-acetylated COX-2 in vascular endothelial cells to 17(R)-hydroxy-DHA which ...

*15-Hydroxyeicosatetraenoic acid

When pretreated with aspirin, however, COX-1 is inactive while COX-2 attacks arachidonic acid to produce almost exclusively 15( ... 13E-eicosatetraenoic acid synthesis within the cyclooxygenase active site of murine COX-2. Why acetylated COX-1 does not ... Lee, S. H.; Rangiah, K; Williams, M. V.; Wehr, A. Y.; Dubois, R. N.; Blair, I. A. (2007). "Cyclooxygenase-2-mediated metabolism ... Lee, S. H.; Williams, M. V.; Dubois, R. N.; Blair, I. A. (2005). "Cyclooxygenase-2-mediated DNA damage". Journal of Biological ...

*Battle of Reading (1688)

Cox. Collier, John Payne; Percy Society (1840). "The Reading Skirmish". Early English poetry, ballads, and popular literature ...

*Stage17.tv

Cox, Gordon. "New Digital Platform, Stage 17, Bets on the Broadway Demographic". Variety.com. Retrieved 2 September 2014. ... Retrieved 2 September 2014. McElroy, Steve. "If You Can't Get Onstage, Go Online Stage Actors Between Gigs Stay Busy With Web ...

*Kenneth Kruszewski

Cox, Harold. "House Members K". Wilkes University Election Statistics Project. Wilkes University. ...

*John T. Wilder

Eicher, p. 569; Cox, p. 11. Baumgartner, Richard A. Blue Lightning: Wilder's Mounted Infantry Brigade in the Battle of ... Cox, Steven. Chattanooga Was His Town: The Life of General John T. Wilder, presentation to the Chattanooga Area Historical ... ISBN 978-1-885033-35-2. Terrell, W.H.H. (1866). Report of the Adjutant General of the State of Indiana (Volume III ed.). ... ISBN 978-1-885033-35-2. Cozzens, Peter (1992). This Terrible Sound. ISBN 0-252-01703-X. Cozzens, pp. 14-15. Cozzens, p. 15; ...

*NEET

Simon Cox of BBC News said the word is "the latest buzzword for teenage drop-outs". He says "Neets are 20 times more likely to ... 8-9. Cox, Simon. "A 'Neet' solution". BBC News. Accessed 24 August 2011. See also: Abrams, Adam. Learning to Fail: How Society ... Cox, Simon. "A 'Neet' solution". BBC News. Accessed 24 August 2011. Smith, David. "Nobody Neets this lazy lot any more". The ... The NEET rate in the province (13,5%) is similar to the Canadian rate (13,2%). The report also stated that the decrease of the ...

*Archdeacon of Chester

COX, Ven. William Lang Paige. ukwhoswho.com. Who Was Who. 1920-2008 (December 2007 online ed.). A & C Black, an imprint of ... Retrieved 2 January 2013. TUBBS, Rt Rev. Norman H. ukwhoswho.com. Who Was Who. 1920-2008 (December 2012 online ed.). A & C ... Retrieved 2 January 2013. BARBER, Ven. Edward. ukwhoswho.com. Who Was Who. 1920-2008 (December 2007 online ed.). A & C Black, ... Retrieved 2 January 2013. FISHER, Ven. Leslie Gravatt. ukwhoswho.com. Who Was Who. 1920-2008 (December 2012 online ed.). A & C ...

*Joseph M. Gaydos

Cox, Harold. "Senate Members "G"". Wilkes University Election Statistics Project. Wilkes University. Obituary-Joseph M. Gaydos ... Cox, Harold (2004). "Pennsylvania Senate - 1967-1968" (PDF). Wilkes University Election Statistics Project. Wilkes University. ...

*Claybank Log Church

Cox, Dale. "Historic Claybank Church - Ozark, Alabama". exploresouthernhistory.com. Archived from the original on March 3, 2014 ... Retrieved March 2, 2014. See also: "Accompanying photos" (PDF). Archived (PDF) from the original on March 2, 2014. Retrieved ... Archived (PDF) from the original on March 2, 2014. ...

*18th Guards Motor Rifle Brigade

Cox, Matthew; Sisk, Richard (15 April 2014). "NATO Builds Plan as Violence Increases in Ukraine". Military.com. Retrieved 12 ... Between 1 and 2 February, a combined formation of the brigade and other Russian units were involved in combat near Debaltseve. ... Sutyagin, Igor (March 2015). "RUSI Briefing Paper: Russian Forces in Ukraine" (PDF). Royal United Services Institute: 2-7. ...

*EGF-like domain

COX-2; CRB1; CRB2; CSPG3; CUBN; DLK1; DLL1; DLL3; DLL4; DNER; EDIL3; EGF; EGFL11; EGFL8; EGFL9; EGFLAM; EPGN; EREG; F7; F9; F10 ... 1477 (1-2): 51-63. doi:10.1016/s0167-4838(99)00262-9. PMID 10708848. Glanville RW, Qian RQ, McClure DW, Maslen CL, et al. (1994 ... 2 (6): 504-9. doi:10.1038/nsb0695-504. PMID 7664114. Sunnerhagen M, Olah GA, Stenflo J, Forsen S, Drakenberg T, Trewhella J ( ... 29 (2): 119-67. doi:10.1017/S0033583500005783. PMID 8870072. Wouters MA, Rigoutsos I, Chu CK, Feng LL, Sparrow DB, Dunwoodie SL ...

*Altamaha-ha

Cox, Dale. "The Altamaha-ha - Sea Monster of the Georgia Coast". www.exploresouthernhistory.com. Retrieved 2 April 2017. ...

*American wigeon

Cox, Cameron; Barry, Jessie. "Aging of American and Eurasian Wigeons in female-type plumages" (PDF). Birding. 37 (2): 156-164. ... 96 (1): 2-22. ISSN 0007-0335. Harrop, A. (1994). "Field identification of American Wigeon". Birding World. 7: 50-56. Jiquet, F ...

*Precycling

Cox, Jayne; Giorgi, Sarah; Veronica, Sharp; Strange, Kit; Wilson, David C.; Blakey, Nick (2010). "Household waste prevention - ... Cox, Jayne; Giorgi, Sarah; Veronica, Sharp; Strange, Kit; Wilson, David C.; Blakey, Nick (2010). "Household waste prevention - ... Cox, Jayne; Giorgi, Sarah; Veronica, Sharp; Strange, Kit; Wilson, David C.; Blakey, Nick (2010). "Household waste prevention - ... Cox, Jayne; Giorgi, Sarah; Veronica, Sharp; Strange, Kit; Wilson, David C.; Blakey, Nick (2010). "Household waste prevention - ...

*Robert Whitney (conductor)

Cox, Dwayne; Morison, William James (2000). The University of Louisville at Google Books. University Press of Kentucky. p. 119 ... "WorldCat Identities Page for Robert Sutton Whitney". Retrieved 2 March 2009. "Louisville Orchestra Founder, Conductor Robert ... access-date= requires ,url= (help) "Cedille Records Notes". Retrieved 2 March 2009. ...

*Hayling Island Lifeboat Station

ISBN 0-907605-89-3. Cox, Barry. "FESTING, Francis Worgan, Major, Royal Marine Artillery". Lifeboat Gallantry - RNLI Medals and ... Cox, Barry. "GOLDRING, William, FARMER, David, and SPRAGG, James". Lifeboat Gallantry - RNLI Medals and how they were won. ... The decision was made at an RNLI management committee meeting held on 2 February 1865. The following week the District ... ISBN 978-0-319-24079-3. Leach, Nicholas (1999). "Hayling Island". Part 2, South Coast of England - Eastbourne to Weston-super- ...

*Cake (band)

Cox Enterprises. ,access-date= requires ,url= (help) Finan, Chris (April 10, 1999). "Reviews - For Records Released On April 19 ... Cox Enterprises. August 2, 2001. ,access-date= requires ,url= (help) "Billboard 200". Business Wire. August 6, 2001. ,access- ... "Short Skirt/Long Jacket" hit number 2 on the Bear Rock Top 10 in Canada and number 7 on the Billboard Modern Rock Tracks; the ... Montgomery, James (August 2, 2001). "Cake man talks about economic importance of short skirts". UWIRE. ,access-date= requires , ...

*Public health

Lampos, Vasileios; Yom-Tov, Elad; Pebody, Richard; Cox, Ingemar J. (2 July 2015). "Assessing the impact of a health ... 27 (2): 133-136. doi:10.1016/j.det.2008.11.010. PMID 19254656. "Public Health 2.0: Spreading like a virus" (PDF). 24 April 2007 ... In a June 2010 editorial in the medical journal The Lancet, the authors opined that "The fact that type 2 diabetes, a largely ... 2: 183-191. "What is Public Health". Centers for Disease Control Foundation. Atlanta, GA: Centers for Disease Control. ...

*Alister Clark Memorial Rose Garden

Cox, Peter (1999). Australian roses : roses and rose breeders of Australia. Hawthorn, Vic.: Bloomings Books. pp. 7-18. ISBN 1- ... Retrieved 2 February 2014. "Madge Taylor". Help Me Find. Retrieved 25 November 2013. "'Margaret Turnbull'". Help Me Find. ...

*St Michael, Cornhill

Cox, H. (1867). Modern churches: church furniture and decoration. London: Horace Cox. pp. 31-2. Retrieved 21 October 2011. "The ... 2. London: J. Stratford. p. 129. Ash, Russell (1973). Folklore, Myths and Legends of Britain. Reader's Digest Association ...

*Ketone

Nelson, D. L.; Cox, M. M. (2000) Lehninger, Principles of Biochemistry. 3rd Ed. Worth Publishing: New York. ISBN 1-57259-153-6. ... R2CH(OH) + O → R2C=O + H2O. Typical strong oxidants (source of "O" in the above reaction) include potassium permanganate or a ... The most widely used member of this class of compounds is methyl vinyl ketone, CH3C(O)CH=CH2, which is useful in the Robinson ... The simplest class have the formula (CH2)nCO, where n varies from 2 for cyclopropanone to the teens. Larger derivatives exist. ...

*Frank Riethmuller

Peter Cox and others have pointed out that 'Carabella,' like 'Titian,' can easily be grown as a pillar rose, some examples ... Cox, Peter (1999). Australian Roses. Melbourne: Bloomings Books. pp. 36-7. ISBN 1-876473-02-9. Personal communication from ... 34 (2): 38-41. Statutory declaration made to internment tribunal 23 August 1940, National Archive A12102/37. "Police Court". ... It is available online as part of the Australian National Archive: NAA document MP1103/2, PWN1389 National Archive A12102/37 ...
Prostaglandin-endoperoxide synthase (PTGS), also known as cyclooxygenase, is the key enzyme in prostaglandin biosynthesis, and acts both as a dioxygenase and as a peroxidase. There are two isozymes of PTGS: a constitutive PTGS1 and an inducible PTGS2, which differ in their regulation of expression and tissue distribution. This gene encodes the inducible isozyme. It is regulated by specific stimulatory events, suggesting that it is responsible for the prostanoid biosynthesis involved in inflammation and mitogenesis. [provided by RefSeq, Feb 2009 ...
TY - JOUR. T1 - Store-operated Ca2+ Entry Facilitates the Lipopolysaccharide-induced Cyclooxygenase-2 Expression in Gastric Cancer Cells. AU - Wong, Jhen Hong. AU - Ho, Kuo Hao. AU - Nam, Sean. AU - Hsu, Wen Li. AU - Lin, Chia Hsien. AU - Chang, Che Mai. AU - Wang, Jaw Yuan. AU - Chang, Wei Chiao. PY - 2017/12/1. Y1 - 2017/12/1. N2 - Helicobacter pylori has been identified as one of the major causes of chronic gastritis, gastric and duodenal ulcers, and gastric cancer. Lipopolysaccharide (LPS) is a major component of the outer membrane of gram-negative bacteria, and H. pylori LPS might play an exclusively important role in activating inflammatory pathways in monocytes and macrophages. To study the role of LPS in the underlying mechanism of inflammatory responses, we established an in vitro model using the human AGS gastric cancer cell line. We found that LPS mediates inflammation through setting off a cascade of events: activation of the store-operated calcium (SOC) channel, initiation of ...
PTGS2 (COX-2) is unexpressed under normal conditions in most cells, but elevated levels are found during inflammation. PTGS1 (COX-1) is constitutively expressed in many tissues and is the predominant form in gastric mucosa and in the kidneys. Inhibition of PTGS1 (COX-1) reduces the basal production of cytoprotective PGE2 and PGI2 in the stomach, which may contribute to gastric ulceration. Since PTGS2 (COX-2) is generally expressed only in cells where prostaglandins are upregulated (e.g., during inflammation), drug-candidates that selectively inhibit PTGS2 (COX-2) were suspected to show fewer side-effects[25] but proved to substantially increase risk for cardiovascular events such as heart attack and stroke. Two different mechanisms may explain contradictory effects. Low-dose aspirin protects against heart attacks and strokes by blocking PTGS1 (COX-1) from forming a prostaglandin called thromboxane A2. It sticks platelets together and promotes clotting; inhibiting this helps prevent heart ...
The size of the PCR products from cyclooxygenase-1 and cyclooxygenase-2 are 524 and 583 base pairs, respectively. The specificity of the PCR reaction for cyclooxygenase-1 and cyclooxygenase-2 complementary deoxyribonucleic acid (cDNA) was confirmed by digestion of PCR products by sequence-specific restriction enzymes (cyclooxygenase-1: Sac I and Sma I; cyclooxygenase-2: Pst I and Nco I). For quantitation of cyclooxygenase-1 and cyclooxygenase-2 mRNA levels, the Escherichia coli plasmid pT2M containing specific internal standards for cyclooxygenase-1 and cyclooxygenase-2 was constructed by internal deletion of sequences: The truncated fragments (320 base pairs) from cyclooxygenase-1 and cyclooxygenase-2 PCR products were incorporated into the E. coli cloning plasmid pBSII SK(+)(Stratagene, La Jolla, CA) at the EcoR I and Kpn I restriction sites and multiplied as plasmids in an E. coli strain Dh5 alpha. Plasmid solutions were adjusted to 1 x 104molecules/micro liter after double digestion by ...
bom:102287995 K00509 prostaglandin-endoperoxide synthase 1 [EC:1.14.99.1] , (RefSeq) PTGS1; prostaglandin-endoperoxide synthase 1 (A) MSRQGISLRFPLLLLLLSPSPVLPADPGAPAPVNPCCYYPCQHQGICVRFGLDRYQCDCT RTGYSGPNCTIPEIWTWLRTTLRPSPSFVHFLLTHGRWLWDFVNATFIRDTLMRLVLTVR SNLIPSPPTYNIAHDYISWESFSNVSYYTRILPSVPRDCPTPMGTKGKKQLPDAEFLSRR FLLRRKFIPDPQGTNLMFAFFAQHFTHQFFKTSGKMGPGFTKALGHGVDLGHIYGDNLER QYQLRLFKDGKLKYQMLNGEVYPPSVEEAPVLMHYPRGIPPQSQMAVGQEVFGLLPGLML YATIWLREHNRVCDLLKAEHPTWGDEQLFQTARLILIGETIKIVIEEYVQQLSGYFLQLK FDPELLFGAQFQYRNRIAMEFNQLYHWHPLMPDSFRVGPQDYSYEQFLFNTSMLVDYGVE ALVDAFSRQPAGRIGGGRNIDHHILHVAVDVIKESRELRLQPFNEYRKRFGMKPYTSFQE LTGEKEMAAELEELYGDINALEFYLGLLLEKCHPNSIFGESMIEMGAPFSLKGLLGNPIC SPEYWKASTFGGDVGFNLVKTATLKKLVCLNTKTCPYVSFHVPDPHREDRPGVERPPTEL ...
bom:102271174 K11987 prostaglandin-endoperoxide synthase 2 [EC:1.14.99.1] , (RefSeq) PTGS2; prostaglandin-endoperoxide synthase 2 (A) MLARALLLCAAVALSGAANPCCSHPCQNRGVCMSVGFDQYKCDCTRTGFYGENCTTPEFL TRIKLLLKPTPNTVHYILTHFKGVWNIVNKISFLRNMIMRYVLTSRSHLIESPPTYNVHY SYKSWEAFSNLSYYTRALPPVPDDCPTPMGVKGRKELPDSKEVVKKVLLRRKFIPDPQGT NLMFAFFAQHFTHQFFKTDFERGPAFTKGKNHGVDLSHIYGESLERQHKLRLFKDGKMKY QMINGEMYPPTVKDTQVEMIYPPHVPEHLKFAVGQEVFGLVPGLMMYATIWLREHNRVCD VLKQEHPEWGDEQLFQTSRLILIGETIKIVIEDYVQHLSGYHFKLKFDPELLFNQQFQYQ NRIAAEFNTLYHWHPLLPDVFQIDGQEYNYQQFIYNNSVLLEHGLTQFVESFTRQRAGRV AGGRNLPVAVEKVSKASIDQSREMKYQSFNEYRKRFLLKPYESFEELTGEKEMAAELEAL YGDIDAMEFYPALLVEKPRPDAIFGETMVEAGAPFSLKGLMGNPICSPEYWKPSTFGGEV GFKIINTASIQSLICSNVKGCPFTSFSVQDTHLTKTVTINASSSHSGLDDINPTVLLKER STEL ...
Cyclooxygenase (COX), officially known as prostaglandin-endoperoxide synthase (PTGS), is an enzyme that is responsible for formation of important biological mediators called prostanoids, including prostaglandins, prostacyclin and thromboxane. Pharmacological inhibition of COX can provide relief from the symptoms of inflammation and pain. Drugs, like Aspirin, that inhibit cyclooxygenase activity have been available to the public for about 100 years. Two cyclooxygenase isoforms have been identified and are referred to as COX-1 and COX-2. Under many circumstances the COX-1 enzyme is produced constitutively (i.e., gastric mucosa) whereas COX-2 is inducible (i.e., sites of inflammation). Non-steroidal anti-inflammatory drugs (NSAID), such as aspirin and ibuprofen, exert their effects through inhibition of COX. The main COX inhibitors are the non-steroidal anti-inflammatory drugs (NSAIDs).. ...
PTGS2 is the inducible isozyme of prostaglandin-endoperoxide synthase, also known as cyclooxygenase. It has been linked to numerous conditions, especially involving inflammation or cancer. Also known as COX2. [PMID 17479405] Haplotypes A-1195G-765T8473 and A-1195C-765T8473 variants of COX-2 were associated with 1.3X increased risk of breast cancer in a Chinese population [PMID 16361272] Relative to individuals with a PTGS2 Ex10 +837 TT genotype, those carrying the C allele (TC or CC genotype) had a 1.8-fold risk of bile duct cancer in a Chinese population [PMID 12920574] In a group of Pima Indians, individuals with the variant PTGS2 rs20417 CC genotype had a 30% higher Type 2 diabetes prevalence compared with subjects with the GG genotype ...
Cystic fibrosis (CF) is one of the most common autosomal recessive diseases among Caucasians caused by a mutation in the CFTR gene. However, the clinical outcome of CF pulmonary disease varies remarkably even in patients with the same CFTR genotype. This has led to a search for genetic modifiers located outside the CFTR gene. The aim of this study was to evaluate the effect of functional variants in prostaglandin-endoperoxide synthase genes (COX1 and COX2) on the severity of lung disease in CF patients. To the best of our knowledge, it is the first time when analysis of COX1 and COX2 as potential CF modifiers is provided. The study included 94 CF patients homozygous for F508del mutation of CFTR. To compare their clinical condition, several parameters were recorded, e.g. a unique clinical score: disease severity status (DSS). To analyse the effect of non-CFTR genetic polymorphisms on the clinical course of CF patients, the whole coding region of COX1 and selected COX2 polymorphisms were analysed. ...
COX1 / Cyclooxygenase 1兔单克隆抗体[EPR5866](ab109025)可与小鼠, 大鼠, 人样本反应并经WB, IP, IHC, Flow Cyt, ICC/IF实验严格验证,被2篇文献引用并得到2个独立的用户反馈。
Cyclooxygenase is the key enzyme in the biosynthetic pathway of prostaglandins (PGs) and thromboxane from arachidonic acid. There are two isozymes of cyclooxygenase; constitutive cyclooxygenase-1 and...
Cyclooxygenase is an enzyme that produces signals that can lead to pain and inflammation. Medications that inhibit cyclooxygenase...
购买我们的人COX1 / Cyclooxygenase 1肽。ab22901可作为ab2338的封闭肽并经过Blocking实验验证。Abcam提供免费的实验方案,操作技巧及专业的支持。中国80%以上现货。
高い抗原親和性、特異性と安定した品質を兼ね備えたアブカムのウサギ・モノクローナル抗体 RabMAb® ab62331 交差種: Ms,Hu 適用: WB,Flow Cyt,ICC/IF
ptgs2, cox-2, cox2, gripghs, hcox-2, pgg/hs, pghs-2, phs-2; prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase); K11987 prostaglandin-endoperoxide synthase 2 [EC:1.14.99.1] ...
Sirtuin 1 (Sirt1) is a NAD+-dependent deacetylase that exerts many of the pleiotropic effects of oxidative metabolism. Due to local hypoxia and hypertonicity, the renal medulla is subject to extreme oxidative stress. Here, we set out to investigate the role of Sirt1 in the kidney. Our initial analysis indicated that it was abundantly expressed in mouse renal medullary interstitial cells in vivo. Knocking down Sirt1 expression in primary mouse renal medullary interstitial cells substantially reduced cellular resistance to oxidative stress, while pharmacologic Sirt1 activation using either resveratrol or SRT2183 improved cell survival in response to oxidative stress. The unilateral ureteral obstruction (UUO) model of kidney injury induced markedly more renal apoptosis and fibrosis in Sirt1+/¨C mice than in wild-type controls, while pharmacologic Sirt1 activation substantially attenuated apoptosis and fibrosis in wild-type mice. Moreover, Sirt1 deficiency attenuated oxidative stress¨Cinduced COX2 ...
Cyclooxygenase 1 (COX-1), also known as prostaglandin G/H synthase 1, prostaglandin-endoperoxide synthase 1 or prostaglandin H2 synthase 1, is an enzyme that in humans is encoded by the PTGS1 gene. In humans it is one of two cyclooxygenases. Cyclooxygenase (COX) is the central enzyme in the biosynthetic pathway to prostaglandins from arachidonic acid. This protein was purified more than 20 years ago and cloned in 1988. There are two isozymes of COX encoded by distinct gene products: a constitutive COX-1 (this enzyme) and an inducible COX-2, which differ in their regulation of expression and tissue distribution. The expression of these two transcripts is differentially regulated by relevant cytokines and growth factors. This gene encodes COX-1, which regulates angiogenesis in endothelial cells. COX-1 is also involved in cell signaling and maintaining tissue homeostasis. A splice variant of COX-1 termed COX-3 was identified in the CNS of dogs, but does not result in a functional protein in humans. ...
Non-steroidal anti-inflammatory drugs (NSAIDs), which include over-the-counter pharmaceuticals such as ibuprofen, naproxen, and aspirin, rank among the most widely used pharmaceuticals worldwide. Their chief mechanism of action is inhibition of two forms of cyclo-oxygenase (COX), namely COX-1 and COX-2 (1). Also known as prostaglandin-endoperoxide synthase (PTGS), COX is responsible for the production of downstream mediators of pain and inflammation, such as thromboxane and prostaglandins. Due to their suppression of prostaglandins, which exert protective roles in the gastrointestinal tract, one of the most frequent adverse effects of NSAIDs is irritation of the gastric mucosa.. Thus, newer generation selective COX-2 drugs, known as the coxibs, were introduced in the 1990s to mitigate the risk of peptic ulceration that results from COX-1 suppression. By 2004, coxibs had dominated the prescription drug market for NSAIDs, with worldwide sales of approximately $10 billion (2). Their development was ...
Ibuprofen is a well-established non-steroidal anti-inflammatory drug, inhibiting the prostaglandin-endoperoxide synthase. One of the key features defining the ibuprofen structure is the doubly intermolecular O-H⋯O [[double bond, length as m-dash]] C hydrogen bond in cyclic dimers as know from carboxylic acids a...
Cyclooxygenase (COX) is a bifunctional enzyme exhibiting coupled peroxidase and dioxygenase activities.1,2 Human COX-1 and COX-2 are two structurally homologous hemoproteins responsible for the biosynthesis of prostaglandin H2 from arachidonic acid (AA).1-3 They have been found to play great roles in certain diseases, including cancer,4 and nervous system5 and apoptosis-related diseases.6 COX-1 is constitutively expressed in a variety of cells,7 whereas COX-2 is induced by various inflammatory and proliferative stimuli. COX enzymes are important drug targets for the non-steroidal anti-inflammatory drugs. Over the past decades, COX-2 inhibitors have widely been used as anti-inflammatory medicine, although they usually elicit potential cardiotoxic side effects. Hence, many efforts have been made in recent years to eliminate or reduce such kinds of adverse effects.6,8,9 Crystal structure studies10,11 reveal that COX-2 has a larger substrate binding pocket than COX-1 (Fig. S1†), providing the ...
Coincident with the FDA approval of refecoxib and celecoxib, FitzGerald et al reported that these drugs suppress the formation of prostacyclin (PGI2), leaving the production of thromboxane A2 (TXA2) unaltered.30 PGI2 is a key COX product in the endothelium that inhibits platelet aggregation, causes vasodilatation, and prevents proliferation of vascular smooth muscle cells.31 Evidence was also provided that PGI2 production in vivo was COX-2 dependent, possibly through COX-2 induction in endothelial cells by shear stress.31 In contrast to PGI2, the COX-1-derived prostanoid TXA2, causes platelet aggregation, vasoconstriction, and vascular proliferation.31 FitzGerald et al speculated that suppression of COX-2-dependent formation of PGI2 by the COX-2 inhibitors left TXA2 generation unopposed, promoting vasoconstriction, thrombosis, and atherogenesis.32 A number of publications began to surface suggesting that the COX-2 inhibitors might be associated with an increased risk of cardiovascular events. ...
The role of NSAIDs in the prevention of colorectal cancer is mediated through various mechanisms including the inhibition of COX-2 and the induction of apoptosis through COX-2 independent pathways (26). Previous studies from our laboratory suggested that ASA partially suppresses the MSI-H phenotype of human colon cancer cell lines through an apoptotic mechanism that appeared to be COX independent (22). In vitro ASA has been shown to arrest colon cancer cells at the G1/S checkpoint and induce apoptosis through activation of ATM, p21, and BAX (27). Among NSAIDS, ASA is still a preferred choice for chemoprevention in average-risk individuals. This is not only because of its shown chemopreventive efficacy but also because of its unique potential in cardiovascular protection (3, 4).. In this study, we investigated the chemopreventive potential of ASA and NO-ASA using a newly developed mouse model of LS/HNPCC. LS/HNPCC mice treated with ASA at 400 mg/kg had an increased median survival time compared ...
Cyclooxygenase-2 (COX-2)-dependent prostaglandin E2 (PGE2) synthesis exacerbates occlusive and aneurysmal vascular disease by inducing macrophage proteinase and...
Sevigny M.B., Li C.F., Alas M., Hughes-Fulford M.. Cyclooxygenase-2 (COX-2) catalyzes the rate-limiting step in the prostanoid biosynthesis pathway, converting arachidonic acid into prostaglandin H(2). COX-2 exists as 72 and 74kDa glycoforms, the latter resulting from an additional oligosaccharide chain at residue Asn(580). In this study, Asn(580) was mutated to determine the biological significance of this variable glycosylation. COS-1 cells transfected with the mutant gene were unable to express the 74kDa glycoform and were found to accumulate more COX-2 protein and have five times greater COX-2 activity than cells expressing both glycoforms. Thus, COX-2 turnover appears to depend upon glycosylation of the 72kDa glycoform.. FEBS Lett. 580:6533-6536(2006) [PubMed] [Europe PMC] ...
Rabbit recombinant monoclonal COX2 / Cyclooxygenase 2 antibody [EPR18376-119] validated for WB, IP, Flow Cyt, ICC/IF and tested in Mouse. Immunogen…
So the problem has to do with the fact that sometimes our understanding of how the body does what it does is incomplete, and when we isolate a chemical or split a natural chemical down to only part of its molecule, it ends up turning off one bad function of the body but unwittingly turning off some beneficial functions, too. For instance, aspirin inhibits cyclooxygenase, the bodys natural chemical that normally mediates the synthesis of natural chemicals that enable platelets to activate and stick together and form a clot when blood vessel damage occurs so you dont bleed out... some people are inappropriately prone to clotting and need to tone that natural process down a bit, so they take aspirin. Well, unfortunately cyclooxygenase also mediates processes that cause your stomach to protect its lining against its own acid... so inhibiting cyclooxygenase will stop platelets of clot-prone people from clotting inappropriately, but at the same time it has the potential to also cause you to get a ...
Interleukin-1 (IL-1) induces hypophagia, which can be reduced by cyclooxygenase (COX) inhibitors. Earlier studies with COX knockout (COXko) mice suggested that COX2 was more important for hypophagia than COX1. However, behavioral responses occur long before COX2 is induced. Hypophagia was assessed in mice by measuring the intake of sweetened milk in a brief period. The intake was reduced within 30 min after intraperitoneal injection of IL-1β and was depressed for about 2 h. When milk intake was measured 30 to 40 min after IL-1β, COX1ko mice showed an attenuated response, whereas COX2ko mice responded more like wild-type animals. By contrast, 90 to 120 min after IL-1β COX1ko mice responded normally, whereas COX2ko mice showed only small responses. The COX2-selective inhibitor, celecoxib, failed to alter the response to IL-1β 30 min after administration, but low doses antagonized the effects of IL-1β at 90 to 120 min. The COX1-selective inhibitor, SC560, attenuated both the early and late ...
Drug Discovery, Drugs, Inflammation, Pain, Therapeutic, Community, Homo, Inhibition, Mechanics, Cyclooxygenase, Cyclooxygenase-1, Literature, Pathologies
Several studies suggest that cyclooxygenase-2 contributes to the delayed progression of ischemic brain damage. In this study we examined whether the highly selective cyclooxygenase-2 inhibitor DFU reduces neuronal damage when administered several hours after 5 min of transient forebrain ischemia in gerbils. The extent of ischemic injury was assessed behaviorally by measuring the increases in locomotor activity and by histopathological evaluation of the extent of CA1 hippocampal pyramidal cell injury 7 days after ischemia. DFU treatment (10 mg/kg, p.o.) significantly reduced hippocampal neuronal damage even if the treatment is delayed until 12 h after ischemia. These results suggest that selective cyclooxygenase-2 inhibitors may be a valuable therapeutic strategy for ischemic brain injury. ...
Background Giardia lamblia trophozoites colonize in the upper small intestine resulting in diarrhea and various clinical manifestations, including abdominal pain, anorexia, and signs of malabsorption. A decrease in the level of trace elements might occur because of this absorption deficiency resulting from giardiasis. Experimentally, the excretory secretory product of G. lamblia trophozoites increased the level of reactive oxygen species in mice enterocytes. The levels of bilirubin, uric acid, and albumin are often used as major nonenzymatic oxidative biomarkers. Objective This study was designed to determine the effect of therapy by metronidazole (MTZ) and artemether (ART) on trophozoite and cyst forms in experimentally Giardia spp.-infected hamsters and to reveal the changes in iron (Fe), manganese (Mn), copper (Cu), and chromium (Cr) serum levels pretreatment and post-treatment. Another objective was to evaluate the impact of this therapy on serum levels of bilirubin, uric acid, and albumin ...
We have recently reported that cyclooxygenase (COX)-2-deficiency affects brain upstream and downstream enzymes in the arachidonic acid (AA) metabolic pathway to prostaglandin E2 (PGE2), as well as enzyme activity, protein and mRNA levels of the reciprocal isozyme, COX-1. To gain a better insight into the specific roles of COX isoforms and characterize the interactions between upstream and downstream enzymes in brain AA cascade, we examined the expression and activity of COX-2 and phospholipase A2 enzymes (cPLA2 and sPLA2), as well as the expression of terminal prostaglandin E synthases (cPGES, mPGES-1, and − 2) in wild type and COX-1-/- mice. We found that brain PGE2 concentration was significantly increased, whereas thromboxane B2 (TXB2) concentration was decreased in COX-1-/- mice. There was a compensatory up-regulation of COX-2, accompanied by the activation of the NF-κB pathway, and also an increase in the upstream cPLA2 and sPLA2 enzymes. The mechanism of NF-κB activation in the ...
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This invention is in the field of antiinflammatory pharmaceutical agents and specifically relates to compounds, compositions and methods for treating disorders mediated by cyclooxygenase-2 or 5-lipoxygenase, such as inflammation. Compounds of particular interest are defined by Formula I wherein A, Y, R1, R2, R3, R4 and R5 are as defined in the specification.
Liu, X., Wong, P.T.-H., Lee, T.L. (2006). Cyclooxygenase-1 inhibition shortens the duration of diazepam-induced loss of righting reflex in mice. Anesthesia and Analgesia 102 (1) : 135-140. [email protected] Repository. https://doi.org/10.1213/01.ane.0000189102.09347. ...
Eicosanoids exert their cellular action through specific G-protein coupled receptors. Prostanoids are the products of cyclooxygenases action on C-20…
hypothetical protein, gbf1, Anapl_04335, AS27_01565, AS28_01193, C79137, C9orf15, CB1_000576027, D623_10025025, gamma-interferon-activated transcriptional element-binding factor 1, GATE-binding factor 1, GBF-1, H920_19196, I79_014770, M91_12705, M959_12051, MDA_GLEAN10019304, membrane-associated prostaglandin E synthase 2, membrane-associated prostaglandin E synthase-2, microsomal prostaglandin E synthase 2, microsomal prostaglandin E synthase-2, Mpges2, MPGES-2, mPGE synthase-2, N300_09271, N301_12743, N302_13172, N303_06092, N305_09010, N306_14810, N307_02442, N308_10508, N311_11677, N312_00533, N320_07005, N321_11509, N322_00413, N324_09565, N325_00199, N326_00389, N327_11175, N328_09700, N329_10988, N330_00570, N331_03110, N332_07603, N333_00239, N334_00603, N335_09322, N336_03658, N339_06101, N340_07113, N341_11017, PAL_GLEAN10012478, PANDA_003194, pges2, prostaglandin E receptor 2, prostaglandin E synthase 2-like protein, prostaglandin-H(2) E-isomerase, TREES_T100004307, UY3_04702, ...
Accepted name: prostaglandin-endoperoxide synthase. Reaction: arachidonate + reduced acceptor + 2 O2 = prostaglandin H2 + acceptor + H2O. Other name(s): prostaglandin synthase; prostaglandin G/H synthase; (PG)H synthase; PG synthetase; prostaglandin synthetase; fatty acid cyclooxygenase; prostaglandin endoperoxide synthetase. Systematic name: (5Z,8Z,11Z,14Z)-icosa-5,8,11,14-tetraenoate,hydrogen-donor:oxygen oxidoreductase. Comments: This enzyme acts both as a dioxygenase and as a peroxidase.. Links to other databases: BRENDA, EXPASY, KEGG, Metacyc, PDB, CAS registry number: 39391-18-9. References:. 1. DeWitt, D.L. and Smith, W.L. Primary structure of prostaglandin G/H synthase from sheep vesicular gland determined from the complementary DNA sequence. Proc. Natl. Acad. Sci. USA 85 (1988) 1412-1416. [PMID: 3125548]. 2. Ohki, S., Ogino, N., Yamamoto, S. and Hayaishi, O. Prostaglandin hydroperoxidase, an integral part of prostaglandin endoperoxide synthetase from bovine vesicular gland microsomes. ...
The potential role of arachidonic acid metabolism in the enhancement (promotion) of malignant transformation of C3H/M2 mouse fibroblasts by the tumor promoter 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was investigated using inhibitors of cyclooxygenase and lipoxygenase activities. The promoting effects of TCDD (1.5 pM) and of the reference tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA; 0.4 mM) on carcinogen (N-methyl-N′-nitro-N-nitrosoguanidine or 3-methylcholanthrene)-pre-treated fibroblasts was abolished by cotreatment with indomethacin, hydrocortisone, caffeic acid or nordihydroguaiaretic acid. A differential inhibition was found with N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide, a selective inhibitor of the cyclooxygenase isoenzyme COX-2: the promoting effect of TPA, but not that of TCDD, was abolished. Therefore, the role of the cyclooxygenase isoenzymes COX-1 and COX-2 during chronic exposure to TCDD was studied in more detail. Long-term treatment with TCDD (4-7 weeks) ...
Inflammation comprises the reaction of the body to injury, in which a series of changes of the terminal vascular bed, blood, and connective tissue tends to eliminate the injurious agent and to repair the damaged tissue. It is a complex process, which involves the release of diverse regulatory mediators. The current anti-inflammatory agents are challenged by multiple side effects and thus, new effective therapies are highly needed. The aim of this review is to summarize the described microsomal prostaglandin E synthase-1 (mPGES-1) inhibitors or transcriptional suppressors from medicinal plants, which could be an ideal approach in the management of inflammatory disorders, but need further clinical trials in order to be ultimately validated ...
This is the first study to demonstrate that a selective COX-2 inhibitor on top of standard therapy improves endothelial function and reduces markers of inflammation and oxidative stress in patients with coronary artery disease. Recognition that COX-2 is an inducible enzyme particularly associated with inflammation led to the development of selective COX-2 inhibitors that offer comparable efficacy and fewer unwanted side effects attributable to COX-1 inhibition, gastric ulceration in particular.1,2 Gastrointestinal safety of selective COX-2 inhibitors, however, may come at the cost of increased cardiovascular events, as suggested by the results of the VIGOR trial.5 Cardiovascular safety of coxibs was additionally challenged by studies in mice deficient in the PGI2 or TXA2 receptor.10 PGI2 receptor-deficient animals showed enhanced injury-induced vascular proliferation and platelet activation that was abolished in mice deficient of both PGI2 and TXA2 receptor, suggesting that PGI2 inhibition with ...
Cyclooxygenase 2 (COX-2) is a key enzyme in the transformation of arachidonic acidity to prostaglandins and COX-2 overexpression has an important function in carcinogenesis. modulation of USF transcriptional activity in the 5? upstream area from the COX-2 gene. Right here we discovered that apigenin treatment also elevated COX-2 mRNA balance as well as the inhibitory aftereffect of apigenin on UVB-induced luciferase reporter gene activity was reliant on the Saxagliptin AU-rich component of the COX-2 3?-untranslated area. Furthermore we discovered two RNA-binding protein HuR as well as the T-cell-restricted intracellular antigen 1-related proteins (TIAR) that have been connected with endogenous COX-2 mRNA in 308 keratinocytes and apigenin treatment elevated their localization to cell cytoplasm. Moreover Saxagliptin reduced amount of HuR amounts by little interfering RNA inhibited apigenin-mediated stabilization of COX-2 mRNA. Cells expressing decreased TIAR showed proclaimed level of resistance ...
The widespread consumption of diets rich in anthocyanin and catechin content prompted the evaluation of their in vitro inhibitory effects on cyclooxygenase (COX) enzymes and on the proliferation .... ...
When we considered all the randomised trial data, selective COX 2 inhibitors were associated with a highly significant 1.4-fold increased risk of serious vascular events, largely due to a twofold increased risk of myocardial infarction. Although we found no significant excesses in the incidence of stroke or vascular death, the confidence intervals for each were wide, so we could not exclude a clinically important excess. If, as some people have suggested (on the basis of the delayed divergence of survival curves), the hazard emerges only after a year or 18 months,4 5 then combining short term and long term trials might underestimate the effects of long term exposure to a selective COX 2 inhibitor. We were not able to assess time dependent variation in the rate ratio because we sought numbers of events and person time only for the whole period of follow-up in each trial. However, as figure 2 clearly shows, when all the long term trials are considered, the summary rate ratio is similar to that ...
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This page contains the abstract- Vitamin E and Macrophage Cyclooxygenase Regulation in the Aged http://www.chiro.org/nutrition/ABSTRACTS/Macrophage_Regulation.shtml
Elevated levels of systemic, liver-derived IGF-I and increased serum IGF-I:IGFBP-3 ratio have emerged as potential risk factors for cancers (19, 20, 21, 22) also known to frequently overexpress COX-2 (10 , 11 , 42, 43, 44) . Furthermore, as a recent study indicates, down-regulation of IGFBP-3 in stage I NSCLC predicts a shorter survival (45) . An IGF-autocrine growth loop also has been shown to operate in a number of tumor cell lines (26 , 46) . Therefore, we speculated that a functional link exists between tumor COX-2 and the IGF axis in NSCLC cells.. As hypothesized, COX-2 enhanced the IGF-related viability and proliferation of NSCLC cells (Figs. 1 ⇓ , 2 ⇓ , and 3 ⇓ ). The COX-2-enhanced viability and mitogenicity of IGFs in A549 cells were accompanied by the following: (1) facilitated autophosphorylation of IGF-IR (Fig. 3B) ⇓ ; (2) up-regulation of class IA PI3k signaling (Fig. 2) ⇓ ; and (3) down-regulation of IGFBP-3 expression (Fig. 6) ⇓ . All of these activities can be ...
Etodolac (Lodine) is a COX inhibitor with an IC50 of 53.5 nM. Find all the information about Etodolac (Lodine) for cell signaling research.
CYCLOOXYGENASE-2: Cyclooxygenase (COX), first purified in 1976 and cloned in 1988, is the key enzyme in the synthesis of prostaglandins (PGs) from arachidonic acid. In 1991, several laboratories identified a product from a second gene with COX activity and called it COX-2. However, COX-2 was inducible, and the inducing stimuli included pro-inflammatory cytokines and growth factors, implying a role for COX-2 in both inflammation and control of cell growth. The two isoforms of COX are almost identical in structure but have important differences in substrate and inhibitor selectivity and in their intracellular locations. Protective PGs, which preserve the integrity of the stomach lining and maintain normal renal function in a compromised kidney, are synthesized by COX-1. In addition to the induction of COX-2 in inflammatory lesions, it is present constitutively in the brain and spinal cord, where it may be involved in nerve transmission, particularly that for pain and fever. PGs made by COX-2 are ...
BACKGROUND: Microsomal prostaglandin (PG) E(2) synthase-1 (mPGES-1) catalyzes isomerization of the cyclooxygenase product PGH(2) into PGE(2). Deletion of mPGES-1 modulates experimentally evoked pain and inflammation and retards atherogenesis. The role of mPGES-1 in abdominal aortic aneurysm is unknown. METHODS AND RESULTS: The impact of mPGES-1 deletion on formation of angiotensin ...
Celecoxib belongs to the group of medications called selective COX-2 inhibitors, which is a kind of nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs work by reducing a substance in the body that leads to inflammation (swelling) and pain.
Celecoxib belongs to the group of medications called selective COX-2 inhibitors, which is a kind of nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs work by reducing a substance in the body that leads to inflammation (swelling) and pain.
Coxs Bazar will be a testing ground for the UN Secretary-Generals Prevention Agenda and for the concept of preventing violent extremism.
The expression of gonadotropin-releasing hormone (GNRH) receptor (GNRHR) and the direct role of GNRH1 on corpora lutea function were studied in Mediterranean buffalo during diestrus. Immunohistochemistry evidenced at early, mid, and late luteal stages the presence of GNRHR only in large luteal cells and GNRH1 in both small and large luteal cells. Real-time-PCR revealed GNRHR and GNRH1 mRNA at the three luteal stages, with lowest values in late corpora lutea. In vitro corpora lutea progesterone production was greater in mid stages and less in late luteal phases, while prostaglandin (PG) F2alpha (PGF2alpha) increased from early to late stages, and PGE2 was greater in the earlier-luteal phase. Cyclooxygenase 1 (prostaglandin-endoperoxide synthase 1, PTGS1) activity did not change during diestrus, while PTGS2 increased from early to late stages, and PGE2-9-ketoreductase (PGE2-9-K) was greater in late corpora lutea. PTGS1 activity was greater than PTGS2 in early corpora lutea and less in late luteal ...
Nonsteroidal anti-inflammatory drugs selective for inhibition of cyclooxygenase 2 (COX-2) were developed to conserve the analgesic and anti-inflammatory efficacy of older nonsteroidal anti-inflammatory drugs that inhibited cyclooxygenase 1 and COX-2, while reducing the likelihood of gastrointestinal adverse effects. Although this objective was broadly attained, COX-2 inhibitors, which turned out to include some older nonsteroidal anti-inflammatory drugs like diclofenac, also caused thrombotic events, hypertension, and cardiac failure attributable to suppression of COX-2-derived PGI2. The microsomal prostaglandin E synthase-1 (mPGES-1) enzyme is downstream of COX-2 and accounts for most of the prostaglandin E2 that is formed in humans. Some, but not all studies in mice lacking mPGES-1 suggest analgesic and anti-inflammatory efficacy similar to nonsteroidal anti-inflammatory drugs. Most, but not all studies suggest that unlike COX-2 disruption or inhibition, global mPGES-1 deletion does not ...
Inhibition of neuronal cyclooxygenase-2 (COX-2) and hence prostaglandin E2 (PGE2) synthesis by non-steroidal anti-inflammatory drugs has been suggested to protect neuronal cells in a variety of pathophysiological situations including Alzheimers disease and ischemic stroke. Ascorbic acid (vitamin C) has also been shown to protect cerebral tissue in a variety of experimental conditions, which has been attributed to its antioxidant capacity. In the present study, we show that ascorbic acid dose-dependently inhibited interleukin-1beta (IL-1beta)-mediated PGE2 synthesis in the human neuronal cell line, SK-N-SH. Furthermore, in combination with aspirin, ascorbic acid augmented the inhibitory effect of aspirin on PGE2 synthesis. However, ascorbic acid had no synergistic effect along with other COX inhibitors (SC-58125 and indomethacin). The inhibition of IL-1beta-mediated PGE2 synthesis by ascorbic acid was not due to the inhibition of the expression of COX-2 or microsomal prostaglandin E synthase ...
Background: Nonsteroidal anti-inflammatory drugs (NSAIDs) have been known to cause renal dysfunction in healthy patients and more pronounced renal effects in patients with cirrhosis and ascites. The use of NSAIDs have been associated with hepatorenal syndrome, a serious and often fatal complication associated with acute decline in renal function in the context of cirrhosis. However, renal safety of selective cyclo-oxygenase-2 (COX-2) and non-selective COX inhibitors has not been well delineated in current research with regards to patients with cirrhosis. This literature review seeks to compare the renal safety of selective and non-selective COX inhibitors in patients with cirrhosis. Methods: A thorough multi-database search was conducted using various combinations of keywords. Each study was evaluated using the Grading of Recommendations, Assessments, Development and Evaluation (GRADE) system. Results: Selective COX-2 inhibitor did not produce statistically significant decrements in renal function,
Prostaglandin E synthase (PGES) including isoenzymes of membrane-associated PGES (mPGES)-1, mPGES-2, and cytosolic PGES (cPGES) is the recently identified terminal enzyme of the arachidonic acid cascade. PGES converts prostaglandin (PG)H2 to PGE2 downstream of cyclooxygenase (COX). We investigated the expression of PGES isoenzyme in articular chondrocytes from patients with osteoarthritis (OA). Chondrocytes were treated with various cytokines and the expression of PGES isoenzyme mRNA was analyzed by the reverse transcription-polymerase chain reaction and Northern blotting, whereas Western blotting was performed for protein expression. The subcellular localization of mPGES-1 was determined by immunofluorescent microscopy. Conversion of arachidonic acid or PGH2 to PGE2 was measured by enzyme-linked immunosorbent assay. Finally, the expression of mPGES-1 protein in OA articular cartilage was assessed by immunohistochemistry. Expression of mPGES-1 mRNA in chondrocytes was significantly induced by
It is well-established that prostaglandins (PGs) affect tumorigenesis, and evidence indicates that PGs also are important for the reduced food intake and body weight loss, the anorexia-cachexia syndrome, in malignant cancer. However, the identity of the PGs and the PG producing cyclooxygenase (COX) species responsible for cancer anorexia-cachexia is unknown. Here, we addressed this issue by transplanting mice with a tumor that elicits anorexia. Meal pattern analysis revealed that the anorexia in the tumor-bearing mice was due to decreased meal frequency. Treatment with a non-selective COX inhibitor attenuated the anorexia, and also tumor growth. When given at manifest anorexia, non-selective COX-inhibitors restored appetite and prevented body weight loss without affecting tumor size. Despite COX-2 induction in the cerebral blood vessels of tumor-bearing mice, a selective COX-2 inhibitor had no effect on the anorexia, whereas selective COX-1 inhibition delayed its onset. Tumor growth was ...
Several lines of evidence support the role of COX-2-dependent PGE2 in colon tumorigenesis (Wang and Dubois, 2010). Thus, in FAP, the administration of the selective COX-2 inhibitor celecoxib (400 mg/b.i.d.) was associated with a significant reduction of the number of colorectal polyps by approximately one-third (Steinbach et al., 2000). However, marked variability in the response to celecoxib was noted (Steinbach et al., 2000). We hypothesized that the inhibition of vascular COX-2-dependent PGI2 may contribute to the variable response to celecoxib in this setting. In fact, PGI2 may control angiogenesis by preventing endothelial activation and platelet release of angiogenic factors present in α-granules (Menter et al., 1987). Thus, we performed the present study to investigate the biosynthesis of PGI2 and TXA2, two key mediators of CV homeostasis (Grosser et al., 2006), and PGE2, a well known mediator of inflammation and tumorigenesis (Wang and Dubois, 2010) in intestinal neoplasia. We aimed to ...
Microsomal prostaglandin E synthase-1 (mPGES-1) constitutes a drug target for inflammation, fever and pain. mPGES-1 catalyzes the biosynthesis of prostaglandin (PG) E2 from cyclooxygenase (Cox) -derived PGH2, which in turn is derived from arachidonic acid. mPGES-1 is mainly associated with inflammation and it is known to be up regulated by various pro-inflammatory cytokines like IL-1 beta and TNF-alpha. Mice devoid of mPGES-1 activity display resistance to development of experimental arthritis, fever, pain, symptoms following stroke, atherosclerosis and breathing anomalies induced by hypoxia. Conversely, the enzyme seems to have a protective role in wound healing and remodeling following myocardial infarction. Inhibitors of mPGES-1 have been developed by several groups. However, their characterization in animal models of inflammation, or other models previously used to study mPGES-1 knock-out mice, remains limited. One reason is the fact that a majority of the potent inhibitors of human mPGES-1 ...
Inducible cyclooxygenase (COX-2) has been implicated in the process of inflammation and carcinogenesis. Chamomile has long been used in traditional medicine for the treatment of inflammatory diseases. In this study we aimed to investigate whether chamomile interferes with the COX-2 pathway. MAIN METHODS: We used lipopolysaccharide (LPS)-activated RAW 264.7 macrophages as an in vitro model for our studies. KEY FINDINGS: Chamomile treatment inhibited the release of LPS-induced prostaglandin E(2) in RAW 264.7 macrophages. This effect was found to be due to inhibition of COX-2 enzyme activity by chamomile. In addition, chamomile caused reduction in LPS-induced COX-2 mRNA and protein expression, without affecting COX-1 expression. The non-steroidal anti-inflammatory drug, sulindac and a specific COX-2 inhibitor, NS398, were shown to act similarly in LPS-activated RAW 264.7 cells. Our data suggest that chamomile works by a mechanism of action similar to that attributed to non-steroidal ...
Preventive intervention of colorectal cancer has become essential as a major portion of the population may develop the disease at some points during their lives. Diet and nutrition play an important role during this multistep colon carcinogenic process. Inhibitory activity of aqueous suspensions of garlic and tomato, individually and in combination, were tested on azoxymethane induced colon carcinogenesis in Sprague-Dawley rats. The effect was observed on aberrant crypt foci (ACF), the preneoplastic lesion. To investigate the mechanism of action of the agents used, cell proliferation and the level of apoptosis were determined and the expression of cyclooxygenase-2 (COX-2) protein was analyzed in the colon. Following treatment, significant inhibition of the level of cell proliferation (P|0.01 in garlic; P|0.001 in tomato and P|0.001 in combination treatment group with respect to the carcinogen control group), significant induction of apoptosis (P|0.01 in garlic treated; P|0.01 in tomato treated and P|0
MAA699Hu22, PGG/HS; PGHS2; PHS2; HCox2; COX2; Cyclooxygenase 2; Prostaglandin G/H Synthase And Cyclooxygenase; Prostaglandin H2 synthase 2 | Products for research use only!
Malignant mesothelioma (MM) is an uncommon neoplasm that arises from the cells lining the body cavities, in particular the pleural and peritoneal cavities. The treatment of MM is a major challenge with frustrating results for clinicians and patients alike. Despite the adoption of newly developed radiotherapic and chemotherapic regimens, the prognosis remains dismal and only modest improvements have been obtained thus far. In this scenario, a better comprehension of the molecular patterns is of paramount importance. Cyclooxygenases catalyze the rate limiting step in the production of prostanoids. Accumulating data demonstrate that overexpression of these enzymes, and in particular of cyclooxygenases- 2, promotes multiple events involved in tumorigenesis; in addition, numerous studies show that inhibition of cyclooxygenases- 2 can delay or prevent certain forms of cancer. Aim of this review is to discuss the current state of the art in mesothelioma, with a particular emphasis on the recent ...
Synthesizing these two pieces of data, the researchers confirmed that individuals estimated to have high adenoma PGE2 levels at baseline, based on high COX-2 expression and/or absence of 15-PGDH, attained a 41% reduction in adenoma detection with Celecoxib treatment as opposed to placebo ( RR 0.59; p less than 0.0001 ...
Introduction Cyclooxygenase-2 (COX-2) is frequently over-expressed in primary breast cancer. In transgenic breast cancer models, over-expression of COX-2 leads to tumour formation while COX-2...
Several lines of evidence show that production of PGE2 is enhanced during inflammation, and this lipid mediator can dramatically modulate the immune response (43). Given these observations and because myeloid-derived cells produce large amounts of proinflammatory lipid mediators, we investigated COX expression, PGE2 synthesis, and cytokine production by BM-DC. We reported that production of AA-derived metabolites did not require the addition of exogenous substrate, because BM-DC are able to produce PGE2 and LTB4 under the two experimental conditions, and these APC express cytosolic PLA2, which catalyzes the release of endogenous AA from the cell membrane. The expression of cPLA2 is up-regulated by LPS in a dose-dependent fashion, and an important liberation of AA was observed in LPS-treated BM-DC compared with control cells. These data are consistent with previous studies, which reported induction of cPLA2 by LPS in human leukocytes (44, 45). Analysis of COX expression shows that resting BM-DC ...
Buy our Natural Sheep COX2 / Cyclooxygenase 2 protein. Ab81696 is a full length protein produced in Nativesyntheticaly and has been validated in WB. Abcam…
The present invention provides compositions and methods for the treatment of pain, inflammation or inflammation mediated disorders in a subject. More particularly, the invention provides a combination therapy for the treatment of pain, inflammation or inflammation mediated disorders comprising the administration to a subject of a potassium ion channel modulator in combination with a cyclooxygenase-2 selective inhibitor.
The use of nonsteroidal anti-inflammatory drugs (NSAIDs) may confer a long-term risk of adverse cardiovascular events, a Danish population study found.
Priva-Celecoxib: Celecoxib belongs to the group of medications called selective COX-2 inhibitors, which is a kind of nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs work by reducing a substance in the body that leads to inflammation (swelling) and pain.
Riva-Celecoxib: Celecoxib belongs to the group of medications called selective COX-2 inhibitors, which is a kind of nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs work by reducing a substance in the body that leads to inflammation (swelling) and pain.
S-2474 is an inhibitor of COX-2 and 5-lipoxygenase (5-LO), with IC50s of 11 nM and 27 μM for COX-2 and COX-1 in human intact cells, and used as a nonsteroidal anti-inflammatory drug. - Mechanism of Action & Protocol.
Breast, Breast Cancer, Cancer, Cyclooxygenase, Cyclooxygenase-2, Developed Countries, Disease, Disease-free Survival, Estrogen, Human, Matrix Metalloproteinase-2, Membrane, Metastasis, Mt1-mmp, Multivariate Analysis, Neoplasm, Patients, Progesterone, Progesterone Receptor, Prognosis
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COX1_DICDI (O21042 ), COX2_ACHDO (P29870 ), COX2_ACOIG (Q38S50 ), COX2_ACOWI (P50672 ), COX2_ADABI (P29871 ), COX2_AEDAE (P50692 ), COX2_AILFU (Q3L6W7 ), COX2_AILME (Q2Y0B9 ), COX2_ALBCA (P48889 ), COX2_ALBTU (Q09334 ), COX2_ALLMI (O47870 ), COX2_ALOPA (P98024 ), COX2_ANAPL (P98019 ), COX2_ANIIM (Q38S38 ), COX2_ANOGA (P34840 ), COX2_ANOQU (P33505 ), COX2_ANTAM (Q37369 ), COX2_AOTNI (Q7IC90 ), COX2_APIFL (P50267 ), COX2_APIKO (P50268 ), COX2_APILI (P20375 ), COX2_APOMY (Q38S35 ), COX2_APOSM (Q38S29 ), COX2_APOSY (P50673 ), COX2_APTAU (O03889 ), COX2_ARATH (P93285 ), COX2_ARTSF (Q37706 ), COX2_ARVSO (Q38S26 ), COX2_ASCSU (P24882 ), COX2_ASHGO (Q7YFV7 ), COX2_ATEMI (Q7J6G4 ), COX2_BACP3 (Q03438 ), COX2_BACPE (Q04441 ), COX2_BACSU (P24011 ), COX2_BALBO (Q599A0 ), COX2_BALMU (P41294 ), COX2_BALPH (P24986 ), COX2_BATGR (Q38S23 ), COX2_BERBO (Q38S20 ), COX2_BETVU (P98012 ), COX2_BISBI (Q37416 ), COX2_BISBO (P68296 ), COX2_BOSGA (P68295 ), COX2_BOSIN (P68553 ), COX2_BOSJA (P68294 ), COX2_BOSMU (P68554 ...
TY - JOUR. T1 - Subepithelial myofibroblasts express cyclooxygenase-2 in colorectal tubular adenomas. AU - Adegboyega, Patrick A.. AU - Ololade, Omiyosoye. AU - Saada, Jamal. AU - Mifflin, Randy. AU - Di Mari, John F.. AU - Powell, Don W.. PY - 2004/9/1. Y1 - 2004/9/1. N2 - Purpose: Recent data support the hypothesis that the inducible isoform of cyclooxygenase (COX-2) plays a role in the early stages of colonic carcinogenesis and that nonsteroidal anti-inflammatory drugs (NSAIDs) retard the development of colon cancer by modulating COX-2. However, the cell types responsible for producing COX-2 in colorectal adenomas remain a subject of controversy. Experimental Design: COX-2 expression in normal colonic mucosa (n = 50), hyperplastic polyps (n = 43), sporadic adenomas (n = 67), and invasive colonic adenocarcinoma (n = 39) was studied in formalin-fixed and paraffin-embedded tissue sections from endoscopy biopsy and colonic resection specimens. Immunohistochemistry (avidin-biotin complex technique ...
In recent years evidence has accumulated which suggests that prostaglandins are involved in spinal nociceptive processing. Several studies have shown that spinally-administered prostaglandins evoke characteristic pain behaviour in rats. Non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin, inhibit the enzyme cyclooxygenase (COX) and thus prevent the formation of prostaglandins. It has been hypothesised that a component of the analgesic properties of NSAIDs may be due to an action in the spinal cord, a theory which is supported by behavioural and electrophysiological studies. The current study shows by Western blotting that the two isoforms of COX, COX-1 and COX-2, are present in rat spinal cord tissue. Furthermore, using immunocytochemical techniques, we have localised COX-2-like immunoreactivity to regions of the spinal cord associated with nociceptive processing, namely the superficial and deep dorsal horn and around the central canal. Spinal COX-2, but not COX-1 is bilaterally ...
The results of this study demonstrate that single doses of celecoxib, a highly selective COX-2 inhibitor in vitro, are well tolerated by healthy volunteers. All doses inhibited LPS-stimulated monocyte PGE2 formation ex vivo, an index of COX-2 activity, to a degree that approximated that attained after 800 mg ibuprofen, a therapeutic dose of a nonselective, conventional NSAID. Although interindividual differences in response were apparent and the biochemical selectivity of Celecoxib for COX-2 was relative, rather than absolute, in humans, it did not influence TxA2-dependant platelet aggregation ex vivo. Surprisingly, celecoxib and ibuprofen had comparable suppressive effects on the excretion of PGI-M. Celecoxib also suppressed urinary 6-keto PGF1α. This implies a major role for COX-2 in the biosynthesis of both systemic and renal PGI2 under physiological conditions in young volunteers.. The two COX isoforms are distinct gene products prone to differential patterns of regulation (5-9, 13-17). ...
1. Health Technol Assess. 2008 Apr12(11):1-278, iii. Cyclooxygenase-2 selective non-steroidal anti-inflammatory drugs (etodolac, meloxicam, celecoxib, rofecoxib
NS-398 inhibits COX-2 enzyme activity in a concentration dependent manner, the IC50 being 3.8 μM, whereas NS-398 at 100μM has no effect on COX-1 activity[1]. At 10 μM, NS-398 treatment results in increased production of COX-2 and the pro-inflammatory cytokine. NS-398 (10 μM) induces apoptosis in LNCaP cells, but not in the more aggressive, androgen-unresponsive C4-2b cells. The C4-2b cells are observed to continue to proliferate when treated with NS-398 and continues to retain malignant phenotype characteristics. NS-398 treatment results in C4-2b cell differentiation into an unusual neuroendocrinelike cell. These neuroendocrine-like cells produces both epithelial (cytokeratin 18 and prostate specific antigen) and neuronal (neuron-specific enolase and chromogranin A) proteins. Furthermore, this C4-2b cellular response to NS-398 is mediated by NF-kB transcription factor activation. NS-398 induces NF-kB and down-regulates Ikβ-α protein expression in LNCaP C4-2b cells[2]. ...
A child with a fever is every parents nightmare and is usually the first indication that a child is ill.. Watching the thermometer steadily increasing, feeling the heat radiating from the child and the listlessness is a simply horrible experience for everyone.. What to do?. A common practice is to reach for the ibuprofen and dose the child up as quickly and as often as possible. But how efficacious and safe is this practice?. What is Ibuprofen?. Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID). Ibuprofen is commonly taken to alleviate mild to moderate pain and to minimise the impact of fever in children over 3 months of age.. Ibuprofen blocks the production of prostaglandins, substances our body releases in response to illness and injury. Ibuprofen blocks the enzyme cyclooxygenase that makes these prostaglandins, resulting in lower levels of prostaglandins being produced. As a consequence, inflammation, pain and fever are reduced.. Ibuprofens painkilling effects work very quickly ...
Fukai, A.; Kamekura, S.; Chikazu, D.; Nakagawa, T.; Hirata, M.; Saito, T.; Hosaka, Y.; Ikeda, T.; Nakamura, K.; Chung, U-il.; Kawaguchi, H., 2012: Lack of a chondroprotective effect of cyclooxygenase 2 inhibition in a surgically induced model of osteoarthritis in mice
Cheung S-Y, Werner M, Esposito L, Troisi F, Cantone V, Liening S, König S, Gerstmeier J, Koeberle A, Bilancia R, Rizza R, Rossi A, Roviezzo F, Temml V, Schuster D, Stuppner H, Schubert-Zsilavecz M, Werz O, Hanke T, Pace S (2018) Discovery of a benzenesulfonamide-based dual inhibitor of microsomal prostaglandin E2 synthase-1 and 5-lipoxygenase that favorably modulates lipid mediator biosynthesis in inflammation. Eur J Med Chem 156:815-830. ...
Cyclooxygenasen regulieren die Produktion von Prostaglandinen und spielen eine Rolle bei der Entstehung und Progression maligner Tumore. Versuche mit COX Inhibitoren (NSAIDs) zeigten im Tiermodell eine deutliche Reduktion von Inzidenz und Größe der Tumoren in einer dosisabhängigen Weise. Das Ziel der vorliegenden Arbeit war, das Expressionsmuster der induzierbaren Isoform COX-2 und der konstitutiven Isoform COX-1 im Mammakarzinom zu untersuchen. Die Grundlage der Untersuchung bildeten Tumorproben von 221 Patientinnen mit primärem Mammakarzinom. Diese wurden mittels immunhistochemischer Methoden auf beide COX-Isoenzyme untersucht. Eine erhöhte COX-2 Expression wurde in 36% der untersuchten Mammakarzinome festgestellt. Sie korrelierte signifikant mit verschiedenen klinisch-pathologischen Parametern, insbesondere mit einem positiven Lymphknotenstatus, einer geringen Differenzierung und einer Tumorgröße ,20 mm. Eine erhöhte COX-1 Expression wurde in 45% der untersuchten Tumoren gefunden und ...
Prognostic role of host cyclooxygenase and cytokine genotypes in a Caucasian cohort of patients with gastric adenocarcinoma. ...
Find patient medical information for Celecoxib Oral on WebMD including its uses, side effects and safety, interactions, pictures, warnings and user ratings.
Accepted name: 15-hydroxyprostaglandin dehydrogenase (NAD+). Reaction: (5Z,13E,15S)-11α,15-dihydroxy-9-oxoprost-5,13-dienoate + NAD+ = (5Z,13E)-11α-hydroxy-9,15-dioxoprost-5,13-dienoate + NADH + H+. Other name(s): NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (type I); PGDH; 11α,15-dihydroxy-9-oxoprost-13-enoate:NAD+ 15-oxidoreductase; 15-OH-PGDH; 15-hydroxyprostaglandin dehydrogenase; 15-hydroxyprostanoic dehydrogenase; NAD-specific 15-hydroxyprostaglandin dehydrogenase; prostaglandin dehydrogenase; 15-hydroxyprostaglandin dehydrogenase (NAD). Systematic name: (5Z,13E,15S)-11α,15-dihydroxy-9-oxoprost-5,13-dienoate:NAD+ 15-oxidoreductase. Comments: Acts on prostaglandin E2, F2α and B1, but not on prostaglandin D2. cf. EC 1.1.1.196 15-hydroxyprostaglandin-D dehydrogenase (NADP+) and EC 1.1.1.197 15-hydroxyprostaglandin dehydrogenase (NADP+).. Links to other databases: BRENDA, EXPASY, GTD, KEGG, Metacyc, PDB, CAS registry number: 9030-87-9. References:. 1. Änggård, E. and Samuelsson, ...
In this study, we demonstrate that curcumin exerts potent effects on the angiogenic properties of microvascular endothelial cells isolated from the human intestine, inhibiting multiple stages in the angiogenic process. We have demonstrated that (1) COX-2 induction as well as prostanoid production induced by VEGF were blocked by curcumin; (2) VEGF-induced growth, proliferation, transmigration and tube formation in HIMECs, an in vitro strategy for modelling angiogenesis, were also inhibited by curcumin; (3) the COX-2-specific inhibitor NS398, inhibited HIMEC growth, proliferation, transmigration and tube formation induced by VEGF; and (4) MAPK family members are involved in VEGF-induced upregulation of COX-2 and PGE2 production in HIMECs.. The cyclo-oxygenase enzymes COX-1 and COX-2 have been shown to play an important role in the regulation of angiogenesis.33 These enzymes catalyse the conversion of arachidonic acid to PGH2, the first step in the biosynthesis of the PGs thromboxane and ...
A dermally deliverable pharmaceutical composition comprises at least one selective cyclooxygenase-2 (COX-2) inhibitory drug or prodrug thereof solubilized in a pharmaceutically acceptable carrier that comprises a low molecular weight monohydric alcohol, and exhibits a skin permeation rate of the therapeutic agent at least equal to that exhibited by a reference solution of the therapeutic agent in 70% aqueous ethanol. A method of effecting targeted delivery of a selective COX-2 inhibitory drug to a site of pain and/or inflammation in a subject comprises topically administering such a composition to skin of the subject, preferably at a locus overlying or adjacent to the site of pain and/or inflammation. A method of effecting systemic treatment of a subject having a COX-2 mediated disorder comprises transdermally administering such a composition, preferably by contacting the composition with an area of skin of the subject not greater than about 400 cm2.
Varas-Lorenzo, C., Castellsague, J., Stang, M. R., Perez-Gutthann, S., Aguado, J. and Rodriguez, L. A. G. (2009), The use of selective cyclooxygenase-2 inhibitors and the risk of acute myocardial infarction in Saskatchewan, Canada . Pharmacoepidem. Drug Safe., 18: 1016-1025. doi: 10.1002/pds.1815 ...
Topical corticosteroids and topical nonsteroidal antiinflammatory drugs (NSAIDs) are the two main options at surgeons disposal for controlling postoperative ocular inflammation. While both drug classes decrease inflammation, they have different properties and different mechanisms of action.Steroids block the inflammatory cascade at an early stage: the arachidonic acid pathway activated by tissue damage. But to be effective, steroids need to pass through cell membranes and enter the nucleus, which is limited because of their lipophobic nature. In addition, steroid side effects include intraocular pressure (IOP) elevation, delayed wound healing, and increased susceptibility to infection.NSAIDs block cyclooxygenase (COX-1 and COX-2), enzymes that convert arachidonic acid into the prostaglandins that directly mediate inflammation. NSAIDs enter cells readily and effectively shut down prostaglandin formation; within its class, the brominated NSAID bromfenac penetrates cells particularly well. ...
The present study was performed to investigate the effects of chronic administration of nonylphenol (NP) on the expression of inflammation-related genes in the brains of mice. NP was given orally by gavages at 0, 50, 100, and 200 mg/kg/d. The expression of inflammatory enzymes, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), was evaluated by immunohistochemistry and immunoblotting assays. The nitric oxide (NO) level and nitric oxide synthase (NOS) activity were also measured by biochemical analyses. The results showed that NP at a high dose (200 mg/kg/d) significantly increased the expression of iNOS and COX-2 in both the hippocampus and cortex. In parallel with the increase in iNOS expression, the NO level was significantly greater at the dose of 200 mg/kg/d, compared to the control. The activity of NOS was also increased in the brain of mice at the dose of 100 and 200 mg/kg/d. These findings demonstrate that NP may have the potential to induce the chronic inflammation or cause
Th17 cells are critically involved in autoimmune disease induction and severity. Recently, we showed that Th17 cells from patients with rheumatoid arthritis (RA) directly induced a proinflammatory loop upon interaction with RA synovial fibroblasts (RASF), including increased autocrine IL-17A production. To unravel the mechanism driving this IL-17A production, we obtained primary CD4+CD45RO+CCR6+ (Th17) cells and CD4+CD45RO+CCR6− (CCR6−) T cells from RA patients or healthy individuals and cocultured these with RASF. IL-1β, IL-6, IL-23p19, and cyclooxygenase (COX)-2 expression and PGE2 production in Th17-RASF cultures were higher than in CCR6− T cell-RASF cultures. Cytokine neutralization showed that IL-1β and IL-6, but not IL-23, contributed to autocrine IL-17A induction. Importantly, treatment with celecoxib, a COX-2 inhibitor, resulted in significantly lower PGE2 and IL-17A, but not IFN-γ, production. Combined celecoxib and TNF-α blockade more effectively suppressed the ...
BioAssay record AID 162654 submitted by ChEMBL: Inhibitory activity against human recombinant Prostaglandin G/H synthase 2 expressed in microsomes taken from baculovirus infected Sf9 cells.
A 740003 tumor development and angiogenesis had been first examined using sarcoma 180 cells that are allogeneic for ddy mice (Fig. 1) . In charge ddy mice treated with automobile solid tumors had been obvious 14 d after cell implantation. Daily oral administration of SC-560 the inhibitor functioning on COX-1 had simply no significant influence on tumor mass selectively. On the other hand the COX-2-selective inhibitors JTE-522 and NS-398 considerably decreased tumor mass as do aspirin a non-selective COX inhibitor (Fig. 1 A and D). The level of tumor-induced angiogenesis was evaluated based on hemoglobin items (Fig. 1 C) which correlated well using the vascular thickness in the tumor under histological evaluation (Fig. 1 B). In keeping with the proclaimed red color from the tumors angiogenesis was significant in vehicle-treated mice (Fig. 1 C and B. Like the results in tumor mass angiogenesis was significantly decreased by treatment with COX-2 inhibitors or aspirin however not with SC-560 (Fig. 1 ...
Looking for online definition of prostaglandin endoperoxide synthase in the Medical Dictionary? prostaglandin endoperoxide synthase explanation free. What is prostaglandin endoperoxide synthase? Meaning of prostaglandin endoperoxide synthase medical term. What does prostaglandin endoperoxide synthase mean?
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Decreasing tumor-induced immune suppression. Secreted proteins released by tumors that lead to immune escape can be targets to monoclonal antibody blockade. For example, the anti-VEGF antibody bevacizumab, in addition to its effect of tumor vasculature, may decrease VEGF-induced inhibition of DC and T-cell function (32). Monoclonal antibodies to transforming growth factor-β and IL-10 are also potential means to reverse immune escape induced by tumor-released molecules. In addition, anti-inflammatory drugs such as aspirin and other nonsteroidal anti-inflammatory drugs, including the specific cyclooxygenase-2 inhibitor celecoxib, could be means to inhibit cyclooxygenase-2 that leads to prostaglandin E2 production (33).. Depletion of immunosuppressive cells. T regulatory cells, myeloid suppressor cells, and IDO-positive plasmacytoid DC have emerged as major immunosuppressive cells reported to be implicated in escape of tumors from immune control (34, 35). Depletion of CD4/CD25/FoxP3-positive ...

Alzforum: 
    AlzRisk Risk Factor DiscussionAlzforum: AlzRisk Risk Factor Discussion

The two COX isoforms appear to play different roles in neuroinflammation. COX-1 (inhibited only by traditional NSAIDs such as ... COX-1 and COX-2), which catalyze the synthesis of prostaglandins.. ... COX-2, but not COX-1, activity is necessary for the induction of perforant path long-term potentiation and spatial learning in ... COX-2 (inhibited by the selective COX-2 inhibitors like celecoxib and rofecoxib, as well as by traditional NSAIDs) is expressed ...
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Alzforum: 
    AlzRisk Risk Factor DiscussionAlzforum: AlzRisk Risk Factor Discussion

The two COX isoforms appear to play different roles in neuroinflammation. COX-1 (inhibited only by traditional NSAIDs such as ... COX-1 and COX-2), which catalyze the synthesis of prostaglandins.. ... COX-2, but not COX-1, activity is necessary for the induction of perforant path long-term potentiation and spatial learning in ... COX-2 (inhibited by the selective COX-2 inhibitors like celecoxib and rofecoxib, as well as by traditional NSAIDs) is expressed ...
more infohttp://szgene.org/riskfactordoc.aspx?rfid=13

COX-2 inhibitor - WikipediaCOX-2 inhibitor - Wikipedia

... cyclooxygenase. Prostaglandins whose synthesis involves the cyclooxygenase-I enzyme, or COX-1, are responsible for maintenance ... 170-fold more potent in inhibiting COX-1 than COX-2. Studies of meloxicam 7.5 mg per day for 23 days find a level of gastric ... "Evaluation of natural products on inhibition of inducible cyclooxygenase (COX-2) and nitric oxide synthase (iNOS) in cultured ... Some COX-2 inhibitors are used in a single dose to treat pain after surgery. Etoricoxib appears as good as if not better than ...
more infohttps://en.wikipedia.org/wiki/COX-2_inhibitor

Discovery and development of cyclooxygenase 2 inhibitors - WikipediaDiscovery and development of cyclooxygenase 2 inhibitors - Wikipedia

Cyclooxygenases have two main isoforms that are called COX-1 and COX-2 (as well as a COX-3). COX-1 is responsible for the ... COX enzyme proved to be difficult to purify and was not sequenced until 1988. In 1991 the existence of the COX-2 enzyme was ... The side-chain of Leu384, at the top of the receptor channel, is oriented into the active site of COX-1, but, in COX-2, it is ... The same laboratory showed that this gene truly expressed a novel COX enzyme. The two enzymes were renamed COX-1, referring to ...
more infohttps://en.wikipedia.org/wiki/Discovery_and_development_of_cyclooxygenase_2_inhibitors

COX-2 inhibitor - WikipediaCOX-2 inhibitor - Wikipedia

Prostaglandins whose synthesis involves the cyclooxygenase-I enzyme, or COX-1, are responsible for maintenance and protection ... 170-fold more potent in inhibiting COX-1 than COX-2.[32] Studies of meloxicam 7.5 mg per day for 23 days find a level of ... "COX-2 Inhibitors and Cancer". Fact Sheet. United States National Cancer Institute. Archived from the original on May 9, 2008.. ... COX-2 up-regulation has also been linked to the phosphorylation and activation of the E3 ubiquitin ligase HDM2, a protein that ...
more infohttps://en.wikipedia.org/wiki/COX_inhibitor

Cyclooxygenase-2 inhibitors: promise or peril?Cyclooxygenase-2 inhibitors: promise or peril?

... Laurel J. Mengle-Gaw and Benjamin D. Schwartz ... Laurel J. Mengle-Gaw and Benjamin D. Schwartz, "Cyclooxygenase-2 inhibitors: promise or peril?," Mediators of Inflammation, vol ...
more infohttps://www.hindawi.com/journals/mi/2002/864195/cta/

Cox-2 - Drugs.comCox-2 - Drugs.com

A list of US medications equivalent to Cox-2 is available on the Drugs.com website. ... Cox-2 is a medicine available in a number of countries worldwide. ... Cox-2 may be available in the countries listed below.. Ingredient matches for Cox-2. Celecoxib. Celecoxib is reported as an ...
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Transgenic cyclooxygenase-2 overexpression sensitizes mouse skin for carcinogenesis | PNASTransgenic cyclooxygenase-2 overexpression sensitizes mouse skin for carcinogenesis | PNAS

a) COX isozyme expression in epidermis from wt mice and the transgenic lines K5.COX-2/19+/− (19) and K5.COX-2/667+/− (667). (b ... Although COX-1 expression does not change in the course of tumor development, aberrant expression of COX-2 is also a consistent ... In contrast to the constitutively and ubiquitously expressed COX-1, COX-2 is not expressed in most tissues but becomes ... Nonsteroidal antiinflammatory drugs (NSAIDs) prevent prostaglandin (PG) biosynthesis through inhibition of cyclooxygenase (COX ...
more infohttps://www.pnas.org/content/99/19/12483?ijkey=279082762c89da4ffaa8b609f69cbcbe32ce15b6&keytype2=tf_ipsecsha

Cox 2 Inhibitor News, ResearchCox 2 Inhibitor News, Research

Cox 2 Inhibitor News and Research. RSS Cox-2 Inhibitors are nonsteroidal anti-inflammatory drugs used to relieve pain and ... The cyclooxygenase-2 enzyme is just such a protein, as the concentration of COX-2 is greater in cancer cells than in adjacent ... COX-2 inhibitor extends sunitinib activity in renal cell carcinoma The effectiveness of sunitinib for the treatment of renal ... COX-2 inhibitors are being studied in the prevention of colon polyps, and as anticancer drugs. Also called cyclo-oxygenase-2 ...
more infohttps://www.news-medical.net/?tag=/Cox-2+Inhibitor

Glycosylation regulates turnover of cyclooxygenase-2.Glycosylation regulates turnover of cyclooxygenase-2.

... Sevigny M.B., Li C.F., Alas M., Hughes-Fulford M. ... COS-1 cells transfected with the mutant gene were unable to express the 74kDa glycoform and were found to accumulate more COX-2 ... Cyclooxygenase-2 (COX-2) catalyzes the rate-limiting step in the prostanoid biosynthesis pathway, converting arachidonic acid ... Thus, COX-2 turnover appears to depend upon glycosylation of the 72kDa glycoform. ...
more infohttp://www.uniprot.org/citations/17113084

COX-2 | ALZFORUMCOX-2 | ALZFORUM

If you know of any papers that use this antibody, please contact us at antibodies [at] alzforum [dot] org for consideration in the References section.. ...
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Role of cyclooxygenase 2 in acute spinal cord injury.  - PubMed - NCBIRole of cyclooxygenase 2 in acute spinal cord injury. - PubMed - NCBI

Role of cyclooxygenase 2 in acute spinal cord injury.. Resnick DK1, Graham SH, Dixon CE, Marion DW. ... COX-2 was expressed in the normal adult rat spinal cord. COX-2 mRNA and protein production were increased following injury with ... Cyclooxygenase, or prostaglandin G/H synthase, is the rate-limiting step in the production of prostaglandins. A new isoform, ... Selective inhibition of COX-2 activity with SC58125 resulted in improved mean Basso, Beattie, and Bresnahan scores in animals ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/9872457

COX-2 expression in pseudomyxoma peritonei.  - PubMed - NCBICOX-2 expression in pseudomyxoma peritonei. - PubMed - NCBI

COX-2 expression in pseudomyxoma peritonei.. Gatalica Z1, Loggie B.. Author information. 1. Department of Pathology, Creighton ... COX-2 expression was studied using an immunohistochemical method in 75 patients with pseudomyxoma peritonei (PMP). Twenty-five ... In addition, COX-2 was detected in stromal, endothelial, inflammatory cells and reactive mesothelium. This preliminary ... COX-2 was expressed in neoplastic mucinous epithelium of 30 cases (40%): 20 in PMCA (40%), 10 in DPAM (40%). Weak COX-2 ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/16427185

Cyclooxygenase-2 expression in human colon cancer cells increases metastatic potential | PNASCyclooxygenase-2 expression in human colon cancer cells increases metastatic potential | PNAS

Two isoforms for COX have been described, COX-1 and COX-2. We and others have shown that COX-2 levels are markedly increased in ... Two isoforms of COX have been characterized, COX-1 and COX-2. COX-2 is expressed at high levels in intestinal tumors in humans ... Two COX isoforms have been characterized, COX-1 and COX-2. COX-1 is expressed in normal intestine, but its levels do not change ... COX,. cyclooxygenase;. NSAID,. nonsteroidal antiinflammatory drug;. MMP-2,. metalloproteinase-2;. MT MMP,. membrane-type ...
more infohttps://www.pnas.org/content/94/7/3336?ijkey=e424c58772e5981d30fcce89688b119c125aa7c5&keytype2=tf_ipsecsha

Castigata Dal Boss 2 by Samantha Cox (eBook) - LuluCastigata Dal Boss 2 by Samantha Cox (eBook) - Lulu

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Efficacy and safety of COX 2 inhibitors | The BMJEfficacy and safety of COX 2 inhibitors | The BMJ

Two large pivotal trials have been published, in which the efficacy and safety of the COX 2 inhibitors celecoxib and rofecoxib ... Efficacy and safety of COX 2 inhibitors New data are encouraging but the risk:benefit ratio remains unclear ... with more specific inhibitory effects on cyclo-oxygenase 2 (COX 2) pathways, promised equivalent efficacy with greater safety ... Efficacy and safety of COX 2 inhibitors. BMJ 2002; 325 doi: https://doi.org/10.1136/bmj.325.7365.607 (Published 21 September ...
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Expression der Cyclooxygenase-2 im MammakarzinomExpression der Cyclooxygenase-2 im Mammakarzinom

Cyclooxygenases regulate the production of prostaglandins and play a role in tumor development and progression. COX-inhibitors ... In this study, we investigated the prognostic impact of expression of both COX-isoforms as well as the association of COX ... Diese wurden mittels immunhistochemischer Methoden auf beide COX-Isoenzyme untersucht. Eine erhöhte COX-2 Expression wurde in ... The expression of COX-1 and -2 was determined by immunohistochemistry retrospectivly in a cohort of 221 women. An elevated ...
more infohttps://edoc.hu-berlin.de/handle/18452/15897

Patent US6696477 - Heterocyclo substituted hydroxamic acid derivatives as cyclooxygenase-2 and ... - Google PatentsPatent US6696477 - Heterocyclo substituted hydroxamic acid derivatives as cyclooxygenase-2 and ... - Google Patents

... compositions and methods for treating disorders mediated by cyclooxygenase-2 or 5-lipoxygenase, such as inflammation. Compounds ... a. Preparation of recombinant COX baculoviruses. Recombinant COX-1 and COX-2 were prepared as described by Gierse et al, [J. ... Evaluation of COX-1 and COX-2 activity in vitro. The compounds of this invention exhibited inhibition in vitro of COX-2. The ... b. Assay for COX-1 and COX-2 and COX-2 activity ... to generate the baculovirus transfer vectors for COX-1 and COX- ...
more infohttp://www.google.com/patents/US6696477?dq=6480844

Prognostic significance of cyclooxygenase-2 protein in pancreatic cancer: a meta-analysis | SpringerLinkPrognostic significance of cyclooxygenase-2 protein in pancreatic cancer: a meta-analysis | SpringerLink

COX-2) protein and the prognosis of pancreatic cancer. The following electronic... ... We conducted a meta-analysis of relevant cohort studies to investigate the relationships between cyclooxygenase-2 ( ... Cyclooxygenase in normal human tissues-is COX-1 really a constitutive isoform, and COX-2 an inducible isoform? J Cell Mol Med. ... shRNA-targeted cyclooxygenase (COX)-2 inhibits proliferation, reduces invasion and enhances chemosensitivity in laryngeal ...
more infohttps://link.springer.com/article/10.1007/s13277-014-2260-y

Cox-2 inhibitor | Define Cox-2 inhibitor at Dictionary.comCox-2 inhibitor | Define Cox-2 inhibitor at Dictionary.com

Cox-2 inhibitor definition at Dictionary.com, a free online dictionary with pronunciation, synonyms and translation. Look it up ... cox-2 inhibitor in Medicine Expand. COX-2 inhibitor n. Any of a class of nonsteroidal anti-inflammatory drugs thought to have ...
more infohttp://www.dictionary.com/browse/cox-2-inhibitor

Natural Sheep COX2 / Cyclooxygenase 2 protein (ab81696)Natural Sheep COX2 / Cyclooxygenase 2 protein (ab81696)

Cyclooxygenase 2 protein. Ab81696 is a full length protein produced in Nativesyntheticaly and has been validated in WB. Abcam… ... References for Natural Sheep COX2 / Cyclooxygenase 2 protein (ab81696). ab81696 has not yet been referenced specifically in any ... Natural Sheep COX2 / Cyclooxygenase 2 protein. See all COX2 / Cyclooxygenase 2 proteins and peptides. ...
more infohttp://www.abcam.com/natural-sheep-cox2-cyclooxygenase-2-protein-ab81696.html

Recombinant Human COX2 / Cyclooxygenase 2 protein (ab159280)Recombinant Human COX2 / Cyclooxygenase 2 protein (ab159280)

Cyclooxygenase 2 protein. Ab159280 is a full length protein produced in Wheat germ and has been validated in WB, ELISA. Abcam… ... Recombinant Human COX2 / Cyclooxygenase 2 protein. See all COX2 / Cyclooxygenase 2 proteins and peptides. ...
more infohttps://www.abcam.com/recombinant-human-cox2-cyclooxygenase-2-protein-ab159280.html

COX-2 gene promoter haplotypes and prostate cancer risk.  - PubMed - NCBICOX-2 gene promoter haplotypes and prostate cancer risk. - PubMed - NCBI

COX-2 gene promoter haplotypes and prostate cancer risk.. Panguluri RC1, Long LO, Chen W, Wang S, Coulibaly A, Ukoli F, Jackson ... Cyclooxygenase-2 (COX-2) is a key rate-limiting enzyme that converts arachidonic acid into pro-inflammatory prostaglandins. COX ... Three of the SNPs in the promoter region of COX-2 gene create at least three putative transcription factor binding sites and ... However, little is known about the role that sequence variation of the COX-2 gene contributes to prostate cancer. Thus, we ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/14754878

COX-2 inhibitors and gastroduodenal toxicity: Major clinical trialsCOX-2 inhibitors and gastroduodenal toxicity: Major clinical trials

Two related isoforms of the cyclo-oxygenase (COX) enzyme have been described: COX-1 (PGHS-1) and COX-2 (PGHS-2). COX-1 is ... COX-2 inhibitors and gastroduodenal toxicity: Major clinical trials. Author. Mark Feldman, MD, MACP, AGAF, FACG. Mark Feldman, ... COX-2 inhibitors. Lancet 1999; 353:307.. *Simon LS, Weaver AL, Graham DY, et al. Anti-inflammatory and upper gastrointestinal ... Other COX-2 inhibitors are available in some countries. Parecoxib is a prodrug that is converted to valdecoxib. Etoricoxib and ...
more infohttp://www.uptodate.com/contents/pulse-oximetry-in-adults/abstract/10
  • An elevated expression of COX-2 as the inducible form of the cyclooxygenases was detected in 36% of tumors and was significantly associated with several clinicopathological parameters, for example positive nodal status, poor differentiation and larger tumor size. (hu-berlin.de)
  • Genetic and pharmacological evidence suggests that overexpression of cyclooxygenase-2 (COX-2) is critical for epithelial carcinogenesis and provides a major target for cancer chemoprevention by nonsteroidal antiinflammatory drugs. (pnas.org)
  • To delineate COX-2 functions for carcinogenesis, we have used the initiation-promotion model ( 2 ) for the induction of skin tumors in wild-type (wt) NMRI mice and COX-2 transgenic mouse lines. (pnas.org)
  • COX-2 is expressed at high levels in intestinal tumors in humans and rodents. (pnas.org)
  • 7 COX-2 exerts an angiogenic effects in tumors 8,9 and in corneal neovascularization. (ahajournals.org)
  • In contrast to the constitutively and ubiquitously expressed COX-1, COX-2 is not expressed in most tissues but becomes transiently induced in response to growth factors, proinflammatory cytokines, mechanical tissue damage, and UV light ( 1 , 3 ). (pnas.org)
  • An elevated expression of COX-1 had no significant influence on patient prognosis. (hu-berlin.de)
  • Our findings provide empirical evidence that abnormal COX-2 expression may be strongly correlated with poor prognosis for patients with pancreatic cancer. (springer.com)
  • Although COX-1 expression does not change in the course of tumor development, aberrant expression of COX-2 is also a consistent feature of nonmelanoma skin cancer in man and mice. (pnas.org)
  • Data from gene knockout ( 13 , 14 ) and transgenic mice ( 15 , 16 ) provide support for the hypothesis that there is a causal relationship between COX-2 overexpression and tumor development. (pnas.org)
  • The Caco-2 cells, which constitutively expressed COX-2, acquired increased invasiveness compared with the parental Caco-2 cells or the vector transfected control cells. (pnas.org)
  • We found that the Caco-2 cells, programmed to constitutively expressed COX-2, acquired increased invasiveness compared with the parental Caco-2 cells or the vector transfected control cells. (pnas.org)
  • Some of these analogs retained COX-2 inhibitory activity, whereas many others didn't. (wikipedia.org)
  • Conclusion- These findings point to an important role for COX-2 in ischemic proliferative retinopathy, as in diabetes. (ahajournals.org)
  • As shown here, overexpression of COX-2 targeted to basal keratinocytes contributes to skin-tumor promotion and progression by establishing an autopromoted skin phenotype, i.e., the initiating dose of DMBA is sufficient to induce skin carcinogenesis in COX-2 transgenic mice. (pnas.org)
  • however, COX-2 is undetectable in normal intestine ( 15 ) and its levels are elevated in up to 85% of colorectal adenocarcinomas ( 16 - 18 ). (pnas.org)
  • COX-2 appears to be related to cancers and abnormal growths in the intestinal tract. (wikipedia.org)
  • Zhang H, Xu Y, Zhang Z, Liu R, Ma B. Association between COX-2 rs2745557 polymorphism and prostate cancer risk: a systematic review and meta-analysis. (springer.com)
  • Methods and Results- We describe here that COX-2 is induced in retinal astrocytes in human diabetic retinopathy, in the murine and rat model of ischemic proliferative retinopathy in vivo, and in hypoxic astrocytes in vitro. (ahajournals.org)