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Artykuły w czasopismach na temat „Cox”

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Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 1 sierpnia 2024

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1

Zada, Muhammad, Desalegn Demise Sage, Qiuyue Zhang, Yanping Ma, Gregory A. Solan, Yang Sun i Wen-Hua Sun. "Thermally Stable and Highly Efficient N,N,N-Cobalt Olefin Polymerization Catalysts Affixed with N-2,4-Bis(Dibenzosuberyl)-6-Fluorophenyl Groups". Catalysts 12, nr 12 (2.12.2022): 1569. http://dx.doi.org/10.3390/catal12121569.

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The cobalt(II) chloride N,N,N-pincer complexes, [2-{(2,4-(C15H13)2-6-FC6H2)N=CMe}-6-(ArN=CMe)C5H3N]CoCl2 (Ar = 2,6-Me2C6H3) (Co1), 2,6-Et2C6H3 (Co2), 2,6-i-Pr2C6H3 (Co3), 2,4,6-Me3C6H2 (Co4), 2,6-Et2-4-MeC6H2 (Co5), and [2,6-{(2,4-(C15H13)2-6-FC6H2)N=CMe}2C5H3N]CoCl2 (Co6), each containing at least one N-2,4-bis(dibenzosuberyl)-6-fluorophenyl group, were synthesized in good yield from their corresponding unsymmetrical (L1–L5) and symmetrical bis(imino)pyridines (L6). The molecular structures of Co1 and Co2 spotlighted their distorted square pyramidal geometries (τ5 value range: 0.23–0.29) and variations in steric hindrance offered by the dissimilar N-aryl groups. On activation with either MAO or MMAO, Co1–Co6 all displayed high activities for ethylene polymerization, with levels falling in the order: Co1 > Co4 > Co5 > Co2 > Co3 > Co6. Indeed, the least sterically hindered 2,6-dimethyl Co1 in combination with MAO exhibited a very high activity of 1.15 × 107 g PE mol−1 (Co) h−1 at the operating temperature of 70 °C, which dropped by only 15% at 80 °C and 43% at 90 °C. Vinyl-terminated polyethylenes of high linearity and narrow dispersity were generated by all catalysts, with the most sterically hindered, Co3 and Co6, producing the highest molecular weight polymers [Mw range: 30.26–33.90 kg mol−1 (Co3) and 42.90–43.92 kg mol−1 (Co6)]. In comparison with structurally related cobalt catalysts, it was evident that the presence of the N-2,4-bis(dibenzosuberyl)-6-fluorophenyl groups had a limited effect on catalytic activity but a marked effect on thermal stability.

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Guo, Jingjing, Zheng Wang, Wenjuan Zhang, Ivan Oleynik, Arumugam Vignesh, Irina Oleynik, Xinquan Hu, Yang Sun i Wen-Hua Sun. "Highly Linear Polyethylenes Achieved Using Thermo-Stable and Efficient Cobalt Precatalysts Bearing Carbocyclic-Fused NNN-Pincer Ligand". Molecules 24, nr 6 (25.03.2019): 1176. http://dx.doi.org/10.3390/molecules24061176.

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Six examples of 2-(1-arylimino)ethyl-9-arylimino-5,6,7,8-tetrahydrocycloheptapyridine-cobalt(II) chloride complexes, [2-(1-ArN)C2H3-9-ArN-5,6,7,8-C5H8C5H3N]CoCl2, (Ar = 2-(C5H9)-6-MeC6H3 Co1, 2-(C6H11)-6-MeC6H3 Co2, 2-(C8H15)-6-MeC6H3 Co3, 2-(C5H9)-4,6-Me2C6H2 Co4, 2-(C6H11)-4,6-Me2C6H2 Co5, and 2-(C8H15)-4,6-Me2C6H2 Co6), were synthesized by the direct reaction of the corresponding ortho-cycloalkyl substituted carbocyclic-fused bis(arylimino)pyridines (L1–L6) and cobalt(II) chloride in ethanol with good yields. All the synthesized ligands (L1–L6) and their corresponding cobalt complexes (Co1–Co6) were fully characterized by FT-IR, 1H/13C-NMR spectroscopy and elemental analysis. The crystal structure of Co2 and Co3 revealed that the ring puckering of both the ortho-cyclohexyl/cyclooctyl substituents and the one pyridine-fused seven-membered ring; a square-based pyramidal geometry is conferred around the metal center. On treatment with either methylaluminoxane (MAO) or modified methylaluminoxane (MMAO), all the six complexes showed high activities (up to 4.09 × 106 g of PE mol−1 (Co) h−1) toward ethylene polymerization at temperatures between 20 °C and 70 °C with the catalytic activities correlating with the type of ortho-cycloalkyl substituent: Cyclopentyl (Co1 and Co4) > cyclohexyl (Co2 and Co5) > cyclooctyl (Co3 and Co6) for either R = H or Me and afforded strictly linear polyethylene (Tm > 130 °C). The narrow unimodal distributions of the resulting polymers are consistent with single-site active species for the precatalyst. Furthermore, compared to the previously reported cobalt analogues, the titled precatalysts exhibited good thermo-stability (up to 70 °C) and possessed longer lifetime along with a higher molecular weight of PE (Mw: 9.2~25.3 kg mol−1).

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3

Domoki, Ferenc, James V. Perciaccante, Roland Veltkamp, Greg Robins, Ferenc Bari, Thomas M. Louis i David W. Busija. "Cycloheximide rapidly inhibits cortical COX activity and COX-dependent pial arteriolar dilation in piglets". American Journal of Physiology-Heart and Circulatory Physiology 277, nr 3 (1.09.1999): H1113—H1118. http://dx.doi.org/10.1152/ajpheart.1999.277.3.h1113.

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We have previously shown that cycloheximide (CHX) preserved neuronal function after global cerebral ischemia in piglets, in a manner similar to indomethacin. To elucidate the mechanism of this protection, we tested the hypothesis that CHX would inhibit cyclooxygenase (COX) activity in the piglet cerebral cortex and vasculature. Pial arteriolar responses to hypercapnia, arterial hypotension, and sodium nitroprusside (SNP) were determined before and 20 min after treatment with CHX (0.3–1 mg/kg iv) using a closed cranial window and intravital microscopy. We also determined baseline and arachidonic acid (AA)-stimulated cortical PGF2αand 6-keto-PGF1α production before and 20–60 min after CHX (1 mg/kg iv) treatment, using ELISA kits. CHX did not affect baseline diameters (∼100 μm) but significantly decreased arteriolar dilation to COX-dependent stimuli, such as hypercapnia and hypotension, but not to COX-independent SNP. In the 1 mg/kg CHX-treated group, increases in vascular diameters were reduced from 22 ± 2 to 10 ± 2%, from 49 ± 5 to 31 ± 3% (means ± SE, 5 and 10% CO2, respectively, n = 8), from 12 ± 3 to 3 ± 1%, and from 26 ± 5 to 6 ± 2% (∼25 and 40% decreases in blood pressure, respectively, n = 6). CHX also inhibited conversion of exogenous AA to both PGF2αand 6-keto-PGF1α; for example, 20 min after CHX treatment 10 μg/ml AA-stimulated PGF2α concentrations in the artificial cerebrospinal fluid decreased from 14.28 ± 3.04 to 5.90 ± 1.26 ng/ml ( n = 9). Thus CHX rapidly decreases COX activity in the piglet cerebral cortex. This result may explain in part the preservation of neuronal function of CHX in cerebral ischemia.

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4

de Oliveira, Ricardo Cunha, Sávio Pinho dos Reis i Giovanna C. Cavalcante. "Mutations in Structural Genes of the Mitochondrial Complex IV May Influence Breast Cancer". Genes 14, nr 7 (18.07.2023): 1465. http://dx.doi.org/10.3390/genes14071465.

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Although it has gained more attention in recent years, the relationship between breast cancer (BC) and mitochondrial oxidative phosphorylation (OXPHOS) is still not well understood. Importantly, Complex IV or Cytochrome C Oxidase (COX) of OXPHOS is one of the key players in mitochondrial balance. An in silico investigation of mutations in structural genes of Complex IV was conducted in BC, comprising 2107 samples. Our findings show four variants (rs267606614, rs753969142, rs199476128 and rs267606884) with significant pathogenic potential. Moreover, we highlight nine genes (MT-CO1, MT-CO2, MT-CO3, CO4I2, COX5A, COX5B, COX6A2, COX6C and COX7B2) with a potential impact on BC.

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5

Wang, Yizhou, Zheng Wang, Qiuyue Zhang, Song Zou, Yanping Ma, Gregory A. Solan, Wenjuan Zhang i Wen-Hua Sun. "Exploring Long Range para-Phenyl Effects in Unsymmetrically Fused bis(imino)pyridine-Cobalt Ethylene Polymerization Catalysts". Catalysts 13, nr 10 (23.10.2023): 1387. http://dx.doi.org/10.3390/catal13101387.

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Unsymmetrical 11-phenyl-1,2,3,7,8,9,10-heptahydrocyclohepta[b]quinoline-4,6-dione, incorporating a para-phenyl substituted pyridine unit fused by both 6- and 7-membered carbocyclic rings, has been prepared on the gram-scale via a multi-step procedure involving cyclization, hydrogenation and oxidation. Templating this diketone, in the presence of cobalt(II) chloride hexahydrate, with the corresponding aniline afforded in good yield five examples of doubly fused bis(arylimino)pyridine-cobalt(II) chlorides, Co1 (aryl = 2,6-dimethylphenyl), Co2 (2,6-diethylphenyl), Co3 (2,6-diisopropylphenyl), Co4 (2,4,6-trimethylphenyl) and Co5 (2,6-diethyl-4-methylphenyl). Structural characterization of Co1, Co2 and Co3 highlights the flexible nature of the inequivalent fused rings on the NNN’-ligand and the skewed disposition of the para-phenyl group. On activation with MAO, Co1–Co5 exhibited high activity for ethylene polymerization at 30 °C (up to 5.66 × 106 g (PE) mol−1 (Co) h−1) with the relative order being as follows: Co4 > Co1 > Co5 > Co3 > Co2. All polyethylenes were strictly linear, while their molecular weights and dispersities showed some notable variations. For Co1, Co2, Co4 and Co5, all polymerizations were well controlled as evidenced by the narrow dispersities of their polymers (Mw/Mn range: 1.8–2.7), while their molecular weights (Mw range: 2.9–10.9 kg mol−1) steadily increased in line with the greater steric properties of the N-aryl ortho-substituents. By contrast, the most hindered 2,6-diisopropyl counterpart Co3 displayed a broad distribution with bimodal characteristics (Mw/Mn = 10.3) and gave noticeably higher molecular weight polymer (Mw = 75.5 kg mol−1). By comparison, the MMAO-activated catalysts were generally less active, but showed similar trends in molecular weight and polymer dispersity. End group analysis of selected polymers via 13C and 1H NMR spectroscopy revealed the presence of both saturated and unsaturated polyethylenes in accordance with competing chain transfer pathways. Notably, when comparing Co3/MAO with its non-phenyl substituted analogue (E2,6-iPr2Ph)CoCl2/MAO, the former, though less controlled, displayed higher activity and molecular weight, a finding that points towards a role played by the remote para-phenyl group.

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6

Sade, Aslı, Seda Tunçay, İsmail Çimen, Feride Severcan i Sreeparna Banerjee. "Celecoxib reduces fluidity and decreases metastatic potential of colon cancer cell lines irrespective of COX-2 expression". Bioscience Reports 32, nr 1 (26.09.2011): 35–44. http://dx.doi.org/10.1042/bsr20100149.

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CLX (celecoxib), a selective COX-2 (cyclo-oxygenase-2) inhibitor, has numerous pleiotropic effects on the body that may be independent of its COX-2 inhibitory activity. The cancer chemopreventive ability of CLX, particularly in CRC (colorectal cancer), has been shown in epidemiological studies. Here we have, for the first time, examined the biophysical effects of CLX on the cellular membranes of COX-2 expressing (HT29) and COX-2 non-expressing (SW620) cell lines using ATR-FTIR (attenuated total reflectance–Fourier transform IR) spectroscopy and SL-ESR (spin label–ESR) spectroscopy. Our results show that CLX treatment decreased lipid fluidity in the cancer cell lines irrespective of COX-2 expression status. As metastatic cells have higher membrane fluidity, we examined the effect of CLX on the metastatic potential of these cells. The CLX treatment efficiently decreased the proliferation, anchorage-independent growth, ability to close a scratch wound and migration and invasion of the CRC cell lines through Matrigel. We propose that one of the ways by which CLX exerts its anti-tumorigenic effects is via alterations in cellular membrane fluidity which has a notable impact on the cells' metastatic potential.

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7

Niiro, H., T. Otsuka, T. Tanabe, S. Hara, S. Kuga, Y. Nemoto, Y. Tanaka, H. Nakashima, S. Kitajima i M. Abe. "Inhibition by interleukin-10 of inducible cyclooxygenase expression in lipopolysaccharide-stimulated monocytes: its underlying mechanism in comparison with interleukin-4". Blood 85, nr 12 (15.06.1995): 3736–45. http://dx.doi.org/10.1182/blood.v85.12.3736.bloodjournal85123736.

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Both interleukin-10 (IL-10) and IL-4 inhibited the prostanoid synthesis of lipopolysaccharide (LPS)-stimulated human monocytes, and their inhibition was shown to be based on a common mechanism to suppress the gene expression of inducible cyclooxygenase (COX). COX has been shown to exist in at least two distinct isoforms, designated COX-1 and COX-2, and their gene expressions exhibit different profiles. At both the protein and mRNA levels, the expression of COX-1 was constitutive and was not modulated by treatments with LPS, IL-10, or IL-4. In contrast, the expression of COX-2 was observed only after stimulation with LPS. IL-10 and IL-4 significantly inhibited LPS-induced COX-2 expression. Kinetic studies showed that they inhibited COX-2 mRNA expression within 1 hour after stimulation and that maximal inhibition was consistently observed at 5 hours. Moreover, the addition of cycloheximide (CHX) to LPS-stimulated monocytes resulted in a superinduction of COX-2 mRNA, whereas CHX almost abrogated the abilities of IL-10 and IL-4 to inhibit this gene expression. Experiments with actinomycin D showed that both cytokines accelerated the degradation of COX-2 mRNA. Furthermore, nuclear run-on experiments showed that both cytokines modestly inhibited LPS-induced COX-2 gene transcription. Thus, both cytokines seemed to regulate the COX-related pathway in a similar manner, although their receptor systems did not show any structural similarities. Considering recent findings showing that the drugs that exhibit a selective effect on COX-2 may be more preferable in inflammatory conditions, such biologic activities of IL-10 and IL-4 described above may offer useful tools in controlling inflammatory disorders in the future.

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8

Khalil, Hany Ezzat, Hairul-Islam Mohamed Ibrahim, Emad A. Ahmed, Promise Madu Emeka i Ibrahim A. Alhaider. "Orientin, a Bio-Flavonoid from Trigonella hamosa L., Regulates COX-2/PGE-2 in A549 Cell Lines via miR-26b and miR-146a". Pharmaceuticals 15, nr 2 (27.01.2022): 154. http://dx.doi.org/10.3390/ph15020154.

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Cancer is a severe health condition and considered one of the major healthcare issues and is in need of innovative strategy for a cure. The current study aimed to investigate the chemical profile of Trigonella hamosa L. and a potential molecular approach to explain its regulation in cancer progression through an inflammatory mediator (COX-2) in A549 non-small lung cancer cell lines via in silico, mechanistic and molecular aspects. T. hamosa was extracted and then subjected to a CCK-8 cell viability assay in different cancer cell lines including MDA-MB-231, A549 and HCT-116. Total extract was subjected to several chromatographic techniques to yield orientin (OT); the structure was elucidated by inspection of NMR spectroscopic data. To achieve anticancer effects of OT, a cell viability assay using a CCK-8 kit, immunoprecipitation by Western blot, cell migration using a wound healing assay, cell invasion using a Matrigel-Transwell assay, apoptosis by AO/EB dual staining, flow cytometric analysis and DAPI staining, a silenced COX-2 model to determine PGE-2 production and real-time PCR and Western blot of BCL-2, CYP-1A1, iNOS and COX-2 markers were carried out. The results demonstrated that OT decreased the cell proliferation and controlled cell migration and invasive properties. OT destabilized the COX-2 mRNA and downregulated its expression in A549 cell lines. Virtual binding showed interaction (binding energy −10.43) between OT and COX-2 protein compared to the selective COX-2 inhibitor celecoxib (CLX) (binding energy −9.4). The OT-CLX combination showed a superior anticancer effect. The synergistic effect of OT-CLX combination was noticed in controlling the migration and invasion of A549 cell lines. OT-CLX downregulated the expression of BCL-2, iNOS and COX-2 and activated the proapoptotic gene CYP-1A1. OT mitigated the COX-2 expression via upregulation of miR-26b and miR-146a. Interestingly, COX-2-silenced transfected A549 cells exhibited reduced expression of miR-26b and miR-146a. The findings confirmed the direct interaction of OT with COX-2 protein. PGE-2 expression was quantified in both naïve and COX-2-silenced A549 cells. OT downregulated the release of PGE-2 in both tested conditions. These results confirmed the regulatory effect of OT on A549 cell growth in a COX-2-dependent manner. OT activated apoptosis via activation of CYP-1A1 expression in an independent manner. These results revealed that the OT-CLX combination could serve as a potential synergistic treatment for effective inflammatory-mediated anticancer strategies.

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9

Bradbury, D. A., R. Newton, Y. M. Zhu, J. Stocks, L. Corbett, E. D. Holland, L. H. Pang i A. J. Knox. "Effect of bradykinin, TGF-β1, IL-1β, and hypoxia on COX-2 expression in pulmonary artery smooth muscle cells". American Journal of Physiology-Lung Cellular and Molecular Physiology 283, nr 4 (1.10.2002): L717—L725. http://dx.doi.org/10.1152/ajplung.00070.2002.

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Prostanoids are major regulators of smooth muscle function that are generated by cyclooxygenase (COX). Here we hypothesized that cytokines and mediators that regulate the pulmonary circulation would alter COX expression and prostanoid generation in pulmonary artery smooth muscle cells. Bradykinin, transforming growth factor-β1 (TGF-β1), and interleukin-1β (IL-1β) increased inducible COX-2 expression and prostaglandin E2 (PGE2) release. Transfection studies using a COX-2 promoter construct demonstrated that all three agents acted transcriptionally. Constitutive COX-1 protein expression was unchanged. The COX inhibitor indomethacin, the COX-2 inhibitor NS-398, the protein synthesis inhibitor cycloheximide, and the glucocorticoid dexamethasone abrogated the increased PGE2levels. Dexamethasone and cycloheximide prevented COX-2 induction. Hypoxia (3% O2-5% CO2-92% N2) for 24 h selectively augmented TGF-β1-stimulated PGE2 production and COX-2 induction but had no effect alone. Prolonged hypoxic culture alone for 48 and 72 h enhanced COX-2 induction and increased PGE2. These studies show that a number of stimuli are capable of inducing COX-2 in pulmonary artery smooth muscle cells. The interaction between hypoxia and TGF-β1 may be particularly relevant to pulmonary hypertension.

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10

Botting, Regina. "COX-1 and COX-3 inhibitors". Thrombosis Research 110, nr 5-6 (czerwiec 2003): 269–72. http://dx.doi.org/10.1016/s0049-3848(03)00411-0.

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Hawkey, C. J. "COX-1 and COX-2 inhibitors". Best Practice & Research Clinical Gastroenterology 15, nr 5 (październik 2001): 801–20. http://dx.doi.org/10.1053/bega.2001.0236.

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12

NAKAMURA, Hideo. "Cyclooxygenase (COX)-2 selective inhibitors: aspirin, a dual COX-1/COX-2 inhibitor, to COX-2 selective inhibitors". Folia Pharmacologica Japonica 118, nr 3 (2001): 219–30. http://dx.doi.org/10.1254/fpj.118.219.

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13

Ferreri, Nicholas R., Shao-Jian An i John C. McGiff. "Cyclooxygenase-2 expression and function in the medullary thick ascending limb". American Journal of Physiology-Renal Physiology 277, nr 3 (1.09.1999): F360—F368. http://dx.doi.org/10.1152/ajprenal.1999.277.3.f360.

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The medullary thick ascending limb (MTAL) metabolizes arachidonic acid (AA) via cytochrome P-450 (CyP450)- and cyclooxygenase (COX)-dependent pathways. In the present study, we demonstrated that the COX-2-selective inhibitor, NS-398, prevented tumor necrosis factor-α (TNF)- and phorbol myristate acetate (PMA)-mediated increases in PGE2 production by cultured MTAL cells. Accumulation of COX-2, but not COX-1, mRNA increased when cells were challenged with TNF (1 nM) or PMA (1 μM). Pretreatment of cells for 30 min with actinomycin D (AcD, 1 μM) had little effect on COX-2 mRNA accumulation in unstimulated cells or in cells challenged with either TNF or PMA. Moreover, a posttranscriptional mechanism(s) appears to contribute significantly to COX-2 mRNA accumulation as pretreatment for 15 min with cycloheximide (CHX, 1 μM) caused a superinduction of COX-2 mRNA accumulation in unstimulated cells as well as in cells challenged with either TNF or PMA. Expression of COX-2 protein in unstimulated MTAL cells was attenuated by preincubation for 2 h with dexamethasone (Dex, 2 μM); however, Dex had little or no effect on COX-2 expression in cells challenged with either PMA or TNF. The time-dependent inhibition of86Rb uptake by MTAL cells challenged with TNF was diminished by pretreating cells with NS-398. These data suggest that TNF-mediated induction of COX-2 protein expression accounted for the lag-time required for this cytokine to inhibit 86Rb uptake in MTAL cells.

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14

Rodrigues, Josilene Aparecida Vieira, Luide Rodrigo Martins, Laís Milagres Furtado, Amália Luísa Pedrosa Xavier, Francine Tatiane Rezende de Almeida, Ana Luísa da Silva Lage Moreira, Tânia Márcia Sacramento Melo, Laurent Frédéric Gil i Leandro Vinícius Alves Gurgel. "Oxidized Renewable Materials for the Removal of Cobalt(II) and Copper(II) from Aqueous Solution Using in Batch and Fixed-Bed Column Adsorption". Advances in Polymer Technology 2020 (10.01.2020): 1–17. http://dx.doi.org/10.1155/2020/8620431.

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Batch and continuous adsorption of Co2+ and Cu2+ from aqueous solutions by oxidized sugarcane bagasse (SBox) and oxidized cellulose (Cox) were investigated. The oxidation reaction of sugarcane bagasse and cellulose was made with a mixture of H3PO4‒NaNO2 to obtain SBox and Cox, with the introduction of high number of carboxylic acid functions, 4.5 and 4.8 mmol/g, respectively. The adsorption kinetics of Co2+ and Cu2+ on SBox and Cox were modeled using two models (pseudo-first-order and pseudo-second-order) and the rate-limiting step controlling the adsorption was evaluated by Boyd and intraparticle diffusion models. The Sips and Langmuir models better fitted the isotherms with values of maximum adsorption capacity Qmax of 0.68 and 0.37 mmol/g for Co2+ and 1.20 and 0.57 mmol/g for Cu2+ adsorption on Cox and SBox, respectively. The reuse of both spent adsorbents was evaluated. Adsorption of Cu2+ and Co2+ on SBox in continuous was evaluated using a 22 factorial design with spatial time and initial metal concentration as independent variables and Qmax and effective use of the bed as responses. The breakthrough curves were very well described by the Bohart–Adams original model and the Qmax values for Co2+ and Cu2+ were 0.22 and 0.55 mmol/g. SBox confirmed to be a promising biomaterial for application on a large scale.

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15

Liu, Xing. "Hydrogenation of CO2 Promoted by Silicon-Activated H2S: Origin and Implications". Molecules 26, nr 1 (24.12.2020): 50. http://dx.doi.org/10.3390/molecules26010050.

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Unlike the usual method of COx (x = 1, 2) hydrogenation using H2 directly, H2S and HSiSH (silicon-activated H2S) were selected as alternative hydrogen sources in this study for the COx hydrogenation reactions. Our results suggest that it is kinetically infeasible for hydrogen in the form of H2S to transfer to COx at low temperatures. However, when HSiSH is employed instead, the title reaction can be achieved. For this approach, the activation of CO2 is initiated by its interaction with the HSiSH molecule, a reactive species with both a hydridic Hδ− and protonic Hδ+. These active hydrogens are responsible for the successive C-end and O-end activations of CO2 and hence the final product (HCOOH). This finding represents a good example of an indirect hydrogen source used in CO2 hydrogenation through reactivity tuned by silicon incorporation, and thus the underlying mechanism will be valuable for the design of similar reactions.

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16

Carlson, Robert. "COX 2". Inpharma Weekly &NA;, nr 1195 (lipiec 1999): 9–10. http://dx.doi.org/10.2165/00128413-199911950-00017.

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Champkin, Julian. "Amanda Cox". Significance 9, nr 5 (październik 2012): 28–31. http://dx.doi.org/10.1111/j.1740-9713.2012.00605.x.

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Baker, Monya. "Susan Cox". Nature Methods 9, nr 2 (30.01.2012): 113. http://dx.doi.org/10.1038/nmeth.1866.

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19

Bates, A. "Niall Cox". BMJ 324, nr 7348 (25.05.2002): 1280b—1280. http://dx.doi.org/10.1136/bmj.324.7348.1280/b.

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20

Roy, H. K. "COX 3?" American Journal of Gastroenterology 94, nr 9 (wrzesień 1999): 2343. http://dx.doi.org/10.1111/j.1572-0241.1999.2343a.x.

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Roy, H. "COX 3?" American Journal of Gastroenterology 94, nr 9 (wrzesień 1999): 2343. http://dx.doi.org/10.1016/s0002-9270(99)00474-8.

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Pang, Pitt, Petkova i Knox. "The COX-1/COX-2 balance in asthma". Clinical & Experimental Allergy 28, nr 9 (wrzesień 1998): 1050–58. http://dx.doi.org/10.1046/j.1365-2222.1998.00311.x.

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23

Morrison, Janet A. "Save the Planet 1992.Roger Cox , Kathy Cox". Quarterly Review of Biology 68, nr 4 (grudzień 1993): 649. http://dx.doi.org/10.1086/418425.

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Whelton, Andrew. "COX-1 Sparing and COX-2 Inhibitory Drugs". American Journal of Therapeutics 7, nr 3 (maj 2000): 151–52. http://dx.doi.org/10.1097/00045391-200007030-00002.

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25

Morita, Ikuo. "Distinct functions of COX-1 and COX-2". Prostaglandins & Other Lipid Mediators 68-69 (sierpień 2002): 165–75. http://dx.doi.org/10.1016/s0090-6980(02)00029-1.

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Emery, Paul. "COX-1, COX-2: So What?: EDITORIAL REVIEW". Scandinavian Journal of Rheumatology 28, nr 1 (styczeń 1999): 6–9. http://dx.doi.org/10.1080/03009749950155715.

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Mitra, Manu. "Usage of COX-1 and COX-2 Nanomedicines in Nanotechnology". Nanomedicine & Nanotechnology Open Access 8, nr 3 (2023): 1–13. http://dx.doi.org/10.23880/nnoa-16000245.

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Nanomedicine is the branch of medical applications in nanotechnology. Nanomedicine ranges from medical applications of nanomaterials, biological devices to nanoelectronic biosensors, molecular nanotechnology such as biological machines. It utilizes knowledge and tools of nanotechnology to prevention and treatment of disease. Nanomedicine involves use of nanoscale materials such as biocompatible nanoparticles for delivery, sensing or actuation in a living organism. COX inhibitors are a class of pharmaceutical compounds that selectively target and inhibit the activity of the enzymes cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). These enzymes are key players in the synthesis of prostaglandins, which are important mediators of inflammation, pain, and fever in the body. By modulating prostaglandin production, COX inhibitors have significant therapeutic implications in the management of various inflammatory conditions, pain relief, and fever reduction. COX-1 is constitutively expressed in many tissues and is involved in maintaining normal physiological functions, including the protection of the stomach lining and platelet aggregation. In contrast, COX-2 is induced at sites of inflammation and is primarily responsible for producing prostaglandins involved in the inflammatory response. The selective inhibition of COX-2 allows for targeted suppression of inflammation while preserving the beneficial functions of COX-1. Moreover, recent research has shed light on the complex interplay between COX-1 and COX-2 in health and disease. Emerging evidence suggests that the balance between COX-1 and COX-2 inhibition may have implications beyond pain and inflammation. Investigating the diverse roles of these enzymes in different tissues and pathologies may open up new avenues for drug development and personalized medicine. COX inhibitors represent an important therapeutic class with a profound impact on managing pain, inflammation, and related disorders. Understanding the differential regulation and functions of COX-1 and COX-2 is crucial for optimizing the clinical use of COX inhibitors and developing novel strategies for targeted and safer anti-inflammatory therapies.

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WHITTLE, B. J. R. "COX-1 and COX-2 products in the gut: therapeutic impact of COX-2 inhibitors". Gut 47, nr 3 (1.09.2000): 320–25. http://dx.doi.org/10.1136/gut.47.3.320.

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Willoughby, Derek A., Adrian R. Moore i Paul R. Colville-Nash. "COX-1, COX-2, and COX-3 and the future treatment of chronic inflammatory disease". Lancet 355, nr 9204 (luty 2000): 646–48. http://dx.doi.org/10.1016/s0140-6736(99)12031-2.

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Shurdumov, Gazali K., Zaur A. Cherkesov i Laura I. Mokaeva. "EFFECT OF MASS TRANSFER OF SYSTEMS Mn(Fe,Co)Mo(W)O4–Na2CO3 AND ENVIRONMENT AND NEED FOR HIS ACCOUNT WHEN IDENTIFYING MOLYBDATES AND TUNGSTATES OF MULTIVALENT d-ELEMENTS, Mn, Fe, Co, ON BASIS OF THERMOGRAVIMETRIC DATA". IZVESTIYA VYSSHIKH UCHEBNYKH ZAVEDENII KHIMIYA KHIMICHESKAYA TEKHNOLOGIYA 62, nr 4 (7.04.2019): 111–20. http://dx.doi.org/10.6060/ivkkt.20196204.5761.

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The paper presents the experimental and calculated data for study of exchange reactions in the systems Mn(Fe,Co)Mo(W)O4–Na2CO3 with methods of thermodynamics, thermogravimetry, kinetics topochemically reactions and stoichiometry, analysis and synthesis which led to the identification of the effect of mass transfer between the system and the environment – a phenomenon characteristic of molybdates (tungstates) polyvalent d-elements (Mn,Fe,Co) in contrast to similar derivatives of d-elements (Ni, Zn, Cd, Ag) with constant valency. It identified the genesis and the mechanism of manifestation of this phenomenon, which, as shown by theoretical analysis and experimental data, due to polivalentes Mn (Fe,Co) and hence the possibility of occurrence in the systems Mn(Fe,Co)Mo(W)O4–Na2CO3 exchange reactions of Mn(Fe, Co)Mo(W)O4+Na2CO3→ →Mn(Fe,Co)CO3+Na2Mo(W)O4, dissociation of Mn(Fe,Co)CO3=Mn(Fe,Co)O+CO2 and redox Mn(Fe,Co)O+1/2О2→Mnx(Feх,Cox)Oy where y=x+1/2О2, leading to the loss of CO2 and the conversion of Mn(Fe,Co)O – degradation products of Mn(Fe,Co)CO3 at the expense of the oxygen of environment to the oxide type-Mnx(Feх,Cox)Oy, the composition of which is determined by the process temperature. It is established that the above reactions form the basis of the unique phenomenon in solid state chemistry of molibdates (wolframates) of polyvalent d-elements discovered for the first time, in the opinion of the authors. This phenomenon is associated with the proceeding of Mn(Fe,Co)Mo(W)O4–Na2CO3 processes in their heat treatment. It is shown that successive thermal dissociation reactions of Mn(Fe,Co)CO3 lead to their loss of CO2 (mass reduction) and oxidation of the formed Mn(Fe,Co)O by air oxygen to Mnх(Feх,Coх)Oу=x+1/2О2 (mass growth): CO2 donor systems and O2 acceptors, and the medium (air) – O2 donor and CO2 acceptor. The proposed methodology is a reasonable choice of the reaction from the expected, the occurrence of which is absolutely reliable in given physicochemical conditions.

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Adelizzi, Raymond A. "COX-1 and COX-2 in health and disease". Journal of the American Osteopathic Association 99, nr 11_suppl (1.11.1999): S7. http://dx.doi.org/10.7556/jaoa.1999.99.11.s7.

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Marnett, Lawrence J., Scott W. Rowlinson, Douglas C. Goodwin, Amit S. Kalgutkar i Cheryl A. Lanzo. "Arachidonic Acid Oxygenation by COX-1 and COX-2". Journal of Biological Chemistry 274, nr 33 (13.08.1999): 22903–6. http://dx.doi.org/10.1074/jbc.274.33.22903.

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Loftin, Charles D., Howard F. Tiano, Darshini B. Trivedi, Christopher A. Lee, James A. Clark, Scott Morham i Robert Langenbach. "The development of COX-1/COX-2 double knockouts". Prostaglandins & Other Lipid Mediators 59, nr 1-6 (grudzień 1999): 109. http://dx.doi.org/10.1016/s0090-6980(99)90344-1.

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Mungo, David V., Xinping Zhang, Regis J. O'Keefe, Randy N. Rosier, J. Edward Puzas i Edward M. Schwarz. "COX-1 and COX-2 expression in osteoid osteomas". Journal of Orthopaedic Research 20, nr 1 (styczeń 2002): 159–62. http://dx.doi.org/10.1016/s0736-0266(01)00065-1.

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Hinz, Burkhard, i Kay Brune. "COX-1 und COX-2: Funktionen und pharmakologische Beeinflussung". Pharmazie in unserer Zeit 28, nr 1 (23.07.2007): 21–29. http://dx.doi.org/10.1002/pauz.19990280108.

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Agarwal, Banke, Prabhakar Swaroop, Petr Protiva, Ram Chuttani, William G. Ramey i Peter R. Holt. "Cox-2 selective inhibitors induce apoptosis by both Cox-2 dependent and Cox-2 independent mechanisms". Gastroenterology 118, nr 4 (kwiecień 2000): A52. http://dx.doi.org/10.1016/s0016-5085(00)82279-9.

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Schmassmann, Adrian, Georg Zoidl, Brigitta M. Peskar, Bea Waser, Diana Schmassmann-Suhijar, Jan-Olaf Gebbers i Jean Claude Reubi. "Role of the different isoforms of cyclooxygenase and nitric oxide synthase during gastric ulcer healing in cyclooxygenase-1 and -2 knockout mice". American Journal of Physiology-Gastrointestinal and Liver Physiology 290, nr 4 (kwiecień 2006): G747—G756. http://dx.doi.org/10.1152/ajpgi.00416.2005.

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Traditional NSAIDs, selective cyclooxygenase (COX)-2 inhibitors, and inhibitors of nitric oxide synthase (NOS) impair the healing of preexisting gastric ulcers. However, the role of COX-1 (with or without impairment of COX-2) and the interaction between COX and NOS isoforms during healing are less clear. Thus we investigated healing and regulation of COX and NOS isoforms during ulcer healing in COX-1 and COX-2 deficiency and inhibition mouse models. In this study, female wild-type COX-1−/− and COX-2−/− mice with gastric ulcers induced by cryoprobe were treated intragastrically with vehicle, selective COX-1 (SC-560), COX-2 (celecoxib, rofecoxib, and valdedoxib), and unselective COX (piroxicam) inhibitors. Ulcer healing parameters, mRNA expression, and activity of COX and NOS were quantified. Gene disruption or inhibition of COX-1 did not impair ulcer healing. In contrast, COX-2 gene disruption and COX-2 inhibitors moderately impaired wound healing. More severe healing impairment was found in dual (SC-560 + rofecoxib) and unselective (piroxicam) COX inhibition and combined COX impairment (in COX-1−/− mice with COX-2 inhibition and COX-2−/− mice with COX-1 inhibition). In the ulcerated repair tissue, COX-2 mRNA in COX-1−/− mice, COX-1 mRNA in COX-2−/− mice, and, remarkably, NOS-2 and NOS-3 mRNA in COX-impaired mice were more upregulated than in wild-type mice. This study demonstrates that COX-2 is a key mediator in gastric wound healing. In contrast, COX-1 has no significant role in healing when COX-2 is unimpaired but becomes important when COX-2 is impaired. As counterregulatory mechanisms, mRNA of COX and NOS isoforms were increased during healing in COX-impaired mice.

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Abbasi, Amirali, i Jaber Jahanbin Sardroodi. "Theoretical investigation of the adsorption behaviors of CO and CO2 molecules on the nitrogen-doped TiO2 anatase nanoparticles: Insights from DFT computations". Journal of Theoretical and Computational Chemistry 16, nr 01 (luty 2017): 1750005. http://dx.doi.org/10.1142/s0219633617500055.

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Over the past years, an interest has arisen in resolving the problems of the increased carbon monoxide and carbon dioxide emissions, leading to the serious air pollution and many detrimental effects. A convenient solution would be a process that could utilize metal oxide nanoparticles such as TiO2 to control the concentration of atmospheric pollutants. The chemisorption of CO and CO2 molecules over the semiconductor titanium dioxide (TiO[Formula: see text] is such a process. In this way, density functional theory (DFT) calculations were performed to investigate CO and CO2 adsorptions on undoped and N-doped TiO2 anatase nanoparticles. The supercell approach is conducted to construct the considered nanoparticles and the adsorption of COx molecule was simulated by use of these chosen nanoparticles. By including van der Waals (vdW) interactions between COx molecule and TiO2 nanoparticle, we found that both CO and CO2 molecules can bind strongly to the N-doped nanoparticles. The adsorption on the five-fold coordinated titanium site of TiO2 nanoparticles including the bond lengths, bond angles, adsorption energies, density of states (DOSs), Mulliken population analysis and molecular orbitals has been broadly studied in this work. Based on the obtained results, it can be concluded that the adsorption on the N-doped nanoparticle is more energetically favorable than the adsorption on the pristine one, representing the higher tendency of N-doped nanoparticles for COx detention, compared to the undoped ones. Therefore, the results indicate that the N-doped TiO2 would be an ideal COx gas sensor in the environment.

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&NA;. "COX-2 inhibitors". Inpharma Weekly &NA;, nr 1216 (grudzień 1999): 14. http://dx.doi.org/10.2165/00128413-199912160-00033.

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Watts, Geoff. "David Roxbee Cox". Lancet 399, nr 10332 (kwiecień 2022): 1298. http://dx.doi.org/10.1016/s0140-6736(22)00575-x.

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Brooks, Peter M., i Richard O. Day. "COX‐2 inhibitors". Medical Journal of Australia 173, nr 8 (październik 2000): 433–36. http://dx.doi.org/10.5694/j.1326-5377.2000.tb139277.x.

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Lawrie, Malcolm M. "COX‐2 inhibitors". Medical Journal of Australia 174, nr 7 (kwiecień 2001): 367. http://dx.doi.org/10.5694/j.1326-5377.2001.tb143321.x.

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McKeough, Gregory N. "COX‐2 inhibitors". Medical Journal of Australia 174, nr 7 (kwiecień 2001): 367. http://dx.doi.org/10.5694/j.1326-5377.2001.tb143322.x.

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Jones, D. Brian. "COX‐2 inhibitors". Medical Journal of Australia 174, nr 7 (kwiecień 2001): 368. http://dx.doi.org/10.5694/j.1326-5377.2001.tb143323.x.

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Brooks, Peter M., i Richard O. Day. "COX‐2 inhibitors". Medical Journal of Australia 174, nr 7 (kwiecień 2001): 368–69. http://dx.doi.org/10.5694/j.1326-5377.2001.tb143324.x.

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Uyeda, S. "Obituary (A. Cox)". Journal of geomagnetism and geoelectricity 40, nr 9 (1988): 1043–45. http://dx.doi.org/10.5636/jgg.40.1043.

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Collignon, P., H. C. Wegener, H. P. Braam i C. Butler. "Reply to Cox". Clinical Infectious Diseases 42, nr 7 (1.04.2006): 1053–54. http://dx.doi.org/10.1086/501134.

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Houston, Avril Melissa, i Stephen J. Teach. "COX-2 Inhibitors". Pediatric Emergency Care 20, nr 6 (czerwiec 2004): 396–99. http://dx.doi.org/10.1097/01.pec.0000133618.36861.73.

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Mazhar, D., R. Gillmore i J. Waxman. "COX and cancer". QJM: An International Journal of Medicine 98, nr 10 (1.10.2005): 711–18. http://dx.doi.org/10.1093/qjmed/hci119.

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KERMODE, FRANK. "C. B. Cox". Critical Quarterly 50, nr 1-2 (kwiecień 2008): 5–7. http://dx.doi.org/10.1111/j.1467-8705.2008.00809.x.

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